The Practice of Clinical Echocardiography

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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The Practice of Clinical Echocardiography III

Second Edition Catherine M. Otto MD Professor of Medicine Acting Director, Division of Cardiology Director, Training Programs in Cardiovascular Disease Associate Director, Echocardiography Laboratory University of Washington Seattle, Washington

W.B. SAUNDERS COMPANY An Imprint of Elsevier Science Philadelphia•London•New York•St. Louis•Sydney•Toronto

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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W.B. SAUNDERS COMPANY An Imprint of Elsevier Science The Curtis Center Independence Square West Philadelphia, Pennsylvania 19106 Library of Congress Cataloging-in-Publication Data The practice of clinical echocardiography / [edited by] Catherine M. Otto.—2nd ed. p. cm. Includes bibliographical references and index. ISBN 0-7216-9204-4 1. Echocardiography. I. Otto, Catherine M. [DNLM: 1. Echocardiography. WG 141.5.E2 P8942 2002] RC683.5.U5 C57 2002 616.1'207543-dc21 2001049709 Acquisitions Editor: Richard Zorab Production Editor: Robin E. Davis Production Manager: Mary Stermel Illustration Specialist: Rita Martello Book Designers: Catherine Bradish and Lynn Foulk THE PRACTICE OF CLINICAL ECHOCARDIOGRAPHY, Second Edition ISBN 0-7216-9204-4

Copyright © 2002, 1997 by W.B. Saunders Company. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

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Contributors

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Gerard P. Aurigemma MD Professor of Medicine and Radiology, University of Massachusetts Medical School; Director, Noninvasive Cardiology, University of Massachusetts Medical Center, Worcester, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas J. Benedetti MD Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Ann F. Bolger MD Associate Clinical Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco General Hospital, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of

Echocardiography Hans G. Bosch MSc Senior Staff Member, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Ian G. Burwash MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Benjamin F. Byrd III MD Associate Professor of Medicine, Division of Cardiology, Vanderbilt University School of Medicine; Director, Echocardiography Laboratory, Vanderbilt University Medical Center, Nashville, Tennessee Maintaining Quality in the Echocardiography Laboratory Kwan-Leung Chan MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Edmond W. Chen MD Fellow, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic

Embolic Event John S. Child MD Professor, University of California, Los Angeles, School of Medicine; Co-Chief, Division of Cardiology, Director, Ahmanson/UCLA Adult Congenital Heart Disease Center, UCLA Medical Center, Los Angeles, California Echocardiographic Evaluation of the Adult with Postoperative Congenital Heart Disease Joseph A. Diamond MD Assistant Professor of Medicine, Mount Sinai School of Medicine; Assistant Attending, The Mount Sinai Medical Center, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Pamela S. Douglas MD Tuchman Professor of Medicine; Head, Cardiovascular Medicine Section, University of Wisconsin Medical School, Madison, Wisconsin Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas R. Easterling MD Associate Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Peter J. Fitzgerald MD, PhD Associate Professor of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical

Applications Kirsten E. Fleischman MD, MPH Assistant Professor in Residence, University of California, San Francisco, School of Medicine; Attending Physician, University of California, San Francisco, Medical Center, San Francisco, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome Elyse Foster MD Professor of Clinical Medicine, University of California, San Francisco, School of Medicine; Director, Adult Echocardiography Laboratory, Moffitt-Long Hospital, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myicardial Infarction, Detection of Complications, and Prognostic Implications

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William H. Gaasch MD Professor of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts; Director, Cardiovascular Research, Lahey Clinic, Burlington, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Edward F. Gibbons MD Assistant Clinical Professor of Medicine, University of Washington School of Medicine; Director of Echocardiography, Director of Inpatient Cardiology Services, Virginia Mason Medical Center, Seattle, Washington

Education and Training of Physicians and Sonographers John S. Gottdiener MD Professor of Medicine, State University of New York at Stony Brook, School of Medicine; Director, Noninvasive Cardiac Imaging, St. Francis Hospital, Roslyn, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Brian P. Griffin MD Director, Cardiovascular Disease Training Program, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning and Intraoperative Evaluation of Mitral Valve Repair Sheila K. Heinle MD Clinical Assistant Professor of Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas Quantitation of Valvular Regurgitation: Beyond Color Flow Mapping Mary Etta E. King MD Associate Professor of Pediatrics, Harvard Medical School; Director, Pediatric Echocardiography, Massachusetts General Hospital, Boston, Massachusetts Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Tim Kinnaird MB Fellow in Cardiovascular Medicine, London Chest Hospital, London, United Kingdom Pericardial Disease

Katsuhiro Kitamura MD Research Fellow in Medicine, Stanford University Medical Center, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Allan L. Klein MD Professor of Medicine, Ohio State University College of Medicine; Director, Cardiovascular Imaging Research, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Carol Kraft RDCS Lead Cardiac Sonographer, Virginia Mason Medical Center, Seattle, Washington Education and Training of Physicians and Sonographers Carolyn K. Landolfo MD Assistant Professor of Medicine, Duke University School of Medicine; Director, Adult Echocardiography, Duke University Medical Center, Durham, North Carolina The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation Jannet F. Lewis MD Professor of Medicine, George Washington University Medical Center; Director of Echocardiography, George Washington University Hospital, Washington, D.C. Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient David T. Linker MD

Associate Professor of Medicine, Division of Cardiology; Adjunct Associate Professor of Bioengineering; University of Washington School of Medicine, Seattle, Washington Principles of Intravascular Ultrasound Warren J. Manning MD Associate Professor of Medicine and Radiology, Harvard Medical School; Section Chief, Non-invasive Cardiac Imaging, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Pamela A. Marcovitz MD Director, Clinical Cardiology Fellowship Program; Director, Echocardiographic Research, William Beaumont Hospital, Royal Oak, Michigan Exercise Echocardiography: Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Roy W. Martin PhD Research Professor, Department of Anesthesiology and Center for Bioengineering, Applied Physics Laboratory, University of Washington School of Medicine, Seattle, Washington Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Thomas H. Marwick MD, PhD Professor of Medicine, Head of Section, University of Queensland Department of Medicine; Director of Echocardiography, Princess Alexandra Hospital, Brisbane, Queensland, Australia Stress Echocardiography with Nonexercise Techniques: Principles, Protocals, Interpretation, and Clinical Applications David J. Meier MD

Cardiology Fellow, University of Michigan Health System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention of Chronic Mitral and Aortic Regurgitation

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Bradley I. Munt MD Clinical Instructor, The University of British Columbia Department of Medicine; Cardiologist, Providence Healthcare and St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Danielle Noll MD Department of Cardiology, Echocardiography, Medizinische Klinik, Klinikum Innentadt, Munich, Germany Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Catherine M. Otto MD Professor of Medicine; Acting Director, Division of Cardiology; Director, Training Programs in Cardiovascular Disease; Associate Director, Echocardiography Laboratory, University of Washington School of Medicine, Seattle, Washington Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making; The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy; Echocardiographic Findings in Acute and Chronic Pulmonary Disease Donald C. Oxorn MD

Associate Professor of Anesthesiology, Adjunct Associate Professor of Medicine, University of Washington School of Medicine, Seattle, Washington Monitoring Ventricular Function in the Operating Room: Impact on Clinical Outcome Abraham C. Parail MD Fellow in Cardiology, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Robert A. Phillips MD, PhD Associate Professor of Medicine, Mount Sinai School of Medicine; Director, Department of Medicine, Lenox Hill Hospital, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Thomas R. Porter MD Associate Professor, University of Nebraska College of Medicine, Diagnostic Cardiac Ultrasound and Noninvasive Diagnostics, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Harry Rakowski MD Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Rita F. Redberg MD

Associate Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Johan H. C. Reiber PhD Professor of Medical Imaging, Director, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographi Digital Image Processing and Approaches to Endocardial Edge Detection Cheryl L. Reid MD Associate Professor of Medicine, University of California, Irvine College of Medicine; Director, Non-invasive Cardiology, University of California, Irvine, Medical Center, Orange, California Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy: Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Carlos A. Roldan MD Associate Professor of Medicine, University of New Mexico School of Medicine; Staff Cardiologist, Director, Echocardiography Laboratory, Veterans Affairs Medical Center; Staff Cardiologist, University of New Mexico Health Sciences Center, Albuquerque, New Mexico Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Elizabeth W. Ryan MD

Research Fellow in Cardiology, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of Echocardiography Kiran B. Sagar MD Professor of Cardiology and Medicine, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Nelson B. Schiller MD Professor of Medicine, Radiology, and Anesthesia, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco Veterans Affairs Medical Center; Attending Physician, Cardiology, Echocardiography, and Adult Congenital Heart Disease, Moffitt-Long Hospital, San Francisco, California Clinical Decision Making in Endocarditis Ingela Schnittger MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Douglas S. Segar MD Clinical Associate Professor of Medicine, Indiana University School of Medicine, Indiana Heart Institute, Indianapolis, Indiana The Digital Echocardiography Laboratory

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David M. Shavelle MD

Interventional Cardiology Fellow, Good Samaritan Hospital, Los Angeles, California Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making Florence H. Sheehan MD Research Professor of Medicine, Division of Cardiology, University of Washington School of Medicine, Seattle, Washington Quantitative Evaluation of Regional Left Ventricular Systolic Function; Three-Dimensional Echocardiography: Approaches and Applications Bruce K. Shively MD Associate Professor of Cardiology, Oregon Health and Science University; Co-Director, Echocardiography Laboratory, Oregon Health and Science University Hospital, Portland, Oregon Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Mikel D. Smith MD Professor of Internal Medicine/Cardiology, University of Kentucky College of Medicine; Director, Adult Echocardiography Laboratory, Gill Cardiovascular Institute, Albert B. Chandler Medical Center, Lexington, Kentucky Left Ventricular Diastolic Function: Clinical Utility of Doppler Echocardiography A. Rebecca Snider MD Consultant, Pediatric Cardiology, Monmouth Junction, New Jersey General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease Mark R. Starling MD Professor of Internal Medicine,

Director of Cardiology Training Program, Associate Chief of Cardiology, University of Michigan Medical School; Chief, Cardiology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation William J. Stewart MD Associate Professor of Medicine, Department of Cardiology, Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Marcus F. Stoddard MD Professor of Medicine, University of Louisville School of Medicine; Director, Noninvasive Cardiology, University of Louisville Hospital, Louisville, Kentucky Echocardiography in the Evaluation of Cardiac Disease Due to Endocinopathies, Renal Disease, Obesity, and Nutritional Deficiencies Maran Thamilarasan MD Assistant Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Christopher R. Thompson MD, CM Clinical Associate Professor of Medicine (Cardiology), Director, Echocardiography Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Aneesh V. Tolat MD

Clinical Fellow in Medicine, Harvard Medical School; Clinical Fellow in Cardiovascular Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Brandon R. Travis PhD School of Chemical Engineering, Georgia Institute of Technology, Atlanta, Georgia Fluid Dynamics of Prosthetic Valves Zian H. Tseng MD Cardiology Fellow, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Hannah A. Valantine MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Samuel Wang MD Assistant Professor of Clinical Internal Medicine, University of California, Davis, School of Medicine; Attending Physician, University of California, Davis, Medical Center, Sacramento, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome E. Douglas Wigle MD Professor of Medicine, University of Toronto; Staff Cardiologist,

Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Selwyn P. Wong MD Cardiologist, Middlemore Hospital, Auckland, New Zealand Echocardiographic Findings in Acute and Chronic Pulmonary Disease Anna Woo MD Assistant Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy

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Feng Xie MD Research Assistant Professor, Cardiology, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Paul G. Yock MD Professor of Medicine, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Ajit P. Yoganathan PhD Regents Professor of Biomedical Engineering, The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia

Fluid Dynamics of Prosthetic Valves Miguel Zabalgoitia MD Professor of Medicine; Director, Echocardiography Laboratory, University of Texas Health Science Center, San Antonio, Texas Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction William A. Zoghbi MD Professor of Medicine, Director of Echocardiography Research, Baylor College of Medicine; Associate Director, Echocardiography Laboratory, The Methodist Hospital, Houston, Texas Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Preface Echocardiography increasingly has become a key component in the routine evaluation of patients with suspected or known cardiovascular disease. As this technique has evolved and matured, the role of the echocardiographer has shifted from simply providing a description of images to providing an integrated assessment of echocardiographic data in conjunction with the other clinical data from each patient. In effect, echocardiography has become a specialized type of cardiology consultation. The information now requested by the referring physician includes not only the qualitative and quantitative interpretation of the echocardiographic images and Doppler flow data but also a discussion of how this information might affect clinical decision making. Specific examples include decisions regarding medical or surgical therapy (e.g., treatment of endocarditis, surgery for aortic dissection), optimal timing of intervention in patients with chronic cardiac diseases (e.g., valvular regurgitation, mitral stenosis), prognostic implications (e.g., heart disease in pregnancy, heart failure patients), and the possible need for and frequency of periodic diagnostic evaluation (e.g., congenital heart disease, the postoperative patient). This book reflects our role as clinicians with specialized expertise in echocardiography and is of value to cardiology fellows pursuing advanced training in echocardiography, cardiologists in clinical practice, researchers using echocardiographic techniques, and other individuals using echocardiographic approaches in the clinical setting (including anesthesiologists, radiologists, emergency medicine physicians, and obstetricians), as well as to cardiac sonographers, cardiovascular technologists, and nursing professionals.

Each chapter provides an advanced level of discussion, written by an expert in the field, building upon the basic material in the Textbook of Clinical Echocardiography (C. M. Otto, 2nd Edition, WB Saunders, Philadelphia, 2000). The emphasis is on optimal data acquisition, results of recent studies, quantitative approaches to data analysis, potential technical limitations, and areas of active research, in addition to a detailed discussion of the impact of echocardiographic data on patient management. Tables, line drawings, echocardiographic images, and Doppler tracings are used to summarize and illustrate key points. In this Second Edition, the text has been revised to reflect recent advances, illustrations and tables have been updated, and new references have been added to each chapter. The book is organized into sections based on major diagnostic categories. In this new edition, an introductory section on transesophageal echocardiography has been added. Chapters include basic principles of transesophageal imaging, monitoring of ventricular function in the operating room, and a discussion of echocardiographic evaluation of aortic dissection and trauma. Other detailed information on the role of transesophageal echocardiography is integrated into subsequent chapters, which are organized by disease categories. The next section focuses on the left ventricle, with chapters spanning the spectrum from emerging new techniques (e.g., myocardial contrast echocardiography, automated edge detection, tissue characterization, three-dimensional echocardiography) to critical appraisals of quantitative techniques (e.g., left ventricular geometry and systolic function, evaluation of regional function, and assessment of diastolic function). The section on ischemic heart disease includes chapters on the role of echocardiography in the emergency room and coronary care unit, stress echocardiography (exercise and nonexercise), and the basic principles, instrumentation, and clinical applications of intravascular ultrasound in patients with coronary artery disease. The critical role that echocardiography now plays in management of patients with valvular heart disease is evident in a section of chapters on technical aspects of echocardiographic evaluation, optimal timing of surgery and periodic evaluation of patients with valvular regurgitation, management of patients undergoing balloon mitral commissurotomy, clinical decision making in patients with endocarditis, evaluation of disease severity, progression in valvular aortic stenosis, and evaluation of prosthetic valves. The following clinically oriented sections bring together data from both the

echocardiographic and general cardiology literature to discuss the role of echocardiography in patients with cardiomyopathies (heart failure, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and the posttransplant patient) and pericardial disease, pregnant patients with cardiac disease, and a wide range of other vascular and systemic diseases that lead to cardiac dysfunction (hypertension, aortic dissection, pulmonary disease, systemic immune-mediated diseases, renal disease, aging, systemic embolic events, and cardiac arrhythmias). In recognition of the increasing number of adult patients presenting with congenital heart disease, either as a new diagnosis or following prior surgical procedures, three chapters are devoted to this topic. In addition, a new section has been added on the echocardiography laboratory to address issues that increasingly affect our clinical practice, including education and training of echocardiographers, quality improvement in the echocardiography laboratory, and the transition to a digital laboratory. It is hoped that this book will provide the needed background to support and supplement clinical experience and expertise. Of course, competency in the acquisition and interpretation of echocardiographic and Doppler data depends on appropriate clinical education and training as detailed in accreditation requirements for both physicians and technologists, and as recommended by professional societies including the American Society of Echocardiography, the American College of Cardiology, and the American Heart Association. I strongly support these educational requirements and training recommendations; XII

readers of this book are urged to review the relevant documents. In addition, there continue to be advances both in the the technical aspects of image and flow data acquisition and in our understanding of the clinical implications of specific echocardiographic findings. This book represents our knowledge base at one point in time; readers should consult the current literature for the most up-to-date information. Although an extensive list of carefully selected references is provided with each chapter, the echocardiographic literature is so robust that it is impractical to include all relevant references; the reader can use an online medical literature search if an all-inclusive listing is desired. Catherine M. Otto MD

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Acknowledgments

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Sincere thanks are due to the many individuals who made this book possible. Primary recognition goes to the chapter contributors who provided scholarly, thoughtful, and insightful discussions and who integrated the clinical and echocardiographic information into a format that benefits our readers. The support staff at each of our institutions deserves our appreciation for manuscript preparation and providing effective communication, with special thanks to Sharon Kemp and Bev Bubela. The many research subjects who contributed to the data on which our current understanding is based certainly are worthy of our appreciation. The cardiac sonographers at the University of Washington Medical Center (Rachel Elizalde, RDCS; Michelle C. Fujioka, RDMS; Carolyn J. Gardner, RDCS; Caryn D'Jang, RDCS; Scott Simicich, RDCS; David Stolte, RDCS; Rebecca G. Schwaegler, RDMS; Erin Trent, RDCS; and Todd R. Zwink, RDMS) merit acknowledgment. In addition, gratitude is due to Richard Zorab and the production team at W.B. Saunders. Finally, I thank my family for their constant encouragement and support.

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NOTICE Medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. THE PUBLISHER

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Section 1 - Transesophageal Echocardiography

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Chapter 1 - Indications, Procedure, Image Planes, and Doppler Flows Ian G. Burwash MD Kwan-Leung Chan MD

Transesophageal echocardiography (TEE) has become a valuable diagnostic imaging modality for the dynamic assessment of cardiac anatomy and function. Since the initial description of esophageal echocardiography in 1976,[1] the potential role and utility of TEE in the evaluation of diseases of the heart and great vessels have expanded to involve all aspects of cardiac disease. The close proximity of the esophagus to the heart and great vessels provided the echocardiographer with an easily accessible window with the potential for excellent visualization of cardiac structures, avoiding the intervening lung and chest wall tissues that limit transthoracic imaging. The potential of TEE to provide a valuable imaging tool became widely recognized in the 1980s with advancements in TEE probe technology, including the availability of single-plane phased array transducers and the addition of color flow and continuous wave Doppler imaging technology. TEE does not supplant transthoracic echocardiography

(TTE), however; it is a complementary imaging modality with its own strengths and weaknesses. The 2

introduction of biplane TEE transducers in the late 1980s and multiplane transducers in the 1990s has resulted in a further expansion of potential diagnostic applications. Perhaps the best evidence of TEE's diagnostic utility and value in patient management is the widespread use of this technology. TEE is found in the inpatient and outpatient ambulatory setting, in the operating room, in the intensive care unit, and in the emergency department. Currently, TEE accounts for approximately 5% to 10% of all echocardiography studies performed. The indications and utility of TEE will likely expand in the future with new technologic advancements such as three-dimensional echocardiography.

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Performance of Transesophageal Echocardiography Transesophageal echocardiography is a semi-invasive procedure that should be performed only by a properly trained physician who understands the indications for and potential complications of the procedure. Both technical and cognitive skills are required for the competent performance and interpretation of TEE studies (Table 1-1) , and guidelines on training have been published.[2] The physician should be assisted by an experienced sonographer whose tasks are to ensure that optimal images are obtained by adjusting the controls of the echocardiographic system and to ensure safety by monitoring the responses of the patient during the procedure. Although family members or friends are usually not allowed in the room when the procedure is being performed, there are situations in which their presence can be helpful. The presence of a parent can have a calming effect when one is dealing with an apprehensive teenager. A friend or a relative who speaks the same language can relieve much of the anxiety when dealing with an anxious patient who is not fluent in English. Transesophageal echocardiography should be performed in a spacious room that can comfortably accommodate a stretcher. The room should be equipped with an oxygen outlet and suction facilities. A pulse oximeter should be available, to be used mainly in cyanotic patients and patients with severe lung disease. The TEE probe should be carefully examined prior to each use. In addition to visual inspection, it is important to palpate the probe, particularly the flexion portion, to ensure that there is no unusual wear and tear of the probe.[3] Stretching of the steering cables may result in increased flexibility and mobility of the probe tip with buckling of the probe tip within the esophagus.[4] This phenomenon is associated with a poor TEE image and resistance to probe withdrawal. The probe should be advanced into the stomach and straightened by retroflexion of the extreme antiflexed probe tip. We have also detected perforation of the TEE probe sheath by a ruptured steering cable and recommend inspection of the casing for any protruding wires prior to probe insertion.[3] The flexion controls

need to be tested on a regular basis. Anterior flexion should exceed 90 degrees, and right and left flexion should approach 90 degrees. TABLE 1-1 -- Cognitive and Technical Skills Required for the Performance of Transesophageal Echocardiography (TEE) Cognitive Skills Knowledge of appropriate indications, contraindications, and risks of TEE Understanding of differential diagnostic considerations in each clinical case Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Familiarity with the operation of the ultrasonographic instrument, including the function of all controls affecting the quality of the data displayed Knowledge of normal cardiovascular anatomy, as visualized tomographically Knowledge of alterations in cardiovascular anatomy resulting from acquired and congenital heart diseases Knowledge of normal cardiovascular hemodynamics and fluid dynamics Knowledge of alterations in cardiovascular hemodynamics and blood flow resulting from acquired and congenital heart diseases Understanding of component techniques for general echocardiography and TEE, including when to use these methods to investigate specific clinical questions Ability to distinguish adequate from inadequate echocardiographic data and to distinguish an adequate from an inadequate TEE examination Knowledge of other cardiovascular diagnostic methods for correlation with TEE findings Ability to communicate examination results to patient, other health care professionals, and medical record Technical Skills Proficiency in performing a complete standard echocardiographic examination, using all echocardiographic modalities relevant to the case Proficiency in safely passing the TEE transducer into the esophagus and

stomach and in adjusting probe position to obtain the necessary tomographic images and Doppler data Proficiency in correctly operating the ultrasonographic instrument, including all controls affecting the quality of the data displayed Proficiency in recognizing abnormalities of cardiac structure and function as detected from the transesophageal and transgastric windows, in distinguishing normal from abnormal findings, and in recognizing artifacts Proficiency in performing qualitative and quantitative analysis of the echocardiographic data From Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. Preparation of Patient Patients should be contacted at least 12 hours before the procedure and instructed to fast for at least 4 hours before the procedure. They are informed that they should be accompanied, because they will not be able to drive or return to work for several hours owing to the lingering effect of sedation. On the day of the study, the procedure is explained in greater detail, and informed consent is obtained. Patients are told to expect mild abdominal discomfort and gagging following the insertion of the probe and are reassured that these responses are transient. A 20-gauge intravenous cannula is then inserted for administration of medications and contrast agents, if necessary. Lidocaine hydrochloride spray is routinely used for topical anesthesia, which should cover the posterior pharynx and the tongue. We usually use diazepam 2 to 10 mg intravenously 3

for sedation.[5] Midazolam at 0.05 mg/kg, with a total dose between 1 and 5 mg, can also be used. Sedation is used in about 85% of our patients and should be more sparingly used in elderly patients, because they tend to be more stoic and the effect of sedation is more likely prolonged. On the other hand, sedation is essential in young anxious patients and when the study is expected to be protracted. We aim for light sedation so that at the end of the procedure the patients are awake and can leave with an escort. Heavy sedation is needed in situations in which blunting the hemodynamic responses to the procedure is desirable. One obvious example is a patient undergoing TEE for suspected aortic

dissection.[6] It has not been our practice to use anticholinergic agents such as glycopyrrolate to decrease salivation. In the rare circumstances in which there is excessive salivation, it is usually adequate to simply instruct the patient to let the saliva dribble onto the towel placed under the chin, or the saliva can be removed by intermittent suction. Bacteremia is not a significant risk in TEE, and we do not use antibiotic prophylaxis to prevent endocarditis even in patients with prosthetic heart valves.[7] [8] Esophageal Intubation We perform the TEE study with the patient in the left decubitus position. The physician, the sonographer, and the echocardiographic system are all positioned on the left-hand side of the patient.[5] Artificial teeth or dentures are routinely removed. The flexion controls should be unlocked to allow for maximum flexibility of the probe when it is being inserted. The patient's head should be in a flexed position. The tip of the probe is kept relatively straight and gently advanced to the back of the throat. It should be maintained in a central position, because deviation to either side increases the likelihood that it may become lodged in the piriform fossa. The operator can facilitate this process by inserting one or two fingers into the patient's oropharynx to direct the path of the probe. Gentle pressure is exerted and the patient is instructed to swallow. The swallowing mechanism helps guide the probe into the esophagus. In older patients, cervical spondylosis with prominent protrusion into the posterior pharynx can create difficulty with passage of the probe.[5] Manually depressing the back of the tongue provides more room, allowing the TEE probe to assume a less acute angle and facilitating the intubation of the esophagus. If significant resistance is encountered when the probe is advanced, it is prudent to withdraw the probe and then initiate a new attempt. Esophageal intubation is more difficult with the multiplane probe than with the smaller monoplane and biplane probes.[9] [10] The latter can be used, if available, when esophageal intubation cannot be achieved with a multiplane probe. In experienced hands, the rate of failure of esophageal intubation should be less than 2%.[5] [9] [11]

A bite guard should always be used, except in edentulous patients. Our practice is to put it between the patient's teeth after the TEE probe has been successfully passed into the esophagus. Patients with a very sensitive pharynx may close their mouths involuntarily during esophageal intubation. In these patients, it is safer to insert the bite guard before the insertion of

the TEE probe. The patient should be instructed to keep the guard between the teeth throughout the procedure, and regular checks should be made to ensure that it is in the proper position to prevent damage to the probe or injury to the patient. Even when the probe is inserted without difficulties, it is not uncommon for the patient to develop nausea with or without mild retrosternal or abdominal discomfort. We find it useful to pause for 10 to 15 seconds to allow these symptoms to subside before proceeding with echocardiographic imaging. Our practice is to start with images acquired from the esophagus before advancing the probe into the stomach for the gastric views. The gastroesophageal sphincter is usually reached when the probe is advanced 40 cm from the teeth. Gentle pressure is all that is required to advance the probe through the gastroesophageal sphincter. The patient may again experience nausea and mild discomfort, and it may be advisable to pause momentarily for these symptoms to subside. Imaging of the proximal descending thoracic aorta and aortic arch is generally reserved for the end of the study, because the probe needs to be positioned in the upper esophagus and the patient is generally more aware of the probe at this position and tends to have more discomfort and gagging. Inadvertent passage of the probe into the trachea can occur, particularly in deeply sedated patients. The development of stridor and incessant cough should alert the operator of this possibility. Furthermore, it would be difficult to advance the probe beyond 30 cm from the teeth and the image quality is usually poor.[5] In patients on mechanical ventilation, esophageal intubation is more difficult. We usually introduce the probe with the patient lying supine, because the airway is protected and aspiration is unlikely. The probe is positioned behind the endotracheal tube and gently advanced. It is helpful to have the patient's mandible pulled forward when the probe is being advanced. If there is undue resistance at about 25 to 30 cm from the teeth, slight deflation of the cuff of the endotracheal tube can be considered to ease the passage of the probe. We do not usually remove the gastric tube, which can be used as a guide to help in the proper positioning and passage of the TEE probe. In a minority of intubated patients, successful esophageal intubation may be achieved only with direct laryngoscopy. Image Format There is no general agreement on how the imaging planes should be

displayed. Our preference is to orient the images such that the right-sided structures are on the left side of the screen and the left-sided on the right. The apex of the imaging plane with the electronic artifact is at the top of the screen. Thus, in the longitudinal views, superior structures are to the right of the screen and the inferior to the left.[12]

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TABLE 1-2 -- Standard Imaging Planes with Multiplane Transesophageal Echocardiography (TEE) at the University of Ottawa Heart Institute

Imaging View Basal

Fourchamber

Standard Imaging Plane Aortic valve

Angle of Imaging Array (degrees) 0–60

Atrial septum

90–120

Pulmonary bifurcation

0–30

Left ventricle

0–180

Mitral valve

0–180

Left ventricular outflow tract

120–160

Transgastric Left ventricle Mitral valve

0–150 0–150

Main Cardiac Structures Aortic valve, coronary arteries, left atrial appendage, pulmonary veins Fossa ovalis, superior vena cava, inferior vena cava Pulmonic valve, main and right pulmonary arteries, proximal left pulmonary artery Left ventricle (regional and global function), right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles, chords Aortic valve, ascending aorta, left and right ventricular outflow tracts, pulmonic valve, main pulmonary artery Left ventricle, right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles,

Aortic

Coronary sinus Descending thoracic aorta Aortic arch

0

chords Coronary sinus, tricuspid valve

0

Entire descending thoracic aorta

90

Aortic arch, arch vessels, left pulmonary artery

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Standard Imaging Planes Advances in TEE transducer technology have culminated in the development of the multiplane probe capable of two-dimensional and color flow imaging in multiple planes. The imaging plane can be steered electronically from 0 to 180 degrees by means of a pressure-sensitive switch, providing views unattainable by monoplane and biplane probes. The following discussion focuses only on standard imaging views routinely performed at the University of Ottawa Heart Institute using multiplane TEE (Table 1-2) . These views are considered "standard" because they have important clinical relevance and can be obtained in most patients with specific imaging planes. Four basic maneuvers are used to obtain specific tomographic views with TEE.[13] The first relates to the positioning of the probe by advancement or withdrawal of the probe. Although this is a simple maneuver, it is the most crucial, and the imaging views can be conveniently categorized according to the location of the TEE probe within the esophagus or stomach (Fig. 11) . The second maneuver involves rotation of the probe from side to side. This is particularly useful when using longitudinal imaging planes, which provide a better demonstration of the continuity between vertically aligned structures such as the superior vena cava and the arch vessels.[12] [13] Steering the imaging plane using the pressure-sensitive switch is the third maneuver to obtain different tomographic views. The ability to image cardiac structures from 0 to 180 degrees not only enhances understanding of cardiac anatomy but also provides a ready means for three-dimensional reconstruction. [14] [15] The fourth maneuver involves manipulation of the anterior-posterior and right-left flexion control knobs. The availability of a steerable imaging plane has drastically reduced the need to use the flexion knobs, but there are situations in which these knobs play a crucial role in obtaining proper tomographic views.[10] [13] The versatility of multiplane TEE provides an almost infinite number of

imaging planes. In our experience, it is useful to categorize them into four groups: basal, four-chamber, transgastric, and aortic views (see Fig. 1-1) . Table 1-2 summarizes the standard imaging planes and the cardiac structures evaluated in these four groups of views. Basal Views The basal group of views is obtained with the TEE probe located in the midesophagus. The base of the heart, Figure 1-1 Diagram showing the transesophageal echocardiography transducer locations for the four standard imaging views: basal (A), fourchamber (B), transgastric (C), and aortic (D).

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particularly the aortic valve, is well seen. The relationship of the two great arteries can be very well defined and followed cephalad to at least the level of the pulmonary bifurcation. Beyond this level, the interposing trachea make imaging impossible. Three tomographic planes are found to be particularly useful and are routinely performed at our laboratory. Aortic Valve

A short-axis view of the aortic valve can be obtained with the probe at about 30 to 35 cm from the teeth. The left coronary cusp often appears to have nodular thickening if the aortic valve is cut obliquely, which is often the case at 0 degrees.[12] Steering the imaging plane to 30 to 60 degrees should eliminate this artifact by providing an optimal short-axis view of the aortic valve (Fig. 1-2) . [13] A slight pull-back of the transducer should allow visualization of both the left and right coronary arteries. The left coronary artery can be followed to its bifurcation into the left anterior descending and circumflex arteries (Fig. 1-3) . The right coronary artery is more difficult to display, and usually only the proximal 2 to 3 cm is seen (Fig. 14) . Other structures well seen in this view are the left atrial appendage and the left pulmonary veins. The partition between these structures can be quite bulbous and should not be confused with an abnormal intracardiac mass (see Fig. 1-4) .[16] Rotating the probe to the right should reveal the right pulmonary veins.

We like the horizontal plane in imaging the four pulmonary veins. The left and right pulmonary veins are imaged separately. It is difficult to image the upper and lower pulmonary veins, left or right, in the same view because the veins are not located in the same plane with the lower pulmonary veins posterior and inferior to the upper pulmonary veins.[17] When one pulmonary vein is identified, a slight translational movement of the probe should bring out the other, because the orifices of the upper and Figure 1-2 The aortic valve was imaged with the imaging plane at about 60 degrees, showing the three cusps in systole. LA, left atrium; RA, right atrium; RV, right ventricle.

Figure 1-3 The left coronary artery (arrows) was imaged at 0 degrees. Ao, aorta; LA, left atrium.

lower pulmonary veins are in close proximity. The lower pulmonary veins run horizontal to the imaging plane, whereas the upper veins are more anterior and at an obtuse angle, making them more suitable for Doppler assessment. The right and left atrial appendages wrap around the great arteries anteriorly. The left atrial appendage is more prominent and can consist of multiple lobes.[18] A comprehensive interrogation using multiple imaging planes should be performed to exclude left atrial appendage thrombus in the appropriate clinical setting. The right atrial appendage is smaller and triangular in shape (Fig. 1-5) . The endocardial surfaces of both appendages are corrugated and should not be confused with small thrombi.[16] A long-axis view of the aorta can be achieved with the imaging plane at about 120 degrees. A more rightward imaging plane, such as 150 degrees, may be Figure 1-4 The proximal right coronary artery (small arrows) and the bulbous partition between the left atrial appendage and the left upper pulmonary vein (large arrow) are demonstrated. Ao, aorta; LA, left atrium.

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Figure 1-5 The atrial septum was preferentially imaged using the longitudinal plane to demonstrate its relation with the superior vena cava (SVC). LA, left atrium; RA, right atrium; RAA, right atrial appendage.

needed if the ascending aorta is dilated and tortuous. This view allows the visualization of a longer length of the ascending aorta and thus significantly reduces the blind spot caused by the interposing trachea. Atrial Septum

We prefer to image the atrial septum using the longitudinal plane at 90 to 120 degrees. The fossa ovalis, which is the thinnest part of the atrial septum, and the continuity of the superior vena cava with the right atrium are very well demonstrated in this view (see Fig. 1-5) . This view is particularly valuable in demonstrating the sinus venosus atrial septal defect, which is usually located just inferior to the entrance of the superior vena cava.[19] [20] The foramen ovale, if present, is located at the superior aspect of the fossa ovalis and is readily seen in this view. It is important to advance the probe to the level of the inferior vena cava so as not to neglect the inferior aspect of the atrial septum.[21] Careful sweep of the atrial septum with left-right rotation is needed to visualize the entire atrial septum. Continuous rotation from right to left will sequentially demonstrate the left ventricular outflow tract and the right ventricular outflow tract. Rotating the probe to the right shows the right upper pulmonary vein and provides parallel alignment for Doppler assessment. Pulmonary Bifurcation

The pulmonary bifurcation view is achieved by withdrawal of the probe with the imaging plane at 0 degrees. The pulmonic valve and main pulmonary artery are best seen slightly superior to the aortic valve (Fig. 16) . The pulmonic valve is thinner than the aortic valve and is usually difficult to image in a true cross section. Further slight withdrawal allows imaging the pulmonary bifurcation. The entire length of the right pulmonary artery but only the very proximal portion of the left pulmonary artery can be seen. The right pulmonary artery can usually be followed to its first bifurcation by rotation of the probe rightward, but this maneuver is better performed with the longitudinal plane at 90 degrees. Gradual rotation from left to right provides good visualization in cross section of the entire right pulmonary artery and its first bifurcation. This is an important view in

the detection of proximal pulmonary emboli.[22] [23] Four-Chamber Views Four-chamber views are obtained with the transducer within the middle to lower esophagus. It is difficult to image the left ventricle in its true long axis. Excessive anterior flexion should be avoided to prevent foreshortening of the ventricles. Indeed, to optimize visualization of the left ventricle, it is advisable to withdraw the probe slightly and at the same time attempt gentle retroflexion while maintaining adequate contact between the imaging surface and the esophagus. In the setting of a dilated and unfolded aorta, rotating the imaging plane to about 20 to 30 degrees may be necessary to obtain the four-chamber view without the aorta obscuring the tricuspid valve and part of the right ventricle. Left Ventricle

The inferior septum and anterolateral wall are usually seen in the fourchamber view (Fig. 1-7) . The left ventricular apex is difficult to visualize, particularly in patients with a dilated left ventricle. In addition to retroflexion, rightward flexion can often be helpful to minimize foreshortening of the left ventricle. Far-field imaging can be improved by decreasing the transmission frequency. A continuous sweep from 0 to 180 degrees should be performed to examine the different left ventricular segments Figure 1-6 The bifurcation of the main pulmonary artery (MPA) into the right (RPA) and left (LPA) pulmonary arteries was imaged using the transverse plane. Ao, aorta.

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Figure 1-7 The four-chamber view showing the left ventricle (LV) and mitral valve. LA, left atrium; RA, right atrium; RV, right ventricle.

so as to have a comprehensive assessment of left ventricular global and regional function (Fig. 1-8) .

Mitral Valve

The mitral valve is well seen using the four-chamber view, but the depth of the imaging plane should be reduced to enhance the resolution of the image ( see Fig. 1-7 and Fig. 1-8 ). To identify the individual scallops of the anterior and posterior mitral leaflets, a careful sweep from 0 to 180 degrees should be made. The technique of visualizing specific scallops of the mitral leaflets have been published,[24] but patient-to-patient variation should be kept in mind. The presence of a good long-axis view of the aortic valve and proximal ascending aorta, usually at Figure 1-8 The left ventricle and mitral valve can be comprehensively assessed by a continuous sweep of the imaging plane, which was about 100 degrees in this example. LA, left atrium; LV, left ventricle.

120 degrees, is a good indication that the middle scallops of both the anterior and the posterior mitral leaflets are imaged and provides the internal reference for the analysis of the other imaging planes. Both papillary muscles can be imaged but usually not in the same plane. The subvalvular chords are seldom completely imaged because they are frequently obscured by the mitral leaflets. The morphologic information obtained from this view should be corroborated by the short-axis view of the mitral valve obtained from the transgastric view, which also allows a better assessment of the subvalvular structures, including the papillary muscles and chords. Four-chamber views are ideal for the assessment of mitral regurgitation in relation to the number of regurgitant jets, the direction of the regurgitant jets, and the severity of regurgitation. [25] [26] Left Ventricular Outflow Tract

We like to image the left ventricular outflow tract at 120 to 160 degrees, because the outflow tract has a horizontal alignment in this plane that may allow optimal imaging even in the setting of a prosthetic aortic valve (Fig. 1-9) . The opening and closing of the aortic valve as well as the presence or absence of aortic regurgitation can be well visualized. The proximal ascending aorta is present in this view. A slight withdrawal of the probe will allow more of the ascending aorta to be visualized (Fig. 1-10) . A slight rotation to the left will show the right ventricular outflow tract with the thin pulmonic valve. Both the motion of the pulmonic valve and the presence or absence of pulmonic regurgitation can be adequately assessed

using this view. Transgastric Views There is slight resistance during the passage of the TEE probe through the gastroesophageal junction, and the Figure 1-9 The left ventricular outflow tract was well seen with the imaging plane at about 120 degrees. Ao, aorta; LA, left atrium; LV, left ventricle; RVOT, right ventricular outflow tract.

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Figure 1-10 Slight withdrawal of the probe relative to the probe position used to acquire the image shown in Figure 1-9 showed the right pulmonary artery (RPA) in short axis and more of the ascending aorta (Ao). LA, left atrium.

appearance of the liver is a clear indication that the probe is in the stomach. Anterior flexion, often with leftward rotation and flexion, is required to achieve good contact between the imaging surface and the gastric wall. Extreme anterior flexion with further advancement of the probe can sometimes produce images similar to the five-chamber views obtained from the subxiphoid surface approach. Left Ventricle

Multiple cross sections of the left ventricle can usually be obtained using the transgastric approach ( Fig. 1-11 and Fig. 1-12 ). These are the views commonly used in the intraoperative assessment of left ventricular function.[24] Optimization of the short-axis views of the left ventricle Figure 1-11 Transgastric short-axis view of the left ventricle (LV) at the papillary muscle level.

Figure 1-12 Transgastric long-axis view of the left ventricle (LV) with

visualization of the apex.

can be achieved with leftward rotation accompanied by leftward flexion. To visualize the left ventricular apex, gentle advancement of the probe is required together with slight retroflexion. In our experience, the short-axis view of the left ventricular apex can be obtained in about 60% of cases. Another way to visualize the left ventricular apex is to use the longitudinal plane at about 90 degrees (see Fig. 1-12) . Careful lateral rotation can be used to obtain comprehensive regional assessment of the left ventricle. Leftward rotation of this imaging plane can yield a good alignment with the left ventricular outflow tract and aortic valve to allow accurate measurement of the transaortic pressure gradients in the setting of aortic stenosis (Fig. 1-13) . [27] The right ventricle can be seen with rightward rotation of the probe. Both short- and long-axis views of the tricuspid valve are achievable, although Figure 1-13 Transgastric transesophageal echocardiography approach to assess the severity of aortic stenosis using continuous wave Doppler echocardiography.

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the tricuspid valve and its papillary muscles are better assessed with the long-axis plane. Mitral Valve

The mitral valve can be best assessed using the horizontal imaging plane with the transducer brought up to near the gastroesophageal junction (Fig. 1-14) . Anterior flexion and leftward flexion are usually required to optimize this view. Adjusting the imaging plane to about 20 degrees will help to bring out the lateral commissure. This view provides unambiguous assessment of the individual scallops of both the anterior and posterior mitral leaflets and thus should be attempted in all patients with myxomatous mitral valve degeneration. In our experience, this view is achievable in about 70% of patients. Both the papillary muscle and chords can be demonstrated, and the continuity between these structures and the mitral leaflets is best seen in the long-axis plane. Coronary Sinus

The coronary sinus comes into view when the probe is withdrawn to be near the gastroesophageal junction and the flexion knobs are in relatively neutral positions (Fig. 1-15) . This view can also be achieved by retroflexion with the probe in the lower esophagus. The coronary sinus is seen as a vascular structure located posterior to the left ventricle at the atrioventricular groove draining into the right atrium. The tricuspid valve can be visualized to the right and anterior. A dilated coronary sinus should raise the possibility of the presence of a persistent left superior vena cava, which is the most common cause. Leftward rotation while following the coronary sinus may sometimes demonstrate this anomalous vein. In the esophageal views, the left superior vena cava is usually sandwiched between the left atrial appendage and the left upper pulmonary vein.[28] Figure 1-14 The mitral valve was demonstrated in the short axis showing the anterior (arrows) and posterior (arrowheads) mitral leaflets.

Figure 1-15 The coronary sinus (CS) was demonstrated with the probe at the gastroesophageal junction. LV, left ventricle; RV, right ventricle.

Aortic Views The thoracic aorta is well assessed by TEE because of its close proximity to the esophagus. Descending Thoracic Aorta

The best way to assess the descending thoracic aorta is to use the horizontal imaging plane with the transducer rotated leftward and posterior, followed by slow withdrawal from the level of the diaphragm to the aortic arch (Fig. 1-16) .[16] Because of the relationship between the Figure 1-16 The descending aorta was imaged in the short axis to allow good visualization of entire circumference.

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Figure 1-17 The aortic arch (AA) was imaged using the longitudinal plane, showing the origin of the left subclavian artery (LSA).

esophagus and the aorta, slight rotational adjustment is required to visualize the entire circumference of the aortic wall as the probe is slowly withdrawn.[29] If the aorta is dilated or tortuous, proper short-axis views of the descending aorta will require adjustment of the imaging plane by 0 to 90 degrees. Aortic Arch

The longitudinal imaging plane at 90 degrees is preferred in imaging the aortic arch because it allows visualization of the entire circumference of the aorta (Fig. 1-17) .[29] Anterior rotation of the longitudinal plane should visualize the entire aortic arch, but the proximal aortic arch may not be visualized when the aortic arch is unfolded. The transducer will need to be withdrawn slightly to image the arch vessels, which course superiorly. In one third of patients, all three arch vessels can be imaged, but in the other two thirds of patients, only the two distal arch vessels can be imaged. It is rare not to be able to image at least one arch vessel. As a rule, the brachiocephalic artery, which is anterior and more rightward, is the most difficult to image because of the interposing trachea. The transverse plane in a more superior location may sometimes show the three arch vessels in their short axis. Advancing the probe by 1 to 2 cm so that the imaging plane is just inferior to the aortic arch can frequently image the proximal left pulmonary artery. It is sometimes possible to follow it to the first bifurcation. This view should be sought in the assessment of patients suspected of having pulmonary embolism.

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Doppler Examination Transesophageal echocardiography can be used to assess the flow patterns across the four cardiac valves, but it does not provide additional information to TTE. Furthermore, good alignment with the transvalvular flows may not be feasible because of the anatomic confines of the esophagus. On the other hand, intracardiac flows such as pulmonary vein flow and left atrial appendage flow are best evaluated by TEE and provide important insight into intracardiac hemodynamics. Pulmonary Vein Flow The pulmonary veins are imaged from the midesophagus level. Pulmonary vein flow can be assessed by placing the pulsed Doppler = sample=20 volume 0.5 to 1.0 cm into the pulmonary veins. The anterior to posterior = direction of the left and right upper pulmonary veins allows the Doppler = ultrasound beam to be aligned parallel to blood flow. This often cannot = be=20 achieved when interrogating the left and right lower pulmonary = veins. The normal pulmonary venous flow pattern can be = divided=20 into three phases: (1) antegrade systolic flow, (2) antegrade diastolic = flow,=20 and (3) retrograde atrial contraction flow reversal (F= ig.=20 1-18) . Two phases of antegrade systolic flow can usually be = appreciated on=20 transesophageal study. Systolic flow is dependent on apical displacement = of the=20 annulus, which is predominantly determined by left ventricular function, = atrial=20 relaxation, and atrial compliance.[3= 0]=20 [3= 1]=20 Left atrial pressure also affects antegrade systolic flow, with = increases in=20 left atrial pressure reducing systolic flow.[3= 0]=20 [3= 1]=20 Mitral regurgitation increases left atrial pressure during systole and = may=20 result in systolic flow reversal in one or all pulmonary=20 veins.[3= 0]=20 [3= 1] =20 Diastolic antegrade flow occurs as the mitral valve opens and left = atrial=20 pressure falls. The diastolic flow profile is dependent on left atrial = pressure,=20 left ventricular relaxation, and ventricular compliance. = [3= 0] =20 [3= 1]=20 Atrial contraction flow reversal is dependent on atrial contractility, = atrial=20 systolic pressure, and left ventricular compliance. The normal pulmonary = venous=20 flow pattern is dependent on heart rate and age.[3= 1]=20 [3= 2]=20 Higher systolic pulmonary venous flow velocities, higher atrial reversal = velocities, and smaller diastolic flow velocities=20

Figure = 1-18 Normal pulmonary venous flow showing two antegrade = flows in=20 ventricular systole and diastole, with a diminutive retrograde flow = caused by=20 atrial contraction. .

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patients younger than 50 years of=20 age.[3= 1]=20 [3= 2]=20 Left Atrial Appendage Flow The left atrial appendage can be imaged from = the=20 midesophagus

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aortic valve short-axis view (30 to 60 degrees) or the = midesophagus=20 two-chamber view (80 to 100 degrees). Left atrial appendage flow should = be=20 recorded by positioning the color flow sector over the left atrial = appendage and=20 placing the pulsed-Doppler sample volume at the site of maximal flow = velocity.=20 This usually occurs in the proximal or middle third of the left atrial=20 appendage. Velocity recordings from the distal third of the left atrial=20 appendage frequently incorporate wall motion artefacts and are usually=20 unsatisfactory. Low-velocity flow may be present, and wall filters = should be set=20 low. The pattern of left atrial appendage flow is = dependent on=20 cardiac rhythm.[3= 3]=20 In patients with sinus rhythm, four left atrial appendage flow waves = have been=20 described (F= ig.=20 1-19) : (1) a large positive wave after the electrocardiographic = P-wave,=20 which represents left atrial appendage contraction and emptying; (2) a = large=20 negative early systolic wave immediately following the QRS complex = representing=20 left atrial appendage filling; (3) alternating positive and negative = waves of=20 decreasing velocity throughout the remainder of systole representing = passive=20 flow in and out of the appendage; and (4) a low-velocity positive = emptying wave=20 in early diastole coinciding with rapid left ventricular filling. In = addition, a=20 low-velocity middiastolic negative filling wave representing appendage = filling=20 from the pulmonary veins may follow the early diastolic atrial appendage = emptying wave. The normal velocities are as follows: left atrial = appendage=20 contraction, 60 =B1 14; left atrial appendage filling, 52 =B1 13; and = early=20 diastolic filling, 20 =B1 11 cm per second.[3= 3]=20 [3= 4] =20 In patients with atrial fibrillation, a regular = atrial=20 contraction wave is absent. However, the left atrial appendage continues = to=20 contract, resulting in irregular oscillating positive and negative = emptying and=20 filling waves with variable velocities. The velocities are usually = larger during=20 ventricular diastole when the mitral valve is open, and=20

Figure = 1-19 Normal left atrial appendage flow pattern in sinus = rhythm,=20 showing prominent atrial emptying and filling = velocities.

smaller during systole when the mitral valve is closed. = Of note,=20 mean left atrial appendage velocities tend to be lower with higher heart = rates=20 because of the smaller proportion of time spent during diastole.

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The = early=20 diastolic appendage emptying wave, which coincides with early rapid left = ventricular filling, may still be visualized in atrial fibrillation. In = patients=20 with atrial flutter, the velocity waves are more regular and tend to be = of=20 greater velocity because of the slower atrial contraction rate.=20 Factors other than cardiac rhythm that may = affect left=20 atrial appendage velocities have recently been reviewed and include age, = heart=20 rate, left atrial contractility, left atrial pressure, left ventricular = systolic=20 and diastolic function, mitral stenosis, and mitral=20 regurgitation.[3= 3]=20 The potential clinical utility of assessing = left atrial=20 appendage velocities relates to the association of left atrial appendage = velocities with left atrial spontaneous echo contrast and left atrial = appendage=20 thrombus.[3= 3]=20 [3= 5]=20 [3= 6]=20 Atrial fibrillation patients with a left atrial appendage contraction = velocity=20 of less than 20 cm per second are more likely to have left atrial = appendage=20 thrombus and have a greater risk of ischemic stroke compared with = patients with=20 left atrial appendage velocities of 20 cm per second or=20 greater.[3= 5]=20 [3= 6]=20 Lower left atrial appendage velocity has also been observed in stroke = patients=20 with normal sinus rhythm.[3= 7]=20 Other potential utilities may relate to an ability of left atrial = appendage=20 velocities to predict the success of maintaining sinus rhythm following=20 cardioversion of atrial fibrillation.[3= 3]=20 [3= 8]=20 Coronary Artery Flow The assessment of coronary artery flow may be = limited by=20 motion of the heart during the cardiac cycle and difficulties aligning = the=20 Doppler ultrasound beam parallel to coronary blood flow. Coronary artery = blood=20 flow and coronary artery blood flow reserve are best measured in the = distal left=20 main coronary artery or proximal left anterior descending artery using = the=20 midesophagus aortic valve short-axis view, in which the pulsed-Doppler=20 ultrasound beam can be aligned parallel to coronary blood flow. The = ultrasound=20 beam can only rarely be aligned parallel to flow in the left circumflex = artery,=20 and the right coronary artery cannot be imaged in up to half of all = patients.=20 The normal Doppler flow signal is characterized by a large diastolic = component=20 and small systolic component moving away from the transducer. In = general, normal=20 diastolic velocities are 60 cm per second or less, and diastolic = velocities=20 greater 100 cm per second

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suggest significant obstruction in the=20 artery.[3= 9]=20 [4= 0]=20 [4= 1]=20 Additionally, coronary artery flow reserve can be assessed by measuring = peak or=20 mean diastolic coronary flow velocities at rest and then following = dipyridamole=20 or adenosine infusion. [4= 0]=20 [4= 2]=20 Transaortic and Transpulmonary Flow Transaortic flow can be assessed by imaging the = left=20 ventricular outflow tract and aortic valve in the transgastric long-axis = view=20 (100 to 135 degrees) or deep transgastric long-axis view (0 degrees), in = which=20 the probe is=20 12

advanced deep into the stomach = adjacent=20 to the left ventricular apex and anteflexed until the imaging plane is = directed=20 superiorly to the base of the heart. In these views, the pulsed-Doppler = or=20 continuous wave Doppler beam can be aligned parallel to blood flow to = measure=20 transaortic velocity. Stroke volume can be derived with the additional=20 measurement of either the midesophagus left ventricular outflow tract = diameter=20 or the short-axis aortic valve orifice area at valve leaflet=20 level.[4= 3]=20 [4= 4]=20 In patients with aortic stenosis or other forms of left ventricular = outflow=20 tract obstruction, the transvalvular pressure gradients can be derived = using the=20 simplified Bernoulli equation and continuous wave Doppler signals = obtained from=20 the transgastric longaxis or deep transgastric long-axis view.=20 [2= 7]=20 Transpulmonary flow has been measured by = combining either=20 pulsed Doppler or continuous wave Doppler velocity measurements of = pulmonary=20 artery flow obtained from mid-esophagus short- axis images of the main = pulmonary=20 artery and measurements of the main pulmonary artery=20 diameter.[4= 5]=20 [4= 6]=20 Transmitral and Transtricuspid Flow In the midesophageal four-chamber view or = long-axis view,=20 the pulsed Doppler ultrasound beam can be aligned parallel to = transmitral flow=20 to accurately measure transmitral filling velocities. The pulsed Doppler = sample=20 volume should be kept small (3 to 5 mm) and positioned at the mitral = valve=20 leaflet tips for the evaluation of diastolic function and filling=20 pressures.[3= 0]=20 In contrast, transmitral stroke volume is measured by placing the sample = volume=20 at the mitral

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valve annulus, so that velocity and annular dimensions are = measured at the same location.[4= 7]=20 [4= 8]=20 Transtricuspid filling can be assessed by = pulsed Doppler=20 measurements obtained in the midesophageal four-chamber view. However, = it is=20 frequently not possible to align the Doppler ultrasound beam parallel to = blood=20 flow. The transtricuspid filling pattern is similar to the transmitral = filling=20 pattern, although lower velocities are present.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Indications for Transesophageal Echocardiography The potential utility of TEE in the assessment and management of patients with suspected and overt cardiac disease is wide-ranging and encompasses the spectrum of cardiac problems encountered in clinical cardiology. TEE can be performed on patients in the ambulatory setting, intensive care unit, coronary care unit, or operating room. In general, TTE should be employed as the initial diagnostic investigation, as this technique is noninvasive and will entail no risk to the patient. Patient factors such as obesity, emphysema, or chest deformities frequently limit ultrasound penetration, resulting in nondiagnostic TTE studies. Surgical bandages may limit the number of available acoustic windows, and mechanical ventilation and surgical devices, such as traction and intra-aortic balloon pumps, may limit the ability to properly position the patient. Subcutaneous emphysema may result in the complete TABLE 1-3 -- Common Indications for Transesophageal Echocardiography Nondiagnostic transthoracic echocardiogram Assessment of native valve disease Assessment of prosthetic valves Assessment of infective endocarditis Assessment of a suspected cardioembolic event Assessment of cardiac tumors Assessment of atrial septal abnormalities Assessment of aortic dissection, intramural hematomas, and aortic rupture Evaluation of congenital heart disease Detection of anatomic coronary artery disease Stress echocardiography

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Evaluation of pericardial disease Evaluation of critically ill patients Intraoperative monitoring Monitoring during interventional procedures inability of TTE to visualize cardiac structures. TEE should be considered in these patients to obtain the necessary diagnostic information. Despite an adequate TTE study, TEE may be indicated to assess cardiac structures not usually seen by TTE, such as the superior vena cava, pulmonary veins, and the descending thoracic aorta, or to provide improved anatomic details such as the detection of flail mitral valve leaflet scallops and valvular vegetations, which are not consistently detected by TTE. Finally, TEE has important applications in the operating room, which are discussed in Chapter 2 and Chapter 19 . The common clinical indications for TEE are given in Table 1-3 . Native Valve Disease The presence, etiology, and severity of native valve disease can usually be determined by TTE. TEE should be reserved for the clinical situation in which TTE findings are inconclusive or a more precise characterization of the valve lesion will alter the patient management plan. Excellent visualization of the mitral valve anatomy is possible by TEE because of the close proximity of the mitral valve to the TEE transducer and the ability to image with high-frequency transducers. The mitral annulus, leaflets, chordal structures, and papillary muscles can all be visualized and evaluated. The use of a multiplane transducer allows a comprehensive, detailed examination of the valve to determine the location and mechanism of mitral regurgitation (see Chapter 19) . Ruptured chordae tendineae can be visualized, and precise anatomic localization of prolapsing or flail leaflet scallops is possible to predict the potential for successful mitral valve repair.[25] [49] [50] Abnormalities of the papillary muscles, such as a partial or complete rupture, are better visualized by TEE than TTE.[51] The severity of mitral valve regurgitation can be quantified using the methods employed for TTE,[52] but color Doppler velocity regurgitant jet areas tend to be larger in size on TEE than TTE because higher transducer frequencies are used and because of the close proximity of the transducer to

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the regurgitant jet.[53] Pulmonary vein flow can be assessed in nearly all patients and provides 13

a valuable measure of mitral regurgitation severity.[54] [55] Regurgitant vena contracta width, regurgitant volumes, and regurgitant orifice areas using the proximal flow convergence zone can be obtained by TEE.[56] [57] In mitral stenosis, TTE is usually satisfactory in assessing the valve morphology and severity of stenosis (see Chapter 20) . TEE appears equivalent to TTE in assessing valve mobility and leaflet thickening, but subvalvular disease and calcification may be underestimated owing to the shadowing effect of thickening and calcification of the mitral leaflets and annulus in the esophageal views.[58] Transvalvular pressure gradients can be measured by aligning the continuous wave Doppler beam parallel to left ventricular inflow through the mitral valve in the midesophageal views.[59] Effective orifice areas can be derived by the pressure half-time method,[59] the proximal flow convergence method, or orifice planimetry.[60] Orifice planimetry requires a tomographic cut of the distal or most narrow mitral orifice, however, which is technically more difficult to obtain by TEE and frequently not possible. The potential suitability of a patient for percutaneous balloon mitral valvuloplasty usually incorporates a detailed TEE assessment of the left atrial chamber and appendage to identify thrombus, in addition to an evaluation of the mitral valve morphology score and mitral regurgitation severity.[61] Transthoracic echocardiography can adequately visualize most aortic valve abnormalities, and only rarely is TEE required for assessment. However, subvalvular abnormalities such as subaortic membranes frequently require TEE for definitive diagnosis. [62] The assessment of aortic regurgitation severity only rarely necessitates a TEE evaluation (see Chapter 17) . Standard Doppler methods used for TTE may be employed using TEE.[63] One of the best measures, the ratio of color jet area to left ventricular outflow tract area, can be obtained from esophageal short-axis images of the outflow tract immediately inferior to the aortic valve. Jet height to outflow tract height can be obtained from esophageal long-axis images. Holodiastolic flow reversal in the descending aorta is always present with severe aortic regurgitation and can be detected by biplane or multiplane TEE using pulsed Doppler.[64] Aortic regurgitation severity may also be quantified by TEE using proximal flow convergence methods and vena

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contracta width.[65] [66] The severity of aortic stenosis is best quantified using transvalvular pressure gradients or valve areas derived by TTE (see Chapter 22) . Continuous wave Doppler interrogation of the aortic valve is possible by TEE using the transgastric long-axis view (100 to 135 degrees) or deep transgastric long-axis view (0 degrees) in which the probe is advanced deep into the stomach adjacent to the left ventricular apex and anteflexed until the imaging plane is directed superiorly to the base of the heart (see Fig. 113) . Good correlations between TTE and TEE gradients have been reported, despite the limited TEE windows.[27] Anatomic orifice area can be derived by planimetry of the maximum systolic aortic valve orifice visualized from esophageal short-axis images. Proper transducer position should be confirmed by rotating to the longitudinal plane and verifying that the leaflet tips are being imaged. Aortic valve areas derived by orifice planimetry correlate well with valve areas derived by TTE using the continuity equation and Gorlin equation valve areas.[27] , [67] [68] Valve calcification may affect the accuracy of TEEmeasured orifice areas.[69] Importantly, orifice planimetry is often more feasible and accurate using multiplane than biplane TEE.[68] Prosthetic Valves Transesophageal echocardiography is an extremely valuable technique in the assessment of prosthetic valve function, because TTE visualization of the prosthetic valve components and function is often limited by the echogenicity of the prosthetic components (see Chapter 24 and Chapter 25) . Reverberation artifacts, attenuation artifact, and acoustic shadowing obscure visualization of the prosthetic components and limit the visualization of structures beyond the prosthesis. Thickening and calcification of the leaflets, or the presence of a torn or flail bioprosthetic leaflet, are better appreciated on TEE. The structure and motion of the occluding device of a mechanical prosthesis may also be better evaluated. TEE provides increased sensitivity for detecting abnormalities of bioprosthetic and mechanical prostheses when compared to TTE.[70] [71] Small abnormalities of prosthetic valves such as leaflet thickening, flail leaflets, vegetations, thrombi, and filamentous strands can be missed on TTE but appreciated on TEE.[70] [71] [72] [73] [74] [75] [76] [77] TEE can be used to distinguish pannus from thrombus formation[78] and to guide thrombolytic therapy use in patients with the latter condition.[79] TEE is especially valuable in assessing mitral prostheses, as the transducer's posterior

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position provides excellent visualization of vegetations and thrombi, which usually locate on the left atrial aspect of the prosthesis.[70] [73] However, the ventricular aspect of a mitral prosthesis may not be adequately seen, and so TTE should complement the TEE assessment. [80] Transesophageal echocardiography can differentiate between normal variant and pathologic prosthetic valve regurgitation.[71] [72] [73] [74] [75] [81] Prosthetic mitral regurgitation is frequently better evaluated by TEE than TTE,[71] [72] [74] because TEE provides excellent visualization of the left atrial cavity without any intervening prosthetic material. TEE should be performed in patients in whom significant mitral regurgitation is not seen on TTE but is a clinical concern. Importantly, TEE allows characterization of mitral regurgitation jets as paravalvular or transvalvular in origin, which may modify the surgical procedure.[72] [74] [82] Multiplane TEE appears to better delineate paraprosthetic mitral regurgitation as compared with biplane TEE.[82] The incremental benefit of TEE in the assessment of regurgitation severity is less clear for aortic prostheses because the aortic regurgitation jet is usually well seen on TTE, and TEE visualization of prosthetic aortic regurgitation may be compromised by partial obstruction of the aortic regurgitation jet by either a mitral or aortic prosthesis in the esophageal views.[75] All bioprostheses and mechanical prostheses are inherently stenotic. The degree of stenosis is dependent on the prosthesis type and size and the presence of an associated pathologic condition such as leaflet calcification, pannus formation, or valve thrombosis.[83] In general, TTE is sufficient to assess the severity of prosthetic aortic or mitral 14

stenosis, but only TEE has sufficient resolution to distinguish these pathologic conditions.[78] In patients with inadequate TTE findings, TEE can quantify prosthetic mitral stenosis by measuring diastolic pressure gradients, pressure half-time, and effective orifice area using the proximal flow convergence method, as described for native mitral stenosis.[60] [84] Prosthetic aortic stenosis can be assessed by measuring transvalvular pressure gradients, as described for native aortic stenosis. [27] Importantly, flow through certain mechanical aortic prostheses results in localized pressure gradients and significant pressure recovery, which may lead to a discrepancy between Doppler and catheterization pressure gradients and an apparent "overestimation" of Doppler gradients.[85]

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Infective Endocarditis The presence of a vegetation is a hallmark finding of infective endocarditis, and its identification in the clinical setting of suspected endocarditis confirms the diagnosis[86] (see Chapter 21) In native valve endocarditis, the sensitivity of TTE for the detection of vegetations was 28% to 63%, and the sensitivity of TEE was 86% to 98%. [87] [88] [89] [90] [91] The specificity of the TTE and TEE findings for a vegetation appears similar and exceeds 90% when strict echocardiographic criteria are used for diagnosis.[87] [88] [90] Smaller vegetations are more likely to be detected by TEE than TTE.[88] Isolated case reports have suggested that pulmonic valve vegetations may also be better seen by TEE.[92] TEE does not appear to have an increased sensitivity compared with TTE, however, in the detection of tricuspid valve vegetations.[93] Prosthetic valve endocarditis is more difficult to diagnose using either TTE or TEE. The reported sensitivity of TTE for detecting vegetations was 0 to 43%, and the sensitivity of TEE was superior at 33% to 86%.[70] [89] [94] , [95] Thus, TEE should be performed in patients with suspected prosthetic valve endocarditis if the TTE procedure does not identify a vegetation. Although TEE has an improved sensitivity for detecting vegetations compared with TTE, the impact of TEE on diagnosis appears to be greatest in patients with suspected endocarditis with an intermediate clinical probability of endocarditis, especially patients with prosthetic valves.[96] Importantly, the absence of a vegetation on TEE makes the diagnosis of endocarditis unlikely (<10%), and alternative diagnoses should be considered.[95] [97] However, false-negative TEE studies have been reported, and patients with a high index of suspicion of endocarditis, prosthetic valves, or a persistent bacteremia may benefit from follow-up TEE if the initial study was negative.[95] [97] The complications of infective endocarditis, including abscess formation, leaflet diverticula, leaflet perforation, fistula tracts, mycotic aneurysms, and pseudoaneurysm formation, are better detected by TEE than TTE.[89] [98] [99] [100] [101] In a large series of patients with infective endocarditis, only 28% of surgically or autopsy confirmed abscess cavities were identified by TTE, as opposed to an 87% detection rate by TEE.[98] The specificity of both techniques in the detection of abscess formation exceeded 90%. Thus, patients with a suspected abscess based on clinical grounds or persistent bacteremia should undergo TEE.

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The role or potential utility of TEE in uncomplicated confirmed endocarditis is controversial. TEE may provide the clinician with prognostic information. Larger, mobile vegetations on TEE are associated with systemic embolization.[91] Additionally, complications including embolism, abscess formation, need for valve replacement, and death may be more likely to occur in patients with a vegetation that fails to decrease in size with therapy.[102] At this time, we do not perform routine follow-up TEE for cases of uncomplicated confirmed endocarditis. Suspected Cardioembolic Event The potential for a cardioembolic event should be considered in patients suffering cerebral ischemia or a peripheral arterial embolus. The Cerebral Embolism Task Force has suggested that cardiac emboli account for 15% of cerebral ischemic events.[103] Several cardiac abnormalities have a strong association with cardioembolic events and are considered a major risk source (see Chapter 37) . These abnormalities include atrial fibrillation, left atrial or left ventricular thrombi, vegetations, intracardiac tumor, mitral stenosis, mechanical valves, recent myocardial infarction, dilated cardiomyopathy, and intra-aortic debris.[104] Minor risk sources with weaker associations include cardiac abnormalities such as atrial septal aneurysms, patent foramen ovale, spontaneous echo contrast, mitral annular calcification, and mitral valve prolapse.[104] Many of these conditions can be diagnosed by clinical assessment, but echocardiography is frequently required for the diagnosis of many of the anatomic abnormalities. Approximately 7% of patients with a suspected cardioembolic event will have left atrial thrombus in the absence of atrial fibrillation and mitral stenosis. [105] The thrombus is frequently located in the left atrial appendage, a region poorly visualized on TTE. The sensitivity of TTE in detecting left atrial thrombus has been reported to be only 0 to 53%, whereas TEE has a sensitivity of 93% to 100% and a specificity exceeding 95%.[106] [107] In contrast, left ventricular thrombi may be better appreciated by TTE than TEE because of the close proximity of the left ventricular apex to the TTE transducer and the far field position and frequent apical foreshortening of the left ventricular apex on TEE.[108] However, TEE assessment may be beneficial if the TTE findings are inconclusive. [109] Left atrial spontaneous echo contrast is rarely appreciated on TTE, but well seen on TEE because of the close proximity of the left atrium to the TEE transducer and use of higher frequency transducers.[110] TEE may better detect small myxomas and aid in the diagnosis and management by better characterizing the

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attachment site.[111] [112] Similarly, TEE is superior in the detection of patent foramen ovale and atrial septal aneurysms.[113] [114] The size of the patent foramen ovale is associated with the cardioembolic risk and can better be appreciated by TEE.[115] A comprehensive characterization of aortic arch atheroma is rarely possible by TTE alone and requires TEE assessment.[35] [116] [117]

The indication for performing a TEE in patients with a suspected cardioembolic event is controversial. Although TEE has a better sensitivity than TTE for detecting potential 15

cardioembolic abnormalities, the yield for identifying a major risk source is limited. An analysis of pooled data from more than 30 cross-sectional studies suggested an overall detection rate for intracardiac masses of 4% for TTE and 11% for TEE.[104] However, the yield was greater in patients with evidence of cardiac disease. TTE and TEE identified an intracardiac mass in 13% and 19% of patients with cardiac disease and only 0.7% and 1.6% in patients without cardiac disease, respectively. In addition, the information obtained by TEE, which may include the identification of minor risk sources, may not significantly alter patient management.[104] [118] Many management decisions will be predetermined by the clinical setting (e.g., the patient with atrial fibrillation requires anticoagulation), and the management of patients with minor-risk cardiac abnormalities is frequently controversial. Thus, TEE should only be performed if the results have a reasonable chance of altering patient management or therapy. In this regard, TEE may have the greatest impact on patient management in the clinical setting of patients younger than 55 years of age with unexplained cerebral ischemia, in patients having recurrent events, or in patients with suspected endocarditis. Atrial Septal Abnormalities Transesophageal echocardiography provides excellent visualization of the atrial septum because of the atrial septum's close proximity to the transducer and perpendicular orientation to the ultrasound beam. Abnormalities of the atrial septum, including atrial septal defects, atrial septal aneurysms, and patent foramen ovale, are identified more frequently by TEE than by TTE.[19] [113] [114] , [119] [120] Sinus venosus defects and associated anomalous pulmonary venous drainage are frequently not

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identified on transthoracic imaging but can be easily detected on TEE study. [19] [20] TEE can be used to assess the severity of left-to-right shunting across the defect, determine the potential for percutaneous closure by accurate localization and characterization of the defect, and be used to assist in proper device placement during percutaneous closure.[121] [122] TEE can also detect thrombus formation within an atrial septal aneurysm and paradoxic emboli across an atrial septal defect.[115] [120] Cardiac Tumors For detecting intracardiac tumors, TEE appears superior to TTE, computed tomography, angiography, and magnetic resonance imaging.[112] [123] The sensitivity of TTE and TEE for the detection of atrial myxomas has been reported to be 95% and 100%, respectively.[123] Nonmyxomatous intracardiac tumors are identified by TTE and TEE in 91% and 100% of patients, respectively.[123] Pericardial or paracardial tumors are detected in only 67% by TTE and 97% by TEE.[123] TEE appears especially valuable in the detection of tumors located at the base of the heart, adjacent to the great vessels, or adjacent to the right heart.[112] [123] In addition, TEE is superior to TTE in characterizing features of a cardiac tumor that may assist in the diagnosis and management, such as the involvement of multiple chambers, the site of tumor attachment, the presence of multiple tumors, infiltration of adjacent structures, tumor calcification, or cyst formation.[112] [123] TEE has been used to guide percutaneous biopsy of intracardiac tumors.[124] However, the size and extent of paracardial involvement is not well assessed by TTE or TEE. In this setting, tomographic imaging with a wider field of view (magnetic resonance imaging or computed tomography) is needed. Aortic Dissection, Intramural Hematoma, and Rupture Aortic dissection can be detected by TEE with a high degree of accuracy and is the diagnostic investigation of choice for suspected aortic dissection in many institutions (see Chapter 3) . [125] The ascending aorta, aortic arch, and descending thoracic aorta can be visualized with excellent resolution owing to the close proximity of the aorta to the transducer and the use of high-frequency transducers. Importantly, a small segment of the superior ascending aorta cannot be visualized using TEE owing to the interposition of the air-filled trachea and bronchus. The sensitivity of monoplane and biplane TEE for the diagnosis of aortic dissection has been reported to be 97% to 100%, with a specificity that has ranged from 77% to 100%.[125] [126] [127] [128] The specificity was found to be greater than 95%, except in one

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study.[126] Multiplane TEE has been associated with similar sensitivities and specificities of 98% to 100% and 94% to 95%, respectively.[129] [130] The sensitivity and specificity of TEE compares favorably with those of other technologies, including aortography, computed tomography, and magnetic resonance imaging.[126] [127] [128] In addition to diagnosis, TEE can determine the extent of the dissection, differentiate the true and false lumens, identify thrombus within the false lumen, identify the site of the intimal tear, and assess for aortic valve involvement. [125] , [126] Involvement of the arch vessels and coronary arteries can also be determined.[125] Additionally, TEE can detect findings of aortic rupture, such as a pericardial effusion, pleural effusion, or mediastinal hematoma, which may significantly alter surgical therapy.[125] Aortic complications after repair may also be detected.[131] Associated aortic abnormalities, such as intramural hematoma and penetrating aortic ulcers, may have a similar presentation to aortic dissection and can be diagnosed using TEE.[128] [129] [132] TEE appears to have a high sensitivity and specificity for the detection of intramural hematoma, [129] but the diagnostic accuracy in the detection of penetrating aortic ulcers is unclear. In the largest series of 12 patients, penetrating aortic ulcers were identified by TEE in 83% of patients.[132] Transesophageal echocardiography has been used in the setting of chest trauma for the diagnosis of traumatic aortic rupture. The reported sensitivity and specificity for the detection of traumatic aortic rupture has ranged from 63% to 100% and 84% to 100%, respectively.[117] [133] However, TEE cannot consistently visualize the superior ascending aorta and aortic arch branch vessels, a frequent site of traumatic injury.[134] Thus, the role of TEE in the diagnostic evaluation of chest trauma patients remains undefined. Congenital Heart Disease

16

Transesophageal echocardiography commonly adds information to the preoperative, intraoperative, and postoperative assessment and management of patients with congenital heart disease[135] [136] (see Chapter 39 , Chapter 40 , Chapter 41 ). TEE can better appreciate abnormalities of the atrial septum and pulmonary veins, and it can be used to guide percutaneous

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closure of atrial septal defects.[19] [20] [119] , [121] [122] [124] In patients with atrioventricular canal defects, the atrioventricular valves and site of chordal insertion can be visualized to determine the potential for surgical valvuloplasty. [137] TEE provides good visualization of an atrial baffle and can detect stenoses or leaks.[138] Complications of a Fontan procedure, such as obstruction or thrombosis, can be evaluated.[139] TEE can characterize right and left ventricular outflow tract obstructions.[62] [135] [137] Abnormalities of the aorta, including aortic coarctation and patent ductus arteriosus, are also better appreciated by TEE than by TTE.[140] [141] Coronary Artery Disease Transesophageal echocardiography can be employed for the diagnosis of coronary artery disease by (1) visualization of coronary stenoses in the proximal vessels or (2) detection of stress-induced regional wall motion abnormalities. The left main coronary artery can be visualized in more than 85% of patients.[39] [142] [143] [144] [145] The proximal left anterior descending artery and proximal left circumflex artery can also be visualized in most patients.[142] [143] [144] The proximal right coronary artery is more difficult to visualize but may still be seen in 50% of patients or more.[142] [144] Several studies have examined the accuracy of TEE in identifying coronary stenoses in the proximal segments of the coronary arteries using two-dimensional and color flow imaging. In patients with visualized vessels, the sensitivity of TEE in identifying significant left main coronary stenoses has been reported to be 91% to 100%, with specificities greater than 90%.[39] [142] [143] [144] [145] The sensitivity for detecting significant proximal left anterior descending artery disease, left circumflex artery disease, and right coronary artery disease has been reported to be 78% to 100%, 50% to 89%, and 82% to 100%, respectively.[142] [143] [144] The sensitivity for detecting coronary artery stenoses significantly decreases, however, if patients with nonvisualized segments are included in the analysis.[144] One author has reported employing TEE and the continuity equation to quantify the severity of stenoses in the left anterior descending artery.[41] In addition, coronary artery flow reserve can be measured using TEE, and differences in flow reserve can be detected in patients with left anterior descending artery stenoses.[40] [42] TEE should not replace coronary angiography in the diagnosis of proximal coronary artery stenoses, but it may be useful in assessing angiographically questionable stenoses involving the left main ostium or the left anterior descending artery in centers in which

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intravascular ultrasonography is not available.[146] Stress echocardiography with TEE imaging has been used to evaluate patients with suspected or confirmed coronary artery disease.[147] [148] TEE provides high-quality images with excellent endocardial resolution. Stress techniques employed to induce ischemia have included transesophageal atrial pacing and pharmacologic methods using either dobutamine or dipyridamole.[147] [148] These techniques have been shown to be highly accurate in the detection of coronary artery disease and to provide information useful in risk stratification, and they may be useful in the assessment of myocardial viability in patients with left ventricular dysfunction.[147] [148] TEE is an invasive procedure with potential risks, however, and stress echocardiography with TEE imaging should be reserved for patients who have poor TTE images. Additional applications of TEE in the assessment of coronary artery disease include the detection of anomalous coronary arteries and the detection and mapping of coronary artery fistulas.[149] Pericardial Disease Pericardial effusions and cardiac tamponade are usually easily diagnosed on TTE and do not require TEE (see Chapter 29) . However, the detection of cardiac tamponade after cardiac surgery can be difficult to diagnose by TTE. Local compression of the right atrium by extracardiac thrombus may not be apparent on TTE because of the posterior position of the thrombus and poor TTE images related to suboptimal patient position, surgical bandages, and drainage tubes. TEE circumvents these problems and can better detect extracardiac compression.[150] Constrictive pericarditis and restrictive physiologic diseases can usually be differentiated on TTE using respiratory monitoring. In patients with nondiagnostic TTE, however, TEE with respiratory monitoring may be useful in differentiating these diseases. [151] Pericardial thickening can be measured by TEE and correlates with computed tomography. [152] In one study, TEE was shown to be superior to TTE in assessing pericardial thickening, intrapericardial metastases, intrapericardial thrombus, and pericardial cysts.[150] Intensive Care Unit The TTE images obtained in the intensive care unit are frequently inadequate because of poor acoustic penetration, limited windows from surgical bandages and drains, mechanical ventilation, and an inability to

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properly position patients. In this setting, TEE can provide essential information that alters patient management. TEE has been shown to be valuable in the assessment of the patient with unexplained hypotension, pulmonary edema, and hypoxia.[153] [154] TEE provides information on myocardial function, valve function, and volume status, which is critical in evaluating the patient with unexplained hypotension or unexplained pulmonary edema. TEE can detect right-to-left intracardiac shunting through a patent foramen ovale, which may occur in ventilated patients requiring high levels of pressure support and right ventricular infarction. [155] [156] The presence of massive or proximal pulmonary emboli can be diagnosed by TEE.[22] [23] Potential complications of myocardial infarction, including left ventricular 17

dysfunction, papillary muscle rupture, and myocardial rupture, may be detected. Intraoperative Monitoring Intraoperative TEE can provide detailed information on cardiac anatomy and function not obtainable by other monitoring technologies and can obtain this information without disrupting the surgical procedure.[157] [158] TEE can evaluate global and segmental left ventricular function, detect intraoperative myocardial ischemia, and monitor hemodynamics, including cardiac output, left ventricular filling pressures, and volume status. The cause of hemodynamic disturbances can be determined and intraoperative complications identified. Importantly, the adequacy of valve repairs or replacements and surgical reconstructions for congenital and acquired diseases can be evaluated prior to leaving the operating room. In 1996, the American Society of Anesthesiologists published recommendations for performing TEE based on the strength of supporting evidence and expert opinion that TEE improved clinical outcome.[157] The complete list of potential indications for TEE in the intraoperative period is extensive and is discussed in more detail in Chapter 2 and Chapter 19 . Monitoring During Interventional Procedures Transesophageal echocardiography is a valuable adjunct to percutaneous mitral valvuloplasty. TEE can guide catheter placement during trans-septal puncture, assist in proper balloon placement, evaluate the valvuloplasty result, identify complications, and shorten procedure and fluoroscopy

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times.[121] [159] It has been used to assist in right ventricular biopsies and biopsies of intracardiac masses.[124] [160] TEE may assist in trans-septal puncture and proper catheter position for radiofrequency ablation.[161] TEE has been used to guide catheter position for percutaneous closure of atrial septal defects, patent ductus arteriosus, ventricular septal defects, and coronary artery fistulas.[122] [162] [163] [164] TEE has also been found to be useful in the pediatric population during creation or enlargement of an interatrial communication or balloon dilation of obstructive left heart lesions. [165] Electrical cardioversion of atrial fibrillation without prolonged anticoagulation has been proposed as a safe procedure if TEE excludes left atrial thrombus.[166] However, this management scheme is controversial and requires further investigation (see Chapter 38) .[167]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Contraindications to Transesophageal Echocardiography Patients undergoing TEE should be kept on NPO (nothing by mouth) status for 4 to 6 hours prior to the procedure because of the potential for vomiting and aspiration. However, urgent procedures can likely be performed earlier with minimal risk of vomiting and aspiration if there has been only clear fluid intake up to 2 hours prior to the procedure.[168] TEE should not be performed in the uncooperative patient. Patients who are uncooperative should either have the study deferred or be sedated and paralyzed, if necessary. Patients with a tenuous cardiorespiratory status should be intubated and ventilated to avoid decompensation during the procedure. To avoid esophageal rupture, TEE should not be attempted in a patient with esophageal obstruction caused by a stricture or mass. The presence of an esophageal diverticulum should also be considered a relative contraindication because of the possibility of the probe entering and perforating the diverticulum. TEE is contraindicated in the patient with a perforated viscus or active gastrointestinal bleed. Esophageal varices are not a contraindication to TEE. However, the potential additive information should be weighed against the small risk of major bleeding. Severe cervical arthritis or dislocation of the atlantoaxial joint, in which flexion of the neck is severely limited or impossible, should be considered a relative contraindication to TEE. TEE can be performed safely in patients receiving anticoagulation therapy.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Complications of Transesophageal Echocardiography Transesophageal echocardiography is a relatively safe procedure with a low complication rate. Procedural complications have been observed in 0.47% to 2.80% of patients with successful esophageal intubation, however (Table 1-4) .[5] [9] [11] [169] The vast majority of complications are minor. Major complications, defined in one study as death, laryngospasm, sustained ventricular tachycardia, or congestive heart failure, occur in approximately 0.3% of patients.[169] In the Multicenter European Survey of 10,419 examinations, the TEE examination had to be interrupted prior to completion in 0.88% of studies.[11] Patient TABLE 1-4 -- Procedural Complications with Transesophageal Echocardiography Major Complications Death Esophageal rupture Laryngospasm or bronchospasm Congestive heart failure or pulmonary edema Sustained ventricular tachycardia Minor Complications Excessive retching or vomiting Sore throat Hoarseness Minor pharyngeal bleeding Blood-tinged sputum Nonsustained or sustained supraventricular tachycardia Atrial fibrillation

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Nonsustained ventricular tachycardia Bradycardia or heart block Transient hypotension Transient hypertension Angina Transient hypoxia Parotid swelling Tracheal intubation

18

intolerance of the probe, including excessive retching or vomiting, was the most common complication, resulting in premature termination of the procedure.[11] In the largest series, deaths have been reported in 0 to 0.03% of patients.[5] [9] [11] , [169] Cardiac complications reported include nonsustained and sustained supraventricular tachycardias or atrial fibrillation, nonsustained and sustained ventricular tachycardia, bradycardia, transient hypotension or hypertension, angina pectoris, congestive heart failure, and pulmonary edema. Pulmonary complications have included transient hypoxia and laryngospasm. Bleeding complications have included minor pharyngeal bleeding or blood-tinged sputum, MalloryWeiss tear, and severe hematemesis in a patient with a malignant tumor invading the esophagus. A minor sore throat may be present for 24 hours after the procedure. Adverse reactions may occur as a result of intravenous sedation, topical anesthesia, or drying agents such glycopyrrolate. Intravenous sedation may result in respiratory depression and hypoxia, hypotension, or paradoxical reactions. Topical anesthesia with benzocaine or lidocaine may result in acute toxic methemoglobinemia, a rare condition in which hemoglobin is oxidized by the topical anesthesia agent and is unable to carry oxygen to the tissues.[170] The partial pressure of oxygen in the blood is normal, but oxyhemoglobin levels are decreased. Patients usually develop cyanosis and dyspnea. On pulse oximetry, oxygen saturation often appears only mildly reduced because this technique cannot distinguish methemoglobin and reduced hemoglobin. The diagnosis can be confirmed with an arterial blood gas sample with measurement of methemoglobinemia. Methylene blue (1

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Transesophageal echocardiography is a very powerful tool that provides a unique acoustic window to assess cardiac structure and function. In our view, a comprehensive study should include the standard views discussed in this chapter. When dealing with specific clinical problems, additional views should be used to obtain the necessary diagnostic information. In critically ill patients, we believe that the initial views should be those that are most pertinent to the clinical question. Adequate diagnostic information would then have been obtained even if the study needs to be terminated prematurely. Finally, we need to be mindful that TEE is a semi-invasive procedure and is not free of risks. Clear and convincing indications should be present before a TEE study is performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Frazin L, Talano JV, Stephanides L, et al: Esophageal echocardiography.

Circulation 1976;54:102–108. 2. Pearlman AS, Gardin JM, Martin RP, et al: Guidelines for physician training in

transesophageal echocardiography: Recommendations of the American Society of Echocardiography Committee for physician training in echocardiography. J Am Soc Echocardiogr 1992;5:187–194. 3. Chan K, Burwash I: Unusual structural abnormality in a biplane transesophageal

transducer with normal imaging function. Am Soc Echocardiog 1998;11:310–312. 4. Kronzon I, Cziner DG, Katz ES, et al: Buckling of the tip of the transesophageal

echocardiography probe: A potentially dangerous technical malfunction. J Am Soc Echocardiogr 1992;5:176–177. 5. Chan KL, Cohen GI, Sochowski RA, et al: Complications of transesophageal

echocardiography in ambulatory adult patients: Analysis of 1500 consecutive examinations. J Am Soc Echocardiogr 1991;4:577–582. 6. Chan K: Impact of transesophageal echocardiography on the management of

patients with aortic dissection. Chest 1991;101:406–410. 7. Steckelberg JM, Khandheria BK, Anhalt JP, et al: Prospective evaluation of the risk

of bacteremia associated with transesophageal echocardiography. Circulation 1991;84:177–180. 8. Melendez L, Chan K, Cheung P, et al: Incidence of bacteremia in transesophageal

echocardiography: A prospective study of 140 consecutive patients. J Am Coll Cardiol 1991;18:1650–1654. 9. Tam JW, Burwash IG, Ascah KJ, et al: Feasibility and complications of single-plane

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and biplane versus multiplane transesophageal imaging: A review of 2947 consecutive studies. Can J Cardiol 1997;13:81–84. 10. Yvorchuk K, Sochowski R, Chan K: A prospective comparison of the multiplane

probe with the biplane probe in structure visualization and Doppler examination during transesophageal echocardiography. J Am Soc Echocardiog 1995;8:111–120. 11. Daniel WG, Erbel R, Kasper W, et al: Safety by transesophageal

echocardiography: A multicenter survey of 10,419 examinations. Circulation 1991;83:817–821. 12. Cohen G, Chan K: Biplane transesophageal echocardiography: Clinical

applications of the long-axis plane. J Am Soc Echocardiogr 1991;4:155–163. 13. Seward JB, Khandheria BK, Freeman WK, et al: Multiplane transesophageal

echocardiography: Image orientation, examination technique, anatomic correlations, and clinical applications. Mayo Clin Proc 1993;68:523–551. 14. Marx GR, Fulton DR, Pandian NG, et al: Delineation of site, relative size and

dynamic geometry of atrial septal defects by real-time three dimensional echocardiography. J Am Coll Cardiol 1995;25:482–490. 15. Flachskampf FA, Chandra S, Gaddipatti A, et al: Analysis of shape and motion of

the mitral annulus in subjects with and without cardiomyopathy by echocardiographic 3-dimensional reconstruction. J Am Soc Echocardiogr 2000;13:277–287. 16. Seward JB, Khandheria BK, Oh JK, et al: Transesophageal echocardiography:

technique, anatomic correlations, implementation, and clinical applications. Mayo Clin Proc 1988;63:649–680. 17. Anderson R, Dussek J, Evans S, et al: Cardiovascular. In Williams PL (ed): Gray's

Anatomy, 38th ed. New York, Churchill Livingstone, 1995, pp 1482–1483. 18. Veinot JP, Harrity PJ, Gentile F, et al: Anatomy of the normal left atrial

appendage: A quantitative study of age-related changes in 500 autopsy hearts— implications for echocardiographic examination. Circulation 1997;96:3112–3115. 19. Kronzon I, Tunick PA, Freedberg RS, et al: Transesophageal echocardiography is

superior to transthoracic echocardiography in the diagnosis of sinus venosus atrial septal defect. J Am Coll Cardiol 1991;17:537–542. 20. Pascoe RD, Oh JK, Warnes CA, et al: Diagnosis of sinus venosus atrial septal

defect with transesophageal echocardiography. Circulation 1996;94:1049–1055.

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21. Fagan S, Veinot JP, Chan KL: Residual sinus venosus atrial septal defect following

surgical closure of atrial septal defect. J Am Soc Echocardiogr 2001 (in press). 22. Wittlich N, Erbel R, Eichler A, et al: Detection of central pulmonary artery

thromboemboli by transesophageal echocardiography in patients with severe pulmonary embolism. J Am Soc Echocardiogr 1992;5:515–524. 23. Pruszczyk P, Torbicki A, Pacho R, et al: Noninvasive diagnosis of suspected

severe pulmonary embolism: transesophageal echocardiography vs spiral CT. Chest 1997;112:722–728. 19

24. Shanewise JS, Cheung AT, Aronson S, et al: ASE/SCA guidelines for performing a

comprehensive intraoperative multiplane transesophageal echocardiography examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr 1999;12:884–900. 25. Enriquez-Sarano M, Freeman WK, Tribouilloy CM, et al: Functional anatomy of

mitral regurgitation: Accuracy and outcome implications of transesophageal echocardiography. J Am Coll Cardiol 1999;34:1129–1136. 26. Pieper EP, Hellemans IM, Hamer HP, et al: Additional value of biplane

transesophageal echocardiography in assessing the genesis of mitral regurgitation and the feasibility of valve repair. Am J Cardiol 195;75:489–493. 27. Blumberg FC, Pfeifer M, Holmer SR, et al: Transgastric Doppler

echocardiographic assessment of the severity of aortic stenosis using multiplane transesophageal echocardiography. Am J Cardiol 1997;79:1273–1275. 28. Catoire P, Beydon L, Delaunay L, et al: Persistent left superior vena cava

diagnosed by transesophageal echocardiography. J Cardiothorac Vasc Anesth 1993;7:375–379. 29. Seward JB, Khandheria BK, Edwards WD, et al: Biplanar transesophageal

echocardiography: Anatomic correlations, image orientation, and clinical applications. Mayo Clin Proc 1990;65:1193–1213.

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30. Nishimura RA, Tajik AJ: Evaluation of diastolic filling of left ventricle in health

and disease: Doppler echocardiography is the clinician's Rosetta stone. J Am Coll Cardiol 1997;30:8–18. 31. Klein AL, Tajik AJ: Doppler assessment of pulmonary venous flow in healthy

subjects and in patients with heart disease. J Am Soc Echocardiogr 1991;4:379–392. 32. Klein AL, Burstow DJ, Tajik AJ, et al: Effects of age on left ventricular

dimensions and filling dynamics in 117 normal persons. Mayo Clin Proc 1994;69:212–224. 33. Agmon Y, Khandheria BK, Gentile F, et al: Echocardiographic assessment of the

left atrial appendage. J Am Coll Cardiol 1999;34:1867–1877. 34. Tabata T, Oki T, Fukuda N, et al: Influence of aging on left atrial appendage flow

velocity patterns in normal subjects. J Am Soc Echocardiogr 1996;9:274–280. 35. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography: Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med 1998;128:639–647. 36. Goldman ME, Pearce LA, Hart RG, et al: Pathophysiologic correlates of

thromboembolism in nonvalvular atrial fibrillation: I. Reduced flow velocity in the left atrial appendage (The Stroke Prevention in Atrial Fibrillation [SPAFF-III] study). J Am Soc Echocardiogr 1999;12:1080–1087. 37. Kamalesh M, Copeland TB, Sawada S: Severely reduced left atrial appendage function: A cause of embolic stroke in patients in sinus rhythm? J Am Soc Echocardiogr 1998;11:902–904. 38. Verhorst PM, Kamp O, Welling RC, et al: Transesophageal echocardiographic

predictors for maintenance of sinus rhythm after electrical cardioversion of atrial fibrillation. Am J Cardiol 1997;79:1355–1359. 39. Yamagishi M, Yasu T, Ohara K, et al: Detection of coronary blood flow associated

with left main coronary artery stenosis by transesophageal Doppler color flow echocardiography. J Am Coll Cardiol 1991;17:87–93. 40. Kozakova M, Palombo C, Pratali L, et al: Assessment of coronary reserve by

transoesophageal Doppler echocardiography: Direct comparison between different modalities of dipyridamole and adenosine administration. Eur Heart J 1997;18:514– 523.

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41. Isaaz K, da Costa A, de Pasquale JP, et al: Use of the continuity equation for

transesophageal Doppler assessment of severity of proximal left coronary artery stenosis: A quantitative coronary angiography validation study. J Am Coll Cardiol 1998;32:42–48. 42. Redberg RF, Sobol Y, Chou TM, et al: Adenosine-induced coronary vasodilation during transesophageal Doppler echocardiography: Rapid and safe measurement of coronary flow reserve ratio can predict significant left anterior descending coronary stenosis. Circulation 1995;92:190–196. 43. Feinberg MS, Hopkins WE, Davila-Roman VG, et al: Multiplane transesophageal

echocardiographic Doppler imaging accurately determines cardiac output measurement in critically ill patients. Chest 1995;107:679–673. 44. Katz WE, Gasior TA, Quinlan JJ, et al: Transgastric continuous-wave Doppler to

determine cardiac output. Am J Cardiol 1993;71:853–857. 45. Gorscan J III, Diana P, Ball BA, et al: Intraoperative determination of cardiac

output by transesophageal continuous wave Doppler. Am Heart J 1992;123:171–176. 46. Muhiudeen IA, Kuecherer HF, Lee E, et al: Intraoperative estimation of cardiac

output by transesophageal pulsed Doppler echocardiography. Anesthesiology 1991;74:9–14. 47. Hozumi T, Shakudo M, Applegate R, et al: Accuracy of cardiac output estimation

with biplane transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:62– 68. 48. Pu M, Griffin BP, Vandervoort PM, et al: Intraoperative validation of mitral inflow

determination by transesophageal echocardiography: Comparison of single-plane, biplane and thermodilution techniques. J Am Coll Cardiol 1995;26:1047–1053. 49. Foster GP, Iselbacher EM, Rose GA, et al: Accurate localization of mitral

regurgitation defects using multiplane transesophageal echocardiography. Ann Thorac Surg 1998;65:1025–1031. 50. Grewal KS, Malkowski MJ, Kramer CM, et al: Multiplane transesophageal

echocardiographic identification of the involved scallop in patients with flail mitral valve leaflet: Intraoperative correlation. J Am Soc Echocardiogr 1998;11:966–971. 51. Moursi MH, Bhatnagar SK, Vilacosta I, et al: Transesophageal echocardiographic

assessment of papillary muscle rupture. Circulation 1996;94:1003–1009. 52. Schiller NB, Foster E, Redberg RF: Transesophageal echocardiography in the

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evaluation of mitral regurgitation: The twenty-four signs of severe mitral regurgitation. Cardiol Clin 1993;11:399–408. 53. Smith MD, Harrison MR, Pinton R, et al: Regurgitant jet size by transesophageal

compared with transthoracic Doppler color flow imaging. Circulation 1991;83:79–86. 54. Klein AL, Obarski TP, Stewart WJ, et al: Transesophageal Doppler echocardiography of pulmonary venous flow: A new marker of mitral regurgitation severity. J Am Coll Cardiol 1991;18:518–526. 55. Hynes MS, Tam JL, Burwash IG, et al: Predictive value of pulmonary venous flow

patterns in detecting mitral regurgitation and left ventricular abnormalities. Can J Cardiol 1999;15:665–670. 56. Grayburn PA, Fehske W, Omran H, et al: Multiplane transesophageal

echocardiographic assessment of mitral regurgitation by Doppler color flow mapping of the vena contracta. Am J Cardiol 1994;74:912–917. 57. Pu M, Vandervoort PM, Griffin BP, et al: Quantification of mitral regurgitation by

the proximal convergence method using transesophageal echocardiography: Clinical validation of a geometric correction for proximal flow constraint. Circulation 1995;92:2169–2177. 58. Marwick TH, Torelli J, Obarski T, et al: Assessment of the mitral valve splitability

score by transthoracic and transesophageal echocardiography. Am J Cardiol 1991;68:1106–1107. 59. Stoddard MF, Prince CR, Tuman WL, et al: Angle of incidence does not affect accuracy of mitral stenosis area calculation by pressure half-time: Application to Doppler transesophageal echocardiography. Am Heart J 1994;127:1562–1572. 60. Degertekin M, Basaran Y, Gencbay M, et al: Validation of flow convergence

region method in assessing mitral valve area in the course of transthoracic and transesophageal echocardiographic studies. Am Heart J 1998;135:207–214. 61. Cormier B, Vahanian A, Michel PL, et al: Transesophageal echocardiography in

the assessment of percutaneous mitral commissurotomy. Eur Heart J 1991;12(suppl B):61–65. 62. Essop MR, Skudicky D, Sareli P: Diagnostic value of transesophageal versus

transthoracic echocardiography in discrete subaortic stenosis. Am J Cardiol 1992;70:962–963. 63. Meyerowitz CB, Jacobs LE, Kotler MN, et al: Assessment of aortic regurgitation

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Pagina 7 di 16

by transesophageal echocardiography: Correlation with angiographic determination. Echocardiography 1993;10:269–278. 64. Sutton DC, Kluger R, Ahmed SU, et al: Flow reversal in the descending aorta: A

guide to intraoperative assessment of aortic regurgitation with transesophageal echocardiography. J Thorac Cardiovasc Surg 1994;108:576–582. 20

65. Sato Y, Kawazoe K, Nasu M, et al: Clinical usefulness of the proximal isovelocity

surface area method using echocardiography in patients with eccentric aortic regurgitation. J Heart Valve Dis 1999;8:104–111. 66. Sato Y, Kawazoe K, Kamata J, et al: Clinical usefulness of the effective regurgitant

orifice area determined by transesophageal echocardiography in patients with eccentric aortic regurgitation. J Heart Valve Dis 1997;6:580–586. 67. Hoffmann R, Flachskampf FA, Hanrath P: Planimetry of orifice area in aortic stenosis using multiplane transesophageal echocardiography. J Am Coll Cardiol 1993;22:529–534. 68. Kim KS, Maxted W, Nanda NC, et al: Comparison of multiplane and biplane

transesophageal echocardiography in the assessment of aortic stenosis. Am J Cardiol 1997;79:436–441. 69. Cormier B, Iung B, Porte JM, et al: Value of multiplane transesophageal

echocardiography in determining aortic valve area in aortic stenosis. Am J Cardiol 1996;77:882–885. 70. Daniel WG, Mugge A, Grote J, et al: Comparison of transthoracic and

transesophageal echocardiography for detection of abnormalities of prosthetic and bioprosthetic valves in the mitral and aortic positions. Am J Cardiol 1993;71:210–215.

71. Alton ME, Pasierski TJ, Orsinelli DA, et al: Comparison of transthoracic and

transesophageal echocardiography in evaluation of 47 Starr-Edwards prosthetic valves. J Am Coll Cardiol 1992;20:1503–1511. 72. Daniel LB, Grigg LE, Weisel RD, et al: Comparison of transthoracic and

transesophageal assessment of prosthetic valve dysfunction. Echocardiography 1990;7:83–95.

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73. Khandheria BK, Seward JB, Oh JK, et al: Value and limitations of transesophageal

echocardiography in the assessment of mitral valve prosthesis. Circulation 1991;83:1956–1968. 74. Chaudhry FA, Herrera C, DeFrino PF, et al: Pathologic and angiographic

correlations of transesophageal echocardiography in the prosthetic heart valve dysfunction. Am Heart J 1991;122:1057–1064. 75. Karalis DG, Chandrasekaran K, Ross JJ Jr, et al: Single-plane transesophageal

echocardiography for assessing function of mechanical or bioprosthetic valves in the aortic valve position. Am J Cardiol 1992;69:1310–1315. 76. Gueret P, Vignon P, Fournier P, et al: Transesophageal echocardiography for the

diagnosis and management of nonobstructive thrombosis of mechanical mitral prosthesis. Circulation 1995;91:103–110. 77. Orsinelli DA, Pearson AC: Detection of prosthetic valve strands by

transesophageal echocardiography: Clinical significance in patients with suspected cardiac source of embolism. J Am Coll Cardiol 1995;26:1713–1718. 78. Barbetseas J, Nagueh SF, Pitsavos C, et al: Differentiating thrombus from pannus

formation in obstructed mechanical prosthetic valves: An evaluation of clinical, transthoracic and transesophageal echocardiographic parameters. J Am Coll Cardiol 1998;32:1410–1417. 79. Ozkan M, Kaymaz C, Kirma C, et al: Intravenous thrombolytic treatment of

mechanical prosthetic valve thrombosis: A study using serial transesophageal echocardiography. J Am Coll Cardiol 2000;35:1881–1889. 80. Tenenbaum A, Fisman EZ, Vered Z, et al: Failure of transesophageal

echocardiography to visualize a large mitral prosthesis vegetation detected solely by transthoracic echocardiography. J Am Soc Echocardiogr 1995;8:944–946. 81. Flachskampf FA, O'Shea JP, Griffin BP, et al: Patterns of transvalvular

regurgitation in normal mechanical prosthetic valves. J Am Coll Cardiol 1991;18:1493–1498. 82. Flachskampf FA, Hoffmann R, Franke A, et al: Does multiplane transesophageal

echocardiography improve the assessment of prosthetic valve regurgitation? J Am Soc Echocardiogr 1995;8:70–78. 83. Reisner SA, Meltzer RS: Normal values of prosthetic valve Doppler

echocardiographic parameters: A review. J Am Soc Echocardiogr 1998;11:201–210.

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84. Gorscan J III, Kenny WM, Diana P, et al: Transesophageal continuous-wave

Doppler to evaluate mitral prosthetic stenosis. Am Heart J 1991;121:911–914. 85. Baumgartner H, Khan S, DeRobertis M, et al: Effect of prosthetic aortic design on

the Doppler-catheter gradient correlation: An in vitro study of normal St. Jude, Medtronic-Hall, Starr-Edwards, and Hancock valves. J Am Coll Cardiol 1992;19:324– 332. 86. Durak DT, Lukes AS, Bright DK: New criteria for diagnosis of infective

endocarditis: Utilization of specific echocardiographic findings. Am J Med 1994;96:200–209. 87. Birmingham GD, Rahko PS, Ballantyne FE: Improved detection of infective

endocarditis with transesophageal echocardiography. Am Heart J 1992;123:774–781. 88. Erbel R, Rohmann S, Drexler M, et al: Improved diagnostic value of

echocardiography in patients with infective endocarditis by transesophageal approach: A prospective study. Eur Heart J 1988;9:43–53. 89. Taams MA, Gussenhoven EJ, Bos E, et al: Enhanced morphologic diagnosis in

infective endocarditis by transoesphageal echocardiography. Br Heart J 1990;63:109– 113. 90. Shively BK, Gurule FT, Roldan CA, et al: Diagnostic value of transesophageal

compared with transthoracic echocardiography in infective endocarditis. J Am Coll Cardiol 1991;18:391–397. 91. Mügge A, Daniel WG, Frank G, et al: Echocardiography in infective endocarditis:

Reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol 1989;14:631–638. 92. Shapiro SM, Young E, Ginzton LE, et al: Pulmonic valve endocarditis as an underdiagnosed disease: Role of transesophageal echocardiography. J Am Soc Echocardiogr 1992;5:48–51. 93. San Roman JA, Vilacosta I, Zamorano JL, et al: Transesophageal

echocardiography in right-sided endocarditis. J Am Coll Cardiol 1993;21:1226–1230. 94. Zabalgoitia M, Herrera CJ, Chaudhry FA, et al: Improvement in the diagnosis of

bioprosthetic valve dysfunction by transesophageal echocardiography. J Heart Valve Dis 1993;2:595–603. 95. Lowry RW, Zoghbi WA, Baker WB, et al: Clinical impact of transesophageal

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echocardiography in the diagnosis and management of infective endocarditis. Am J Cardiol 1994;73:1089–1091. 96. Lindner JR, Case RA, Dent JM, et al: Diagnostic value of echocardiography in

suspected endocarditis: An evaluation based on the pretest probability of disease. Circulation 1996;93:730–736. 97. Sochowski RA, Chan K-L: Implication of negative results on a monoplane

transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol 1994;21:216–221. 98. Daniel WG, Mugge A, Martin RP, et al: Improvement in the diagnosis of abscesses

associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:795–800. 99. Massey WM, Samdarshi TE, Nanda NC, et al: Serial documentation of changes in

a mitral valve vegetation progressing to abscess rupture and fistula formation by transesophageal echocardiography. Am Heart J 1992;124:241–248. 100. Castro SD, Cartoni D, d'Amati G, et al: Diagnostic accuracy of transthoracic and

multiplane transesophageal echocardiography for valvular perforation in acute infective endocarditis: Correlation with anatomic findings. Clin Infect Dis 2000;30:825–826. 101. Vilacosta I, San Roman JA, Sarria C, et al: Clinical, anatomic, and

echocardiographic characteristics of aneurysms of the mitral valve. Am J Cardiol 1999;84:110–113. 102. Rohmann S, Erhel R, Darius H, et al: Effect of antibiotic treatment on vegetation

size and complication rate in infective endocarditis. Clin Cardiol 1997;20:132–140. 103. Cerebral Embolism Task Force: Cardiogenic brain embolism: The second report

of the Cerebral Embolism Task Force. Arch Neurol 1989;46:727–743. 104. Kapral MK, Silver FL, with the Canadian Task Force on Preventive Health Care:

Preventive health care, 1999 update: 2. Echocardiography for the detection of a cardiac source of embolus in patients with stroke. Can Med Assoc J 1999;161:989– 996. 105. Dressler FA, Labovitz AJ: Systemic arterial emboli and cardiac masses:

Assessment with transesophageal echocardiography. Cardiol Clin 1993;11:447–460. 106. Hwang JJ, Chen JJ, Lin SC, et al: Diagnostic accuracy of transesophageal

echocardiography for detecting left atrial thrombi in patients with rheumatic heart

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disease having undergone mitral valve operations. Am J Cardiol 1993;72:677–681. 107. Manning WJ, Weintraub RM, Wakomonski CA, et al: Accuracy of

transesophageal echocardiography for identifying left atrial thrombi. A prospective intraoperative study. Ann Intern Med 1995;123:817–822. 21

108. Mugge A, Daniel WG, Haverich A, et al: Diagnosis of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 109. Chen C, Koschyk D, Hamm C, et al: Usefulness of transesophageal

echocardiography in identifying small left ventricular apical thrombus. J Am Coll Cardiol 1993;21:208–215. 110. Black IW, Hopkins AP, Lee LCL, et al: Left atrial spontaneous echo contrast: A

clinical transesophageal echocardiographic analysis. J Am Coll Cardiol 1991;18:398– 404. 111. Rittoo D, Cotter L: Detection of a small left atrial myxoma: Value and limitations

of four imaging modalities. J Am Soc Echocardiogr 1997;10:874–876. 112. Mügge A, Daniel WG, Haverich A, et al: Diagnoses of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 113. Siostrzonek P, Zangeneh M, Gössinger H, et al: Comparison of transesophageal

and transthoracic contrast echocardiography for detection of a patent foramen ovale. Am J Cardiol 1991;68:1247–1249. 114. Pearson AC, Nagelhout D, Castello R, et al: Atrial septal aneurysm and stroke: A

transesophageal echocardiographic study. J Am Coll Cardiol 1991;18:1223–1229. 115. Hausmann D, Mügge A, Daniel WG: Identification of patent foramen ovale

permitting paradoxical embolism. J Am Coll Cardiol 1995;26:1030–1038. 116. Tunick PA, Kronzon I: Atheromas of the thoracic aorta: Clinical and therapeutic

update. J Am Coll Cardiol 2000;35:545–554. 117. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

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diseases of the thoracic aorta: Part II—atherosclerotic and traumatic diseases of the aorta. Chest 2000;117:233–243. 118. Rauh G, Fischereder M, Spengel FA: Transesophageal echocardiography in

patients with focal cerebral ischemia of unknown cause. Stroke 1996;27:691–694. 119. Mehta RH, Helmcke F, Nanda NC, et al: Transesophageal Doppler color flow

mapping assessment of atrial septal defect. J Am Coll Cardiol 1990;16;1010–1016. 120. Mugge A, Daniel WG, Angermann C, et al: Atrial septal aneurysm in adult

patients: A multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;91:2785–2792. 121. Rittoo D, Sutherland GR, Shaw TR: Quantification of left-to-right shunting and

defect size after balloon mitral commissurotomy using biplane transesophageal echocardiography, color flow Doppler mapping, and the principle of proximal flow convergence. Circulation 1993;87:1591–1603. 122. Ewert P, Berger F, Daehnert I, et al: Transcatheter closure of atrial septal defects

without fluoroscopy: Feasibility of a new method. Circulation 2000;101:847–849. 123. Engberding R, Daniel WG, Erbel R, et al: Diagnosis of heart tumours by

transoesophageal echocardiography: A multicentre study in 154 patients. Eur Heart J 1993;14:1223–1228. 124. Beaver TA, Robb JF, Teufel EJ, et al: Right ventricular outflow tract obstruction

in an older woman: Facilitated diagnosis with transesophageal echocardiographyguided biopsy. J Am Soc Echocardiogr 2000;13:622–625. 125. Cigarrao JE, Isselbacher EM, DeSanctis RW, et al: Diagnostic imaging in the

evaluation of suspected aortic dissection: Old standards and new directions. N Engl J Med 1993:328:35–43. 126. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic

dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9. 127. Bansal RC, Chandrasekaran K, Ayala K, et al: Frequency and explanation of false

negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393–1401. 128. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

diseases of the thoracic aorta: Part I—aortic dissection, aortic intramural hematoma, and penetrating atherosclerotic ulcer of the aorta. Chest 2000;116:1772–1779.

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129. Keren A, Kim CB, Hu BS, et al: Accuracy of biplane and multiplane

transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol 1996;28:627–636. 130. Sommer T, Fehske W, Holzkuecht N, et al: Aortic dissection: A comparative

study of diagnosis with spiral CT, multiplanar transesophageal echocardiography and MR imaging. Radiology 1996;199:347–352. 131. Masani ND, Banning AP, Jones RA, et al: Follow-up of chronic thoracic aortic

dissection: Comparison of transesophageal echocardiography and magnetic resonance imaging. Am Heart J 1996;131:1156–1163. 132. Vilacosta I, San Roman JA, Aragoncillo P, et al: Penetrating atherosclerotic aortic

ulcer: Documentation by transesophageal echocardiography. J Am Coll Cardiol 1998;32:83–89. 133. Smith MD, Cassidy JM, Souther S, et al: Transesophageal echocardiography in

the diagnosis of traumatic rupture of the aorta. N Engl J Med 1995;332:356–362. 134. Ahrar K, Smith DC, Bansal RC, et al: Angiography in blunt thoracic aortic injury.

J Trauma 1997;42:665–669. 135. Ritter SB: Transesophageal real-time echocardiography in infants and children

with congenital heart disease. J Am Coll Cardiol 1991;18:569–580. 136. Weintraub R, Shiota T, Elkadi T, et al: Transesophageal echocardiography in

infants and children with congenital heart disease. Circulation 1992;86:711–722. 137. Sreeram N, Stumper OF, Kaulitz R, et al: Comparative value of transthoracic and

transesophageal echocardiography in the assessment of congenital abnormalities of the atrioventricular junction. J Am Coll Cardiol 1990;16:1205–1214. 138. Kaulitz R, Stümper OFW, Geuskens R, et al: Comparative values of the

precordial and transesophageal approaches in the echocardiographic evaluation of atrial baffle function after an atrial correction procedure. Am J Coll Cardiol 1990;16:686–694. 139. Stümper O, Sutherland GR, Geuskens R, et al: Transesophageal echocardiography

in evaluation and management after a Fontan procedure. J Am Coll Cardiol 1991;17:1152–1160. 140. Engvall J, Sjoqvist L, Nylander E, et al: Biplane transoesophageal

echocardiography, transthoracic Doppler, and magnetic resonance imaging in the

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assessment of coarctation of the aorta. Eur Heart J 1995;10:1399–1409. 141. Andrade A, Vargas-Barron J, Rijlaarsdam M, et al: Utility of transesophageal

echocardiography in the examination of adult patients with patent ductus arteriosus. Am Heart J 1995;130:543–546. 142. Tardif JC, Vannon MA, Taylor K, et al: Delineation of extended lengths of coronary arteries by multiplane transesophageal echocardiography. J Am Coll Cardiol 1994;24:909–919. 143. Reichert SL, Visser CA, Koolen JJ, et al: Transesophageal examination of the left

coronary artery with a 7.5 MHz annular array two-dimensional color flow Doppler transducer. J Am Soc Echocardiogr 1990;3:118–124. 144. Samdarshi TE, Nanda NC, Gatewood RP Jr, et al: Usefulness and limitations of

transesophageal echocardiography in the assessment of proximal coronary artery stenosis. J Am Coll Cardiol 1992;19:572–580. 145. Yoshida K, Yoshikawa J, Hozumi T, et al: Detection of left main coronary artery

stenosis by transesophageal color Doppler and two-dimensional echocardiography. Circulation 1990;81:1271–1276. 146. Firstenberg MS, Greenberg NL, Lin SS, et al: Transesophageal echocardiography

assessment of severe ostial left main coronary stenosis. J Am Soc Echocardiogr 2000;13:696–698. 147. Panza JA: Transesophageal echocardiography with stress for the evaluation of

patients with coronary artery disease. Cardiol Clin 1999;17:501–520. 148. Madu EC: Transesophageal dobutamine stress echocardiography in the evaluation

of myocardial ischemia in morbidly obese subjects. Chest 2000;117;657–661. 149. Lin FC, Chang HJ, Chern MS, et al: Multiplane transesophageal

echocardiography in the diagnosis of congenital coronary artery fistula. Am Heart J 1995;130:1236–1242. 150. Hutchison SJ, Smalling RG, Albornoz M, et al: Comparison of transthoracic and

transesophageal echocardiography in clinically overt or suspected pericardial heart disease. Am J Cardiol 1994;74:962–965. 151. Klein AL, Cohen GI, Pietrolungo JF, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943.

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152. Ling LH, Oh JK, Tei C, et al: Pericardial thickness measured with

transesophageal echocardiography: Feasibility and potential clinical usefulness. J Am Coll Cardiol 1997;29:1317–1323. 153. Heidenreich PA, Stainback RF, Redberg RF, et al: Transesophageal

echocardiography predicts mortality in critically ill patients with unexplained hypotension. J Am Coll Cardiol 1995;26:152–158. 154. Vignon P, Mentec H, Terre S, et al: Diagnostic accuracy and therapeutic impact of

transthoracic and transesophageal echocardiography in mechanically ventilated patients in the ICU. Chest 1994;106;1829–1834. 155. Dewan NA, Gayasaddin M, Angelillo VA, et al: Persistent hypoxemia due to

patent foramen ovale in a patient with adult respiratory distress syndrome. Chest 1986;89:611. 156. Bansal RC, Marsa RJ, Holland D, et al: Severe hypoxemia due to shunting

through a patent foramen ovale: A correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;15:499–504. 157. American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography: Practice guidelines for perioperative transesophageal echocardiography. Anesthesiology 1996;84:986–1006. 158. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767–773. 159. Park SH, Kim MA, Hyon MS: The advantages of on-line transesophageal

echocardiography guide during percutaneous balloon mitral valvuloplasty. J Am Soc Echocardiogr 2000;13:26–34. 160. Pytlewski G, Georgeson S, Burke J, et al: Endomyocardial biopsy under

transesophageal echocardiographic guidance can be safely performed in the critically ill cardiac transplant recipient. Am J Cardiol 1994;73:1019–1020. 161. Kantoch MJ, Frost GF, Robertson MA: Use of transesophageal echocardiography

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in radiofrequency catheter ablation in children and adolescents. Can J Cardiol 1998;14:519–523. 162. Tumbarello R, Sanna A, Cardu G, et al: Usefulness of transesophageal

echocardiography in the pediatric catheterization laboratory. Am J Cardiol 1993;71:1321–1325. 163. van der Velde ME, Sanders SP, Keane JF, et al: Transesophageal

echocardiographic guidance of transcatheter ventricular septal defect closure. J Am Coll Cardiol 1994;23:1660–1665. 164. McElhinney DB, Burch GH, Kung GC, et al: Echocardiographic guidance for

transcatheter coil embolization of congenital coronary arterial fistulas in children. Pediatr Cardiol 2000;21:253–258. 165. Cheung YF, Leung MP, Lee J, et al: An evolving role of transesophageal

echocardiography for the monitoring of interventional catheterization in children. Clin Cardiol 1999;22:804–810. 166. Manning WJ, Silverman DI, Gordon SP, et al: Cardioversion from atrial

fibrillation without prolonged anticoagulation with use of transesophageal echocardiography to exclude the presence of atrial thrombi. N Engl J Med 1993;328:750–755. 167. Moreyra E, Finkelhor RS, Cebul RD: Limitations of transesophageal

echocardiography in the risk assessment of patients before nonanticoagulated cardioversion from atrial fibrillation and flutter: An analysis of pooled trials. Am Heart J 1995:129:71–75. 168. Greenfield SM, Webster GJ, Brar AS, et al: Assessment of residual gastric

volume and thirst in patients who drink before gastroscopy. Gut 1996;39:360–362. 169. Khandheria BK, Seward JB, Tajik AJ: Concise review for primary-care

physicians: Transesophageal echocardiography. Mayo Clin Proc 1994;69:856–863. 170. Grauer SE, Giraud GD: Toxic methemoglobinemia after topical anesthesia for

transesophageal echocardiography. J Am Soc Echocardiogr 1996;9:874–876.

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23

Chapter 2 - Monitoring Ventricular Function in the Operating Room Impact on Clinical Outcome Donald C. Oxorn MD

Since being introduced into anesthetic practice in the late 1980s, transesophageal echocardiography (TEE) for intraoperative monitoring during cardiac surgery has gained wide acceptance. In 1995, Poterack[1] reported a national survey of anesthesia residency program directors in which 91% reported its use. TEE is relatively noninvasive, can be used in the vast majority of patients, and does not interfere physically with most surgical procedures. In some centers, TEE is used routinely for all cases involving cardiopulmonary bypass, whereas it is used more selectively at others. The usefulness of TEE during noncardiac surgery has been less thoroughly investigated, although if one extrapolates from the experience with hemodynamically unstable intensive care unit patients,[2] its utility in the differential diagnosis of intraoperative hemodynamic instability would appear intuitive. In this chapter, after I offer a general approach to and a personal philosophy on intraoperative TEE, the focus will be on the assessment of cardiac

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function in the setting of both cardiac and noncardiac surgery. In addition, the impact intraoperative TEE has had on the quality of perioperative care is discussed. Intraoperative assessment of valvular function, chamber size, masses, and great vessels are covered in other sections of the book.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

An Approach to Intraoperative Transesophageal Echocardiography Intraoperative TEE has become inextricably linked with cardiac anesthesiology. Over the past decade, guidelines for physician training in TEE have been directed primarily at cardiologists[3] [4] [5] and have stressed a background in transthoracic echocardiography, the acquisition of both cognitive and technical skills, and an ongoing program of maintenance of competence (see Chapter 42) . What is the standard that anesthesiologists should hold themselves up to? No written standard exists, although there are several distinct levels of expertise. Some individuals have taken advanced training that has included the performance and interpretation of surface studies under the tutelage of cardiologists and sonographers; others have studied TEE in the operating room during cardiac anesthesiology fellowships or "on the job"; and many have taught themselves by observation in the operating room, attendance at educational symposia, and the study of text and videotape. The educational program for intraoperative TEE at the Cleveland Clinic is a joint effort between cardiac anesthesiologists and cardiologists and is designed to train individuals to the highest level.[6] There are now two examinations of special competence under the auspices of the National Board of Echocardiography. The curriculum for the intraoperative examination focuses primarily on TEE, whereas the curriculum for the examination in general echocardiography emphasizes a broad knowledge of most aspects of echocardiography, both transthoracic and transesophageal. I believe that anesthesiologists who wish to practice intraoperative TEE should adhere to several tenets. Firstly, although attendance at lectures and reviewing written matter is important, didactic material should not

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replace direct interaction with knowledgeable colleagues. My personal experience suggests that beginning with transthoracic echocardiography is an invaluable first step. Secondly, it must be recognized that there will be different comfort levels among practitioners, and consultation with more skilled colleagues, be they anesthesiologists or cardiologists, should be encouraged. Even if intraoperative TEE is used solely as a monitor of ventricular function, it behooves the practitioner to perform a complete examination and to recognize that unexpected pathologic lesions, when present, may necessitate consultation. And lastly, all practitioners who are involved with TEE would serve themselves and their institutions by striving to pass one of the examinations of special competence. A working group of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists developed guidelines for performing a comprehensive intraoperative TEE examination.[7] Their recommendations are summarized in Figure 2-1 (Figure Not Available) . It is the committee's contention that if the practitioner performs a careful and systematized examination every time the probe is inserted, the chance of missing important findings is minimized, and the potential for teaching is enhanced. Figure 2-1 (Figure Not Available) Twenty cross-sectional views composing the recommended comprehensive transesophageal echocardiography examination. The icon adjacent to each view indicates the approximate multiplane angle. ME, midesophageal; LAX, long axis; TG, transgastric; SAX, short axis; AV, aortic valve; RV, right ventricle; asc, ascending; desc, descending; UE, upper esophageal. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870.)

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Intraoperative Ventricular Function Left Ventricular Filling In the operating room, rapidity is needed in the assessment of preload during periods of hemodynamic instability. Since the introduction of the pulmonary artery catheter in the 1970s, measurement of pulmonary capillary wedge pressure as a surrogate of left ventricular end diastolic volume has been the intraoperative practice standard; however, it is recognized that especially in situations of decreased ventricular compliance, the pulmonary capillary wedge pressure is an inaccurate estimate of preload.[8] TEE has the potential to refine this measurement by allowing Doppler estimation of left atrial pressure, two-dimensional measurement of left ventricular cross-sectional area, and calculation of left ventricular volume. Left Atrial Pressure

Left atrial pressure can be estimated with Doppler TEE by several methods. If mitral regurgitation is present, 25

measurement of the peak velocity of the regurgitant jet and application of the modified Bernoulli equation allows calculation of the left ventriculoatrial pressure gradient; subtraction of this number from the peak systolic blood pressure yields left atrial pressure[9] (Fig. 2-2) . Certain mitral inflow and pulmonary venous variables also correlate with left atrial pressure; Kuecherer et al[10] found that in patients undergoing cardiovascular surgery, changes in the systolic fraction of the pulmonary venous tracing correlated inversely and strongly with pulmonary capillary wedge pressure, and they theorized that this related to decreased atrial compliance. Nomura et al[11] found that in patients with ejection fractions

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less than 35%, the deceleration time of the early velocity of mitral inflow correlated with pulmonary capillary wedge pressure, and that a deceleration time greater than 150 msec was strongly predictive of a pulmonary capillary wedge pressure of less than 10 mm Hg. There are a number of caveats related to the intraoperative estimation of left atrial pressure with TEE. Patients with a rhythm other than sinus or with valvular regurgitation were excluded in most studies; these are the very patients in whom preload estimates are often crucial. In suitable patients, correlations but not absolute values of left atrial pressure are usually yielded. Use of the mitral regurgitation jet to calculate left atrial pressure dictates that mitral regurgitation must be present. And finally, an estimate of left atrial pressure, whether obtained by Doppler echocardiography or by pulmonary artery catheter, may still yield inaccurate estimates of preload in patients with decreased ventricular compliance. End-Diastolic Area and End-Systolic Area

A number of authors have examined the intraoperative relationship between end-diastolic and end-systolic area Figure 2-2 Measuring the peak velocity (V) of the mitral regurgitation (MR) jet and applying the modified Bernoulli equation yields a pressure gradient (PG) between the left atrium and ventricle of 56 mm Hg. Subtracting this value from the systolic arterial pressure of 86 mm Hg gives a left atrial pressure (LAP) of 30 mm Hg. BP, blood pressure.

measured at the transgastric midpapillary level and cardiac volume status. Cheung et al[12] performed an elegant study examining the effect of graded hypovolemia produced by autologous blood collection on hemodynamic and TEE-derived indices of left ventricular preload in patients undergoing coronary artery bypass surgery. Patients with valvular insufficiency, rhythms other than sinus, and overt congestive heart failure were excluded. Patients were stratified on the basis of resting left ventricular function. Enddiastolic area, end-systolic area, pulmonary capillary wedge pressure, and measures of end-diastolic and end-systolic wall stress decreased linearly as blood volume was reduced from 0 to 15% in all patients; however, in patients with impaired left ventricular function, only the TEE-derived indices maintained linearity (Fig. 2-3) (Figure Not Available) . Other studies have also demonstrated that single plane areas, although not

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predictive of absolute left ventricular volumes,[13] [14] can generally be used to monitor for a trend toward increased or decreased volume.[15] [16] [17] It must also be remembered that the presence of a small end-diastolic area or end-systolic area does not always reflect decreased intravascular volume. Small left ventricular volumes can be seen with restrictions to filling, as in pericardial disease, or decreased right heart function, as in right ventricular infarction or large pulmonary embolus[18] (Fig. 2-4) . Patients presenting for cardiac surgery often have preexisting impairment of diastolic function. De Hert et al[19] obtained transmitral flow signals with TEE and high-fidelity recordings of left ventricular pressure in patients anesthetized for coronary bypass. A subset of patients was identified in whom leg elevation resulted in a decreased dP/dt; those same patients developed a restrictive pattern on mitral inflow. Diastolic function is worsened to a variable degree following cardiopulmonary bypass.[20] This explains the frequent inadequacy of left ventricular filling despite seemingly adequate filling pressures.

26

The presence of end-systolic obliteration of the left ventricular cavity, although usually associated with hypovolemia (Fig. 2-5) , may also be associated with increased inotropy, or redistribution of blood out of the thoracic cavity.[21] Left Ventricular Volumes

In an in vitro study using silicone rubber models of the left ventricle, the calculation of left ventricular volumes using multiplane TEE and the disk summation method[22] was found to be highly accurate.[23] However, problems related to the moving heart, exclusion of akinetic segments of the left ventricle, and difficulty in getting a true long-axis view of the left ventricle have led to disappointing Figure 2-3 (Figure Not Available) End-diastolic area (EDA) and end-systolic area (ESA) in response to graded hypovolemia yielded estimated blood volume (EBV) deficits of 0 to 15%. Patients had either normal left ventricular (LV) function or reduced LV function. Control patients were not subjected to hypovolemia. (From Cheung AT, Savino JS, Weiss SJ, et al: Anesthesiology 1994;81:376–387.)

Figure 2-4 Transgastric image of a transesophageal echocardiography

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scan obtained in a patient who had suffered massive fat embolism. Increased pulmonary vascular resistance and subsequent right ventricular (RV) dilation led to impaired left ventricular (LV) filling.

results when used in the perioperative setting.[14] [24] Technologic advances such as three-dimensional TEE,[25] harmonic imaging,[26] and automated border detection may lead to improved intraoperative accuracy. In summary, the assessment of preload with intraoperative TEE is in most cases a semiquantitative estimate based on visual inspection of enddiastolic and end-systolic areas and on temporal comparison with the use of videotape or stored cine loops. Confounding conditions such as right ventricular failure or the administration of inotropic agents must be considered. Global Systolic Function Cardiac Output

Ventricular filling, contractility, wall stress, and heart rate all influence cardiac output. Thus, cardiac output is the measurement most often used in anesthetic and critical care practice as a guide to therapeutic manipulations of cardiac function. Despite its limitations,[27] [28] thermodilution cardiac output measurement has been considered the "gold standard" since being popularized in the early 1970s. Doppler transesophageal echocardiography has the potential to be used in the intraoperative setting for the continuous measurement of cardiac output. These methods utilize the concept that the cross-sectional area of a conduit within the cardiovascular system multiplied by the Doppler-derived timevelocity integral yields the stroke volume through that conduit. When the result is multiplied by heart rate, the product is cardiac output. Several important assumptions are inherent to this approach. Valid area formulas must be applicable to the anatomic site being analyzed. The velocity profile across the valve must be flat and devoid of skew.[29] [30] Whichever anatomic area is chosen, the ability to consistently obtain the image and to interrogate parallel to flow is mandatory. Pulmonary Artery.

With the probe at 0 degrees and retroflexed, the main pulmonary artery and pulmonic valve can be imaged at the base of the heart (Fig. 2-6) . This

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Figure 2-5 Transesophageal echocardiogram from a hypovolemic patient. During systole, the posteromedial and anterolateral papillary muscles touch. LV, left ventricle; RV, right ventricle.

Figure 2-6 Imaging at the base of the heart of the main pulmonary artery (PA) and its branches. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; PV, pulmonary valve; Vmax, maximum velocity.

28

site has been examined with pulsed wave Doppler,[30] [31] [32] and in a study by Gorcsan et al,[33] using both pulsed wave and continuous wave methodologies, pulmonary artery diameter was measured just distal to the pulmonic valve. Interobserver variability was low in all studies, and correlation with thermodilution was strong in all but the study by Muhiudeen et al,[31] in which patients with inaccurate thermodilution measurements may have been included. The major limitation with using the pulmonary artery is the inability to obtain an adequate two-dimensional image for diameter measurement in up to 25% of patients. Right Ventricular Outflow Tract.

With the probe turned rightward and flexed, the right ventricular outflow tract is imaged from the stomach between 0 and 120 degrees (Fig. 2-7) . Imaging frequency must usually be reduced to ensure optimal penetration. Maslow et al[34] found excellent correlation between cardiac output calculated with pulsed wave Doppler and thermodilution. Patients with pulmonary hypertension, significant tricuspid regurgitation, and non-sinus rhythms were excluded. Again, in a significant percentage (16%) of patients, the two-dimensional image was not suitable. Left Ventricular Outflow Tract.

With the probe in the stomach, turned leftward, in the flexed position, and at low imaging frequency, the aortic valve and left ventricular outflow tract

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can usually be imaged between 0 and 140 degrees (Fig. 2-8) (Figure Not Available) . Imaging from the stomach allows parallel pulsed Doppler interrogation of the left ventricular outflow tract, and its diameter, obtained from either the stomach or the midesophageal 120-degree view, allows calculation of the cross-sectional area and cardiac output (Fig. 2-9) . Strong correlation with thermodilution and low interobserver variability have been described.[35] [36] To avoid contamination of the Doppler signal by the region of flow acceleration adjacent to the aortic Figure 2-7 Pulsed wave (PW) Doppler measurement from the right ventricular outflow tract (RVOT) (color plate). RV, right ventricle.

valve orifice, the sample volume must be placed precisely in the left ventricular outflow tract. Aortic Valve.

Using the transgastric view described for left ventricular outflow tract, several investigators have studied the combination of continuous wave Doppler positioned through the left ventricular outflow tract and aortic valve and cross-sectional area of the aortic valve using the triangle method (Fig. 2-10) .[37] [38] In brief, the triangular shape of the aortic valve orifice at mid-systole is assumed to represent the time averaged value for the aortic valve area. Strong correlation with thermodilution and low interobserver variability were again obtained (Fig. 2-11) . As continuous wave Doppler is used, it is important to confirm that the maximal peak velocity is occurring at the aortic valve. The triangle method is limited to patients with unrestricted aortic valve opening. Mitral Valve.

Using the mitral valve for calculation of cardiac output has the advantages of consistent imaging and parallel Doppler alignment. However, the saddle shape of the mitral annulus makes the area measurement unpredictable, and the cross-sectional velocity skew[29] is of concern when using pulsed wave Doppler. Practical Considerations.

For intraoperative transesophageal Doppler calculation of cardiac output, the left ventricular outflow tract method is the most reproducible. Adjustments in the degree of probe flexion and imaging angle should be

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made to ensure that the aortic valve and ascending aorta are clearly visualized and that the Doppler intercept angle is small (see Fig. 2-9) . Several measurements should be made and averaged, this being especially important when dealing with rhythms other than sinus. In practical terms, Doppler measurement of cardiac output is used when a pulmonary artery catheter is not in place, or when conditions such as severe tricuspid regurgitation render thermodilution inaccurate. There is a need for 29

Figure 2-8 (Figure Not Available) Transesophageal echocardiography imaging from the stomach allows parallel alignment with the ascending aorta. (From Perrino AC Jr., Harris SN, Luther MA: Anesthesiology 1998;89:350–357.) Figure 2-9 Transgastric imaging of the left ventricular outflow tract (LVOT). The ascending aorta is well visualized, and the Doppler intercept angle is small. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; Vmax, maximum velocity.

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Figure 2-10 The triangle method of aortic valve area measurement. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796–805.)

further validation of this approach in patients with a spectrum of cardiovascular diseases. Ejection Fraction and Stroke Volume

Although it is somewhat load dependent and therefore not a pure index of "left ventricular function,"[39] ejection fraction is often assumed to reflect ventricular contractility. During intraoperative TEE, the fractional area of change measured at the transgastric midpapillary level is often used interchangeably with ejection fraction, although gauging volume in a potentially asymmetric Figure 2-11 Regression analysis: thermodilution cardiac output (TCO)

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and Doppler cardiac output (DCO) using the aortic valve triangle method. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796– 805.)

chamber based on a measure of area has obvious limitations.[40] [41] A number of studies report the relationship between TEE-derived fractional area of change and radionuclide-derived ejection fraction. Clements et al[42] examined the relationship in 12 patients having abdominal aortic aneurysm surgery. There was excellent correlation in patients with both normal and abnormal left ventricular function. In patients with ventricular dyssynergy, fractional area of change led to a slight overestimate of ejection fraction. Urbanowicz et al[13] found strong correlation in 10 patients following coronary artery bypass grafting. In a series of 15 patients following coronary artery bypass grafting, Ryan et al[14] measured TEE ejection fraction using volumes calculated from the modified Simpson's and arealength methods[43] in addition to TEE-derived fractional area of change and radionuclide-derived ejection fraction. Unlike previous studies, variability was calculated and found to be small and not significantly different between the three measurement techniques. Not surprisingly, the TEE volumetric results were more representative of radionuclide ejection fraction than fractional area of change. Smith et al[24] also found that ejection fraction based on TEE volumetric methods were comparable to those obtained with angiography. In an attempt to develop online methods of intraoperative functional assessment, the technique of automated border detection has been used (see Chapter 7) . Automated border detection is based on the principle of acoustic quantification of ultrasonic back scatter signals to detect the bloodtissue interface and thereby define the endocardial edge.[44] Measurements correlate closely to those obtained by manual tracing of the endocardial border. [45] [46] [47] Gorcsan et al[17] examined stroke area, defined as the difference between end-systolic area and end-diastolic area measured at the midpapillary level, and compared the results to stroke volume measured in the ascending aorta by an electromagnetic flow probe in nine patients undergoing coronary artery bypass. Preoperative left ventricular function was largely preserved. Measurements were made before and after cardiopulmonary bypass. There was a strong correlation between the measurements at all periods of the study. Katz et al[48] compared stroke volume as measured by thermodilution to stroke volume obtained with automated border detection determination of end-systolic and end-diastolic areas and volumetric formulas (Fig. 2-12) ; these latter measurements were

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made at the two-chamber and four-chamber midesophageal views. There was a close correlation between stroke volumes obtained by the two methods, but whereas the two-chamber view led to an average underestimate of 0.4 L, the four-chamber view led to an average underestimate of 1.9 L. In a similar study, Greim et al[49] used the twochamber view alone. Directional changes in stroke volume between thermodilution and automated border detection again correlated closely; however, the automated border detection technique significantly underestimated stroke volume. Ejection fraction has been estimated using automated border detection derived measurements of fractional area of change at the midpapillary level and compared to radionuclide-derived ejection fraction.[45] [46] [47] Although the directionality of change was significantly 31

Figure 2-12 An example of transesophageal echocardiography automated border detection from the four-chamber view with ventricular volume estimated on line by the area length method. (From Katz WE, Gasior TA, Reddy SC, et al: Am Heart J 1994;128:389–396.)

correlated, fractional area of change derived by automated border detection consistently overestimated radionuclide-derived ejection fraction. It would appear that fractional area of change more closely estimates ejection fraction in patients with normal ventricular function. The use of TEE-derived volumetric data to estimate ejection fraction is more accurate, but the cumbersome calculations involved do not lend themselves to rapid intraoperative derivation. The use of automated border detection algorithms and programmed volume calculations may prove superior but are largely untested in clinical practice. At present, the intraoperative assessment of ejection fraction is impractical, and stroke volume measurement is best accomplished with either Doppler or thermodilution methodology. Contractility

The end-systolic pressure-volume relationship and resultant end-systolic elastance defines contractility in a load-independent fashion[50] and would therefore be of potential use in the estimation of intraoperative left ventricle contractility and in the quantification of changes resulting from manipulations such as cardiopulmonary bypass.

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A number of surrogates of this relationship have been described to facilitate the practical acquisition of this information in an operating room setting. The substitution of femoral arterial pressure for left ventricular end-systolic pressure,[51] end-systolic area for end-systolic volume,[20] [52] [53] and endsystolic wall stress for end-systolic pressure[53] have been made. Although these substituted measurements are not construed as replacements for traditional measures of pressure and volume, their directional change suggests that in cardiac surgical patients undergoing cardiopulmonary bypass, they may be used as an alternative way of assessing loadindependent left ventricular function. The changes in contractility as a result of cardiopulmonary bypass[20] [54] and the administration of anesthetic agents[52] appear better assessed with estimates of end-systolic elastance than with more traditional indices of ventricular performance such as fractional area of change. Figure 2-13 illustrates the decrease in elastance (Ees) and increased chamber stiffness (Kc) that occur following cardiopulmonary bypass, and the mitigating effect of volume loading prior to bypass termination. At present, the methods for data analysis are prohibitively complex.[55] [56] Right Ventricular Function

In the setting of cardiopulmonary bypass, the evaluation of right ventricular function is important. Right ventricular dysfunction often occurs secondary to the inadequate delivery of cardioplegia[57] and to the embolization of intracardiac air down the right coronary artery following separation from cardiopulmonary bypass. The triangular shape of the right ventricle makes its global function hard to quantitate with TEE, and the abnormal septal motion often seen following cardiopulmonary bypass[58] compounds this difficulty. Rafferty et al[59] measured planimetered areas and major and minor axes in both long-axis and short-axis images of the right ventricle with TEE, before and after cardiopulmonary bypass. Unfortunately, the echo measurements, obtained offline, were not compared in a meaningful way to results obtained by thermodilution. Semiquantitative analysis of right ventricular function with TEE has also been attempted with the analysis of hepatic venous flow.[60] Many factors other than right ventricular systolic function, however, affect hepatic venous flow. In patients with diverse causes of right ventricular dysfunction, Vignon et al[61] demonstrated the ability to 32

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Figure 2-13 Effect of cardiopulmonary bypass (CPB) on elastance (Ees) and chamber stiffness (Kc) of the left ventricle. Times of measurement were before the start of CPB (baseline); immediately after separation from CPB (time 0); and 5 minutes (time 5), 10 minutes (time 10), and 15 minutes (time 15) later. In protocol 1, preload was optimized just before the start of the separation procedure from CPB. In protocol 2, preload was optimized 10 minutes before the anticipated separation time. Data are shown as mean ± SEM. In protocol 1, ventricular function after separation from CPB was impaired, with a decrease in Ees and an increase in Kc, and a progressive improvement of ventricular function within the first 10 minutes after separation from CPB. These findings were not seen in protocol 2, in which ventricular function remained unchanged and comparable to baseline values. *Difference between both groups is statistically significant at P < 0.01. (From De Hert SG, Rodrigus IE, Haenen LR, et al: Anesthesiology 1996;85:1063–1075.)

quantitate right ventricular function with color kinesis and surface echocardiography. This method of examining right ventricular function has not been evaluated in an intraoperative setting with TEE. At the present time, TEE assessment of intraoperative right ventricular function is best accomplished by visual inspection and semiquantitative assessment in both the transgastric and the four-chamber views. Excellent transgastric views of all three leaflets of the tricuspid valve and the entire free wall of the right ventricle are best obtained by scanning at approximately 40 degrees (Fig. 2-14) . Regional Wall Motion The suggestion of a link between perioperative myocardial ischemia and cardiac morbidity[62] [63] has led to an intensive search for accurate methods of its intraoperative detection (Fig. 2-15) (Figure Not Available) . Visual inspection of ST segment changes has been the foundation upon which the newer technologies of automated ST analysis and TEE detection of regional wall motion abnormalities have been added. There are several points on which to judge the merits of TEE: Applicability, accuracy, reproducibility, cost, expertise required for interpretation, and prognostic importance. Segmental analysis is most frequently undertaken using the 16-segment model first proposed by Schiller et al[64] and later modified for TEE by Shanewise et al[7] (Fig. 2-16) (Figure Not Available) . Excellent inter- and intraobserver variability has been documented when six segments at the midpapillary level were analyzed offline by an anesthesiologist trained in

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TEE and an echocardiographer.[65] The recognition that coronary occlusion leads to the immediate development of regional wall motion abnormalities[66] and their frequent regression following revascularization[67] has prompted investigators to examine the usefulness of intraoperative TEE as a monitor of ischemia. The paucity of contraindications to TEE means that it can be used in most patients undergoing general anesthesia. The midpapillary view is generally easy to obtain and demonstrates areas of myocardium subtended by the three major coronary arteries. Interpretation is rarely confounded by rhythm disturbances, as is the case for automated ST analysis. TEE cannot be used, however, in patients receiving regional anesthesia, and, because the probe is not inserted until after anesthetic induction, it cannot detect changes during this vulnerable period. Assessment of the accuracy of TEE in the detection of myocardial ischemia has been limited somewhat by the lack of a reliable reference standard. Smith et al[68] found that in patients at high risk of myocardial ischemia who were analyzed offline, wall motion changes could be detected Figure 2-14 Transgastric image of the right ventricular (RV) free wall, septum, and the leaflets of the tricuspid valve.

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Figure 2-15 (Figure Not Available) Causes of ischemic changes on intraoperative monitors (color plate). (From Fleisher LA: Anesthesiology 2000;92:1183–1188.)

more quickly and commonly than ST segment changes. Conflicting studies[69] [70] regarding the prognostic importance of regional wall motion abnormalities were subsequently published. In a study by London et al,[69] 156 patients undergoing noncardiac surgery who were at high risk for coronary artery disease were studied. Specific clinical, electrocardiographic, or hemodynamic events prompted analysis of stored images. The number of new wall motion abnormalities detected was low, and discordance with electrocardiographic findings was significant (Table 2-1) . The number of postoperative cardiac complications was low. In the

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study by Leung et al,[70] patients undergoing coronary artery bypass were examined with electrocardiography and TEE. Although prebypass ischemia was rare, postbypass ischemia was more common and postoperative cardiovascular complications were associated more closely with TEE findings than with electrocardiography alone. It is now accepted that regional wall motion abnormalities, although often the result of myocardial ischemia, may be due to hypovolemia, tethering of nonischemic myocardium, and myocardial stunning after cardiopulmonary bypass.[71] [72] Offline analysis has been employed in most of the large-scale studies involving comparison of TEE with other methods of ischemia detection, but extrapolation to the accuracy of real-time TEE analysis should not be assumed. Regional wall motion abnormalities that subtend the anatomic distribution of coronary TABLE 2-1 -- Comparison of Transesophageal Echocardiography (TEE) and Intraoperative Electrocardiography (ECG) Monitoring for Myocardial Ischemia * TEE + TEE ECG + 8 (1 MI) 11 ECG 24 (2 MI, 1 UA) MI, myocardial infarction; UA, unstable angina. From London MJ, Tuban JF, Wong MG, et al: Anesthesiology 1990;73 (4):644. * P < 0.05.

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Figure 2-16 (Figure Not Available) A 16-segment model of the left ventricle. A, Fourchamber views show the three septal and three lateral segments. B, Two-chamber views show the three anterior and three inferior segments. C, Long-axis views show the two anteroseptal and two posterior segments. D, Middle short-axis views show all six segments at the midpapillary level. E, Basal short-axis views show all six segments at the basal level. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870–884.)

artery flow are more often a result of ischemia than those that do not.

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Comunale et al[73] also documented the poor concordance between the TEE and electrocardiography and attributed this finding to the lack of standard definitions of significant regional wall motion abnormalities and ischemic ST changes, the exclusion of longitudinal TEE views, and the use of different models of segment nomenclature. The role of intraoperative monitoring of myocardial ischemia with TEE remains unclear. Intraoperative TEE monitoring is better suited to patients undergoing cardiac as opposed to noncardiac surgery and to those patients in whom more traditional methods of ischemia are deemed inadequate. The ability to monitor additional tomographic planes,[74] [75] the use of cine loops for comparison, and the advent of new technologies such as automated border detection and Doppler tissue imaging should improve accuracy. Regional wall motion abnormalities precede electrocardiographic changes, [76] and, once ischemia is diagnosed, TEE can be used to directly monitor the effects of intervention. Personnel with expertise in the online assessment of wall motion abnormalities are needed, however. Lastly, studies examining the outcomes of patients monitored for myocardial ischemia with TEE are needed. Intraoperative Assessment of Coronary Reserve Dobutamine stress echocardiography is a well-established technique for diagnosing coronary artery disease and predicting the improvement of dysfunctional myocardium postoperatively (see Chapter 14) .[77] [78] The ability to predict the reversibility of left ventricular dysfunction with the use of intraoperative low-dose dobutamine TEE was examined by Aronson et al[79] in the setting of coronary artery bypass grafting. The odds ratios for early and late improvement in myocardial function were 20.7 and 34.6 times higher if preoperative low-dose dobutamine produced improved function than if it did not. The instances when this intraoperative strategy might supplant the normal preoperative assessment of myocardial viability by transthoracic dobutamine stress echocardiography[78] or low-dose dobutamine technetium-99m sestamibi scintigraphy[80] have yet to be determined.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Use of Transesophageal Echocardiography to Monitor Intraoperative Cardiac Function in Specific Clinical Entities The use of TEE has improved our ability to intelligently manage postcardiopulmonary bypass instability. It has allowed us to understand the intraoperative changes that occur during some of the newer techniques in coronary revascularization and can guide us in placement of numerous intracardiac and intravascular devices. Its use in monitoring cardiac function during noncardiac surgery is most advantageous in the diagnosis of sudden and unexplained hemodynamic instability. Separation from Cardiopulmonary Bypass At the time of separation of the patient from cardiopulmonary bypass, the use of TEE may guide the anesthesiologist in the use of pharmacologic and nonpharmacologic therapies and can maximize the likelihood of a smooth transition. Intracardiac Air

Left-sided intracardiac air is ubiquitous following procedures in which leftsided chambers have been open to atmosphere and is identified by its characteristic "firefly" appearance. Air is often seen entering the left atrium from the pulmonary veins or enmeshed in the mitral subvalvular apparatus (Fig. 2-17) . Echocardiographic inspection is carried out in the fourchamber and transgastric long-axis views. Careful evacuation by the surgeon is important and involves suctioning on the aortic root vent or needle aspiration of the left ventricular apex to evacuate trapped pockets. As well as guiding evacuation, TEE is 35

Figure 2-17 Four-chamber midesophageal view. As the patient is being

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separated from cardiopulmonary bypass (CPB), a pocket of air enmeshed in the left ventricular subvalvular apparatus is noted (asterisk), with numerous bubbles emanating from it. LA, left atrium; LV, left ventricle.

useful in diagnosing the consequences of embolization through the right coronary ostium, which results in ventricular dysfunction in a right coronary distribution. Cardiac Output

There are a number of potential causes of low cardiac output immediately following cardiopulmonary bypass: perioperative infarction, coronary air emboli, metabolic abnormalities, hypovolemia, left ventricular outflow tract obstruction, and inadequate myocardial protection. It seems intuitive that the yield of TEE when it is used during hemodynamic instability during and after cardiac surgery would be high. Two published series[81] [82] have demonstrated the myriad diagnoses that have been made TABLE 2-2 -- Relevant Intraoperative Transesophageal Echocardiograph Findings Categorized by Indication Indication, n

Finding Severe left ventricular dysfunction ± regional wall motion abnormality Aortic dissection ± aortic regurgitation Significant mitral regurgitation Intracardiac/great vessel shunt Hyperdynamic left ventricular function

HEMODYNAMIC SURGICAL INSTABILITY PLANNING TRAUMA HYPOXEMIA 15 2

1

13

4

2

1

1

2

TOTA NO. O PATIE

2 1

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Severe right 2 1 ventricular dysfunction Extracardiac clot 2 Significant aortic 2 regurgitation Significant 1 tricuspid regurgitation Pericardial 1 tamponade No relevant 5 1 4 3 findings From Brandt RR, Oh JK, Abel MD, et al: J Am Soc Echocardiogr 1998;1 (10):972. and the ability to intervene on many (Table 2-2) . No attempt was made to compare TEE with other diagnostic modalities, although the speed with which information is made available appears hard to supersede. The use of myocardial contrast echocardiography has improved our understanding of the distribution of cardioplegia delivered by both anterograde and retrograde routes. The ability to predict the adequacy of delivery based on knowledge of coronary anatomy and the presence of angiographically demonstrated collateral flow is marginal at best.[83] It is also clear that retrograde cardioplegia does not reliably perfuse the right ventricular free wall,[57] [84] and, in some centers, this observation has led to a strategy of early cardioplegia administration down a vein graft to the right coronary artery.[85] In the future, the use of myocardial contrast echocardiography may help to 36

Figure 2-18 A, Transesophageal echocardiography to investigate hypoxia revealed an expanding ascending aortic aneurysm with main pulmonary artery (PA) compression. B, Normal image for comparison. LA, left atrium; SVC, superior vena cava.

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differentiate postbypass stunning, which would be treated with cardiopulmonary support, from graft obstruction, which would be treated with surgical correction.[86] [87] Off-Pump Coronary Bypass Surgery The off-pump bypass surgical approach to coronary revascularization involves bypassing coronary arteries without cardiopulmonary bypass, otherwise known as the "beating heart" operation. TEE can detect regional wall motion abnormalities during intermittent coronary occlusion and cardiac lifting, which, if persistent, may necessitate the institution of cardiopulmonary bypass. The use of color kinesis to better define regional wall motion abnormalities intraoperatively has been described [88] but is limited somewhat by cardiac translocation during surgical manipulation. Cardiac Function in Noncardiac Surgery The use of TEE to monitor cardiac function in noncardiac surgery has been described largely in anecdotal form. In most of the case reports, unexplained hypotension prompted the use of TEE, and subsequent diagnoses have included massive pulmonary embolism,[89] [90] intracardiac tumor extension,[91] retroperitoneal hemorrhage,[92] cardiac tamponade,[93] main pulmonary artery obstruction by an expanding aortic aneurysm[94] (Fig. 2-18) , traumatic cardiac injury,[95] [96] [97] ventilator-induced systemic air embolism,[98] [99] and a case of venous air embolism during pelvic surgery, which resulted in pulseless electrical activity until open cardiac aspiration was undertaken (Fig. 2-19) . Positioning of Intravascular Devices Intraoperative TEE can be used to guide the positioning of a number of intravascular devices: Central Venous Pressure Air Aspiration Catheters.

These are often used during sitting craniotomies to aspirate air that has gained access to the venous circulation. Correct positioning is at the right atrial-superior vena caval junction, and imaging is best in the midesophagus with rightward rotation and a transducer angle of approximately 90 degrees (Fig. 2-20) . Intra-aortic Balloon Pump.

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The benefits of intra-aortic balloon pump have been demonstrated with TEE and include improved left ventricular function and decreased wall stress. [100] [101] The balloon pump is best imaged in the descending aorta in a vertical plane. Correct positioning is at the inferior border of the transverse aortic arch.[102] Once the tip of the balloon is visualized at a transducer angle of approximately 90 degrees, the probe marking at the teeth is noted. The probe is slowly withdrawn until the left subclavian artery orifice is seen; the marking is again noted. The distance between the balloon and the subclavian orifice should be approximately 5 cm (Fig. 2-21) . Left Ventricular Assist Device.

As the left ventricular assist device withdraws blood from the left ventricle, left atrial pressure falls below right atrial pressure. It is important Figure 2-19 During pelvic surgery, massive amounts of air are seen entering the right atrium (RA) via the inferior vena cava (IVC).

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Figure 2-20 A catheter inserted from the arm is positioned at the junction of the right atrium (RA) and superior vena cava (SVC) to evacuate any air that gains access to the venous circulation during sitting craniotomy. LA, left atrium.

to determine whether a patent foramen ovale is present, as right-to-left shunting will invariably occur. The orifice of the ventricular apical cannula should be imaged in the four-chamber view, and the lack of obstruction by adjacent walls should be ascertained[103] (Fig. 2-22) . Right Ventricular Assist Device.

In positioning the right atrial drainage cannula, it is preferable to avoid impingement on the tricuspid valve (Fig. 2-23) . Minimally Invasive Cardiac Surgery.

Port access surgery

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Figure 2-21 Intra-aortic balloon pump (IABP) positioned in the descending thoracic aorta. The left subclavian artery is visualized and not encroached upon.

involves the performance of a variety of surgical procedures through small thoracic ports or very limited incisions. Cannulation for the purposes of cardiopulmonary bypass and cardioplegic arrest is achieved percutaneously. TEE is used to position the various endovascular catheters and to monitor their position during surgery[104] [105] (Fig. 2-24) (Figure Not Available) . Some surgeons prefer an upper sternotomy incision. Cannulation is then achieved directly, except for the retrograde cardioplegia cannula, 38

Figure 2-22 The drainage component of the left ventricular assist device (LVAD) is seen to freely enter the apical region of the left ventricle (LV). LA, left atrium.

which is inserted through blind right atrial puncture and maneuvered into the coronary sinus under TEE guidance[106] (Fig. 2-25) . Left Ventricular Vent.

A left ventricular vent is placed through the right upper pulmonary vein into the left atrium and advanced through the mitral valve into the left ventricle to drain excess ventricular volume on bypass (Fig. 2-26) . Transplant Surgery Transesophageal echocardiography can be used to assess the function of the donor heart prior to procurement and after separation from cardiopulmonary bypass, when Figure 2-23 (color plate.) The drainage component of the right ventricular assist device (RVAD) enters the right atrium (RA) through the appendage (left, arrow). The tip is seen in the right atrium and free of the tricuspid valve on TEE (right). PA, pulmonary artery. Figure 2-24 (Figure Not Available) The various endovascular cardiopulmonary

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bypass catheters for post-access surgery are depicted. (From Siegel LC, St. Goar FG, Stevens JH, et al.: Circulation 1997;96:562–568.)

the effects of the ischemic time may become evident. During lung transplantation, the use of TEE has been described in the evaluation of vascular anastomoses,[107] and a recent case report documented a diagnosis of post-transplant pulmonary venous obstruction.[108] Laparoscopic Surgery As laparoscopic surgery has grown in its application, so has the realization that the associated pneumoperitoneum 39

Figure 2-25 During minimally invasive cardiac surgery, the coronary sinus catheter is seen entering the right atrium (RA) and passing into the coronary sinus. LA, left atrium.

leads to increased left ventricular wall stress[109] and decreased fractional area of change.[110] Following release of the pneumoperitoneum, higher than baseline fractional area of change has been described.[110] These hemodynamic alterations have been attributed to the physical effect of increased intra-abdominal pressure and to the associated neurohumoral changes. TEE has also been used to monitor for intraoperative gas embolization.[111]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transesophageal Echocardiography as a Monitor of Intraoperative Ventricular Function: Impact on Perioperative Complications and Cost-Effectiveness Medical technology assessment has become an important step in the introduction and clinical use of increasingly sophisticated and costly methods of monitoring and diagnosis.[112] In anesthetic and critical care practice, no technology has engendered more controversy than the use of pulmonary artery catheterization, which has become an established monitor of cardiovascular function, despite the lack of significant outcome and costeffectiveness data.[113] [114] The use of TEE to monitor intraoperative ventricular function varies significantly between institutions[1] [115] and relates in part to the experience of the operator, the type of surgical procedure, and the cardiopulmonary reserve of the patient. For TEE to be deemed an effective mode of intraoperative monitoring, it must be shown to provide at least the same if not more information than currently accepted monitoring techniques, have a reasonable cost profile, involve acceptable risk, and alter outcome in a positive way. Kato et al[116] demonstrates the ability to diagnose and effectively manage intraoperative ischemia under TEE guidance, but, as is the case with many subsequent studies, their study falls short in not evaluating the effects of intraoperative TEE monitoring on patient outcome. Several studies have addressed the impact of intraoperative TEE monitoring of ventricular function during coronary bypass surgery. Bergquist et al[117] studied the concordance between real-time intraoperative TEE interpretation by five cardiac anesthesiologists and offline analysis by two blinded investigators in the assessment of left ventricular filling, ejection fraction area, and regional wall motion. Results obtained by the two methods were within 10% of each other 75% of the time with respect to ejection fraction and filling. The accuracy of regional assessment

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Figure 2-26 A left ventricular (LV) vent is seen passing into the left atrium (LA) via a right-sided pulmonary vein. MV, mitral valve.

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TABLE 2-3 -- Surgical Management Alterations During Coronary Artery Bypass Grafting Based on Transesophageal Echocardiographic Findings

Before CPB, n 2 NA NA 0 8

Before CPB After CPB After Total No. Separation, Separation, CC, of n n n Patients NA NA NA 2 NA 3 1 4 NA NA 2 2 0 0 1 1 2 3 1 12

Alteration Rush to CPB Return to CPB Reopen LVAD/ECMO Additional redo grafts IABP 4 3 2 0 9 CC, chest closure; CPB, cardiopulmonary bypass; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; NA, not applicable. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997;64(2):368. was variable: more accurate for normal than for abnormal wall motion and better in anesthesiologists with more advanced echocardiographic training. In the second part of the study,[118] TEE was found to be the most important factor in guiding hemodynamic interventions in 17% of cases examined. What is lacking is a clear demonstration that the TEE assessments were correct and that the same interventions would not have been undertaken if guided by more traditional monitors. Cost and outcome were not examined. Savage et al,[87] at the Cleveland Clinic, examined the use of intraoperative

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TEE monitoring in a group of high-risk patients undergoing coronary artery bypass grafting. As well as documenting numerous management changes related to TEE-derived information (Table 2-3) , they documented lower short-term morbidity and mortality rates as compared with a historical group of patients with similar severity scores[119] who were not monitored with TEE (Table 2-4) . An individual not part of the anesthetic or surgical team read the TEE scan; it is uncertain whether someone involved in direct patient management would have as readily garnered the information. In studies from Australia,[120] Europe,[121] Canada,[122] and India,[123] the realtime accrual of information with TEE was demonstrated to be of value in the management of hemodynamic perturbations and the planning of the surgical procedure in coronary bypass grafting as well as other cardiac surgical procedures Table 2-5 , Table 2-6 , and Table 2-7 ). No assessment of the effect of intraoperative TEE TABLE 2-4 -- Patient Outcomes with and without Intraoperative Transesophageal Echocardiography (TEE) Management without TEE 478 64.8 5.9 18 (3.8) 14 (3.5)

Variable Management with TEE Patients, n 82 Age, y 68.4 Severity score 6.1 Hospital deaths, n (%) 1 (1.2) Myocardial Infarction, n 1 (1.2) (%) Cardiac morbidity, n (%) 1 (1.2) 7 (1.5) ICU CNS morbidity, n (%) 3 (3.6) 18 (3.8) Hospital CNS morbidity, n 1 (1.2) 16 (3.3) (%) CNS, central nervous system; ICU, intensive care unit. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997; 64(2):368.

monitoring on patient outcome was made. These studies are summarized in Table 2-8 . The impact of monitoring of ventricular function during noncardiac surgery

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has not been studied as closely. In a retrospective review by Suriani et al, [124] the use of TEE was associated with some alterations in anesthetic and surgical management in a majority of cases. However, the indications for TEE were subjective, and neither the cost-effectiveness nor the effect on outcome was studied.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Has the burden of proof been met with respect to intraoperative TEE as a monitor of ventricular function? If one adopts the premise that rigorously designed, randomized, controlled clinical trials are society's benchmark,[125] TABLE 2-5 -- Impact of Routine Transesophageal Echocardiographic (TEE) Findings on Medical and Surgical Management: Coronary Artery Bypass Grafting After Cardiopulmonary Bypass (N = 120) Clinical Problem/TEE Finding (no. of patients) Consequence (no. of patients) Acute SWMA (8), acute Graft revision (3), papaverine (1), SWMA and medical therapy (5) moderate/severe mitral regurgitation (1) IABP not in optimal position (2) IABP not in descending aorta ST depression (II and V5)/no SWMA (3) Pulmonary

Impact E (3) * †

IABP advanced

I (6) V (2) ‡

IABP reinserted

V (1)

De-cannulation-good outcome

I (3)

Medical therapy for ischemia, not protamine reaction

I (1)

hypertension 3 minutes post protamine/

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widespread SWMA, moderate to severe mitral regurgitation E, essential; I, informative; IABP, intra-aortic balloon pump; SWMA, segmental wall motion abnormality; V, valuable. From Sutton DC, Kluger R: Anaesth Intensive Care 1998;26(3):287. * One patient also classified as valuable for IABP not in descending aorta. † One patient also classified as informative for ST depression without SWMA. ‡ Two patients also classified as informative in problems separating from CPB.

41

TABLE 2-6 -- Influence of Intraoperative Transesophageal Echocardiogra as the Driving Force on Interventions Compared with Other Monito Monitor Intervention, n (%) TEE ELECTROCARDIOGRAPHY Fluid bolus 275 0 (28) Anti-ischemic 207 114 (31) therapy (56) Vasopressor 56 3 (1) or inotrope (16) therapy Change in 4 0 anesthetic (2) depth Vasodilator 6 9 (6) therapy (4) Antiarrythmic 0 55 (89) therapy

ARTERIAL CATHETER 129 (13)

PULMONARY ARTERY OTH CATHETER 73 (7)

11 (3)

31 (8)

183 (51)

27 (7)

164 (78)

2 (1)

96 (68)

13 (9)

0

0

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Surgical 9 17 (33) 12 (23) 0 intervention (17) Miscellaneous 3 2 (6) 27 (75) 3 (8) (8) Total 560 200 (9) 622 (28) 149 (7) (25) From Kolev N, Brase R, Swanefelder J, et al: Anaesthesia 1998;53(8):76 *Indicates that the interventions were not based on information from the four monitors studied. More than half of these interventions were transfusion of blood for low hematocrit.

TABLE 2-7 -- Summary of Surgical Modifications Related to the Intraoperative Use of Transesophageal Echocardiography Modification Number Return on bypass for revision of coronary artery bypass graft 4 Modification of planned surgery: Valvular replacement cancelled 5 Valvular replacement or repair 11 Pleural drainage 3 Detection of air emboli before aortic unclamping 2 Surgical exploration for hemodynamic instability 7 Femoral artery bypass for aortic dissection 2 Others: Ventricular aneurysm resection 1 Aortoplasty 1 Cancellation of aortic dissection (diagnostic error) 1 Left ventricular assist device 1 Total 38 From Couture P, Denault AY, McKenty S, et al: Can J Anaesth 2000;47 (1):20.

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TABLE 2-8 -- Summary of Studies Examining the Alterations in Therapy During Cardiac Surgery with the Use of Intraoperative Transesophageal Echocardiography Altered Therapy, Study Population Surgery n/% 98/17% of all Bergquist n = 75, 584 C[118] Interventions revasc interventions et al Savage et n = 82 "High CSurgical change: [87] al risk" revasc 27/33% of patients Hemodynamic change: 42/51% of patients Sutton & n = 120 C16/13% of all patients Kluger revasc

Outcome Reported No Compared to historical controls

No

[120]

C-all 560/25% of all No Kolev et n = 224, [121] 2232 NC interventions al interventions Couture n = 851 C-all 125/15% of all No [122] et al patients Mishra et n = 5016 C-all 1146/23% of all No [123] al patients C-all, coronary and non-coronary cardiac surgery; C-revasc, coronary revascularizations; NC, noncardiac surgery.

42

then the jury is still out. The cost-effectiveness data that have been generated by studies of the use of TEE in congenital cardiac surgery,[126] preparation for elective cardioversion,[127] and determination of antibiotic treatment duration in endocarditis[128] have not yet demonstrated the benefits of monitoring of ventricular function in cardiac or noncardiac surgery. The data collected for studies are often reviewed offline, whereas clinical utility comes from online interpretation. Outcome data are scarce and sometimes conflicting. The "division of labor" in the operating room is also important, as too much attention to TEE may distract the anesthesiologist from other

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monitoring tasks.[129] Transesophageal echocardiography is an expensive undertaking and is not practically carried into the postoperative phase of patient management. Case studies and observational data cannot be dismissed, however. [130] [131] TEE has a unique ability to facilitate the rapid diagnosis of circulatory instability, and a number of observational studies show that information gained during intraoperative TEE frequently guides subsequent therapeutic maneuvers. In response, most fellowships in cardiac anesthesiology have incorporated instruction in the monitoring of ventricular function with intraoperative TEE. It must be emphasized that appropriate physician training and quality assurance[132] are crucial to the correct interpretation of data. Further technologic advancements such as color kinesis, automated border detection, and the use of loop storage for comparison should improve accuracy. Studies examining cost-effectiveness and outcome are needed.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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References 1. Poterack KA: Who uses transesophageal echocardiography in the operating room?

Anesth Analg 1995;80:454. 2. Poelaert JI, Trouerbach J, De Buyzere M, et al: Evaluation of transesophageal

echocardiography as a diagnostic and therapeutic aid in a critical care setting. Chest 1995;107:774. 3. Chan KL, Alvarez N, Cujec B, et al: Standards for adult echocardiography training.

Canadian Cardiovascular Society Committee. Can J Cardiol 1996;12:473. 4. Eisenberg MJ, Rice S, Schiller NB: Guidelines for physician training in advanced

cardiac procedures: The importance of case mix [editorial]. J Am Coll Cardiol 1994;23:1723. 5. Pearlman AS, Gardin JM, Martin RP, et al: Guidelines for physician training in

transesophageal echocardiography: Recommendations of the American Society of Echocardiography Committee for Physician Training in Echocardiography. J Am Soc Echocardiogr 1992;5:187. 6. Savage RM, Licina MG, Koch CG, et al: Educational program for intraoperative

transesophageal echocardiography. Anesth Analg 1995;81:399. 7. Shanewise JS, Cheung AT, Aronson S, et al: ASE/SCA guidelines for performing a

comprehensive intraoperative multiplane transesophageal echocardiography examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. Anesth Analg 1999;89:870. 8. Hoeft A, Schorn B, Weyland A, et al: Bedside assessment of intravascular volume

status in patients undergoing coronary bypass surgery. Anesthesiology 1994;81:76.

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Pagina 2 di 13

9. Gorcsan JD, Snow FR, Paulsen W, et al: Noninvasive estimation of left atrial

pressure in patients with congestive heart failure and mitral regurgitation by Doppler echocardiography. Am Heart J 1991;121(3 Pt 1):858. 10. Kuecherer HF, Muhiudeen IA, Kusumoto FM, et al: Estimation of mean left atrial

pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow. Circulation 1990;82:1127. 11. Nomura M, Hillel Z, Shih H, et al: The association between Doppler transmitral

flow variables measured by transesophageal echocardiography and pulmonary capillary wedge pressure. Anesth Analg 1997;84:491. 12. Cheung AT, Savino JS, Weiss SJ, et al: Echocardiographic and hemodynamic

indexes of left ventricular preload in patients with normal and abnormal ventricular function. Anesthesiology 1994;81:376. 13. Urbanowicz JH, Shaaban MJ, Cohen NH, et al: Comparison of transesophageal

echocardiographic and scintigraphic estimates of left ventricular end-diastolic volume index and ejection fraction in patients following coronary artery bypass grafting. Anesthesiology 1990;72:607. 14. Ryan T, Burwash I, Lu J, et al: The agreement between ventricular volumes and ejection fraction by transesophageal echocardiography or a combined radionuclear and thermodilution technique in patients after coronary artery surgery. J Cardiothorac Vasc Anesth 1996;10:323. 15. Tousignant CP, Walsh F, Mazer CD: The use of transesophageal echocardiography

for preload assessment in critically ill patients. Anesth Analg 2000;90:351. 16. Hinder F, Poelaert JI, Schmidt C, et al: Assessment of cardiovascular volume status

by transoesophageal echocardiography and dye dilution during cardiac surgery. Eur J Anaesthesiol 1998;15:633. 17. Gorcsan JD, Gasior TA, Mandarino WA, et al: On-line estimation of changes in

left ventricular stroke volume by transesophageal echocardiographic automated border detection in patients undergoing coronary artery bypass grafting. Am J Cardiol 1993;72:721. 18. Jardin F, Dubourg O, Bourdarias JP: Echocardiographic pattern of acute cor

pulmonale. Chest 1997;111:209. 19. De Hert SG, Vander Linden PJ, ten Broecke PW, et al: Assessment of lengthdependent regulation of myocardial function in coronary surgery patients using

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 3 di 13

transmitral flow velocity patterns. Anesthesiology 2000;93:374. 20. De Hert SG, Rodrigus IE, Haenen LR, et al.: Recovery of systolic and diastolic left

ventricular function early after cardiopulmonary bypass. Anesthesiology 1996;85:1063. 21. Leung JM, Levine EH: Left ventricular end-systolic cavity obliteration as an

estimate of intraoperative hypovolemia. Anesthesiology 1994;81:1102. 22. Erbel R, Krebs W, Henn G, et al: Comparison of single-plane and biplane volume

determination by two-dimensional echocardiography. 1. Asymmetric model hearts. Eur Heart J 1982;3:469. 23. Krebs W, Klues HG, Steinert S, et al: Left ventricular volume calculations using a

multiplanar transoesophageal echoprobe; in vitro validation and comparison with biplane angiography. Eur Heart J 1996;17:1279. 24. Smith MD, MacPhail B, Harrison MR, et al: Value and limitations of transesophageal echocardiography in determination of left ventricular volumes and ejection fraction. J Am Coll Cardiol 1992;19:1213. 25. Hozumi T, Yoshikawa J, Yoshida K, et al: Three-dimensional echocardiographic

measurement of left ventricular volumes and ejection fraction using a multiplane transesophageal probe in patients. Am J Cardiol 1996;78:1077. 26. Rocchi G, de Jong N, Galema TW, et al: Effect of harmonic imaging without

contrast on image quality of transesophageal echocardiography. Am J Cardiol 1999;84:1132. 27. Schuster AH, Nanda NC: Doppler echocardiographic measurement of cardiac

output: Comparison with a non-golden standard. Am J Cardiol 1984;53:257. 28. Levett JM, Replogle RL: Thermodilution cardiac output: A critical analysis and

review of the literature. J Surg Res 1979;27:392. 29. Samstad SO, Torp HG, Linker DT, et al: Cross sectional early mitral flow velocity

profiles from colour Doppler. Br Heart J 1989;62:177. 30. Savino JS, Troianos CA, Aukburg S, et al: Measurement of pulmonary blood flow

with transesophageal two-dimensional and Doppler echocardiography. Anesthesiology 1991;75:445. 43

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 4 di 13

31. Muhiudeen IA, Kuecherer HF, Lee E, et al: Intraoperative estimation of cardiac

output by transesophageal pulsed Doppler echocardiography. Anesthesiology 1991;74:9. 32. Izzat MBB, Regragui IA, Wilde P, et al: Transesophageal echocardiographic measurements of cardiac output in cardiac surgical patients. Ann Thorac Surg 1994;58:1486. 33. Gorcsan JD, Diana P, Ball BA, et al: Intraoperative determination of cardiac output

by transesophageal continuous wave Doppler. Am Heart J 1992;123:171. 34. Maslow A, Comunale ME, Haering JM, et al: Pulsed wave Doppler measurement

of cardiac output from the right ventricular outflow tract. Anesth Analg 1996;83:466. 35. Stoddard MF, Prince CR, Ammash N, et al: Pulsed Doppler transesophageal

echocardiographic determination of cardiac output in human beings: Comparison with thermodilution technique. Am Heart J 1993;126:956. 36. Descorps-Declere A, Smail N, Vigue B, et al: Transgastric, pulsed Doppler

echocardiographic determination of cardiac output. Intensive Care Med 1996;22:34. 37. Perrino AC Jr, Harris SN, Luther MA: Intraoperative determination of cardiac

output using multiplane transesophageal echocardiography: A comparison to thermodilution. Anesthesiology 1998;89:350. 38. Darmon PL, Hillel Z, Mogtader A, et al: Cardiac output by transesophageal

echocardiography using continuous-wave Doppler across the aortic valve. Anesthesiology 1994;80:796. 39. Robotham JL, Takata M, Berman M, et al: Ejection fraction revisited.

Anesthesiology 1991;74:172. 40. Schiller NB, Acquatella H, Ports TA, et al: Left ventricular volume from paired

biplane two-dimensional echocardiography. Circulation 1979;60:547. 41. Teichholz LE, Kreulen T, Herman MV, et al: Problems in echocardiographic

volume determinations: Echocardiographic-angiographic correlations in the presence or absence of asynergy. Am J Cardiol 1976;37:7. 42. Clements FM, Harpole DH, Quill T, et al: Estimation of left ventricular volume

and ejection fraction by two-dimensional transoesophageal echocardiography:

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Pagina 5 di 13

Comparison of short axis imaging and simultaneous radionuclide angiography. Br J Anaesth 1990;64:331. 43. Wyatt HL, Haendchen RV, Meerbaum S, et al: Assessment of quantitative methods

for 2-dimensional echocardiography. Am J Cardiol 1983;52:396. 44. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313. 45. Cahalan MK, Ionescu P, Melton HE Jr, et al: Automated real-time analysis of

intraoperative transesophageal echocardiograms. Anesthesiology 1993;78:477. 46. Liu N, Darmon PL, Saada M, et al: Comparison between radionuclide ejection

fraction and fractional area changes derived from transesophageal echocardiography using automated border detection. Anesthesiology 1996;85:468. 47. Perrino AC Jr, Luther MA, O'Connor TZ, et al: Automated echocardiographic analysis. Examination of serial intraoperative measurements. Anesthesiology 1995;83:285. 48. Katz WE, Gasior TA, Reddy SC, et al: Utility and limitations of biplane

transesophageal echocardiographic automated border detection for estimation of left ventricular stroke volume and cardiac output. Am Heart J 1994;128:389. 49. Greim CA, Roewer N, Laux G, et al: On-line estimation of left ventricular stroke

volume using transoesophageal echocardiography and acoustic quantification. Br J Anaesth 1996;77:365. 50. Sagawa K: The end-systolic pressure-volume relation of the ventricle: Definition,

modifications and clinical use. Circulation 1981;63:1223. 51. Gorcsan J 3rd, Denault A, Gasior TA, et al: Rapid estimation of left ventricular

contractility from end-systolic relations by echocardiographic automated border detection and femoral arterial pressure. Anesthesiology 1994;81:553. 52. Declerck C, Hillel Z, Shih H, et al: A comparison of left ventricular performance

indices measured by transesophageal echocardiography with automated border detection. Anesthesiology 1998;89:341. 53. O'Kelly BF, Tubau JF, Knight AA, et al: Measurement of left ventricular

contractility using transesophageal echocardiography in patients undergoing coronary artery bypass grafting. The Study of Perioperative Ischemia (SPI) Research Group. Am Heart J 1991;122(4 Pt 1):1041.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 6 di 13

54. Gorcsan J 3rd, Gasior TA, Mandarino WA, et al: Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressurearea relations. Circulation 1994;89:180. 55. Deneault LG, Kancel MJ, Denault A, et al: A system for the on-line acquisition,

visualization, and analysis of pressure-area loops. Comput Biomed Res 1994;27:61. 56. Shih H, Hillel Z, Declerck C, et al: An algorithm for real-time, continuous

evaluation of left ventricular mechanics by single-beat estimation of arterial and ventricular elastance. J Clin Monit 1997;13:157. 57. Winkelmann J, Aronson S, Young CJ, et al: Retrograde-delivered cardioplegia is not distributed equally to the right ventricular free wall and septum. J Cardiothorac Vasc Anesth 1995;9:135. 58. Wranne B, Pinto FJ, Siegel LC, et al: Abnormal postoperative interventricular

motion: New intraoperative transesophageal echocardiographic evidence supports a novel hypothesis. Am Heart J 1993;126:161. 59. Rafferty T, Durkin M, Harris S, et al: Transesophageal two-dimensional

echocardiographic analysis of right ventricular systolic performance indices during coronary artery bypass grafting. J Cardiothorac Vasc Anesth 1993;7:160. 60. Nomura T, Lebowitz L, Koide Y, et al: Evaluation of hepatic venous flow using

transesophageal echocardiography in coronary artery bypass surgery: An index of right ventricular function. J Cardiothorac Vasc Anesth 1995;9:9. 61. Vignon P, Weinert L, Mor-Avi V, et al: Quantitative assessment of regional right

ventricular function with color kinesis. Am J Respir Crit Care Med 1999;159:1949. 62. Slogoff S, Keats AS: Does perioperative myocardial ischemia lead to postoperative

myocardial infarction? Anesthesiology 1985;62:107. 63. Fleisher LA: Real-time intraoperative monitoring of myocardial ischemia in

noncardiac surgery. Anesthesiology 2000;92:1183. 64. Schiller NB, Shah PM, Crawford M, et al: Recommendations for quantitation of

the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of TwoDimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358. 65. Couture P, Denault AY, Carignan SHP, et al: Intraoperative detection of segmental

wall motion abnormalities with transesophageal echocardiography. Can J Anaesth

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Book Text

Pagina 7 di 13

1999;46:827. 66. Tennant R, Wiggers CJ: The effect of coronary occlusion on myocardiol

contraction. Am J Physiol 1935;112:351. 67. Koh TW, Pepper JR, Gibson DG: Early changes in left ventricular anterior wall

dynamics and coordination after coronary artery surgery. Heart 1997;78:291. 68. Smith JS, Cahalan MK, Benefiel DJ, et al: Intraoperative detection of myocardial

ischemia in high-risk patients: Electrocardiography versus two-dimensional transesophageal echocardiography. Circulation 1985;72:1015. 69. London MJ, Tubau JF, Wong MG, et al: The "natural history" of segmental wall

motion abnormalities in patients undergoing noncardiac surgery. S.P.I. Research Group. Anesthesiology 1990;73:644. 70. Leung JM, O'Kelly B, Browner WS, et al: Prognostic importance of postbypass

regional wall-motion abnormalities in patients undergoing coronary artery bypass graft surgery. SPI Research Group. Anesthesiology 1989;71:16. 71. Leung JM, O'Kelly BF, Mangano DT: Relationship of regional wall motion

abnormalities to hemodynamic indices of myocardial oxygen supply and demand in patients undergoing CABG. Anesthesiology 1990;73:802. 72. Seeberger MD, Cahalan MK, Rouine-Rapp K, et al: Acute hypovolemia may cause

segmental wall motion abnormalities in the absence of myocardial ischemia. Anesth Analg 1997;85:1252. 73. Comunale MEHP, Body SC, Ley C, et al: The concordance of intraoperative left ventricular wall-motion abnormalities and electrocardiographic S-T segment changes: Association with outcome after coronary revascularization. Multicenter Study of Perioperative Ischemia (McSPI) Research Group. Anesthesiology 1998;88:945. 44

74. Koide Y, Keehn L, Nomura T, et al: Relationship of regional wall motion

abnormalities detected by biplane transesophageal echocardiography and electrocardiographic changes in patients undergoing coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth 1996;10:719. 75. Rouine-Rapp K, Ionescu P, Balea M, et al: Detection of intraoperative segmental

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wall-motion abnormalities by transesophageal echocardiography: The incremental value of additional cross sections in the transverse and longitudinal planes. Anesth Analg 1996;83:1141. 76. Hauser AM, Gangadharan V, Ramos RG, et al: Sequence of mechanical,

electrocardiographic and clinical effects of repeated coronary artery occlusion in human beings: Echocardiographic observations during coronary angioplasty. J Am Coll Cardiol 1985;5(2 Pt 1):193. 77. Geleijnse ML, Fioretti PM, Roelandt JR: Methodology, feasibility, safety and

diagnostic accuracy of dobutamine stress echocardiography. J Am Coll Cardiol 1997;30:595. 78. Elhendy A, Cornel JH, Roelandt JR, et al: Impact of severity of coronary artery

stenosis and the collateral circulation on the functional outcome of dyssynergic myocardium after revascularization in patients with healed myocardial infarction and chronic left ventricular dysfunction. Am J Cardiol 1997;79:883. 79. Aronson S, Dupont F, Savage R, et al: Changes in regional myocardial function

after coronary artery bypass graft surgery are predicted by intraoperative low-dose dobutamine echocardiography. Anesthesiology 2000;93:685. 80. Leoncini M, Marcucci G, Sciagra R, et al: Comparison of baseline and low-dose

dobutamine technetium-99m sestamibi scintigraphy with low-dose dobutamine echocardiography for predicting functional recovery after revascularization. Am J Cardiol 2000;86:153. 81. Chan KL: Transesophageal echocardiography for assessing cause of hypotension

after cardiac surgery. Am J Cardiol 1988;62:1142. 82. Brandt RR, Oh JK, Abel MD, et al: Role of emergency intraoperative

transesophageal echocardiography. J Am Soc Echocardiogr 1998;11:972. 83. Aronson S, Jacobsohn E, Savage RHP, et al: The influence of collateral flow on the

antegrade and retrograde distribution of cardioplegia in patients with an occluded right coronary artery. Anesthesiology 1998;89:1099. 84. Allen BS, Winkelmann JW, Hanafy H, et al: Retrograde cardioplegia does not

adequately perfuse the right ventricle. J Thorac Cardiovasc Surg 1995;109:1116. 85. Borger MA, Wei KS, Weisel RD, et al: Myocardial perfusion during warm

antegrade and retrograde cardioplegia: A contrast echo study. Ann Thorac Surg 1999;68:955.

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86. Aronson S, Savage R, Toledano A, et al: Identifying the cause of left ventricular

systolic dysfunction after coronary artery bypass surgery: The role of myocardial contrast echocardiography. J Cardiothorac Vasc Anesth 1998;12:512. 87. Savage RM, Lytle BW, Aronson S, et al: Intraoperative echocardiography is

indicated in high-risk coronary artery bypass grafting. Ann Thorac Surg 1997;64:368. 88. Kotoh K, Watanabe G, Ueyama K, et al: On-line assessment of regional ventricular

wall motion by transesophageal echocardiography with color kinesis during minimally invasive coronary artery bypass grafting. J Thorac Cardiovasc Surg 1999;117:912. 89. Langeron O, Goarin JP, Pansard JL, et al: Massive intraoperative pulmonary

embolism: Diagnosis with transesophageal two-dimensional echocardiography. Anesth Analg 1992;74:148. 90. Pharo GH, Andonakakis A, Chandrasekaren K, et al: Survival from catastrophic

intraoperative pulmonary embolism. Anesth Analg 1995;81:188. 91. Plowman AN, Bolsin SN, Patrick AJ: Unusual cause of intraoperative hypotension

diagnosed with transoesophageal echocardiography in a patient with renal cell carcinoma. Anaesth Intensive Care 1999;27:63. 92. Yamaura K, Okamoto H, Maekawa T, et al: Detection of retroperitoneal

hemorrhage by transesophageal echocardiography during cardiac surgery. Can J Anaesth 1999;46:169. 93. Hsin ST, Luk HN, Lin SM, et al: Detection of iatrogenic cardiac tamponade by

transesophageal echocardiography during vena cava filter procedure. Can J Anaesth 2000;47:638. 94. Jacka M, Oxorn DC: Pulmonary artery obstruction by aortic aneurysm mimicking

pulmonary embolism. Anesth Analg 1995;80:185. 95. Chavanon O, Dutheil V, Hacini R, et al: Treatment of severe cardiac contusion

with a left ventricular assist device in a patient with multiple trauma. J Thorac Cardiovasc Surg 1999;118:189. 96. Weiss RL, Brier JA, O'Connor W, et al: The usefulness of transesophageal

echocardiography in diagnosing cardiac contusions. Chest 1996;109:73. 97. Tousignant C: Transesophageal echocardiographic assessment in trauma and

critical care. Can J Surg 1999;42:171.

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98. Ibrahim AE, Stanwood PL, Freund PR: Pneumothorax and systemic air embolism

during positive-pressure ventilation. Anesthesiology 1999;90:1479. 99. Ho AM, Ling E: Systemic air embolism after lung trauma. Anesthesiology

1999;90:564. 100. Cheung AT, Savino JS, Weiss SJ: Beat-to-beat augmentation of left ventricular

function by intraaortic counterpulsation. Anesthesiology 1996;84:545. 101. Reichert CL, Koolen JJ, Visser CA: Transesophageal echocardiographic

evaluation of left ventricular function during intraaortic balloon pump counterpulsation. J Am Soc Echocardiogr 1993;6:490. 102. Shanewise JS, Sadel SM: Intraoperative transesophageal echocardiography to

assist the insertion and positioning of the intraaortic balloon pump. Anesth Analg 1994;79:577. 103. Scalia GM, McCarthy PM, Savage RM, et al: Clinical utility of echocardiography

in the management of implantable ventricular assist devices. J Am Soc Echocardiogr 2000;13:754. 104. Siegel LC, St. Goar FG, Stevens JH, et al: Monitoring considerations for port-

access cardiac surgery. Circulation 1997;96:562. 105. Coddens J, Deloof T, Hendrickx J, et al: Transesophageal echocardiography for

port-access surgery. J Cardiothorac Vasc Anesth 1999;13:614. 106. Secknus MA, Asher CR, Scalia GM, et al: Intraoperative transesophageal

echocardiography in minimally invasive cardiac valve surgery. J Am Soc Echocardiogr 1999;12:231. 107. Michel-Cherqui M, Brusset A, Liu N, et al: Intraoperative transesophageal

echocardiographic assessment of vascular anastomoses in lung transplantation. A report on 18 cases. Chest 1997;111:1229. 108. Huang YC, Cheng YJ, Lin YH, et al: Graft failure caused by pulmonary venous

obstruction diagnosed by intraoperative transesophageal echocardiography during lung transplantation. Anesth Analg 2000;91:558. 109. Branche PE, Duperret SL, Sagnard PE, et al: Left ventricular loading

modifications induced by pneumoperitoneum: A time course echocardiographic study. Anesth Analg 1998;86:482.

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110. Harris SN, Ballantyne GH, Luther MA, et al: Alterations of cardiovascular

performance during laparoscopic colectomy: A combined hemodynamic and echocardiographic analysis. Anesth Analg 1996;83:482. 111. Fahy BG, Hasnain JU, Flowers JL, et al: Transesophageal echocardiographic

detection of gas embolism and cardiac valvular dysfunction during laparoscopic nephrectomy. Anesth Analg 1999;88:500. 112. Fleisher LA, Mantha S, Roizen MF: Medical technology assessment: An

overview. Anesth Analg 1998;87:1271. 113. Connors AF Jr, Speroff T, Dawson NV, et al: The effectiveness of right heart

catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889. 114. Robin ED: Death by pulmonary artery flow-directed catheter: Time for a

moratorium? Chest 1987;92:727. 115. London MJ, Shroyer AL, Grover FL, et al: Evaluating anesthesia health care

delivery for cardiac surgery: The role of process and structure variables. Med Care 1995;33(10 suppl):OS66. 116. Kato M, Nakashima Y, Levine J, et al: Does transesophageal echocardiography

improve postoperative outcome in patients undergoing coronary artery bypass surgery? J Cardiothorac Vasc Anesth 1993;7:285. 117. Bergquist BD, Leung JM, Bellows WH: Transesophageal echocardiography in

myocardial revascularization: I. Accuracy of intraoperative real-time interpretation. Anesth Analg 1996;82:1132. 118. Bergquist BD, Bellows WH, Leung JM: Transesophageal echocardiography in

myocardial revascularization: II. Influence on intraoperative decision making. Anesth Analg 1996;82:1139. 45

119. Higgins TL, Estafanous FG, Loop FD, et al: Stratification of morbidity and

mortality outcome by preoperative risk factors in coronary artery bypass patients: A clinical severity score. JAMA 1992;267:2344. 120. Sutton DC, Kluger R: Intraoperative transoesophageal echocardiography: Impact

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on adult cardiac surgery. Anaesth Intensive Care 1998;26:287. 121. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767. 122. Couture P, Denault AY, McKenty S, et al: Impact of routine use of intraoperative

transesophageal echocardiography during cardiac surgery. Can J Anaesth 2000;47:20. 123. Mishra M, Chauhan R, Sharma KKHP, et al: Real-time intraoperative

transesophageal echocardiography: How useful? Experience of 5,016 cases. J Cardiothorac Vasc Anesth 1998;12:625. 124. Suriani RJ, Neustein S, Shore-Lesserson L, et al: Intraoperative transesophageal

echocardiography during noncardiac surgery. J Cardiothorac Vasc Anesth 1998;12:274. 125. Pocock SJ, Elbourne DR: Randomized trials or observational tribulations?

[editorial; comment]. N Engl J Med 2000;342:1907. 126. Siwik ES, Spector ML, Patel CR, et al: Costs and cost-effectiveness of routine

transesophageal echocardiography in congenital heart surgery. Am Heart J 1999;138(4 Pt 1):771. 127. Seto TB, Taira DA, Tsevat J, et al: Cost-effectiveness of transesophageal

echocardiographic-guided cardioversion: A decision analytic model for patients admitted to the hospital with atrial fibrillation. J Am Coll Cardiol 1997;29:122. 128. Rosen AB, Fowler VG Jr, Corey GR, et al: Cost-effectiveness of transesophageal

echocardiography to determine the duration of therapy for intravascular catheterassociated Staphylococcus aureus bacteremia. Ann Intern Med 1999;130:810. 129. Weinger MB, Herndon OW, Gaba DM: The effect of electronic record keeping

and transesophageal echocardiography on task distribution, workload, and vigilance during cardiac anesthesia. Anesthesiology 1997;87:144. 130. Benson K, Hartz AJ: A comparison of observational studies and randomized,

controlled trials [see comments]. N Engl J Med 2000;342:1878. 131. Concato J, Shah N, Horwitz RI: Randomized, controlled trials, observational

studies, and the hierarchy of research designs. N Engl J Med 2000;342:1887. 132. Rafferty T, LaMantia KR, Davis E, et al: Quality assurance for intraoperative

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46

Chapter 3 - Aortic Dissection and Trauma Value and Limitations of Echocardiography Elizabeth W. Ryan MD Ann F. Bolger MD

The rate of mortality with acute aortic dissection escalates hourly, [1] reaching 50% by 48 hours. Immediate diagnosis and therapy are critical for survival. Two thousand new cases of acute dissection are reported in the United States per year[2] the true incidence, including the large numbers of patients who die from unrecognized dissection, has been estimated at more that 10,000 per year.[3] Further, 10% to 30% of acute dissections occurring in the hospital may be misdiagnosed. Prompt diagnosis is a clinical challenge because patient's presenting symptoms may be nonspecific or even misleading. Aortic dissection must be included in the differential diagnosis of chest pain in many patients at risk for dissection and also when simultaneous acute involvement of multiple organ systems does not have a ready explanation. Acute dissection of the aorta can share many of the features of acute myocardial infarction: pain (related to the dissection itself or to myocardial ischemia), electrocardiographic abnormalities consistent with ischemia (resulting from involvement of the coronary ostia in proximal dissection),[4] and elevated serum creatinine kinase levels.[5] True myocardial ischemia is a potential component of the syndrome of aortic dissection. On pathologic examination, Hirst et al[6] found

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involvement of the coronary arteries in 39 of 505 cases of acute dissection (7.7%). Confusion of acute dissection with myocardial infarction not only delays appropriate treatment but also may lead to disastrous consequences if thrombolytic agents are administered.[7] [8] Thrombolysis impedes compensatory thrombosis of the false channel and promotes uncontrollable hemorrhage in the event of aortic rupture. Given that the incidence of aortic dissection is far less than that of myocardial infarction (0.26% of 5011 patients in the Anglo-Scandinavian Study of Early Thrombolysis trial[7] ) and that ST segment elevation is a relatively rare finding in patients with aortic dissection, classic electrocardiographic changes without physical findings suggesting dissection will rarely mislead clinicians toward thrombolysis.[9] Maintenance of a high suspicion for dissection must be paired with highly reliable tests to avoid such infrequent but catastrophic misdiagnoses. The optimal diagnostic test for acute aortic dissection, therefore, must be accurate, safe, and immediately applicable in a broad range of medical environments. The limited sensitivity of echocardiography for dissection from the transthoracic approach has been greatly improved by transesophageal approaches; transesophageal examinations can be performed within minutes in the emergency department, operating room, or intensive care unit and provides high-quality images of the thoracic aorta as well as of other cardiac and vascular structures at risk. The advantages and limitations of echocardiographic techniques 47

in the management of patients with aortic dissection have been carefully investigated at many centers, and, as a result, their strengths and weaknesses relative to other imaging techniques are being better defined. Ongoing advances in transesophageal probe technology and other ultrasonographic imaging methods are proceeding rapidly, with smaller transducers, multiple and variable imaging planes, and wider ranges of frequencies being made available. These improvements are solidifying the already well-established role of echocardiography in the diagnosis and follow-up of aortic dissection.

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Pathophysiology of Aortic Dissection Anatomy and Histology The aortic wall consists of three layers: the intima, which is a single layer of vascular endothelium; the media, with concentric layers of smooth muscle cells, collagen, elastin, and extracellular matrix proteoglycans; and the peripheral adventitia, consisting of loose connective tissue that anchors the aorta in surrounding tissues. The vaso vasorum, which perfuses the aortic wall, is contained within the adventitia. Of the three layers of the aortic wall, the structure of the media dominates the wall's mechanical properties.[10] Medial smooth muscle directly influences wall stiffness by contraction. In addition, smooth muscle cells are the major source of the extracellular matrix components. These include the elastin fibers, which can be stretched to 300% of their resting length without rupturing[11] and are important contributors to the normal pulsatile behavior of the vessel. Elastin is less important to the overall strength of the aorta than collagen, however, which is both stiffer and much stronger than elastin. The components of the media vary from vessel to vessel and change with age. In the aortas of older patients, the elastin content decreases and the collagen content increases, resulting in increased vascular stiffness.[12] The mechanical properties of the vasculature are also almost always disturbed in cases of systemic hypertension.[13] Mechanical and Shear Stresses The aortic wall is subjected to mechanical stresses of several forms. Stress, which is expressed as force per unit area, may occur in radial, circumferential, or longitudinal directions.[14] The normal intima bears little of the aorta's stress load. It is exposed to shear stresses, however, which are forces applied parallel to the vessel wall as a result of the viscous effects of blood flow. The amount of these shear stresses varies with the distribution of velocity across the vessel lumen and with local vessel geometry.

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Circumferential stress predominantly affects the media. This type of stress (δ) increases with the radial pressure from the aortic lumen (P) and the aortic radius (r), and decreases with increasing wall thickness (h): δ = Pr/h The danger of aortic dilation can therefore be understood: in dilated, thinwalled aortas, the circumferential stresses may be increased many times above normal. In addition, the geometry of the dilating aorta changes progressively from the normal cylinder to an ellipsoidal or even spherical shape. This slowly increases the circumferential stress but quickly exacerbates longitudinal stress. Most atraumatic aortic tears are caused by longitudinal stress, which explains why they are generally transverse in orientation.[15] The ascending aorta experiences additional longitudinal stress owing to the motion of the aortic annulus. Finally, dilated or aneurysmal vessels demonstrate marked stiffness, in part because of loss of elastin.[16] Combined aortic dilation, wall thinning, and shape change sets the stage for intimal rupture and the initiation of dissection. Intimal or medial abnormalities of the aorta increase the resistance to both shear and circumferential stresses. Stress failures of both types may play a role in aortic dissection. Circumferential stress failure can occur when the stresses caused by intraluminal pressure are greatly magnified in the thin fibrous cap of an atheromatous lesion. If the lesion fractures and a small crack develops, the circumferential stress will cause it to extend through the wall.[10] Shear stress failure is due to inhomogeneity in the properties of the vessel wall. Even under normal conditions, mural stresses are greater on the inner than on the outer wall.[15] In the presence of atherosclerosis, incremental variations in the shear resistance between contiguous regions of diseased and normal wall occur. The progression of aortic dissection probably represents an example of shear failure, in which the interface between two such aortic segments with different stiffness leads to separation of medial and intimal layers: the two layers slide relative to one another, because the "glue" of the extracellular matrix cannot withstand the shear stress.[10] Once initiated, dissections behave like a two-ply tube. The intima and the internal elastic lamina of the media form the inner layer, and the outer layer consists of the external elastic lamina and the adventitia. A velocitydependent shear force will then further separate the two layers, creating a false lumen separated from the true lumen by the intima and internal elastic

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lamina.[15] Experimentally, it has been demonstrated that the work per unit area of tissue required to propagate a tear in the aorta is small (15.9 ± 0.9 mJ cm2 ), and independent of the depth of the tear.[17] These concepts of shear and tensile failure are the basis for understanding why different patient populations are at increased risk for aortic dissection. Medial elastic tissue degeneration resulting from hereditary defects of the arterial wall creates the substrate for dissection in patients with Marfan's syndrome, Turner's syndrome,[18] Noonan's disease, Ehlers-Danlos syndrome, and osteogenesis imperfecta.[15] [19] In these patients, as well as in other groups, dilation of the aorta is an important source of tensile failure and a precursor to dissection. Both wall abnormalities (shear failure) and increased wall stress (tensile failure) caused by dilation are important in nonhereditary risk groups. Dissection occurring in hypertensive patients is generally based on 48

high blood pressure, moderate aortic dilation, and medial muscular degeneration predisposing the internal layer to tear.[15] The contribution of shear stress in those patients is infrequent and unpredictable. Atherosclerosis In atherosclerosis, both generalized and focal manifestations can predispose to dissection. True aortic aneurysms are caused by atherosclerotic degeneration of the media and progress to involve all three layers of the vessel wall and to gradual dilation. Increasing risk accompanies diameters exceeding 10 cm, rapid expansion, or symptoms. Formation of laminar thrombus within the aneurysm does not decrease the wall stress. The 1-year survival rate in patients with thoracic aortic aneurysms is less than 60%, and the 5-year survival rate is approximately 20%. False aneurysms are created by through-and-through disruption of the media, with the adventitia alone confining the extravasation.[20] The risk of rupture is even higher in this setting. A third type of atherosclerotic aortic abnormality is penetrating aortic ulceration.[21] [22] In this case, rupture of atherosclerotic plaque causes fissuring into the media and creation of an intramural hematoma, which may progress to rupture or pseudoaneurysm formation. Trauma

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Trauma is another important cause of dissection. Dissection may occur in external, accidental trauma and be difficult to assess in the setting of major multisystem injuries. The region most prone to traumatic injury is the aortic isthmus, where relative tethering by the spinal arteries and ligamentum arteriosum resists abrupt deceleration more than the more mobile transverse arch.[23] Other vulnerable sites include the origin of the innominate artery, particularly with vertical forces from falls, and the ascending aorta above the sinus of Valsalva. [24] Traumatic injuries to the aorta may result in intimal tears, recognizable on transesophageal echocardiography (TEE) scans as mobile flaps. Thrombus may be seen protruding into the lumen; in other cases, intramural hematoma without apparent intimal discontinuity is seen. Although very minor lesions such as minimal hematomas may regress spontaneously, the prognosis of significant aortic trauma is grave. Without repair, there is a 30% rate of mortality within the first 24 hours. Within 1 week, the mortality rate is greater than 50%.[25] Prompt recognition is therefore critical to patient outcome. TEE has been shown to be safe and highly sensitive for aortic trauma after motor vehicle accidents, equivalent to angiography and more expeditiously applied.[26] TEE may also detect other signs of cardiac trauma, including wall motion abnormalities, pericardial effusion, and valvular insufficiency. When the suspicion of aortic rupture in the territory of the transverse arch remains high, computed tomography (CT) may provide better images of those territories. Other sources of trauma include the Heimlich maneuver for respiratory obstruction and cardiovascular procedures. Operative sources of tears in the aorta include cannulation sites for cardiopulmonary bypass, aortic transections for valve or aortic segment replacement, and proximal anastomotic sites for coronary bypass grafts.[27] [28] Very uncommonly, aortic catheterization for angiography may traumatize an atherosclerotic region and prompt dissection.[29] Angioplasty procedures of coronary or renal vessels can also initiate the process.[30] A history of these procedures may be important in alerting the clinician to the possibility of dissection in these patients. Pregnancy Although aortic dissection is mostly a disease of middle-aged or elderly men, women and children can also experience dissection. It has been claimed that half of all aortic dissections occurring in women younger than 40 years of age are associated with pregnancy, particularly during the third trimester or the postpartum period.[31] [32] [33] This finding has been disputed

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by Oskoui and Lindsay,[34] who reviewed their own experience and published a series of 1253 dissections in consecutive patients (868 men and 385 women), with no cases occurring in pregnancy. They concluded that most women experiencing aortic dissection in pregnancy had other risk factors such as hypertension or Marfan's syndrome, and that the apparent association could result from selective reporting and coincidental occurrence of dissection with the very common condition of pregnancy. There are also other well-recognized causes of aortic dissection (Table 31) .[35] [36] [37] [38] [39] [40] [41] [42] [43] Genetic Diseases Of the genetic causes of aortic medial disease and aortic dissection, Marfan's syndrome is the most common and best studied. Although a clinical diagnosis, Marfan's syndrome can be confirmed by linkage to the dominantly inherited gene MFS-1 on 15q21 or by determination of the specific family mutation.[44] Histologic examination of the aortic wall in patients with Marfan's syndrome reveals fragmentation of aortic components, especially the elastic fibers,[45] and abnormal accumulation of collagenous and mucoid materials in the media.[46] Fragmentation of elastinassociated microfibrils also occurs in aortic valve leaflets. [47] The disruption and loss of elastic tissue of the media is attributed to a deficiency of fibrillin, a microfibrillar protein that scaffolds the elastic lamellae in the aortic wall.[48] [49] These changes are greatest in the ascending aorta, which is subject to the greatest pulsatile expansion and therefore the highest stress in systole.[15] The alterations in aortic wall components are associated with abnormal functional properties: aortic elasticity is abnormal in patients with Marfan's syndrome, irrespective of the aortic diameter. [50] A comparative study of aortic wall dynamics between patients with Marfan's syndrome and normal control subjects confirmed that, in both groups, stiffness of the wall increases with age and aortic diameter, but at all ages the patients in the Marfan's syndrome group exhibit a stiffer aorta for a given diameter than the control subjects do.[51] Furthermore, Marfan's syndrome patients have large ascending aortic diameters, but not 49

TABLE 3-1 -- Patient Populations at Risk for Aortic Dissection Genetic disorders (medial abnormalities)

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Marfan's syndrome Turner's syndrome Noonan's disease Ehlers-Danlos syndrome Osteogenesis imperfecta Congenital disorders Aortic coarctation Unicuspid or bicuspid aortic valve Degenerative disorders Hypertension Atherosclerotic vascular disease Aortic ulcer Aortic aneurysm Non-Marfan's syndrome cystic medial necrosis Traumatic causes Deceleration injury Penetrating injury Heimlich maneuver Postprocedural causes Cardiac surgery Cannulation Cross-clamping Aortic valve replacement Angioplasty Coronary Renal Inflammatory disorders Syphilis Giant cell arteritis Other conditions

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Pregnancy Weight lifting Cocaine use Discontinuation of beta blockers Polycystic kidney disease abdominal aortic size, after correction for body surface area.[50] Dissection occurs in Marfan's syndrome patients because of this dilation in combination with wall weakness; mural stress increases dramatically with increasing radius and becomes self-perpetuating[15] (Fig. 3-1) . Echocardiographic evidence of aortic root dilation is present in 60% to 80% of patients with Marfan's syndrome.[52] [53] In one series, aortic dilation was generalized in 51% and localized in 28% of patients.[54] Localized dilation did not appear to represent an earlier stage of aortic involvement, as the patient ages in both groups were identical, as was the duration of follow-up. It could not be determined whether generalized dilation reflected more severe underlying cystic medial necrosis from different specific mutations in fibrillin. Generalized dilation, however, was associated with higher rates of expansion as well as aortic regurgitation. In Marfan's syndrome patients, aortic insufficiency has been associated with decreased survival.[43] The existence of mitral valve prolapse does not appear to be an independent predictor of outcome. The clinical course of patients with Marfan's syndrome with respect to progressive aortic dilation and dissection is variable[55] increased risk has been associated with older age,[54] [55] male gender, aortic root diameters exceeding 60 mm,[56] aortic growth rate,[54] [55] and a family history of dissection.[57] Of great concern is the observation that aortic dissection can occur in Marfan's syndrome patients even in the absence of aortic root dilation.[58] Medical management of Marfan's syndrome patients with aortic dilatation involves beta blockers and observation of aortic root diameter to determine the timing of elective surgery aimed at preventing aortic dissection. Longterm fatality rates are improved with prophylactic aortic root replacement; the 5-year survival rate approximates 97% for elective surgery versus only 51% with emergency surgery for dissection.[59] Operative mortality in experienced centers for elective surgery in Marfan's syndrome patients is low (1.3% to 1.5% 30-day mortality rate versus 11.7% for emergency surgery).[60] [61] In patients with normal aortic valve leaflets, elective aortic valve-sparing surgery may provide better clinical outcomes than aortic root

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replacement,[62] although in this retrospective review, patients undergoing aortic root replacement with aortic valve replacement had more cardiac comorbidities than the patients in whom valve-sparing surgery was possible. The size of aneurysm often determines the feasibility of valvesparing surgery; therefore, some centers recommend elective surgery when the aortic root reaches 50 mm.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Spectrum of Aortic Dissection The primary entry tear that initiates aortic dissection is usually transverse and involves more than half of the circumference of the aorta. In 65% of cases, it occurs within 3 cm of the coronary ostia. Ten percent of tears occur in the descending thoracic aorta and another 10% in the arch. Primary tears are rare in the abdominal aorta.[63] Whatever the location of the initial tear, dissections may extend caudally, proximally, or occasionally in both directions. Figure 3-1 Type A aortic dissection (arrows indicate intimal flap) in a patient with Marfan's syndrome. Prolapse of the posterior mitral valve leaflet is also noted.

Anatomic Classification

50

There are several widely used classification systems for dissection (Table 3-2) . The DeBakey classification divides dissections with involvement of the ascending aorta into type I, which extends into the transverse arch and distal aorta, type II, which is confined to the ascending aorta, and type III, which involves the descending aorta only.[64] The Stanford classification[65] was developed from a functional approach based on whether the ascending aorta is involved, regardless of the site of primary intimal tear and irrespective of the extent of distal propagation. This reflects clinical observations that the biologic behavior of the dissection, the clinical prognosis, and how the patient should be managed pivot almost exclusively on whether the ascending aorta is involved.[66] [67] [68] This system of nomenclature describes type A dissections as any with involvement of the

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ascending aorta (including DeBakey types I and II), and type B dissections as dissection limited to the descending aorta (DeBakey type III). The clinical classification schemes described do not emphasize the location of the primary entry tear or the extent of the distal propagation of the dissection. These two factors are of less prognostic value and can be technically difficult to determine.[69] [70] When identification of the entry site is possible, the culprit primary intimal tear is more easily resected. Although successful resection of the primary tear does not appear to affect early or late survival rates, it may decrease the incidence of late reoperation.[71] Some cases of aortic dissection will present with multiple "primary" tears. Two separate dissections in the same patient may be more common than previously reported. Roberts and Roberts[72] reported that 3 of 40 necropsy patients had separate proximal and distal thoracic dissections. Although all fatal events were caused by rupture of the acute proximal dissections, a separate distal dissection may still pose a risk for late complications, and therefore recognizing two separate dissections may have important implications in terms of follow-up and therapy.[73] Multiple distal "exit" tears, which decompress the false lumen, are extremely common. Time Course Dissections are also differentiated with respect to their time course. Acute dissections are detected within 14 days of the onset of initial symptoms. Chronic dissections TABLE 3-2 -- Nomenclature of Aortic Dissection Dissection Type Ascending aorta involved

Ascending aorta not involved

Classification Stanford type A DeBakey I DeBakey II University of Alabama "ascending"[56] Massachusetts General Hospital "proximal"[57] Stanford type B DeBakey III University of Alabama "descending"[56] Massachusetts General Hospital "distal"[57]

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present more than 2 weeks after onset.[68] [74] This division is arbitrary; it may primarily reflect the fact that the majority of type A dissection patients will die within 2 weeks if untreated.[75] Chronic dissections may be detected because of symptoms or may be an incidental finding. They are differentiated from aortic aneurysms by the presence of an intimal flap and false lumen. These may not be easy to recognize when the false lumen is largely thrombosed. Pronounced atherosclerotic changes may be present in the false lumen in chronic dissections, even when the true lumen walls appear normal and hyperlipidemia is absent.[76] Sequelae The concomitant sequelae of aortic dissection are many and varied. Obstruction of branch vessels may explain acute myocardial ischemia and infarction of cerebral, spinal, bowel, and renal territories. Aortic valve dehiscence with regurgitation, cardiac tamponade from retrograde extension into the pericardium, and frank aortic rupture are all highly morbid consequences.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in Aortic Dissection Time is of the essence when aortic dissection is suspected, and the entire thoracic aorta must be visualized. Transthoracic echocardiography is immediately available, and, in some cases of proximal dissection, it may visualize the ascending aortic intimal flap and false lumen, or a flap in the descending aorta may be visible from the suprasternal (Fig. 3-2) or subcostal windows. Other clues to dissection available from transthoracic approaches include pericardial effusion with or without tamponade, aortic valve insufficiency with or without leaflet dehiscence, aortic root dilation, or regional wall motion abnormalities. Given the variable occurrence of any of these abnormalities, it is not surprising that the sensitivity of transthoracic echocardiography has been limited (Table 3-3) . Transesophageal Imaging Transesophageal echocardiography has elevated ultrasonic diagnosis of dissection into the first line of clinical options (Fig. 3-3) . Multiple studies have documented specificity and sensitivity in the range of 98% and 99%, respectively. The recognized blind spot of TEE, involving the distal ascending aorta and superior aspect of the arch, is an important limitation, especially because entry tears in this region are important to clinical management. The goal of imaging the entire thoracic aorta may therefore require a combination of modalities and approaches, including transthoracic views (often from the suprasternal notch), transesophageal windows, and often direct epiaortic or epicardial views at the time of surgery. Transesophageal echocardiography has many discrete advantages in the diagnosis of acute aortic dissection, the most important of which is its documented accuracy. Erbel 51

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Figure 3-2 Suprasternal views of the transverse and descending aorta demonstrate the intimal flap (A, arrows) as well as an entry tear with systolic flow from the true lumen into the false lumen (B) (color plate).

et al,[77] reporting for the European Cooperative Study Group for Echocardiography on a series of 164 patients suspected of acute dissection, demonstrated sensitivity and specificity rates of 99% and 98%, respectively. Another large study by Nienaber et al[78] compared TEE with magnetic resonance imaging (MRI). Both TEE and MRI had perfect sensitivity; the 100% specificity of MRI exceeded the 68% specificity of TEE. The authors suggested that TEE's limited visualization of common ascending aorta pathologic lesions might have accounted for the higher rate of false-positive findings. In that study, strict criteria for diagnosing dissection were not applied (see later discussion); more stringent criteria could minimize false-positive results. Transthoracic echocardiography TABLE 3-3 -- Imaging Modalities for Aortic Dissection

Study Appelbaum et al[67] Miller[66] Daily et al

Modality TTE

Positive Negative Sensitivity, Specificity, Predictive Predictive A % % Value, % Value, % 77 93 — —

TTE TTE

59 83

83 63

— 80

— 70

Miller[66] TEE Chirillo et TEE al[1] Daily et al TEE

98 98

77 97

— 98

— 97

100

68

82

100

88

94

96

84

88

97

97

85

100

100

100

100

98

98

—

—

[65]

[65]

DeBakey Aortography et al[64] Chirillo et Aortography al[1] Daily et al MRI [65]

Miller[66]

MRI

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83

100

100

86

94

87

—

—

[83]

Erbel et al CT [94]

CT, computed tomography; MRI, magnetic resonance imaging; TE transesophageal echocardiography; TTE, transthoracic echocardiograp from the suprasternal notch provides additional views of this vulnerable area. The sequential use of TEE and CT, aortography, or MRI is clearly extremely powerful in clarifying suspicious or clinically incongruous results.[79] [80] Transesophageal echocardiography provides additional information about left and right ventricular wall motion and global function and aortic and mitral valve competence. Importantly, with acute type A dissections, TEE is able to detect and determine the severity and mechanism of aortic valve regurgitation[81] and may influence the decision to replace or repair the valve. An important advantage of TEE in cases of dissection is its rapid and safe performance in a wide range of clinical environments, including emergency departments, 52

Figure 3-3 Examining the aorta in multiple planes is essential. In this case, the short-axis view (A) suggests an abscess cavity. The long-axis view (B), however, demonstrates a longitudinal dissection flap (arrows). Ao, aorta; LA, left atrium.

intensive care units, and the operating room. TEE requires minimal patient preparation, avoids the contrast agent and x-ray exposure associated with CT and angiography, and eliminates the time delays and practical encumbrances of MRI. Choice of a "best test" must always take into account the individual center's track record with each modality, as well as access issues. Safety of Transesophageal Echocardiography The safety of transesophageal examinations depends on adequate patient

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preparation with respect to pain, anxiety, and airway protection. Careful monitoring of the electrocardiogram and blood pressure is critical to avoiding adverse affects of TEE. In a study of 54 ambulatory patients, TEE was accompanied by an increase in systolic pressure in 77% of patients. This elevation was moderate (average increase of 16 mm Hg) in most patients, but some patients had acute increases of as much as 51 mm Hg.[82] Abrupt increases of blood pressure must clearly be avoided in any patient suspected of having a dissection. Serial blood pressure monitoring, pulse oximetry, intravenous sedation, topical anesthesia, and control of blood pressure with intravenous vasodilators and beta blockers, if needed, are important to patient safety. With these precautions, the majority of patients can undergo esophageal intubation with minimal distress and good hemodynamic stability. Even so, there has been a reported case of aortic rupture occurring during TEE in a patient with an acute dissection, which might have been elicited by retching and elevated blood pressure.[83] Other commonly reported adverse events during transesophageal studies that must be anticipated and avoided are nonsustained atrial and ventricular arrhythmias, excessive vagotonia with transient atrioventricular block, and arterial hypoxemia.[84] Diagnostic Features The diagnosis of aortic dissection is most secure when very specific criteria are met. Identification of an intimal flap, seen as a mobile, linear echo within the vascular lumen, and flow in the true and false channels on either side of the flap are highly sensitive features of dissection. The motion of the intimal flap toward the false lumen during systole may be a helpful feature. A thickening of the aortic wall in excess of 15 mm has also been used as a sign of dissection, suggesting thrombosis of a false channel, which makes the intimal flap difficult to recognize.[85] Strict adherence to these criteria can avoid confusion with imaging artifacts and manifestations of other types of disease and minimize false-positive results.[86] This is particularly important because most patients suspected of having an aortic dissection have evidence of vascular disease involving the thoracic aorta. In one series of 40 patients evaluated for dissection, abnormal aortic findings (including atherosclerotic plaques, intravascular and extravascular masses, thrombi, and dilation) were found in 16 of 17 patients in whom aortic dissection and coronary artery disease were excluded as explanations for their chest pain.[87] Other underlying aortic abnormalities such as coarctation or prior surgical repair may affect clinical management, but they are also important potential sources of misdiagnosis.

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Doppler Findings Color Doppler flow imaging during TEE is an excellent descriptor of aortic flow patterns with acute dissection. Flow in the false channel is variable and complicated; the true lumen, which is often dwarfed by the false channel, is identified by forward systolic flow (Fig. 3-4) . With large proximal entry tears, flow in the nearby segments of the false lumen may have the same direction and timing as the true lumen flow and may reverse in diastole.[88] [89] With 53

Figure 3-4 A short-axis transesophageal echocardiographic view of the descending aorta shows a small anterior true lumen and a larger posterior false lumen that is partially thrombosed (left, arrow). A pulsed Doppler signal from the true lumen, oriented from a long-axis view (right), demonstrates forward systolic flow.

smaller or more distal tears, false lumen flow is less similar to true lumen flow: it may be directed in the opposite direction, and peak velocity may occur later in the cardiac cycle, representing delay of flow into the false lumen. Many areas will show extremely slow, swirling flow with spontaneous echo contrast or partial thrombosis (Fig. 3-5) . These segments tend to be remote from large entry or exit sites, where high-velocity flow keeps these changes from occurring. Finally, areas of complete thrombosis are also seen, and care must be taken to ascertain that the hematoma is entirely intravascular and not actually Figure 3-5 Transesophageal echocardiogram of the descending thoracic aorta demonstrates the true lumen anteriorly and a thrombosing false lumen posteriorly in a patient with acute aortic dissection. As the false lumen thrombosis proceeds, the only clue to dissection may be the apparent "thickening" of the aortic wall.

the result of adventitial rupture, pseudoaneurysm formation, or intramural hematoma (Fig. 3-6) . Multiple communications between the true and false lumens are often identified on careful scanning of the entire thoracic aorta. Some will represent entry sites with flow from the true toward the false channel, and others will be exit sites or have bidirectional flow (Fig. 3-7) . Exit tears,

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where flow re-enters the true lumen from the false lumen, may occur at one or multiple sites. The exact location of a given tear can be estimated from the depth of probe insertion from the incisors, an arbitrary but 54

Figure 3-6 Transesophageal view of the descending aorta at 40 cm from the incisors in a patient with a prior proximal dissection and repair. There is discontinuity of the posterior aortic wall and a large thrombus extending into the periaortic tissues. This was confirmed to be a descending thoracic aortic rupture on subsequent surgery.

convenient reference point. Recording this information at the time of the procedure and on the written report not only is helpful in the surgical correction of dissection, but also is extremely important for comparison with postoperative follow-up TEE studies, in which many of the original tears may still be detectable. Identification of the primary entry site must be deduced from location, size, and flow patterns. In some cases, the primary tear cannot clearly be assigned to any one tear, either because of multiple tears as described Figure 3-7 A short-axis transesophageal echocardiographic view of the descending aorta with a large entry tear in the intimal flap. Pulsed Doppler echocardiography demonstrates flow from true to false lumen during systole. FL, false lumen; TL, true lumen.

earlier or, in some cases, because of the TEE blind spot. Adachi et al[90] were able to identify the entry site in 50 of 57 patients with acute dissection. They were more successful in this with type B dissections (90%) than with type A (83%). As mentioned previously, identification of the primary tear is mostly important because ensuring that the surgical repair resects the primary entry site may decrease the incidence of late reoperation. Complications of Dissection An important goal of echocardiographic imaging in aortic dissection is identifying associated complications. Type A dissections may produce acute aortic insufficiency because of annular dilation or disruption of leaflet suspension. TEE can provide detailed morphologic information regarding

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the quality of the leaflet tissue and the mechanism of aortic insufficiency; these can help in the decision regarding valve resuspension versus replacement. Pericardial effusion and tamponade are manifestations of aortic rupture with dissection and are often readily identified on transthoracic views. The Doppler manifestations of pericardial tamponade may be best obtained from external apical views and may obviate preoperative TEE in the interest of moving the patient emergently to the operating room. Small effusions unassociated with tamponade physiology may not be related to rupture and can be evaluated with contrast echocardiography if time and patient stability allow (Fig. 3-8) . Other rupture syndromes can occur at different sites. Uncontained rupture into the mediastinum or pleural space causes sudden death. Some ruptures are contained by the aortic adventitia, resulting in pseudoaneurysm formation or hematoma. In these cases, TEE can detect the intimal breach as well as the extension of the hematoma into the surrounding tissues; contrast can be helpful in delineating protuberant thrombus and rupture (Fig. 3-9) . An important proviso is to image the aorta at an adequate imaging depth so that such a hematoma 55

Figure 3-8 A four-chamber transesophageal echocardiographic view during contrast injection (Optison) shows contrast in the left ventricular cavity but not in the small pericardial effusion (arrow), which was unassociated with tamponade physiology.

can be recognized. These extravasations can be missed if the imaging field is restricted to the expected aortic contours; disastrous consequences can ensue if the site of the extravasation is not corrected along with the proximal aortic repair. Intramural Hematoma A small number of aortic dissections, estimated at 3% to 5%, occur without apparent intimal disruption.[6] [91] The pathologic process in these cases is rupture of the vasa vasorum into a region of medial degeneration, or possibly rupture of atherosclerotic plaque. Patients with this form of disease tend to be older (mean age, 70 years versus 56 years for communicating dissection) and have frequently had long-term hypertension. Transesophageal images

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Figure 3-9 A transesophageal echocardiographic view of the ascending aorta suggests an intimal flap with possible lumen rupture. Contrast injection (A, Optison) does not confirm extravasation outside the aorta (B, arrow).

demonstrate a thickened aortic wall with intramural echo-free spaces, an increased distance from the TEE probe to the inner aortic wall, and focal distortion of the transverse circular configuration of the aorta. This process has been described on CT images as well, seen as circular high-intensity areas along the aortic wall. [92] In their series, Mohr-Kahaly et al[93] described this type of noncommunicating aortic dissection as a dissection membrane without intimal tear and often involving the entire descending thoracic aorta. Early prognosis in those patients was somewhat better than in those with acute "communicating" dissections; this may reflect the tendency for the noncommunicating medial space to heal with complete thrombus formation.[94] These intramural hematomas may progress to typical dissection (in 33%) or to rupture (in 27%) and therefore usually require surgical rather than medical management.[95] Coronary Artery Involvement Involvement of coronary arteries by aortic dissection is an important issue, and one that raises the question of whether preoperative coronary angiography is mandatory. Involvement of one or both coronary arteries by acute aortic dissection has been estimated to occur in 10% to 20% of cases. [96] In a series of 34 aortic dissection patients, Ballal et al[97] detected coronary involvement with TEE in six of seven surgically documented dissected coronary arteries. Of note, electrocardiographic changes were demonstrated in only two of the six patients with coronary involvement. Adequate views of the ostia and proximal vessel were obtained for 88% of left main arteries and 50% of right coronary arteries overall. Visualization of the ostia and proximal coronary arteries continues to improve as variable imaging plane TEE probes are utilized and higher frequencies become available (Fig. 3-10) . A separate but related issue is whether concomitant coronary artery disease, independent of coronary dissection, is an important consideration that should prompt routine angiography. Given the underlying vascular disease 56

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Figure 3-10 A short-axis transesophageal echocardiographic view of the aortic root demonstrates an intimal flap in proximity to the left coronary ostium. LC, left coronary.

that affects many patients with dissection, it is not surprising that coronary disease has been found in up to 43% of patients with aortic dissection. The benefits of addressing potentially important coronary stenoses must be weighed against the risk of delays and aortic manipulation during acute dissection and adjusted for the patient's baseline likelihood of coronary disease. A series of 122 patients from the Cleveland Clinic found no difference in the in-hospital mortality rate between patients who had emergency coronary arteriography before dissection repair and those who did not. Three fourths of all coronary artery bypass procedures performed in that series were done because of coronary dissection rather than obstruction owing to coronary artery disease.[98]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Surgical Considerations The planning of surgical correction of aortic dissection is heavily influenced by many of the features discussed earlier. The extent of the dissection, the location of primary tears, and concomitant valvular insufficiency and coronary disease are all critically important to the surgical team. In addition, safe cannulation sites, aortic valve repair strategies, need for coronary reimplantation with root replacement, and confirmation of adequate cardiopulmonary bypass and even intra-aortic balloon function can all be addressed with intraoperative ultrasonography (Table 3-4) . Transesophageal imaging during surgery has the advantage of being nonobtrusive (at least for the surgeon, if not for the anesthesiologist) and is commonly also used as an accurate monitor of left ventricular wall motion and volume status. Intraoperative Echocardiographic Monitoring An additional tool for completing the scan of the aorta is intraoperative imaging from the epicardium or surface of the aorta. The unlimited number of acoustic windows from this approach allows careful interrogation of the aortic root, origins of the great vessels, cardiac valves, and left ventricular wall motion. The transesophageal blind spots in the ascending aorta and transverse arch can be thoroughly inspected from the epicardium, and potential aortic cannulation sites can be evaluated from the exterior aortic surface (Fig. 3-11) . Epicardial views give much greater freedom of visualization and measurement of the aortic valve and allow precise annular sizing before cardiopulmonary bypass to expedite selection of the valvular prosthesis. The position of the coronary ostia relative to the dissection and the annulus can be defined precisely with epicardial views, which may also aid in surgical decisions regarding valve-graft conduit placement or coronary ostial reimplantation. The amount of time required for imaging in the surgical field can be limited

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to a few minutes, but this achievement requires an experienced team with a surgeon or cardiologist familiar with the epicardial techniques and TABLE 3-4 -- Operative Uses of Transesophageal Echocardiography in Aortic Dissection Site Feature Pre–Cardiopulmonary Bypass Assessment Aorta Intimal flap Entry tear * Intramural hematoma Aortic rupture Aortic pseudoaneurysm Distal extent of extension Additional tears False lumen flow patterns, including thrombus Branch vessel involvement * Coronary situs and dissection Involvement of origins of great vessels Underlying pathologic condition Atheromatous disease Coarctation Sites of previous repairs Cannulation and cross-clamp sites Aortic valve Insufficiency Suitability for repair vs. replacement Sizing for allograft replacement Mitral valve Insufficiency Suitability for repair vs. replacement Left and right ventricle Wall motion abnormalities Pericardium Effusion Post–Cardiopulmonary Bypass Assessment Aorta Confirm competency of proximal anastomosis

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Establish baseline for false lumen flow and distal tears Aortic valve Confirm competency of repaired valve Mitral valve Confirm competency Left and right ventricle Wall motion Intra-aortic balloon Confirm position in true lumen * Epicardial and/or epiaortic scanning may be important in fully defining these features.

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Figure 3-11 Intraoperative epiaortic view of the transverse aortic arch in a patient with acute proximal aortic dissection. The intima is widely dissected and highly mobile. Note the linear streaking artifact from electrocautery.

views. The combination of epicardial and transesophageal techniques ensures that a high-quality ultrasonographic image is acquired of all segments of the aorta above the diaphragm and eliminates any uncertainty regarding involvement of the ascending aorta. Post-cardiopulmonary bypass images from the epicardium can also be extremely helpful in reassessing proximal tears and interrogating suture lines between aorta and conduit. Transesophageal views at the conclusion of cardiac surgery confirm aortic valve or prosthetic valve competency and allow prompt reinstitution of support if significant aortic insufficiency demands surgical revision. Intraaortic balloon pump position can be assessed with TEE (Fig. 3-12) ; accidental placement of the balloon in the false lumen can be disastrous if not immediately recognized.[99] Finally, postoperative TEE images of the graft and native aorta create a baseline for subsequent follow-up studies. Choice of Surgical Procedure The goal of surgical correction of aortic dissection is to prevent the most common causes of death. For type A dissections, death is caused by

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intrapericardial rupture and tamponade in 80% to 90% of cases and by extrapericardial rupture in 5% to 10%. For type B dissection, rupture causes 60% to 70% of deaths. A localized and conservative operative procedure prevents most deaths and is associated with the lowest number of operative risks. This generally consists of resection of a limited segment of aorta containing the worst damage, including the primary intimal tear if possible, and reconstruction of the local pathologic lesion. If required, however, extensive aortic reconstruction for dissection has been reported with longterm survival rates of 88.5% at 1 year and 81.7% at 9 years in a small series of Marfan's syndrome patients.[100] Coexisting Aortic Insufficiency Aortic valve insufficiency complicating aortic dissection has negative effects on outcome and may dictate important issues in the surgical approach. Preservation of the native aortic valve is possible in 86% of type A dissections with excellent results.[101] If the aortic annulus is abnormal because of Marfan's syndrome or annuloaortic ectasia, aortic valve replacement is preferred because of the limited long-term durability of aortic valve reconstruction in these patients. Initiation of cardioplegia for cardiopulmonary bypass usually depends on a competent aortic valve to allow antegrade perfusion of the coronary arteries; in the presence of significant aortic insufficiency, therefore, individual ostial cannulation or coronary sinus retroperfusion may be indicated. The specific causes of aortic insufficiency are also important[81] normal-appearing leaflets with a prolapsing cusp caused by avulsion of the leaflet base may be amenable to aortic repair with resuspension. Other cases may require aortic valve replacement. The specific involvement of the adjacent aortic root is also critical and may require a variable extent of prosthetic conduit. In some cases, human aortic allografts are used, which have the advantage of supplying both natural aortic valve and root. In proximal aortic involvement, the position and involvement of the coronary ostia are important. Ostial reimplantation may be necessary; coronary bypass grafting may be unavoidable if the coronary arteries are dissected. Coronary arteries may be reattached by direct reimplantation with or without a surrounding button of aortic tissue, reattached to a piece of prosthetic conduit (the Cabrol procedure), or completely bypassed with saphenous vein or internal mammary artery grafts. Figure 3-12 The position of the intra-aortic balloon pump (bright echo,

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upper right) can be confirmed with transesophageal echocardiography. This balloon is placed correctly in the anterior true lumen.

Coexisting Mitral Regurgitation

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Mitral regurgitation is a different example of a valvular abnormality associated with aortic dissection. New insufficiency may result from wall motion abnormalities induced by coronary involvement in the dissection, or from acute left ventricular dilation induced by aortic insufficiency. In other cases, mitral regurgitation is part of the underlying disorder, as is the case with Marfan's syndrome with mitral valve prolapse. Identification of the etiologic factors in the mitral insufficiency (e.g., leaflet degeneration, ventricular dilation, papillary muscle ischemia) will influence the need for repair or prosthetic replacement. Confirmation of results on early postcardiopulmonary bypass images is important, especially when the decision is made to leave the mitral valve alone despite some insufficiency in hopes that correction of acute ischemia or dilation will remedy it. Perfusion of Distal Vascular Beds In an acute aortic dissection, organs may be perfused by either the true or the false lumen flow. Organ under-perfusion may occur if flow to the source lumen is compromised. During surgery, malperfusion may be caused by flow reversal when cardiopulmonary bypass is established by cannulation of the femoral artery, with obliteration of major communications between the two lumens from cross-clamping, or with repair of the dissection itself. Neustein et al[102] describe a case in which femoral cardiopulmonary bypass compressed the true lumen and created severe malperfusion once the dissection was repaired. Perfusion through the new ascending aortic graft allowed immediate reinstitution of forward flow.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Follow-up of Patients after Repair of Aortic Dissection Persistent Intimal Flaps Despite successful surgical repair of aortic dissection, the aorta retains many abnormalities of structure and Figure 3-13 (color plate.) Distal tears are frequently present in aortic dissection. A, During systole, flow crosses from the true lumen into the false lumen. B, During diastole, flow reverses as the false lumen decompresses. C, Tears are usually multiple; here, two discrete tears with systolic flow into the false lumen are seen at the same level of the aorta. TRUE, true lumen; FALSE, false lumen; DESC AO, descending aorta.

flow. Distal to the repair, the intimal flap and false lumen persist. The false lumen may thrombose, or it may retain flow along with entry and exit flow through multiple fenestrations (Fig. 3-13) . One study detected persistent flap and false lumen in 100% of post-repair patients by MRI.[103] Persistent flow in the false lumen can be detected with TEE in the majority of patients after surgical repair. Mohr-Kahaly et al[89] found persistence of the false lumen in 71% of their postoperative patients at a follow-up interval of 1 to 41 months, and in 82% of their medically treated patients. Dinsmore and Willerson[104] have suggested that long-term survival is poorer in patients with persistent flow in the false lumen. Thrombosis of the false channel seems to be protective, a "natural buttress against future or further extension of the dissection." TEE confirms that sites without communications develop low-velocity flow and thrombus, whereas "healing" changes are less likely to occur in regions with significant tears and persistent flow. TEE also demonstrates aggressive atherosclerotic changes and calcification of the "neointima" lining the false channel. Progression of Disease

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Patients with previous dissection may develop progressive abnormalities of both operated and nonoperated aortic segments. Twenty-five to 40% of original dissections will enlarge over time, and the rate and extent of enlargement are primary factors driving the need for reoperation.[96] In addition, dilation of noncontiguous, nonoperated aortic segments develops in 17% of patients with prior acute type A dissections. Early recognition of this progressive downstream aortic pathology allows reoperation in hopes of preventing rupture or redissection.[105] The concern regarding disease progression commits these patients to routine follow-up studies indefinitely. Pseudoaneurysm Formation Pseudoaneurysms form in 7% to 25% of patients with composite grafts, such as a Bentall procedure, secondary to hemorrhage at a suture line dehiscence. [106] Blood between 59

the graft and aortic wall can create supravalvular aortic stenosis.[107] Both of these complications can be detected and completely delineated by TEE,[108] as well as by CT, angiography, and MRI.[109] [110] Color flow Doppler will demonstrate blood flow into the echo-free space between the graft and the aortic wall. Other postoperative complications include endocarditis and the development of an aneurysm in the sinus of Valsalva.[111] Recurrent Disease Because the symptoms of acute redissection or expansion of a chronic dissection are nonspecific, the ability to reassess rapidly and compare the current findings with previous images is extremely important. Younger patients, those with Marfan's syndrome, and those with primary tears involving the transverse arch are particularly prone to progression of their disease.[112] Because TEE may not be able to reproducibly measure the true transverse diameter of an ectatic aorta, suspicion of chronic expansion usually requires additional confirmatory tests such as CT or MRI. Excellent definition of the intimal flap, false channel thrombi and flow patterns, and consistent reference landmarks for serial sizing over time make MRI a highly reliable method. When recurrent chest pain or hemodynamic instability suggests acute redissection, TEE can rapidly define the new pathologic abnormality and its extent. Changes from baseline postoperative or postdissection images can be extremely helpful in clarifying the etiologic

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Limitations of Transesophageal Echocardiography False-Negative Results The interposition of the trachea between the esophagus and the heart creates a blind spot that obscures portions of the distal ascending aorta, superior transverse arch, and origins of the great vessels. As a result, a dissection limited to these areas could be missed by transesophageal imaging alone. This is of concern because the clinical behavior and therapeutic approach to the patient depends largely on whether the proximal aorta is involved in the dissection. The occurrence of this extremely limited type of dissection must be very rare, because the incidence of false-negative studies has been minimal in large series.[76] In addition, large series have not confirmed a positive angiographic or CT result when the initial TEE result was negative. The involvement of the great vessels may not modify the surgical approach and can be assessed at operation.[113] The combination of transesophageal imaging with transthoracic imaging from suprasternal and parasternal windows yields a much more thorough assessment of the arch. CT, MRI, or angiography can also be used to assess this area when there is persistent clinical suspicion of a dissection that is not detectable by TEE. False-Positive Results The path of ultrasound through the esophageal wall and surrounding tissues may generate near-field artifacts that are often disconcertingly linear and run parallel to the aortic wall, mimicking an intimal flap. In patients with severe atherosclerotic disease, calcification in the wall can present similar artifacts and shadows. Abrupt aortic dilation can create a "shelf," which can resemble a flap as well. Determining that these do not represent true intimal flaps depends on recognizing the minimal mobility of these "structures" and the homogeneity of flow on both sides of the line. The ability to change to a second imaging plane, as is possible with biplane or multiple-plane TEE

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probes, is extremely helpful in resolving the issue of artifactual "flaps."[86] [114] Multiple-plane imaging also allows better visualization of the proximal ascending aorta, where atherosclerosis and ectasia can be misinterpreted as dissection.[77] Aneurysmal dilation of the aorta is another source of false-positive TEE studies for dissection. Flow in aneurysmal areas is often low-velocity and swirling, similar to the flow in false channels. The absence of an intimal flap is important in avoiding misdiagnosis in this situation. The possibility that the intimal flap is not seen because the false channel has thrombosed must be excluded by carefully scanning up and down the aorta from the abnormal site. An intimal layer identified proximally or distally may be followed back to the suspicious dilated segment to suggest dissection.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Alternative Approaches to the Diagnosis of Dissection Echocardiography is only one of several diagnostic tests for dissection. The choice of imaging procedure, as well as the clinical confidence in positive or negative results, needs to be gauged relative to the test's performance (see Table 3-3) . Angiography is a time-honored diagnostic method for aortic dissection that may identify the intimal flap and false lumen. In addition, it can define coronary and great vessel ostial involvement. Its sensitivity and specificity for dissection (88% and 94%, respectively) are limited by false lumen thrombosis, intramural hematomas, and equal flow in true and false lumens.[115] [116] The last case is also an important limitation for CT studies, in which differential flow may not be detectable even with dynamic CT imaging.[117] The lower sensitivity (83%) of CT reflects its poor definition of the intimal flap and entry tear. Despite CT's high specificity (90% to 100%), a negative CT result in the presence of high clinical suspicion of dissection requires a second confirmatory test. Extremely slow, swirling flow within a segment of the false channel may not be completely differentiated from thrombus by MRI.[118] MRI's excellent definition of the important components of aortic dissection have resulted in its excellent sensitivity, however, which approaches 100%.[119] The pragmatic issues of imaging acutely ill patients with needs for hemodynamic monitoring or infusion of medications or those at risk for hemodynamic collapse continue to make TEE preferable in many acute settings. As mentioned earlier, MRI may be the procedure of choice for the follow-up of patients with repaired or chronic dissections.

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In their comparison of angiography, TEE, CT, and MRI techniques for aortic dissection, Barbant et al[120] used data from several published series to compare the accuracy and predictive value of these tests in populations

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with high, intermediate, and low prevalence of disease. For populations with a high risk of dissection, positive predictive values for all tests exceeded 85%. In intermediaterisk populations (prevalence, 10%), positive predictive values were greater than 90% for CT, MRI, and TEE but less than 65% for angiography. When the disease prevalence was low (1%), as it probably is in most clinical applications of these tests, the positive predictive values were less than 50% for angiography, CT, and TEE, and remained high only for MRI (100%). In any population, the negative predictive value was greater than or equal to 85% for all tests. These results suggest that TEE and other imaging techniques may not perform as well in a low-risk ambulatory population, as suggested by published results from higher-prevalence populations.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications and Future Directions Transesophageal echocardiographic images provide excellent spatial resolution, especially with the higher frequencies that are becoming available. Combining this with the high temporal resolution of M-mode methods has allowed investigation of aortic distensibility in normal patients, in patients at risk for vascular disease, and after repair of aneurysms or dissection. These types of methods have documented decreases in elastic aortic properties after aortic surgery, which predispose patients to redissection.[121] Two-dimensional echocardiographic assessments of aortic distensibility have been shown to estimate changes in aortic mechanical properties resulting from increasing age[122] Doppler estimates of pulse wave velocity Figure 3-14 Three-dimensional constructed views of the aorta in shortaxis (left) and long-axis (right) orientations demonstrate the intimal flap separating true and false lumens.

are also being investigated as measures of aortic compliance.[123] Animal models for validation of these parameters include chronic models of accelerated atherogenesis, as well as acute aortic ischemia and decreased distensibility generated by removal of the vasa vasorum.[124] High-frequency ultrasonic integrated backscatter methods are also being applied to the aortic wall (see Chapter 9) . Recchia et al[125] detected sixfold decreases in backscatter and 15-fold decreases in anisotropy, suggesting marked disorganization of the three-dimensional aortic architecture in the aortas of Marfan's syndrome patients as compared with the aortas of normal patients. These types of functional and structural investigations may improve our recognition of aortic disease of many stages and refine our prediction of risk of dissection. Technologic advances in aortic visualization are occurring based on

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improved transducer designs with more elements, greater freedom in imaging plane, and higher frequencies. These will be the basis for expanding the role of echocardiography in caring for aortic dissection patients, who will be undergoing new types of surgery involving new developments such as stents, balloon fenestration, and aortic valve resuspension.[126] Intravascular ultrasonography has become an extremely important imaging technique within the coronary vessels ( see Chapter 15 Chapter 16 ). Expanding this technology to the larger vessels and cardiac chambers has required lower-frequency transducers.[127] The potentially powerful role of intravascular ultrasonography in combination with angiography may have an important effect on the sensitivity of that technique. Similarly, tissue characterization with ultrasonography may be useful in identifying abnormalities of vessel wall composition, architecture, and material properties and aid in the prediction of primary or secondary dissection events. New ultrasonographic contrast agents that pass from venous injections through the pulmonary bed and into 61

the left-sided circulation may potentially aid in defining entry tears and important communications between true and false lumens.[128] [129] This improved spatial information will also be greatly aided by threedimensional constructs that can be generated from tomographic echocardiographic acquisitions (Fig. 3-14) .[130]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary The grim prognosis of patients with undetected acute aortic dissection demands a rapid, highly sensitive, and efficient diagnostic approach. Transesophageal imaging has excellent sensitivity for aortic dissection, its multiple complications, and its imitators. Intraoperatively, TEE or epicardial imaging identifies surgically relevant features of aortic valve damage and ventricular function. Patients with postoperative or chronic dissection can be followed with TEE, and serious events such as expansion or redissection can be quickly defined when symptoms of recurrent pain appear. Echocardiography is already established as a mainstay in the emergent diagnosis, treatment, and follow-up of patients with acute and chronic aortic dissection, and new technologies and applications will continue to expand its role in the future.

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References 1. Chirillo F, Marchiori MC, Andriolo L, et al: Outcome of 290 patients with aortic

dissection: A 12 year multicentre experience. Eur Heart J 1990;11:311–319. 2. Demos TC, Posniak HV, Marsan RE: CT of aortic dissection. Semin Roentgenol

1989;24:22–37. 3. Lilienfeld DE, Gunderson PD, Sprafka JM, et al: Epidemiology of aortic aneurysms:

1. Mortality trends in the United States, 1951–1981. Arteriosclerosis 1987;7:637–643. 4. Satler FL, Levine S, Kent KM, et al: Aortic dissection masquerading as acute

myocardial infarction: Implication for thrombolytic therapy without cardiac catheterization. Am J Cardiol 1984;54:1134–1145. 5. Davidson E, Weinberger I, Rotenberg Z, et al: Elevated serum creatinine kinase

levels: An early diagnostic sign of acute dissection of the aorta. Arch Intern Med 1988;148:2184–2186. 6. Hirst AE, Johns VJ, Kime SW: Dissecting aneurysm of the aorta: A review of 505

cases. Medicine 1958;37:217–279. 7. Wilcox RG, Olsson CG, Skene AM, et al: Trial of plasminogen activator for

mortality reduction in acute myocardial infarction. Lancet 1988;2:525–530. 8. Butler J, Davies AH, Westaby S: Streptokinase in acute aortic dissection. Br Med J

1990;300:517–519. 9. Weiss P, Weiss I, Zuber M, Ritz R: How many patients with acute dissection of the

thoracic aorta would erroneously receive thrombolytic therapy based on the electrocardiographic findings on admission? Am J Cardiol 1993;72:1329–1330.

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10. Lee RT, Kamm RD: Vascular mechanics for the cardiologist. J Am Coll Cardiol

1994;23:1289–1295. 11. Mukherjee DP, Kagan HM, Jordan RE, Franzblau C: Effect of hydrophobic elastin

ligands on the stress-strain properties of elastin fibers. Connect Tissue Res 1976;4:177–179. 12. Buntin CM, Silver FH: Noninvasive assessment of mechanical properties of

peripheral arteries. Ann Biomed Eng 1990;18:549–566. 13. Dzau VJ, Safar ME: Large conduit arteries in hypertension: Role of the vascular

renin-angiotensin system. Circulation 1988;77:947–954. 14. Yoganathan AP, Cape EG, Sung HW, et al: Review of hydrodynamic principles for

the cardiologist: Applications to the study of blood flow and jets by imaging techniques. J Am Coll Cardiol 1988;12:1344–1353. 15. Robicsek F, Thubrikar MJ: Hemodynamic considerations regarding the mechanism

and prevention of aortic dissection. Ann Thorac Surg 1994;58:1247–1253. 16. MacSweeney ST, Young G, Greenhalgh RM, Powell JT: Mechanical properties of

the aneurysmal aorta. Br J Surg 1992;79:1281–1284. 17. Carson MW, Roach MR: The strength of the aortic media and its role in the

propagation of aortic dissection. J Biomech 1990;23:579–588. 18. Rubin K: Aortic dissection and rupture in Turner syndrome. J Pediatr

1993;122:670. 19. Ashraf SS, Shaukat N, Masood M, et al: Type I aortic dissection in a patient with

osteogenesis imperfecta. Eur J Cardiothorac Surg 1993;7:665–666. 20. Singer A, Cooke JP: Aortic aneurysm. In Cooke JP, Frolich ED (eds): Current

Management of Hypertensive and Vascular Diseases. Philadelphia, BC Decker, 1992, pp 166–171. 21. Cooke JP, Kazimer FJ, Orszulak TA: The penetrating aortic ulcer: Pathology,

diagnosis and management. Mayo Clin Proc 1988;63:718–725. 22. Harris JA, Bis KG, Glover JL, et al: Penetrating atherosclerotic ulcers of the aorta

[discussion, pp 98–99]. J Vasc Surg 1994;19:90–98. 23. Pretre R, Chilcott M: Blunt trauma to the heart and great vessels. N Engl J Med

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 3 di 11

1997;336:626–632. 24. Vlahakes GJ, Warren RL: Traumatic rupture of the aorta. N Engl J Med

1995;332:389–390. 25. Parmley LF, Mattingly TW, Manion WC, et al: Nonpenetrating traumatic injury of

the aorta. Circulation 1958;17:1086–1101. 26. Smith MD, Cassidy JM, Souther S, et al: Transesophageal echocardiography in the

diagnosis of traumatic rupture of the aorta. N Engl J Med 1995;332:356–362. 27. Pieters FA, Widdershoven JW, Gerardy AC, et al: Risk of aortic dissection after

aortic valve replacement. Am J Cardiol 1993;72:1043–1047. 28. Katz ES, Tunick PA, Colvin SB, et al: Aortic dissection complicating cardiac

surgery: Diagnosis by intraoperative biplane transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:217–222. 29. Sakamoto I, Hayashi K, Matsunaga N, et al: Aortic dissection caused by

angiographic procedures. Radiology 1994;191:467–471. 30. Dorsey DM, Rose SC: Extensive aortic and renal artery dissection following

percutaneous transluminal angioplasty. J Vasc Interv Radiol 1993;4:493–495. 31. Braunwald E: Heart Disease. Philadelphia, WB Saunders, 1992, pp 1536–1551. 32. Nolte JE, Rutherford RB, Nawaz S, et al: Arterial dissections associated with

pregnancy. J Vasc Surg 1995;21:515–520. 33. Roberts WC: Aortic dissection: Anatomy, consequences and causes. Am Heart J

1981;101:195–241. 34. Oskoui R, Lindsay J Jr: Aortic dissection in women less than 40 years of age and

the unimportance of pregnancy. Am J Cardiol 1994;73(11):821–823. 35. McDermott JC, Schuster MR, Crummy AB, Acher CW: Crack and aortic

dissection. Wisc Med J 1993;92:453–455. 36. Das G: Cardiovascular effects of cocaine abuse. Int J Clin Pharmacol Ther Toxicol

1993;31:521–528. 37. Biagini A, Maffei S, Baroni M, et al: Familiar clustering of aortic dissection in

polycystic kidney disease. Am J Cardiol 1993;72:741–742.

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Pagina 4 di 11

38. Schor JS, Horowitz MD, Livingstone AS: Recreational weight lifting and aortic

dissection: Case report. J Vasc Surg 1993;17:774–776. 39. Chauvel C, Cohen A, Albo C, et al: Aortic dissection and cardiovascular syphilis:

Report of an observation with transesophageal echocardiography and anatomopathologic findings. J Am Soc Echocardiogr 1994;7:419–421. 40. Eber B, Tscheliessnigg KH, Anelli-Monti M, et al: Aortic dissection due to

discontinuation of beta-blocker therapy. Cardiology 1993;83:128–131. 41. Evans JM, Bowles CA, Bjornsson J, et al: Thoracic aortic aneurysm and rupture in

giant cell arteritis: A descriptive study of 41 cases. Arthritis Rheum 1994;37:1539– 1547. 62

42. Gersbach P, Lang H, Kipfer B, et al: Impending rupture of the ascending aorta due

to giant cell arteritis. Eur J Cardiothorac Surg 1993;7:667–670. 43. Marsalese DL, Moodie DS, Lytle BW, et al: Cystic medial necrosis of the aorta in

patients without Marfan's syndrome: Surgical outcome and long-term follow-up. J Am Coll Cardiol 1990;16:68–73. 44. Child AH: Marfan syndrome—current medical and genetic knowledge: How to

treat and when. J Card Surg 1997;12(2 suppl):131–135. 45. McDonald GR, Schaff HV, Pyeritz RE, et al: Surgical management of patients with

Marfan syndrome and dilatation of the ascending aorta. J Thorac Cardiovasc Surg 1981;81:180–186. 46. Murdoch JL, Walker BA, Halpern BL, et al: Life expectancy and causes of death in

the Marfan syndrome. N Engl J Med 1972;286:804–808. 47. Gott VL, Laschinger JC, Cameron DE, et al: The Marfan syndrome and the

cardiovascular surgeon. Eur J Cardiothorac Surg 1996;10:149–158. 48. Pyeritz RE, McKusick VA: The Marfan syndrome diagnosis and management. N

Engl J Med 1979;300:772–777. 49. Hollister DW, Godfrey M, Sakai LY, Pyeritz RE: Immunohistologic abnormalities

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 5 di 11

of the microfibrillar-fiber system in the Marfan syndrome. N Engl J Med 1990;323:152–159. 50. Hirata K, Triposkiadis F, Sparks E, et al: The Marfan syndrome: Abnormal aortic

elastic properties. J Am Coll Cardiol 1991;18:57–63. 51. Jeremy RW, Huang H, Hwa J, et al: Relation between age, arterial distensibility,

and aortic dilatation in the Marfan syndrome. Am J Cardiol 1994;74:369–373. 52. Come PC, Fortuin NJ, White RI, McKusick VA: Echocardiographic assessment of

cardiovascular abnormalities in the Marfan syndrome: Comparison with clinical findings and with roentgenographic estimation of aortic root size. Am J Med 1983;74:465–474. 53. Brown OR, DeMots H, Kloster FE, et al: Aortic root dilatation and mitral valve

prolapse in Marfan's syndrome: An echocardiographic study. Circulation 1975;52:651–657. 54. Roman MJ, Rosen SE, Kramer-Fox R, Devereux RB: Prognostic significance of

the pattern of aortic root dilation in the Marfan syndrome. J Am Coll Cardiol 1993;22:1470–1476. 55. Legget ME, Unger TA, O'Sullivan CK, et al: Aortic root complications in the

Marfan's syndrome: Identification of a lower risk group. Heart 1996;75:389–395. 56. Gott VL, Pyeritz RE, Magovern GJ Jr, et al: Surgical treatment of aneurysms of the

ascending aorta in the Marfan syndrome: Results of composite-graft repair in 50 patients. N Engl J Med 1986;314:1070–1074. 57. Pyeritz RE: Predictors of dissection of the ascending aorta in Marfan syndrome

[abstract]. Circulation 1991;84(suppl II):II-351. 58. Roberts WC, Honig HS: The spectrum of cardiovascular disease in the Marfan

syndrome: A clinicomorphologic study of 18 necropsy patients and comparison to 151 previously reported necropsy patients. Am Heart J 1982;104:115–135. 59. Groenink M, Lohuis TA, Tijssen JG, et al: Survival and complication free survival

in Marfan's syndrome: Implications of current guidelines. Heart 1999;82:499–504. 60. Gott VL, Greene PS, Alejo DE, et al: Replacement of the aortic root in patients

with Marfan's syndrome. N Engl J Med 1999;29;340:1307–1313. 61. Coselli JS, LeMaire SA, Buket S: Marfan syndrome: The variability and outcome

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of operative management. J Vasc Surg 1995;21:432–443. 62. Tambeur L, David TE, Unger M, et al: Results of surgery for aortic root aneurysm

in patients with the Marfan syndrome. Eur J Cardiothorac Surg 2000;17:415–419. 63. Svensson LG, Labib SB: Aortic dissection and aortic aneurysm surgery. Curr Opin

Cardiol 1994;9:191–199. 64. DeBakey ME, McCollum CH, Crawford ES, et al: Dissection and dissecting

aneurysms of the aorta: Twenty year follow-up of five hundred twenty seven patients treated surgically. Surgery 1982;92:1118–1134. 65. Daily PO, Trueblood HW, Stinson EB, et al: Management of acute aortic

dissections. Ann Thorac Surg 1970;10:237–247. 66. Miller DC: Surgical management of aortic dissections: Indications, perioperative

management, and long term results. In Doroghazi RM, Slater EE (eds): Aortic Dissection. New York, McGraw-Hill, 1983, pp 193–243. 67. Applebaum A, Karp RB, Kirklin JW: Ascending vs. descending aortic dissections.

Ann Surg 1976;183:296. 68. DeSanctis RW, Doroghazi RM, Austen WG, Bucklet MJ: Aortic dissection. N

Engl J Med 1987;317:1060–1067. 69. Miller DC: Acute dissection of the descending thoracic aorta. Chest Surg Clin

North Am 1992;2:347–378. 70. Dinsmore RE, Willerson JT: Dissecting aneurysms of the aorta: Angiographic

features affecting prognosis. Radiology 1972;105:567. 71. Miller DC: Improved follow-up for patients with chronic dissections. Semin

Thorac Cardiovasc Surg 1991;3:270–276. 72. Roberts CS, Roberts WC: Aortic dissection with the entrance tear in the

descending thoracic aorta: Analysis of 40 necropsy patients. Ann Surg 1991;213:356– 368. 73. Duch PM, Chandrasekaran K, Karalis DG, Ross JJ Jr: Improved diagnosis of

coexisting types II and III aortic dissection with multiplane transesophageal echocardiography. Am Heart J 1994;127:699–701. 74. Slater EE: Aortic dissection: Presentation and diagnosis. In Doroghazi RM, Slater

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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EE (eds): Aortic Dissection. New York, McGraw-Hill, 1983, pp 61–70. 75. Wheat MW Jr: Intensive drug therapy. In Doroghazi RM, Slater EE (eds): Aortic

Dissection. New York, McGraw-Hill, 1983, pp 165–192. 76. Grossman CM, D'Agostino AN: Advanced atherosclerosis in false channels of

chronic aortic dissection. Lancet 1993;342:1428–1429. 77. Erbel R, Engberding R, Daniel W, et al: Echocardiography in diagnosis of aortic

dissection. Lancet 1989;1:457–461. 78. Nienaber CA, Spielmann RP, von Kodolitsch Y, et al: Diagnosis of thoracic aortic

dissection: Magnetic resonance imaging versus transesophageal echocardiography. Circulation 1992;85:434–447. 79. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic

dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9. 80. Victor MF, Mintz GS, Kotler MN, et al: Two-dimensional echocardiographic

diagnosis of aortic dissection. Am J Cardiol 1981;48:1155–1159. 81. Movsowitz HD, Levine RA, Hilgenberg AD, et al: Transesophageal

echocardiographic description of the mechanisms of aortic regurgitation in acute type A aortic dissection: Implications for aortic valve repair. J Am Coll Cardiol 2000;36:884–890. 82. Geibel A, Kasper W, Behroz A, et al: Risk of transesophageal echocardiography in

awake patients with cardiac diseases. Am J Cardiol 1988;62:337–339. 83. Silvey SV, Stroughton TL, Pearl W, et al: Rupture of the outer partition of aortic

dissection during transesophageal echocardiography. Am J Cardiol 1991;68:286–287. 84. Pearson AC, Castello R, Labovitz AJ: Safety and utility of transesophageal

echocardiography in the critically ill patient. Am Heart J 1990;119:1083–1089. 85. Iliceto S, Nanda NC, Rizzon P, et al: Color Doppler evaluation of aortic dissection.

Circulation 1987;75:748–755. 86. Appelbe AF, Walker PG, Yeoh JK, et al: Clinical significance and origin of

artifacts in transesophageal echocardiography of the thoracic aorta. J Am Coll Cardiol 1993;21:754–760. 87. Chan KL: Usefulness of transesophageal echocardiography in the diagnosis of

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conditions mimicking aortic dissection. Am Heart J 1991;122:495–504. 88. Erbel R, Mohr-Kahaly S, Rennollet H, et al: Diagnosis of aortic dissection: The

value of transesophageal echocardiography. Thorac Cardiovasc Surg 1987;35:126– 133. 89. Mohr-Kahaly S, Erbel R, Rennollet H, et al: Ambulatory follow-up of aortic dissection by transesophageal two-dimensional and color-coded Doppler echocardiography. Circulation 1989;80:24–33. 90. Adachi H, Kyo S, Takamoto S, et al: Early diagnosis and surgical intervention of

acute aortic dissection by transesophageal color flow mapping. Circulation 1990;82 (suppl 4):19–23. 91. Eichelberger JP: Aortic dissection without intimal tear: Case report and findings on

transesophageal echocardiography. J Am Soc Echocardiogr 1994;7:82–86. 63

92. Yamada T, Tada S, Harada J: Aortic dissection without intimal rupture: Diagnosis

with MR imaging and CT. Radiology 1988;168:347–352. 93. Mohr-Kahaly S, Erbel R, Kearney P, et al: Aortic intramural hemorrhage

visualized by transesophageal echocardiography: Findings and prognostic implications. J Am Coll Cardiol 1994;23:658–664. 94. Erbel R, Oelert H, Meyer J, et al: Effect of medical and surgical therapy on aortic

dissection evaluated by transesophageal echocardiography: Implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993;87:1604–1615. 95. Robbins RC, McManus RP, Mitchell RS, et al: Management of patients with

intramural hematoma of the thoracic aorta. Circulation 1993;88:II1–II10. 96. Crawford ES: The diagnosis and management of aortic dissection. JAMA

1990;264:2537–2541. 97. Ballal RS, Nanda NC, Gatewood R, et al: Usefulness of transesophageal

echocardiography in assessment of aortic dissection. Circulation 1991;84:1903–1914. 98. Penn MS, Smedira N, Lytle B, et al: Does coronary angiography before emergency

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aortic surgery affect in-hospital mortality? J Am Coll Cardiol 2000;35:889–894. 99. Nakatani S, Beppu S, Tanaka N, et al: Application of abdominal and

transesophageal echocardiography as a guide for insertion of intraaortic balloon pump in aortic dissection. Am J Cardiol 1989;64:1082–1083. 100. Niinami H, Aomi S, Tagusari O, et al: Extensive aortic reconstruction for aortic

aneurysms in Marfan syndrome. Ann Thorac Surg 1999;67:1864–1867. 101. Mazzucotelli JP, Deleuze PH, Baufreton C, et al: Preservation of the aortic valve

in acute aortic dissection: Long-term echocardiographic assessment and clinical outcome. Ann Thorac Surg 1993;55:1513–1517. 102. Neustein SM, Lansman SL, Quintana CS, et al: Transesophageal Doppler

echocardiographic monitoring for malperfusion during aortic dissection repair. Ann Thorac Surg 1993;56:358–361. 103. Laissy JP, Blanc F, Soyer P, et al: Thoracic aortic dissection: Diagnosis with

transesophageal echocardiography versus MR imaging. Radiology 1995;194:331–336.

104. Dinsmore RE, Willerson JT: Dissecting aneurysms of the aorta: Angiographic

features affecting prognosis. Radiology 1972;105:567–572. 105. Heinemann M, Laas J, Karck M, Borst HG: Thoracic aortic aneurysms after acute

type A aortic dissection: Necessity for follow-up. Ann Thorac Surg 1990;49:580–584.

106. Barbetseas J, Crawford S, Safi HJ, et al: Doppler echocardiographic evaluation of

pseudoaneurysms complicating composite grafts of the ascending aorta. Circulation 1992;85:212–222. 107. Vilacosta I, Camino A, San Roman JA, et al: Supravalvular aortic stenosis after

replacement of the ascending aorta. Am J Cardiol 1992;70:1505–1507. 108. San Roman JA, Vilacosta I, Castillo JA, et al: Role of transesophageal

echocardiography in the assessment of patients with composite aortic grafts for therapy in acute aortic dissection. Am J Cardiol 1994;73:519–521. 109. Nath PH, Zollikofer C, Castaneda-Zuniga WR, et al: Radiological evaluation of

composite aortic grafts. Radiology 1979;131:43–51. 110. Pucillo AL, Schechter AG, Moggio RA, et al: Postoperative evaluation of

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ascending aortic prosthetic conduits by magnetic resonance imaging. Chest 1990;97:106–110. 111. Simon P, Owen AN, Moidl R, et al: Sinus of Valsalva aneurysm: A late

complication after repair of ascending aortic dissection. Thorac Cardiovasc Surg 1994;42:29–31. 112. Haverich A, Miller DC, Scott WC, et al: Acute and chronic aortic dissections:

Determinant of long-term outcome for operative survivors. Circulation 1985;72(suppl 2):22–34. 113. Chan KL: Impact of transesophageal echocardiography on the treatment of

patients with aortic dissection. Chest 1992;101:406–410. 114. Adachi H, Omoto R, Kyo S, et al: Emergency surgical intervention of acute aortic

dissection with the rapid diagnosis by transesophageal echocardiography. Circulation 1991;84(suppl 3):14–19. 115. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA: Diagnostic imaging in

the evaluation of suspected aortic dissection: Old standards and new directions. N Engl J Med 1993;328:35–43. 116. Bansal RC, Chandrasekaran K, Ayala K, Smith DC: Frequency and explanation of

false negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393–1401. 117. Mugge A, Daniel WG, Laas J, et al: False-negative diagnosis of proximal aortic

dissection by computed tomography or angiography and possible explanations based on transesophageal echocardiographic findings. Am J Cardiol 1990;65:527–529. 118. Barzilai B, Waggoner AD: Diagnosis of aortic dissection with transesophageal

echocardiography. Cardiology 1991;91:73–83. 119. Laissy JP, Blanc F, Soyer P, et al: Thoracic aortic dissection: Diagnosis with

transesophageal echocardiography versus MR imaging. Radiology 1995;194:331–336.

120. Barbant SD, Eisenberg MJ, Schiller NB: The diagnostic value of imaging

techniques for aortic dissection. Am Heart J 1992;124:541–543. 121. Imawaki S, Maeta H, Shiraishi Y, et al: Decrease in aortic distensibility after an

extended aortic reconstruction for Marfan's syndrome as a cause of postoperative acute aortic dissection DeBakey type I: A report of two cases. Surg Today

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1993;23:1010–1013. 122. Lacombe F, Dart A, Dewar E, et al: Arterial elastic properties in man: A

comparison of echo-Doppler indices of aortic stiffness. Eur Heart J 1992;13:1040– 1045. 123. Lehmann ED, Hopkins KD, Gosling RG: Aortic compliance measurements using Doppler ultrasound: In vivo biochemical correlates. Ultrasound Med Biol 1993;19:683–710. 124. Stefanadis CI, Karayannacos PE, Boudoulas HK, et al: Medial necrosis and acute

alterations in aortic distensibility following removal of the vasa vasorum of canine ascending aorta. Cardiovasc Res 1993;27:951–956. 125. Recchia D, Sharkey AM, Bosner MS, et al: Sensitive detection of abnormal aortic

architecture in Marfan syndrome with high-frequency ultrasonic tissue characterization. Circulation 1995;91:1036–1043. 126. Peterson AH, Williams DM, Rodriguez JL, Francis IR: Percutaneous treatment of

a traumatic aortic dissection by balloon fenestration and stent placement. Am J Roentgenol 1995;164:1274–1276. 127. Weintraub AR, Schwartz SL, Pandian NG, et al: Evaluation of acute aortic

dissection by intravascular ultrasonography. N Engl J Med 1990;323:1566–1567. 128. McRee D, Matsuda M, Stratton J, et al: Transthoracic contrast echocardiographic

detection of ascending aortic dissection. J Am Soc Echocardiogr 1999;12:1122–1124. 129. Kimura BJ, Phan JN, Housman LB: Utility of contrast echocardiography in the

diagnosis of aortic dissection. J Am Soc Echocardiogr 1999;12:155–159. 130. Sugeng L, Cao QL, Delabays A, et al: Three-dimensional echocardiographic

evaluation of aortic disorders with rotational multiplanar imaging: Experimental and clinical studies. J Am Soc Echocardiogr 199;10:120–132.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Section 2 - The Left Ventricle 65

Chapter 4 - Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Gerard P. Aurigemma MD Pamela S. Douglas MD William H. Gaasch MD

The quantitation of left ventricular (LV) systolic function, size, and geometry is critical to the proper evaluation and management of patients with all types of heart disease.[1] For example, the assessment of LV function in patients with coronary artery disease provides better prognostic information than does knowledge of the number of diseased vessels (Fig. 41) . Even when only one or two vessels are diseased, a low ejection fraction (EF) is associated with a higher mortality than that seen in patients with three-vessel disease and a normal EF.[2] Large LV systolic and diastolic volumes are also associated with a poor prognosis[3] [4] thus, a patient with a reduced EF after a myocardial infarction can be categorized according to subsequent risk based on the absolute end-systolic volume (Fig. 4-2) . Furthermore, information concerning LV size and geometry has important

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therapeutic implications, in view of the salutary effects of therapy with angiotensin converting enzyme inhibitors on postinfarction remodeling and prognosis in patients with a reduced EF.[5] Similarly, in cardiomyopathy of any cause, mortality remains high in patients with an EF less than 35%,[6] [7] even with medical therapy. A depressed EF is uniformly present in patients with idiopathic dilated cardiomyopathy and is due to a combination of afterload excess and depressed contractility. In this setting, indices of LV geometry, such as the relative wall thickness or the mass/volume ratio (Fig. 4-3) , provide prognostic information that is independent of the EF.[8] Conversely, it is important to identify the significant percentage of patients with congestive heart failure symptoms who have a normal EF.[9] [10] Measurement of LV volume, mass, and function can provide data that are necessary to define the optimal time for surgery in patients with volume overload hypertrophy owing to chronic, severe mitral or aortic regurgitation. In this regard, the prognostic usefulness of ventricular enddiastolic and end-systolic volumes, the EF, the ratio of end-diastolic volume to mass, systolic stress-shortening relations, and end-systolic pressure-volume relations has been tested in a variety of clinical studies. The end-systolic volume and EF appear to provide the most useful clues to prognosis.[11] [12] [13] [14] [15] [16] [17] [18] [19] [20] Certainly, a most important determinant of postoperative survival is the level of LV systolic function (Fig. 4-4) (Figure Not Available) . In pressure overload hypertrophy owing to aortic stenosis, an assessment of systolic function is perhaps less important than in the regurgitant lesions. Although severe depression of the EF may indicate an increased surgical risk, patients with an EF as low as 20% to 25% can show substantial clinical improvement after aortic valve replacement.[21] [22] [23] In such patients, excessive systolic loads are usually responsible for the low EF; this situation is termed inadequate hypertrophy or afterload excess. Alternatively, 66

Figure 4-1 The relation between left ventricular ejection fraction (EF) and survival in patients with single-, double-, and triple-vessel coronary artery disease (CAD). The negative impact of a low EF is seen in all three groups. Survival is better in patients with three-vessel CAD and a

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normal EF than in those with one- or two-vessel disease and a low EF. (Adapted from Mock MB, Rindqvist I, Fisher LD, et al: Circulation 1982;66:562–567. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:368.) Figure 4-2 The relation between left ventricular end-systolic volume (ESV) and survival in patients with normal, near-normal, and abnormal ejection fraction (EF). Data were obtained from patients with a history of myocardial infarction. ESV is a major predictor of survival when the EF is less than 50%. (Adapted from White HD, Norris RM, Brown MA, et al: Circulation 1987;76:44–51. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:369.) Figure 4-3 The relation between left ventricular mass/volume (M/V) ratio and survival in patients with an ejection fraction (EF) higher than and less than 20%. Data were obtained from patients with dilated cardiomyopathy. Patients with a normal M/V ratio exhibit better survival than those with a low ratio; this trend is seen in EF categories. (Adapted from Feild BJ, Baxley WA, Russell RO Jr, et al: Circulation 1973;47:1022–1031. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:370.)

67

Figure 4-4 (Figure Not Available) Relation of preoperative ventricular function to postoperative survival. These and other published data (see text) indicated that preoperative ventricular function is an important determinant of postoperative survival. ESD (echo), end-systolic dimension by echocardiography; SEF (angio), systolic ejection fraction by angiography; SEF (echo), systolic ejection fraction by echocardiography. (Adapted from Hoshino PK, Gaasch WH: Arch Intern Med 1986;146:349–352. Copyright © 1986 American Medical Association. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:371.)

excessive or inappropriate hypertrophy, indicated by a high relative wall thickness, appears to identify a group of patients having a high perioperative risk[24] [25] in this situation, a normal or high EF does not seem to be beneficial. In aortic stenosis, therefore, indices of LV geometry[26] (relative wall thickness) appear to provide prognostic clues that are not reflected in the EF. It is well established that increased LV mass is a strong predictor of

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cardiovascular morbidity as well as cardiovascular and all-cause mortality, even when age, blood pressure, and other risk factors are considered[27] [28] [29] [30] [31] [32] (see Chapter 32) . Some investigators have suggested that LV geometry provides prognostic information that is incremental to the extent of LV hypertrophy.[29] [30] [31] For example, an increased ratio of LV wall thickness to cavity dimension[32] identifies patients at higher risk for cardiovascular morbidity and mortality (Table 4-1) ; whether this incremental risk is truly independent of LV mass has been called into question by other data.[33] Thus, a substantial body of clinical research has demonstrated the prognostic value of indices of LV volume, mass, geometry, and function. Most if not all of these indices are routinely available to the clinician from standard M-mode and two-dimensional (2D) and Doppler echocardiography. In this chapter the echocardiographic techniques for evaluating LV geometry, stress, and systolic function are reviewed. Principles and methods are discussed, TABLE 4-1 -- Relation Between Morbid Events and the Pattern of Left Ventricular Geometry Normal LV Mass LVH P RWT ≥ RWT < RWT ≥ RWT < 0.45 (N = 0.45 (N = 0.45 (N = 0.45 (N = 29) 40) 34) 150) 0 3 10 21 < .001

CV deaths (%) CV events 11 15 23 31 .03 (%) All deaths 1 6 10 24 < .01 (%) The prognostic value of LVH for morbid events in men (at an average of 10.2 years of follow-up) is striking. For all end points, the RWT provides incremental value for assessing risk. P-value obtained by analysis of variance. CV, cardiovascular; LVH, left ventricular hypertrophy; RWT, relative wall thickness. From Koren M, Devereux R, Casale PN, et al: Ann Intern Med 1991;114:345–352.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Definitions and Theoretical Considerations The systolic pumping of the left ventricle is a complex process that involves a coordinated contraction of subendocardial, midwall, and subepicardial muscle fibers. These fibers are arranged in a complex, helical fashion. At the equator of the ventricle, midwall fibers are oriented circumferentially; contraction of these fibers mainly contributes to a decrease in the minor axis (or dimension) of the ventricle and is responsible for generation of much of the stroke volume (Fig. 4-5) . Longitudinally oriented fibers in the subendocardium and subepicardium contribute to shortening of the long axis of the ventricle, also contributing to stroke volume. In addition to circumferential and long-axis shortening, the apex of the left ventricle rotates counterclockwise during systolic contraction, and the base rotates clockwise (as viewed from the apex).[34] [35] Such "twist," like fiber shortening, appears to be influenced by the contractile state of the myocardium. In concert with these shortening and twisting motions, wall thickening contributes to volume displacement and generation of the stroke volume.[36] Preload, afterload, contractility, and geometry influence shortening and thickening.[37] The pumping activity of the left ventricle provides oxygenated blood to the tissues of the body; therefore, the stroke volume can be used as a parameter of the pump performance of the ventricle (Table 4-2) . Because LV systolic pressure and stroke volume are inversely related, using stroke work as an index of ventricular performance can be more appropriate; a stroke work parameter credits the ventricle for the development of pressure and for shortening. When performance is assessed relative to end-diastolic fiber length or a related parameter, ventricular function can be described. Thus, a ventricular function curve can be generated by plotting stroke work against end-diastolic pressure, diameter, volume, or wall stress. Volume loading therefore produces an increment in stroke work (i.e., performance) through use of the Frank-Starling

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68

Figure 4-5 Circumferential and longitudinal fibers contribute to wall thickening and volume displacement. These functions are influenced by left ventricular preload, afterload, contractile state, and geometry. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:374.)

mechanism. By contrast, increased myocardial contractility also can produce an increment in stroke work, but in this case performance is augmented through a change in inotropic state rather than by a change in end-diastolic fiber length. In other words, contractility refers to a basic property of the myocardium that reflects the intensity of its active state. The use of the term contractility should be restricted to situations in which a change in performance or EF cannot be ascribed to a change in preload or afterload. Contractile function is a more general term used to describe changes in performance or function that could be affected by changes in inotropic state, fiber length, or loads. Thus, a change in the EF might best be classified as a change in contractile function; this term is often used interchangeably with systolic function. To fully describe the ventricle, it is necessary to define several additional terms that refer to its mechanical properties. Stress is defined as the force per unit cross-sectional area of a material. It is an engineering term used to compare loads borne by different-sized elements of a material; the total load is less important than the load per unit of material. If the same load is borne by a smaller amount of material, the stress on that material is higher. In a spherical model of the left ventricle, wall stress (σ) is directly proportional to the transmural pressure (P) and inversely proportional to the product of chamber radius (R) and wall thickness (Th): σ = PR/2Th In the left ventricle, geometry is much more complex, and several components of stress exist within the wall (Fig. 4-6) . Of these, meridional and circumferential TABLE 4-2 -- Aspects of Ventricular Function Pump performance The pumping activity of the left ventricle that results in the delivery of oxygenated blood to the tissues. Stroke volume and stroke work are

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parameters of pump performance Ventricular function Left ventricular performance assessed relative to end-diastolic fiber length (or related parameter) Myocardial contractility A basic property of the myocardium that reflects its active state, rather than loading conditions Contractile function A descriptor of ventricular performance or function that is affected by inotropic state, fiber length, or load stresses have most commonly been used in the analysis of LV mechanics. The meridional stress vector is oriented in the longitudinal or apex-to-base direction and represents the component of the load resisting long-axis shortening; circumferential stress is oriented along the equator, perpendicular to the long axis (see Fig. 4-6) and represents the component of the load resisting minor-axis shortening. Meridional stress (σm ) can be calculated as

σm = P · LVID / [4 · Th(1 + LVID/Th)] where P is pressure (mm Hg), Th is wall thickness, and LVID is cavity dimension.[38] This stress parameter does not require measurement of the long axis of the LV cavity. Circumferential stress (σc ) can be calculated as σc = P · a2 [1 + (b2 /r2 )]/(b2 − a2 ) where P is end-systolic pressure (mm Hg), a is the internal (endocardial) radius, b is the external (epicardial) radius, and r is the midwall radius.[39] Other approaches to the calculation of circumferential stress, using minorand major-axis dimensions, have been evaluated.[40] Formulas for calculation of meridional and circumferential stress using 2D echocardiographic data are as follows:[41] σm = 1.33P Am /Ac · 103 kdyn/cm2

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where At is the short-axis area subtended by the LV epicardium and right

side of the septum, Ac is the cavity (endocardial) area, and Am = At − Ac or

myocardial area, and L is the LV cavity length, obtained from the apical four-chamber view. Two-dimensional and M-mode methods yield somewhat different results, with M-mode-derived σm being higher than 2D-

derived values, even in normal subjects. In spherical ventricles, σm by any method tends to overestimate afterload.[42]

The determination of wall stress requires assessment of LV pressure. Invasively determined values may be combined with echocardiographic dimensions, but they are often not available or simultaneously obtained. Three methods have been proposed for using noninvasive recordings to ascertain LV systolic pressures; LV diastolic 69

Figure 4-6 Schematic of the left ventricle (LV) (represented as a truncated ellipsoid) illustrating the major stress vectors. Meridional stress (σm ) is the force acting along the long axis of the LV; meridional stress opposes long-axis shortening. Circumferential stress (σc ) is the force acting in the equatorial direction; circumferential stress opposes circumferential fiber shortening, and circumferentially oriented fibers are located in the midwall of the left ventricle. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:375.)

pressures (and therefore diastolic stress) cannot be reliably determined noninvasively. Although these methods assume that there is no LV outflow gradient, the first and easiest method assumes that end-systolic LV pressure can be approximated by peak arterial pressure.[38] Thus, cuff systolic blood pressure is substituted for LV end-systolic pressure. The second method involves calibration of an externally recorded pulse recording using cuff systolic and diastolic pressures, with calculation of arterial pressures at the dicrotic notch.[43] The third involves the substitution of mean arterial pressure, derived from cuff recording, for end-systolic pressure, given the

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close correlation between these two values, as shown by Rozich.[44] Because wall stress parameters incorporate appropriate size normalization, they allow comparison among the mechanical properties of different hearts. End-systolic wall stresses, calculated using end-systolic pressures (or the surrogates discussed earlier) and dimensions, are taken as indices of LV afterload, whereas end-diastolic wall stress, calculated using end-diastolic pressure and dimension, is a measure of LV preload. Preload is the force (i.e., load) acting to stretch the resting myofibril. Preload is commonly estimated as the LV end-diastolic pressure, diameter, or volume, but to be more precise, this force should be normalized for each unit cross-sectional area of muscle and expressed as end-diastolic wall stress. In this manner, LV preload is analogous to the preload on a strip of isolated cardiac muscle in a myograph. This force, which acts to stretch the myocardium, is resisted by the stiffness of the muscle. Thus, the extent to which the myocardial fiber is stretched depends on an interaction between preload and muscle stiffness. [45] Because preload influences initial fiber length, it affects LV systolic performance. This phenomenon, which operates on a beat-to-beat basis, is generally referred to as Starling's law of the heart or the Frank-Starling mechanism. The preload reserve of the ventricle depends on the baseline hemodynamic conditions and the stiffness of the myocardium. Thus, in the upright posture, normal human subjects exhibit a substantial preload reserve, whereas in the recumbent posture they may exhibit a minimal preload reserve. The difference in preload reserve is related to difference in the baseline end-diastolic volume, which is lower in the upright posture than it is when the subject is recumbent, owing to the differences in venous return. This fact should be kept in mind when interpreting exercise studies; the end-diastolic volume of the normal left ventricle generally increases during upright exercise, but it may not during recumbent exercise. Moreover, the ability to recruit the Frank-Starling mechanism may also be limited in hypertrophied ventricles that have abnormal ventricular compliance characteristics. Thus, in patients with aortic stenosis or hypertensive heart disease, there may be little or no increment in LV end-diastolic volume during exercise, and consequently the EF may not increase normally.[46] [47] [48] Such limited preload reserve occurs as a result of a steep diastolic pressure-volume relation in which large changes in filling pressure cause only small changes in volume.[49] This mechanism may even underlie marginal LV function in the basal state.[45]

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Despite a low EF, many dilated hearts (particularly those with compensated mitral or aortic regurgitation) generate a normal or high stroke volume. In this instance, although the Frank-Starling mechanism may be a contributing factor, the large stroke volume is primarily a function of the large enddiastolic volume. In other words, the presence of a large LV chamber does not necessarily indicate use of preload reserve at the fiber level. Many such hearts retain the ability to use preload reserve to augment stroke volume. By contrast, in end-stage heart failure, preload reserve may be exhausted (Fig. 4-7) . Afterload can be thought of as the force (i.e., stress) developed by the myocardium after the onset of contraction. As described by the Laplace relation, afterload (systolic wall stress) is directly related to LV systolic pressure and radius, and inversely related to wall thickness. Afterload varies with time, and thus it can be calculated at the instant of aortic valve opening, at the end of ejection, or at any instant throughout systole. Whereas LV systolic pressure and systemic vascular resistance can affect afterload, neither of these should be considered the equivalent of afterload. [50] [51] [52] Likewise, aortic input impedance influences systolic pressure and stress, but impedance is not the equivalent of afterload.[53] In aortic stenosis, the LV systolic pressure may exceed 250 mm Hg, but if there is an appropriate increase in LV wall thickness, the force borne by each unit of heart muscle might remain near normal (i.e., afterload is normal). [51] [52] , [54] On the other hand, an acute increase in systolic pressure or chamber size can result in an increased afterload.[55] By virtue of the inverse relation between load and shortening, an acute increase in afterload generally causes a decrease in shortening, and vice versa (see Fig. 4-7) . Contractility can be defined as the quality of cardiac muscle that determines performance independent of loading conditions. Contractility is easiest to study and define in isolated heart muscles when loading conditions are held constant. For example, if resting length is held constant, the addition of digitalis or norepinephrine to an isolated muscle preparation results in an increase in the 70

Figure 4-7 Left, The relation between left ventricular afterload and fiber shortening. Two coordinates of afterload are shown on a normal curve. If preload is constant, an acute increase in afterload will cause a decrease in

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shortening. During acute interventions in a clinical setting, the relation between aortic pressure and stroke volume is similar to this schematic afterload-shortening curve. A failing ventricle exhibits a depressed curve with reduced shortening; thus, the ejection fraction and stroke volume can be depressed despite a normal afterload. Middle and right, Afterload-shortening relations in moderate and severe left ventricular dysfunction. In moderate dysfunction (middle), shortening in the basal state (A) is depressed; if some preload reserve is present, mild pressor stress does not substantially reduce shortening (B); more marked pressor stress will depress shortening (C). In severe dysfunction (right), inotropic state is markedly depressed and preload reserve is exhausted; under these circumstances, any pressor stress will cause a decrease in shortening. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:377–378.)

extent and velocity of force development and shortening; such increased performance under constant loading conditions reflects an augmented inotropic state (i.e., increased contractility). In many cardiac diseases, abnormal LV pump function may be caused by disordered loading conditions, depression of contractility, or both. For this reason, it may be difficult to determine the exact cause of decreased fiber shortening. Accordingly, there has been considerable interest in the development of a sensitive index of contractility that is not affected by changes in loading conditions.[56] [57] Unfortunately, there is no completely load-independent index of basal contractile state. Thus, directional changes in contractility (during acute hemodynamic interventions) are relatively easy to demonstrate, but it is not possible to define a basal level of contractility in patients with chronic heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Mass, Volume, and Geometry Remodeling of the left ventricle in valvular heart disease, heart failure, and hypertensive heart disease is characterized by changes in LV mass and geometry. Descriptors of LV geometry include the relative wall thickness, short axis/long axis ratio, and volume/mass ratio. These descriptors are easily obtained by M-mode and 2D echocardiography. As suggested earlier, alterations in LV geometry have been used to assist risk stratification in a variety of diseases and to describe more completely remodeling changes effected by valve replacement. In patients with idiopathic dilated cardiomyopathy, for example, a poorer survival is associated with larger short-axis dimension and a greater ratio of short/long axes (i.e., a more spherical LV geometry).[58] The relative wall thickness, when used to estimate the "adequacy" of LV hypertrophy in patients with idiopathic dilated cardiomyopathy, also predicts the increase in contractility in response to dobutamine infusion[59] cardiomyopathy patients with a diminution in relative wall thickness appear to have an attenuated contractile response to dobutamine infusion. In the following section, the methods used to calculate LV mass and describe LV geometry are reviewed. M-mode Echocardiography Mass

Whereas newer and more costly tomographic methods, such as ultrafast computed tomography (CT) and magnetic resonance imaging (MRI), permit more precise quantitation, echocardiography remains the most commonly used technique for estimating LV mass and geometry. M-mode echocardiography is universally available and relatively low cost, and there is a considerable body of evidence supporting its accuracy in LV mass quantitation.[60] [61] [62] [63] Quantitation of mass (see also Chapter 32) is based on the geometric assumption that the ventricle is a prolate ellipsoid with a

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2:1 long axis/short axis ratio.[60] [61] [62] [63] [64] [65] In practical terms, LV mass estimates are most accurate in ventricles with normal shape,[64] [65] specifically, a long axis/short axis ratio that approximates 2:1. It is assumed, of course, that minor axis dimensions are measured in a region free of wall motion abnormalities. This assumption is invalidated in ischemic heart disease with focal wall motion abnormality or in right ventricular overload. Estimates of myocardial mass and volume are derived from LV minor axis dimensions obtained with the transducer in the parasternal position (Fig. 4-8) . Under 2D echocardiographic guidance, the ultrasound beam is aligned so that it is perpendicular to the interventricular septum and 71

Figure 4-8 Schematic of an M-mode echocardiogram obtained using two-dimensional echocardiographic guidance. Measurements are made coincident with the Q wave of the simultaneous electrocardiogram. LVIDd, left ventricular internal dimensions in diastole; LVIDs, left ventricular internal dimensions in systole; PWTd, posterior wall thickness in diastole; PWTs, posterior wall thickness in systole; STd, ventricular septal thickness in diastole; STs, ventricular septal thickness in systole. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:381.)

posterior wall at a level slightly below the mitral leaflet tips; the transducer is then rotated to obtain a short-axis view. This approach maximizes the LV cavity dimension and ensures that proper beam orientation with respect to the papillary muscles is obtained. LV mass is estimated from measurements of septal and posterior wall thickness and LV cavity dimensions at enddiastole using the anatomically validated cube formula[60] [61] [62] [63] [64] [65] LV mass = 0.8{1.04(STd + LVIDd + PWTd )3 − LVIDd 3 } + 0.6 g where STd is the diastolic septal thickness, LVIDd is the diastolic LV cavity dimension, PWTd is the diastolic posterior wall thickness, and 1.04 is the

specific gravity of myocardium. The measurements are made using the American Society of Echocardiography standard technique.[60] As shown by Devereux et al,[61] LV mass estimates made with American Society of Echocardiography measurements overestimate true anatomic LV weights by 20%, necessitating a correction factor of 0.8.

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Volume

A simple estimate of LV volume may be obtained from the minor-axis dimension, derived by M-mode echocardiography as V = LVID3 The geometric assumptions are similar to those used for LV mass calculation. However, in the dilated, spherical left ventricle encountered in long-standing valvular regurgitation or dilated cardiomyopathy, the ratio of length to minor-axis dimension decreases, leading to significant overestimation of LV volumes by this simple method. Teichholz et al[66] derived a formula that attempts to correct for this problem: Vd = [7/(2.4 + LVIDd )] · LVIDd 3 LV volumes derived with this formula correlate well with single-plane angiographic estimates.[64] The Teichholz method produces the most accurate volume estimates of any of the M-mode formulas.[67] Because Mmode echocardiography provides minor-axis dimensions of the left ventricle in systole and diastole, the Teichholz method may be used to compute LV volumes at end-systole and end-diastole, and thus to derive stroke volume and cardiac output. A compelling advantage of this method is that LV volume can be determined rapidly from easily obtained M-mode measurements. Relative Wall Thickness

M-mode estimates of myocardial mass and volume are derived from LV minor-axis dimensions obtained with the transducer in the parasternal position (see Fig. 4-8) . These same measurements are used to describe LV geometry. Although the amount of LV mass is an important 72

predictor of subsequent cardiac events in hypertensive disease, the geometry and pattern of LV hypertrophy also provide insight into the pathophysiology of hypertensive hypertrophy[68] and may confer prognostic information. [29] [30] [31] The most commonly used index of the pattern of hypertrophy is the relative wall thickness (RWT),[32] [68] which is calculated as

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RWT ± 2 · PWT/LVID where PWT is the posterior wall thickness and LVID is the LV internal dimension, respectively; relative wall thickness may be measured in diastole or systole. Relative wall thickness also has been expressed as h/R, where h is wall thickness and R is cavity radius. Ford[69] and others[52] [54] have shown that in the normal or compensated ventricle, the relative wall thickness increases in direct proportion to elevations in systolic pressure (Fig. 4-9) . Assuming that there is not a substantial shape change as the ventricle enlarges (i.e., during normal growth), the relation is independent of absolute chamber size. [52] It is also assumed that the magnitude and transmural distribution of stresses are the same in normal ventricles of different size. Systolic dysfunction with dilation is usually associated with a lower relative wall thickness; in contrast, chronic pressure overload produces an increment in wall thickness with little change in the chamber radius (a high relative wall thickness).[70] In untreated hypertensive patients, LV mass and relative wall thickness determinations may be used to subdivide Figure 4-9 Relationship between relative wall thickness (RWT, equivalent to the ratio of thickness to radius) and level of systolic pressure in patients with aortic stenosis (black circles). In normal hearts (open diamonds), RWT increases in direct proportion to the level of systolic pressure. Individuals with a higher thickness-to-radius ratio than predicted by the level of pressure are considered to have inappropriate (or excessive) hypertrophy; by contrast, individuals whose thickness-to-radius ratio is less than that predicted by the level of pressure have inadequate hypertrophy. In normal hearts the relationship between peak pressure (P) and RWT, as defined by Ford,[69] is RWT = 0.0027P.

the population into four general categories (Fig. 4-10) : 1. Concentric hypertrophy (elevations in both LV mass and relative wall thickness) 2. Eccentric hypertrophy (elevation in LV mass with normal relative wall thickness) 3. Concentric remodeling (normal mass but abnormally high relative wall thickness) 4. Normal LV mass and relative wall thickness

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In a population of untreated hypertensive patients, the majority had normal LV mass and normal relative wall thickness; concentric hypertrophy was the least common abnormal pattern observed. [68] What is the clinical relevance of the mass and geometry subcategories? Patients with concentric hypertrophy have a relatively high incidence of adverse cardiovascular and noncardiovascular events compared with patients with eccentric hypertrophy.[30] [31] [32] In addition, concentric geometry, even without hypertrophy, appears to be associated with adverse consequences during follow-up (see Table 4-1) , although not all studies have confirmed that the incremental risk is independent of LV mass. [71] Thus, in hypertensive disease, as noted earlier, incremental information regarding risk for both cardiovascular and noncardiovascular events is provided by assessing geometry as well as LV mass. The relative wall thickness may provide insight into the appropriateness of hypertrophy. There is occasionally more muscle mass than would be required for the observed pressure; thus, a very high relative wall thickness, such as is encountered in hypertrophic cardiomyopathies, "hypertensive hypertrophic cardiomyopathy of the elderly,"[72] [73] [74] [75] uncommonly in hypertension, and not infrequently in aortic stenosis,[70] indicates excessive or inappropriate LV hypertrophy. In our experience, relative wall thickness values greater than 0.8 are uncommon in aortic stenosis, but when present, they appear to represent inappropriate hypertrophy. Indeed, values exceeding 0.8 predict a systolic pressure in excess of 300 mm Hg, a pressure rarely seen, even in adults with aortic stenosis[70] (see Fig. 4-9) . Extreme concentric hypertrophy, with exceedingly high values for relative wall thickness, has been described in elderly patients undergoing aortic valve replacement for aortic stenosis.[25] The interaction among shape, load, and function is complex and important, because each one may influence the others. A decompensated heart clearly demonstrates abnormalities of all three—low relative wall thickness, high afterload, and reduced function—yet it is not possible to state which abnormality is primary. Does the ventricle dilate, thereby raising afterload and reducing pump performance, or is shortening impaired first, leading to dilation, which then raises afterload? Human studies shed little light because of the lengthy time course of disease and other confounding factors; animal studies suggest that all three events may occur in concert.[76] Two-Dimensional Echocardiography Two-dimensional echocardiography permits acquisition of data with

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excellent spatial orientation, because the left 73

Figure 4-10 Left ventricular (LV) volume, mass, and geometry, stress, and systolic shortening in various cardiac disorders. Different cardiac disorders are classified with respect to LV mass, volume, relative wall thickness (RWT), and volume/mass (V/M) ratio, as well as stress and shortening. (Redrawn from Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:385.)

ventricle can be sampled in real time at multiple levels. In many laboratories, therefore, 2D echocardiography is the principal noninvasive means for quantitation of LV volume as well as for the assessment of global and regional systolic function. LV mass and volume quantitation by 2D echocardiography requires high-quality images and true long- and short-axis images of the left ventricle. A variety of geometric models is used to approximate the shape of the left ventricle and to compute LV volumes, including the prolate ellipse model, the hemiellipse model, and others that represent a combination of geometric shapes. Detailed review of the geometric principles underlying these volumes for formulas may be found elsewhere.[64] [65] [77] This chapter emphasizes the applications most suited for clinical use. Mass

Theoretically, 2D echocardiographic assessment of LV mass can improve on the limitations of M-mode methods; mean wall thickness can be backcalculated from planimetered short-axis myocardial area, which helps avoid reliance on single-dimensional determinations. One of the most practical 2D methods for mass calculation, the area-length method, approximates the left ventricle as a cylinder-hemiellipsoid; volume is calculated for both the inner and outer "shells" (the LV cavity and total myocardial area, respectively), as shown schematically in Figure 4-11 : V = 5/6 A × L where A is planimetered short-axis area obtained at the high papillary muscle level and L is the LV length obtained from the apical four-chamber view; area and length measurements are made at end-diastole. In this way, total LV and internal (LV cavity) volume are determined; myocardial

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volume is the difference between the inner and outer shells. [65] [77] [78] [79] Myocardial volume is then multiplied by the specific gravity of myocardium (1.04 g/cc) to compute myocardial mass. The model has been validated by comparing echocardiographic and anatomic LV mass in 21 patients who underwent 2D echocardiographic studies shortly before death [79] there was an excellent correlation between anatomic and echocardiographic mass (r = 0.93 and SEE = 31 g). It is important to note that phantom-generated regression equations were used to correct clinical mass measurements for each 2D echocardiographic machine. Although more complicated 2D echocardiographic methods for mass determination have been associated with greater accuracy, the cylinder-hemiellipsoid area-length method represents a relatively simple and practical approach that yields acceptable results.[64] [65] Volume

As noted earlier, a variety of geometric approaches is described for the quantitation of LV volume from 2D 74

Figure 4-11 Schematic illustrating the technique used to calculate left ventricular (LV) mass with the area-length method. Endocardial and epicardial borders are traced (and papillary muscles excluded). Mean wall thickness (t) is back-calculated from the LV cavity area (A2 ) and total area (A1 ), and minor axis radius (b). The sum a + d is equivalent to the diastolic LV cavity length, which is measured from the apical four-chamber view. (Adapted from Schiller N, Shah P, Crawford M, et al: J Am Soc Echocardiogr 1989;2:358–367. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:389.)

echocardiography. There are theoretical advantages for use of the Simpson's rule algorithm, and this approach is preferable when ventricular shape is distorted, such as with an apical aneurysm. The Simpson's rule approach, also known as the method of discs, is predicated on the fact that the volume of the whole left ventricle (or of any object) may be computed as the sum of individual "slice" volumes. In general, the accuracy of the measurement varies directly with the number of slices:

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V is total volume (cavity or myocardial), A is planimetered area, and T is slice thickness. Myocardial volume is then multiplied by the specific gravity of myocardium to estimate myocardial mass. It is best to compute LV volume from two orthogonal apical views with the LV length divided equally along that length[74] [75] [76] [77] [78] [79] apical four- and two-chamber views at end-diastole should be recorded to maximize ventricular length. The use of the cylinder-hemiellipsoid (area-length) method for calculating the volume component represents a reasonable alternative to the method of discs. The method described by Tortoledo et al[80] allows for the computation of end-diastolic volume from 2D-derived minor- and majoraxis dimension and has been shown to correlate closely with single-plane angiographic volumes: EDV = (Dmax × Lmax × 3.42) − 6.44 where Dmax and Lmax are maximal minor- and major-axis dimensions

derived from apical views.

In general, LV volumes derived from 2D echocardiographic measurements are smaller than those obtained by contrast angiography.[64] [65] There are many explanations for these findings, including foreshortening of the maximal length of the left ventricle on 2D echocardiography; differences in measurement of the LV long axis; and the fact that angiographic contrast material fills intermyocardial interstices, contributing to overall LV cavity volume, whereas echocardiography does not account for this volume.[64] Geometry

Compared with M-mode echocardiography, 2D echocardiography offers improved spatial orientation, because the left ventricle can be sampled in real time at multiple levels. Accordingly, 2D echocardiography may be used to quantify the LV mass and chamber volumes of abnormally shaped ventricles, and, because measurements of LV length are possible, this technique provides more extensive description of LV geometry. Estimates of both the short axis/long axis ratio and the volume/mass ratio[81] [82] [83] [84] are possible with 2D echocardiography. In patients with normal LV mass and function, the short axis/long axis ratio ranges from 0.45 to 0.62.[82] [83]

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In untreated hypertensive patients with normal LV systolic function, the short axis/long axis ratios range from 0.52 ± 0.04 in patients with concentric remodeling to 0.63 ± 0.03 in patients with eccentric hypertrophy.[68] The short axis/long axis ratio also provides information regarding ventricular compensation in valvular heart disease. As in patients with dilated cardiomyopathy, in whom the ventricle becomes more spherical, patients with poorly compensated aortic stenosis and regurgitation (those with low EFs) tend to have higher short axis/long axis ratios. [84] A high ratio in turn alters the relationship of meridional to circumferential stresses, a change in the distribution of afterload that may affect overall pump performance[84] (see Fig. 4-10) . [84]

The end-diastolic volume/mass ratio in normal men and women, as defined by 2D echocardiography, is approximately 0.8.[83] It has been traditionally assumed that the ratio of LV volume to mass is relatively constant from 75

the most basal to the most apical slices of the left ventricle. A study using the technique of ultrafast CT, which can provide approximately eight tomographic slices through the left ventricle, showed that in normal subjects, the volume/mass ratio decreased from approximately 0.8 at the most basal slice, a finding consistent with results of 2D echocardiography, to approximately 0.25 at the most apical slice. LV mass exceeds LV volume at each slice location.[85] It is important to emphasize that 2D echocardiographic methods have limitations that militate against their routine use for quantitation in the clinical setting[64] [65] (Table 4-3) . M-mode echocardiography samples at approximately 1000 frames per second, whereas the frame rate for 2D echocardiography is orders of magnitude less: 30 to 60 frames per second under optimal conditions. There is considerable image degradation when stop frames are used, making precise endocardial definition problematic. Near-field artifact and poor lateral resolution make it difficult to reliably identify endocardium around the entire ventricular perimeter. Apical views often do not yield images of sufficient quality for manual tracing.[86] Computations tend to be tedious. It is likely that digital technology, which has permitted the growth of stress echocardiography, will be routinely used for LV volume quantitation; at present, however, it appears that most 2D quantitation performed clinically is still subjective.[86] [87]

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In view of the limitations discussed earlier, there is considerable interest in the development of online, beat-to-beat volumetric quantitation. One potential solution is the technique of automated boundary detection, which uses integrated backscatter to define a border between echocardiographic picture elements (pixels) assigned to myocardium or LV cavity.[88] [89] [90] Thus, the area of the LV cavity can be displayed for each frame, plotted with respect to time, and the fractional area change computed; the technique may be applied to images obtained from either parasternal or apical windows. Several validation studies have been performed with this technique[88] [89] [90] and have shown an excellent correlation between online LV cavity areas and offline manual planimetry of the corresponding 2D echocardiographic images (Fig. 4-12) . Further software development now permits online estimation of beat-to-beat LV volumes (using the arealength or TABLE 4-3 -- Limitations of Ultrasound Methods for Mass and Volume Quantitation General All methods require high-quality images with good endocardial definition Most methods require geometric assumptions about left ventricular shape and are applicable only to normally shaped hearts M-mode echocardiography Small errors in measurement may lead to large errors in mass/volume determinations May be insensitive to small changes in mass (20–40 g) observed in response to antihypertensive treatment Two-dimensional echocardiography Limited frame rate, making timing of cardiac events difficult Considerable degradation when images are stop-framed Apical images may foreshorten true left ventricular length Tedious, labor-intensive computations Simpson's rule methods), dV/dt, time to peak positive dV/dt, and time to peak negative dV/dt. Software upgrades, such as beat selection and signal averaging, may enhance the application of the automated border detection system for clinical use, which is currently somewhat limited by a significant percentage of technically inadequate studies[86] and other

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technical problems. Assuming these problems will be solved, automated border detection has particular promise for online quantitation of LV volumes obtained by intraoperative transesophageal echocardiography, in view of the generally excellent image quality with this technique. Other automated edge detection systems are in development, and this remains an area of active investigation. Another area of active research is that of three-dimensional (3D) echocardiography (see Chapter 10) . This technique promises to provide the most accurate ultrasound determination of LV volume, mass, and EF, largely because the need for geometric assumptions and on-axis views will be eliminated.[91] [92] [93] [94] Alternative Methods for Quantitation of Left Ventricular Structure and Function In addition to cardiac ultrasound, the clinician may use other noninvasive and invasive techniques to measure LV size and function. A brief review of some of the more commonly used techniques is therefore appropriate. Doppler Echocardiography

Routine Doppler measurements of flow velocity may be combined with echocardiographic dimensional data to determine stroke volume and cardiac output. [94] [95] [96] This technique is known as the time velocity integral (TVI) method. The appeal of this method is that, unlike M-mode and 2D echocardiographic measurements, TVI measurements do not require geometric assumptions about cardiac shape. To compute stroke volume using the TVI method, an integral of the systolic pulsed wave flow envelope in the aortic outflow tract is computed (Fig. 413) . To obtain this velocity spectrum, the transducer is placed in the apical position with the sample volume positioned at the level of the aortic valve annulus. Although the TVI may be obtained in other locations, such as the pulmonary artery or LV inflow, accuracy seems to be best with measurements made in the proximal ascending aorta.[65] The cross-sectional linear dimension of the proximal ascending aorta is obtained in the same approximate location that the pulsed or continuous wave Doppler velocity spectrum is recorded, using the parasternal long-axis window (see Fig. 413) . Stroke volume (SV) is then the product of the TVI and cross-sectional area of the aortic annulus, which is assumed to be circular:

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CSA = π(D/22 ) SV = CSA · TVI

76

Figure 4-12 Technique of automated boundary detection and its application to the study of cardiac volumes and ejection fraction (EF) in clinical practice. Top, A parasternal short-axis image with corresponding enddiastolic and end-systolic areas (EDA and ESA, respectively); the fractional area change for each beat is also displayed below the two-dimensional image. Bottom, In an apical four-chamber view, the corresponding beat-to-beat volume display is shown. From these measurements, the EF can be computed beat to beat. End-diastolic and end-systolic volumes (EDV and ESV, respectively) are given in milliliters.

where CSA is the cross-sectional area of the aortic annulus, D is the linear dimension of the annulus, and TVI is the time velocity integral. Stroke volume and cardiac output obtained by the TVI method correlate well with results of concurrent thermodilution cardiac output determinations in patients who were without left-sided valvular regurgitation.[95] [96] The Doppler TVI method is highly dependent on accurate measurements of aortic annular diameter, because the CSA formula involves squaring the annular dimension; it is also assumed that the Doppler beam is oriented parallel to flow. This method can be particularly useful for following changes in a single patient—beat to beat, or over weeks to months. Doppler echocardiographic assessments of LV function do not depend on measurements of ventricular size (and thus avoid the attendant geometric assumptions and sources of error); they rely on information derived from flow velocities.[96] This information includes measurement of LV stroke volume, cardiac output, and peak flow velocity of aortic ejection, all of which, being ejection phase indices, are dependent on afterload. One approach to the noninvasive assessment of dP/dt has used the continuous wave profile of the mitral regurgitant flow.[97] [98] [99] As we have seen, stroke volume, and thereby cardiac output, may be calculated by measuring the area under the flow velocity contour and multiplying it by the cross-sectional

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77

Figure 4-13 Calculation of cardiac output using the time velocity integral (TVI) method. The continuous wave Doppler-derived TVI (also called velocity time integral [VTI]) is displayed. The cross-sectional area is 3.14 cm2 (π times the square of the annular radius, which is 1 cm2 in this instance) and the TVI is 24.7 cm by planimetry. The stroke volume is 78 cc per beat by equation, yielding a cardiac output of 4.3 L/min at the patient's heart rate of 55.

area of the annulus.[94] [95] Accuracy is dependent on recording velocity parallel to flow and, most importantly, on the aortic diameter measurement used to calculate the cross-sectional area. This method also requires that there be no significant aortic or mitral valve disease. Aortic acceleration and peak flow velocity are both reduced in cardiomyopathy,[94] but this has not received widespread clinical acceptance as a diagnostic tool. Magnetic Resonance Imaging

In many respects, MRI is the ideal method to quantitate LV mass and volume. It combines the attributes of ultrafast CT (noninvasive and permitting true tomographic imaging throughout the entire cardiac volume) with several unique advantages. MRI does not require contrast administration or ionizing radiation, and there is no limitation to image plane selection; thus, the heart may be imaged not only in the familiar contrast ventriculography views but also in the long- and short-axis planes used in standard transthoracic echocardiography. MRI usually provides images with excellent contrast between myocardium and the blood pool so that manual or even semiautomated computerized mass and volume quantitation is possible.[100] For these reasons, MRI has provided the most accurate noninvasive estimates of LV mass and volume to date,[101] even in ventricles distorted by myocardial infarction.[102] A more recent advance, gradient-echo magnetic resonance techniques, displays the heart in cine loop fashion at up to 64 frames per cardiac cycle; this technique can be used to quantitate EF and regional function and to estimate the severity of valvular regurgitation. [103] [104] [105] Although MRI can be used to estimate mass, volume, and EF,[36] [106] [107] ultrasound and radionuclide techniques are currently much more commonly used for this purpose. If technologic advances in MRI lead to shorter scan times and reduced scan costs and permit routine, accurate assessment of coronary anatomy, it is not hard to conceive that this technique will be

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widely used to provide a comprehensive assessment of cardiac structure and function. At present, however, the use of MRI in adult clinical practice is usually confined to answering questions regarding anatomic abnormalities, such as disorders involving the aorta, the pericardium, congenital heart disease, cardiac masses, and RV dysplasia.[108]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Systolic Function As shown in Figure 4-5 , the major factors affecting LV systolic performance and function are preload, afterload, myocardial contractile (or inotropic) state, and heart rate. Nonuniform contraction can also be important; thus, regional variations in mechanical function, as occur in coronary heart disease or even with electronic ventricular pacing, can affect stroke volume. Only if synchronous contraction is present, heart rate is stable, and loading conditions are constant does a change in performance indicate a change in contractility. These traditional concepts relating preload, afterload, and contractility are generally considered in the assessment of an acute response to altered hemodynamic conditions. Thus, an isolated increase in preload is said to produce an increment in performance through the Frank-Starling mechanism, whereas an isolated increase in afterload is said to produce 78

TABLE 4-4 -- Clinical Methods Used to Evaluate Systolic Function Ejection fraction Fractional shortening at endocardium and midwall Stress-shortening relations Pressure-volume analysis a decrease in the stroke volume (or EF) by virtue of the inverse forceshortening relation. Unfortunately, in the intact heart, especially in patients with chronic heart disease, it is virtually impossible to produce an isolated change in preload or afterload. For example, nitrates are classified as vasodilators and agents that primarily affect preload, but the associated decrease in LV volume and arterial pressure leads to a reduction in

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afterload. Likewise, a pure arterial vasodilator also reduces heart size (and preload) by augmenting the stroke volume. It is apparent, therefore, that preload and afterload are intimately related, and that it is an oversimplification to assume that isolated changes in preload or afterload occur in patients with chronic heart disease. Most interventions that produce an acute change in preload or afterload also result in a length-dependent change in intrinsic myocardial contractility, [109] which further complicates the assessment of global systolic function. Therefore, acute changes in preload produce changes in performance through the Frank-Starling mechanism and through this length-dependent activation. The importance of this phenomenon in the chronically enlarged or diseased heart is unknown. It is usually not difficult to detect an acute change in LV performance or contractile function, but it is harder to determine the major mechanism or mechanisms responsible for the change. Chronic changes in LV volume, mass, and geometry are even more difficult to interpret because such changes tend to limit our use of the traditional interrelationships of preload, afterload, and contractility. Indeed, there is no acceptable index of basal contractility that can be used in patients with chronic heart disease, nor can LV end-diastolic pressure or even absolute end-diastolic volume be used as a surrogate for fiber stretch in chronically diseased hearts. For these and other reasons, the evaluation of contractile function and the distinction between a compensated and a decompensated ventricle often rest on empiric observations coupled with analyses based on physiologic principles. In the following section the use and limitations of several clinically useful approaches to the evaluation of contractile function are discussed (Table 4-4) . Ejection Fraction The EF is perhaps the most widely used measure of LV systolic function. This parameter is defined as the change in LV volume (i.e., stroke volume) divided by the initial volume (i.e., end-diastolic volume): EF = (EDV − ESV)/EDV where EDV is end-diastolic volume and ESV is end-systolic volume; these may be obtained by either M-mode or 2D echocardiography. In addition, there are other published algorithms that use minor-axis dimensions and an estimate of long-axis shortening derived from 2D echocardiography to

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derive EF directly.[110] The EF, representing volume strain, is appropriately normalized; it can be used as an index of systolic function that is independent of the size of the patient or the ventricle. The normal ventricle ejects more than half of its end-diastolic volume; the average EF, as determined by 2D echocardiography, varies from 63% to 69%.[81] In patients with coronary disease or idiopathic cardiomyopathy, it is generally conceded that values in the range of 40% to 50% are abnormal but of little clinical significance.[1] However, in patients with mitral regurgitation, an EF in this range may denote significant depression in contractile function.[111] Hemodynamic Determinants of the Ejection Fraction

Acute changes in LV loading conditions are known to exert a major influence on the EF. Thus, an acute increase in preload and/or a decrease in afterload results in a higher EF. By contrast, an acute decrease in preload and/or an increase in afterload reduces the EF. Under such circumstances, it can be difficult to decide whether a change in contractility has occurred. If, however, alterations in load are associated with a change in the EF that is opposite to the expected result, it is possible to conclude that a simultaneous change in contractility (i.e., inotropic state) also occurred. For example, an increased EF in the presence of increased afterload likely represents increased contractility, because an increase in afterload would normally be expected to cause a lower EF. Despite its load sensitivity, the EF can therefore provide useful information, even during acute hemodynamic interventions. In this regard, the concept of preload reserve is important. In patients with chronic heart disease, the EF can be an important index of contractile function, in part because of its sensitivity to increased afterload. As LV dysfunction develops and dilation occurs, afterload tends to increase, as dictated by the Laplace relationship, and the EF falls.[55] Such a decline in the EF can be useful in identifying LV dysfunction very early in the course of a disease; it does not, however, identify the underlying mechanism or mechanisms. Therefore, in patients with chronic heart disease, the EF must be interpreted with consideration of the magnitude and time course of changes in loading conditions that evolve during progression of the disease.[111] For example, very early in the course of aortic regurgitation, LV preload and afterload tend to be increased; these changes affect the EF in opposite directions, and it remains within the normal range. As the ventricle remodels and eccentric hypertrophy develops, the loads

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normalize despite LV enlargement; if myocardial contractility is preserved, the EF remains normal. As the hemodynamic burden increases (or contractile dysfunction develops), the afterload increases and the EF decreases. Thus, 79

even a modest decline in the EF can be an important early marker of LV dysfunction. In decompensated aortic stenosis, LV systolic pressures increase in parallel with an increase in wall stress, as predicted by the Laplace relationship. As wall stress progressively rises, EF decreases. Carabello et al[21] have shown that patients with critical aortic stenosis, congestive heart failure, and decreased EF owing to high levels of wall stress ("afterload mismatch") may anticipate improvement in systolic function following afterload reduction associated with valve replacement[21] [111] [112] (Fig. 4-14) . In contrast, those patients whose reduction in EF is out of proportion to the high levels of wall stress are thought to have developed cardiomyopathic changes in addition to excess afterload; such patients generally do not experience functional improvement after valve replacement.[21] [112] This subgroup of patients may be identifiable by a low transvalvular gradient (usually less than 30 mm Hg) in association with severe stenosis of the aortic valve.[21] In the clinical setting, making the proper diagnosis can be challenging. Because the Gorlin equation is flow dependent, patients with primary LV dysfunction and coexistent (mild) calcific aortic stenosis can be difficult to distinguish from those with LV dysfunction caused by unrelieved severe aortic stenosis. Dobutamine echocardiography is increasingly used to help make this distinction and to assess prognosis.[113] Fractional Shortening and Related Indices The fractional change (percentage) in minor-axis dimension is a widely used index of systolic performance; fractional shortening is usually derived from M-mode echocardiographic tracings (see Fig. 4-8) . This measurement Figure 4-14 Relationship between ejection fraction (EF) and endsystolic stress in patients undergoing cardiac catheterization for critical aortic stenosis and severe congestive heart failure. All patients were free of significant coronary artery disease. Patients falling close to the regression line relating EF to stress (open circles) are thought to have

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LV dysfunction owing to excessive wall stress (afterload). These patients experienced a gratifying functional recovery after aortic valve replacement. In contrast, the four subjects who fell below the regression line (dark circles) have depressed EF beyond that predicted by the level of afterload and are considered to have depressed contractility as well. These patients did not experience functional recovery after valve replacement. (Adapted from Carabello BA, Green LH, Grossman W, et al: Circulation 1980;62:42. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:416.)

is particularly useful because LV circumferential fiber shortening is responsible for most of the stroke volume. In this regard, fractional shortening is similar to the EF; in the absence of focal wall motion abnormalities, the two indices correlate closely, although the absolute values for fractional shortening are obviously less than that for EF. Fractional shortening, measured at the endocardium (FSendo [%]), is

calculated as

FSendo = 100 × (LVIDd − LVIDs )/(LVIDd ) Normal values for FSendo exceed 30%. As is the case with EF, FSendo is

influenced by factors in addition to contractile state and should be interpreted in the light of loading conditions; increases in preload and decreases in afterload increase fractional shortening.

A refinement of fractional shortening, the velocity of circumferential shortening (Vcf ) reflects the mean velocity of ventricular shortening at the level of the LV minor axis, and it is also calculated from M-mode echocardiographic dimensions: Vcf = FSendo /ET where ET is the ejection time derived either from the duration of aortic valve opening, from the period of aortic forward flow (pulsed or continuous wave Doppler), or from a carotid pulse tracing.[65] The Vcf is expressed in circumferences per second (the lower limit of normal is 1.1 c/sec); because Vcf measures the velocity rather than the extent of shortening, it is

theoretically a more sensitive index of contractility than FSendo and may be

an earlier marker of abnormality in chronic disease states. As with the EF and fractional shortening, this parameter is normalized for LV chamber size

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and may be used to make comparisons between patients. Vcf has been

shown to be

80

relatively insensitive to acute changes in preload.[114] [115] However, it is also possible that this preload insensitivity may be a result of acute elevations in preload increasing heart size (and pressure) and thus increasing afterload. Thus, augmentation in afterload may offset the increased shortening caused by the increased preload. A further refinement in Vcf , the rate-corrected

Vcf ,[64] [65] [113] may be obtained by dividing Vcf by the square root of the

preceding RR interval. This index is designed to allow comparison between patients with differing heart rates. The incremental value of velocity of shortening methods (e.g., Vcf , rate-corrected Vcf ), compared with extent of shortening (e.g., fractional shortening) may be marginal.[116]

Standard M-mode measurements also may be used to estimate circumferential fractional shortening at the midwall (FSmw [%]), using the

same standard M-mode echocardiographic measurements. FSmw is

calculated using a modified two-shell cylindrical model.[37] This method assumes constant LV mass throughout the cardiac cycle and does not require the assumption that inner and outer wall thickening fractions are equal.[37] [117] [118] Most important, in contrast to FSendo , FSmw is not

influenced by LV geometry (relative wall thickness) and therefore has particular use in the evaluation of the hypertrophied heart with increased relative wall thickness (see Fig. 4-16) . Normal systolic function includes the excursion of the mitral annulus toward the relatively immobile apex; thus, the long axis of the left ventricle shortens during systole. An assessment of the longitudinal (or long-axis) shortening of the left ventricle can be made using M-mode measurements under 2D echocardiographic guidance.[119] [120] Using the apical window, the transducer is oriented to maximize apical endocardial to mitral annular distance. M-mode tracings are made with the cursor directed through the lateral aspects of the mitral annulus; recordings of multiple cardiac cycles are made on strip chart paper,[118] [120] and mitral annular excursion is normalized for initial diastolic length. Several investigators have used mitral annular excursion and long-axis

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shortening as a descriptor of ventricular systolic function. Keren and LeJemtel [119] showed that the principal systolic mitral annular excursion toward the apex coincides with the systolic component of pulmonary venous flow; this systolic phase of mitral annular motion is markedly attenuated in patients with dilated cardiomyopathy. Jones and Gibson[120] showed that, in the normal left ventricle, mitral annular excursion toward the apex precedes circumferential shortening, leading to a more spherical LV shape early in systole.[120] These investigators also showed that mitral annular descent was reduced in patients with mitral disease who had undergone valve replacement.[120] In patients with "compensated" hypertensive heart disease, that is, LV hypertrophy and normal EF, longaxis shortening is depressed compared with normal controls.[118] Similar findings have been reported using the technique of MRI tagging, as described later.[121] Other ultrasound techniques have been employed in recent years to investigate LV systolic and diastolic function. Doppler tissue imaging applies a modification of pulsed Doppler methods to the assessment of myocardial systolic and diastolic motion.[122] [123] In this way, the velocity of myocardial tissue or of the mitral annulus, and not just the total excursion, may be measured. The velocity of the diastolic mitral annular motion has been applied to the study of LV diastolic function (see Chapter 6) .[122] [123] Nagueh et al[123] have demonstrated that mitral annular velocity information, when coupled with more traditional mitral inflow velocity data, can be used to reliably predict diastolic pressure. Similarly, more qualitative assessment of ventricular function can be obtained using color Doppler imaging.[124] Stress-Shortening Relations On the basis of extensive experimental and clinical experience, the myocardial force-velocity relation provides a framework for evaluating the contractile state and function of the left ventricle. A most important advantage of assessing function with a stress-shortening analysis is that it avoids afterload dependency, the major limitation of the EF alone. Unfortunately, end-diastolic fiber length (or the degree to which the resting fiber is stretched) is difficult if not impossible to measure; LV end-diastolic pressure or volume or even wall stress fails to provide an absolute measure of fiber length. For this reason, length is generally omitted and the simpler force-velocity or stress-shortening relation is used as a substitute for the force-length-velocity relation. Both systolic stress (the force per unit cross-sectional area of myocardium)

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and shortening (fractional change in length or volume) are appropriately normalized and allow accurate comparisons among hearts of different sizes. [125] Therefore, contractile function in pressure overload hypertrophy, volume overload hypertrophy, and dilated as well as hypertrophic cardiomyopathies may be assessed within the framework of the stressshortening relation. A major limitation of the simple stress-shortening analysis is the assumption that differences in resting length do not substantially influence the stress-shortening relation. In this regard, a distinction must be made between acute interventions and chronic steady-state conditions. Changes in fiber length and appropriate use of preload reserve certainly occur during acute or short-term hemodynamic interventions. However, under chronic conditions (e.g., chronic compensated volume overload), this may not be the case.[126] After the acute or subacute phase, when the compensatory remodeling process is complete and chronic changes in LV volume and mass are established, end-diastolic fiber length may not be substantially different from normal.[127] In pressure overload or concentric hypertrophy, end-diastolic sarcomere lengths may even be less than normal.[128] [129] In such hearts, high chamber stiffness apparently limits use of the preload reserve. It appears, therefore, that assumptions about chronic changes in fiber length are unwarranted. Midwall Stress-Shortening Analysis

The analysis of midwall stress-shortening relations may be superior to that of endocardial stress-shortening relations, especially for comparison of contractile state between 81

hearts differing in LV geometry ( Fig. 4-15 and Fig. 4-16 ). The first advantage of midwall measurements is that the (circumferential) stress vector and the shortening transient are oriented in the same direction, because circumferential fibers predominate in the midwall of the LV.[130] [131] Second, the values for midwall (but not endocardial) shortening are consonant with experimental data indicating that myocardial fibers shorten by approximately 15% to 20%. Circumferential midwall strain ranges from 9% ± 2% in the anesthetized, open chest dog (implanted markers[132] ) to 30% ± 7% in conscious humans (MRI tagging).[133] We believe that the experimental results represent an underestimate of strain, but MRI

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techniques likely overestimate true myocardial shortening. All methods indicate that circumferential shortening at the endocardium exceeds that seen at the midwall. Third, significant differences in chamber radius or circumference may be caused by differences in LV relative wall thickness. [37] By contrast, midwall shortening is independent of relative wall thickness. We believe that studies designed to assess myocardial contractile function should ideally be based on midwall stress-shortening data, not on endocardial Figure 4-15 Left ventricular (LV) shortening in normal LV (top) and in concentric left ventricular hypertrophy (LVH) (bottom), illustrating the added insight into systolic function provided by midwall shortening. LV endocardial dimension (LVID), wall thickness (Th), relative wall thickness (RWT), and LV mass are measured in diastole (d). The systolic dimensions (s) are shown at right. The midwall circumference is indicated by the dotted line. Systolic shortening refers to the percent reduction in the circumference that occurs from diastole to systole. FS endo, the percent reduction of the endocardial circumference (dark inner circle) and FS mw, the percent reduction of the midwall circumference (dotted line), are in the normal range. However, concentric LVH (elevated RWTd and LV mass) is associated with an increased value for FS endo, but a diminution in FS mw, compared with normal LV, owing to the nonuniformity of systolic thickening. Myocardial fibers in the inner (subendocardial) layers contribute more to systolic thickening than those in the outer (epicardial) layers; this effect is exaggerated when concentric geometry is present.

shortening parameters, which may be contaminated by altered ventricular geometry. An example of the usefulness of a midwall stress-shortening analysis is shown in Figure 4-17 . The endocardial stress-shortening relation is normal in patients with pressure overload hypertrophy owing to aortic stenosis; thus, LV function is normal. By contrast, the midwall stress-shortening relation is abnormal in approximately one third of the patients, indicating a subtle depression of myocardial function in these individuals. Pressure-Volume Analysis By plotting LV pressure against volume throughout the entire cardiac cycle, a pressure-volume loop can be generated (Fig. 4-18) . The height of the loop is determined by systolic pressure, and its width is determined by stroke volume; thus, the area within the loop is a measure of stroke work. By definition, such loops incorporate end-diastolic and end-systolic volumes; thus, the stroke volume and the EF are displayed. The bottom

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limb of the loop (i.e., the diastolic pressure-volume curve) 82

Figure 4-16 Endocardial and midwall stress-shortening relations in pressure overload hypertrophy. The top panel shows fractional shortening at the endocardium versus circumferential stress in a consecutive series of patients with severe, symptomatic aortic stenosis who were free of segmental wall motion abnormalities. All patients fall within the 95% confidence intervals of the stress-shortening relationship, suggesting normal contractile function. In contrast, the bottom panel shows midwall shortening versus circumferential stress in the same population. A substantial portion (approximately one third) of these patients demonstrates a diminution in contractility by the midwall analysis.

describes ventricular diastolic compliance. Therefore, the pressure-volume loop can provide a simple yet comprehensive description of ventricular pump function. [134] Such loops can be generated from a variety of techniques that provides ventricular volume data in conjunction with LV pressure. [135] [137] Online, beat-to-beat determinations of LV volumes with automated edge detection can be combined with LV pressure measurements to yield real-time pressure-volume loops, useful in both clinical and research settings[137] [138] [139] (Fig. 4-19) . Pressure-dimension loops derived from M-mode echocardiographic data are adequate surrogates for pressurevolume loops, and they provide the added advantage of simplicity and widespread availability. If only the systolic portion is of interest, calibrated carotid pulse tracings may be substituted for intraventricular pressure, and the data can be obtained entirely noninvasively.[43] By manipulating LV volume and/or arterial pressure, multiple coordinates of the maximal ratio of pressure to volume or dimension (which occurs near end-ejection) can be obtained; these coordinates exhibit a nearly linear direct relation. The slope of this relation (Emax ) is relatively insensitive to

acute changes in loading conditions. The relation shifts upward and to the left during positive inotropic interventions, and it shifts downward to the right when the ventricle is depressed; the slope of the relation generally increases with the former and decreases with the latter ( see Fig. 4-18 and Fig. 4-19 ).

This end-systolic index of contractility is sensitive to acute changes in contractility, but its reliability is diminished in chronically diseased hearts, especially dilated hearts. In large ventricles the end-systolic pressure-

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volume curve can be displaced down and to the right (depressed Emax ), in

the absence of a depressed contractility. For this reason, Emax should be

normalized for heart size,[140] [141] [142] as illustrated in Figure 1-19 . In this example of chronic aortic regurgitation, there is modest LV enlargement, the end-systolic volume is less than 60 mL/m2 , the EF is normal, and the total stroke volume is high. Such data indicate that the ventricle is compensated, albeit larger than normal. However, the depressed slope of the end-systolic pressure-volume relation inappropriately suggests depressed contractility. These disparate conclusions can be reconciled if the effect of chamber dilation on Emax is considered.[140] [141] [142] Thus, if the slope is normalized for chamber size, it approximates that seen in the normal heart.

Recognizing this limitation, end-systolic stress-volume or stress-dimension relations should not be a major criterion for the diagnosis of chronic contractile dysfunction. Certainly, it is not useful as a measure of basal contractility and it has limited applicability in comparisons among normal and diseased hearts. The raw pressure-volume or stress-dimension data provide important diagnostic information and, with few exceptions, the simple measurement of the end-systolic volume or dimension identifies a depressed ventricle. An example of the usefulness of echocardiography pressure-dimension loops is shown in Figure 4-20 . This example illustrates the effect of mitral valve replacement on LV size and function in compensated and decompensated chronic mitral regurgitation. In compensated mitral regurgitation the chamber is enlarged but the end-systolic dimension is only 42 mm, systolic stress is minimally increased, and the fractional shortening is normal (35%). After valve replacement the stress-dimension loop returns to near normal. In decompensated mitral regurgitation the end-diastolic and end-systolic volumes are markedly increased and fractional shortening is low (26%). After mitral valve replacement there is persistent LV enlargement and a further decline in shortening. A similar analysis has been used in patients with aortic regurgitation.[143] (See also Chapter 18.)

83

Figure 4-17 Left ventricular pressure-volume (P-V) loops. The dashed

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line indicates a normal ventricle. An acute decrease in contractile state is shown; the loop is displaced to the right, and the end-systolic P-V line shifts downward and to the right. The effect of an acute increase in contractile state is illustrated by the line on the left; the slope of the end-systolic P-V line is increased (the corresponding loop is not shown). (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:418.) Figure 4-18 Pressure-volume loops with inferior vena caval occlusion at baseline and with 3 µg/kg/min of dobutamine infusion in an intact canine model. Volume was assessed online with transesophageal echocardiographic border detection using a Simpson's rule algorithm. End-systolic elastance (Ees ), or the slope of the end-systolic P-V relation, increased with positive inotropic modulation, which is consistent with increased contractility. (Courtesy of Dr. John Gorcsan III.) Figure 4-19 LV pressure-volume loops and end-systolic pressure volume lines illustrate the effects of chronic aortic regurgitation on ventricular size and function. Moderate ventricular enlargement is present, ejection fraction (EF) is normal, and stroke volume (SV) is high. Such data are consistent with compensated aortic regurgitation. However, the slope of the end-systolic P-V relation (Emax ) is reduced. This apparent inconsistency may be resolved by considering the effect of chamber size on Emax . If the slope is normalized for chamber size (end-diastolic volume), the result indicates that Emax is similar in the two ventricles. (Adapted from Shen WF, Roubin G, Choong CYP, et al: Circulation 1985;71:31–38. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:420.)

84

Figure 4-20 Left ventricular (LV) stress-dimension loops in two cases of mitral regurgitation, before (Preop) and after (Post) mitral valve replacement. In the left panel the preoperative loop indicates compensated ventricular function; the end-diastolic dimension is 6.5 cm, the end-systolic dimension is 4.2 cm, systolic stress is minimally elevated, and fractional shortening is normal (35%). After valve replacement the end-diastolic dimension and end-systolic wall stress return to normal, but fractional shortening decreases (29%). In the right panel the preoperative loop indicates a decompensated ventricle; the end-diastolic and end-systolic dimensions are markedly increased (7.3 cm and 5.4 cm, respectively) and fractional shortening is low (26%). After valve replacement there is persistent LV enlargement and a further decline in fractional shortening. These examples illustrate the LV response to mitral valve replacement in

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Gaasch WH: Diagnosis and treatment of heart failure based on LV systolic or

diastolic dysfunction. JAMA 1994;271:1276–1280. 2. Mock MB, Rindqvist I, Fisher LD, et al: Survival of medically treated patients in

the coronary artery surgery (CASS) registry. Circulation 1982;66:562–567. 3. Hammermeister KE, De Rouen TA, Dodge HT: Variables predictive of survival in

patients with coronary disease. Circulation 1979;59:421–430. 4. White HD, Norris RM, Brown MA, et al: Left ventricular end systolic volume as the

major determinant of survival after recovery from myocardial infarction. Circulation 1987;76:44–51. 5. Pfeffer MA, Braunwald E, Moye LA, et al: Effect of captopril on mortality and

morbidity in patients with left ventricular dysfunction after myocardial infarction: Results of the survival and ventricular enlargement trial. N Engl J Med 1992;327:669– 677. 6. The SOLVD Investigators: Effect of enalapril on survival in patients with reduced

left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325:293–302. 7. Bestetti RB, Dalbo CMR, Freitas OC, et al: Non-invasive predictors of mortality for

patients with Chagas heart disease: A multivariate stepwise logistic regression study. Cardiology 1994;84:261–267. 8. Feild BJ, Baxley WA, Russell RO Jr, et al: Left ventricular function and

hypertrophy in cardiomyopathy with depressed ejection fraction. Circulation 1973;47:1022–1031. 9. Vasan RS, Larson MG, Benjamin EJ, et al: Congestive heart failure in subjects with

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 2 di 14

normal versus reduced left ventricular ejection fraction: Prevalence and mortality in a population-based cohort. 1999;33:1948–1955. 10. Gottdiener JS, Arnold AM, Aurigemma GP, et al: Predictors of congestive heart

failure in the elderly: The Cardiovascular Health Study. J Am Coll Cardiol 2000;35:1628–37. 85

11. Schuler G, Peterson KL, Johnson A, et al: Temporal response of left ventricular

performance to mitral valve surgery. Circulation 1979;59:1218–1231. 12. Borow KM, Green LH, Mann T, et al: End-systolic volume as a predictor of post-

operative left ventricular performance in volume overload from valvular regurgitation. Am J Med 1980;68:655–663. 13. Gaasch WH, Carroll JD, Levine HJ, et al: Chronic aortic regurgitation: Prognostic

value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 1983;1:775–782. 14. Zile MR, Gaasch WH, Carroll JD, et al: Chronic mitral regurgitation: Predictive

value of preoperative echocardiographic indexes of left ventricular function and wall stress. J Am Coll Cardiol 1984;3:235–242. 15. Hoshino PK, Gaasch WH: When to intervene in chronic aortic regurgitation. Arch

Intern Med 1986;146:349–352. 16. Bonow RO, Epstein SE: Is preoperative left ventricular function predictive of

survival and functional results after aortic valve replacement for chronic aortic regurgitation? J Am Coll Cardiol 1987;10:713–716. 17. Carabello BA, Usher BW, Hendrix GH, et al: Predictors of outcome for aortic

valve replacement in patients with aortic regurgitation and left ventricular dysfunction: A change in the measuring stick. J Am Coll Cardiol 1987;10:991–997. 18. Crawford MH, Souchek J, Oprian CA, et al: Determinants of survival and left

ventricular performance after mitral valve replacement. Circulation 1990;81:1173– 1181. 19. Cunha CLP, Giuliani ER, Fuster V, et al: Preoperative M-mode echocardiography as a predictor of surgical results in chronic aortic insufficiency. J Thorac Cardiovasc

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 3 di 14

Surg 1980;79:256–265. 20. Bonow RO, Rosing DR, Kent KM, Epstein SE: Timing of operation for chronic

aortic regurgitation. Am J Cardiol 1982;50:325–336. 21. Carabello BA, Green LH, Grossman W, et al: Hemodynamic determination of

prognosis of aortic valve replacement in critical aortic stenosis and advanced congestive heart failure. Circulation 1980;62:42. 22. Connolly HM, Oh JK, Schaff HV, et al: Severe aortic stenosis with low

transvalvular gradient and severe left ventricular dysfunction: Result of aortic valve replacement in 52 patients. Circulation 2000;101:1940–1946. 23. Collinson J, Henein M, Flather M, et al: Valve replacement for aortic stenosis in

patients with poor left ventricular function: Comparison of early changes with stented and stentless valves. Circulation 1999;100(19 suppl):II1–5. 24. Orsinelli DA, Aurigemma GP, Battista S, et al: Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis: A high risk subgroup identified by preoperative relative wall thickness. J Am Coll Cardiol 1993;22:1679– 1683. 25. Aurigemma G, Battista S, Orsinelli D, et al: Abnormal left ventricular intracavitary

flow acceleration in patients undergoing aortic valve replacement for aortic stenosis: A marker for high postoperative morbidity and mortality. Circulation 1992;86:926– 936. 26. Casale PN, Devereux RB, Milner M, et al: Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Ann Intern Med 1986;105:173–178. 27. Levy D, Garrison RJ, Savage D, et al: Prognostic implications of

echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322:1561–1566. 28. Levy D, Garrison RJ, Savage D, et al: Left ventricular mass and incidence of

coronary heart disease in an elderly cohort. Ann Intern Med 1990;110:101–107. 29. Koren M, Devereux R, Casale PN, et al: Relation of LV mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991;114:345–352. 30. Verdecchia P, Schillaci G, Borgioni C, et al: Adverse prognostic significance of

concentric remodeling of the left ventricle in hypertensive patients with normal left

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 4 di 14

ventricular mass. J Am Coll Cardiol 1995;25:871–878. 31. Devereux R: Left ventricular geometry, pathophysiology and prognosis. J Am Coll

Cardiol 1995;25:885–887. 32. Savage DD, McGhee DL, Oster G: Hypertension associated heart disease among

black Americans. Milbank Q 1987;65:297–321. 33. Krumholz HM, Larson M, Levy D: Prognosis of left ventricular geometric patterns

in the Framingham Heart Study. J Am Coll Cardiol 1995;25:879. 34. Reichek N: Magnetic resonance imaging for assessment of myocardial function.

Magn Reson Q 1991;7:255–274. 35. Buchalter MB, Weiss JL, Rogers WJ, et al: Noninvasive quantification of left

ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging. Circulation 1990;81:1236–1244. 36. Dumesnil J: A mathematical model of the dynamic geometry of the intact left

ventricle and its application to clinical data. Circulation 1979;59:1024–1034. 37. deSimone G, Devereux RB, Roman MJ, et al: Assessment of left ventricular

function by the midwall fractional shortening/end systolic stress relation in human hypertension. J Am Coll Cardiol 1994;23:1444–1451. 38. Reichek N, Wilson J, St. John Sutton M, et al. Noninvasive determination of left

ventricular end-systolic stress: Validation of the method and initial application. Circulation 1982;65:99–108. 39. Gaasch WH, Zile MR, Hoshino PK, et al: Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure overload hypertrophy. Circulation 1989;79:872–883. 40. St. John Sutton M, Plappert T, Hirshfeld JW, et al: Assessment of left ventricular

mechanics in patients with asymptomatic aortic regurgitation: A two-dimensional echocardiographic study. Circulation 1984;69:259–270. 41. Mirsky I: Review of the various theories for evaluation of left ventricular wall

stress. In Mirsky I, Chiston DN, Sandler H, (eds): Cardiac Mechanics: Physiological, Chemical, and Mathematical Considerations. New York, John Wiley, 1974. 42. Douglas PS, Reichek N, Plappert T, et al: Comparison of echocardiographic

methods for assessment of left ventricular shortening and wall stress. J Am Coll

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 5 di 14

Cardiol 1987;9:945–951. 43. Colan SD, Borow KM, Neumann A: Use of the calibrated carotid pulse tracing for

calculation of left ventricular pressure and wall stress throughout ejection. Am Heart J 1985;109:1306–1310. 44. Rozich JD, Carabello BA, Usher BW, et al: Mitral valve replacement with and without chordal preservation in patients with chronic mitral regurgitation. Circulation 1992;86:1718–1726. 45. Gaasch WH, Battle WE, Oboler AD, et al: Left ventricular stress and compliance

in man: With special reference to normalized ventricular function curves. Circulation 1972;45:746–762. 46. Clyne CA, Arrighi JA, Maron BJ, et al: Systemic and LV responses to exercise

stress in asymptomatic patients with valvular aortic stenosis. Am J Cardiol 1991;68:1469–1476. 47. Cuocolo A, Sax F, Brush J, et al: Left ventricular hypertrophy and impaired

diastolic filling in essential hypertension. Circulation 1990;81:978–986. 48. Kitzman D, Higginbotham M, Cobb F, et al: Exercise intolerance in patients with

heart failure and preserved LV systolic function. J Am Coll Cardiol 1991;7:1065– 1072. 49. Bonow RO, Udelson JE: LV diastolic dysfunction as a cause of congestive heart

failure. Ann Intern Med 1992;117:502–510. 50. Schwinger RH, Bohm M, Koch A, et al: The failing heart is unable to use the

Frank-Starling mechanism. Circ Res 1994;74:959–969. 51. Ross J Jr: Afterload mismatch and preload reserve: A conceptual framework for

the analysis of ventricular function. Prog Cardiovasc Dis 1976;18:255–264. 52. Grossman W, Jones D, McLaurin LP: Wall stress and patterns of hypertrophy in

the human left ventricle. J Clin Invest 1975;56:56–64. 53. Pouleur H, Covell JW, Ross J Jr: Effects of alterations in aortic input impedance on

the force-velocity-length relationship in the intact canine heart. Circ Res 1979;45:126– 135. 54. Gaasch WH: LV radius to wall thickness ratio. Am J Cardiol 1979;43:1189–1194.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 6 di 14

55. Goldfine H, Aurigemma GP, Zile MR, Gaasch WH: Left ventricular length-force-

shortening relations before and after surgical correction of chronic mitral regurgitation. J Am Coll Cardiol 1998;31:180–185. 56. Carabello BA, Spann JF: The uses and limitations of end-systolic indices of left

ventricular function. Circulation 1984;69:1058–1064. 57. Sagawa K: The end-systolic pressure-volume relationship of the ventricle:

Definitions, modifications, and clinical use. Circulation 1981;61:1223–1227. 86

58. Douglas PS, Morrow R, Ioli A, et al: Left ventricular shape, afterload and survival

in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989;13:311–315. 59. Borow KM, Lang RM, Neumann A, et al: Physiologic mechanisms governing

hemodynamic responses to positive inotropic therapy in patients with dilated cardiomyopathy. Circulation 1988;77:625–637. 60. Devereux R, Reichek N: Echocardiographic determination of left ventricular mass

in man. Anatomic validation of the method. Circulation 1977;55:613–618. 61. Devereux RB, Alonso D, Lutas E, et al: Echocardiographic assessment of left

ventricular hypertrophy: Comparison to necropsy findings. Am J Cardiol 1986;57:450–458. 62. Devereux R: Detection of LV hypertrophy by M-mode echocardiography:

Anatomic validation, standardization and comparison to other methods. Hypertension 1987;9(suppl II):19–26. 63. Reichek N: Standardization in the measurement of left ventricular wall mass.

Hypertension 1987;9(suppl II):II27–29. 64. Vuille C, Weyman AE: Left ventricle I: General considerations, assessment of

chamber size and function. In Weyman AE (ed): Principles and Practice of Echocardiography, 2nd ed. Philadelphia, Lea & Febiger, 1994, pp 575–624. 65. Borow K: An integrated approach to the noninvasive assessment of left ventricular

systolic and diastolic performance. In St. John Sutton M, Oldershaw P (eds): Textbook of Echocardiography. Boston, Blackwell Scientific Publications, 1989, pp 97–152.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 7 di 14

66. Teichholz LE, Kreulen T, Herman MV, et al: Problems in echocardiographic

volume determinations: Echocardiographic-angiographic correlations in the presence or absence of asynergy. Am J Cardiol 1976;37:7–12. 67. Kronik G, Slany J, Mosslacher H: Comparative value of eight M-mode

echocardiographic formulas for determining left ventricular stroke volume. Circulation 1979;60:1308–1316. 68. Ganau A, Devereux R, Roman M, et al: Patterns of LV hypertrophy and geometric

remodeling in essential hypertension. J Am Coll Cardiol 1992;19:1550–1560. 69. Ford LE: Heart size. Circ Res 1976;39:297. 70. Aurigemma G, Silver K, McLaughlin M, et al: Impact of chamber geometry and

gender on LV systolic function in patients over 60 years of age with aortic stenosis. Am J Cardiol 1994;74:794–798. 71. Krumholz HM, Larson M, Levy D: Prognosis of left ventricular geometric patterns

in the Framingham Heart Study. J Am Coll Cardiol 1995;25:879–884. 72. Topol E, Traill T, Fortuin N: Hypertensive hypertrophic cardiomyopathy of the

elderly. N Engl J Med 1985;312:277–283. 73. Pearson AC, Gudipati CV, Labovitz A: Systolic and diastolic flow abnormalities in

elderly patients with hypertensive hypertrophic cardiomyopathy. J Am Coll Cardiol 1988;12:989–995. 74. Lewis JF, Maron BJ: Elderly patients with hypertrophic cardiomyopathy: A subset

with distinctive LV morphology and progressive clinical course late in life. J Am Coll Cardiol 1989;13:36–45. 75. Fay WP, Taliercio CP, Ilstrup DM, et al: Natural history of hypertrophic

cardiomyopathy in the elderly. J Am Coll Cardiol 1990;16:821–826. 76. Litwin SE, Katz SE, Weinberg EO, et al: Serial echocardiographic Doppler

assessment of left ventricular geometry and function in rats with pressure-overload hypertrophy: Chronic angiotensin converting enzyme inhibition attenuates the transition to heart failure. Circulation 1995;91:2642–2649. 77. Schiller N, Shah P, Crawford M, et al: Recommendations for quantitation of the

left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358–367.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 8 di 14

78. Schiller NB: Considerations in the standardization of measurement of LV

myocardial mass by two-dimensional echocardiography. Hypertension 1987;9(suppl II):II33–35. 79. Reichek NR, Helak J, Plappert T, et al: Anatomic validation of left ventricular

mass from clinical two-dimensional echocardiography: Initial results. Circulation 1983;67:348–352. 80. Tortoledo FA, Quinones MA, Fernandez GC, et al: Quantification of left

ventricular volumes by two dimensional echocardiography: A simplified and accurate approach. Circulation 1982;67:579–584. 81. Wahr DW, Schiller NB: Left ventricular volumes determined by two-dimensional

echocardiography in a normal adult population. J Am Coll Cardiol 1983;1:863–868. 82. St. John Sutton MG, Plappert T, Crosby L, et al: Effects of reduced left ventricular

mass on chamber architecture, load, and function: A study of anorexia nervosa. Circulation 1985;72:991–1000. 83. Byrd BF, Wahr D, Wang YS, et al: Left ventricular mass and volume/mass ratio

determined by two-dimensional echocardiography in normal adults. J Am Coll Cardiol 1985;6:1021–1025. 84. Douglas PS, Reichek N, Hackney K, et al: Contribution of afterload, hypertrophy,

and geometry to left ventricular ejection fraction in aortic valve stenosis, pure aortic regurgitation and idiopathic dilated cardiomyopathy. Am J Cardiol 1987;59:1398– 1404. 85. Feiring A, Rumberger J, Reiter S, et al: Determination of left ventricular mass in

dogs with rapid-acquisition cardiac computed tomographic scanning. Circulation 1985;72:1355–1364. 86. Martin RP: Real time ultrasound quantitation of ventricular function: Has the

eyeball been replaced or will the subjective become objective? J Am Coll Cardiol 1993;19:321–323. 87. Amico AF, Reisner SA, Stone CK, et al: Superiority of visual versus computerized

echocardiographic estimation of radionuclide left ventricular ejection fraction. Am Heart J 1989;118:1259–1265. 88. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular

function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313–320.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 9 di 14

89. Perez JE, Klein SC, Prater DM, et al: Automated on-line quantitation of left

ventricular dimensions and function by echocardiography with backscatter imaging and lateral gain compensation. Am J Cardiol 1992;70:1200–1205. 90. Vandenburg BF, Rath LS, Stuhlmiller P, et al: Estimation of left ventricular cavity

area with an on-line semiautomated echocardiographic edge detection system. Circulation 1992;86:159–166. 91. King DL: Three-dimensional echocardiography: Use of additional spatial data for

measuring left ventricular mass. Mayo Clin Proc 1994;69:293–295. 92. King DL, Gopal AS, Keller AM, et al: Three-dimensional echocardiography

advances for measurement of ventricular volume and mass. Hypertension 1994;23:172. 93. King DL, Harrison MR, King DL Jr, et al: Ultrasound beam orientation during

standard two-dimensional imaging: Assessment by three dimensional echocardiography. J Am Soc Echocardiogr 1992;5:567–576. 94. Schmidt MA, Ohazama CJ, Agyeman KO, et al: Real-time three-dimensional

echocardiography for measurement of left ventricular volumes. Am J Cardiol 1999;84:1434–1439. 95. Gardin JM, Tomasso CL, Talano JV: Evaluation of dilated cardiomyopathy by

pulsed Doppler echocardiography. Am Heart J 1983;106:1057–1065. 96. Lewis JF, Kuo LC, Nelson JG, et al: Pulsed Doppler echocardiographic

determination of stroke volume and cardiac output: Clinical validation of two new methods using the apical window. Circulation 1984;70:425–431. 97. Bargiggia GS, Bertucci C, Recusani F, et al: A new method for estimating left

ventricular dP/dt by continuous wave Doppler-echocardiography: Validation studies at cardiac catheterization. Circulation 1989;80:1287–1292. 98. Pai RG, Bansal RC, Shah P: Doppler-derived rate of left ventricular pressure rise.

Circulation 1990;82:514–520. 99. Chen C, Rodriguez L, Guererro JL, et al: Noninvasive measurement of the

instantaneous first derivative of left ventricular pressure using continuous wave Doppler echocardiography. Circulation 1991;83:2101–2110. 100. Aurigemma GP, Reichek N, Venugopal R, et al: Automated left ventricular mass,

volume, and shape from 3D MRI: In vitro validation. Am J Card Imaging 1991;5:257– 263.

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101. Maddahi J, Crues J, Berman DS, et al: Noninvasive quantification of left ventricular myocardial mass by gated proton nuclear magnetic resonance imaging. J Am Coll Cardiol 1987;10:682–692. 102. Shapiro EP, Rogers WJ, Beyar R, et al: Determination of left ventricular mass by

magnetic resonance imaging in hearts deformed by acute infarction. Circulation 1989;79:706–711. 103. Utz JA, Herfkens RJ, Heinsimer JA: Cine MR determination of left ventricular

ejection fraction. AJR Am J Roentgenol 1987;148:839–849. 87

104. Aurigemma G, Reichek N, Schiebler M, Axel L: Evaluation of mitral

regurgitation by cine magnetic resonance imaging. Am J Cardiol 1990;66:621–625. 105. Aurigemma G, Reichek N, Schiebler M, Axel L: Evaluation of aortic

regurgitation by cardiac cine magnetic resonance imaging: Planar analysis and comparison to Doppler echocardiography. Cardiology 1991;78:340–347. 106. Cranney G, Lotan C, Dean L, et al: Left ventricular volume measurements using

cardiac axis nuclear magnetic resonance imaging. Circulation 1990;82:154–163. 107. Aurigemma GP, Davidoff A, Silver K, Boehmer J: Left ventricular mass

quantitation using single-phase cardiac MRI. Am J Cardiol 1992;70:259–262. 108. Carlson MD, White RD, Trohman RG, et al: Right ventricular outflow tract

ventricular tachycardia: Detection of previously unrecognized anatomic abnormalities using cine magnetic resonance imaging. J Am Coll Cardiol 1994;24:720–727. 109. Allen DG, Kentish JC: The cellular basis of the length tension relation in cardiac

muscle. J Mol Cell Cardiol 1985;17:821–828. 110. Quinones MA, Waggoner AD, Nelson JG, et al: A new simplified and accurate

method for determining ejection fraction with two dimensional echocardiography. Circulation 1981;64:744–752. 111. Ross J Jr: Afterload mismatch in aortic and mitral valve disease: Implications for

surgical therapy. J Am Coll Cardiol 1985;5:811–826.

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112. St. John Sutton M, Plappert T, Spiegel A, et al: Early post-operative changes in

LV chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: A prospective twodimensional echocardiographic study. Circulation 1987;76:77–89. 113. DeFilippi CR, Willett DL, Brickner ME, et al: Usefulness of dobutamine

echocardiography in distinguishing severe from non-severe valvular aortic stenosis in patients with depressed left ventricular function and low transvalvular gradients. Am J Cardiol 1995;75:191–194. 114. Colan SD, Borow KM, Neuman AS: The left ventricular end-systolic wall stress-

velocity of fiber shortening relation: A load independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715–724. 115. Quinones MA, Gaasch WH, Alexander JK: Influences of acute changes in

preload, afterload, contractile state, and heart rate on ejection and isovolumic indices of myocardial contractility in man. Circulation 1976;53:293–300. 116. Aurigemma GP, Meyer TE, Sharma M, et al: Evaluation of extent of shortening

versus velocity of shortening at the endocardium and midwall in hypertensive heart disease. Am J Cardiol 1999;83:792–794. 117. Shimizu G, Zile M, Blaustein AS, Gaasch WH: Left ventricular chamber filling

and midwall fiber lengthening in patients with left ventricular hypertrophy: Overestimation of fiber velocities by conventional midwall measurements. Circulation 1985;71:266–272. 118. Aurigemma GP, Silver KH, Fox MA, et al: Depressed midwall and long axis

shortening in hypertensive left ventricular hypertrophy with normal ejection fraction. J Am Coll Cardiol 1995;26:195–202. 119. Keren G, LeJemtel T: Mitral annulus motion: Relation to pulmonary venous and

transmitral flows in normal subjects and in patients with dilated cardiomyopathy. Circulation 1988;78:621–629. 120. Jones CR, Gibson D: Functional importance of the long axis dynamics of the

human left ventricle. Br Heart J 1990;65:215–220. 121. Palmon L, Reichek N, Yeon S, et al: Intramural myocardial shortening in

hypertensive left ventricular hypertrophy with normal pump function. Circulation 1994;89:122–131. 122. Sohn DW, Chai IH, Lee DJ, et al: Assessment of mitral annulus velocity by

Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am

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Coll Cardiol 1997;30:474–480. 123. Nagueh SF, Middleton KJ, Kopelen HA, et al: Doppler tissue imaging: a

noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527–1533. 124. Sutherland GR, Stewart MJ, Groundstroem KWE, et al: Color Doppler

myocardial imaging: A new technique for the assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 125. Mirsky I, Pasternac A, Ellison RC: General index for the assessment of cardiac

function. Am J Cardiol 1972;30:483–491. 126. Ross J Jr: Adaptations of the left ventricle to chronic valvular overload. Circ Res

1974;35:64–70. 127. Ross J Jr, Sonnenblick EH, Taylor RR, et al: Diastolic geometry and sarcomere

lengths in the chronically dilated canine left ventricle. Circ Res 1971;28:49–56. 128. Sonnenblick EH: Correlation of myocardial ultrastructure and function.

Circulation 1968;38:29–44. 129. Laks MM, Morady F, Swan HJC: Canine right and left ventricular cell and

sarcomere lengths after banding the pulmonary artery. Circ Res 1969;24:705–710. 130. Greenbaum R, Ho S, Gibson D: Left ventricular fibre architecture in man. Br

Heart J 1981;45:248–263. 131. Streeter D, Spotnitz H, Patel D: Fiber orientation in the canine left ventricle

during diastole and systole. Circ Res 1969;24:339–346. 132. Villareall FJ, Lew WYW, Waldman LK et al: Transmural myocardial deformation

in the ischemic canine left ventricle. Circ Res 1991;68:368–381. 133. Clark NR, Reichek N, Bergey P, et al: Circumferential myocardial shortening in

the normal human left ventricle. Assessment by magnetic resonance imaging using spatial modulation of magnetization. Circulation 1991;84:67–74. 134. Sagawa K, Maughan L, Suga H, Sunagawa K: Cardiac Contractility and the

Pressure-Volume Relationship. New York, Oxford University Press, 1988. 135. Magorien DJ, Shaffer P, Bush CA, et al: Assessment of left ventricular pressure-

volume relations using gated radionuclide angiography, echocardiography and

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micromanometer pressure recordings. Circulation 1983;67:844–852. 136. McKay RG, Aroesty JM, Heller GV, et al: Left ventricular pressure-volume

diagrams and end-systolic pressure-volume relations in human beings. J Am Coll Cardiol 1984;3:301–312. 137. Gorcsan J III, Gasior TA, Mandarino WA: Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressure-area relations. Circulation 1994;89:180–190. 138. Gorcsan J III, Denault A, Gasior TA, et al: Rapid estimation of LV contractility

from end systolic relations by echocardiographic automated border detection and femoral artery pressure. Anesthesiology 1994;81:553–562. 139. Katz WE, Gasior TA, Reddy SC, Gorcsan J III: Utility and limitations of biplane

transesophageal echocardiography for estimation of LV stroke volume. Am Heart J 1994;128:389–396. 140. Sagawa K: The ventricular pressure-volume diagram revisited. Circ Res

1978;43:677–680. 141. Bogen DK, Ariel Y, McMahon TA, Gaasch WH: Measurement of peak systolic

elastance in intact canine circulation with servo pump. Am J Physiol 1985;249:H585– H593. 142. Berko B, Gaasch WH, Tanigawa N, et al: Disparity between ejection and end

systolic indexes of left ventricular contractility in mitral regurgitation. Circulation 1987;75:1310–1319. 143. Gaasch WH, Carroll JD, Levine HJ, et al: Chronic aortic regurgitation: Prognostic

value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 1983;1:775–782. 144. Gottdiener JS, Livengood SV, Meyer PS, et al: Should echocardiography be

performed to assess the effects of antihypertensive therapy? Test-retest reliability of echocardiography for measurement of left ventricular mass and function. J Am Coll Cardiol 1995;25:424–430. 145. Dahloff B, Pennert K, Hanson L: Reversal of left ventricular hypertrophy in

hypertensive patients: A meta-analysis of 109 treatment studies. Am J Hypertens 1992;5:95–110.

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88

Chapter 5 - Quantitative Evaluation of Regional Left Ventricular Systolic Function Florence H. Sheehan MD

Two-dimensional (2D) echocardiography is well suited to the assessment of regional left ventricular systolic function for both clinical and research applications. Every region of the ventricle can be examined at high spatial and temporal resolution, allowing a more comprehensive visualization than with other imaging modalities. Furthermore, echocardiography is portable, safe, and relatively inexpensive, so serial studies can be obtained without risk to the patient to follow disease progression or response to therapy. Quantitative methods have been developed for measurement of systolic function both for diagnosis and for evaluation of treatment efficacy and prognosis in patients with ischemic heart disease. These methods also allow analysis of the structure-function relationship of the left ventricle and mitral valve, of asynchrony in the timing of contraction, and of the heart's compensatory response to disease processes. Thus, echocardiographic examination offers high informational content for both clinical and research applications.

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Semiquantitative Assessment of Regional Systolic Function In clinical practice, visual assessment provides a rapid evaluation of regional systolic function. In each imaging plane, the ventricular contour is divided into several segments. Each segment is assigned a numeric value that indicates its degree of asynergy. Methodology Segmentation of Ventricle

Several schemata have been devised for dividing the ventricle into 14 to 20 segments.[1] [2] The American Society of Echocardiography's most recent recommendation is for a 16-segment model (Fig. 5-1) .[2] The goal is to obtain sufficient detail to characterize the pattern of dysfunction 89

Figure 5-1 Sixteen-segment model for visual assessment of regional wall motion, recommended by the American Society of Echocardiography. A, anterior; AL, anterolateral; AS, anteroseptal; PL or IL, postero-or inferolateral; I or P, inferior or posterior; IS or PS, infero- or postero-septal; RV, right ventricle; L, lateral; S, septal. (From Schiller NB, Shah PM, Crawford M, et al: Am Soc Echocardiogr 1989;2:358–367.)

in patients with ischemic heart disease without overburdening the clinician. The locations of the segments follow the perfusion territory of the three major epicardial arteries (Fig. 5-2) to facilitate the diagnosis of ischemic dysfunction. Wall Motion Score

The severity of dysfunction is scored visually in each segment. The recommended standard assigns a score of 1 for normal contraction or

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hyperkinesis, 2 for hypokinesis, 3 for akinesis, 4 for dyskinesis, and 5 for aneurysmal segments. [2] Some investigators use the system developed for angiography by Herman and Gorlin,[3] which assigns 1 for normal motion, 2 for mild or moderate hypokinesis, 3 for severe hypokinesis or akinesis, 4 for dyskinesis, and 5 for aneurysmal segments. Gibson et al[4] recommended evaluating wall thickening as well as motion in scoring segmental function because of reports that wall motion varies widely in normal subjects. However, wall thickening evaluation is not included in the American Society of Echocardiography's recommendation for regional function assessment.[2] Hyperkinesis can be distinguished from normal motion and may be assigned a negative value (e.g., -1) to indicate that its contribution to global function is opposite to that of segments with depressed function.[5] A global wall motion score is then calculated by summing or averaging the readings in all of the segments. The region of infarction can be evaluated separately from the noninfarct region by averaging the scores in the appropriate subset of segments. [6] Validation Comparison with Other Imaging Modalities

In clinical validation studies, the echocardiographic score agreed exactly with the score obtained from contrast ventriculograms in 44% of segments; agreement within one functional class was seen in 68% to 88% (Table 5-1) [7] [8] [9] [10] [11] [12] that is, agreement is higher for distinguishing normal from abnormal contraction than in identifying grades of abnormality. Comparable results were obtained in comparisons of radionuclide ventriculography versus 2D echocardiography (see Table 5-1) .[9] [13] In a significant minority of patients, however, the discordance is two or three classes. In one study, the global wall motion score by 2D echocardiography and angiography correlated with r = .70.[11] Factors Affecting Diagnostic Accuracy

Many factors influence the apparent accuracy of qualitative assessment of wall motion. Obvious direct factors are image quality and correct positioning of the image plane relative to the left ventricle. Another important factor is the difference between imaging modalities. Unlike contrast and radionuclide ventriculography, 2D echocardiography is tomographic, producing images of discrete slices of the heart; therefore, the different modalities do not obtain exactly comparable views of each

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segment. The training and experience of the observer are also important, both in recognizing normality and in differentiating classes of abnormality. Even with adequate training, significant intra- and interobserver variability exists in visual assessment. In general, variability increases with the number of grades. Exact agreement within and between observers ranges from 81% to 95%.[14] [15] [16] [17] However, allowance of a one-grade error (e.g., combining normal with hypokinesis or dyskinesis with aneurysm) improves intra- and interobserver agreement to 98% to 99%. These variability rates are comparable to those reported for the 90

Figure 5-2 Regions of single-vessel infarct asynergy. The maximum predicted area of infarct akinesis or dyskinesis and adjacent, noninfarct hypokinesis is depicted for each coronary artery. The ventricular model is based on 11 segments evaluated from short-axis sections obtained at the level of the mitral valve, papillary muscles, and apex. The mitral and papillary level sections were each divided into five segments. LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery. (From Stamm RB, Gibson RS, Bishop HL: Circulation 1983;67:232– 244.)

visual assessment of wall motion from contrast ventriculograms.[18] [19] To minimize the impact of observer variability, most studies report readings made by consensus between two or more observers. Variability reduces the sensitivity of qualitative assessment in diagnosing abnormality or detecting change in function. In patients studied after bypass surgery, wall motion in the revascularized segments improved significantly from baseline values when measured quantitatively, but they did not improve significantly when assessed visually.[20] Nevertheless, the global wall motion score has been repeatedly shown to predict survival in patients with acute or chronic myocardial infarction.[11] [21] Other clinical applications TABLE 5-1 -- Diagnostic Accuracy of Semiquantitative Echocardiography Analysis: Agreement Analysis: Agreement with Other with Other Imaging Modalities No. of Patients Echo Views No. of Classes

% Concordance ±1 COMPLETE CLASS Reference

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Comparison with contrast ventriculography 105 4 SAX, 1 apical 66 2 apical 24 2 parast, 2 apical 47 2 parast, 2 apical 47 2 parast, 2 apical 50 3 SAX, 3 LAX 20 2 parast, 2 apical Comparison with radionuclide ventriculography 24 2 parast, 2 apical 39 Subcostal

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2: normal vs. abnormal 4: nl, hypo, ak, dys

— 94

2: nl/hypo, ak/dys

—

87 Kisslo et al[7] 100 Ohuchi et al[8] 68 Hecht et al [9]

2: normal vs. abnormal 4: nl, hypo, ak, dys

—

5: nl, hypo, ak, dys, aneur 2: normal vs. abnormal

44

2: nl/hypo, ak/dys

—

69

—

79 Freeman et al[10] 94 Freeman et al[10] 88 Shiina et al[11] 77 Lundgren et al[12]

64 Hecht et al [9]

5: hyper, nl, hypo, 86 98 Ginzton et ak, dys al[13] ak, akinesis; aneur, aneurysm; dys, dyskinesis; hypo, hypokinesis; LAX, long axis (include apical views and parasternal long-axis view); nl, normal; parast, parasternal; SAX, short axis. are diagnosis of acute infarction in patients with nondiagnostic electrocardiograms, estimation of infarct size, and prediction of complications of infarction.[4] [22] [23]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of Regional Systolic Function Overview of Calculable Parameters As a tomographic imaging modality, 2D echocardiography allows delineation of both the endocardial and epicardial contours of the left ventricle. Consequently, it is 91

possible to calculate not only those parameters reflecting endocardial displacement, such as are used to analyze contrast ventriculograms, but also parameters based on measuring wall thickness. For clinical applications, the most commonly measured parameters are wall motion and wall thickening. The velocity of wall motion can also be measured by analyzing the Doppler signals generated by myocardial tissue. For research, other parameters of interest include midwall shortening, epicardial motion, shape, and wall stress. These measurements can be performed not only in two dimensions, within the plane of imaging, but also in three dimensions and even in four dimensions, with time. Through multiplanar image acquisition, echocardiography provides more complete visualization of the left ventricle than can be provided by either radionuclide or contrast ventriculography. Methods have been developed for three-dimensional (3D) reconstruction of the endocardium and epicardium and for performing 3D analysis of left ventricular dimensions, shape, and regional and global function (see Chapter 10) . Unlike with other imaging modalities, the visibility of landmarks on echocardiogram images (e.g., the papillary muscles, valve planes, and right ventricular septal insertion) helps to localize functional defects on the ventricle. From a multiplanar analysis of function, an estimate of infarct size can be derived by mapping the location of the dysfunctional region on the endocardial surface.

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The analysis of function, both regional and global, measures the alteration of the left ventricle between two time points in the cardiac cycle. For clinical purposes, the contours at end-diastole and end-systole are generally compared. Some investigators have also studied the extent of contraction at specific phases such as during isovolumic contraction or relaxation.[24] Frame-by-frame analysis through the cardiac cycle provides information on the synchrony of regional function. This can be taken to the "fourth dimension" by performing 3D analyses of the left ventricle at multiple time points through the cardiac cycle. Four-dimensional analysis is feasible with currently available fast computer technology and is being undertaken for teaching purposes. Application to clinical medicine will require automated border detection (see Chapter 7) to relieve the labor and tedium associated with analyzing so many images. Wall Motion Wall motion analysis measures the displacement of the left ventricular endocardium. To normalize for patient-to-patient differences in heart size, the measured motion is divided by the left ventricular dimension at enddiastole. The resulting unitless shortening fraction is analogous, on a local and linear level, to the global volume ejection fraction. Unlike the ejection fraction, however, wall motion may have negative values, which indicate paradoxical outward motion during systole. Implicit Assumptions

There are two major assumptions implicit in wall motion analysis. The first is that a one-to-one correspondence can be made from anatomic points on the left ventricular contour at end-diastole to the same points at end-systole. Second, the location of the patient relative to the imaging equipment remains stable. In fact, both assumptions are compromised in 2D image analysis. Nevertheless, the methods developed for wall motion analysis attempt to deal with these sources of imprecision. Methods for Wall Motion Analysis

Because it is not possible to track specific points on the left ventricle over time, there is no gold standard for judging the accuracy of methods for measuring wall motion. As a consequence, there is a plethora of methods, all of which model rather than measure wall motion. Almost all methods available for analysis of wall motion from echocardiogram images were developed initially for contrast ventriculograms. Ventriculograms have

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only one clearly visible landmark—the aortic valve—although some investigators attempt to identify the apex as a second landmark even though it is not an anatomic structure. Because the aortic valve is the only structure whose motion can be tracked over time, all other points on the ventricle have to be identified by their distance from the aortic valve. Echocardiograms display more anatomic landmarks, but they have not been used to make additional correspondences between the endocardial contour at end-diastole and end-systole, probably because the descent of the base toward the apex during systole moves different "slices" of the ventricle into and out of the imaging plane, so that the landmarks cannot be tracked over time. Most wall motion analysis methods for echocardiography employ a radial coordinate system. Motion is assumed to proceed from all points on the endocardial contour toward a single point, the center of area (Fig. 5-3) . There is little evidence supporting this assumption, although some data suggest a multicentric motion pattern.[25] However, the radial approach seems inherently suited to analysis of short-axis images. The radial method has also been applied to contours from apical views.[26] In methods based on a rectangular coordinate system, motion is measured along hemiaxes constructed at intervals along and perpendicular to the long axis of the ventricle. Rectangular coordinate system methods are applied only to apical views.[27] [28] [29] The apex is the least well visualized part of the contour; therefore, construction of a coordinate system based on identification of the apex may be subject to variability. One author justified the coordinate system approach by its similarity at the apex to a method derived by tracking endocardial landmarks felt to represent trabeculae.[30] The concept in these two methods is that endocardial displacement at the apex results from apical obliteration as the lateral walls contract toward the long axis. However, a study that also tracked endocardial landmarks found that apical wall motion proceeds toward the base, that is, 90 degrees off from the direction dictated by the first endocardial landmark method.[31] An angiographic analysis of the motion of surgically implanted metallic markers also reported that apical wall motion proceeds toward the base.[32] Thus, the 92

Figure 5-3 Method used for analysis of regional left ventricular

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contraction in a schematic of a short-axis two-dimensional echocardiographic image. The junction between the posterior right ventricular free wall endocardium and right ventricular septal endocardium was chosen as a landmark and a line drawn to the farthest point on the lateral left ventricular wall epicardium. From the midpoint of this line (1–7), 12 equidistant radii are drawn to separate the image into 12 cavity and wall segments. Percentage area change of each cavity segment and percentage thickening of the wall along each radius during systole are calculated. Solid lines, end-diastole; interrupted lines, end-systole. (From Pandian NG, Skorton DJ, Collins SM, et al: Am J Cardiol 1983; 51:1667–1673. Reprinted with permission from Excerpta Medica Inc.)

rectangular coordinate system, endocardial landmark, and midwall marker methods produce radically different descriptions of the direction of endocardial displacement at the apex. Only part of this discrepancy can be explained by the differing motions of the endocardium versus the midwall, which become separated during systole owing to relatively greater thickening of the inner myocardium.[33] Little of the discrepancy can be attributed to left ventricular torsion that rotates different layers of myocardium to different extents around the long axis of the left ventricle.[34] The Figure 5-4 Centerline method for regional wall motion analysis. Left, End-diastolic (ED) and end-systolic (ES) endocardial contours of the left ventricle from the apical long-axis echocardiographic view with the centerline midway between the two contours. Right, One hundred equidistant chords (not all shown) are constructed perpendicular to the centerline and numbered counterclockwise from the anterior aortic valve. The motion at each chord is normalized by the end-diastolic perimeter to yield a dimensionless chord fractional shortening. (From Wohlgelernter D, Cleman M, Highman A, et al: J Am Coll Cardiol 1986;7:1245–1254. Reprinted with permission from the American College of Cardiology.)

disagreement between these studies illustrates the current lack of knowledge and forms the justification for modeling rather than attempting to measure regional wall motion, at least until more definitive results can be obtained. Two methods have been developed for modeling wall motion without using a coordinate system. Gibson et al[35] divide the end-diastolic contour into a number of evenly spaced points and measure the distance from each to the nearest point on the end-systolic contour. In the centerline method, a centerline is drawn midway between the end-diastolic and end-systolic contours. Motion is measured along 100 chords evenly spaced along and

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perpendicular to the centerline and normalized by the end-diastolic perimeter length (Fig. 5-4) .[36] [37] [38] [39] Because they make no assumptions concerning the geometry of the left ventricular contour, both methods can be applied to chambers of diverse shapes. For example, the centerline method has been used to measure wall motion in the right ventricle as well as from different views of the left ventricle, unaffected by distortions of ventricular shape resulting from disease processes. Wall Motion Parameters

Motion can be measured in one dimension as the linear distance between the end-diastolic and end-systolic contours and normalized to yield a shortening fraction. Alternatively, function can be measured in regions of the left ventricle: the change in the area of a region between end-diastole and end-systole normalized by the end-diastolic area yields a regional ejection fraction (Fig. 5-5) . Studies have shown that such an area parameter is less subject to variability in delineating the endocardial contour, probably because the variability at individual contour points is averaged out over the region.[29] [40] [41] The principal drawback to regional assessment lies in the definition of the regions. Although the perfusion territories of the major epicardial coronary arteries have been mapped,[42] studies have shown that dysfunction in 93

Figure 5-5 Schematic of diastolic and systolic left ventricular outlines subdivided into octants, showing different approaches to measuring regional contraction. A, regional area change; H, hemiaxis shortening; P, segmental endocardial perimeter contraction. Similar measurements can be made for other approaches of segmenting the ventricular contour. (From Moynihan PF, Parisi AF, Feldman EL: Circulation 1981;63:752–760.)

patients with ischemic heart disease may extend beyond the defined territory of the stenosed artery.[5] [43] [44] [45] [46] [47] This result may be due to multivessel disease, border zone dysfunction, and/or variable coronary anatomy. In patients with multiple critical stenoses or infarctions, there may be multiple regions of dysfunction that run together and cannot be distinguished from each other.[5] The only distinguishing feature about border zone dysfunction is that it is less severe than dysfunction in the central ischemic region.[48] [49]

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The impact of variable coronary anatomy on the measurement of regional left ventricular function is significant, because dysfunction may be underestimated if the central ischemic region straddles two adjacent segments, each of which also containing some normally contracting myocardium.[36] One solution to this problem is to measure wall motion at many discrete points around the ventricular contour and then average the motion of points lying within the region of interest. This approach is flexible enough to adjust for variable coronary anatomy while retaining the advantage of lower variability for regional analyses, and it has been applied successfully using the centerline method to analyze function in the center of, on the periphery of, and remote from the ischemic region.[36] [50] It is important to note that the motion of multiple points from different locations on the contour cannot be averaged validly unless the motion values have comparable distributions. For wall motion, the normal mean and standard deviation vary by location on the ventricle (see "Definition of Normal Values"). One solution is to convert the shortening fraction values to a Z score (i.e., to units of standard deviations from the mean of a normal reference population).[41] After conversion, a value of zero indicates normal motion, positive values indicate hyperkinesis, and negative values indicate hypokinesis. The magnitude of the wall motion value indicates the clinical significance of the abnormality. These standardized wall motion values can be averaged over regions and compared among different regions and different patients. Validation Using Empirical Criteria

The various methods for wall motion analysis have been "validated" clinically using empirical criteria. The principal criteria are high sensitivity and specificity in distinguishing patients with diseased hearts from normal subjects. The problem with this approach is that the demonstrated diagnostic accuracy depends not only on the parameter but also on the patient populations used for testing. For example, the diagnostic accuracy of a new method will appear to be much higher if the diseased patients have myocardial infarction than if they merely suffer from chronic stable angina, simply because the latter have near-normal function. For this reason, the relative merits of the various methods of wall motion analysis are best assessed from comparative studies of two or more methods. Most comparisons have been made on contours drawn from contrast ventriculograms (Table 5-2) . These studies have shown that the radial and centerline methods have higher diagnostic accuracy than methods based on a rectangular coordinate system. One study of 2D echocardiograms in the

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subcostal view reported that the centerline method is less likely to diagnose abnormality in normal subjects than the radial method.[26] In contrast, another echocardiographic study found that a rectangular coordinate system approach yielded higher diagnostic accuracy than either the radial or centerline methods.[28] The homogeneity of the normal group is the second empirical criterion. A narrow normal range, reflected by a small standard deviation, enhances sensitivity in diagnosing TABLE 5-2 -- Comparison of Sensitivity and/or Specificity of Methods of Wall Motion Analysis in Detecting Regional Dysfunction Methods RadialED COM > radialES COM, LA

Reference Papapietro et al[122]

RadialLA > radialES COM, ED + ES COM

Karsch et al *

Radial > area > rectangular Area, radialmidwall >> radialED + ES COM ,

Karsch et al * Lorente et al †

rectangular in anterior MI RadialED + ES COM , radialmidwall >>

Lorente et al †

rectangular, area in inferior MI Radialmidwall > rectangular > radialED + ES Colle et al ‡ COM

Area > radialLA , rectangular

Gelberg et al[41]

Centerline, rectangular >> radialmidwall

Sheehan et al §

Centerline = radialmidwall = rectangular

Lamberti et al

Centerline >> radialmidwall

Ginzton et al[26]

Radialmidwall > radialLA , radialES COM ,

Ingels et al ¶

rectangular Rectangular > centerline, radial Assmann et al[28] A >> B, C indicates that method A was significantly better than methods B and C, and that B and C do not differ from each other; A > B indicates method A was better than method B but not compared statistically; Area

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specifies that regional ejection fractions were measured; Radialmidwall

refers to the method of Ingels et al; Centerline refers to the centerline method of Sheehan et al; ED COM, origin at end-diastolic center of mass; ES COM, origin at end-systolic center of mass; ED + ES COM, origin of each contour at that contour's center of mass; LA, origin at midpoint of long axis; MI, myocardial infarction.

*Clin Cardiol 1980;3:123. †Int J Cardiol 1985;7:361. ‡Arch Mal Coeur 1982;75:395. §In Sigwart U, Heintzen PH, (eds): Ventricular Wall Motion. Stuttgart, Georg Thieme Verlag, 1984, p 139. In Computers in Cardiology. Long Beach, Calif., IEEE Computer Society, 1985, p 467. ¶Circulation 1980;61:966.

94

abnormality (Fig. 5-6) . For example, in calculating sample size for a clinical trial, the number (n) of patients per group is proportional to the square of the standard deviation (σ):

One way to evaluate a method quickly is to divide the value for the normal mean by the normal standard deviation. If the quotient is greater than 2, then akinesis is unlikely to lie within the normal range (defined as the mean ± 2 SD). If akinesis differs from the normal mean by less than 2 SD, then a patient's motion must be dyskinetic or aneurysmal to be considered definitely abnormal. Such a method is relatively insensitive to lesser degrees of dysfunction. Additional considerations in selecting a method of wall motion analysis are its ability to focus on a user-defined region of interest and its applicability to other chambers of the heart or to particularly distorted ventricular

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contours. The importance of these considerations depends on the intended application. Effect of Cardiac Translation on Wall Motion Analysis

The second assumption implicit in wall motion—that the heart's position is stable—is particularly problematic for 2D echocardiography. During systole, the left ventricle rotates about its long axis and translates anteriorly. [51] [52] There is no easy way to distinguish contraction from the translational motion of the heart. Several empirical methods have been proposed to "correct for" translation by realigning the end-systolic contour relative to the end-diastolic contour (Fig. 5-7) . For contrast ventriculography, Figure 5-6 Effect of variability on diagnostic accuracy. Bottom, Probability distribution functions for a normal (—) and disease (---) population. When the variability of the measurement is low and the standard deviation (SD) is narrow, virtually no overlap exists between the two groups. Top, When variability is greater, as indicated by a higher SD, the overlap between the same two populations increases from 11% to 68%. (From Sheehan FH: Measurement of left ventricular function from contrast angiograms in patients with coronary disease. In Brundage B [ed]: Comparative Cardiac Imaging-Function, Flow, Anatomy, Quantitation. Rockville, Md, Aspen Publications, 1990, pp 101–118.)

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Figure 5-7 Reference systems. The method of reregistration of the contours is shown on the left; the resulting superimposition of contours is shown on the right. Top, Fixed external reference system. There was no realignment of the drawn outlines between extension of radii from (in this example) the enddiastolic center of the area. Middle, Floating reference system with translation. The center of area in end-diastole and the center of area in end-systole were superimposed. Bottom, Floating reference system with translation and rotation. The centers of area in end-diastole and end-systole were superimposed for translation. The long axis from the center of the area to the apex at end-diastole was superimposed over the long axis in end-systole for rotation. □, end-diastolic center of area; •, endsystolic center of area. (From Schnittger I, Fitzgerald P, Gordon E, et al: Circulation 1984;70:242–254.)

realignment methods have no theoretical advantage over using a fixed reference system (i.e., analyzing the motion of the endocardial contour relative to the image frame [53] ) and may even worsen the reproducibility of the analysis.[40]

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For echocardiographic analysis, the question of realignment has not been definitively answered because of conflicting evidence. There are data to show that use of a fixed reference system may cause artifactual hypokinesis in a normal heart[54] however, using a floating reference (i.e., realigning) may present a dysfunctional segment as normal.[54] Parisi et al[55] found that fixed and floating reference systems yield equal accuracy in detecting the presence of wall motion abnormalities, but the fixed reference system was superior for localizing the abnormality. Schnittger et al[56] performed a detailed analysis of several methods for correcting for translation and rotation. They reported that the optimal analysis method differs by view. In the apical four-chamber view, correction for translation by superimposing the center of mass in the enddiastolic and end-systolic contours yielded the highest sensitivity and specificity in distinguishing patients with diseased hearts from normal subjects. However, in the short-axis view at the papillary muscle level, optimal results were obtained with a fixed reference. Zoghbi et al[57] reaffirmed the superior performance of the fixed over the floating reference analysis for the short-axis view, but they found that realignment using an epicardial centroid yielded the best correlation between wall motion and regional wall thickening. The need for realignment in the four-chamber view was reiterated by Force et al,[54] who found that patients with normal function studied after bypass surgery developed artifactual septal hypokinesis when analyzed using a fixed reference system. Feneley et al[58] [59] also found that a fixed reference causes artifactual dyskinesis in the septum when measured from short-axis images in patients with right ventricular volume overload or after bypass surgery. Wall Thickening In analyzing wall thickening, the thickness of the myocardium is measured at two or more time points in the cardiac cycle, then the measurements are compared. The thickness change is normalized by the end-diastolic dimension, as for wall motion. Normal myocardium thickens during systole. Dysfunctional myocardium exhibits decreased thickening or even thinning. Because each measurement of wall thickening is made from a single time point, thickening analysis is independent of artifact owing to cardiac translation. For this reason, many investigators prefer thickening for analyzing regional systolic function.[60] Experimental Basis

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The validity of wall thickening as a parameter of regional systolic function was initially demonstrated in experimental animals. In a series of acute and chronic studies, Ross and Franklin[61] showed a linear relationship between wall thickening and subendocardial fiber shortening measured using implanted ultrasonic crystals. Heikkila and Nieminen[62] reported that wall thickening is preferable because of its larger signal and lower variability compared with epicardial segment shortening. The accuracy of wall thickness measurements from echocardiograms was established initially using M-mode imaging of postmortem specimens.[62] The accuracy of wall thickening measurements from 2D echocardiograms has been validated for the calculation of ventricular mass.[63] [64] Subsequently, several investigative groups demonstrated 96

the feasibility of noninvasive regional wall thickening analysis by 2D echocardiography [44] [55] , [65] [66] and explored the potential clinical usefulness of this method for diagnosis of infarction, estimation of infarct size, and assessment of recovery and response to treatment. Measurements of wall thickening obtained from analyzing 2D echocardiograms are higher than those obtained using implanted ultrasonic crystals. This discrepancy is due to placement of the crystals in the subendocardium, whose movement underestimates true endocardial excursion.[63] Implicit Assumptions

Two assumptions are made in analysis of regional wall thickening. The first assumption is that wall thickness is measured along a vector orthogonal to the myocardial wall; that is, the imaging plane should be orthogonal to the wall and thickness should be measured in a radial direction within that plane, because analysis at oblique angles overestimates wall thickness. Some investigators advocate 3D analysis to ensure orthogonality.[67] In practice, the problem of oblique imaging pertains primarily to magnetic resonance imaging and computed tomography, which image in parallel planes, rather than to echocardiography, which offers greater flexibility in selecting each imaging plane. Nevertheless, this potential source of error should not be overlooked. The second assumption is the same as for wall motion: that a one-to-one correspondence be made between points on the ventricular contour at enddiastole and at end-systole. Actually, a strict correspondence is not possible

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because different slices of ventricle are imaged in systole and diastole owing to the translational motion of the heart through the imaging plane and the descent of the base toward the apex.[51] [52] However, the methods developed to date provide an estimated correspondence that has served well for both clinical and research applications. Figure 5-8 Measurement of wall thickening by the centerline method. The epicardial and endocardial contours of the left ventricular wall are displayed at end-diastole (left) and end-systole (right). Thickness is measured as the length of each of 100 chords constructed perpendicular to and evenly spaced along a line in the center of the myocardial wall (not shown), midway between the epicardial and endocardial contours. The end-diastolic endocardial contour is reproduced on the end-systolic plot to illustrate the extent of endocardial wall motion. (Redrawn from Sheehan FH, Feneley MP, DeBruijn NP, et al: J Thorac Cardiovasc Surg 1992;103:347–354.) Methods for Analyzing Regional Wall Thickening

Two methods are used for wall thickening analysis. The radial method measures wall thickness along radii extending from an origin usually located at the center of area, or at the midpoint of an anatomically defined diameter.[29] [51] [54] This method is most suitable for analyzing short-axis views with their near-circular contours, but it has also been applied to apical views.[68] In the centerline method, a centerline is drawn midway between the endocardial and epicardial contours. Wall thickness is measured along chords constructed perpendicular to and evenly spaced along the centerline (i.e., in the direction of the local radial vector[38] [69] [70] ) (Fig. 5-8) . In both methods the correspondence between end-diastole and end-systole relies on even distribution of points around the ventricular contour. No attempt has yet been made to anchor the point numbering system to available anatomic landmarks other than those used to define the start and end of the border. In short-axis views, border tracing usually begins at the junction of the right ventricle and septum, because the papillary muscles are not visible at all levels. In apical views, the border begins and ends at the valve planes. Wall thickening may be affected by cardiac motion if the wall thickness measurements are not performed independently at each time point. For example, Pandian et al[51] measured wall thickening using a radial coordinate system defined at end-diastole and superimposed on the end-

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systolic contours. In a patient with marked translational motion, the origin of this coordinate system may deviate from the center of the end-systolic contour. However, these investigators measured the translation and rotation of short-axis "slices" and found that the mean rotation in their 12 normal subjects was 1.0 ± 7.6 degrees counterclockwise, and translation averaged 1.7 ± 21.4 mm to the right and 6.7 ± 37 mm anteriorly. Realignment to correct for translation and rotation did not alter the mean or range of normal thickening.[51] Force 97

et al[54] reported that rotation in the dog averages 3.5 degrees and also recommended against corrective realignment. However, it is not clear how much translation affects wall thickening measurements in patients with diseased hearts. Comparison of Wall Motion and Wall Thickening Several studies have been performed that compare wall motion, wall thickening, and other parameters. Because no test has yet been developed for anatomic validation of methods for wall motion analysis, the comparisons with wall thickening have used empirical criteria. In deciding between these two parameters, theoretical and practical considerations are also worthy of attention. Theoretical Considerations

When the left ventricle is modeled as a thick-walled cylinder contracting radially and longitudinally, it can be shown mathematically that wall thickening, midwall shortening, and longitudinal axis shortening are related, but internal radius shortening (i.e., wall motion) is significantly influenced by the degree of left ventricular hypertrophy.[71] In ventricles with normal wall thickness, wall motion and wall thickening correlate closely.[72] However, the relative contribution of wall thickening, but not of wall motion, to ventricular power during ejection increases with increasing hypertrophy.[73] Thus, for example, wall motion may be inappropriately elevated in patients with hypertrophy owing to chronic valvular disease or cardiomyopathy. The discordance between wall motion and either wall thickening or midwall fiber shortening, both of which do not display hyperkinesis in these patients, is related to the relative wall thickness (compared with the chamber radius).[71] [74] [75] Thus, analysis of regional wall thickening more accurately reflects the functional status of

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hypertrophied ventricles than does endocardial wall motion. TABLE 5-3 -- Heterogeneity of Wall Motion and Wall Thickening in Normal Subjects *

N 10 10 12 12 12 10 14 14 14 9 9 9 9

% Wall % Wall Motion Thickening MEAN COEF. MEAN COEF. ± SD OF VAR. ± SD OF VAR. Reference Method View Hemiaxis SAX 30 ± 7 0.29 — — Moynihan shortening mitral et al[29] Hemiaxis SAX 35 ± 0.36 — — Moynihan shortening papillary 13 et al[29] Radius SAX 44 ± 0.39 52 ± 0.52 Pandian et shortening mitral 17 27 al[51] Radius SAX 49 ± 0.39 53 ± 0.43 Pandian et shortening chordal 19 23 al[51] Radius SAX 53 ± 0.34 53 ± 0.45 Pandian et shortening papillary 18 24 al[51] Radius SAX 24 ± 5 0.21 18 ± 0.72 Sandor et shortening papillary 13 al[76] Area change SAX 39 — — — Haendchen mitral et al[78] Area change SAX 56 — — — Haendchen papillary et al[78] Area change SAX 61 — — — Haendchen apical et al[78] Area change SAX 61 ± 0.16 38 ± 0.45 Ren et al[77] mitral 10 17 Area change 4CH: 69 ± 0.23 37 ± 0.38 Ren et al[77] apex 16 14 Area change 4CH: 62 ± 0.26 25 ± 0.40 Ren et al[77] postlateral 16 10 Area change 4CH: 70 ± 0.19 35 ± 0.43 Ren et al[77] septum 13 15

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4CH, apical four chamber; Coef. of Var., coefficient of variation (calculated as standard deviation/mean); N, number of subjects; SAX, short axis; SD, standard deviation. *Table displays representative data only from cited references; for complete data, see reference.

In addition to being independent of the degree of hypertrophy, wall thickening analysis is independent of translational artifact; therefore, no empirical realignment needs to be performed to correct for cardiac translation or rotation, and patients can be evaluated serially before and after bypass surgery without having to adjust for the effect of pericardiectomy on septal motion. The disadvantage of measuring wall thickening is that it does not reflect the contribution of epicardial motion to stroke volume.[57] Practical Considerations

Wall thickening analysis requires delineation of the epicardial contours as well as the endocardial contours. This doubling of work is not merely time consuming but also introduces additional opportunity for error. Imaging must be performed with the intent to quantify regional wall thickening, so that care is taken to include the epicardium within the scan sector throughout the cardiac cycle. Empirical Comparisons

The final arbiter between wall motion and wall thickening, each with its theoretical advantages and practical disadvantages, is performance. Because diagnostic accuracy is intimately related to normal variability, several investigators have performed comparative studies (Table 5-3) .[29] , [51] [69] [76] [77] [78] In general, although both akinesis and the absence of wall thickening are rare in normal subjects, wall thickening is more heterogeneous (i.e., has a higher coefficient of variation). The normal range, defined as mean ± 2 standard deviations, is more likely to encompass 0% thickening than 0% motion. The higher wall thickening variability is due in large part to point-to-point differences in end-diastolic wall thickness and can be reduced by using the end-diastolic perimeter length to normalize the observed change in wall thickness.[69]

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In diagnosing myocardial infarction, both parameters perform well (see "Diagnosis of Myocardial Infarction" 98

and "Assessment of Infarct Size"). Wall motion is slightly more sensitive in detecting dysfunction (96% vs. 93%), and wall thickening is slightly better in identifying normally functioning regions (100% vs. 83%) (Table 5-4) . In clinical studies, wall thickening has proved to be more sensitive in detecting dysfunction.[77] [79] For estimation of infarct size, both parameters yield comparable results (Table 5-5) . Tissue Doppler Imaging of Myocardial Velocity Low-velocity Doppler signals returned by myocardial tissue can be analyzed to assess regional ventricular function without the need for border delineation. [80] The velocities are presented visually using color coding, but they can also be quantified. The M-mode format provides higher temporal resolution. For accuracy 2D tissue Doppler imaging should be performed at a frame rate fast enough to capture changes in velocity.[80] Although it is a form of mapping rather than imaging, the pulsed wave Doppler mode allows peak velocity to be measured with high temporal and spatial resolution within the sample volume.[81] The accuracy of velocity measurements by tissue Doppler imaging has been validated in phantoms against M-mode echocardiography, in experimental animals by comparison with sonomicrometry, and in normal subjects versus M-mode.[80] [82] [83] The artifactual velocity contributed by the heart's translational motion can be canceled by computing a myocardial velocity gradient as the difference TABLE 5-4 -- Accuracy of Regional Systolic Function Analysis in Dia Myocardial Infarction Diagnosis Study Group Human: 37 acute MI Human:

Locatio SENSITIVITY SPECIFICITY Accurac Method Threshold (%) (% (%) Semiquantitative Abnormal 100 — 9

Semiquantitative Hypo, ak,

—

—

9

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26 TMMI, 6 SEMI Human: 66 acute MI Human: 20 MI, 18 normal Human: 20 MI, 18 normal Human: 20 MI, 18 normal Human: 15 MI Human: 48 acute MI Human: 18 angina, 12 SEMI Human: 18 angina, 12 SEMI Human: 32 angina, 33 acute MI Dog: 27 Dog: 27

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dys

Semiquantitative Hypo, ak, dys

—

—

9

Area change

<2 SD

95

89

—

Hemiaxis shortening

<2 SD

85

78

—

Perimeter shortening

<2 SD

90

72

—

Semiquantitative Hypo, ak, dys Semiquantitative Hypo, ak, dys

90

54

—

—

—

9

Semiquantitative Akinesis

50

100

—

Semiquantitative Severe hypo

83

100

—

Semiquantitative Abnormal

94

84

—

Area change

<2 SD

77

83

7

Wall thickening <2 SD

81

100

8

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— Human: 9 Wall motion <2 SD 100 — TMMI 6 Wall motion <2 SD 33 — — SEMI 9 Wall thickening <2 SD 89 — — TMMI 6 Wall thickening <2 SD 83 — — SEMI 6 Epicardial <2 SD 0 — — SEMI motion Human: Semiquantitative Hypo, ak, 94 — 9 95 acute dys MI Human: Semiquantitative Hypo, ak, 100 — — 31 TMMI dys 9 Semiquantitative Hypo, ak, 56 — — SEMI dys Dog: 24 Wall thickening ≤0 71 100 — MI, 5 nl Dog: 24 Wall motion ≤0 63 80 — MI, 5 nl Human: Semiquantitative Hypo, ak, 100 — 9 32 acute dys MI Human: Semiquantitative Hypo, ak, — — 8 73 TMMI dys Human: Semiquantitative Hypo, ak, 93 — 7 92 acute dys MI ak, akinesis; dys, dyskinesis; hypo, hypokinesis; MI, myocardial infarctio normal; SD, standard deviation; SEMI, subendocardial MI; TMMI, transmu between the endocardial and epicardial velocities normalized by the local wall thickness. [84] This correction, however, can only be applied to the anterior and posterior segments in the parasternal short-axis view, whose motion parallels the direction of the ultrasound beam.

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The normal range differs between the base and apex, the anterior and posterior walls, and the endocardium, midwall, and epicardium regardless of whether it is measured in M-mode as a tissue velocity, in 2D as a myocardial velocity gradient, or by pulsed wave Doppler as a peak velocity.[84] [85] [86] Variability is not lower than for other echocardiographic indices of ventricular function.[87] Several clinical applications have been proposed[88] even though the technology is limited to ventricular segments lying within ± 15 degrees of the incidence angle. In apical views, tissue Doppler imaging captures only longitudinal shortening. Tissue velocities measured from the apex failed to correlate with visual wall motion scores in infarct patients, although the velocity gradient between base and apex did reflect the number of dysfunctional segments. [89] A more recent study indicated that velocity measurement by pulsed Doppler improves diagnostic accuracy of viability assessment by dobutamine stress echocardiography.[90] In contrast, another study found this mode unable to discriminate control versus scar tissue when systolic velocity was measured, although diastolic velocities proved to be useful. [91] Clinical acceptance of tissue Doppler imaging is currently inhibited by the lack of consensus or standardization among the various acquisition and quantification modes. This modality's greatest contribution may be to applications for which it offers unique information. For example, 2D tissue Doppler acceleration 99

TABLE 5-5 -- Evaluation of Myocardial Infarction by Two-Dimensio Study No. of Echo Group Subjects Timing View Method Estimation of infarct size Dog 25 5.5 hr 1 Semiquant LAX +3 SAX Human 20 2–4 4 Semiquant days SAX Human 29 2–4 4 Semiquant days SAX

Infarct Size Threshold Parameter Hypo, ak, Tc99 dys

Hypo, ak, Thallium 201 dys Hypo, ak, Tc99 dys

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Human

60

Human

15

Human

48

Dog

20

Dog

20

Dog

24

Dog

24

Dog

27

Dog

27

Dog

10

Human

61

Dog

11

Human

20

<12 hr 3 LAX +5 SAX Varied 3 SAX <12 hr 3 apical 2 hr 1 LAX +3 SAX 48 hr 1 LAX +3 SAX 20 min 2 SAX 2 days 2 SAX Varied 3 SAX Varied 3 SAX 6 hr 4 SAX <12 hr 4 LAX +3 SAX 6 hr 3 SAX +3 apical <1 yr 3 SAX

Semiquant

Hypo, ak, Peak CK-MB dys

Semiquant

Ak, dys

Semiquant

Hypo, ak, Peak CK-MB dys <0 Histopatholog

Wall thickening

Postmortem

Wall thickening

<0

Histopatholog

Wall thickening Wall thickening Area change

<0

Histopatholog

<0

Histopatholog

<2 SD

Histopatholog

Wall thickening Semiquant

<2 SD

Histopatholog

Semiquant

Hypo, ak, Peak CK dys

Semiquant; endocardial surface map

Abnormal Histopatholog

Semiquant; endocardial

Abnormal Postmortem

Abnormal Histopatholog

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+ 2 surface map apical Dog 10 72 hr 5 Radial SAX shortening at ES Dog 10 72 hr 5 Radial SAX shortening over cardiac cycle Correlation with the size of the risk region Dog 24 20 min 2 Wall SAX thickening Dog 24 2 days 2 Wall SAX thickening Dog 10 6 hr 4 Semiquant SAX Dog 11 3 hr 4 Wall motion SAX Dog 11 3 hr 4 Wall motion SAX Dog 11 3 hr 4 Circumference SAX Dog 11 3 hr 4 Wall motion SAX over cardiac cycle Wall Dog 12 2 hr 1 SAX thickening: referenced to contrast defect Dog 12 2 hr 1 Wall SAX thickening: COM method

<15%

Histopatholog

<15%

Histopatholog

<0

Angiography

<0

Angiography

Abnormal Echo contrast <10%

Echo contrast

<20%

Echo contrast

Ak, dys

Echo contrast

<95% CI

Echo contrast

<95% CI

Echo contrast

<95% CI

Echo contrast

Risk Study No. of Echo Group Subjects Timing View Method

Infarct Size Threshold Parameter ESTIM

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Dog

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18

60 min 1 Wall <95% CI Microsphere SAX thickening Dog 16 60 min 1 Wall <2 SD Microsphere SAX motion Dog 16 60 min 1 Wall <95% CI Microsphere SAX motion Dog 16 60 min 1 Wall Dys Microsphere SAX motion Dog 16 60 min 1 Wall <2 SD Microsphere SAX thickening Wall <95% CI Microsphere Dog 16 60 min 1 SAX thickening Dog 16 60 min 1 Wall Dys Microsphere SAX thickening ak, akinesis; CI, confidence interval; CK, creatine kinase; CK-MB, creati COM, center of mass (method of realignment for translation); Corr. Coef., c dys, dyskinesis; ES, end-systole; hypo, hypokinesis; LAX, long axis; SAX, deviation; SEE, standard error of estimate; semiquant, semiquantitative anal Tc 99m pyrophosphate scintigraphy. * Percentage circumference.

100

imaging can localize the onset of mechanical contraction for electrophysiology testing. [92] Epicardial Motion The motion of the epicardium can be measured as a parameter of regional systolic function by applying methods for wall motion analysis to the epicardial contour. Compared with endocardial motion, however, epicardial motion is much lower in magnitude,[76] [78] [79] because thickening of the wall during systole contributes about half of what is measured as endocardial displacement.[93] Because measurement of epicardial motion is subject to the same sources of error and variability as endocardial motion, its lower

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magnitude results in an unfavorably high coefficient of variation,[76] which may explain its low sensitivity in detecting the presence of myocardial infarction.[79] Shape Analysis It has long been established that the left ventricle becomes more spherical when it dilates and decompensates.[94] [95] This compensatory mechanism allows a more even distribution of regional stress and improves ventricular efficiency. More recently it has been recognized that similar changes occur on a regional level in patients with recent myocardial infarction. Measurement of the magnitude of these changes provides information on the mechanism, magnitude, and time course of remodeling and its effect on prognosis. Global Shape

The analysis of global left ventricular shape is performed using general mathematical models. Most commonly, the ventricle is assumed to be elliptic, and its degree of sphericity is assessed by determining the ratio of the long-axis length to the short-axis diameter.[96] This parameter is subject to variability in measuring the axis lengths. Other parameters of global shape have also been developed, such as the ratio of the end-diastolic volume to the volume of a sphere with equivalent long-axis length, the ratio of the end-diastolic volume to the volume of the sphere with equivalent surface area, or the following ratio[97] [98] [99] 4π(Area)/(Perimeter2 ) In an experimental heart failure model, shape measurements based on axis length and area-to-perimeter ratios were less sensitive to incipient ventricular decompensation than the volume-to-surface area ratio.[99] Regional Shape

In patients with regional dysfunction (e.g., secondary to myocardial infarction), the left ventricular contour may develop regional abnormalities in curvature. [97] Curvature is a major determinant of wall tension, and changes in ventricular shape have been attributed to acute elevation in stress at the time of infarction; remodeling redistributes these stresses to improve efficiency. [100] [101] Analysis of regional curvature has been shown to provide diagnostic information when measured from contrast

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ventriculograms.[102] However, relatively little investigation has been performed in measuring regional curvature from 2D echocardiograms. [103] This lack of investigation may be because the apparent shape of the left ventricle in 2D echocardiography is greatly influenced by the imaging plane and is therefore dependent on the skill and care of the sonographer acquiring the images. It may be preferable, when analyzing echocardiograms, to measure regional shape using a method that is relatively insensitive to oblique imaging. One approach is to compare the lengths of the contour segments between the papillary muscles in the shortaxis view (Fig. 5-9) . This simple but effective method has proved useful for studying ventricular remodeling in patients with myocardial infarction. [104] Expansion (lengthening) of the infarct region is accompanied by thinning of the myocardium; therefore, the ratio of wall thickness in the diseased and normal regions provides another parameter of left ventricular geometry.

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Imaging and Image Analysis for Quantification Image Acquisition Technique

Unlike contrast ventriculography, in which the view angles are fixed, 2D echocardiography relies on the skill Figure 5-9 Method of measuring the expansion index and thinning ratio, shown in a midventricular section from a patient with anterior infarction and asynergy. Segment lengths were measured between midpoints of papillary muscle landmarks. a, average thickness of asynergic zone; b, average thickness of nonasynergic zone; LV, left ventricle; RV, right ventricle; x, endocardial length of asynergy-containing segment; y, endocardial length of segment without asynergy. Expansion index, x/y; thinning ratio, a/b. (Copyrighted and reprinted with the permission of Clinical Cardiology Publishing Company, Inc., and/or the Foundation for Advances in Medicine & Science, Inc. From Jugdutt BI, Michorowski BL: Clin Cardiol 1987;10:641–652.)

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of the sonographer in locating the desired anatomic slice in each patient. It is important to locate the various "standard" views with precision, reduce heterogeneity in the normal population, enhance diagnostic accuracy, and reduce variability between repeated studies in the same patient. The quality of quantitative analysis improves if the person performing image acquisition also performs the analysis. A sonographer with experience in quantification can recognize images that will be difficult to analyze and will enhance them as much as possible during acquisition. The American Society of Echocardiography has published recommendations concerning imaging for quantitative analysis of the endocardial contour. [2]

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Additional attention also may be needed to ensure visualization of the epicardium (e.g., increasing depth to ensure that the epicardium and anatomic landmarks are visible within the sector scan throughout the cardiac cycle and increasing lateral gain to improve edge definition along walls parallel to the beam). In patients with poor endocardial edge definition, intravenous injection of a contrast agent (e.g., albumin microbubbles) opacifies the chamber and improves endocardial depiction. [105]

An electrocardiographic rhythm strip should be acquired and recorded with the image to facilitate selection of a normal sinus beat (not following a premature beat) for analysis. Analog versus Digital Imaging

Echocardiograms are traditionally recorded on videotape at 30 frames per second. Because of the nature of analog imaging, only half of the scan lines are laid down at this rate; the other half of the lines, which alternate between the first set, are recorded 1/60 second later. Thus, each image frame consists of two half-resolution fields offset by 1/60 second. In analog-to-digital conversion, the convention is to treat each frame as a single image, regardless of the component fields. Digital images have a resolution of 256 × 256 or 512 × 512 pixels. Using the higher format retains the original image's resolution, but it requires four times as much computer memory. In practice, digitization at the 256 × 256 pixel resolution produces acceptable results. Digitization is necessary for quantitative analysis and facilitates comparison of serial studies.[106] As the speed of computer workstations increases and the price of digital memory decreases, the use of digital imaging will increase to take advantage of these benefits. This scenario is best exemplified by imaging systems intended for exercise echocardiography, which acquire and display up to four cine loops at a time, so that small changes in wall motion can be more easily appreciated. The same technology can be used to compare serial studies on the same patient. Networking between computers will allow images to be accessed from different locations in the hospital. Indeed, it may be possible in the near future to transmit and receive cardiac images over long distances for consultations. Image Analysis

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Frame Selection

When the objective is to select a representative cardiac cycle of images for quantitative analysis, the principal consideration is to find a beat in which the endocardial and epicardial contours are clearly visible throughout the cardiac cycle. In general, images acquired near end-expiration are clearer because there is less respiratory motion artifact and less lung interposition between the transducer and the heart. During inspiration, the beat-to-beat variability is higher than at end-expiration, especially at the apex (Fig. 510) .[107] The electrocardiographic rhythm strip assists in selecting a normal sinus beat or a beat of average RR interval in patients with atrial fibrillation. The end-diastolic frame is that with maximum cavity area and generally lies on or one frame after the R wave. The end-systolic frame is that with minimum cavity area. Identification of end-systole may be difficult in patients with asynchronous wall motion, because the timing of minimum cavity area may differ between views. End-systole can be identified from the second heart sound if a phonocardiogram is recorded during imaging. [108] Alternatively, the average time of minimum cavity area can be determined from reviewing all views and then applied to each view by noting its timing on the electrocardiogram. Border Tracing

The objective of border tracing is to delineate the left ventricular endocardial and epicardial contours. The endocardial edge is the interface between the bright echoes at the edge of the myocardium and the darker region of the ventricular cavity. Deciding where the endocardium lies among the bright echoes may be difficult, particularly when the contour is roughened by trabecular reflections. Contributing to the roughness is the relatively poorer resolution parallel to the echo beam. Studies in postmortem hearts have shown that tracing the leading edge of the endocardial echoes reduces underestimation of the cavity area compared with tracing the innermost black-white border.[109] In practice, this approach is associated with unacceptable variability, because the leading edge of the wall nearest to the transducer is separated from the trailing edge at the lumen by the bright border pixels.[109] [110] Some investigators suggest that the trailing edge of the nearer wall be traced and then corrected using image processing techniques to approximate the leading edge. [110] Along walls parallel to the echo beam, phantom studies have shown that accuracy is greatest when the midpoint of the leading edge is traced.[109]

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By convention, the papillary muscles are included in the cavity (Fig. 5-11) . It is recommended that the trabeculae also be included in the cavity, for two reasons. First, this is the approach used for analyzing contrast ventriculograms, which have a high accuracy for volume determination.[111] Indeed, the reported underestimation of volume by 2D echocardiography techniques may be related in part to inclusion of trabeculae with the myocardium in 102

Figure 5-10 Variability in the analysis of regional wall motion. Top, The effect of respiration on variability in 10 normal subjects. The regional ejection fraction between two consecutive beats from an inspiratory phase (variability Insp) is compared with the variability between two beats from the end-expiratory phase of two consecutive respiratory cycles (variability Exp). The variability is expressed as the mean of the absolute differences. In addition, the mean values for regional ejection fraction are presented from the second of the two consecutive beats from the inspiratory phase (mean Insp) and from an end-expiratory phase (mean Exp). Bottom, Variability in regional left ventricular function as measured at end-expiration in 20 normal subjects. The intraobserver, interobserver, and interbeat variability in regional ejection fraction are expressed as the mean of the absolute differences. In addition, the 10th to 90th percentile range for the regional ejection fraction in normal subjects is presented. Note that the interbeat variability is comparable to the intraobserver and interobserver variability. REF, regional ejection fraction. (From Assmann PE, Slager CJ, van der Borden SG, et al: J Am Soc Echocardiogr 1990;3:478–487.)

earlier studies.[112] Second, the borders traced for volume analysis can be applied to analysis of regional function as well. If trabeculae are traced, the borders of the endocardium are extremely noisy, and the resulting measurements of wall motion or wall thickening suffer from wide point-topoint variability. Some automated border detection programs have been developed. [113] As these methods become available commercially, it is important to remember that the physician ultimately must take responsibility for verifying that the border is drawn correctly. One image processing technique does not attempt to define a continuous endocardial contour such as a human observer would trace, but rather detects all blood-tissue interfaces lying within a user-defined region of interest.[114] Because the process can be performed in real time, the displacement of the interfaces through the cardiac cycle can be computed. Using color coding, an image is generated

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representing regional wall motion.[115] The method has been validated for measurement of volume and ejection fraction; for wall motion assessment its segmental analysis does not differ more from the consensus of two human observers than the humans do from each other.[115] Assistance from Digital Workstations

Digital workstations were initially developed for acquisition and display of image loops for exercise echocardiogram interpretation. With the increased interest in quantitation, workstation software is currently available for reviewing images and tracing the borders of the left ventricle and other structures. A properly programmed digital workstation can assist image analysis in a number of ways.

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Figure 5-11 (color plate.) Border tracing. In the initial tracing of the endocardial contour, the papillary muscles are included with the chamber, which produces a smooth contour for analyzing wall motion and wall thickening. Then the papillary muscle borders are traced separately and can be inserted for calculation of left ventricular volume. The epicardial contour is also shown. Cine Loop.

Few images are of such high quality that they can be analyzed entirely from a single stopped frame; therefore, it is essential to be able to review the full cardiac cycle in cine loop format, because watching wall motion helps to identify the endocardial and epicardial borders. The ability to watch wall motion is particularly important in analyzing images of borderline quality. Sometimes it is helpful to toggle quickly between the frame being analyzed and the preceding or following frame to look for a flash of movement that might help to identify an elusive border. Having control over the gray scale and contrast level also may assist in identifying a dim border segment. Review of the cine loop should be available not only before tracing but also during tracing so that the border can be traced in segments as they are identified. Cine loop review is also needed to double-check the tracing, which is most easily accomplished by alternately hiding and displaying the border while viewing the images. Tracing and Editing.

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There are two main methods of tracing: continuous drawing and dot entry. Continuous drawing allows direct delineation of complex border shapes, but it requires good hand-eye coordination. With dot entry, the spaces between the dots are filled in using spline curves. Dot entry is easier for the user and faster over regions that have a simple shape. However, in highly curved regions, the spline curve may not put the border where it was intended; in this case, the border would need to be edited. The workstation software should allow editing of any part of the traced border. Programs that allow selected border segments to be stretched in or out to a new position ("rubber banding") are easier to use than programs that delete the border segment and redraw it, because the latter requires more steps, and connecting the new segment smoothly to the raw ends of the remaining original border is difficult. As a final check, the observer should turn off the border overlay, review the cine loop again, and then turn the overlay back on to confirm the accuracy of the border placement. A custom program developed at the University of Washington allows the user to enter additional points on the border to demarcate segments whose definition is of low confidence. This customized option may help in the subsequent data interpretation. These warning points can also be used to omit the affected segments from regional function analysis. The ability to retain partial borders for analysis makes maximum use of the data by reducing the number of patients whose studies are rejected. The use of digital workstations does not reduce the fatigue associated with image analysis. Paying careful attention to details such as ambient lighting, ergonometrically sound furnishings, and periodic rest periods helps to maximize observer attention to detail and improve accuracy. Because of the possibility of fatigue, observers should not trace more than four hours per day on a regular basis. Variability Many factors affect the accuracy of quantitative image analysis and the precision or repeatability of a measurement. One must be aware of these sources of variability so that measures can be taken to minimize their impact. Beat-to-Beat Variability

Because patients are living, breathing subjects, there is variability between

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different cardiac cycles. This variability can be minimized by averaging over multiple consecutive cardiac cycles. Sandor et al[76] reported that threebeat averaging reduced the normal standard deviation for wall motion and wall thickening by 34% and 38%, respectively. Variability is higher during inspiration than expiration; end-expiratory cardiac cycles are least subject to motion artifact (see Fig. 5-10) . [107] Intraobserver and Interobserver Variability

In general, variability is higher for wall thickening than wall motion.[51] [69] [77] This difference is due mostly to point-to-point variability in enddiastolic wall thickness, because normalization of thickness change by enddiastolic perimeter length reduces variability to that of wall motion.[69] Variability in measuring wall thickening can also be reduced if thickness change is normalized by the end-diastolic wall thickness computed over a local region rather than at a discrete point on the ventricular contour.[70] The magnitude of inter- and intraobserver variability is low, ranging from 5% to 10% of the mean measurement for both wall motion and wall thickening, and it is not significantly higher than the variability between consecutive cardiac cycles (see Fig. 5-10) .[57] [77] , [107] [116] Pandian et al[51] reported intraobserver variability exceeding 50% of the mean for wall thickening, perhaps because the 104

beat and frame selection were not held constant between repeated tracings. Variability in measuring regional function is highest at the apex.[52] Pertinent to methods that use a coordinate system based on anatomic landmarks, the intra- and interobserver variability for landmark identification is 4.4% and 3.5% of the ventricular circumference, respectively.[44] Study-to-Study Variability

Echocardiography is the imaging modality most suitable for serial studies (e.g., to follow a patient's response to treatment), because it is safe, portable, and inexpensive. Study-to-study variability is low for 2D echocardiography, ranging from 7% to 15%.[16] [56] Some of the contributing factors cannot be controlled, such as changes in hemodynamic or emotional state. In stable patients, however, day-to-day changes in heart rate and blood pressure are small and do not significantly affect measurement of the ejection fraction.[117] Variability is 5% between studies acquired by different

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sonographers but analyzed by the same observer, which is lower than the 7% variability for images acquired by the same sonographer but analyzed by different observers.[117]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications Two-dimensional echocardiography is particularly useful as a research tool because of its large informational content. Regional function can be assessed qualitatively or measured quantitatively in terms of endocardial wall motion, wall thickening, or epicardial motion. From wall thickness measurements it is possible to measure mass, wall stress, and even regional stroke work, a parameter of local oxygen consumption.[165] To this list can be added 108

measurement of left ventricular shape, a major determinant of stress and function. The ability to clearly visualize the valve allows assessment of the relationship between valvular and ventricular function.[166] [167] [168] Frameby-frame analysis can be performed to analyze the synchrony of regional function through the cardiac cycle.[116] [169] By infusing echo contrast or performing tissue characterization analysis, the functional status of the myocardium can be related to its perfusion and pathology.[170] [171] By incorporating knowledge of spatial position and orientation of imaging planes, the 2D data can be used to create 3D reconstructions of the left ventricle,[172] which provide a more comprehensive view of this complex organ and allow for more detailed and accurate analysis of spatial relationships. Thus, left ventricular volume can be measured without geometric assumptions concerning its shape, wall thickness can be measured without error from oblique imaging, and shape can be better appreciated in three dimensions. These tools facilitate research to improve understanding of the pathophysiology of the disease process, the mechanisms by which the left ventricle attempts to compensate, and the beneficial effect of therapeutic interventions. However, it is important for investigators interested in applying these techniques to understand the limitations of the method as

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well as its potential benefits. It is generally known that spatial resolution within the imaging plane is higher in the direction of the echo beam than parallel to it. It is equally important to understand that spatial resolution is lowest orthogonal to the imaging plane: the so-called slice thickness owing to finite beam width causes inaccuracy in delineating complex curved surfaces.[173] [174] The temporal resolution, up to 30 frames per second, allows for comparisons of end-diastole to end-systole and analysis of asynchrony,[116] [169] but it may not be adequate for patients with high heart rates (e.g., infants). Two-dimensional echocardiography has been used to acquire the end point measurements in several clinical trials. For example, echocardiographic assessment of wall motion was performed to evaluate functional recovery after angioplasty or thrombolytic therapy for acute myocardial infarction and after coronary artery bypass surgery for angina.[17] [175] [176] [177] Other applications are to test drugs for side effects and to study the effects of anesthetics and surgical procedures.[178] [179] In general, however, echocardiography has not been considered the imaging modality of choice for clinical trials. This fact may be due to poor echogenicity in up to 25% of patients, usually as a result of coexistent lung disease. Another reason may be the reliance on skill, training, and reproducibility of sonographers in acquiring images in comparable imaging planes between patients. New technologic advances in imaging equipment may alleviate this problem in the future, for example, by displaying the position of each imaging plane online to actively assist in properly orienting each acquisition.[180] [181] [182] These sources of data loss and variability are greater than for other imaging modalities, but they are more than compensated for by the much greater informational content of echocardiographic examinations. It can be anticipated that echocardiography will be increasingly employed for clinical investigation in the future.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Edwards WD, Tajik AJ, Seward JB: Standardized nomenclature and anatomic basis

for regional tomographic analysis of the heart. Mayo Clin Proc 1981;56:479–497. 2. Schiller, NB, Shah PM, Crawford M, et al: Recommendations for quantitation of the

left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of TwoDimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358–367. 3. Herman MV, Gorlin R: Implications of left ventricular asynergy. Am J Cardiol

1969;23:538–547. 4. Gibson RS, Bishop HL, Stamm RB, et al: Value of early two dimensional

echocardiography in patients with acute myocardial infarction. Am J Cardiol 1982;49:1110–1119. 5. Stamm RB, Gibson RS, Bishop HL, et al: Echocardiographic detection of infarct-

localized asynergy and remote asynergy during acute myocardial infarction: Correlation with the extent of angiographic coronary disease. Circulation 1983;67:233–244. 6. Bourdillon PDV, Broderick TM, Sawada SG, et al: Regional wall motion index for

infarct and noninfarct regions after reperfusion in acute myocardial infarction: Comparison with global wall motion index. J Am Soc Echocardiogr 1989;2:398–407. 7. Kisslo J, Robertson D, Gilbert B, et al: A comparison of real-time, two-dimensional

echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 1977;55:134–141. 8. Ohuchi Y, Kuwako K, Umeda T, Machii K: Real-time, phased-array, cross-sectional

echocardiographic evaluation of left ventricular asynergy and quantitation of left ventricular function: A comparison with left ventricular cineangiography. Jpn Heart

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1980;21:1–15. 9. Hecht HS, Taylor R, Wong M, Shah PM: Comparative evaluation of segmental

asynergy in remote myocardial infarction by radionuclide angiography, twodimensional echocardiography, and contrast ventriculography. Am Heart J 1981;101:740–749. 10. Freeman AP, Giles RW, Walsh WF, et al: Regional left ventricular wall motion

assessment: Comparison of two-dimensional echocardiography and radionuclide angiography with contrast angiography in healed myocardial infarction. Am J Cardiol 1985;56:8–12. 11. Shiina A, Tajik AJ, Smith HC, et al: Prognostic significance of regional wall

motion abnormality in patients with prior myocardial infarction: A prospective correlative study of two-dimensional echocardiography and angiography. Mayo Clin Proc 1986;61:254–162. 12. Lundgren C, Bourdillon PDV, Dillon JC, Feigenbaum H: Comparison of contrast

angiography and two-dimensional echocardiography for the evaluation of left ventricular regional wall motion abnormalities after acute myocardial infarction. Am J Cardiol 1990;65:1071–1077. 13. Ginzton L, Conant R, Brizendine M, et al: Exercise subcostal two-dimensional

echocardiography: A new method of segmental wall motion analysis. Am J Cardiol 1984;53:805–811. 14. Bhatnagar SK, Al-Yusuf AR: Significance of early two-dimensional

echocardiography after acute myocardial infarction. Int J Cardiol 1984;5:575–84. 15. Loh IK, Yzhar C, Beeder C, et al: Early diagnosis of nontransmural myocardial

infarction by two-dimensional echocardiography. Am Heart J 1982;104:963–968. 16. Deutsch HJ, Curtius JM, Leischik R, et al: Reproducibility of assessment of left

ventricular function using intraoperative transesophageal echocardiography. Thorac Cardiovasc Surg 1993;41:54–58. 17. Otto C, Stratton JR, Maynard C, et al: Echocardiographic evaluation of segmental

wall motion early and late after thrombolytic therapy in acute myocardial infarction: The Western Washington Tissue Plasminogen Activator Emergency Room Trial. Am J Cardiol 1990;65:132–138. 18. Chaitman BR, DeMots H, Bristow JD, et al: Objective and subjective analysis of

left ventricular angiograms. Circulation 1975;52:420–425.

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19. Wexler LF, Lesperance J, Ryan TJ, et al: Interobserver variability in interpreting

contrast left ventriculograms (CASS). Cathet Cardiovasc Diagn 1982;8:341–355. 109

20. Lazar HL, Plehn JF, Schick EM, et al: Effects of coronary revascularization on

regional wall motion. J Thorac Cardiovasc Surg 1989;98:498–505. 21. Kan G, Visser CA, Koolen JJ, Dunning AJ: Short and long term predictive value of

admission wall motion score in acute myocardial infarction. A cross sectional echocardiographic study of 345 patients. Br Heart J 1986;56:422–427. 22. Nixon JV, Narahara KA, Smitherman TC: Estimation of myocardial involvement

in patients with acute myocardial infarction by two-dimensional echocardiography. Circulation 1980;62:1248–1255. 23. Horowitz RS, Morganroth J, Parrotto C, et al: Immediate diagnosis of acute

myocardial infarction by two-dimensional echocardiography. Circulation 1982;65:323–329. 24. Gibson DG, Prewitt TA, Brown DJ: Analysis of left ventricular wall movement

during isovolumic relaxation and its relation to coronary artery disease. Br Heart J 1976;38:1010–1019. 25. Goodyear AVN, Langou RA: The multicentric character of normal left ventricular

wall motion. Implications for the evaluation of regional wall motion abnormalities by contrast angiography. Cathet Cardiovasc Diagn 1982;8:225–232. 26. Ginzton LE, Berntzen R, Lobodzinski S, et al: Computerized quantitative segmental wall motion analysis during exercise: Radial vs. centerline left ventricular segmentation. In Ripley KL (ed): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1985, pp 157–160. 27. Rein A, Sapoznikov D, Lewis N, et al: Regional left ventricular ejection fraction

from real-time two-dimensional echocardiography. Int J Cardiol 1982;2:61–70. 28. Assmann PE, Slager CJ, van der Borden SG, et al: Comparison of models for

quantitative left ventricular wall motion analysis from two-dimensional echocardiograms during acute myocardial infarction. Am J Cardiol 1993;71:1262– 1269.

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29. Moynihan PF, Parisi AF, Feldman EL: Quantitative detection of regional left

ventricular contraction abnormalities by two-dimensional echocardiography: I. Analysis of methods. Circulation 1981;63:752–760. 30. Slager CJ, Hooghoudt TEH, Serruys PW, et al: Quantitative assessment of regional

left ventricular motion using endocardial landmarks. J Am Coll Cardiol 1986;7:317– 327. 31. Caiani EG, Cerutti S: Analysis of left ventricular wall motion using dynamic

alignment. Comput Cardiol 2000 (in press). 32. Ingels NB Jr, Mead CW II, Stinson EB, Alderman EL: A new method for

assessment of left ventricular wall motion In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1978, pp 57–61. 33. Homans DC, Sublett E, Lindstrom P, et al: Subendocardial and subepicardial wall

thickening during ischemia in exercising dogs. Circulation 1988;78:1267–1276. 34. Young AA, Kramer CM, Ferrari VA, et al: Three-dimensional left ventricular

deformation in hypertrophic cardiomyopathy. Circulation 1994;90:854–867. 35. Gibson DG, Sanderson JE, Trail TA, et al: Regional left ventricular wall movement

in hypertrophic cardiomyopathy. Br Heart J 1978;40:1327–1333. 36. Sheehan FH, Bolson EL, Dodge HT, et al: Advantages and applications of the

centerline method for characterizing regional ventricular function. Circulation 1986;74:293–305. 37. Wohlgelernter D, Cleman H, Highman A, et al: Regional myocardial dysfunction during coronary angioplasty: Evaluation by two-dimensional echocardiography and 12 lead electrocardiography. J Am Coll Cardiol 1986;7:1245–1254. 38. McGillem MJ, Mancini GBJ, DeBoe SF, Buda AJ: Modification of the centerline

method for assessment of echocardiographic wall thickening and motion: A comparison with areas of risk. J Am Coll Cardiol 1988;11:861–866. 39. Ginzton, LE: Stress echocardiography and myocardial contrast echocardiography.

Cardiol Clin 1989;7:493–509. 40. Sheehan FH, Stewart DK, Dodge HT, et al: Variability in the measurement of

regional ventricular wall motion from contrast angiograms. Circulation 1983;68:550– 559.

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41. Gelberg HJ, Brundage BH, Glantz S, Parmley WW: Quantitative left ventricular

wall motion analysis: A comparison of area, chord and radial methods. Circulation 1979;59:991–1000. 42. Jugdutt BI, Hutchins GM, Bulkley BH, Becker LC: Myocardial infarction in the

conscious dog: Three-dimensional mapping of infarct, collateral flow and region at risk. Circulation 1979;60:1141–1150. 43. Kerber RE, Marcus ML, Ehrhardt J, et al: Correlation between

echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion. Circulation 1975;52:1097–1104. 44. Lieberman AN, Weiss JL, Jugdutt BI, et al: Two-dimensional echocardiography

and infarct size: Relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog. Circulation 1981;63:739–746. 45. Wyatt HL, Meerbaum S, Heng MK, et al: Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography. Circulation 1981; 63:607–614. 46. Pandian NG, Kyoanagi S, Skorton DJ: Relations between 2-dimensional

echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. Am J Cardiol 1983;52:1318–1325. 47. Hutchins GM, Bulkley BH, Ridolfi RL, et al: Correlation of coronary arteriograms

and left ventriculograms with postmortem studies. Circulation 1977;56:32–37. 48. Homans DC, Asinger R, Elsperger KJ, et al: Regional function and perfusion at the

lateral border of ischemic myocardium. Circulation 1985;71:1038–1047. 49. Buda AJ, Zotz RJ, Gallagher KP: Characterization of the functional border zone

around regionally ischemic myocardium using circumferential flow-function maps. J Am Coll Cardiol 1986;8:150–158. 50. Sheehan FH, Doerr R, Schmidt WG, et al: Early recovery of left ventricular

function after thrombolytic therapy for acute myocardial infarction: An important determinant of survival. J Am Coll Cardiol 1988;12:289–300. 51. Pandian NG, Skorton DJ, Collins SM, et al: Heterogeneity of left ventricular

segmental wall thickening and excursion in 2-dimensional echocardiograms of normal human subjects. Am J Cardiol 1983;51:1667–1673. 52. Assmann PE, Slager CJ, Dreysse ST, et al: Two-dimensional echocardiographic

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analysis of the dynamic geometry of the left ventricle: The basis for an improved model of wall motion. J Am Soc Echocardiogr 1988;1:393–405. 53. Clayton PD, Jeppson GM, Klausner SC: Should a fixed external reference system

be used to analyze left ventricular wall motion? Circulation 1982;65:1518–1521. 54. Force T, Kemper A, Perkins L, et al: Overestimation of infarct size by quantitative

two-dimensional echocardiography: The role of tethering and of analytic procedures. Circulation 1986;73:1360–1368. 55. Parisi A, Moynihan P, Folland E, Feldman C: Quantitative detection of regional

left ventricular contraction abnormalities by two-dimensional echocardiography. II. Accuracy in coronary artery disease. Circulation 1981;63:761–767. 56. Schnittger I, Fitzgerald P, Gordon E, et al: Computerized quantitative analysis of

left ventricular wall motion by two-dimensional echocardiography. Circulation 1984;70;242–254. 57. Zoghbi WA, Charlat ML, Bolli R, et al: Quantitative assessment of left ventricular

wall motion by two-dimensional echocardiography: Validation during reversible ischemia in the conscious dog. J Am Coll Cardiol 1988;11:851–860. 58. Feneley M, Farnsworth A, Shanahan M, Cheng V: Mechanisms of the

development and resolution of paradoxical interventricular septal motion after uncomplicated cardiac surgery. Am Heart J 1987;114:106–114. 59. Feneley M, Gavaghan T: Paradoxical and pseudoparadoxical interventricular septal

motion in patients with right ventricular volume overload. Circulation 1986;74:230– 238. 60. Kittleson MD, Knowlen GG, Johnson LE: Early and late global and regional left

ventricular function after experimental transmural myocardial infarction: Relationships of regional wall motion, wall thickening, and global performance. Am Heart J 1987;114:70–78. 61. Ross J Jr, Franklin D: Analysis of regional myocardial function, dimensions, and

wall thickness in the characterization of myocardial ischemia and infarction. Circulation 1976;53:I88–I92. 62. Heikkila J, Nieminen MS: Echoventriculography in acute myocardial infarction.

IV. Infarct size and reliability by pathologic anatomic correlations. Clin Cardiol 1980;3:26–35.

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110

63. Feneley M, Hickie J. Validity of echocardiographic determination of left

ventricular systolic wall thickening. Circulation 1984;70:226–232. 64. Weiss RJ, Buda AJ, Pasyk S, et al: Noninvasive quantification of jeopardized

myocardial mass in dogs using 2-dimensional echocardiography and thallium-201 tomography. Am J Cardiol 1983;52:1340–1344. 65. Nieminen M, Parisi AF, O'Boyle JE, et al: Serial evaluation of myocardial

thickening and thinning in acute experimental infarction: Identification and quantification using two-dimensional echocardiography. Circulation 1982;66:174– 180. 66. Heikkila J, Tabakin BS, Hugenholtz PG: Quantification of function in normal and

infarcted regions of the left ventricle. Cardiovasc Res 1972;6:516–531. 67. Beyar R, Shapiro EP, Graves WL, et al: Quantification and validation of left

ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach. Circulation 1990;81:297–307. 68. Erbel R, Schweizer P, Meyer J, et al: Sensitivity of cross-sectional

echocardiography in detection of impaired global and regional left ventricular function: Prospective study. Int J Cardiol 1985;7:375–389. 69. Sheehan FH, Feneley MP, DeBruijn NP, et al: Quantitative regional wall

thickening analysis by transesophageal echocardiography. J Thorac Cardiovasc Surg 1992;103:347–354. 70. Yang P, Otto C, Sheehan F: The effect of normalization in reducing variability in

regional wall thickening. J Am Soc Echocardiogr 1997;10:197–204. 71. Dumesnil J, Shoucri R, Laurenceau J, Turcot J: A mathematical model of the

dynamic geometry of the intact left ventricle and its application to clinical data. Circulation 1979;59:1024–1034. 72. Sasayama S, Franklin D, Ross J Jr, et al: Dynamic changes in left ventricular wall

thickness and their use in analyzing cardiac function in the conscious dog: A study based on a modified ultrasonic technique. Am J Cardiol 1976;38:870–879. 73. Azancot I, Masquet C, Bourthoumieux A, et al: Myocardial hypertrophy, rate of

change of free wall thickness and directional components of ventricular power in man.

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J Physiol (Paris) 1981;77:695–703. 74. Aurigemma GP, Silver KH, McLaughlin M, et al: Impact of chamber geometry and

gender on left ventricular systolic function in patients >60 years of age with aortic stenosis. Am J Cardiol 1994;74:794–798. 75. Dong SJ, MacGregor JH, Crawley AP, et al: Left ventricular wall thickness and regional systolic function in patients with hypertrophic cardiomyopathy: A threedimensional tagged magnetic resonance imaging study. Circulation 1994;90:1200– 1209. 76. Sandor T, Henschke C, Risser TA, et al: Quantitative analysis of left ventricular

wall motion and thickness using two-dimensional echocardiography. Int J Biomed Comput 1983; 14:431–439. 77. Ren JF, Kotler Mn, Kakki, AH, et al: Quantitation of regional left ventricular

function by two-dimensional echocardiography in normals and patients with coronary artery disease. Am Heart J 1985;110:552–560. 78. Haendchen RV, Wyatt HL, Maurer G, et al: Quantitation of regional cardiac

function by two-dimensional echocardiography. I. Patterns of contraction in the normal left ventricle. Circulation 1983;67:1234–1245. 79. Henschke CI, Risser TA, Andor T, et al: Quantitative computer-assisted analysis of

left ventricular wall thickening and motion by 2-dimensional echocardiography in acute myocardial infarction. Am J Cardiol 1983;52:960–964. 80. Miyatake K, Yamagishi M, Tanaka N, et al: New method for evaluating left ventricular wall motion by color coded tissue doppler imaging: In vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 81. Isaaz K, Thompson A, Ethevenot G, et al: Doppler echocardiographic

measurement of low velocity motion of the left ventricular posterior wall. Am J Cardiol 1989;64:66–75. 82. Gorcsan J III, Strum DP, Mandarino WA, et al: Quantitative assessment of

alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography: Comparison with sonomicrometry and pressure-volume relations. Circulation 1997;95:2423–2433. 83. Donovan CL, Armstrong WF, Bach DS: Quantitative Doppler tissue imaging of the

left ventricular myocardium: Validation in normal subjects. Am Heart J 1995;130:100–104.

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84. Uematsu M, Miyatake A, Tanaka N, et al: Myocardial velocity gradient as a new

indicator of regional left ventricular contraction: Detection by a two-dimensional tissue doppler imaging technique. J Am Coll Cardiol 1995;26:217–223. 85. Palka P, Lange A, Fleming AD, et al: Doppler tissue imaging: Myocardial wall

motion velocities in normal subjects. J Am Soc Echocardiogr 1995;8:659–668. 86. Galiuto L, Ignone G, DeMaria AN: Contraction and relaxation velocities of the

normal left ventricle using pulsed-wave tissue Doppler echocardiography. Am J Cardiol 1998;81:609–614. 87. Vinereanu D, Khokhar A, Fraser AG: Reproducibility of pulsed wave tissue

Doppler echocardiography. J Am Soc Echocardiogr 1999;12:492–499. 88. Rambaldi R, Poldermans D, Vletter WB, et al: Doppler tissue imaging in the new

era of digital echocardiography. G Ital Cardiol 1997;27:827–839. 89. Jamal F, Derumeaux G, Douillet R, et al: Analysis and quantification of

longitudinal contraction of the left ventricle in myocardial infarction. Value of Doppler myocardial tissue imaging. Arch Mal Coeur Vaiss 1999;92:315–322. 90. Rambaldi R, Poldermans D, Bax JJ, et al: Doppler tissue velocity sampling

improves diagnostic accuracy during dobutamine stress echocardiography for the assessment of viable myocardium in patients with severe left ventricular dysfunction. Eur Heart J 2000;21:1091–1098. 91. von Bibra HV, Tuchnitz A, Klein A, et al: Regional diastolic function by pulsed

Doppler myocardial mapping for the detection of left ventricular ischemia during pharmacologic stress and perfusion testing: A comparison with stress echocardiography and perfusion scintigraphy. J Amer Coll Cardiol 2000;36:444–452. 92. Yin L-X, et al: Ventricular excitation maps using tissue Doppler acceleration

imaging: Potential clinical application. J Amer Coll Cardiol 1999;33:782–787. 93. Gould KL, Lipscomb K, Hamilton GW, Kennedy JW: Relation of left ventricular

shape, function and wall stress in man. Am J Cardiol 1974;34:627–634. 94. Burton AC: The importance of the shape and size of the heart. Am Heart J

1957;54:801–810. 95. Dodge HT, Frimer M, Stewart DK: Functional evaluation of the hypertrophied

heart in man. Circ Res 1974; 34–35(suppl II), II122–II127.

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Pagina 10 di 18

96. D'Cruz IA, Aboulatta H, Killam H, et al: Quantitative two-dimensional

echocardiographic assessment of left ventricular shape in ischemic heart disease. J Clin Ultrasound 1989;17:569–572. 97. Gibson DG, Brown DJ: Continuous assessment of left ventricular shape in man. Br

Heart J 1975;37:904–910. 98. Lamas GA, Vaughan DE, Parisi AF, Pfeffer MA: Effects of left ventricular shape

and captopril therapy on exercise capacity after anterior wall acute myocardial infarction. Am J Cardiol 1989;63:1167–1173. 99. Tomlinson CW: Left ventricular geometry and function in experimental heart

failure. Can J Cardiol 1987;3:305–310. 100. Bogen DK, Rabinowitz SA, Needleman A, et al: An analysis of the mechanical

disadvantage of myocardial infarction in the canine left ventricle. Circ Res 1980;47:728–741. 101. Mitchell GF, Lamas GA, Vaughan DE, Pfeffer MA: Left ventricular remodeling

in the year after first anterior myocardial infarction: A quantitative analysis of contractile segment lengths and ventricular shape. J Am Coll Cardiol 1992;19:1136– 1144. 102. Mancini GBJ, DeBoe SF, Anselmo E, LeFree MT: A comparison of traditional

wall motion assessment and quantitative shape analysis: A new method for characterizing left ventricular function in humans. Am Heart J 1987;114:1183–1191. 103. Sawada H, Fujii J, Takata H, et al: Quantitation of regional left ventricular wall motion by curvature: Two dimensional echocardiographic analysis. J Cardiogr 1986;16:789–798. 104. Jugdutt BI, Michorowski BL: Role of infarct expansion in rupture of the ventrical

septum after acute myocardial infarction: A two-dimensional echocardiographic study. Clin Cardiol 1987;10:641–652. 105. Crouse LJ, Cheirif J, Hanly DE, et al: Opacification and border delineation

improvement in patients with suboptimal endocardial border definition in routine echocardiography: Results of the phase III Albunex Multicenter trial. J Am Coll Cardiol 1993;22:1494–1500. 111

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Pagina 11 di 18

106. Feigenbaum H: Digital echocardiography in myocardial infarction. Aust NZ J

Med 1992;22:521–526. 107. Assmann PE, Slager CJ, van der Borden SG, et al: Quantitative echocardiographic

analysis of global and regional left ventricular function: A problem revisited. J Am Soc Echocardiogr 1990;3:478–487. 108. Moynihan PF, Parisi AF, Folland ED, et al: A system for quantitative evaluation

of left ventricular function with two-dimensional ultrasonography. Med Instrum 1980;14:111–116. 109. Conetta DA, Geiser EA, Skorton DJ, et al: In-vitro analysis of boundary

identification techniques used in quantification of two-dimensional echocardiograms. Am J Cardiol 1984;53:1374–1379. 110. Garcia E, Gueret P, Bennett M, et al: Real time computerization of two-

dimensional echocardiography. Am Heart J 1981;101:783–792. 111. Dodge HT, Sandler H, Ballew DW, Lord JD Jr: The use of biplane

angiocardiography for the measurement of left ventricular volume in man. Am Heart J 1960;60:762–776. 112. Helak JW, Reichek N: Quantitation of human left ventricular mass and volume by

two-dimensional echocardiography: In vitro anatomic validation. Circulation 1981;63:1398–1407. 113. Geiser EA, Wilson DC, Wang DA, et al: Autonomous epicardial and endocardial

boundary detection in echocardiographic short-axis images. J Amer Soc Echocardiogr 1998;11:338–348. 114. Vandenberg BF, Rath LS, Stuhlmuller P, et al: Estimation of left ventricular

cavity area with an on-line, semiautomated echocardiographic edge detection system. Circulation 1992;86: 159–166. 115. Lang RM, Vignon P, Weinert L, et al: Echocardiographic quantification of

regional left ventricular wall motion with color kinesis. Circulation 1996;93:1877– 1885. 116. Gillam LD, Hogan RD, Foale RA, et al: A comparison of quantitative

echocardiographic methods for delineating infarct-induced abnormal wall motion. Circulation 1984;70:113–122. 117. Himelman RB, Cassidy MM, Landzberg JS, Schiller NB: Reproducibility of

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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quantitative two-dimensional echocardiography. Am Heart J 1988;115:425–431. 118. Brutsaert DL: Nonuniformity: A physiologic modulator of contraction and

relaxation of the normal heart. J Am Coll Cardiol 1987;9:341–348. 119. Azancot I, Vannier D, Vannier A, et al: Utilisation of a minicomputer for analysis

and database management of hemodynamic parameters for routine and research applications. In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1979, pp 441–444. 120. Huhmann W, Duangphung K: Left ventricular wall motion. A comparison of six

evaluation methods. Z Kardiol 1980;69:818–826. 121. Karsch KR, Lamm U, Blanke H, Rentrop KP: Comparison of nineteen

quantitative models for assessment of localized left ventricular wall motion abnormalities. Clin Cardiol 1980;3:123–128. 122. Papapietro SE, Smith LR, Hood WP Jr, et al: An optimal method for angiographic

definition and quantification of regional left ventricular contraction. In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1978, pp 293–296. 123. Falsetti HL, Marcus ML, Kerber RE, Skorton DJ: Quantification of myocardial

ischemia and infarction by left ventricular imaging. 1981;63:747–751. 124. Rozanski A, Diamond GA, Forrester JS, et al: Alternative referent standards for

cardiac normality. Ann Intern Med 1984;101:164–171. 125. Gerstenblith G, Grederiksen J, Yin FCP, et al: Echocardiographic assessment of a

normal adult aging population. Circulation 1977;56:273–278. 126. Tennant R, Wiggers CJ: Effect of coronary occlusion on myocardial contraction.

Am J Physiol 1935;112:351–361. 127. Gould KL, Lipscomb K, Hamilton GW: Physiologic basis for assessing critical

coronary stenosis. Am J Cardiol 1974;33: 87–94. 128. Schwarz F, Flameng W, Thiedemann K-U, et al: Effect of coronary stenosis on

myocardial function, ultrastructure and aortocoronary bypass graft hemodynamics. Am J Cardiol 1978;42:193–201. 129. Sheehan FH, Brown BG, Dodge HT, et al: Quantitative analysis of the

relationship between coronary artery stenosis and regional left ventricular wall

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motion. In Sigwart U, Heintzen PH (eds): Ventricular Wall Motion. Georg Thieme Verlag, Stuttgart, 1984, pp 198–205. 130. McMahon MM, Brown BG, Cukingnan R, et al: Quantitative coronary

angiography: Quantitation of the critical stenosis in patients with unstable angina and single-vessel disease without collaterals. Circulation 1979;60:106–113. 131. Sheehan FH, Mathey DG, Schofer J, et al: Factors determining recovery of left

ventricular function following thrombolysis in acute myocardial infarction. Circulation 1985;71:1121–1128. 132. Harrison DG, Ferguson DW, Collins SM, et al: Rethrombosis after reperfusion

with streptokinase: Importance of geometry of residual lesions. Circulation 1984;69:991–999. 133. Braunwald E, Rutherford JD: Reversible ischemic left ventricular dysfunction:

Evidence for the "hibernating myocardium." J Am Coll Cardiol 1986;8:1467–1470. 134. Cohen M, Charney R, Hershman R, et al: Reversal of chronic ischemic

myocardial dysfunction after transluminal coronary angioplasty. J Am Coll Cardiol 1988;12:1193–1198. 135. Heger JJ, Weyman AE, Wann LS, et al: Cross-sectional echocardiography in

acute myocardial infarction: Detection and localization of regional left ventricular asynergy. Circulation 1979;60:531–538. 136. Nieminen M, Heikkila J: Echoventriculography in acute myocardial infarction II:

Monitoring of left ventricular performance. Br Heart J 1976;38:271–281. 137. Meltzer RS, Woythaler JN, Buda AJ, et al: Two dimensional echocardiographic

quantification of infarct size alteration by pharmacologic agents. Am J Cardiol 1979;44:257–262. 138. Visser CA, Lie KI, Kan G, et al: Detection and quantification of acute, isolated

myocardial infarction by two dimensional echocardiography. Am J Cardiol 1981;47:1020–1025. 139. Weiss JL, Bulkley BH, Hutchins GM, Mason SJ: Two-dimensional

echocardiographic recognition of myocardial injury in man: Comparison with postmortem studies. Circulation 1981;63:401–408. 140. Visser CA, Kan G, Lie KI, et al: Apex two dimensional echocardiography:

Alternative approach to quantification of acute myocardial infarction. Br Heart J 1982;47:461–467.

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141. O'Boyle JE, Parisi AF, Nieminen M, et al: Quantitative detection of regional left

ventricular contraction abnormalities by 2-dimensional echocardiography: Comparison of myocardial thickening and thinning and endocardial motion in a canine heart. Am J Cardiol 1983;51:1732–1738. 142. Van Reet RE, Quinones MA, Poliner LR, et al: Comparison of two-dimensional

echocardiography with gated radionuclide ventriculography in the evaluation of global and regional left ventricular function in acute myocardial infarction. J Am Coll Cardiol 1984;3:243–252. 143. Widimsky P, Gregor P, Cervenka V, Visek V: Two-dimensional

echocardiography in acute transmural and non-transmural myocardial infarction. Cor Vasa 1984;26:12–19. 144. Pandian NG, Skorton DJ, Collins SM, et al: Myocardial infarct size threshold for

two-dimensional echocardiographic detection: Sensitivity of systolic wall thickening and endocardial motion abnormalities in small versus large infarcts. Am J Cardiol 1985;55:551–555. 145. Aebischer N, Bise AC, Gabathuler J, Lerch R: Prognostic value of bidimensional

echocardiography in the acute phase of myocardial infarct. Schweiz Med Wochenschr 1985;115:1641–1646. 146. Widimsky P, Kopsa P, Cervenka V, et al: The possibility of non-invasive

identification of occluded coronary artery in acute myocardial infarction. Cor Vasa 1986;28:428–437. 147. Horowitz RS, Morganroth J: Immediate detection of early high-risk patients with

acute myocardial infarction using two-dimensional echocardiographic evaluation of left ventricular regional wall motion abnormalities. Am Heart J 1982;103:814–822. 148. Ideker RE, Behar VS, Wagner GS, et al: Evaluation of asynergy as an indicator of

myocardial fibrosis. Circulation 1978;57:715–725. 149. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB: The wavefront

phenomenon of ischemic cell death. Circulation 1977;56:786–794. 150. TIMI Research Group: Immediate vs delayed catheterization and angioplasty

following thrombolytic therapy for acute myocardial infarction. J Am Med Assoc 1988;260:2849–2858. 151. Kemper AJ, O'Boyle JE, Sharma S, et al: Hydrogen peroxide contrast-enhanced

two-dimensional echocardiography: Real-time in vivo delineation of regional

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myocardial perfusion. Circulation 1983;68:603–611. 112

152. Nishimura RA, Tajik AJ, Shub AC, et al: Role of two-dimensional

echocardiography in the prediction of in-hospital complications after acute myocardial infarction. J Am Coll Cardiol 1984;4:1080–1087. 153. Guyer DE, Foale RA, Gillam LD, et al: An echocardiographic technique for

quantifying and displaying the extent of regional left ventricular dyssynergy. J Am Coll Cardiol 1986; 8:830–835. 154. Wilkins GT, Southern JF, Choong CY, et al: Correlation between

echocardiographic endocardial surface mapping of abnormal wall motion and pathologic infarct size in autopsied hearts. Circulation 1988;77:978–987. 155. Mann DL, Foale RA, Gillam LD, et al: Early natural history of regional left

ventricular dysfunction after experimental myocardial infarction. Am Heart J 1988;115:538–546. 156. Kaul S, Pandian NG, Gillam LD, et al: Contrast echocardiography in acute

myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis. J Am Coll Cardiol 1986;7:383–392. 157. Maroko PR, Libby P, Ginks WR, et al: Coronary artery reperfusion. I. Early

effects on local myocardial function and the extent of myocardial necrosis. J Clin Invest 1972;51:2710–2716. 158. Mock MB, Ringqvist I, Fisher LD, et al: Survival of medically treated patients in

the Coronary Artery Surgery Study (CASS) Registry. Circulation 1982;66:562–568. 159. Schwartz RS, Ilstrup DM, Vlietstra RE, et al: Weighted ventriculographic wall

motion score for improved survival prediction in patients with coronary artery disease. Cathet Cardiovasc Diag 1989;18:79–84. 160. Nishimura RA, Reeder GS, Miller FA Jr, et al: Prognostic value of predischarge

2-dimensional echocardiogram after acute myocardial infarction. Am J Cardiol 1984;53:429–432. 161. Shah PK, Pichler M, Berman DS, et al: Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol

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1980;46:915–921. 162. Bishop HL, Gibson RS, Stamm RB, et al: Role of two-dimensional

echocardiography in the evaluation of patients with ventricular septal rupture postmyocardial infarction. Am Heart J 1981;102:965–971. 163. Jugdutt BI: Identification of patients prone to infarct expansion by the degree of

regional shape distortion on an early two-dimensional echocardiogram after myocardial infarction. Clin Cardiol 1990;13:28–40. 164. Tischler MD, Niggel J, Borowski DT, LeWinter MM: Relation between left

ventricular shape and exercise capacity in patients with left ventricular dysfunction. J Am Coll Cardiol 1993;22:751–757. 165. Nakano K, Sugawara M, Kato T, et al: Regional work of the human left ventricle

calculated by wall stress and the natural logarithm of reciprocal of wall thickness. J Am Coll Cardiol 1988;12:1442–1448. 166. Kono T, Sabbah HN, Rosman H, et al: Left ventricular shape is the primary

determinant of functional mitral regurgitation in heart failure. J Am Coll Cardiol 1992;20:1594–1598. 167. Boltwood CM, Tei C, Wong M, Shah PM: Quantitative echocardiography of the

mitral complex in dilated cardiomyopathy: The mechanism of functional mitral regurgitation. Circulation 1983;68:498–508. 168. Alam M, Rosenhamer G: Atrioventricular plane displacement and left ventricular

function. J Am Soc Echocardiogr 1992;5:427–433. 169. Weyman AE, Hogan TD Jr, Gillam LD, et al: Importance of temporal

heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia. Circulation 1984;70:102–112. 170. Skorton DJ, Melton HE Jr, Pandian NG, et al: Detection of acute myocardial

infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray-level distributions. Circ Res 1983;52:36–44. 171. Armstrong WF, Mueller TM, Kinney EL, et al: Assessment of myocardial

perfusion abnormalities with contrast-enhanced two-dimensional echocardiography. Circulation 1982;66:166–173. 172. Geiser EA, Lupkiewicz SM, Christie LG, et al: A framework for three-

dimensional time-varying reconstruction of the human left ventricle: Sources of error and estimation of their magnitude. Comput Biomed Res 1980;13:225–241.

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173. Geiser EA, Skorton DJ, Conetta DA: Quantification of left ventricular function by two-dimensional echocardiography: Consideration of factors restricting image quality. Am Heart J 1982;103:905–910. 174. Garrison JB, Weiss JL, Maughan WL, et al: Quantifying regional wall motion and

thickening in two-dimensional echocardiography with a computer-aided contouring system. In Ostrow HG, Ripley KL (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1977, pp 25–35. 175. Presti CF, Gentile R, Armstronf WF, et al: Improvement in regional wall motion

after percutaneous transluminal coronary angioplasty during acute myocardial infarction: Utility of two-dimensional echocardiography. Am Heart J 1988;115:1149– 1155. 176. Touchstone D, Beller GA, Nygaard TW, et al: Effects of successful intravenous

reperfusion therapy on regional myocardial function and geometry in humans: A tomographic assessment using two-dimensional echocardiography. J Am Coll Cardiol 1989;13:1506–1513. 177. Bourdillon PDV, Broderick TM, Williams ES, et al: Early recovery of regional

left ventricular function after reperfusion in acute myocardial infarction assessed by serial two-dimensional echocardiography. Am J Cardiol 1989;63:641–646. 178. Nakashima Y, Maldareli W, Oka Y, Sisto DA: Evaluation of the effects of

different cardioplegic techniques on left ventricular function during coronary artery bypass surgery using transesophageal echocardiography. Cardiovasc Surg 1993;1:587–593. 179. Slavik JR, LaMantia KR, Kopriva CJ, et al: Does nitrous oxide cause regional

wall motion abnormalities in patients with coronary artery disease? Anesth Analg 1988;67:695–700. 180. King DL, Harrison MR, King DL Jr, et al: Improved reproducibility of left atrial

and left ventricular measurements by guided three-dimensional echocardiography. J Am Coll Cardiol 1992;20:1238–1245. 181. Sheehan FH: Measurement of left ventricular function from contrast angiograms

in patients with coronary disease. In Brundage BH (ed): Comparative Cardiac Imaging—Function, Flow, Anatomy, Quantitation. Rockville, Md, Aspen Publications, 1990, pp 101–118. 182. Kloner RA: Coronary angioplasty: A treatment option for left ventricular

remodeling after myocardial infarction? J Am Coll Cardiol 1992;20:314–316.

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113

Chapter 6 - Left Ventricular Diastolic Function Clinical Utility of Doppler Echocardiography Mikel D. Smith MD

Left ventricular diastolic function is recognized as an important contributing factor in the pathophysiology of many common cardiovascular diseases. The clinical manifestations of cardiomyopathy, hypertension, and coronary artery disease are often the result of abnormalities of left ventricular filling. Diastolic dysfunction may be present prior to, or concomitant with, systolic dysfunction. Although treatments are often aimed at improving left ventricular contractile performance, they may conflict with appropriate therapy for diastolic abnormalities. Recently, attention has been increasingly directed toward the diagnosis, evaluation, and treatment of diastolic dysfunction. Although catheterization measurements of diastolic performance remain the standard, these invasive parameters have proved technically challenging and tedious to acquire. In recent years, a large body of literature has accrued describing various Doppler echocardiographic techniques for assessing diastolic function. These methods have given new insight into the flow dynamics of the left ventricle, mitral valve, and pulmonary veins and have allowed a more practical noninvasive assessment of diastolic function. Several features of Doppler flow patterns have emerged as having

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important diagnostic and therapeutic implications. This chapter reviews the state of the art in the Doppler echocardiographic assessment of left ventricular diastolic function, relates these methods to the physiology of left ventricular filling, and describes the use of these techniques in clinical decision making.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Physiology of Diastole Definition. Traditionally, diastole has been described as the portion of the cardiac cycle that begins with aortic closure (S2 ) and ends with mitral closure (S1 ). Importantly, this definition includes the isovolumic relaxation phase. Normal diastolic function may be clinically defined as the ability of the left ventricle to accommodate an adequate filling volume to maintain cardiac output while operating at a low pressure. Phases of Diastole. For descriptive purposes, the diastolic period can be divided into four stages (Fig. 6-1) . [1] After systolic ejection is complete and left ventricular 114

Figure 6-1 Schematic of intracardiac pressures and volumes to define the four stages of diastole. The periods of isovolumic relaxation, rapid filling, slow filling (diastasis), and atrial filling are shown. See text for description. AVC, aortic valve closure; AVO, aortic valve opening; LV, left ventricle; MVC, mitral valve closure; MVO, mitral valve opening. (From Zile M: Mod Concepts Cardiovasc Dis 1989;58:67.)

pressure falls below aortic pressure, the aortic valve closes. This marks the beginning of isovolumic relaxation, which subsequently ends at mitral valve opening. During this interval, pressure continues to fall at a rapid rate, while ventricular volume remains constant. Events occurring during this phase have been attributed mainly to myocardial relaxation and have been shown to be an energy-requiring process. At this time, myofibrils return to their resting state from the contracted state. The left ventricular cavity changes in geometry, while volume remains constant.

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When left ventricular pressure falls below left atrial pressure (crossover point) the mitral valve opens, and the rapid filling phase begins. The peak rate of filling is directly related to the magnitude of the left atrial-left ventricular pressure gradient. Even though relaxation continues, the rapid increase in left ventricular volume counterbalances this effect and results in a gradual rise in pressure. Physiologically, this appears to represent a complex interaction between left ventricular suction (active relaxation),[2] and passive viscoelastic properties of the myocardium (compliance). As relaxation slows and the atrium empties, the atrioventricular pressure gradient gradually dissipates, and this phase of left ventricular filling ends. The third phase of diastole consists of passive filling during diastasis. In this period, the left atrial and ventricular pressures are nearly equal, so filling is mainly the result of pulmonary venous flow, with the left atrium essentially acting as a passive conduit. The amount of filling is directly proportional to left ventricular compliance. The final phase of diastole is atrial contraction. This active process contributes approximately 15% of left ventricular filling in normal subjects and possibly more in patients in various disease states. This phase is most affected by left ventricular stiffness and external pericardial restraint (as a resistance to left atrial ejection), atrial contractility, and left atrial-left ventricular synchrony (i.e., the PR interval). This final phase of diastole is terminated with the subsequent rise in ventricular pressure and mitral valve closure. The last three phases after mitral valve opening have also been termed auxotonic relaxation, since left ventricular volume continues to increase, although pressure changes are variable.[3]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Invasive Measures of Diastolic Function From the description just given, it should be evident that no single parameter can be derived that will adequately describe diastolic performance. Left ventricular filling is the result of a variety of complex forces, including myocardial relaxation, ventricular suction, ventricular stiffness, viscoelastic properties of the myocardium, erectile filling of the coronary arteries, atrial contraction, ventricular interdependence, and pericardial restraint. To understand the role of Doppler echocardiographic information in assessing diastolic function, it is necessary to have a working knowledge of other conventional methods. Traditionally, catheterization-based methods for studying diastolic events have focused on evaluation of the relationship between left ventricular pressure and volume. Because of the dynamic nature of diastole, measurements have been derived to describe the function of the ventricle during its isolated phases. The indices of function have centered on the evaluation of relaxation, filling, or compliance (Fig. 6-2) . As shown, these measurements are not interchangeable and, like Doppler descriptors, describe different phenomena during the sequential phases of diastole. They may also be variably influenced by changes in factors such as load or heart rate (Table 6-1) . Hemodynamic indices describing early diastolic events include peak -dP/dt, the time constant of isovolumic left ventricular pressure decay or tau (τ), the isovolumic relaxation time (IVRT), and the half-time of ventricular pressure decline (T1/2 ).[4] [5] Peak -dP/dt. Just after aortic valve closure and early during the isovolumic phase, left ventricular pressure falls exponentially. The maximal rate of this rapid pressure decline (peak -dP/dt) can be obtained with high-fidelity,

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micromanometer-tipped catheters in the ventricular cavity. This value is taken as the lowest value of the first derivative of left ventricular pressure (see Fig. 6-2) and typically yields values in the range of 2000 ± 400 mm Hg per second for normal subjects.[6] [7] The index becomes decreased (less negative) with impaired relaxation due to ischemia. [7] However, the peak dP/dt is dependent on sympathetic tone and absolute aortic pressure and reflects properties of left ventricular relaxation at a single point in time.[8] [9] Tau. Weiss' group and others[7] , [9] [9] have proposed the use of a time constant of relaxation (tau, τ) to describe pressure fall throughout isovolumic diastole. The measurement 115

Figure 6-2 Schematic showing the relationship of pressures, rate of pressure change (dP/dt), volumes, and Doppler transmitral and pulmonary venous flows. The portion of the cardiac cycle and index of diastolic function are shown in block letters and include tau, isovolumic relaxation time (IVRT), peak -dP/dt, peak filling rate (PFR), rapid filling fraction (RFF), and atrial filling fraction (AFF) along with the corresponding Doppler measures of transmitral and pulmonary venous flow. The derivation of these indices is described in the text, and the characteristics and limitations of these parameters are listed in Table 6-1 . Kv, modulus of chamber stiffness.

assumes a monoexponential decay in left ventricular pressure from aortic closure (taken as peak -dP/dt) to an arbitrary point 5 mm Hg above enddiastolic pressure (approximating mitral valve opening). The pressure values are converted to a logarithmic scale and fitted to a straight line (Fig. 6-3) . The negative reciprocal of the slope of this line represents the exponential decay time constant (TL) and is expressed in milliseconds. Normal values for tau range from 25 to 40 msec. Higher values represent reduced early diastolic distensibility due to relaxation at excessively slow rates. Tau may be relatively load independent[6] but does not describe events during any phases of ventricular filling. Nevertheless, the time constant of relaxation remains an accepted standard and widely used invasive descriptor of left ventricular diastolic function. Chamber Stiffness. Catheterization methods have also been derived for pressure-volume events

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during filling. The assessment of diastolic mechanics in the catheterization laboratory requires highly accurate determinations of both pressure and volume. The simultaneous recording of these values allows the calculation of compliance as the rate of change in volume per rate of change in pressure, dV/dP (Fig. 6-4) . The reciprocal of this value, dP/dV (called chamber stiffness), is usually derived by obtaining pressures at different volumes, measured at end-diastole. Since this relationship is exponential for the left ventricle, the rate of change is calculated from a single point and represents the instantaneous slope of the tangent to this curve. Chamber stiffness values are preload dependent, so that an increase in volume from point A to point B will result in an increase in chamber stiffness (see Fig. 64A) . However, when dP/dV is plotted against pressure, a linear relationship exists for a given ventricle (see Fig. 6-4B) . The slope of the line describing chamber stiffness versus pressure is called the modulus of chamber stiffness, or Kv. Although Kv is relatively independent of pressure and volume, comparison between ventricles of different volume must be normalized for chamber stiffness (i.e., VdP/dV). The reciprocal dV/VdP represents specific chamber compliance. Normal values for Kv range from 0.010 to 0.025, and dV/VdP data generally fall between 0.015 and 0.045.[10] Although often difficult to acquire, these values are descriptive of events occurring in late diastole and define the passive components of ventricular filling. The values have not been validated for acute conditions, making comparisons among patients somewhat impractical.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Radionuclide Descriptors of Filling Contrast ventriculography and radionuclide angiography have been used to describe the volume changes that occur with ventricular filling.[11] When volumes are calculated and plotted over time, the resultant curve can readily define the rapid filling, diastasis, and atrial contraction phases of diastole (see Fig. 6-2) . The first derivative of this time-activity curve (dV/dt) describes the peak filling rate and time to peak filling rate. Other available measurements include the atrial filling fraction and early or rapid filling fraction. In summary, there are a number of time-honored methods for describing left ventricular diastolic function. Catheterization methods have the advantage of combining pressures with volume but are tedious, often define only a single point in time, and are load dependent. Although these elegant indices can provide significant insight regarding the physiology of ventricular diastole, their practical application to individual patients remains limited.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Doppler Echocardiographic Indices of Diastolic Function Isovolumic Relaxation Time Dynamic left ventricular relaxation begins at the time of peak systolic pressure.[12] The process continues as ventricular pressure falls below aortic pressure, ejection ceases, and the valve closes. Left ventricular pressure continues to fall even as volume remains constant during the isovolumic phase of diastole but prior to mitral valve 116

TABLE 6-1 -- Description and Limitations of Conventional Diastolic Function Indices Index Description Limitations Catheterization -dP/dt First derivative of LV pressure Sympathetic tone and decay during IVRT afterload dependent No filling data Tau (τ) Time constant of exponential No filling data decay of LV pressure during isovolumic period Kv Modulus of LV chamber Requires multiple stiffness measured at endpressures/volumes diastole Normalized for volume Radionuclide Peak filling Maximal slope of filling curve No pressures

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rate Rapid filling Fraction of early, late filling fraction, atrial filling fracture Transmitral Doppler IVRT Continuous wave Doppler across MV, aortic valve; time between aortic closure, MV opening Peak E, Ei Peak A, Ai

Early filling velocities and integrals Late filling velocities and integrals

No data during IVRT

Age dependent

No filling data Preload dependent Age dependent

Limited by atrial function, heart rate, and rhythm Deceleration Deceleration time from peak E Preload dependent time to baseline velocity Pulmonary vein Doppler Peak S, Si Forward flow velocities from Age and preload atrial relaxation and MV dependent annulus motion Mitral regurgitation Peak D, Di Forward flow velocities due to Age and preload LV relaxation dependent S/D Systolic fraction; ratio (%) Age and preload from Si /Di dependent Atrial reversal

Reverse flow due to atrial contraction

Age dependent

Limited by atrial function, LV compliance A, atrial filling velocity; Ai , integral of atrial filling velocity; D,

diastolic velocity; Di , integral of diastolic velocity; E, early filling

velocity; Ei , integral of early filling velocity; IVRT, isovolumic relaxation

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time; Kv, modulus of left ventricular chamber stiffness; LV, left ventricular; MV, mitral valve; S, systolic velocity; Si , integral of systolic velocity.

Figure 6-3 The derivation of the time constant of relaxation (tau) from left ventricular (LV) pressure recordings. A, Plot of LV pressure over time. The solid line represents the monoexponential decay during the isovolumic period. B, Plot of the log of these LV pressure values over time. The reciprocal of the slope of this line represents tau (TL ) expressed in milliseconds. A, slope of the line; TL , tau.

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Figure 6-4 Derivation of the modulus of chamber stiffness from pressure and volume recordings in the left ventricle. A, Pressure/volume plot for the left ventricle is shown in a hatched line. Pressures are obtained at two separate volume states (A and B). The slope of the tangent of this line at these points represents stiffness, dP/dV. B, The stiffness values at points A and B plotted versus pressure, which gives a straight (dashed) line. The slope of this line is called chamber stiffness, Kv.

opening. M-mode echocardiography with simultaneous phonocardiography traditionally has been used to assess the length of this period between aortic closure and mitral opening.[13] With the aortic closure sound (phono) recorded on a separate channel from but with the same time sweep as mitral leaflet opening (M-mode echo), the aortic closure-mitral opening time interval (representing IVRT) can be readily measured. The IVRT has been described for normal subjects and for subjects in various disease states, including hypertrophic cardiomyopathy and ischemic heart disease.[14] [15] Generally, as relaxation becomes impaired, the IVRT is prolonged, with normal values approximating 65 ± 20 msec.[16] More recently, the phonocardiographic method has been replaced by a continuous wave Doppler echocardiographic method. In this technique, the continuous wave beam is directed from the apical five-chamber view across the region between the aortic outflow tract and the mitral inflow tract (Fig. 6-5) . The Doppler echocardiographic spectrum in this position includes aortic valve flow with valve closure and the onset of mitral inflow, so that

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the aortic closure-mitral opening interval can be determined. Comparisons of Doppler IVRT with catheterization measurements of this time period have shown reasonable correlations.[17] Notably, nuclear scintigraphy conventionally includes the IVRT in the early filling phase, since the volume/count technique is unable to distinguish isovolumic changes.[11] [18] [19]

The IVRT has been demonstrated to be shortened in restrictive cardiomyopathy, probably because of high left atrial pressures resulting in early mitral opening.[20] Although the IVRT describes a limited portion of early diastole, abnormalities of this index have been described as a noninvasive predictor of ventricular diastolic dysfunction in doxorubicininduced cardiomyopathy.[21] However, measurement of the IVRT as the sole predictor of diastolic function is limited, since no information on ventricular filling is provided (see Table 6-1) . Transmitral Flow The use of pulsed Doppler echocardiography to describe events of left ventricular filling is based on the assumption that transmitral blood flow velocities are representative of volumetric flow.[22] According to the law of conservation of mass, true volumetric transmitral flow is equal to the velocity of flow times the area of the orifice (F = A × V). Thus, the dynamic nature of the mitral orifice during diastole plays a role in producing the flow profile. Although the mitral cross-sectional area remains Figure 6-5 Technique for measurement of isovolumic relaxation time by continuous wave Doppler with the beam directed between the aortic outflow tract and mitral inflow. The interval between aortic valve closure (valve click) and onset of mitral flow can be measured in milliseconds (arrow).

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Figure 6-6 Normal pulsed wave Doppler recording taken from mitral valve tips showing peak E (early) and A (late) diastolic flows as well as a low-velocity flow during diastasis (L wave). The integrated area under the early peak (Ei ) and late peaks (Ai ) can be measured, as can the deceleration time (DT).

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relatively constant in size at the annulus level, the diastolic area of flow constantly changes at the leaflet tips.[23] The Doppler velocity profile, therefore, does not represent a direct recording of volumetric flow but is proportional to the atrioventricular pressure gradient, according to the modified Bernoulli equation: P1 − P2 = 4(V2 ), one of the main

determinants of transvalvular blood flow.[24] [25] True volumetric flow rates can be derived when combined with valve area measurements, although a significant benefit of this step in assessing diastolic function has not been well established.

The typical pulsed wave Doppler transmitral spectral pattern is shown in Figure 6-6 . The two phases of forward flow in early diastole and late diastole can be readily identified by their triangular shape and are separated by a brief period of diastasis. The early phase, or E wave, represents flow during the rapid filling phase, while the second peak, or A wave, represents transmitral flow occurring as a result of atrial contraction. The E and A waves are two well-defined peaks within the spectrum and usually display a linear upslope and downslope that can be measured as acceleration and deceleration, respectively, in centimeters per second.[2] Other conventional measurements include the peak E and A velocities, as well as the integrated areas within each phase, Ei and Ai . At slower heart rates, the E and A waves are separated by low, flat velocities during diastasis. These velocities are more readily recorded using low wall filter settings and sweep speeds of 50 or 100 mm per second. Occasionally, a separate distinct and positive inflow wave is seen immediately after the E wave; this wave has been designated the L wave (see Fig. 3-6) . It is thought to represent pulmonary venous flow passing through the left atrium, which acts as a conduit during this period.[26] Studies performed to compare transmitral velocities with ventricular cineangiography have found a significant correlation for both early and late phases. [17] [27] , [28] Studies by Friedman et al[11] and Spirito et al [19] demonstrated similar findings for Doppler versus radionuclide techniques. However, filling time intervals between Doppler and these methods have not correlated well, in part because of the inclusion of IVRT by nuclear methods but not by Doppler echocardiography.[11] Normative data from Doppler transmitral velocities have been reported mainly as control data for studies of various disease states.[29] [30] [31] [32] [33] [33] A normal peak E wave velocity is in the range of 70 to 100 cm per second,

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with a peak A wave of 45 to 70 cm per second, resulting in an E/A ratio of 1.0 to 1.5. The normal deceleration time (DT) for the E wave is 160 to 220 msec. Table 6-2 gives a summary of normal values from various echocardiography laboratories as taken from the literature. The recording methods and the populations sampled vary considerably among centers. Therefore, normative data should be established for each laboratory using standard examination and measurement techniques so that individual subjects can be evaluated against control subjects. Abnormal Transmitral Flow Patterns

Although the ranges for normal values are wide and Doppler parameters are affected by a variety of hemodynamic and physiologic factors, patients with proven diastolic dysfunction have been shown to demonstrate characteristic abnormalities in the spectral flow profile. Rarely is a single finding diagnostic of a specific disease process, but constellations of abnormalities tend to be present for a given pathophysiologic condition.[34] Thus, three distinct clinical patterns of abnormal transmitral flow have been described. [34] [35] [36]

The first pattern consists of a prolonged IVRT and deceleration time with a reduced peak E and an increased peak A wave velocity (Fig. 6-7) . These findings have been associated with normal early diastolic filling pressures and are attributed to impaired left ventricular relaxation.[35] [37] The delay in relaxation directly lengthens the IVRT and produces a smaller atrioventricular gradient in early diastole. The effect is a reduced E wave velocity with a more Figure 6-7 Impaired relaxation pattern of Doppler transmitral flow. A reduced E wave velocity, prolonged deceleration time (DT), and predominant flow during atrial contraction (A) are characteristic of this pattern.

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TABLE 6-2 -- Normal Values Reported for Transmitral Flow b

Study

Age Sample Subjects Range Volume Peak E Ei Peak A Ai (N) (yr) Location (cm/sec) (cm) (cm/sec) (cm) E/A

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Takenaka, et al[14]

16 19–60 Tips

60 ± 9

— 38 ± 8

Gardin, et al[56]

52 21–78 Midleaflet

54 ± 12

— 47 ± 11

Graettinger et al[31]

47 12–14 Tips

Maron et al

35

73 ± 12 6.5 39 ± 7 ± 1.4 69 ± 12 — 27 ± 7

29

[96]

Bryg et al [42]

Gardin et al

Highest recorded

33 30–49 Highest 62 ± 14 recorded

— 33 ± 7

18

— 46 ± 13

50

Highest 59 ± 14 recorded

10 24–29 Annulus 108 ± 10

— 58 ± 15

12 30–49 Annulus 103 ± 16

— 71 ± 17

10 50–68 Annulus 91 ± 16

— 80 ± 15

8 21–30 Tips

66 ± 11

— 41 ± 7

18 61–70 Tips

45 ± 10

— 55 ± 11

[32]

Douglas et al[30]

17 29–60 Annulus 62 ± 9

— 40 ± 8

— 1.52 ± 0.25 — 1.06 ± 0.35 2.2 1.37 ± ± 0.5 0.2 — 2.7 ± 0.7 — 2.0 ± 0.6 — 1.2 ± 0.4 — 1.98 ± 0.53 — 1.52 ± 0.36 — 1.07 ± 0.41 — 1.6 ± 0.31 — 0.82 ± 0.34 — 1.61 ± 0.39

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Appleton et al[35]

40 22–60 Tips

Hatle et al

20 27–63 Tips

1.5 ± 0.32 1.1 ± 0.3 0.89 ± 0.4 0.87 ± 0.17 86 ± 16 13 ± 56 ± 13 5.5 1.6 2.9 ± ± 1.1 0.5 84 ± 18 — 61 ± 14 — —

40 25–65 Tips

86 ± 16

[115]

Drinkovic et al[28]

Pearson et al[89]

24 42–76 Annulus 68 ± 12 8.6 ± 1.8 62 20–66 Tips 64 ± 10 8.9 ±2

48 ± 11 3.6 ± 1.0 59 ± 8 5.3 ± 1.1 Annulus 47 ± 13 6.1 52 ± 10 4.3 ± ± 1.5 0.9 18 65–84 Annulus 58 ± 15 — 69 ± 17 —

[107]

— 1.6 ± 0.5 Kitzman et 10 21–32 Tips 82 ± 12 11 ± 43 ± 10 4.1 1.85 [29] al 2.6 ± ± 1.2 0.25 10 62–73 Tips 56 ± 13 7.9 59 ± 14 5.5 0.92 ± ± ± 2.2 1.2 0.4 25 25–45 Tips 74 ± 8 — 38 ± 3.2 2.5 1.96 Cacciapuoti [33] ± ± et al 0.7 0.2 25 46–65 Tips 73 ± 7 — 38 ± 3 2.4 1.82 ± ± 0.6 0.25 25 66–85 Tips 70 ± 5 — 62 ± 3.1 2.6 1.28 ± ± 0.5 0.24 A, atrial filling velocity; Ai , integral of actual filling velocity; E, early fil Klein et al

— 56 ± 13

[36]

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filling velocity; IVRT, isovolumic relaxation time. gradual downslope (or prolonged deceleration time). The increased peak A wave velocity and Ai are likely the result of diminished early diastolic flow

with a higher left atrial residual volume at the time of atrial contraction.[35]

A second transmitral flow pattern has been termed restrictive (Fig. 6-8) . The characteristics of this pattern are a short (or normal) IVRT and reduced deceleration time, along with increased E wave and diminished A wave Figure 6-8 Restrictive pattern of Doppler transmitral flow. The high early velocity (E), short deceleration time (DT), and diminished atrial velocity (A) are typical of this pattern.

velocities.[20] [36] Thus, filling is predominantly shifted to the rapid filling phase in early diastole and is thought to be due to a high cross-over pressure at the time of mitral valve opening in the presence of a relatively nondistensible left ventricle. The result is a high early velocity of transmitral flow but with rapid equilibration of the atrioventricular pressures and an abrupt cessation of flow (short deceleration time). Late diastole is characterized by diminished atrial transport caused by high left ventricular pressures, poor atrial function, or both.[20] [36] A third pattern has been termed normalized or pseudonormal.[35] This pattern has characteristics of normal transmitral velocities but results from counterbalancing influences of both abnormal relaxation and restrictive forces. This pattern represents an intermediate pattern between the two ends of the pathologic spectrum and may be viewed as a transition from one pattern to another.[34] An example of a pseudonormal pattern is shown in Figure 6-9 . The pseudonormal flow pattern shows nearly equal E and A wave velocities, with a deceleration time that is either normal or shortened. The fact that flow patterns can be seen to change over time within individual patients has caused concern that transmitral Doppler tracings alone may not be used to 120

Figure 6-9 Pseudonormal pattern of Doppler transmitral flow. Nearly equal E and A velocities, with a slightly prolonged deceleration time

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(DT), are shown.

identify diastolic dysfunction.[38] [39] Indeed, it is currently recognized that patients with a pattern of impaired relaxation may convert to "normal" (pseudonormal) as a result of increased mitral regurgitation, hypervolemia, or increased ventricular stiffness resulting from progression of the underlying disease. These physiologic changes can all potentially produce an increased E wave and more rapid deceleration slope. Similarly, the restrictive pattern may be affected by lowering preload.[40] [41] The ability of Doppler flow patterns to mutate as a result of changes in load compromises the use of these recordings from a single examination to assess diastolic function. Thus, serial studies, along with available clinical or direct hemodynamic information, may be beneficial in sorting out findings in individual patients. In addition, studies of Doppler recordings of pulmonary vein flow have contributed to knowledge in this area. Physiologic Factors Affecting Transmitral Flow

A number of physiologic variables have been shown to influence the pattern of flow across the mitral valve during diastole; these include age, heart rate, heart rhythm, loading conditions, systolic function, atrial function, and phases of respiration. The complex interplay of these parameters results in the final spectral Doppler echocardiographic signal. It is therefore important to consider each of these factors to interpret the clinical relevance of the Doppler echocardiographic findings. Age.

Age has been found to be an important determinant of the transmitral flow profile.[32] [42] In studies of normal populations, the peak E wave and integrated E wave (Ei ) velocities have been shown to decrease with advancing age from 20 to 75 years. The peak A and Ai velocities increase

with age, resulting in a decreased E/A ratio.[43] Furthermore, the IVRT and deceleration time have been demonstrated to be progressively longer with age. Thus, Doppler examination of normal, young patients may resemble the restrictive pattern, whereas patients with advanced age often show findings compatible with impaired relaxation. It has been proposed that these changes are due to the development of left ventricular hypertrophy, since wall thickness and mass are known to increase over time in the normal population.[44] An increase in hypertrophy

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and myocardial stiffness could lead to delayed relaxation and result in prolonged IVRT, decreased E wave, and longer deceleration time. This development of a "physiologic state of hypertrophy" remains hypothetical, since Doppler echocardiographic characteristics were not dependent on blood pressure or left ventricular mass in these studies.[29] Heart Rate.

Changes in heart rate affect the resulting transmitral flow pattern by several mechanisms. As heart rate increases and the diastolic interval is shortened, the A wave begins to encroach on the preceding E wave. Studies of patients with dual-chamber pacemakers have shown a decreased E wave peak velocity and Ei , with concomitant increases in A waves with heart rates up to 90 beats per minute. [45] The increase in atrial contribution may be due to a reflex increase in myocardial contractility (the Bowditch phenomenon); a rise in left atrial pressure; or, more simply, the result of higher atrial volume at the onset of atrial systole due to elimination of diastasis.

Similarly, in normal volunteers with atrial pacing via a transesophageal electrode, the peak A wave was seen to increase by a mean value of 8 cm per second for each increment of 10 beats per minute in heart rate.[46] Most studies have shown that at rates greater than 100 beats per minute, the E and A waves become fused, making conventional measurements of peak velocities, velocity integrals, and acceleration or deceleration unobtainable in most cases (Fig. 6-10) . Heart Rhythm.

Changes in atrioventricular synchrony due to alterations in the PR interval, atrial fibrillation, or ectopic rhythms can cause dramatic changes in Doppler transmitral flow. A prolongation of the PR interval usually results in a reduced E wave component, possibly due to more complete atrial emptying and a reduced diastolic time interval, especially during the rapid filling period. Atrial ectopic rhythms and heart block may provide a variety of E and A wave profiles depending on the timing of atrioventricular dyssynchrony (Fig. 6-11) . Atrial fibrillation results in an absence of organized A wave velocities, with variable E waves, depending on the length of the preceding RR interval. Loading Conditions.

Loading conditions have a substantial impact on the Doppler transmitral flow pattern. The most important variable appears to be the left ventricular

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preload, which can have a profound effect on E wave velocities. A study by Choong et al[40] first demonstrated that the administration of nitroglycerin reduced the peak Figure 6-10 Fusion of the E and A waves due to increased heart rate. The peak early (arrow) and late velocities remain distinguishable.

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Figure 6-11 Doppler transmitral flow in a patient with atrial fibrillation. The tracing shows variability in peak E wave velocities depending on RR interval. No A wave velocities are present.

E, Ei , and deceleration rates of the rapid filling phase without significant

changes in A wave parameters. Most importantly, these changes were noted to resemble the pattern of impaired relaxation, even though there was no hemodynamic evidence for diastolic dysfunction. The mechanism for these changes is felt to be related to a decreased left atrium—left ventricle pressure gradient at the time of mitral valve opening ("cross-over pressure"), which results in lower E wave velocities. [47] Other studies using a tilt table or lower body negative pressure have substantiated these findings.[48] Conversely, increasing preload by volume expansion in a canine model has been shown to result in an increased peak E wave velocity, with a lesser effect on the A wave. [49] Of all hemodynamic parameters evaluated, left atrial pressure was the most significant determinant of peak E wave values. Systolic Function.

Left ventricular systolic function also affects the transmitral flow rate during the rapid filling phase. Studies in dogs[50] and humans[51] have shown that left ventricular end-systolic volume is indirectly correlated with peak E wave velocity. Thus, in the presence of systolic dysfunction or increased afterload, the early diastolic velocities can be expected to be reduced, with deceleration time prolonged. These important studies make it clear that one must take volume status and loading conditions into account before classifying patients into categories of diastolic dysfunction. Obviously, patients evaluated in an

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echocardiographic laboratory may be subject to extremes of load and volume due either to the underlying disease process or to treatment with vasoactive drugs. Careful consideration of these circumstances must be given to individual patients during analysis of the Doppler data. Atrial Function.

The size and functional status of the left atrium itself may contribute to changes in the Doppler transmitral flow profile. For example, it has been noted that the reduced atrial contractility (or "atrial stunning") that occurs after cardioversion of patients with atrial fibrillation or flutter results in a reduced peak A-wave velocity.[52] Thus, despite restoration of sinus rhythm, the atrial transport function (and A wave component) of diastole may remain impaired for weeks after cardioversion.[52] , [53] Theoretically, any acute process affecting atrial function (e.g., inflammation, scarring, or infarction) could produce similar abnormalities in transmitral flow. Respiration.

The physiologic intrathoracic pressure changes that occur during normal breathing produce minor changes in transmitral flow. As a result of negative pressures—and, consequently, enhanced peripheral venous return—developed during inspiration, right heart and transtricuspid flows predominate.[54] [55] Concurrently, the transmitral velocity spectrum yields reduced peak E wave velocities in the range of 5% to 10%.[55] Since little or no change is seen in the corresponding A wave, the E/A ratio may fall slightly under that seen in normal circumstances. These changes are compatible with known physiologic reduction of left ventricular preload during inspiration. However, in situations of acute right heart strain or pericardial tamponade, the effect of respiration on transmitral flow has been shown to be much more dramatic. To minimize respiratory changes, most laboratories record the transmitral spectral Doppler echocardiogram with the patient in held, shallow endexpiration. Technical Considerations of Transmitral Flow Measurements Two-Dimensional Imaging Plane.

Doppler recordings of transmitral flow must be performed in a standardized fashion for consistency. Since the Doppler equation includes a term for angle of incidence (cos theta), the technique for recording transmitral flow

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velocities is optimally performed from the apical window (four-chamber, two-chamber, or long-axis views). Most laboratories use the four-chamber view because of its orthogonal relationship to the major diameter of the mitral annulus. Pulsed Wave versus Continuous Wave Doppler.

Because of its superior temporal and range resolution, pulsed wave Doppler echocardiography is the preferred technique for recording transmitral flow. Although the continuous wave method may ensure that the highest velocities are recorded, these signals may arise from other locations along the interrogating beam path (i.e., from aortic insufficiency) rather than via diastolic transmitral flow. In addition, the pulsed wave signal provides a "cleaner" outer border that readily lends itself to tracing peak velocities and slopes. However, the continuous wave Doppler technique is required for obtaining the IVRT, as previously described. Sample Site.

Studies in the literature differ according to optimal location of the pulsed wave sample volume. Some investigators have recommended placing the sample volume near the center of the mitral annulus, just on the ventricular side, using two-dimensional imaging for positioning. This scheme has the advantage of being more reproducible among patient studies and providing a better evaluation of the atrial component.[56] Recordings made between the mitral leaflet tips yield higher velocities of flow and a better assessment of the rapid filling phase.[57] [58] Since no clear consensus currently exists, each laboratory must establish a protocol for recording and analysis, as the spectral profiles often differ at these locations (Fig. 6-12) . As shown in Table 6-2 , normal values are sample site dependent, and published studies must be read carefully if the methods are to be reproduced.

122

Figure 6-12 Pulsed wave Doppler transmitral flow recordings from the two most commonly used sample sites. Top, Spectral pattern recorded from mitral valve leaflet tips shows nearly equal E and A wave components. Bottom, Recording from mitral valve annulus level demonstrating a smaller E wave and predominant A wave. Modal Velocity.

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Flow through the normal mitral orifice with normal cardiac output remains essentially laminar and has a blunt profile.[59] Thus, the border of the pulsed wave velocity spectrum generally exhibits very little spectral dispersion, since at any given instant the red cell targets within the region of interest are moving at nearly the same speed and direction. However, the border does show a finite width. The darkest portion of this band represents the modal velocity and has been suggested as the best location for tracing or measuring the spectrum, as it should be less susceptible to changes in gain. [56]

E and A Waves.

At slower heart rates, the early (E) and late (A) contributions to left ventricular filling can be readily identified, as well as the lower velocities occurring during diastasis (if wall filters are kept low). However, at heart rates above 100 beats per minute, the individual E and A waves often become fused,[46] making measurements of Ei and Ai difficult. At higher

heart rates (around 130 beats per minute), peak velocities may not be readily discriminated and appear as a single large wave (see Fig. 6-10) . Various approaches have been taken to this problem. For example, the E and A waves can be measured by extrapolating the descending and ascending slopes, respectively, through the merged portion of velocity spectrum. Another approach involves dropping a perpendicular line from the point of convergence. Our experience suggests that integrated timevelocity values may be less reliable in this setting and that perhaps only peak velocity values should be used, since these usually remain distinctly visible. The E wave deceleration time can usually be obtained by extrapolating the visible portions of the downslope to the baseline. If Ei and

Ai are to be measured, a convention should be adopted for the laboratory. It should be noted that use of these different methods may account for differences in time-velocity integrals and time intervals between separate examinations and centers. Diastasis.

The velocities recorded between the E and A waves represent the ventricular filling that occurs during diastasis. Normally these velocities are low and represent a very small contribution to overall volume of flow. Indeed, if wall filters are increased to eliminate noise around the baseline, the velocity spectrum during the period may be completely eliminated. Since this portion of the Doppler spectrum may be helpful in understanding

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pulmonary vein flows, the wall filters should be adjusted as low as possible to eliminate noise and yet preserve the outer border of the spectrum during this time period. Deceleration Slope versus Deceleration Time.

Measurements of the descending limb of the transmitral E wave have been reported in terms of both deceleration slope (cm per second squared)[14] [60] and time (msec).[35] [36] The slope is defined by the rate of decline from the peak velocity, whereas deceleration time describes the time interval between peak velocity and the point of intercept of the decay slope (or extrapolated slope) with the baseline. Although these parameters have both been used to describe relaxation events in early diastole, they are not equivalent. The deceleration slope is influenced by and directly related to peak E velocity, whereas deceleration time has the advantage of being more independent of the E velocity.[34] Pulmonary Vein Flow Normal Patterns

Doppler echocardiographic recordings of flow within the pulmonary venous system have been obtained using both transthoracic and transesophageal windows. [61] These spectral patterns have yielded important insight into the physiology of left ventricular filling and diastolic function. The pattern of flow is largely determined by transmitral flow and left atrial function. A typical example of pulsed wave Doppler recording of pulmonary vein velocities is shown in Figure 6-13 . The pattern consists of two forward waves and one reverse (below the baseline) wave. One forward wave occurs during systole (S) and coincides with left atrial relaxation immediately after atrial contraction. The systolic wave occasionally demonstrates two separate components at slow heart rates; these may be distinguished by a notch in the upslope (see Fig. 6-13B) . The early component (SE ) is thought to result from atrial relaxation, and the late systolic wave (SL ) has been described as originating from movement of the mitral annulus toward the apex.[61] [62]

The other forward wave occurs during diastole (D) and coincides with the early transmitral flow and ventricular filling but is delayed by approximately 50 msec.[26] In this

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123

Figure 6-13 Normal Doppler pulmonary vein flow tracings using transthoracic (A) and transesophageal (B) techniques. A, Nearly equal systolic (S) and diastolic (D) waves and a small reverse flow at enddiastole (Ar). B, Transesophageal recording demonstrates laminar flow with well-defined early (SE ) and late (SL ) systolic waves.

context, the diastolic flow can be viewed as produced by ventricular relaxation, resulting in forward pulmonary vein flow, with the left atrium acting as a conduit after mitral valve opening. With short RR intervals, the systolic and diastolic waves may merge, resulting in a single forward-flow wave. Thus, depending on heart rate and rhythm, the pulmonary vein velocities above the baseline may be recorded as monophasic, biphasic, or triphasic.[26] Reverse flow can often be recorded as a small, brief velocity signal below the baseline during atrial contraction (just after the P wave). This wave has been variously designated the pulmonary vein A (PVa) or atrial reversal (Ar) wave and represents retrograde pulmonary vein flow (see Fig. 6-13) . It is usually larger when the atrial afterload is high from left ventricular hypertrophy or restrictive/constrictive processes.[34] [63] Some workers have termed the systolic and diastolic forward waves as J and K waves [26] [64] or X and Y waves, respectively.[65] Although labeling of the pulmonary vein velocity has not yet been standardized as for transmitral flow, most recent investigators have used the S and D designations. This format has the advantage of being readily associated with timing within the cardiac cycle. However, the J and K terminology is more easily associated with the L wave of transmitral flow during diastasis and thus is preferred in some laboratories. Other authors have named these as X and Y waves to correspond to the x and y descent of the pulmonary capillary wedge pressure tracings. In this scheme, the atrial reversal velocity is called the Z wave.[66] Measurements

As with the transmitral flow, the conventional assessment of pulmonary vein velocity waves has included the measurement of peak velocities, as well as the time velocity integral for S (Si ) and D (Di ). The ratio of the

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systolic to diastolic components has also been described by peak S/peak D or expressed as the systolic fraction (percent) by the following equation[63] [66]

The peak Ar velocity, velocity time integral, and duration (Adur , in milliseconds) have also been defined.[41] [63] [66]

Fewer studies of normative data are available for pulmonary vein flow than for transmitral Doppler data. Table 6-3 lists the mean (±SD) values reported from a number of important series in the literature for reference. However, as indicated, some of these investigations were performed in patients undergoing catheterization or elective operations and thus may not reflect values obtained during a routine echocardiographic examination. In general, the S wave is predominant in normal patients, with peak velocities ranging from approximately 40 to 60 (±15) cm per second and time velocity integrals of 15 ± 5 cm. The SE component is usually smaller than SL, with peak velocities of 30 to 40 (±10) cm per second. The diastolic wave has been measured in the range of 35 to 45 (±15) cm per second with a velocity integral of around 7.5 to 9.5 (±4) cm. The ratio of peak S to peak D has been described in normal subjects as 1.3 to 1.5 (±0.3), with a systolic fraction of 60 to 68 (±10%). The peak A wave is normally the smallest of the velocity components at -22 to -32 (±10) cm per second, with integrated values of 2 ± 1 cm. The Ar duration has been found to be helpful in the clinical interpretation of pulmonary vein flow and is approximately 137 ± 31 msec. Abnormal Patterns of Pulmonary Vein Flow

The alterations in transmitral waveforms seen in various cardiac disease states and loading conditions and with aging have also been described for pulmonary vein velocities.[34] , [41] Since pulmonary vein tracings provide additional information about atrial filling and function, these patterns have been used in conjunction with transmitral flows to better define abnormalities of ventricular filling. In patients with impaired left ventricular relaxation, the pulmonary vein

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flow during early diastole (D) becomes smaller, corresponding to decreased E wave velocities at the transmitral site, both being related to a slower rate of ventricular relaxation. As a result, pulmonary vein flow is shifted toward the systolic phase (S) and results in a 124

TABLE 6-3 -- Normal Values Reported for Pulmonary Vein Flow by Pu

Study Keren et al[62] Keren et al[26] Nishimura et al[41] * Kuecherer et al[66] * Castello et al[61]

Age Patients Range Peak S Si Peak D Di Fra (N) (yr) Technique (cm/sec) (cm) (cm/sec) (cm) (% 13 1–83 TTE 44 ± 10 — 53 ± 15 — — 12

26–49 TTE

48 ± 8

— 49 ± 11

—

—

19

45–80 TEE

41 ± 13

— 33 ± 14

—

—

60

35–78 TEE

19

20–65 TEE

41 ± 13 9.2 32 ± 15 ±4 52 ± 15 12 ± 44 ± 14 4.4

12

TTE

Kuecherer et al[65] Arakawa et al[71]

12

33–60 TTE

44

17–70 TEE

Rossvoll and Hatle

28

15–75 TTE

5.2 66 ± ±3 — 7.8 ± 4.4 50 ± 14 11 ± 41 ± 6 2.5 — 1.5 ± 3.1 63 ± 18 — 46 ± 12 — 68 ± —

12.8 — ± 3.3 56 ± 12 — 40 ± 13

— 68 ±

— 65 ±

[63] †

Brunazzi et al[67] †

96

40

TTE

48 ± 13 11.7 57 ± 10 12.7 47 ± ±4 ±2

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41–50

50 ± 11 12.5 46 ± 11 11.4 54 ± ±4 ±2 51–60 55 ± 12 13.3 40 ± 9 10.5 56 ± ±3 ±4 61 60 ± 10 15.1 36 ± 14 9.7 61 ± ±4 ±4 Ar, atrial reversal velocity; Adur, atrial reversal duration; Di , integral of d

systolic velocity; Si , integral of systolic velocity; D, diastolic velocity; TEE echocardiography; TTE, transthoracic echocardiography.

* During coronary artery bypass grafting. † Undergoing diagnostic catheterization with normal pulmonary wedge pressure.

higher peak S, Si , and systolic fraction (Fig. 6-14A and B) . The effect on

the Ar wave is variable, depending on left ventricular distensibility at atrial contraction.[34] [63] If left ventricular compliance remains low, the Ar remains normal or small; however, if compliance is diminished, the Ar wave can become dramatically increased, reflecting Figure 6-14 Transmitral (A) and pulmonary vein flow (B) in a hypertensive patient with impaired relaxation. The transmitral pattern reveals typical peak A greater than peak E and prolonged deceleration time. Pulmonary vein flow shows a predominant systolic (S) wave and a small or absent Ar wave. C and D, Corresponding tracings from a patient with similar history. The transmitral pattern again shows a prolonged deceleration time and prominent A wave, while the pulmonary vein flow demonstrates a large Ar wave and prominent S wave.

more reflux into the pulmonary veins due to a resistance to forward emptying during atrial contraction (see Fig. 6-14C and D) . The pseudonormal pattern is thought to represent a transition between impaired relaxation and restrictive phases and is associated with a normal transmitral flow. Patients 125

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Figure 6-15 Patient with a pseudonormal transmitral flow (A) and corresponding pulmonary vein recording (B). As atrial compliance has become reduced, the pulmonary vein flow demonstrates smaller forward velocities during systole and predominant diastolic flow (D).

in this category often have had progressive increases in left atrial volume and pressure due to decreasing left ventricular compliance over time. Because atrial compliance often becomes gradually reduced in this setting, the pulmonary venous flow during systole (S) is reduced owing to decreased atrial relaxation. Thus, the diastolic (D) wave may become predominant, with Si /Di less than 1 and systolic fraction less than 50%. A characteristic feature to this pattern is also a larger Ar wave, reflecting reduced ventricular compliance (Fig. 6-15) .

The features of pulmonary vein velocity waveforms in patients with restrictive physiology are a small S wave and a large D with an abrupt cessation of flow. The Ar wave size and duration are variable depending on the state of left atrial function. If left atrial contractility is preserved, the pulmonary vein A may be very large and prolonged. However, if left atrial failure has occurred due to chronic dilation, the Ar may become diminutive (Fig. 6-16) . A summary of the combined characteristics of transmitral and pulmonary vein flow changes commonly seen in various disease states is shown in Table 6-4 .[34] Estimation of Left Atrial Pressure

A relationship between pulmonary venous flow variables and mean left atrial or left ventricular diastolic pressures Figure 6-16 Transmitral recording in a patient with restrictive transmitral flow pattern (A) and corresponding pulmonary vein flow (B) from an apical transthoracic approach. Both demonstrate evidence of high velocities during early diastole (arrows). The pulmonary vein recording shows virtually no forward systolic flow and a small or absent Ar wave.

has been described.[63] [66] [67] [68] Kuecherer et al[66] compared pulmonary vein flow variables as well as mitral inflow with mean left atrial pressure (LAP) in 47 consecutive patients undergoing cardiovascular surgery and transesophageal echocardiography. The pulmonary vein systolic fraction correlated best with LAP (r = -.88; SEE = 3.5 mm Hg). The relationship between the two parameters was described by the following equation:

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LAP = 35 − 0.39 × (systolic fraction) The authors believed that the shift from predominant systolic flow to diastolic flow seen with rising left atrial pressure was most likely due to decreased left atrial compliance.[66] Retrospective evaluation of the data also suggested that a systolic fraction less than 55% was 91% sensitive and 87% specific for predicting a mean left atrial pressure of 15 mm Hg or greater. A similar study using transthoracic pulmonary venous flow recordings was reported by Brunazzi et al[67] in 116 consecutive patients undergoing elective catheterization that included measurements of pulmonary capillary wedge pressures (PCWP). The systolic fraction was again noted to correlate best, with r = -.88 and SEE = 3.1 mm Hg. A success rate of 83% was reported in recording 126

TABLE 6-4 -- Characteristic Doppler Findings in Various Stages of Diastolic Dysfunction

E/A DT, msec IVRT, msec S/D AR, cm/sec Vp ,

Normal (young) >1 <220

Normal (older) ≥1 <220

Delayed Pseudonormal Restrictive Relaxation Filling Filling <1 1–2 >2 >220 150–200 <150

<100

<100

>100

60–100

<60

<1 <35

≥1 <35

≥1 <35

<1 ≥35

<1 ≥25

>55

>45

<45

<45

<45

>8

<8

<8

<8

cm/sec Em , >10

cm/sec AR, pulmonary venous peak atrial contraction reversed velocity; DT, early left ventricular filling deceleration time; E/A, early-to-atrial left

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ventricular filling ratio; Em , peak early diastolic myocardial velocity;

IVRT, isovolumic relaxation time; S/D, systolic-to-diastolic pulmonary venous flow rate; Vp , color M-mode flow propagation velocity.

Modified from Garcia MJ, Thomas JD, Klein AL: J Am Coll Cardiol 1998;32:872. pulmonary vein flow from the transthoracic window, and the authors suggested that a systolic fraction of less than 36% percent predicted a mean PCWP of 18 or greater, with a 90% sensitivity and 85% specificity. Rossvoll and Hatle[63] have demonstrated a strong relationship between systolic fraction and the pre-A wave left ventricular end-diastolic pressure (LVEDP). A systolic fraction less than 40% was predictive of LVEDP greater than 18 mm Hg (r = -.70). These investigators also found that the pulmonary A wave duration (Adur ) was frequently prolonged, whereas the transmitral A wave was significantly shortened in patients with increased LVEDP. The difference ([PV − Adur ] − [M − Adur ]) in milliseconds

correlated best with LVEDP (r = -.68). A longer duration of the pulmonary vein A wave than transmitral A wave predicted LVEDP greater than 15 mm Hg with a sensitivity of 85% and specificity of 79%. This study was also recorded using the transthoracic approach in 45 patients undergoing diagnostic catheterization. Factors Affecting Pulmonary Vein Flow

As with transmitral recordings, a number of physiologic factors may affect the pulmonary vein Doppler echocardiographic velocity profile. Age.

Studies of normal subjects with a wide age range have demonstrated that the diastolic components are diminished and the systolic velocities are increased with advancing age.[69] [70] [71] A trend toward a larger atrial flow reversal wave has also been noted, perhaps reflecting abnormalities of left ventricular diastolic performance as part of the normal aging process. Loading Conditions.

The volume of pulmonary venous flow occurring during systole is dependent on preload—that is, with preserved myocardial contractility and increasing preload (i.e., volume loading), the atrial preload will also

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increase, resulting in increased pulmonary venous systolic flow. This increase in S and S/D has been observed in human studies in the operating room[65] and in canine experiments.[72] A direct correlation between both systolic and diastolic forward flows and cardiac output has also been found. [41]

The effect of afterload was studied by Nishimura et al.[41] Patients given phenylephrine in the operating room exhibited variable responses in pulmonary vein flow patterns. Those with a dramatic rise in PCWP (>50%) showed an increase in diastolic pulmonary vein velocities, and a middiastolic flow wave (L) became apparent. Mitral Regurgitation.

Changes in transmitral and pulmonary vein velocity profiles have been found to be useful clinical markers for the estimation of severity of mitral insufficiency. Castello et al[73] found a significantly lower peak S/D velocity ratio (0.4 ± 1.3) in patients with moderate to severe regurgitation compared with patients with less regurgitation (1.4 ± 0.5, P < .0001). This trend toward "systolic blunting" was more remarkable as regurgitation worsened. In patients with severe mitral regurgitation, the systolic flow was reversed (retrograde) into the pulmonary veins. The presence of reversed systolic flow was identified as a sensitive (90%) and specific (100%) marker for severe regurgitation in the 75 patients evaluated.[73] Similar results were reported by Klein et al.[74] An equally high sensitivity and specificity for reversed systolic flow was noted, and the pattern subsequently returned to normal after operative repair in 22 patients. Thus, significant mitral regurgitation may alter the phasic appearance of pulmonary venous flow, with a progressive increase in the diastolic (D) wave component for increasing grades of insufficiency. Technical Considerations in Pulmonary Vein Flow Recordings Transesophageal versus Transthoracic Methods.

The pulmonary vein flow spectrum is generally of superior quality when recorded from the transesophageal window. The transesophageal window has been described as especially helpful in recording reversed flow during atrial contraction (Ar) and in separating the two components of forward systolic flow (SE and SL) (see Fig. 6-13) .[73] Indeed, the transthoracic method may be limited in these areas, yielding Ar recordings of acceptable quality in the minority of patients studied.[69] [73]

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When the transthoracic four-chamber view is used, the right upper (medial) pulmonary vein is recommended for sampling. Spectral data from this site correlate well with velocities recorded from the same vein using the transesophageal technique.[73] The use of color flow or newly available echocardiographic contrast agents may help in identifying the location of the pulmonary vein orifice and in improving Doppler signal intensity from transthoracic studies.[73] Although 127

the esophageal window normally allows imaging of all four pulmonary veins, the upper veins are preferred for sampling because they provide a more parallel flow angle for Doppler interrogation.[70] The advantages of the transesophageal study must be weighed against those of patient discomfort to determine the need for this procedure in each clinical instance. Sample Position.

The ideal position for sampling pulmonary vein velocities and analyzing waveforms is 0.5 to 1 cm from the pulmonary vein orifice into the left atrium.[73] Sampling at greater depths results in spectral broadening, decreased diastolic flow velocities, and loss of phasic characteristics of systolic flow.[64] Pulmonary Vein Size.

One potential factor affecting reproducibility of pulmonary vein inflow velocities is variation of the vein orifice size during the cardiac cycle. Studies of vein dimensions and flow in both dogs and humans have not demonstrated this to be a substantial factor under physiologic conditions.[75] However, in comparisons between mitral and pulmonary vein flow velocities, this factor must certainly be considered.[41]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Applications of Doppler Techniques for Assessing Diastolic Function Transmitral and Pulmonary Vein Recordings: A Combined Approach From the preceding discussion, it should be clear that no single noninvasive or catheterization-derived parameter can be used to describe the complex nature of diastolic function. As with systolic measures of performance, there are general descriptors (e.g., ejection fraction) and more specific measurements (e.g., Vmax , dP/dt, and mean velocity of circumferential

fiber shortening [Vcf ]) that define the process of contractility in greater

detail. Each measurement must be evaluated in the context of the clinical situation so that modifiers such as age, loading conditions, and volume status can be included.

Since the 1980s, diastolic dysfunction has become increasingly recognized as an important part of many clinical syndromes.[76] [77] [78] [79] Consequently, Doppler echocardiography has been recognized as a readily available tool for evaluating left ventricular filling and has given the clinician a method for better understanding these events. However, it must be recognized that the diagnosis of diastolic abnormalities is not routine and requires significant effort and knowledge, even for the experienced echocardiographer. In specific disease states, Doppler variables have provided a conceptual framework for understanding pathophysiology without necessitating cardiac catheterization. Recordings of transmitral and pulmonary vein flows, along with isovolumic relaxation time, should be evaluated in context with other two-dimensional echocardiographic information to best apply these techniques (see Table 6-4) . For example, in the assessment of left ventricular filling, the thickness, cavity size, and systolic function, as well as left atrial size, should be assessed. In other settings, the Doppler

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data may provide more subtle clues that are helpful in distinguishing restrictive from constrictive processes. Thus, although the Doppler information represents a significant advance in the field, its use for detecting abnormal hemodynamics may still be considered part of the "art of medicine." [80] More recent studies also suggest that these noninvasive indices may give insight regarding the prognosis of various heart diseases. [81] Therefore, the following section reflects an attempt to give illustrative case examples of the use of Doppler in various cardiac problems. The cases include a discussion of relevant literature regarding the use of Doppler in these areas; further details can be found in subsequent chapters as noted. Case Examples and Literature Review Hypertensive Heart Disease (Pressure Load Left Ventricular Hypertrophy)

A 74-year-old woman with a history of hypertension presented to the clinic with complaints of dyspnea on exertion. Specifically, for the past 6 months she has had difficulty climbing stairs, carrying laundry, and vacuuming the house. Physical examination revealed a blood pressure of 170/110 with a heart rate of 90 beats per minute. There was no jugular venous distention or evidence of pulmonary congestion. Trace pedal edema was present. The left ventricular impulse was sustained, the carotid pulses were normal, and a grade 2/6 systolic ejection murmur was heard along the left sternal border. A 12-lead electrocardiogram revealed high voltage and secondary ST-T wave changes compatible with left ventricular hypertrophy. Twodimensional echocardiography with Doppler was performed to evaluate left ventricular function. Interpretation.

The Doppler transmitral flow recording from this patient is shown in Figure 6-17 and exhibits several features characteristic of patients with hypertension and left ventricular hypertrophy. The spectral profile shows a reduced E wave, prolonged deceleration time, and predominant A wave. The peak E/A ratio is less than 1.0, and the deceleration time was measured to be 200 msec. The IVRT was also found to be prolonged at 150 msec (see Fig. 6-17B) . These features are consistent with the pattern of impaired relaxation. The reduced velocities of early filling reflect the loss of ability of the

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hypertrophied ventricle to relax quickly and develop a negative pressure gradient ("suction") after mitral opening. The prolonged deceleration time shows that the process of relaxation continues well into diastole, while the increased peak A velocities and Ai show that the atrial volume remains high in late diastole and that atrial contractility is preserved in this case. Although a similar pattern may also be seen in healthy elderly patients, the magnitude of prolongation of deceleration time and IVRT are helpful in distinguishing this as abnormal relaxation. A prolonged IVRT has been reported to be a sensitive sign of this condition, independent of heart rate.[82]

128

Figure 6-17 A, Transmitral pulsed wave recording of a patient with hypertensive heart disease showing delayed deceleration time at 200 ms (arrow) and A greater than E. B, The isovolumic relaxation time (IVRT) (dashed lines) was prolonged at 150 msec. C, Pulmonary vein recordings in the same patient showing absent D wave and prominent Ar velocities suggesting reduced left ventricular (LV) compliance.

The Doppler pulmonary vein flow (see Fig. 6-17C) demonstrates a reduced D component (corresponding to a smaller transmitral E wave) and more prominent S wave (due to larger atrial stroke volume). However, if left ventricular compliance is reduced, a prominent Ar wave may also be seen. [83]

Literature Review.

Several studies of adult patients with hypertensive left ventricular hypertrophy have found this constellation of abnormalities to be present and statistically to be significantly different from findings in control subjects (see Chapter 32) .[84] [85] [86] [87] The pattern of impaired relaxation has also been reported in patients with concentric left ventricular hypertrophy due to aortic stenosis,[88] hypertensive hypertrophic cardiomyopathy of the elderly,[89] and hypertrophy due to obesity heart syndrome.[90] [91] Further evidence that the pathophysiology is related to hypertrophy is available from longitudinal studies in which regression is associated with reversion of this pattern to normal. Progressive improvement in E/A velocities have been demonstrated over 3 to 6 months in patients treated with angiotensin-converting enzyme inhibitors[92] [93] and in patients undergoing aortic valvuloplasty.[94] These effects may be due to

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the direct reduction of afterload or the inhibition of connective tissue protein and collagen production by these drugs.[92] The classic example of impaired relaxation shown (see Fig. 6-17) is not always seen in patients with hypertensive left ventricular hypertrophy. Indeed, patients with high left atrial pressures may have a normal or "pseudonormalized" transmitral flow pattern.[35] [95] Elevated filling pressures result in a higher cross-over pressure gradient in early diastole, resulting in a larger E wave, while left ventricular end-diastolic pressures become elevated to result in smaller atrial contribution. For example, the pseudonormal pattern has also been reported in patients with aortic stenosis and systolic dysfunction[88] and those with chronic hypertension with eccentric hypertrophy.[85] The presence of significant mitral regurgitation may also elevate early filling velocities and result in a normal pattern. However, these exceptions should be apparent from clinical or echocardiographic information. Some authors have suggested that the transmitral flow profile can be used to help choose antihypertensive therapy [95] that is, when delayed relaxation is present, patients are more likely to benefit from a slower heart rate (e.g., beta blockers). Conversely, patients with elevation of diastolic filling pressures may be more likely to respond to diuretics or vasodilator therapy. Clearly, more clinical trials are necessary to assess drug effects on diastolic function and Doppler velocity patterns. Hypertrophic Cardiomyopathy

The diastolic Doppler transmitral velocity profile in patients with hypertrophic cardiomyopathy is variable (see Chapter 27) . Most patients have some evidence of diastolic dysfunction when compared with control subjects. Studies by Maron et al[96] and Lewis et al[97] showed that more than 80% of patients with hypertrophic cardiomyopathy, including those without symptoms or obstruction, had at least one abnormal index of transmitral flow. Typically, the abnormalities were similar to those described for hypertensive hypertrophy: a reduced E velocity, larger A wave component, and prolonged IVRT and deceleration time. These data are concordant with results of nuclear studies of left ventricular filling in patients with hypertrophic cardiomyopathy. Bonow et al[98] described reduced filling during the rapid filling phase, with more filling occurring during atrial systole. However, other investigators have shown that patients with this disorder may present with normal (or pseudonormal) flow profiles.[14] [33] Subgroup analyses in these studies suggest that this pattern may result from mitral regurgitation, a common associated finding.

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Dilated Cardiomyopathy

A 52-year-old man with a long history of an "enlarged heart," diagnosed as idiopathic dilated cardiomyopathy, 129

has been treated with digoxin and diuretics. He presented to the clinic with a history of medical noncompliance and excessive salt and water intake for 3 weeks. Echocardiograms in the past revealed four-chamber enlargement, a dilated hypocontractile left ventricle with thin walls, and an estimated ejection fraction of 30%. Physical examination showed elevated neck veins, bibasilar rales, a pulsatile enlarged liver, and dependent edema to the knees. A grade 2/6 pansystolic murmur was heard at the apex. A two-dimensional echocardiographic and Doppler study was performed to evaluate left ventricular function and rule out pericardial effusion (Fig. 618) and compared with a study performed 1 year earlier. Interpretation.

The tracings in Figure 6-18 demonstrate a number of important findings that can be helpful in the diagnosis and management of this patient. The earlier recording (see Fig. 6-18A) shows a transmitral pattern similar to that shown in Figure 6-7 . The delayed deceleration time and predominant A wave suggest impaired relaxation. However, the spectral Doppler scan now has changed to reflect a restrictive pattern (see Fig. 6-18B) . As the disease process has continued, ventricular compliance has decreased, despite a lack of any evident change in systolic performance. A rising left atrial pressure (higher preload) has resulted in a predominant E component, while the A wave has diminished due to deteriorating contractility and a more noncompliant left ventricle (higher atrial afterload). Most importantly, the availability of serial tracings greatly aids in this assessment of worsening diastolic dysfunction. Literature Review.

Several studies have evaluated left ventricular filling patterns in patients with congestive heart failure due to dilated cardiomyopathy (see Chapter 26) .[81] [99] [100] [101] [102] The combined data suggest that patients with this disorder may present with any of the patterns within the spectrum of

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diastolic abnormalities. Lavine and Arends [100] found that patients with dilated cardiomyopathy and normal left ventricular filling pressures had a prolonged IVRT and reduced E/A ratio, while those with pulmonary capillary pressures greater than 15 mm Hg demonstrated an increased peak E and E/A (2.1 ± 0.4). The two patient groups had similar ages, left ventricular dimensions, and degrees of systolic dysfunction. Mitral regurgitation appeared to be one factor accounting for increased E velocities. Similarly, Takenaka et al[103] found that dilated cardiomyopathy patients without mitral regurgitation typically had a pattern of abnormal relaxation, Figure 6-18 Transmitral flow recordings in a patient with dilated cardiomyopathy. The earlier recording (A) shows a slightly delayed deceleration time and A greater than E, suggesting an impaired relaxation pattern. Transmitral flow recording 1 year later (B) shows markedly an increased E wave and a near-absent A wave typical of the restrictive pattern. Conversion to this pattern suggests a higher preload and has been associated with a poorer prognosis.

whereas patients with mitral regurgitation had a "normalized" pattern. Subjects in the mitral regurgitation group differed from normal subjects in having a shorter deceleration time. Vanoverschelde et al[101] also found the pattern of left ventricular filling to be closely related to both left atrial pressure and the presence of significant mitral regurgitation. Because the majority of patients with dilated cardiomyopathy are studied while on medications, drug effects must also be considered. A study by Makhoul et al[104] demonstrated a direct relationship between PCWP changes induced by intravenous isosorbide dinitrate and the transmitral E/A ratio. The E/A ratio was initially high (restrictive pattern) and was reduced by more than 50% after nitrates in nearly all patients with class IV congestive heart failure. Perhaps the most important clinical information obtainable from Doppler tracings in patients with dilated cardiomyopathy and heart failure relates to functional status and prognosis. Studies by Vanoverschelde et al[101] and Xie et al[105] have demonstrated a clear relationship between transmitral flow pattern and New York Heart Association functional class. Patients with increased peak E velocities or shortened deceleration, or both, had poorer treadmill performance compared with those who had a pattern of impaired relaxation. These clinical data support the idea that the restrictive pattern represents increased preload and abnormal left ventricular compliance.

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Studies by Xie et al[81] and Werner et al[99] have shown the restrictive filling pattern to predict a higher mortality rate in patients with systolic dysfunction. Both series found that patients with a deceleration time of 140 msec or less and an E/A ratio 2.0 or greater had a 2-year survival rate of approximately 50%, compared with heart failure patients with reduced ejection fractions but without this pattern who had a survival rate greater than 90%. Although some authors have correlated an increased peak E wave and higher mortality rate with the degree of mitral regurgitation, [101] two 1994 studies[81] [99] showed no significant difference in this parameter. Thus, the pattern of short IVRT, predominant early diastolic filling (by transmitral peak E wave and pulmonary vein D waves), and a prominent Ar wave and dilated left atrium may all reflect a stage of severely decreased left ventricular compliance and high filling pressures.[34] Findings of this nature may have direct clinical applications, such as encouraging more aggressive medical treatment or consideration of earlier evaluation for heart transplantation.

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In summary, patients with systolic dysfunction, ventricular dilation, and clinical evidence of heart failure may be heterogeneous in their Doppler transmitral or pulmonary venous flow patterns. However, interpretation of these tracings can be extremely helpful if the clinical setting is considered. [102] [106]

Constrictive Pericarditis versus Restrictive Cardiomyopathy

A 38-year-old man presented with severe dyspnea on exertion, worsening over the past year. An earlier evaluation had revealed normal pulmonary function and "no evidence of cardiac disease," based on normal systolic function. Physical examination revealed elevated jugular venous pressure with Kussmaul's sign and pulsus paradoxus of 15 mm Hg; blood pressure was 90/60. The liver was palpably enlarged, with evidence of ascites and 3+ peripheral edema. There were no audible murmurs or gallops. A Doppler echocardiographic examination was obtained to evaluate left ventricular function and to rule out a constrictive or restrictive process. Interpretation.

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The spectral Doppler tracings from this patient are shown in Figure 6-19 . The findings are typical for the "restrictive" transmitral flow pattern: a short IVRT, a high-velocity peak E wave (>100 cm per second) with abrupt cessation of flow and, therefore, extremely short deceleration time (120 msec). The A wave component is nearly absent, with a peak velocity of less than 35 cm per second, and resultant peak E/A of 2.2. The Ei /Ai ratio is also increased at 2.4. The dramatic shift of flow to early diastole along with abrupt cessation of the E wave is compatible with the "dip and plateau" pattern seen in right and left ventricular pressure tracings in patients with constrictive pericarditis. The beat-to-beat variation in E wave size is noteworthy and corresponds to changes during respiration frequently seen with constrictive

Figure 6-19 Spectral Doppler transmitral flow in a patient with constrictive pericarditis. The tracing shows high peak E velocity greater than 100 cm/sec and small A component barely visualized because of high heart rate. The beat-to-beat variation in E wave size shows a greater than 50% change during inspiration (arrows). This finding may be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy.

physiology, but less often with restrictive cardiomyopathy. Literature Review.

Appleton, Hatle, and Popp have published several studies describing the typical Doppler echocardiographic features of patients with restrictive cardiomyopathy. [20] [107] These series included patients with systemic infiltrative disorders (e.g., amyloidosis and Fabry's disease) and postcardiac transplant patients.[107] Comparison of these patients with normal subjects and with a group with coronary artery disease led to the initial description of the patterns of transmitral flow: impaired relaxation, "normalized," and restrictive.[35] Comparison of flow velocity patterns with invasive hemodynamic data showed correlations between transmitral E wave and left ventricular filling pressure (r = .59), and between IVRT and the rapid filling wave (r = -.72). Klein et al[36] demonstrated similar Doppler findings in a large group of 53 patients with biopsy-proven cardiac amyloidosis. This study found the restrictive pattern to be most associated with advanced stages of the disease. Pulmonary vein flows were also recorded by transthoracic echocardiography in 29 patients and showed that those with advanced disease had markedly decreased peak systolic (S) filling and increased diastolic (D) filling compared with normal subjects.

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Atrial systolic function was believed to remain intact (despite left atrial enlargement), since the Ar wave was prominent in 10 patients. A follow-up study of 63 consecutive patients with biopsy-proven cardiac amyloidosis from the same center has shown a high 1-year mortality rate in patients with the restrictive pattern (51%) compared with those who had a deceleration time greater than 150 msec (8%; P < .001). The combination of shortened deceleration time and increased peak E/peak A ratio greater than 2.1 was the most predictive of a high-risk group, whereas the E/A ratio alone exhibited the single best correlation with survival.[108] Fewer clinical data are available from patients with constrictive pericarditis. A study by Hatle et al[107] compared seven patients with constrictive pericarditis, 12 with restrictive cardiomyopathy, and 20 normal subjects. Both constrictive and restrictive groups demonstrated a shorter transmitral deceleration time during held breathing at end-expiration, compared with control subjects. However, during normal inspiration, the patients with constriction showed marked increases in IVRT (50%) and decreases in peak E wave velocity (mean, -33%; all patients, greater than 25%), and these changes were small in the restrictive and control groups (see Fig. 6-19) . Indeed, no patient in the restrictive group had a greater than 15% change in either variable. The transtricuspid flow velocity changes of an increased peak E wave and a peak A wave with shortened deceleration time were also much larger in the constrictive pericarditis patients. The respiratory variation was not seen in five patients who underwent repeat studies after pericardial stripping. The authors theorized that the dramatic changes in transmitral and transtricuspid flow seen during inspiration likely were due to displacement of the interventricular septum and ventricular interdependence in patients with constriction who have a fixed total cardiac volume. Conversely, patients 131

with restrictive cardiomyopathy have a marked reduction in left ventricular compliance that remains relatively constant regardless of the respiratory phase.[107] Thus, patients with abnormalities in ventricular filling due to restrictive muscle disease or pericardial constriction may be readily identified by the "restrictive" Doppler transmitral filling pattern. These data suggest that careful study of diastolic transmitral and transtricuspid velocity during the

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phases of respiration may also be used to separate these groups. Although these results are promising, larger series are needed to confirm these findings. Pericardial Effusion and Cardiac Tamponade

Abnormalities in left ventricular filling have been described in patients with cardiac tamponade. A preliminary report from Pandian et al[109] first described alterations in flow velocity across all four cardiac valves; these alterations coincided with the phases of respiration. The primary study was carried out in a canine model but also included three patients who had documented tamponade physiology and underwent pericardiocentesis. The authors noted an increase in transtricuspid flow velocities and concomitant decrease in transmitral peak E and A waves (-42%) during inspiration. Appleton et al[110] studied seven patients with tamponade compared with 14 patients who had effusion due to malignancy, cardiac surgery, myocardial infarction, chronic renal failure, or cardiac transplantation. The patients with tamponade and severe hemodynamic alterations had a significant change in transmitral filling indices when the first Doppler beat of expiration was compared with the first beat of inspiration: peak E (−43 ± 9%), peak A (−25 ± 12%), IVRT (85 ± 14 msec), Ei (−52 ± 10%), and Ai (−28 ± 22%). Similar decreases were noted in aortic velocities, whereas transtricuspid and transpulmonic flows increased during inspiration. The variation was eliminated after pericardial drainage. Half of the group of patients without tamponade also showed respiratory variations compared with control subjects, but not of the magnitude seen in patients with tamponade. The authors concluded that the Doppler flow abnormalities seen with effusion are extremely sensitive to changes in pericardial pressure and should be viewed as a continuum.

In an animal model described by Gonzales et al,[111] significant respiratory variation in Doppler parameters was noted to occur at low intrapericardial pressures and preceded the echographic findings traditionally associated with clinical tamponade (i.e., right atrial inversion[112] and right ventricular diastolic collapse[113] ). It was concluded that the Doppler findings are sensitive and persist throughout all stages of tamponade but are not predictive of pericardial pressures or the severity of hemodynamic compromise. Picard et al[114] demonstrated similar findings using aortic and pulmonic flow velocities in animals. Their report did not include mitral or tricuspid Doppler data but acknowledged that the E and A waves tended to

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merge in tamponade because of associated tachycardia, and that the transtricuspid Doppler interrogation was often difficult because of compression of the right heart chambers. These limitations may also prove substantial in patients with severe clinical cardiac tamponade. Myocardial Ischemia

Several studies have demonstrated that acute coronary occlusion results in diastolic dysfunction (see Chapter 12) . Most studies have used Doppler indices recorded before and during angioplasty in patients with angina[15] [115] [116] as the clinical model for evaluating the effects of ischemia on diastolic function. Wind et al[115] reported an increased proportion of left ventricular filling during late diastole and a decreased E/A ratio in 34 patients with normal global systolic function who underwent Doppler echocardiographic examination 1 day before and 1 day after coronary angioplasty for angina. These findings were thought to be consistent with impaired relaxation, as previously reported from radionuclide scans in coronary angioplasty patients.[117] The authors provided indirect evidence that the abnormal diastolic indices were due to a prolongation of IVRT, although this was not directly measured. Labovitz et al[116] investigated 32 patients during coronary angioplasty and found that evidence of diastolic left ventricular dysfunction was the earliest change during coronary occlusion with the balloon, preceding electrocardiographic changes, chest pain, or systolic wall motion abnormalities. Impaired relaxation was the pattern most often exhibited and occurred within 15 seconds of balloon inflation but returned to baseline by 15 seconds after deflation. Masuyama et al[118] also found a reduction in peak E-wave velocities and E/A ratio in serial Doppler echocardiographic studies of patients undergoing percutaneous transluminal coronary angioplasty to be a strong predictor of significant coronary restenosis. The most complete comparison of hemodynamic and Doppler indices of diastolic function in patients with coronary disease has been performed by Stoddard et al.[15] Their study evaluated the relationship of chamber stiffness and relaxation (tau) to the traditional transmitral indices in 35 patients undergoing diagnostic catheterization for chest pain. Subjects without coronary artery disease and with normal relaxation were found to have a direct correlation between increasing chamber stiffness and enhanced early filling velocities. Conversely, the group with coronary

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disease showed a significant indirect correlation between impaired relaxation and decreased peak E velocity. Although their findings differ from those of previous studies in that a variety of patterns of transmitral flow were found, they are consistent with early observations by other investigators.[119] The authors concluded that chamber stiffness has a greater influence than relaxation on the pattern of diastolic filling in patients without coronary disease. In contrast, abnormal relaxation appears to be the predominant factor influencing the Doppler pattern in patients with coronary disease and an abnormal tau value. El-Said et al[120] studied the effects of ischemia on left ventricular filling using Doppler transmitral flow recordings 132

during dobutamine stress echocardiography. Their data showed marked decreases in peak E velocities (-22%) and time to peak E acceleration (28%) in ischemic subjects, whereas 10 control subjects had an increase in both values (+33% and +75%, respectively; P < .0001). There was no overlap in the percentage change from baseline to peak dobutamine stress values between normal subjects and patients who had documented singlevessel coronary disease. The authors also found diastolic abnormalities to be more sensitive than induction of wall motion abnormalities for detecting coronary stenoses. Thus, the transmitral Doppler pattern of impaired relaxation appears to be the type most often seen in association with acute (or induced) myocardial ischemic syndromes. Fewer data exist for patients with chronic coronary artery disease or previous myocardial infarction. Fujii et al[121] showed a reduced E/A ratio and prolonged deceleration time to be common in patients with a history of infarction, regardless of location. Other studies comparing inferior with anterior infarct patients have suggested that transtricuspid Doppler echocardiographic recordings may be more sensitive in demonstrating abnormal filling and high right ventricular end-diastolic pressures.[122] One study also suggests a significant relationship among infarct size, degree of systolic dysfunction, and restrictive transmitral flow patterns.[123] This pattern is seen more often in coronary artery disease patients with a worse functional class and poorer prognosis.[81] [105] However, larger studies specifically designed to assess the clinical applicability of Doppler filling patterns in this population are currently not available.

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Another active area of investigation is the use of Doppler echocardiographic techniques to assess changes in left ventricular relaxation produced by commonly used cardioactive drugs. Myreng and Myhre[124] first reported enhanced relaxation and a shift in left ventricular filling toward early diastole in 20 patients given oral verapamil. The patients studied had documented coronary artery disease and showed baseline transmitral filling patterns that did not differ from those of control subjects. After verapamil administration, an increased peak E velocity and E/A ratio and shortening of IVRT were seen. The authors have reported a similar "normalization" of transmitral flow in coronary disease patients after beta blocker treatment.[125] However, the effects of calcium and beta blockade on diastolic function remain controversial.[126] Caramelli et al[127] concluded that the shift in transmitral flow to early diastole can be attributed to effects on heart rate and an increase in pulmonary wedge pressure in a study of 32 patients with anterior wall infarction who were given intravenous atenolol. Nishimura et al[128] have also shown an increase in peak filling rate and a concomitant rise in left ventricular end-diastolic pressure after intravenous verapamil, with no consistent change in tau in 20 patients with coronary artery disease and preserved left ventricular function. Thus, although the use of Doppler echocardiographic methods for assessing pharmacologic effects on diastolic function remains promising, peak filling rates alone should not be used as a marker for improved relaxation. Pulmonary Hypertension

The role of the pericardium and right ventricular function in left heart filling have been recognized from elegant animal studies by Ross,[129] Sonnenblick,[130] and Glantz and coworkers.[131] [132] Patients with primary pulmonary hypertension have also been found to have abnormal left ventricular filling by Doppler echocardiography. [133] Essentially, these patients have been described as having a redistribution of transmitral flow to late diastole, with low E/A ratio (often <0.5), and prolongation of the IVRT. Louie et al[133] have shown this finding to be related to distortion of the left ventricular geometry caused by flattening of the interventricular septum. A subsequent study from the same center showed that patients with right ventricular volume overload (from severe tricuspid insufficiency) had a normal IVRT and reduced atrial component.[134] These effects were related to differences in timing of leftward septal displacement in patients with an intact pericardium. These and other studies[135] point out the importance of diastolic ventricular interaction as a determinant of filling, which may have

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profound effects on relaxation and early diastole (see Chapter 33) . Post-Cardiac Transplantation

The noninvasive evaluation of the transplanted heart has become an integral part of the long-term follow-up of post-cardiac transplantation patients (see Chapter 30) . An increase in left ventricular mass, decreased volume, and evidence of reduced systolic function have all been described in patients who have acute or chronic rejection.[136] [137] [138] Doppler abnormalities of diastolic function have also been described.[137] [139] [140] [141] [142] In a large series of patients, Valantine et al[141] evaluated 64 patients undergoing hemodynamic and Doppler echocardiographic studies as part of the routine follow-up 1 to 13 years (mean, 5 years) after cardiac transplantation. Ten patients were found to have strikingly abnormal (restrictive) transmitral flow patterns. This group had a higher incidence of rejection as the only identifiable clinical difference. Restrictive filling also was associated with impaired systolic performance. Preliminary data comparing Doppler parameter recordings with endomyocardial biopsy findings have shown a relationship between transtricuspid (right ventricular IVRT) and transmitral (left ventricular IVRT) flow patterns and degree of rejection as assessed microscopically.[141] [143] Although preliminary, these data encourage the notion that, in the future, noninvasive examination of transplant patients may help to define which chronic transplant patients have a low likelihood of rejection and thus avoid the need for repeated biopsies.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Newer Doppler Echocardiographic Approaches to Diastolic Function Two-Dimensional Left Ventricular Volume Methods Echocardiographic methods have been described to assess the time course of diastolic changes in left ventricular 133

Figure 6-20 (color plate.) Recording of left ventricular (LV) volume curves (A) using acoustic quantitation. This method allows a real-time assessment of area or volumes and rate of change (B) within a region of interest. The technique provides curves similar to those of radionuclide angiography for assessing the contributions of early and late filling.

volume and dimension.[144] [145] M-mode methods are limited by the need for geometric assumptions to calculate volume and inaccuracies introduced by regional wall motion differences. Traditional two-dimensional techniques require off-line manual tracing of imprecise borders from multiple stillframe images. The frame rate produced at usual scanning depths (around 30 per second) is also slow relative to the instantaneous changes that occur during the isovolumic time period. As a result of these problems, alternative methods have been developed. Research in this area has led to the development of computer-assisted automated border detection algorithms.[146] [147] By differentiating between ultrasound backscatter from myocardium and low-energy reflectances from blood within the left ventricular cavity, these systems can track the motion of the endocardial edge throughout the cardiac cycle. Commercially available programs currently include a real-time assessment of area, volumes, and rate of change within a region of interest (Fig. 6-20) . The accuracy of this method compares well with manual edge tracing and has

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been validated in studies using radionuclide and cineangiographic standards. [148] [149] The main advantage of these methods of quantitation is the on-line availability of data. Comparisons between Doppler and acoustic quantitation in diastolic measurements of the rapid filling and atrial filling phases have shown significant correlations. [150] Therefore, this method has potential uses in evaluating left ventricular filling. However, the technique is gain dependent and requires significant operator experience to acquire reproducible data, especially in patients with characteristics that lead to less than ideal image quality.[151] Noninvasive Measurement of Tau The rate of left ventricular pressure decline has remained a reference standard for the assessment of the relaxation phase of diastole, but its measurement is invasive and requires the use of high-fidelity catheters. A new method has been developed to noninvasively measure tau using continuous wave Doppler spectral recordings of mitral regurgitation.[152] [153] The method involves tracing the deceleration phase of the mitral regurgitant spectral signal and applying the Bernoulli equation to obtain the instantaneous pressure gradient between the left ventricle and the left atrium (Fig. 6-21) . The derivation of tau from this velocity curve has been validated in both animal[152] and human[153] studies using simultaneous catheterization data for corroboration. Although the technique necessitates offline computer analysis of tracings and is not applicable in patients without a complete mitral regurgitant envelope, the results are promising, showing good correlations with results of invasive methods. Additional clinical studies are needed to determine the feasibility of this technique in clinical practice. Color M-Mode Doppler Echocardiography Several investigators have described a new method for relating ventricular inflow velocities to left ventricular relaxation.[154] [155] [156] [157] This method uses color M-mode Doppler echocardiography from apical windows, directed along the longitudinal axis of inflow from mitral valve to apex. The recording typically shows the two waves (early filling and atrial contraction) of flow propagation from the base toward the apex (Fig. 6-22) . The slope of the early filling wavefront has been shown to represent the presence of intraventricular gradients produced from active recoil (suction) of the ventricular myocardium.[156] [158] The velocity of streamlined

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flow propagation into the ventricle (Vp ) is therefore described along the Mmode line by the slope of the color wavefront, in centimeters per second. Measurements of Vp have now been successfully obtained using either the leading edge (transition from black to color) or by tracing along any isovelocity line. More reproducible measurements can be obtained by (1) adjusting 134

Figure 6-21 A, Simultaneous mitral regurgitation Doppler velocity curve and high-fidelity left ventricular (LV) pressure curve. The time constant of relaxation (tau) is calculated from the LV pressure curve using a semilogarithmic model. B, Digitized Doppler velocity curve at 3 msec intervals in which the velocities have been converted to pressure using the modified Bernoulli equation. This new method has been described for the noninvasive assessment of tau. (From Nishimura RA, Schwartz RS, Tajik AJ, Holmes DR: Circulation 1993;88:148.)

the color scale or baseline shift to produce color aliasing, (2) tracing the slope of the first aliasing velocity line, (3) tracing the slope from the mitral leaflet tips to a position 4 cm distally into the left ventricle, and (4) avoiding intracavity flow originating before mitral opening.[159] The method may not be applicable to patients with tachycardia, arrhythmia, or heart block. Young, healthy individuals generally have Vp greater than 55 cm per second, whereas older people have Vp greater than 45 cm per second.[159] Patients with abnormal Figure 6-22 (color plate.) Color M-mode Doppler recording of diastolic flow toward the apex from the four-chamber view. The patient had severe left ventricular (LV) systolic dysfunction and a restrictive transmitral flow pattern. The inflow propagation of velocities (Vp ) is indicated by the slope of the color change during early diastole (dotted white line). The measured slope in this patient was abnormally low at 30 cm/sec.

transmitral filling patterns such as delayed relaxation, restrictive or pseudonormal, will generally have Vp less than 45 cm per second. Thus,

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when combined with other Doppler parameters, measurement of early filling by color M-mode may be useful in distinguishing pseudonormal from normal patterns (see Table 6-4) .[159] This method appears to be less affected by preload than transmitral or pulmonary vein flow.[160] For example, a "pseudonormal" transmitral flow pattern can be produced by increased left atrial pressure in otherwise normal patients. A blunted S wave is commonly seen in young people (especially athletes) in whom the left atrium is functioning as a "passive conduit" and can masquerade as restrictive cardiomyopathy. These situations may be clarified by examining the color M-mode slope during the early filling phase. Another important potential use for color M-mode is in the differential diagnosis of restrictive cardiomyopathy versus constrictive pericarditis.[161] Since color M-mode describes the early inflow of the blood column along the longitudinal axis, this will be rapid in constrictive physiology, whereas filling toward the apex is delayed in restriction. Doppler Tissue Imaging Another promising technique for the noninvasive evaluation of diastolic function involves the direct recording of mitral annulus motion. The technique was first described using M-mode echocardiography[162] but has since evolved to the use of pulsed-wave Doppler spectral recordings, with the sample volume located on the posterolateral portion of the mitral annulus or in the adjacent myocardium.[163] Imaging is usually performed from the apical four-chamber view to minimize the effects of translation 135

and rotation of the heart, while maximizing the longitudinal excursion of the annulus and base. Since tissue Doppler echocardiography involves the assessment of motion of the strong signal reflections (myocardium), the high pass filters are bypassed. Low gain amplification is also used to eliminate the weaker blood flow signals. The result is a triphasic signal with forward velocity toward the apex during systole, and two "away" signals during the early (Em) and the atrial (Am) phases of diastole (Fig. 6-23) . Thus, the diastolic signal appears as a mirror image of the transmitral inflow pattern. The Em wave is also referred to as Ea (for annulus) or E' in the current literature.

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In normal subjects, the Em wave is larger than the Am component, but the ratio falls with age. In restrictive or hypertrophic cardiomyopathies, the early myocardial relaxation phase has been shown to be reduced to less than 8 cm per second. In constrictive pericarditis, the Em values are greater than 8 cm per second, which allows separation of these two groups despite similar tramsmitral flow patterns[164] (see Table 6-4) .[159] A recent study by Sohn et al[165] has shown Em values from tissue Doppler echocardiograms to correlate well with tau as measured during catheterization and to be relatively unaffected by preload changes induced by volume infusion and nitroglycerin. Patients with pseudonormal filling were separated from normal by an Em velocity of less than 8.5 cm per second and an Em/Am ratio less Figure 6-23 Patterns of mitral annulus velocity as recorded by Doppler tissue imaging, with sampling of the septal side of the mitral annulus from the apical view. Note the changes in pattern from normal to restrictive physiology, along with corresponding transmitral flows. The Doppler tissue image may be helpful in differentiating pseudonormal from normal and restrictive transmitral flow patterns. (From Sohn, et al. J Am Coll Cardiol 1997;30:479.)

than 1, with a sensitivity of 88% and a specificity of 67%. Thus, the combination of transmitral flow patterns and color M-mode and tissue Doppler measurements may be helpful in distinguishing patients in various stages of diastolic dysfunction (see Table 6-4) . Estimation of Left Ventricular Filling Pressures As described previously, various Doppler echocardiographic indices of transmitral and pulmonary vein flow have been combined to predict left atrial pressure. Similarly, by combining transmitral E wave velocities with a preload-independent parameter such as the velocity of motion of the lateral mitral annulus (Ea), a reasonable estimate of left atrial pressure can be obtained. Nagueh et al found that an E/Ea ratio of greater than 10 correlated well with a mean pulmonary capillary wedge pressure of greater than 15 mm Hg.[166] The correlation coefficient was 0.87 in 60 patients who had hemodynamic measurements, with the relationship described by the following equation: PCWP (mm Hg) = 1.24[E/Ea] + 1.9 The authors proposed that left ventricular filling pressure can be estimated (with a 95% confidence level of

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± 7.6 mm Hg) from these two simple Doppler measurements. These findings have recently been confirmed by Ommen et al.[167] Their study consisted of 100 consecutive patients who underwent catheterization with micromanometer-tipped catheters and simultaneous Doppler measurements. A ratio of E/E' (or E/Ea) greater than 15 identified patients with elevated LVEDP greater than 12 mm Hg, whereas an E/E' ratio less than 8 accurately predicted normal pressures. Patients with ratios between 8 and 15 had widely variable ventricular diastolic pressures. The authors also noted that, in their experience, adequate signals were more often obtained from the medial or septal portion of the annulus. Although there are currently few such data available, these early and well conducted investigations are highly suggestive that the combination of tissue Doppler and mitral inflow velocities can be used to noninvasively estimate left ventricular filling pressures.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Diastolic dysfunction of the left ventricle has been increasingly appreciated as an important factor in the syndrome of clinical heart failure. The need for noninvasive methods to assess left ventricular filling has led to Doppler echocardiography as a means for describing these events. After a decade of research, it is clear that various patterns of abnormal filling are readily recognized from transmitral and pulmonary vein flow velocity recordings. Although obtaining optimal measurements requires care and diligence on the part of the operator, these data can be obtained in the majority of patients. Further studies of long-term follow-up are needed to determine whether prognostic information can be obtained from Doppler data in subsets of patients. The importance of response of Doppler echocardiographic patterns to drug therapy in patients with heart failure has also not been adequately evaluated. Clearly, this is an active area of investigation and a field in evolution that promises to provide further insight into the pathophysiology and mechanisms of heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Zile MR: Diastolic dysfunction: Detection, consequences, and treatment. Part I:

Definition and determinants of diastolic function. Mod Concepts Cardiovasc Dis 1989;58:67. 2. Sabbah HN, Stein PD: Negative diastolic pressure in the intact canine ventricle:

Evidence of diastolic suction. Circ Res 1981;49:108. 3. Zile MR: Hemodynamic determinants of echocardiographically-derived indices of

left ventricular filling. Echocardiography 1992;9:289. 4. Mirsky I: Assessment of diastolic function: Suggested methods and future

considerations. Circulation 1984;69:836. 5. Mirsky I, Pasipoularides A: Clinical assessment of diastolic function. Prog

Cardiovasc Dis 1990;32:247. 6. Starling MR, Montgomery DG, Mancini GBJ, Walsh RA: Load independence of the

rate of isovolumic relaxation in man. Circulation 1987;76:1274. 7. Weisfeldt ML, Scully HE, Frederiksen J, et al: Hemodynamic determinants of

maximum negative dP/dt and periods of diastole. Am J Physiol 1974;227:613. 8. Gaasch WH, Blaustein AS, Andrias CW, et al: Myocardial relaxation II:

Hemodynamic determinants of the rate of left ventricular isovolumic pressure decline. Am J Physiol 1980;239:41. 9. Weiss JL, Frederiksen JW, Weisfeldt ML: Hemodynamic determinants of the time

course of fall in canine left ventricular pressure. J Clin Invest 1976;58:751. 9A. Gaasch WH, Cole JS, Quinones MA, Alexander JK: Dynamic determinants of left

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 2 di 16

ventricular diastolic pressure-volume relations in man. Circulation 1975;51:317. 10. Karliner JS, Peterson KL, Ross J Jr: Left ventricular myocardial mechanics:

Systolic and diastolic function. In: Grossman W (ed): Cardiac Catheterization and Angiography, 3rd ed. Philadelphia, Lea & Febiger 1988, pp 232–245. 11. Friedman BJ, Drinkovic N, Miles H, et al: Assessment of left ventricular diastolic

function: Comparison of Doppler echocardiography and gated blood pool scintigraphy. J Am Coll Cardiol 1986;8:1348. 12. Brutsaert DL, Rademakers FE, Sys SU, et al: Analysis of relaxation in the

evaluation of ventricular function of the heart. Prog Cardiovasc Dis 1985;28:143. 13. Feigenbaum H: Echocardiographic evaluation of left ventricular diastolic function

[editorial]. J Am Coll Cardiol 1989;13:1027. 14. Takenaka K, Dabestani A, Gardin JM, et al: Left ventricular filling in hypertrophic

cardiomyopathy: A pulsed Doppler echocardiography study. J Am Coll Cardiol 1986;8:1263. 15. Stoddard MF, Pearson AC, Kern MJ, et al: Left ventricular diastolic function:

Comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease. J Am Coll Cardiol 1989;13:327. 16. Rahko PS, Shaver JA, Salerni R, Uretsky BF: Noninvasive evaluation of systolic

and diastolic function in severe congestive heart failure secondary to coronary artery disease or dilated cardiomyopathy. Am J Cardiol 1986;57:1315. 17. Rokey R, Kuo LC, Zoghbi WA, et al: Determinations of parameters of left ventricular diastolic filling with pulsed Doppler echocardiography: Comparison with cineangiography. Circulation 1985;71:543. 18. Magorien DJ, Shaffer P, Bush C, et al: Hemodynamic correlates for timing

intervals, ejection rate, and filling rate derived from the radionuclide angiographic volume curve. Am J Cardiol 1984;53:567. 19. Spirito P, Maron BJ, Bonow RO: Analysis of Doppler echocardiographic and

radionuclide angiographic techniques. J Am Coll Cardiol 1986;7:518. 20. Appleton CP, Hatle LK, Popp RL: Demonstration of restrictive ventricular

physiology by Doppler echocardiography. J Am Coll Cardiol 1988;11:757. 21. Stoddard MF, Seegar J, Liddell NE, et al: Prolongation of isovolumetric relaxation

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 3 di 16

time as assessed by Doppler echocardiography predicts doxyrubicin-induced systolic dysfunction in humans. J Am Coll Cardiol 1992;20:62. 22. DeMaria AN, Wisenbaugh T: Identification and treatment of diastolic dysfunction:

Role of transmitral Doppler recordings [editorial]. J Am Coll Cardiol 1987;9:1106. 23. Fisher DC, Sahn DJ, Friedman MT, et al: The mitral valve orifice method for

noninvasive two-dimensional echo Doppler determination of cardiac output. Circulation 1983;67:872. 24. Holen J, Aaslid R, Landmark K, Simonsen S: Determination of pressure gradient in

mitral stenosis with a noninvasive ultrasound Doppler technique. Acta Med Scand 1976;199:455. 25. Curtois M, Vered Z, Barzilai B, et al: The transmitral pressure-flow velocity

relation, effect of abrupt preload reduction. Circulation 1988;78:1459. 26. Keren G, Meisner JS, Sherez J, Yellin EL: Interrelationship of mid-diastolic mitral

valve motion, pulmonary venous flow, and transmitral flow. Circulation 1986;74:36. 27. Choong CY, Herrmann HC, Weyman AE, Fifer MA: Left ventricular diastolic

pressure-volume relation in man derived from Doppler and two-dimensional echocardiography [abstract]. Circulation 1986;74:II–46. 28. Drinkovic N, Wisenbaugh T, Kwan OL, et al: Assessment of diastolic left

ventricular function by Doppler: Comparison with catheterization measurements [abstract]. J Am Coll Cardiol 1986;7:227A. 137

29. Kitzman D, Sheikh KH, Beere PA, et al: Age related alterations of Doppler left

ventricular filling in normal subjects are independent of left ventricular mass, heart rate, contractility and loading conditions. J Am Coll Cardiol 1991;18:1243. 30. Douglas PS, Berko BA, Iolo A, Reichek N: Variable responses of mitral valve

motion and flow in systemic hypertension and in idiopathic dilated cardiomyopathy. Am J Cardiol 1987;60:363. 31. Graettinger WF, Weber MA, Gardin JM, Knoll ML: Diastolic blood pressure as a

determinant of Doppler left ventricular filling indexes in normal adolescents. J Am Coll Cardiol 1987;10:1280.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 4 di 16

32. Gardin JM, Rohan MK, Davidson DM, et al: Doppler transmitral flow velocity

parameters: Relationship between age, body surface area, blood pressure and gender in normal subjects. Am J Noninvas Cardiol 1987;1:3. 33. Bryg RJ, Pearson AC, Williams GA, Labovitz AJ: Left ventricular systolic and

diastolic flow abnormalities determined by Doppler echocardiography in obstructive hypertrophic cardiomyopathy. Am J Cardiol 1987;59:925. 33A. Cacciapuoti F, D'Avino M, Lanca D, et al: Progressive impairment of left

ventricular diastolic filling with advancing age: A Doppler echocardiographic study. J Am Geriatr Soc 1992;40:245. 34. Appleton CP, Hatle LK: The natural history of left ventricular filling

abnormalities: Assessment by two-dimensional and Doppler echocardiography. Echocardiography 1992;9:437. 35. Appleton CP, Hatle LK, Popp RL: Relation of transmitral flow velocity patterns to

left ventricular diastolic function: New insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12:426. 36. Klein AL, Hatle LK, Burstow DJ, et al: Doppler characterization of left ventricular

diastolic function in cardiac amyloidosis. J Am Coll Cardiol 1989;13:1017. 37. Ishida Y, Meisner JS, Tsujioka K, et al: Left ventricular filling dynamics: Influence

of left ventricular relaxation and left atrial pressure. Circulation 1986;74:187. 38. DeMaria AN, Wisenbaugh T, Smith MD, et al: Doppler echocardiographic

evaluation of diastolic dysfunction. Circulation 1991;84(Suppl I):I–288. 39. Shapiro SM, Bersohn MM, Laks MM: In search of the holy grail: The study of

diastolic ventricular function by the use of Doppler echocardiography. J Am Coll Cardiol 1991;17:517. 40. Choong CY, Herrmann HC, Weyman AE, Fifer MA: Preload dependence of

Doppler derived indexes of left ventricular diastolic function in humans. J Am Coll Cardiol 1987;10:800. 41. Nishimura R, Abel M, Hatle L, Tajik A: Relationship of pulmonary vein to mitral

flow velocities by transesophageal Doppler echocardiography: Effect of different loading conditions. Circulation 1990;81:1488. 42. Bryg RJ, Williams GA, Labovitz AJ: Effect of aging on left ventricular diastolic

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 5 di 16

filling in normal subjects. Am J Cardiol 1987;59:971. 43. Miyatake K, Okamoto M, Kinowhita N, et al: Augmentation of atrial contribution

of left ventricular inflow with aging as assessed by intracardiac Doppler flowmetry. Am J Cardiol 1984;53:586. 44. Sartori MP, Quinones MA, Kuo LC: Relation of Doppler derived left ventricular filling parameters to age and radius/thickness ratio in normal and pathologic states. Am J Cardiol 1987;59:1179. 45. Herzog CA, Elsperger KJ, Manoles M, et al: Effect of atrial pacing on left

ventricular diastolic filling measured by pulsed Doppler echocardiography [abstract]. J Am Coll Cardiol 1987;9(Suppl A):197A. 46. Harrison MR, Clifton ED, Pennell A, DeMaria AN: Effect of heart rate on left

ventricular diastolic transmitral flow velocity patterns assessed by Doppler echocardiography in normal subjects. Am J Cardiol 1991;67:622. 47. Nishimura RA, Abel MD, Hatle LK, Tajik AJ: Assessment of diastolic function of

the heart: Background and current applications of Doppler echocardiography. Part II. Clinical studies. Mayo Clin Proc 1989;64:181. 48. Berk MR, Xie GY, Kwan OL, et al: Reduction of left ventricular preload by lower

body negative pressure alters Doppler transmitral filling patterns. J Am Coll Cardiol 1990;16:1387. 49. Choong CY, Abascal VM, Thomas JD, et al: Combined influence of ventricular

loading and relaxation on the transmitral flow velocity profile in dogs measured by Doppler echocardiography. Circulation 1988;78:672. 50. Curtois M, Mechem C, Barzilai B, Ludbrook P: Factors related to end-systolic

volume are important determinants of peak entry diastolic transmitral flow velocity. Circulation 1992;83:1132. 51. Miki S, Yokota Y, Seo T, Yokoyama M: Dependence of Doppler

echocardiographic transmitral early peak velocity on left ventricular systolic function in coronary artery disease. Am J Cardiol 1991;67:475. 52. Manning WJ, Leeman DE, Gotch PJ, Come PC: Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation. J Am Coll Cardiol 1989;13:617. 53. Grimm RA, Stewart WJ, Maloney JD, et al: Impact of electrical cardioversion of

atrial fibrillation on atrial appendage function and spontaneous echo contrast:

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 6 di 16

Characterization by simultaneous transesophageal echocardiography. J Am Coll Cardiol 1993;22:1359. 54. Riggs TW, Snider AR: Respiratory influence on right and left ventricular diastolic

function in normal children. Am J Cardiol 1989;63:858. 55. Dabestani A, Takenaka K, Allen B, et al: Effects of spontaneous respiration on left ventricular filling as assessed by Doppler echocardiography. Am J Cardiol 1988;61:1356. 56. Gardin JM, Debastani A, Takenaka K, et al: Effect of imaging view and sample

volume location on evaluation of mitral flow velocity pulsed by Doppler echocardiography. Am J Cardiol 1986;57:1335. 57. Drinkovic N, Smith MD, Wisenbaugh T, et al: Influence of sampling site upon the

ratio of atrial to early diastolic transmitral flow velocities by Doppler [abstract]. J Am Coll Cardiol 1987;9:16A. 58. Ding ZP, Oh JK, Klein AL, Tajik AJ: Effect of sample volume location on

Doppler-derived transmitral inflow velocity values. J Am Soc Echocardiogr 1991;4:451. 59. Samstad S, Torp HG, Linker DL, et al: Cross-sectional early mitral flow velocity

profiles from color Doppler. Br Heart J 1989;62:177. 60. Myreng Y, Smiseth DA: Assessment of left ventricular relaxation by Doppler

echocardiography: Comparison of isovolumic relaxation time and transmitral flow velocities with time constant of isovolumic relaxation. Circulation 1990;81;260. 61. Castello R, Pearson A, Lenzen P, Labovitz A: Evaluation of pulmonary venous

flow by transesophageal echocardiography in subjects with a normal heart: Comparison with transthoracic echocardiography. J Am Coll Cardiol 1991;18:65. 62. Keren G, Sherez J, Megedish R, et al: Pulmonary venous flow pattern—its

relationship to cardiac dynamics: A pulsed Doppler echocardiographic study. Circulation 1985;71:1105. 63. Rossvoll O, Hatle LK: Pulmonary venous flow velocities by transthoracic

ultrasound: Relation to left ventricular diastolic pressures. J Am Coll Cardiol 1993;21:1687. 64. Smallhorn JF, Freedom RM, Olley PM: Pulsed Doppler echocardiographic

assessment of extraparenchymal pulmonary vein flow. J Am Coll Cardiol 1987;9:573.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 7 di 16

65. Kuecherer HF, Kusumoto F, Muhiudeen IA, et al: Pulmonary venous flow patterns

by transesophageal echocardiography: Relation to parameters of left ventricular systolic and diastolic function. Am Heart J 1991;122:1683. 66. Kuecherer H, Muhiudeen IA, Kusumoto FM, et al: Estimation of mean left atrial

pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow. Circulation 1990;82:1127. 67. Brunazzi MC, Chirillo F, Pasqualini M, et al: Estimation of left ventricular

diastolic pressures from precordial pulsed-Doppler analysis of pulmonary venous and mitral flow. Am Heart J 1994;128:293. 68. Channer S, Wilde P, Culling W, Jones JV: Estimation of left ventricular end

diastolic pressure by pulsed Doppler ultrasound. Lancet 1986;3:1005. 69. Masuyama T, Lee JM, Tamai M, et al: Pulmonary venous flow pattern as assessed

with transthoracic pulsed Doppler echocardiography in subjects without cardiac disease. Am J Cardiol 1991;67:1936. 70. Klein AL, Tajik AJ: Doppler assessment of pulmonary venous flow in healthy

subjects and in patients with heart disease. J Am Soc Echocardiogr 1991;4:379. 71. Arakawa M, Akamatsu S, Terazawa E, et al: Age-related increase in systolic

fraction of pulmonary vein flow velocity-time integral from transesophageal echocardiography in subjects without cardiac disease. Am J Cardiol 1992;70:1190. 138

72. Hoit B, Shao Y, Gabel M, Walsh R: Influence of loading conditions and contractile

state on pulmonary venous flow: Validation of Doppler velocimetry. Circulation 1992;86:651. 73. Castello R, Pearson AC, Lenzen P, Labovitz A: Effect of mitral regurgitation on

pulmonary venous velocities derived from transesophageal echocardiography colorguided pulsed Doppler imaging. J Am Coll Cardiol 1991;17:1499. 74. Klein A, Obarski TB, Stewart WJ, et al: Transesophageal Doppler

echocardiography of pulmonary venous flow: A new marker of mitral regurgitation severity. J Am Coll Cardiol 1991;18:518.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 8 di 16

75. Rajagopalan B, Friend JA, Stollard T, Lee GJ: Blood flow in pulmonary veins: III. Simultaneous measurements of their dimensions, intravascular pressure and flow. Cardiovasc Res 1979;13:684. 76. Topol EJ, Taill TA, Fortuin NJ: Hypertensive hypertrophic cardiomyopathy of the

elderly. N Engl J Med 1985;312:277. 77. Dougherty AH, Nacarelli GV, Gray EL, et al: Congestive heart failure with normal

systolic function. Am J Cardiol 1984;54:778. 78. Harizi RC, Bianco JA, Alpert JS: Diastolic function of the heart in clinical

cardiology. Arch Intern Med 1988;148:99. 79. Soufer R, Wohlgelertner D, Vita N, et al: Intact systolic left ventricular function in

clinical congestive heart failure. Am J Cardiol 1985;55:1032. 80. Appleton CP: Doppler assessment of left ventricular diastolic function: The

refinements continue [editorial]. J Am Coll Cardiol 1993;21:1697. 81. Xie G, Berk MR, Smith MD, et al: Prognostic value of Doppler transmitral flow

patterns in patients with congestive heart failure. J Am Coll Cardiol 1994;24:132. 82. Bahler RC, Vrobel TR, Martin RL: The relation of heart rate and shortening

fraction to echocardiographic indices of left ventricular relaxation in normal subjects. J Am Coll Cardiol 1983;2:926. 83. Abe H, Yokouchi M, Deguchi F, et al: Measurement of left atrial systolic time

intervals in hypertensive patients using Doppler echocardiography: Relation to fourth heart sound and left ventricular wall thickness. J Am Coll Cardiol 1988;11:800. 84. Pearson AC, Labovitz AJ, Mrosek D, et al: Assessment of diastolic function in

normal and hypertrophied hearts: Comparison of Doppler echocardiography and Mmode echocardiography. Am Heart J 1987;113:1417. 85. Ren JF, Pancholy SB, Iskandrian AS, et al: Doppler echocardiographic evaluation

of the spectrum of left ventricular diastolic dysfunction in essential hypertension. Am Heart J 1994;127:906. 86. Marabotti C, Genovesi-Ebert A, Ghione S, et al: Diastolic function in the different

patterns of left ventricular adaptation to essential hypertension. Int J Cardiol 1994;44:73.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 9 di 16

87. Kuo LC, Quinones MA, Rokey R, et al: Quantitation of atrial contribution to left

ventricular filling by pulsed Doppler echocardiography and the effect of age in normal and diseased hearts. Am J Cardiol 1987;59:1174. 88. Otto CM, Pearlman AS, Amsler LC: Doppler echocardiographic evaluation of left

ventricular diastolic filling in isolated valvular aortic stenosis. Am J Cardiol 1989;63:313. 89. Pearson AC, Gudipati CV, Labovitz AJ: Systolic and diastolic flow abnormalities

in elderly patients with hypertensive hypertrophic cardiomyopathy. J Am Coll Cardiol 1988;12:989. 90. Grossman F, Orem S, Messerli F: Left ventricular filling in the systemic

hypertension of obesity. Am J Cardiol 1991;68:57. 91. Chakko S, Maya M, Allison MD, et al: Abnormal left ventricular diastolic filling in

eccentric left ventricular hypertrophy of obesity. Am J Cardiol 1991;68:95. 92. Kapuka GK, Seto S, Mori H, et al: Reversal of diastolic dysfunction in borderline

hypertension by long-term medical treatment: Longitudinal evaluation by pulsedDoppler echocardiography. Am J Hypertens 1993;6:547. 93. Esper RJ, Burrieza OH, Cacharron JL, et al: Left ventricular mass regression and

diastolic function improvement in mild and moderate hypertensive patients treated with lisinopril. Cardiology 1993;83:76. 94. Stoddard MF, Vandormael MG, Pearson AC, et al: Immediate and short-term

effects of aortic balloon valvuloplasty on left ventricular diastolic function and filling in humans. J Am Coll Cardiol 1989;14:1218. 95. Hatle L: Doppler echocardiographic evaluation of diastolic function in

hypertensive cardiomyopathies. Eur Heart J 1993;14(Suppl J):88. 96. Maron BJ, Spirito P, Green KJ, et al: Noninvasive assessment of left ventricular

diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1987;10:733. 97. Lewis JF, Spirito P, Pelliccia A, Maron BJ: Usefulness of Doppler

echocardiographic assessment of diastolic filling in distinguishing "athlete's heart" from hypertrophic cardiomyopathy. Br Heart J 1992;68:296. 98. Bonow RO, Frederick TM, Bacharach SL, et al: Atrial systole and left ventricular

filling in hypertrophic cardiomyopathy: Effect of verapamil. Am J Cardiol 1983;51:1386.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 10 di 16

99. Werner GS, Schaefer C, Dirks R, et al: Prognostic value of Doppler echocardiographic assessment of left ventricular filling in idiopathic dilated cardiomyopathy. Am J Cardiol 1994;73:792. 100. Lavine S, Arends D: Importance of the left ventricular filling pressure on diastolic

filling in idiopathic dilated cardiomyopathy. Am J Cardiol 1989;64:61. 101. Vanoverschelde JL, Raphael DA, Robert AR, Cosyns JR: Left ventricular filling

in dilated cardiomyopathy: Relation to functional class and hemodynamics. J Am Coll Cardiol 1990;15:1288. 102. Xie GY, Berk MR, Smith MD, et al: The role of the left atrium in heart failure: Assessment by transmitral and pulmonary vein Doppler [abstract]. J Am Soc Echocardiogr 1993;6:34. 103. Takenaka K, Dabestani A, Gardin JM, et al: Pulsed Doppler echocardiographic

study of left ventricular filling in dilated cardiomyopathy. Am J Cardiol 1986;58:143. 104. Makhoul N, Hasanein J, Dagan T, et al: Doppler diastolic transmitral flow

patterns in severe heart failure: Response to controlled changes in filling pressure using intravenous isosorbide dinitrate. Cardiology 1994;85:235. 105. Xie G, Berk MR, Smith MD, DeMaria AN: Relationship of Doppler transmitral

flow patterns to functional status in patients with congestive heart failure. Am Heart J 1996;131:766. 106. Basnight MA, Gonzalez MS, Kershenovitch SC, Appleton CP: Pulmonary venous

flow velocity: Relation to hemodynamics, mitral flow velocity and left atrial volume and ejection fraction. J Am Soc Echocardiography 1991;4:547. 107. Hatle LK, Appleton CP, Popp RL: Differentiation of constrictive pericarditis and

restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357. 108. Klein AL, Hatle LK, Taliercio CP, et al: Prognostic significance of Doppler

measures of diastolic function in cardiac amyloidosis. Circulation 1991;83:808. 109. Pandian NG, Wang SS, McInerney K, et al: Doppler echocardiography in cardiac

tamponade: Abnormalities in tricuspid and mitral flow response to respiration in experimental and clinical tamponade [abstract]. J Am Coll Cardiol 1985;5:485A. 110. Appleton CP, Hatle LK, Popp RL: Cardiac tamponade and pericardial effusion:

Respiratory variation in transvalvular flow velocities studied by Doppler

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 11 di 16

echocardiography. J Am Coll Cardiol 1988;11:1020. 111. Gonzalez MS, Basnight MA, Appleton CP: Experimental pericardial effusion:

Relation of abnormal respiratory variation in mitral flow velocity to hemodynamics and diastolic right heart collapse. J Am Coll Cardiol 1991;17:239. 112. Gillam LD, Guyer DE, Gibson TE, et al: Hydrodynamic compression of the right

atrium: A new echocardiographic sign of cardiac tamponade. Circulation 1983;68:294.

113. Armstrong WI, Schilt BI, Helser DJ, et al: Diastolic collapse of the right ventricle

with cardiac tamponade: An echocardiographic study. Circulation 1982;65:1491. 114. Picard MH, Sanfilippo AJ, Newell JB, et al: Quantitative relation between increased intrapericardial pressure and Doppler flow velocities during experimental cardiac tamponade. J Am Coll Cardiol 1991;18:234. 115. Wind BE, Snider RA, Buda AJ, et al: Pulsed Doppler assessment of left

ventricular diastolic filling in coronary artery disease before and immediately after coronary angioplasty. Am J Cardiol 1987;59:1041. 116. Labovitz AJ, Lewen MK, Kern M, et al: Evaluation of left ventricular systolic and

diastolic dysfunction during transient myocardial ischemia produced by angioplasty. J Am Coll Cardiol 1987;10:748. 139

117. Bonow RO, Bacharach SL, Green MV, et al: Impaired left ventricular diastolic

filling in patients with coronary artery disease: Assessment with radionuclide angiography. Circulation 1981;64:315. 118. Masuyama T, Kodania K, Nakatani S, et al: Effects of changes in coronary

stenosis on left ventricular diastolic filling assessed with pulsed Doppler echocardiography. J Am Coll Cardiol 1988;11:744. 119. Drinkovic N, Wisenbaugh T, Nissen SE, et al: Sensitivity and specificity of

transmitral flow velocity measurements in detecting impaired left ventricular compliance [abstract]. Circulation 1986;74:II-46. 120. El-Said EM, Roelandt JRTC, Fioretti PM, et al: Abnormal left ventricular early

diastolic filling during dobutamine stress Doppler echocardiography is a sensitive

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indicator of significant coronary artery disease. J Am Coll Cardiol 1994;24:1618. 121. Fujii J, Karzaki Y, Sawada H, et al: Noninvasive assessment of left and right

ventricular filling in myocardial infarction with a 2-dimensional Doppler echocardiographic method. J Am Coll Cardiol 1985;5:1155. 122. Isobe M, Yazaki Y, Takaku F, et al: Right ventricular filling detected by pulsed Doppler echocardiography during the convalescent stage of inferior wall acute myocardial infarction. Am J Cardiol 1987;59:1245. 123. Johannessen K, Cerqueria M, Stratton J: Influence of myocardial infarction size

on radionuclide and Doppler echocardiographic measurements of diastolic function. Am J Cardiol 1990;65:692. 124. Myreng V, Myhre E: Effects of verapamil on left ventricular relaxation and filling

dynamics in coronary artery disease: A study by pulsed Doppler echocardiography. Am Heart J 1989;117:870. 125. Myreng Y, Ihlen H, Nitter-Hauge SL: Effects of beta-adrenergic blockade on left

ventricular relaxation and filling dynamics in coronary artery disease: A pulsed Doppler echocardiographic study. Eur Heart J 1988;9:1167. 126. Manning WJ, Shannon RP, Santinga JA, et al: Reversal of changes in left

ventricular diastolic filling associated with normal aging using diltiazem. Am J Cardiol 1991;67:894. 127. Caramelli B, dos Santos RD, Abensur H, et al: Beta-blocker infusion did not

improve left ventricular diastolic function in myocardial infarction: A Doppler echocardiography and cardiac catheterization study. Clin Cardiol 1993;16:809. 128. Nishimura RA, Schwartz RS, Holmes DR, Tajik AJ: Failure of calcium channel

blockers to improve ventricular relaxation in humans. J Am Coll Cardiol 1993;21:182.

129. Ross J Jr: Acute displacement of the diastolic pressure volume curve of the left

ventricle: Role of the pericardium and the right ventricle. Circulation 1979;59:32. 130. Sonnenblick EH: The structural basis and importance of restoring forces and

elastic recoil for the filling of the heart. Eur Heart J 1980;6(Suppl A):107. 131. Glantz SA, Misbach GA, Moores WY, et al: The pericardium substantially affects

the left ventricular diastolic pressure-volume relationship in the dog. Circ Res 1978;42:433.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 13 di 16

132. Alderman EL, Glantz SA: Acute hemodynamic interventricular shift of the

diastolic pressure-volume curve in man. Circulation 1976;54:662. 133. Louie EK, Rich S, Brundage BH: Doppler echocardiographic assessment of

impaired left ventricular filling in patients with right ventricular pressure overload due to primary pulmonary hypertension. J Am Coll Cardiol 1986;8:1298. 134. Louie EK, Rich S, Levitsky S, Brundage B: Doppler echocardiographic

demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol 1992;19:84. 135. Stojnic BB, Brecker SJD, Xiao HB, et al: Left ventricular filling characteristics in

pulmonary hypertension: A new mode of ventricular interaction. Br Heart J 1992;68:16. 136. Dubroff JM, Clark WB, Wong CYH, et al: Changes in left ventricular mass

associated with the onset of acute rejection after cardiac transplantation. Heart Transplant 1983;3:103. 137. Paulsen W, Maid N, Sagar K, et al: Left ventricular function of heart allografts

during acute rejection: An echocardiographic assessment. J Heart Transplant 1985;4:525. 138. Greenberg ML, Uretsky BF, Reddy S, et al: Long-term hemodynamic follow-up

of cardiac transplant patients treated with cyclosporine and prednisone. Circulation 1985;71:487. 139. Popp RL, Schroeder JS, Stinson EB, et al: Ultrasonic studies for the early

detection of acute cardiac rejection. Transplantation 1971;11:543. 140. Dawkins KD, Oldershaw PJ, Billingham ME, et al: Changes in diastolic function

as noninvasive markers of cardiac allograft rejection. Heart Transplant 1984;3:286. 141. Valantine HA, Appleton CP, Hatle LK, et al: A hemodynamic and Doppler

echocardiographic study of ventricular function in long-term cardiac allograft recipients. Circulation 1989;79:66. 142. Boucek MM, Mathis CM, Kanakriyeh MS, et al: Serial echocardiographic

evaluation of cardiac graft rejection after infant heart transplantation. J Heart Lung Transplant 1993;12:824. 143. Xie GY, Morris EJ, Mattson MD, et al: Value of right and left ventricular

diastolic parameters by Doppler echo to predict cardiac rejection after transplantation

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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Pagina 14 di 16

[abstract]. J Am Coll Cardiol 1993;21:41A. 144. Upton MT, Gibson DG: The study of left ventricular filling from digitized

echocardiograms. Prog Cardiovasc Dis 1978;20:359. 145. Shimizu G, Zile MR, Blaustein AS, Gaasch WH: Left ventricular chamber filling

and midwall lengthening in patients with left ventricular hypertrophy: Overestimation of fiber velocities by conventional midwall measurements. Circulation 1985;71:266. 146. Geiser EA, Conetta DA, Limacher MC, et al: A second generation computer-

based edge detection algorithm for short-axis, two-dimensional echocardiographic images: Accuracy and improvement in interobserver variability. J Am Soc Echocardiogr 1990;3:79. 147. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular

function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313. 148. Gorcsan J III, Schulman DS, Koch L, et al: Echocardiographic automated border

detection derived left ventricular ejection fraction: Comparison with radionuclide angiography [abstract]. Circulation 1991;84(Suppl II):II-585. 149. Sapin PM, Kwan OL, Xie GY, et al: The assessment of left ventricular filling

dynamics using an on-line automatic border detection algorithm: Comparison with cineangiography. Echocardiography 1995;12:559. 150. Chenzbraun A, Pinto FJ, Popylisen S, et al: Comparison of acoustic quantification

and Doppler echocardiography in assessment of left ventricular diastolic variables. Br Heart J 1993;70:448. 151. Smith MD, Xie G, Sapin PM, et al: Factors affecting the determination of left

ventricular area by acoustic quantitation [abstract]. J Am Coll Cardiol 1992;19:199A. 152. Chen C, Rodriquez L, Levine RA, et al: Noninvasive measurement of the time

constant of left ventricular relaxation using the continuous-wave Doppler velocity profile of mitral regurgitation. Circulation 1992;86:272. 153. Nishimura RA, Schwartz RS, Tajik AJ, Holmes DR: Noninvasive measurement of

rate of left ventricular relaxation by Doppler echocardiography: Validation with simultaneous cardiac catheterization. Circulation 1993;88:146. 154. Brun P, Tribuoilloy C, Duval AM, et al: Left ventricular flow propagation during

early filling is related to wall relaxation: A color M-mode Doppler analysis. J Am Coll Cardiol 1992;20:420.

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155. Stugaard M, Smiseth DA, Risoe C, Ihlen H: Intraventricular early diastolic filling

during acute myocardial ischemia: Assessment by multigated color M-mode Doppler echocardiography. Circulation 1993;88:2705. 156. Curtois M, Ludbrook PA: Intraventricular pressure gradients during relaxation

and filling. In Gaasch WH, Le Winter MM (eds): Left Ventricular Diastolic Dysfunction and Heart Failure. Philadelphia, Lea and Febiger, 1994, p 150. 157. Greenberg NL, Vandervoort PM, Thomas JD: Estimation of diastolic

intraventricular pressure gradients from color M-mode Doppler spatiotemporal velocities: Analytical Euler equation solution. Los Alamitos, CA, Computers in Cardiology 1994, IEEE Computer Society Press, 1995, p 465. 158. Greenberg NL, Vandervoort PM, Thomas JD: Instantaneous diastolic transmitral

pressure differences from color Doppler M-mode echocardiography. Am J Physiol 1996;271:H-1267. 159. Garcia MJ, Thomas J, Klein AL: New Doppler echocardiographic applications for

the study of diastolic function. J Am Coll Cardiol 1998;32:865. 140

160. Takatsuji H, Mikami T, Urasawa K, et al: A new approach for evaluation of left ventricular diastolic function: Spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography. J Am Coll Cardiol 1996;27:365. 161. Rodriguez L, Ares MA, Vandervoort PM, et al: Does color M-mode flow

propagation differentiate between patents with restrictive vs. constrictive physiology? J Am Coll Cardiol 1996;27:268A. 162. Gibson DG, Prewitt TA, Brown DJ: Analysis of left ventricular wall movement

during isovolumic relaxation and its relation to coronary artery disease. Br Heart J 1976;38:1010. 163. Isaaz K, Munoz del Romeral L, Lee E, Schiller NB: Quantitation of the motion of

the cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr 1993;6:166. 164. Garcia MJ, Rodriguez L, Ares MA, et al: Differentiation of constrictive

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pericarditis from restrictive cardiomyopathy: Assessment of left ventricular diastolic velocities in the longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108. 165. Sohn DW, Chai IH, Lee DJ, et al: Assessment of mitral annulus velocity by

Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474–80. 166. Nagueh SF, Middleton KJ, Kopelen HA, et al: Doppler tissue imaging: A

noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527. 167. Ommen SR, Nishimura RA, Appleton CP, et al: Clinical utility of Doppler

echocardiography and tissue Doppler imaging in the estimation of left ventricular filling presures: A comparative simultaneous Doppler-catheterization study. Circulation 2000;102:1788.

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141

Chapter 7 - Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Hans G. Bosch MSc Johan H.C. Reiber PhD

Digital image processing techniques nowadays can be found in any ultrasonography machine or offline analysis system. Moreover, ultrasonography machines have evolved from mainly analog, video-type technology into fully digital, computer-like systems. Digital image storage and digital processing of echocardiographic images, both for image enhancement and for analysis, are widely practiced. Some forms of automated image analysis and automated border detection (ABD) techniques (also known as edge detection, border delineation, or edge finding) are commercially available. However, automated border detection is still in the process of development. Many issues remain to be solved, but important breakthroughs can be expected soon. Automated border detection can potentially supply the echocardiologist with quantitative, less subjective tools for research and clinical practice. However, ultrasonography is a difficult imaging modality for interpretation, for both humans and computers. Frequently, unrealistic expectations as

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well as unfounded denunciation of the possibilities of image processing and automated analysis are encountered. In this chapter, we want to provide the clinician with some insight into the background of different techniques and supply some practical guidelines for 142

the choice and use of techniques and their possibilities and limitations.

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Digital Image Processing and Endocardial Edge Detection: Why and When? Digital image processing concerns all manipulation of images by a computer. In a more limited sense, it refers to enhancement or analysis of images. Image enhancement aims at improvement of images, for visual interpretation or for further automated analysis. This can range from a simple contrast adjustment up to sophisticated filtering. The user can apply these when all or parts of an image need improved visualization. Image analysis generally involves the derivation of some quantitative measures or parameters from images. In a narrower sense, this often refers to automatic localization and outlining (edge detection, border detection) of certain structures. In echocardiography, the left ventricular (LV) endocardium is of prime interest. Outlining of the LV endocardial border is necessary for quantitative measurements of LV cavity area and calculation of volume, local wall displacement and velocity, and so on. Combination with the epicardial border allows calculation of wall thickness and LV mass. Besides quantitative measurements based on delineated areas or caliper distances, visual estimation of parameters (such as ejection fraction) or semiquantitative classification (e.g., wall motion scoring for stress echocardiography) still plays an important role in clinical practice. Eyeballing can be done fast, without much ado, and some experts reach an admirable accuracy. In general, however, it is inaccurate, irreproducible, and hard to learn.[1] Visual estimation of quantifiable measures should be discouraged for any purpose beyond a rough classification, whenever a quantitative alternative is present. Quantitative analysis is advisable when repetitive interpretations are done, when more subtle differences are sought, when interpretation experience is limited, and whenever scientific research is the goal.

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The classic method of outlining the borders is manual drawing. Any ultrasonography machine or offline analysis system has facilities for this, using a mouse, trackball, or similar device. Manual drawing, however, is known to have high inter- and intraobserver variability; it is strenuous and time consuming for the operator and requires expertise and dexterity. Drawing of all frames in the cardiac cycle, over multiple cycles and over multiple stages (as in stress echocardiography), is especially hard to perform practically, in terms of both consistency and workload. Automated Border Detection (ABD) in principle can provide solutions to these problems. Potentially, any measurement that requires manual drawing of borders or indication of landmark points may benefit from automated detection techniques. Moreover, if ABD can be performed online and in real time, it opens possibilities for real-time monitoring of parameters such as LV area and volume. Procedures such as stress echocardiography that currently rely totally on visual scoring of wall motion and comparison between different stages could benefit enormously from automated analysis; the lack of quantification and the large inter- and intraobserver and interinstitution variabilities[2] are perceived as important limitations. No practical automated method for stress echocardiographic analysis is available yet, but some promising developments are described here.

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Digital Image Storage, Communication, and Compression The basis of digital image processing and analysis is the availability of images in digital form. Digital image storage and related subjects are discussed in more detail in the chapters on the digital echocardiography laboratory; in this chapter, an overview of properties of importance for image processing is given. The generation of ultrasonographic images, including ultrasound physics, radiofrequency signal processing, scan conversion, and the instrumentation of ultrasonography machines, is beyond the scope of this chapter. Excellent descriptions on these subjects can be found in many handbooks.[3] [4] [5] [6] Digital Images Digital images are bitmaps, large rectangular matrices of dots or pixels (picture elements) in which the brightness (or color) at each position is represented by a numeric (digital) value. Brightness level is also referred to as intensity or gray value. Typical sizes for echo images are 640 × 480 × 24-bit, equivalent to an NTSC color image, or 768 × 576 × 8-bit for a PAL black and white image. NTSC and PAL are U.S. and European video standards. This should be read as 640 columns by 480 rows of pixels (width X height), 24 bits per pixel. The composing colors red, green, and blue are each coded by 8 bits, giving 256 levels per color, allowing 16.8 million color combinations. A cineloop or movie is a sequence of such images, typically at a frame-rate of 30 or 25 images per second. A digital representation makes it possible to store images as data files and process these in a computer—hence, digital image processing. Analog images, as they are used in TVs and VCRs, consist of a continuously varying electrical signal (the video signal) that represents the brightness along horizontal lines in the image. Such a signal is subject to noise and degradation when it is transmitted over a line or stored on a VCR tape. On the other hand, digital images do not degrade when copied, transmitted, or stored for longer periods. Digital images can be stored on digital media such as floppy disks,

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MOD, CD-ROM, or DVD, transported over networks, stored in large databases, and linked with any other patient information. The main drawback is still the huge amount of data storage that is involved—a single VCR tape of 2 hours carries the equivalent of about 200 gigabytes of uncompressed color images. With image compression and selection, we can limit the storage requirements considerably, but still we cannot use digital storage simply instead of a VCR now. Inside the ultrasonography system, echo images are 143

always created as digital images. Frame-rates and image size can be very different from the typical video values. For display on a monitor and recording on VCR, these digital images are converted into an analog video signal. Not all ultrasonography machines support the storage or communication of digital images, and some can only store single frames, not cineloops. For digital image processing and analysis, digital images are a prerequisite. If only analog video output or VCR tape is available, it is possible to redigitize the analog signal with the help of computer devices named frame grabbers or video digitizers. Note that this introduces unwanted image deterioration in the form of noise and jitter, loss of spatial and temporal detail, loss of separation between image, graphics and color overlays, and loss of additional information such as calibration and patient information. Storage Formats and Image Communication DICOM

The current method of choice for digital image storage and exchange is DICOM (Digital Imaging and Communications in Medicine [7] ). DICOM 3.0 is a generally accepted international standard for medical images proposed by the DICOM committee, a cooperation of professional organizations such as the American College of Radiology, the American College of Cardiology, and the European Society of Cardiology and experts from the medical imaging industry and standardization organizations such as the National Electrical Manufacturers Association. Originally developed for radiography, DICOM now encompasses extensions for most image modalities, including ultrasonography, magnetic resonance imaging, computed tomography, x-ray angiography, and nuclear imaging. The

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DICOM standard is still being extended and improved to better support stress echocardiography, three-dimensional echocardiography, ultrasonography, and others. DICOM should improve the exchangeability of all medical image data. As its name implies, DICOM is a communication standard rather than a file format—it defines the way in which medical imaging devices such as ultrasonography machines, Picture Archiving and Communications Systems (PACS) servers, and printers communicate to transport, store, retrieve, find, or print images and associated patient information. All major manufacturers have committed themselves to support DICOM; eventually, this should allow easy networking in multivendor environments, workable PACS systems, and easy and transparent offline viewing and analysis. Ultimately, this may lead to the digital integrated patient record, which should contain the full patient file, including patient history, laboratory reports, images of all modalities, and other information. DICOM covers every detail of medical image handling, for a multitude of imaging modalities and uses, all captured in substandards that are defined by subcommittees and working groups. Therefore, DICOM is a very complicated standard: the full description covers several thousands of pages.[8] A very readable explanation of DICOM for echocardiographers is given by Thomas. [9] Note that the statement that devices are "DICOM compliant" is rather meaningless; DICOM defines a multitude of services and imaging modalities. For each piece of equipment, a DICOM Conformance Statement defines precisely which services are supplied and supported for what modalities and to what extent. For ultrasonography, it is good to know that image loop storage is not a part of the standard US (ultrasound) modality, but of the later defined US-MF (Ultrasound-MultiFrame) modality. To verify interoperability between devices, the conformance statements should be compared—not a simple job for a novice in DICOM.[10] Proprietary Formats

Several manufacturers still use or support their own proprietary formats for storage of digital image runs with associated patient and image information. Such formats include HP-TIFF or DSR,[11] DEFF[12] (both TIFF extensions), and VINGMED. Although these digital formats may be adequate or even have certain advantages in a single-vendor environment, they may complicate exchange with other departments or hospitals, use of PACS, offline analysis systems, and so on. General Purpose Formats

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Other widely used general-purpose image formats are BMP, TIF, GIF, and JPEG. These are often used for export of screen shots or single images for use in reports, presentations, and papers. These formats generally lack the possibility for storage of image loops (movies) and additional patient information. For movies, AVI, MPEG, and QuickTime are popular formats. These are also general-purpose formats without possibilities for storage of associated data. Image Compression For reducing the data storage requirements, image compression can be employed. A distinction should be made between lossless and lossy image compression. For lossless compression techniques (such as Run Length Encoding [RLE], Lossless JPEG, or various general-purpose file compression techniques such as LZW [used in the ubiquitous ZIP or TAR]), reversing the compression will produce a perfect copy of the original image. Unfortunately, lossless compression generally only reduces file sizes by a factor of 2 to 5. Lossy compression can reach much higher compression ratios (up to 20 to 100) at the cost of a certain amount of image degradation, generally by eliminating information for which the eye is least sensitive. This degradation may be very acceptable visually (JPEG factor 20 has been found to produce only diagnostically nonsignificant degradation[13] ), especially when compared with the degradation associated with VCR storage. However, the compression 144

artifacts may certainly influence digital image processing and analysis. Severely lossy compression is not advisable for archiving or when digital image postprocessing is foreseen. Lossy compression techniques include Lossy JPEG, fractal and wavelet compression, and MPEG, a popular compression scheme for movies. DICOM currently supports RLE and JPEG (lossless and lossy) compression. MPEG and JPEG 2000 compression schemes have been proposed as extensions to the standard.

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Digital Image Processing Digital image processing[14] [15] is a science by itself and cannot be discussed here in great detail. Medical image processing is a thriving subdiscipline with many applications and innovations that have become valuable tools in the hands of the clinician. Several good handbooks on medical image processing, with special attention to ultrasonography, are available.[16] [17] [18] [19]

Image Enhancement: Level Manipulations, Filtering Image enhancement deals with the improvement of images, either for visual interpretation or as a preprocessing for analysis. Most of the techniques described here are available in any general-purpose program for manipulating digital images, such as photo editors, as well as on most ultrasonography machines and offline analysis programs. The simplest class of operations is level manipulations: operations that change the brightness level or color of each pixel without considering any neighboring pixels. These operations are also known as lookup-table (LUT) operations, because the original brightness of the pixel is simply used to look up the new value in a conversion table. Operations of this class include brightness level manipulations and pseudocoloring. Brightness Level Manipulations

This class includes all one-to-one conversions of image brightness levels (input) to display brightness levels (output), either linear or nonlinear. Examples are digital contrast/brightness adjustments, image inversion, gamma correction, and histogram-based conversions. The histogram H(I) of an image is a function that describes, for each brightness level I, the number or percentage of pixels in the image that have this brightness level. Histogram-based conversions include histogram stretching, a linear contrast stretch between the minimum and maximum values of I (or certain

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percentiles) in the histogram; and histogram equalization, a nonlinear transformation that redistributes the gray levels I so that a flat histogram is obtained, increasing the contrast in brightness ranges with many pixels and reducing the contrast in less frequented ranges. Some examples are given in Figure 7-1 . Note that many level manipulations may result in clipping ( See Fig. 7-1C,D , and E ) and in reduction of the effectively used number of brightness levels. The extreme example is thresholding (see Fig. 7-1E) , in which all brightness levels above a threshold are set to white, and all below to black. Pseudocolors

Pseudocoloring involves a direct conversion of brightness levels to a color scale, generally labeled with fancy names such as Rainbow, Ocean, or Harvest. As the eye is more sensitive to color differences than to intensities, this may reveal subtle contrast differences. It can be visually pleasing but it is highly suggestive, as it clusters similar gray values into color groups. Because brightness levels in ultrasonography by themselves do not represent any physical property (see the section on problems and pitfalls) and are highly dependent on gain, signal attenuation, and time gain control, among other factors, the borders that are suggested visually by these colors have no practical significance.[20] This technique is also applied sometimes to highlight brightness values above some threshold with a color, such as during injection of contrast material. Similar objections apply in such a case. Filtering

Filtering is the generic name for image operations that consider neighborhoods of pixels and deal with the spatial or temporal aspects of the image. Filtering operations include noise reduction, smoothing or blurring, and sharpening or edge enhancement. Smoothing or low-pass filtering (e.g., uniform, Gaussian) is used in many ABD methods (see later discussion) to reduce the speckle noise and get more or less homogeneous regions; highpass edge enhancing or detection filters (e.g., Sobel, Laplacian) are often used to find (candidate) border points. Note that most smoothing methods change the positions of edges and cannot differentiate between noise and weak signals. High-pass filters tend to be very sensitive to noise. In general, filtering does not improve the appearance of ultrasonographic images without simultaneously removing valuable information. Smoothing and sharpening filters may be available on your ultrasonography machine for real-time use: keep the above-mentioned caveats in mind when using this

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option. Many more complex forms of postprocessing exist, including median filters, temporal smoothing, morphologic operators such as opening and closing, region growing, matched filters, texture analyses, wavelet transforms, and Fourier and cosine transforms, all of which have been used as parts of ABD methods. Most of these have little practical value by themselves. Image Interpretation: The Interpretation Pyramid The interpretation of highly complex information like medical images is an extremely complicated task. We humans 145

Figure 7-1 Image brightness conversions (look-up table operations) and their results. A, Identity: no change; B, inversion; C, increased contrast (note clipping, C); D, decreased brightness; E, thresholding; F, histogram equalization.

146

Figure 7-2 The image interpretation pyramid.

tend to underestimate it considerably: for us, vision is a very natural process that we perform instantly and automatically. From the study of human perception, we know that vision is anything but a simple, straightforward process. Think of the many well-known optical illusions: there is a lot of hidden interpretation going on. In the interpretation of images, a certain number of information abstraction levels can be distinguished. This is generally known as the image interpretation pyramid (Fig. 7-2) . The levels of this pyramid give us more insight into the mechanisms of different automated techniques and their limitations. A good analogy is found in the interpretation of handwriting or spoken language. This analogy is described in Table 7-1 . For interpretation of a written text, one has to know about the alphabet, spelling, vocabulary,

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syntax, and semantics, and ultimately about the subject of the text, the intentions of the source, and adornments such as humor, sarcasm, and metaphors. These last aspects concern real-world knowledge that has nothing to do with language—it refers to the domain that the text is discussing. In practice, this is not just a simple bottom-up TABLE 7-1 -- Abstraction Level Hierarchy Associated Level General Speech Image Cardiac Operations 0 Raw data Samples Pixels Pixels Image generation 1 Features Amplitude, Intensity, Intensity, Preprocessin filtering, frequency texture, texture, feature gradients gradients extraction 2 Structures Phonemes Edges, Edges, Linking, regions regions merging, matching, clustering 3 Objects Words World Cardiac Model entities, structures relaxation, borders, (lumen, border objects endocardium finding, valve) classification 4 Object sets Sentences Scene Cardiac Scene scene modeling, interobject relationships 5 Interpretation Significance Scene Interpretation High-level interpretation and interpretatio diagnosis expert systems, rul process of combining letters into words into sentences into significance. Text can be fragmented; there are imperfections such as misspellings and ambiguities, unknown words, and missing domain knowledge that necessitate interactions and feedback between all levels, and even guessing, to come to a consistent interpretation.

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Cardiac Image Interpretation

In image interpretation, we have a similar hierarchy. At the basis, we find the raw image information (pixels). Going up, we encounter image features such as local texture and gradients; structures such as regions (groups of adjacent pixels with similar properties) and edges (lines of sudden change, between regions); objects such as a square or a person; and a scene, such as a football match. At the top we have significance, such as finding out who's winning; this requires very specific knowledge on behavior of the players and audience, rules of the play, and so on.

147

Interpretation of medical images, especially of a complex, dynamic organ like the heart, is still more difficult, as it requires expert knowledge about the three-dimensional anatomic structures in the heart, their dynamic behavior, pathology and anatomic variability between patients, and the intricacies of the imaging modality involved. This last point specifically is not to be underestimated for ultrasonography. Again, interpretation is not a simple bottom-up process. Missing or ambiguous information, disturbances such as noise and artifacts, and higher-level knowledge of anatomy, physiology, and pathology are involved and necessitate feedback and interactions between levels. Clearly, very different sorts of knowledge are applied at each level to come to a valid interpretation, and only the lower levels have to do with image properties: higher levels concern sizes and shapes of cardiac parts, anatomic models of the heart, physiology, congenital or pathologic conditions, and so on. Automated border detection systems generally have very limited knowledge at the higher interpretation levels, and resolve this in one of three ways, as follows: 1. They use simplifying assumptions regarding the objects. For example, the left ventricle is a dark, round object in the middle of the image; the endocardial contour is convex, the endocardium is the strongest edge in the image, the cardiac wall will not move more than x pixels per frame. Most of such assumptions will hold only to some extent or are overly general. 2. They limit themselves to a subset of the problem domain, for aspects like cross sections (e.g., only midpapillary short-axis), image quality

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(no dropouts, low noise), anatomy (e.g., no congenital defects), or imaging equipment or settings (scale, gain, frequency). 3. They require the user to handle the high-level aspects by initializing, steering, or correcting the system. The level of knowledge that a certain system applies, the validity of its assumptions, and the ease of interaction for the user determine the "intelligence" and practical value of the system. Rules for a Well-Behaved Automated Border Detection Method

No practical system can do without the intervention of the user. Ideally, there is only one desired and necessary interaction; in cases in which there is room for multiple interpretations, the user should have the final decision. In practice, a computer system can never have all the high-level knowledge that the physician has, and it requires the physician's intervention to handle these blind spots. Systems with little high-level knowledge and models, however, rely heavily on the user to handle their shortcomings and mistakes (USER = Universal Solution for Error Recovery). With these limitations in mind, we can formulate a few criteria for a good and well-behaved ABD method. 1. The method should generate "correct" contours. Because this judgment may be subjective (in the light of multiple possible interpretations), a system should be able to adapt to the expert user's general ideas about correct contours. 2. The contours should be reproducible; this seems obvious for an automatic system, but almost all systems require some type of user interaction (setting of certain parameters, indicating some start point or region, selection of the images to be analyzed, corrections), which will lead to some variability in results. This inter- and intraobserver difference should possibly be smaller than the considerable inter- and intraobserver variabilities associated with similar manual work. 3. The method should be user-friendly; it should only address the user for high-level expert decisions. It should not require him or her to handle "stupid" mistakes or do repetitive corrections. Some implications are as follows: • It should not generate physically or anatomically impossible solutions; unlikely solutions should be marked as such. It should supply alternative hypotheses (when relevant). • It should not override user-drawn contours, for example, unless

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specifically asked to (apart from clean-up of minor imperfections). • It should allow for easy, intelligent, minimized control and correction (the intent of the correction should be applied throughout the whole image set).

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Automated Border Detection in Echocardiography Problems and Pitfalls of Border Detection in Ultrasonography Ultrasonography is a particularly difficult imaging modality for interpretation. Outsiders mostly find it hard to interpret, contrary to other tomographic modalities such as computed tomography and magnetic resonance imaging. Ultrasonography suffers from several specific drawbacks, which also impede automated analysis. 1. There is no simple physical relation between pixel intensity and any physical property of the tissue visualized, in contrast to the LambertBeer law for radiography or the Hounsfield units for computed tomography. In ultrasonography, images are formed by sound reflection and scattering, resulting in a combination of interference patterns (ultrasound speckle patterns) and reflections at tissue transitions. Different tissues are often distinguishable only by subtle differences in texture (speckle patterns) or behavior of texture over time, rather than by different intensity values. 2. Ultrasonographic image information is very anisotropic and positiondependent, as reflection intensity, spatial resolution, and signal-tonoise (S/N) ratio are very dependent on both the depth and the angle of incidence of the ultrasound beam, as well as on the user-controlled time gain compensation (depth gain) settings. Even the definition of the border position may be direction-dependent (leading edge or trailing edge borders[20] ). 148

3. Image disturbances can occur, such as artifacts caused by side lobes, reverberations, lateral and radial point spread functions, and significant amounts of random noise. Many of these problems are associated with high gain settings, which are often necessary in obese or older patients.

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Speckle noise can be seen as an artifact as well; although it is an inherent part of ultrasound imaging, it often veils anatomic details. 4. Missing information can occur, such as dropouts (for structures parallel to the ultrasound beam), shadowing (behind acoustically dense structures), scan sector limitations, and limited echo windows. Stillframe images generally miss some information; the human eye compensates for this when viewing a sequence of images. It resolves ambiguities and interpolates the missing parts by exploiting the temporal behavior of structures and texture, which allows discrimination between noise, artifacts, and anatomy. 5. Problems can arise that are caused by the limited temporal resolution and the scanning process. The sequential scanning of lines combines information from different time moments into one image. For quickly moving structures, this may lead to spatial distortion. When the scan frame-rate is not synchronous with the video frame-rate of 25 or 30 images per second, sharp transitions between "old" and "new" scan line information may appear in still images. These effects are stronger for lower scan frame-rates. 6. Two-dimensional ultrasonography generally lacks spatial reference information. No exact spatial localization of the cross-sectional plane is known. In three-dimensional techniques such as magnetic resonance imaging or computed tomography, this information is often employed in model positioning for the detection. In cardiac ultrasonography, the choice of the imaged cross section depends both on the skill and precision of the sonographer and on the available echo window, which is limited by ribs or other structures. Apart from volume measurement errors, this may also result in detection problems if the ABD method relies on assumptions of shape, distance between epicardium and endocardium, and the presence or absence of other structures such as valves or papillary muscles. Practical Considerations for Automated Border Detection Practical considerations for appropriate border detection (either automatic or manual) are listed in Table 7-2 , subdivided into three categories. Acquisition and Image Quality

The primary requirement for any analysis, whether automated, manually traced, or visual, is optimal image quality. If the border cannot be seen, it can only be guessed at (more or less intelligently). Therefore, one should optimize image quality, standardize system settings, and reduce variability

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in settings and cross sections. Select a depth such that the object of interest fits well TABLE 7-2 -- Practical Considerations for Automated Border Detection Acquisition and image quality Optimize border visualization Limit variation in system settings (gain, power, time gain control, lateral gain control) Limit variation in cross sections (use landmarks) Proper region of interest/depth High frame-rate Digital storage (preferably lossless); no filtering No spatial/temporal subsampling or small regions of interest for storage Border definitions and consistency Inventory of desired calculations Standardize border drawing definitions: Inclusion or exclusion of papillary muscles, trabecular structures, valves, etc. Position of edges: leading, peak, trailing Exclusion criteria and special cases: Image quality: foreshortening, dropouts, artifacts, noise Pathologies: hypertrophy, dilation, cardiac masses, etc. Congenital deformations, etc. Assess inter- and intraobserver variabilities: To test standardization To check errors against study goal, estimate patient population size for significance Include acquisition protocol? Choice of detection technique Check specifics of technique against problem: Cross sections Cardiac objects (left ventricle, right ventricle, endocardium, epicardium)

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Border definitions Single frame, ED/ES, full-cycle, multicycle Real-time online or offline with corrections Dependence on image quality, artifacts, settings Amount and types of user interaction Is manual analysis a practical alternative? inside the scan sector and fills most of it. Try to adjust acoustic power, overall gain, time gain control, or lateral gain control such that the endocardium is best and most homogeneously visualized. Remember that stop-frame images are much harder to interpret than moving sequences; individual frames may be much less pleasing than the cineloop suggests. Since most detection methods do not use interframe relationships, they actually use single frames and suffer from the higher uncertainty. A high frame-rate (at least 25 frames per second) is advisable, both for full-cycle analysis or for proper selection of end-diastolic (ED) and end-systolic (ES) frames in case of ED/ES analysis. For image storage, use digital images whenever possible—do not store images on videotape to redigitize later. Avoid lossy compression with high compression rates, image subsampling (resolution reduction), and temporal subsampling (frame rate reduction). When selecting a region of interest for storage, make sure that it will contain the object completely over the full time range. Contour Definitions and Consistency

Before attempting manual or automated detection, make sure that proper criteria are defined for the desired contours. This may depend on the desired calculations to 149

be performed from the contour. Trabecular structures, papillary muscles, or valves can either be included or excluded for certain calculations (LV volume, regional wall motion, LV mass). Many points need to be standardized: whether leading, maximum, or trailing edges are drawn; what to do in case of foreshortening, dropout, and so on.[20] [21] When possible, perform inter- and intraobserver comparisons and try to reach consensus before starting a large study. In some cases, this should include the image acquisition, to assess inter- and intraoperator variability in the choice of

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cross section, ultrasonographic system settings, and other factors. Choice of Detection Technique

When considering an automated technique for border detection, it is wise to check the following against the specifications of the automated method: the cross sections involved, the object to be detected (e.g., left ventricle, right ventricle, atrium); single-frame, ED/ES, full-cycle or multicycle analysis; the brand and type of echo machine used; the type of contour to be found (blood-tissue border or other, such as epicardium); online or offline availability of the detection; possibilities for user correction of the boundaries (in offline case); dependency on system gain, image quality, and common artifacts such as dropouts or noise; and amount of user interaction needed. In case no suitable automated technique is found for a certain analysis, manual measurements may (or may not) provide a practical alternative. Overview of Automated Border Detection Methods Ever since the invention of echocardiography, methods have been devised for the automated analysis of these images. Literally hundreds of methods have been reported,[22] [23] most of which have only academic value.[24] [25] We do not try to present a complete taxonomy here and limit ourselves to the main directions of research. We refrain from any comparisons on reported success scores, as there are no standard test data sets for this purpose, nor standard test criteria. It is also difficult to compare the type and extent of user interaction, reproducibility, and so on. Any success scores reported depend very much on the chosen inputs and their quality. Because of lack of a gold standard, contours are generally judged by an expert or compared with contours manually drawn by one or more experts, or derived values such as area or volume are compared with some alternative measurement. Most of these values are hard to compare between studies. A rough measure for the worth of a method could be the number of patients on which it has been tested. Methods that have been tested on fewer than 10 patients probably have no practical value (although their academic value may be high): no matter how naive the method, one can always find a few images on which it will work. A listing of a representative cross section of reported techniques is given in Table 7-3 . For each level, the most basic technique is given first. This one is often applied by methods that focus on other levels. Not surprisingly, older techniques generally operate on a lower level. Of level 5, few true

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examples currently exist. The terms "knowledge-based," "intelligent," and "model-driven" are widely misused, even for the most basic techniques at any level. Feature-Based Method: Integrated Backscatter Method, Advantages, and Limitations

The clinically most widespread method for ABD is by far HewlettPackard's Acoustic Quantification (AQ[26] ), which is installed in several Hewlett-Packard (Philips) ultrasonography machine models (Fig. 7-3) . AQ is not an ABD system in the strict sense as described previously, because it merely does a blood/border/tissue pixel classification (by thresholding) on the basis of the integrated backscatter energy of the radiofrequency ultrasound signal. Therefore, it falls into the lower hierarchical levels of the image interpretation pyramid. However, its use of the radiofrequency data, the online real-time applicability, and widespread availability make it a valuable tool. A real-time lumen area plot and area change (dA/dt) plot can be generated, as well as a real-time frame-to-frame monoplane volume calculation. When used with care in images of good quality, it can give very nice results. However, AQ also suffers from some serious drawbacks, [27] [28] which can be summarized as follows: • The AQ borders are very sensitive to image quality (noise, dropouts) and gain settings (time gain control, lateral gain control), and often difficult to control for the user. Cardiac cycle-dependent intensity changes can influence area change calculations.[27] • AQ uses a fixed, user-drawn region of interest within which the blood pixels are counted. Parts of the ventricle (the valve plane and/or septum) tend to move in and out of such a region throughout the cycle, resulting in considerable measurement errors because of missed parts of the ventricle or included parts of the atrium and the other ventricle. • It is mostly impossible to eliminate tissue parts within the ventricle (valve, papillary muscle, and trabecular structures) or to exclude dropout regions from the ventricle, and noise and artifacts may cause serious problems, especially in difficult patients. Reported success scores in larger patient populations vary widely. • The contours are very noisy, which can be expected for a thresholding-type technique; this implies that they are not directly suitable for regional wall motion calculations. A procedure for extracting and postprocessing these contours has been reported.[29] • The method is real time by nature, as it uses the radiofrequency

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signal, which is available only during image acquisition. Apart from representing a unique advantage, this feature also means that the method cannot be used offline, nor can the same images be reanalyzed with different settings. Whenever radiofrequency data can be stored, this limitation will be resolved. Figure 7-3 (color plate.) Acoustic quantification on Philips (HewlettPackard) equipment. (Courtesy Philips Medical Systems Ultrasound, Andover, Mass.)

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TABLE 7-3 -- Overview of Automated Border Detection Methods at Different Abstraction Levels Level Name Basic Technique(s) 1. Heavy smoothing for Preprocessing noise/speckle reduction[68] Contrast stretching Histogram equalization

2. Edge or region detection

Advanced Techniques Spatiotemporal smoothing[69]

Morphologic filters[70] Texture filters: inverse difference moment[71] wavelet transforms[72] Fourier-based filters[73] Radiofrequency data processing: integrated backscatter (AQ) [26] Global or local thresholding Advanced edge detectors: [69] [74] Marr-Hildreth[77] [78] Canny[79] [80] [81] rank-based operator[82] Simple edge detectors such Pattern or profile matching[51] as difference-of-boxes[65] [75] [76]

Matched filters[83] arc filters [40]

Region detection: region growing[73] fuzzy clustering;

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resolution pyramids; neural nets; Markov random fields [84]

3. Geometric Implicit models: e.g., radial objects or search for candidate points, [68] models interpolation/linking, smoothing/shape filtering

Classification of edge points by fuzzy reasoning[78]

Dynamic Programming optimization[42] [80] [85] [86] [87] Simulated annealing[81] selforganizing maps (SOM, Kohonen)[82] Snakes/balloons/active contours/deformable contours, etc.[75] [79] [80] , [88] Active shape models (ASM) [51] [52]

4. Anatomic None or implicit: Hardstructure or coded scene models Manually positioned

User-drawn

Single geometrical shape models—2D, 2D + T, 3D, 3D + T: Model positioning/landmark finding techniques: row/column sums,[76] [78] arc filters,[40] template matching; Hough transform [81] fuzzy logic[72] Shape parameters (2D + [23] T) 3D shape neural nets[89] Composite models (several objects and their relation, e.g., ventricles and septum)—2D, 2D + T, 3D, 3D + T: Point distribution models [53]

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Multiple active contours[79] Fuzzy neural nets (2D)[90] Adaptation of models to image and user[23]

5. None Interpretation, high-level knowledge User intervention: correction Use of patient group derived of contours, etc models: neural nets,[70] SOM, [82] geometrical eigenvariations (PDM)[51] [53] Learning behavior over all cases analyzed Rule-based analysis Pathology awareness Multiple hypothesis generation 2D, two-dimensional; 3D, three-dimensional; PDM, Point Distribution Models; T, time.

Most of these problems are exemplary for a low-level method that does not use any geometric models or knowledge about cardiac anatomy. Apart from these drawbacks, the use of radiofrequency data supplies superior basic information for blood-tissue classification and may well serve as a basis for higher-level developments, especially when the digital radiofrequency data become available for offline postprocessing. The use of harmonic imaging (see later discussion) has been shown to improve AQ border delineation[30] [31] but does not eliminate most of these problems. A spin-off of AQ is known as color kinesis[32] [33] (Fig. 7-4) . This technique is in essence a method of presenting the time sequence of AQ contours in a single image, by color-coding the lumen area for each time frame and superimposing the images. This method renders a rainbow-like lumen in which each color represents some time-offset from ED. Provided there is little global heart translation, this can give a good impression of wall motion patterns in systole or diastole, especially when these motions are analyzed per region.[33] [34] [35] Of course, all limitations of AQ apply here as

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well, plus the concern of overall heart translation, making this technique also challenging to apply accurately.

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Figure 7-4 (color plate.) Color kinesis image on Philips (HewlettPackard) equipment. (Courtesy Philips Medical Systems Ultrasound, Andover, Mass.) Clinical Use

Acoustic Quantification has been applied in clinical studies for many purposes, especially for looking at left ventricular function (lumen area, volume, and fractional area change). Studies on right ventricular function have been reported as well.[36] Combination of AQ data with invasively measured ventricular pressure has been reported,[37] allowing pressure-area and pressure-volume loops to be constructed, which may hold promise for the assessment of LV mechanical performance. Color kinesis has been used for studying wall motion patterns in several patient groups, systolic and diastolic function, regional wall motion in stress echo, and other parameters.[35] [38] [39] Structure-Based Method: Matched Filters As an example of a structure-based method, we highlight the method by Geiser and Wilson and their group[24] , [40] [41] for automatically detecting endocardial and epicardial borders in short-axis echocardiograms. The method is based on matched filters that respond to arclike structures. The first step applies a filter that responds to the bright epicardial-pericardial interface at the posterior wall. Subsequently, other circular structures along the wall are detected and, after update of the LV center estimate, redetected (an example of high-to-low level feedback). This gives an estimate of epicardial position, which is used as a region of interest. Radial edge detectors are used to locally adjust epicardial edges and to estimate the (relatively strong) anteroseptal endocardial edge. From the estimated wall thickness, the border search is further limited and final endocardial and epicardial edge estimates are found (Fig. 7-5) . This method seems practically useful (it has been validated on a large set of quality-selected patients), and it is clever in the sense that it uses feedback

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between a high-level model of a short-axis cross section and low-level feature data. From a theoretical viewpoint, it is vulnerable because of the cascade of dependent steps, each of which may fail and cause the process to break down. Much of the applied geometrical and expert knowledge (such as the order of strength of expected features) seems to be coded into the steps of the algorithm rather than being captured in a general model. Such an approach may be hard to extend to other views or to certain pathologic conditions that break the assumptions, as this requires redesigning the algorithm. Object-Based Method: Echo-CMS Method

As an example of an object-based (pattern- and geometric model based) ABD method, we describe the Echo-CMS system (MEDIS Medical Imaging Systems, Leiden, The Netherlands) that was developed in our laboratory. The system has been designed for practical use, with the main intent of quantifying endocardial wall motion and lumen volume frame-toframe. A relatively simple circular model-based Dynamic Programming approach is used for short-axis views.[28] [42] An LV center point is indicated by the user, defining a circular model and region of interest in which the strong endocardial edge is found by Dynamic Programming using first derivatives and smoothness and distance constraints. The found border is used as a model in neighboring frames to allow frame-to-frame analysis. In the different long-axis views (apical four-chamber, two-chamber, and parasternal long axis), a more elaborate semiautomated pattern-based approach is used.[23] [43] For the analysis of one or more complete beats (Fig. 7-6A) , one ED and ES contour must be manually drawn (Fig. 7-6B) . Next, three landmark points characterizing the position of the LV (apex and mitral valve attachment points, which are the end points of the contour) are extracted from the contours and interpolated or extrapolated linearly over the cycles. The user is required to inspect these markers over the cycles and may then redefine, if necessary, intermediate positions where the true position deviates from the estimated position. Now, the automated contour detection is started. From the manually drawn ED and ES contours, models are extracted describing the geometrical shape of the ventricle over the cycle and the intensity profiles in a neighborhood of the drawn contours. All models (phase, pose, geometry, and edge profiles) are interpolated over the cycle and extrapolated over other cycles ( see Fig. 7-6C, D andE ). The resulting geometry models are positioned over the images ( Fig. 7-7A and B ), which are resampled along straight lines perpendicular to the models.

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For each point of all scan lines (see Fig. 7-7C, left) , a cost value is calculated representing the likelihood of this point as a contour point: unlikely points will have high costs. The cost is calculated from a combination of edge detectors, match differences with the edge profile models, and local edge reliability measures. Through this rectangular array of cost values (see Fig. 7-7C, center) , an optimal connective path is determined using a Dynamic Programming approach. Cumulative costs for all connective paths are calculated, applying position-dependent penalties for deviation from a straight path. In this way, local stiffness of 152

Figure 7-5 (color plate.) Short-axis border detection with arc filters. Top, Short-axis echocardiographic images at end-diastole and endsystole. Bottom, automatically generated borders at end-diastole and end-systole. (From Sheehan F, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M, Fitzpatrick JM (eds): Handbook of Medical Imaging, vol 2. Medical Image Processing and Analysis. Bellingham, Wash, SPIE—The International Society for Optical Engineering, 2000, p 609.)

parts of the border is modeled. The path with overall lowest cost is selected as optimal (see Fig. 7-7C, right) and by inversion of the resampling process converted into a new contour (see Fig. 7-7D) . After detection of all contours (see Fig. 7-6F) , the user may apply any corrections by overdrawing part of a contour. Consecutively, all models are updated with the extra user-defined information, which is interpolated and extrapolated over the sequence, followed by a redetection of all non-manual contours. In short, this method uses full-cycle models for the two-dimensional pose, shape, and local stiffness properties of the wall and for the intensity profiles of the edges. Case-specific and user-specific information is incorporated by collecting information from all user-defined contours. Drawbacks are the need for two manually defined borders and the marker manipulations. Clinical Use

This method has been applied in studies on wall motion patterns for pacemakers[44] [45] and systolic function.[46] [47] [48] The system has some very strong features, including tracking of structures other than blood-tissue borders (user-defined positions); temporal and spatial coherence; and basic

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knowledge of LV anatomy and appearance. For research purposes, it has been shown to be a valuable tool, but at the moment it is mainly focused on frame-to-frame or multibeat analyses of wall motion patterns. For ED/ES analyses, it offers no extra benefits, as the ED/ES contours need to be defined manually. Population Model-Based Method: Active Appearance Models Great promise is held by a new class of techniques called Active Appearance Models (AAMs). These techniques were originally developed by Cootes and coworkers[49] [50] for facial recognition and medical image analysis, as an extension of the active shape model (ASM[51] [52] [53] ) approach. We have recently applied AAMs to magnetic resonance imaging [54] and echocardiography [55] with very promising results. These techniques derive the typical shape and appearance of an echocardiogram from a large 153

Figure 7-6 Echo-CMS semiautomated border detection procedure. A, Electrocardiogram (ECG) and original images; B, manual drawing of two contours and inspection of markers; C, generation of pose models (landmarks); D, generation of shape models; E, generation of profile models (match patterns); F, automatically detected contours. Figure 7-7 Echo-CMS dynamic programming border detection. A, Original image; B, image with landmarks and shape model; C, scan value matrix (left), cost value matrix (middle), and detected path (right); D, image with detected contour.

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Figure 7-8 Active appearance model: average four-chamber images of left ventricle from 65 patients, at different moments in the cardiac phase. A, End-diastole; B, mid-systole; C, end-systole; D, end of rapid filling; E, start of atrial filling.

set of example images with expert-drawn contours. Principal Component Analysis (PCA) on a point distribution model extracts the average organ shape and the principal variations (so called eigenvariations) of shape. By

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warping all examples to the average shape, an average image (Fig. 7-8) and principal image variations (Fig. 7-9) can be found. By applying another PCA, simultaneous shape and intensity, eigenvariations are modeled in an Appearance Model. Such an appearance model can synthetically generate "probable" echocardiographic images similar to the variations shown in Figure 7-9 . By deforming the model Figure 7-9 (color plate.) Active appearance model eigenvariations: Top to bottom: eigenvariations 1 to 4 of four-chamber left ventricle at end-diastole. Left to right: average minus 3 standard deviations, average, average plus 3 standard deviations. Note the simultaneous shape and intensity variations.

along the characteristic model eigenvariations, using a gradient descent minimization of the difference between the synthetic and the real image, the desired structure can be found (Fig. 7-10) . This can be done fast and fully automatically with good results. This technique has some significant advantages: it models both average organ shape and all variations over a population of examples; it models the complete organ Figure 7-10 Active appearance model matching results on end-systolic left ventricular four-chamber image. A, Image with initial model; B, intermediate iteration; C, final matching result.

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appearance, including typical artifacts; it captures the expert's definition of proper border definition; it can model complex shapes (e.g., LV endocardium plus LV epicardium, right ventricle, valves); it is not limited to blood-tissue borders; and it is easily customizable for different types of images. Limitations of this technique are its dependence on the training data, the selected population of examples, and the quality of the expert contours.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Promise In the near future, serious improvements in the applicability of ABD can be expected. Some instrumental developments will have important effects, and the ABD methods themselves will improve. Impact of Instrumental Developments Harmonic Imaging

Any technical measure that improves visual image quality is likely to improve ABD as well. This is certainly true for harmonic imaging. Originally intended to be used in combination with contrast, harmonic imaging has been shown to improve endocardial visualization in twodimensional echocardiography[56] without contrast as well.[30] It has also been shown to improve endocardial tracking by AQ as rated visually,[30] and by correlating AQ EF measurements to x-ray ventriculography.[31] AQ with harmonic imaging still underestimates absolute volumes and can be technically difficult to perform. Note that harmonic imaging will not improve image quality in all cases, and that it sometimes results in a very grainy image. ABD techniques that rely on image texture may be influenced, but others should certainly benefit from harmonic imaging. Tissue Doppler, Strain Imaging

Tissue Doppler imaging can supply real-time information on tissue velocity in the direction of the ultrasound beam, and thus in itself is a method for quantification of motion.[57] [58] [59] [60] The derived strain rate imaging[61] and strain imaging [62] [63] techniques provide an estimate of local tissue strain, but their practical value remains to be established. For certain purposes, this may become an alternative to border motion detection approaches, but the one-dimensionality of the measurement limits its use considerably. Tissue Doppler information could also well be included in ABD techniques, as it provides clues both on presence and local speed of tissue. ABD might

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supply additional (transversal) motion information. Three-Dimensional and Four-Dimensional Ultrasonography

In principle, three-dimensional image acquisition may provide superior input data for ABD. Border positions can be detected more reliably if information from neighboring slices can be used: spatial continuity, like temporal continuity, may provide additional clues in difficult-to-interpret cases. Furthermore, real volumes can be calculated from three-dimensional data instead of monoplane or biplane estimates. However, the triggered acquisition of such image sets may introduce motion artifacts. Threedimensional smoothing and cut-plane interpolations may also influence border positions. This modality will probably benefit most from an inherently three-dimensional or four-dimensional model-based detection technique. Momentarily, real-time three-dimensional ultrasonography (Volumetrics, Durham, NC) is becoming available[64] [65] this eliminates triggering problems and motion artifacts, but image quality is still limited. With improvement of image quality, real-time 3D echocardiography may become an important substrate for ABD. Contrast

Ultrasonographic contrast agents can be used for luminal opacification to improve visualization of the endocardial border, or for myocardial opacification. Contrary to what is sometimes suggested,[66] it is unlikely that contrast will directly enhance ABD. Although lumen opacification may boost the visual interpretation, application of contrast still has many pitfalls. The transient nature of the opacification, incomplete or inhomogeneous filling of the cavity, shadowing, and local destruction of microbubbles (causing mixing of "white" and "black" blood), especially, make it hard to model the lumen appearance for any detection method. Next-generation contrast agents or special-purpose border detection techniques may provide solutions. Digital Image Storage and Radiofrequency Data

Digital image storage and communication will have a positive effect on general image quality and the availability of additional information (calibration, time, patient age and sex, body surface area, physiologic signals, protocol stages, views) can be a highly important source of a priori information for ABD techniques. As soon as raw radiofrequency information becomes available via digital storage, digital postprocessing of

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these data may provide superior input for ABD methods, effectively combining the strengths of AQ with those of high-level model-based approaches. Developments in Image Processing Model-Based Techniques

As seen in the section on Active Appearance Models, the biggest promises come from new developments in higher-level image processing. These techniques can model the complete appearance of a cardiac echo scene, 156

including patient variabilities. This approach may allow more natural solutions than older, edge-based or geometric model-based approaches. Because both shape variations over a large patient set and image appearance variations can be modeled, these techniques may handle typical artifacts, locally differing edge patterns, and other problems while restricting themselves to probable shapes. Furthermore, it seems possible to separate these models in patient-specific, view-specific, and pathologyspecific parts,[67] allowing more precise and flexible models and opening views to automated classification. The next-generation ABD technique for ultrasonography may well emerge from this family. Intelligent Systems

At the interpretation level, we enter the domain of artificial intelligence. Work in this field, especially in conjunction with image interpretation, is still in its infancy. Many high-level interpretation problems will need techniques from the field of artificial intelligence to be solved: formal reasoning from rule-based expert knowledge; generating multiple hypotheses with measures of confidence; reasoning with pathologic or congenital conditions during detection; checking overall consistency of an interpretation and taking action to resolve conflicts; opportunistically choosing an optimal detection strategy for the image data presented; and learning from operator corrections and actions. Ultimately, such developments may lead to an intelligent "automated image interpretation assistant" for echocardiographers.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Automated border detection for ultrasonography is still undergoing development. Few clinically applicable systems exist, and automation is limited. Positive expectations exist for the future. On the instrumental side, new opportunities will emerge from computer and ultrasonographic hardware improvements, availability of digital images and of raw radiofrequency information, and the perfection of techniques such as harmonic imaging, tissue Doppler imaging, real-time three-dimensional echocardiography, and maybe contrast echocardiography. In the field of ABD, improvements will result from several new technologies at the higher hierarchical levels (especially better three- and four-dimensional geometric modeling, anatomic scene descriptions, and modeling of anatomic interpatient variability and pathologic conditions) and techniques from artificial intelligence.

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References 1. Foster E, Cahalan MK: The search for intelligent quantitation in echocardiography:

"Eyeball," "trackball" and beyond. J Am Coll Cardiol 1993;22:848. 2. Hoffman R, Lethen H, Marwick TH, et al: Analysis of interinstitutional observer

agreement in interpretation of dobutamine stress echocardiograms. J Am Coll Cardiol 1996;27:330. 3. Feigenbaum H: Instrumentation. In Echocardiography. Philadelphia, Lea & Febiger,

1986, p 1. 4. Geiser EA: Echocardiography: Physics and instrumentation. In Skorton DJ,

Schelbert HR, Wolf GL, Brundage BH (eds): Marcus Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1996, p 273. 5. Weyman AE: Physical principles of ultrasound. In Weyman AE (ed): Principles and

Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 3. 6. Weyman AE: Cross-sectional scanning: Technical principles and instrumentation. In

Weyman AE (ed): Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 29. 7. Kennedy TE, Nissen SE, Simon R, et al: Digital Cardiac Imaging in the 21st

Century: A Primer. Bethesda, Md, American College of Cardiology, Cardiac and Vascular Information Working Group, 1997. 8. DICOM Committee: Digital Imaging and Communications in Medicine (DICOM),

1999 ed. Rosslyn, Va, National Electrical Manufacturers Association, 1999. 9. Thomas JD: The DICOM image formatting standard: What it means for

echocardiographers. J Am Soc Echocardiogr 1995;8:319.

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Pagina 2 di 9

10. Waitz AS: An echocardiographer's guide to determining whether DICOM disk

interchange can be achieved between two systems. In Kennedy TE, Nissen SE, Simon R, et al (eds): Digital Cardiac Imaging in the 21st Century: A Primer. Bethesda, Md, American College of Cardiology, Cardiac and Vascular Information Working Group, 1997, p 138. 11. Anonymous: Digital Storage and Retrieval (DSR) File Format Specification V 0.18

(Report Nr. 77450-99000). Andover, Mass, Agilent Technologies, Healthcare Solutions Group, Imaging Systems Division (ISY), 2000. 12. Bono J: Data Exchange File Format (Report Nr. 9062-0085-00 rev B). Bothell,

Wash, ATL Ultrasound, 1992. 13. Karson TH, Chandra S, Morehead AJ, et al.: JPEG compression of digital

echocardiographic images: Impact on image quality. J Am Soc Echocardiogr 1995;8:306. 14. Castleman KR: Digital image processing. Englewood Cliffs, NJ, Prentice-Hall,

1996. 15. Sonka M, Hlavac V, Boyle R: Image Processing, Analysis and Machine Vision,

2nd ed. Pacific Grove, Calif, International Thomson-Brooks/Cole, 1999. 16. Collins SM, Skorton DJ: Cardiac Imaging and Image Processing. New York,

McGraw-Hill, 1986. 17. Skorton DJ, Schelbert HR, Wolf GL, Brundage BH: Marcus Cardiac Imaging: A

Companion to Braunwald's Heart Disease, 2nd ed. Philadelphia, WB Saunders, 1996. 18. Sonka M, Fitzpatrick JM: Handbook of Medical Imaging, vol 2. Medical Image

Processing and Analysis. Bellingham, Wash, SPIE—The International Society for Optical Engineering, 2000. 19. Thomas JD: Digital image processing. In Weyman AE (ed): Principles and Practice

of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 56. 20. Vuille C, Weyman AE: Left ventricle I: General considerations, assessment of

chamber size and function. In Weyman AE (ed): Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 575. 21. Nidorf SM, Weyman AE: Left ventricle II: quantification of segmental

dysfunction. In Weyman AE (ed): Principles and Practice of Echocardiography.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 3 di 9

Philadelphia, Lea & Febiger, 1994. 22. Sher DB, Revankar S, Rosenthal S: Computer methods in quantitation of cardiac

wall parameters from two dimensional echocardiograms: A survey. Int J Card Imaging 1992;8:11. 23. Bosch JG, van Burken G, Nijland F, Reiber JHC: Overview of automated quantitation techniques in 2D echocardiography. In Reiber JHC, van der Wall EE (eds): What's New in Cardiovascular Imaging. Dordrecht, The Netherlands, Kluwer, 1998, p 363. 24. Sheehan F, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M,

Fitzpatrick JM (eds): Handbook of Medical Imaging, vol 2. Medical Image Processing and Analysis. Bellingham, WA, SPIE—The International Society for Optical Engineering, 2000, p 609. 25. Geiser EA: Edge detection and wall motion analysis. In Chambers J, Monaghan M

(eds): Echocardiography: An international review. Oxford, Oxford University Press, 1993, p 71. 157

26. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular

function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313. 27. Marcus R, Bednarz J, Coulden R, et al: Ultrasonic backscatter system for

automated on-line endocardial boundary detection: Evaluation by ultrafast computed tomography. J Am Coll Cardiol 1993;22:839. 28. Bosch JG, Reiber JH, van Burken G, et al: Automated contour detection and

acoustic quantification. Eur Heart J 1995;16 (Suppl J):35. 29. Chandra S, Garcia MJ, Morehead AJ, et al: Spatiotemporal Fourier filtration of

acoustic quantification endocardial border using carthesian vs. polar coordinate system. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 17. 30. Spencer KT, Bednarz J, Rafter PG, et al: Use of harmonic imaging without echocardiographic contrast to improve two-dimensional image quality. Am J Cardiol 1998;82:794.

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Pagina 4 di 9

31. Tsujita-Kuroda Y, Zhang G, Sumita Y, et al: Validity and reproducibility of echocardiographic measurement of left ventricular ejection fraction by Acoustic Quantification with Tissue Harmonic Imaging technique. J Am Soc Echocardiogr 2000;13:300. 32. Lang RM, Vignon P, Weinert L, et al: Echocardiographic quantification of regional

left ventricular wall motion with color kinesis. Circulation 1996;93:1877. 33. Mor-Avi V, Vignon P, Koch R, et al: Segmental analysis of color kinesis images:

New method for quantification of the magnitude and timing of endocardial motion during left ventricular systole and diastole. Circulation 1997;95:2082. 34. Vignon P, MorAvi V, Weinert L, et al: Quantitative evaluation of global and

regional left ventricular diastolic function with color kinesis. Circulation 1998;97:1053. 35. Koch R, Lang RM, Garcia MJ, et al: Objective evaluation of regional left

ventricular wall motion during dobutamine stress echocardiographic studies using segmental analysis of color kinesis images. J Am Coll Cardiol 1999;34:409. 36. Helbing WA, Bosch HG, Maliepaard C, et al: On-line automated border detection

for echocardiographic quantification of right ventricular size and function in children. Pediatr Cardiol 1997;18:261. 37. Gorcsan J, Romand JA, Mandarino WA, et al: Assessment of left ventricular

performance by on-line pressure-area relations using echocardiographic automated border detection. J Am Coll Cardiol 1994;23:242. 38. Carey CF, Mor-Avi V, Koch R, et al: Effects of inotropic stimulation on segmental

left ventricular relaxation quantified by color kinesis. Am J Cardiol 2000;85:1476. 39. Mor-Avi V, Spencer KT, Lang RM: Acoustic quantification today and its future

horizons. Echocardiography 1999;16:85. 40. Geiser EA, Wilson DC, Wang DX, et al: Autonomous epicardial and endocardial

boundary detection in echocardiographic short-axis images. J Am Soc Echocardiogr 1998;11:338. 41. Geiser EA, Wilson DC: Automatic center point determination in 2-dimensional

short-axis echocardiographic images. Pattern Recognition 1992;25:893. 42. Bosch JG, Savalle LH, van Burken G, Reiber JHC: Evaluation of a semiautomatic

contour detection approach in sequences of short-axis two-dimensional

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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Pagina 5 di 9

echocardiographic images. J Am Soc Echocardiogr 1995;8:810. 43. Bosch JG, van Burken G, Reiber JHC: Automatic frame-to-frame contour

detection in echocardiograms using motion estimation. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 351. 44. Auricchio A, Ghanem A, Groethus F, et al: Echocardiographic analysis of left ventricular contraction patterns in left bundle branch block and congestive heart failure [abstract]. J Cardiac Failure 1999;5(Suppl 1):3. 45. Breithardt OA, Kramer A, Schiffgens B, et al: Characteristics of left ventricular

contraction patterns and acute changes with multisite pacing in patients with heart failure as assessed by echocardiographic semiautomatic contour detection [abstract]. Eur Heart J 2000;21:351. 46. Fry SJ, Hunziker PR, Bosch HG, et al: Automated echocardiographic confirmation

of regional wall motion abnormalities: Quantitation of continuous LV volume [abstract]. J Am Coll Cardiol 1998;31:56A. 47. Hunziker PR, Schöb L, Lefkovits M, et al: Automatic border detection in

dobutamine stress echo: How do normal and ischaemic segments behave objectively and quantitatively? [abstract]. Eur Heart J 1999;20:618. 48. Hunziker PR, Yuan D, Schöb L, et al: Objective and quantitative stress echo

analysis to diagnose coronary disease using model-based image processing [abstract]. J Am Coll Cardiol 2000;35:413A. 49. Cootes TF, Edwards GJ, Taylor CJ: Active Appearance Models. In Proceedings,

European Conference Computer Vision. Berlin, Springer, 1998;2:484. 50. Edwards GJ, Taylor CJ, Cootes TF: Interpreting face images using Active

Appearance Models. In Proceedings of the 3rd International Conference on Face and Gesture Recognition. Nara, Japan, IEEE Computer Society Press, 1998, p 300. 51. Cootes TF, Hill A, Taylor CJ, Haslam J: Use of active shape models for locating

structures in medical images. Image Vision Computing 1994;12:355. 52. Cootes TF, Taylor CJ, Cooper DH, Graham J: Active shape models: Their training

and application. Comp Vision Image Understanding 1995;61:38. 53. Parker AD, Hill A, Taylor CJ, et al: Application of point distribution models to the

automated analysis of echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 25.

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Pagina 6 di 9

54. Mitchell SC, Lelieveldt BPF, van der Geest RJ, et al: Segmentation of cardiac MR images: An active appearance model approach. In Proceedings, SPIE Medical Imaging 2000, Image Processing. Bellingham, Wash, SPIE—The International Optical Engineering Society, 2000;3979:224. 55. Bosch JG, Mitchell SC, Lelieveldt BPF, et al: Feasibility of fully automated border

detection on stress echocardiograms by Active Appearance Models [abstract]. Eur Heart J 2000;21:11. 56. van Camp G, Franken PR, Schoors D, et al: Impact of second harmonic imaging on

the determination of the global and regional left ventricular function by 2D echocardiography: A comparison with MIBI gated SPECT. Eur J Echocardiogr 2000;1:122. 57. Isaaz K: What are we actually measuring by Doppler tissue imaging? J Am Coll

Cardiol 2000;36:897. 58. Hunziker PR, Picard MH, Jander N, et al: Regional wall motion assessment in

stress echocardiography by tissue Doppler bull's-eyes. J Am Soc Echocardiogr 1999;12:196. 59. Derumeaux G, Ovize M, Loufoua J, et al: Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging: Characterization of normal, ischemic, and stunned myocardium. Circulation 2000;101:1390. 60. Pasquet A, Armstrong G, Beachler L, et al: Use of segmental tissue Doppler

velocity to quantitate exercise echocardiography. J Am Soc Echocardiogr 1999;12:901. 61. Heimdal A, Stoylen A, Torp H, Skjaerpe T: Real-time strain rate imaging of the

left ventricle by ultrasound. J Am Soc Echocardiogr 1998;11:1013. 62. Armstrong G, Pasquet A, Fukamachi K, et al: Use of peak systolic strain as an

index of regional left ventricular function: Comparison with tissue Doppler velocity during dobutamine stress and myocardial ischemia. J Am Soc Echocardiogr 2000;13:731. 63. Urheim S, Edvardsen T, Torp H, et al: Myocardial strain by Doppler

echocardiography: Validation of a new method to quantify regional myocardial function. Circulation 2000;102:1158. 64. Qin JJX, Jones M, Shiota T, et al: New digital measurement methods for left

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 7 di 9

ventricular volume using real-time three-dimensional echocardiography: Comparison with electromagnetic flow method and magnetic resonance imaging. Eur J Echocardiogr 2000;1:96. 65. Takuma S, Zwas DR, Fard A, et al: Real-time, 3-dimensional echocardiography

acquires all standard 2-dimensional images from 2 volume sets: A clinical demonstration in 45 patients. J Am Soc Echocardiogr 1999;12:1. 66. Kamp O, Sieswerda GT, Visser CA: State-of-the-art: Stress echocardiography

entering the next millennium. In Reiber JHC, van der Wall EE (eds): What's new in cardiovascular imaging. Dordrecht, The Netherlands, Kluwer, 1998, p 351. 67. Costen N, Cootes TF, Edwards GJ, Taylor CJ: Simultaneous extraction of

functional face subspaces. In Proceedings, IEEE Computer Vision & Pattern Recognition. Los Alamitos, Calif, IEEE Computer Society Press, 1999, p 492. 158

68. Grube E, Mathers F, Backs B, Luederitz B: Automatische und halbautomatische

Konturfindung des linken Ventrikels im zweidimensionalen Echokardiogramm: Invitro Untersuchungen an formalinfixierten Schweineherzen. Z Kardiol 1985;74:15. 69. Ezekiel A, Garcia EV, Areeda JS, Corday SR: Automatic and intelligent left

ventricular contour detection from two-dimensional echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1985, p 261. 70. Klingler JW, Vaughan CL, Fraker TD, Andrews LT: Segmentation of

echocardiographic images using mathematical morphology. IEEE Trans Biomed Eng 1988;35:925. 71. Montilla G, Barrios V, Roux C, et al: Border detection in echocardiography images

using texture analysis. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 643. 72. Setarehdan SK, Soraghan JJ: Automatic left ventricular feature extraction and

visualisation from echocardiographic images. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1996, p 9. 73. Verlande M, Flachskampf FA, Schneider W, et al: 3D reconstruction of the beating

left ventricle and mitral valve based on multiplanar TEE. In Proceedings, Computers

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 8 di 9

in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1991, p 285. 74. Han CY, Lin KW, Wee WG, et al: Knowledge-based image analysis for automated

boundary extraction of transesophageal echocardiographic left-ventricular images. IEEE Trans Med Imaging 1991;10:602. 75. Hozumi T, Yoshida K, Yoshioka H, et al: Echocardiographic estimation of left ventricular cavity area with a newly developed automated contour tracking method. J Am Soc Echocardiogr 1997;10:822. 76. Monteiro AP, Marques de Sa JP, Abreu-Lima C: Automatic detection of

echocardiographic LV-contours: A new image enhancement and sequential tracking method. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1988, p 453. 77. Chu CH, Delp EJ, Buda AJ: Detecting left ventricular endocardial and epicardial

boundaries by digital two-dimensional echocardiography. IEEE Trans Med Imaging 1988;7:81. 78. Feng J, Lin W-C, Chen C-T: Epicardial boundary detection using fuzzy reasoning.

IEEE Trans Med Imaging 1991;10:187. 79. Chalana V, Linker DT, Haynor DR, Kim Y: A multiple active contour model for

cardiac boundary detection on echocardiographic sequences. IEEE Trans Med Imaging 1996;15:290. 80. Dong L, Pelle G, Brun P, Unser M: Model-based boundary detection in

echocardiography using dynamic programming technique. In Proceedings, SPIE Medical Imaging V. Bellingham, Wash, SPIE-The International Society for Optical Engineering, 1991, p 178. 81. Friedland N, Adam D: Echocardiographic myocardial edge detection using an

optimization protocol. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1989, p 379. 82. Belohlavek M, Manduca A, Behrenbeck T, et al: Image analysis using modified

self-organizing maps: Automated delineation of the left ventricular cavity in serial echocardiograms. In Proceedings of the 4th International Conference on Visualisation in Biomedical Computing, VBC '96. Berlin, Springer, 1996, p 247. 83. Detmer PR, Bashein G, Martin RW: Matched filter identification of left-ventricular

endocardial borders in transesophageal echocardiograms. IEEE Trans Med Imaging 1990;9:396.

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Pagina 9 di 9

84. Herlin IL, Nguyen C, Graffigne C: Stochastic segmentation of ultrasound images.

In Proceedings of the 11th IAPR International Conference on Pattern Recognition A: Computer Vision and Applications. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 289. 85. Dias JMB, Leitao JMN: Wall position and thickness estimation from sequences of

echocardiographic images. IEEE Trans Med Imaging 1996;15:25. 86. Gustavsson T, Molander S, Pascher R, et al: A model-based procedure for fully

automated boundary detection and 3D reconstruction from 2D echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 209. 87. Maes L, Delaere D, Suetens P, et al: Automated contour detection of the left

ventricle in short axis view and long axis view on 2D echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1990, p 603. 88. Cohen LD: Note on active contour models and balloons. CVGIP Image

Understanding 1991;53:211. 89. Coppini G, Poli R, Valli G: Recovery of the 3-D shape of the left ventricle from

echocardiographic images. IEEE Trans Med Imaging 1995;14:301. 90. Brotherton T, Pollard T, Simpson P, DeMaria A: Echocardiogram structure and

tissue classification using hierarchical fuzzy neural networks. In Proceedings, IEEE Conference on Acoustics, Speech, and Signal Processing. IEEE New York, Computer Society Press, 1994, p 573.

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159

Chapter 8 - Myocardial Contrast Echocardiography Methods, Analysis, and Applications Thomas R. Porter MD Danielle Noll MD Feng Xie MD

Background The use of hand-agitated saline as a source of ultrasonographic contrast was first described in 1968, based on the concept of creating a gas-blood interface for ultrasonic enhancement of blood within the heart. During the following years, bubbles from agitated saline as well as a variety of other substances were used as echocardiographic contrast agents. Because of the large size of the microbubbles, their use was restricted to right heart contrast, when administered via a peripheral vein. This application included the detection of congenital or acquired intracardiac shunts, assessment of right-sided valvular regurgitation, and diagnosis of complex congenital heart defects and pulmonary arteriovenous fistulas. Although color Doppler, echocardiography now provides an easy method of detecting shunts, agitated saline has remained helpful in other areas such as quantifying tricuspid regurgitant velocities. [1] In the past, use of ultrasonographic contrast agents for left-sided imaging, however, could be performed only by direct injection of bubbles into the left atrium or ventricle.

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Initial studies aimed at detecting myocardial contrast used microbubbles produced by hand agitation or solutions containing carbon dioxide gas. Because of the short duration of the contrast, these agents were given either into the aortic root or directly into the coronary artery.[2] [3] [4] [5] [6] Since these studies, however, significant developments have been made in how intravenous microbubbles can be used to study myocardial perfusion. The stimulus for these developments includes an improved understanding of coronary physiology in patients with coronary artery disease, advances in ultrasonographic imaging, and the development of microbubbles that reach the coronary microcirculation after intravenous injection. The purpose of this chapter is to first illustrate the methods used to create ultrasonographic contrast. Second, we examine how these methods have been used to quantify myocardial perfusion, risk area, infarct size, and collateral blood flow with myocardial contrast echocardiography. Finally, 160

Figure 8-1 Effect of incorporating gases with lower diffusivity and solubility into microbubbles. When microbubbles contain only room air (RA) or sulfur hexafluoride (SF), an intravenous injection produces no myocardial contrast compared with baseline (BL). When these microbubbles contain a gas with low diffusivity and solubility such as perfluoropropane (PESDA), intravenous injection produces bright myocardial contrast. (From Porter TR, Xie F, Kilzer K: J Am Soc Echocardiogr 1995;5:710–718.)

the clinical applications of contrast echocardiography are reviewed.

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Characteristics of Microbubbles Microbubbles have to meet numerous physical and chemical standards to reach the left ventricular cavity and myocardium following venous injection. The first requirement is size. Microbubbles of more than 8 µm diameter are filtered from the pulmonary circulation and will not reach the left ventricular cavity.[7] The scattering cross section of a microbubble is related to the sixth power of its radius, and thus the smaller bubbles that reach the left ventricle are less reflective than the bubbles filtered by the pulmonary circulation. To detect the comparatively weak echoes of the bubbles small enough for transpulmonary passage, imaging modalities have been developed that register the more "microbubble-specific" resonant frequencies. The resonant frequency of a microbubble is inversely related to its diameter.[8] Another problem arising with the small microbubble size requirement is surface tension. The internal pressure of gases within microbubbles is increased dramatically as the size of a microbubble decreases to less then 7 µm. Therefore, the gases within the microbubbles are at very high concentrations and rapidly diffuse into blood. This immediately reduces the size and hence the contrast effect, a limitation becoming most evident when attempts are made to obtain myocardial ultrasonographic contrast from an intravenous injection. The transit time required to reach the left ventricular cavity from an intravenous injection is greater than 5 seconds and, therefore, significant amounts of gas will have escaped from the microbubble at this point. Therefore, a second requirement for intravenous microbubbles is to have a method of preventing dissolution after exposure to blood. The gas composition is one of the most important factors for retention of microbubble size in circulation. First-generation contrast agents contained

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room air, which is 78% nitrogen. Since nitrogen rapidly diffuses, these microbubbles survived only seconds.[9] To overcome this problem, slowly diffusing, insoluble gases were incorporated into the microbubbles. This improved the duration of ultrasonographic contrast in blood and even achieved myocardial contrast from an intravenous injection.[10] As shown in Figure 8-1 , by incorporating higher molecular weight gases such as perfluoropropane (molecular weight 188 g/mol) into microbubbles instead of room air, the same intravenous dose of dextrose albumin–coated microbubbles can produce a significantly greater amount of myocardial contrast than the same dose of microbubbles containing room air.

161

A third requirement is safety. Perfluorocarbon-containing microbubbles have been shown to have minimal toxicity in humans. The most frequent side effects noticed with Optison, the first and until now only secondgeneration ultrasonographic contrast agent approved by the Food and Drug Administration (FDA), are headache (5.4%), nausea and vomiting (4.3%), warm sensation or flushing (3.6%), and dizziness (2.5%). [11]

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Ultrasonographic Imaging Techniques Although electromechanical sonication and fluorocarbon gases have rendered the microbubbles more stable, 163

their detection in the myocardium with echocardiographic equipment remained difficult with conventional imaging techniques. The invention of second harmonic imaging, intermittent imaging, harmonic power Doppler and, recently, pulse inversion Doppler and power modulation has dramatically enhanced the myocardial contrast produced from intravenously injected microbubbles. Second Harmonic and Intermittent Imaging Microbubbles in an ultrasonic field have the ability to scatter ultrasound not only linearly but also nonlinearly. At peak incident pressures (above 0.1 megapascals), the microbubbles respond in a nonlinear manner. This physical property is attributable to the fact that gas bubbles are compliant and react to insonification at diagnostic frequencies with compression and rarefaction, thus emitting radial oscillations. The magnitude of compression and rarefaction is not the same with each oscillation, and therefore both linear and nonlinear returning waves occur. [44] The nonlinear responses typically occur in harmonics and can be received and filtered by an appropriate echocardiography system. Since tissue and side lobes exhibit a significantly smaller nonlinear response to ultrasound (Fig. 8-3) , ultrasonic transducers that selectively receive the harmonic frequency produce a much better signal-to-noise ratio and more sensitive detection of microbubbles than conventional imaging.[45] Microbubbles are destroyed by ultrasound when it is transmitted at diagnostic intensities (mechanical indices >0.3). Destruction can be

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reduced by selecting one image out of every one to several cardiac cycles, triggered to the electrocardiogram. This has been referred to as intermittent imaging. When the intermittent ultrasound impulse is at a high intensity (above 0.9 mechanical index), there is a strong and brief nonlinear echo. This transient scattering process is the third mode of action microbubbles show in an ultrasonographic field in addition to linear and harmonic response to ultrasound waves.[46] [47] Interrupting the high-intensity ultrasound for a short period of time allows for replacement of microbubbles, which then produce contrast enhancement for the following (triggered) frame. When microbubbles are administered as a continuous infusion and the ultrasound pulsing interval is incrementally varied, the reappearance of bubbles in the myocardium permits the calculation of mean microbubble velocity and plateau (or peak) myocardial signal intensity.[48] Multiplying these two variables together, one can better estimate myocardial blood flow. Therefore, with a combination of second harmonic and so-called intermittent imaging, it has become possible to noninvasively examine myocardial perfusion in animals and humans using a wide variety of intravenous higher molecular weight microbubbles.[8] [49] [50] [51] [52] (Harmonic) Power Doppler Power Doppler images are based on the integrated power in the Doppler signal instead of its mean frequency Figure 8-3 Illustration of returning signal intensity (indicated by arrow length). Microbubbles have the greatest harmonic signal intensity, but myocardium also has a harmonic response. Fortunately, the side lobe (SL) artifacts have very little harmonic signal intensity and thus do not reduce the image quality of a harmonic image as they do in fundamental images. (From Porter TR: Harmonic ultrasound imaging during routine and contrast-enhance echocardiography. Cardiac Ultrasound Today 1998;4:121.)

shift, as used in conventional color Doppler.[53] The amplitude of the Doppler signal is related to the concentration of scatterers at a particular location. This amplitude is much greater in the presence of microbubbles when compared with the signal of red blood cells.[54] This Doppler signal is more sensitive but, more importantly, is not subject to aliasing and is independent of the angle of insonation. It is, however, subject to flash artifacts, which occur with movement of the heart. Combining power Doppler with intermittent harmonic imaging (harmonic power Doppler) can

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decrease these flash artifacts at the expense of real-time imaging. Harmonic power Doppler has been successfully employed in animal[55] and human myocardial perfusion studies, showing satisfactory concordance in the comparison between echocardiographic and 99m Tc-sestamibi single photon emission computed tomography (SPECT) stress imaging.[56] [57] Low Mechanical Index Imaging Accelerated Intermittent Imaging

As previously mentioned, microbubbles are destroyed when exposed to ultrasound at high power output. Although 164

interrupting the imaging process by taking triggered images helps keep a sufficient concentration of contrast agent in the myocardial capillaries, the dynamic character of the echocardiographic examination cannot be used with triggered or intermittent imaging. If the mechanical index is set low enough to prevent major bubble destruction, while still allowing the microbubbles to resonate, the image acquisition can be performed continuously (because of the higher frame-rate), and real-time data on both wall motion and perfusion can be obtained. This procedure, termed accelerated intermittent imaging, has proven to be extremely helpful, especially during stress echocardiography in humans.[58] [59] Pulse Inversion Doppler and Power Modulation

Another possibility for achieving real-time visualization of myocardial function and perfusion is the application of the recently developed pulse inversion technique. The intention of this new method is the separation of linear and nonlinear scattering using the radiofrequency domain. Alternately positive and negative pulses of identical amplitude are transmitted into the tissue, the sum signal of which is equal to 0 (Fig. 8-4) . The responses of linear scatterers to that kind of pulses, therefore, will be cancelled. On the other hand, the signal from nonlinear scatterers (which do not react to positive and negative pressures in the same way) will be unequal to 0 and can be registered as a bubble-specific response (see Fig. 84) .[60] Although pulse inversion is subject to motion artifacts, pulse inversion Doppler overcomes this by sending multiple pulses of alternating polarity into the myocardium. This allows one to visualize wall thickening and contrast enhancement simultaneously at very low mechanical indices

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(<0.2) while maintaining an excellent signal-to-noise ratio. Initial studies using this technique in humans have demonstrated brilliant myocardial opacification from very small bolus injections of intravenous Optison.[61] [62] Figure 8-4 A depiction of how pulse inversion technology is able to enhance the signal-to-noise ratio from microbubbles at a very low mechanical index (<0.3). By sending pulses of alternating polarity, tissue signals cancel. Microbubbles, however, exhibit a nonlinear response to ultrasound even at these low mechanical indices, and hence the returning signals do not cancel. The resulting returning signal is a pure nonlinear response with almost nonexistent background signal. (Courtesy of Advanced Technology Laboratories, Bothell, Wash.)

Power modulation is another technique that improves the signal-to-noise ratio at very low mechanical indices. This technique, developed by Agilent Technologies (Andover, Mass), is also a multipulse cancellation technique, only here the power of each pulse is varied. The low-power pulses create a linear response, whereas the slightly higher power pulse results in a linear response from tissue but a nonlinear response from bubbles (Fig. 8-5) . The linear responses from the two different pulses (the amplified low-power pulse and the slightly higher power pulse) can be subtracted from each other; the transducer then only sees the nonlinear behavior, which emanates exclusively from the microbubbles. Both pulse inversion Doppler and power modulation can be used at very low mechanical indices to assess myocardial contrast in real time with excellent spatial resolution at higher band-widths.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Application of Ultrasonographic Contrast Via different injection routes, ultrasonographic contrast agents have been used to study various clinical problems in the cardiac catheterization laboratory and operating room, and now in the noninvasive setting (Table 8-2) . Detecting Acute Ischemia/Risk Area With Intracoronary and Aortic Root Injection

Prior to the development of stabilized perfluorocarbon microbubble contrast agents, clinical studies aiming at myocardial perfusion assessment mostly involved administration of air-filled microbubbles in the coronary arteries or aortic root. Bolus injections of air-filled microbubbles have been used to assess infarct size. Since microbubbles only enter regions where capillary integrity is preserved, this approach results in a more direct assessment of viability than definition of the contractile reserve. In several animal and human investigations, intracoronary ultrasonographic contrast injections have successfully delineated the area at risk after acute myocardial infarction, which is defined as the complete transmural extent of the perfusion bed supplied by an occluded coronary artery.[74] [75] [76] These studies have shown that area at risk measured with intracoronary contrast is superior to clinical, electrocardiographic, hemodynamic, or angiographic data in determining actual risk area. TABLE 8-2 -- Specific Clinical Applications of Myocardial Contrast Echocardiography Route of Injection Intracoronary

Clinical Parameters Measured Area at risk

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Perfusion bed size Infarct size Coronary flow reserve Collateral flow Area at risk Infarct size Coronary flow reserve Adequacy of cardioplegic delivery Adequacy of bypass graft perfusion Area at risk Infarct size No reflow Perfusion defect size Myocardial blood volume Myocardial blood flow Red blood cell velocity Subendocardial blood flow

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Figure 8-10 An example of the myocardial ultrasonographic contrast produced with perfluorocarbon-exposed sonicated dextrose albumin (PESDA). A, Short-axis view of the left ventricle in an open chest dog with a left circumflex occlusion before contrast injection. B, Myocardial contrast in the anteroseptal myocardium after intravenous contrast, also illustrating a large contrast defect in the posterolateral left ventricular myocardium. C, After reperfusion, an intravenous injection of this perfluorocarbon-exposed sonicated dextrose albumin produces homogeneous contrast throughout the myocardium. With Intravenous Injection

As previously discussed, intravenous microbubbles encapsulating high molecular weight gases in combination with new imaging techniques have made the noninvasive assessment of myocardial perfusion with

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echocardiography possible. These techniques have already been employed in clinical investigations and extend the findings of contrast studies performed with intracoronary and aortic root injections of contrast material. In several animal experiments, the spatial distribution of hypoperfusion after coronary artery occlusion and reperfusion has been accurately quantified with intravenous myocardial contrast echocardiography (Fig. 810) .[41] [77] [78] [79] Perfusion defects delineated by ultrasonographic contrast were found to correlate well with the extent of wall motion abnormality in the corresponding myocardial segment and postmortem measurement of risk area.[77] Peak myocardial videointensity within the hypoperfused segment following bolus injection of microbubbles has correlated closely with radiolabeled microsphere-derived flow in the infarct area.[41] Continuous infusions of microbubbles have been employed to quantify reductions in myocardial blood flow using the destruction-replenishment techniques described previously.[48] Assessment of the Effect of Myocardial Revascularization Intracoronary and Aortic Root Application

Intracoronary and aortic root injections of air-containing microbubbles have been used to assess the outcome of coronary angioplasty in patients with critical coronary artery stenoses.[80] Mudra et al[81] demonstrated that the half-time of contrast washout from peak myocardial videointensity after intracoronary contrast decreased after successful angioplasty. In their study, this rate of contrast washout from the myocardium returned to abnormal values when restenosis occurred. With intracoronary injection of sonicated albumin, Porter et al[82] described an immediate improvement in antegrade coronary blood flow reserve in a majority of patients who underwent angiographically successful angioplasty. The degree of improvement in diameter stenosis by quantitative angiography correlated closely with the magnitude of improvement in the area under the time intensity curve after intracoronary papaverine injection. Other investigators have demonstrated a correlation between the pressure gradient across a coronary stenosis before and after angioplasty and the degree of improvement in peak myocardial contrast produced by intracoronary contrast.[83] Identification of patients with the "no-reflow" phenomenon has been another important clinical application for intracoronary ultrasonographic contrast. This phenomenon, described first in an animal setting by Kloner et al in 1974,[84] is characterized by a lack of recovery in microvascular

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perfusion although the occluded coronary artery is successfully reopened by angioplasty or thrombolysis. Ito et al[85] were the first to systematically examine myocardial perfusion with intracoronary microbubbles in patients with acute anteroseptal myocardial infarction immediately following restoration of antegrade flow in the left anterior descending artery. Using intracoronary sonicated radiographic contrast, they demonstrated that 23% of the patients had persistent contrast defects (i.e., no reflow) in the area at risk after recanalization. The long-term prognosis of these no-reflow patients was impaired, and there was significant deterioration in regional and global systolic function at follow-up. These findings have been confirmed by other investigators. Visualization of collateral myocardial blood flow before and after revascularization has been demonstrated with intracoronary contrast. In patients with occluded vessels, injection of ultrasonographic contrast material into adjacent coronary arteries can produce myocardial contrast enhancement in the perfusion bed subtended by the occluded vessel.[86] [87] This phenomenon is clinically relevant because it indicates viability of the perfusion bed subtended by the occluded coronary artery.[88] Sabia et al[89] demonstrated that revascularization of an occluded coronary artery after myocardial infarction improved function only when ultrasonographic contrast delivered into the 169

opposite coronary artery resulted in contrast enhancement to the perfusion bed of the occluded artery prior to revascularization.[90] The spatial extent of collateral blood flow as defined by contrast echocardiography correlated closely with improvement in regional function within the infarct zone. These observations suggest that intracoronary contrast echocardiography may be a valuable tool in determining whether revascularization procedures are indicated (Fig. 8-11) . When employed in the operation room during coronary bypass grafting, intracoronary and aortic root injections of ultrasonographic contrast agent have been useful in several aspects. The effectiveness of the saphenous vein graft has been determined by injection of air-filled microbubbles into the cross-clamped aortic root or directly into the graft.[91] [92] [93] Aortic root injections of microbubbles before cardiopulmonary bypass have also guided the sequence of bypassing.[94] The peak myocardial videointensity following intra-aortic contrast-enhanced cardioplegia injections has

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correlated with the eventual improvement in wall motion after bypass grafting.[91] [95] Retrograde (via the coronary sinus) and antegrade cardioplegic delivery have been compared by using myocardial contrast echocardiography. In these small studies, retrograde delivery was found to be superior in providing myocardial perfusion in certain cases.[96] Keller et al[96] investigated the possibility of quantifying myocardial blood flow in the arrested heart during open heart surgery and found that the washout of microbubbles was markedly prolonged during antegrade crystalloid cardioplegia, so that it was no longer correlated with tissue flow (Fig. 812) . The washout delay appeared to be due to albumin microbubble adherence to the venules, suggesting that endothelial damage is caused by the cardioplegic solution.[97] This microvasculature damage could be partly Figure 8-11 Changes in myocardial contrast after intracoronary injection of contrast in both the vessel being dilated (recipient vessel area) and the coronary artery providing angiographic collaterals to the vessel being dilated before and after successful angioplasty in six patients. As can be seen, the amount of recipient vessel area contrast enhanced by the artery supplying collateral flow decreases significantly in most patients immediately after angioplasty. PTCA, percutaneous transluminal coronary angioplasty. (From Grill HP, Brinker JA, Taube JC, et al: J Am Coll Cardiol 1990;16:1594.)

Figure 8-12 Different time intensity curves from the myocardium at the same flow rate demonstrating the effect of the cardioplegia-arrested heart on washout of contrast material. This is markedly different than the washout of contrast material from a beating heart. (From Keller MW, Kaul S, Spotnitz WD, et al: J Am Coll Cardiol 1990;16:1267.)

avoided when cardioplegia was mixed with blood. The greater the amount of blood in the cardioplegic solution, the higher was the observed microbubble transit rate. [98] With Intravenous Injection

By using second-generation contrast agents and intermittent nonlinear detection modalities, several investigators have recently succeeded in detecting the no-reflow phenomenon from intravenous administration of microbubbles in patients with acute myocardial infarction following revascularization. Lepper et al[99] studied myocardial contrast enhancement in patients with acute infarction undergoing angioplasty immediately before

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and 24 hours after recanalization using intravenous perfluorocarboncontaining microbubbles (NC100100; Nycomed Imaging AS) and intermittent harmonic imaging. An improvement of myocardial perfusion within 24 hours after intervention was predictive of functional recovery verified at 4-week follow-up. These investigators found that myocardial contrast imaging performed within an hour after revascularization is likely to lead to an underestimation of the ultimate infarct size. Actual infarct size in this time frame is best assessed following the use of a coronary vasodilatator. [100] Porter et al[101] used intravenous PESDA to identify patients with the noreflow phenomenon following successful restoration of antegrade flow after acute myocardial infarction (Fig. 8-13) . In concordance with previous studies using intracoronary contrast, lack of contrast enhancement in the perfusion bed of the infarct-related artery was predictive of a subsequent lack of recovery in both regional and global myocardial function. There are no human studies evaluating intravenous ultrasonographic contrast imaging for the detection of 170

Figure 8-13 Examples from two different patients who had anteroseptal and apical myocardial infarctions and similar wall motion score indexes following restoration of epicardial flow in the left anterior descending artery. The patient on the right had a persistent perfusion defect (no reflow, arrowheads), whereas the patient on the left demonstrated reflow in the same regions (arrowheads). MI, myocardial infarction. (From Porter TR, Li S, Oster R, Deligonul U: Am J Cardiol 1998;82:1173. Reprinted with permission from Excerpta Medica Inc.)

collateral vessels. However, Mills et al[102] studied the development of coronary collaterals flow in a canine model by examining the spatial and temporal course of a contrast defect following acute coronary occlusion using intravenous echocardiographic contrast and second harmonic intermittent imaging modalities. Thus, intravenous myocardial contrast echocardiography may be useful in assessing myocardial viability in the perfusion beds of patients with occluded coronary arteries. Detection of Coronary Artery Disease With Intracoronary and Aortic Root Contrast Injections

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Early attempts to determine perfusion defects in patients with coronary artery disease were restricted to the catheterization laboratory. Cheirif et al [25] described in a canine model a close correlation between dipyridamole contrast echocardiography and thallium-201 SPECT in assessing the extent of jeopardized myocardium when moderate to severe degrees of coronary stenosis were present. DeFilippi et al[103] compared intracoronary myocardial ultrasonographic contrast enhancement with wall motion responses to dobutamine (contractile reserve) in 35 patients with chronic coronary artery disease. They found that both contractile reserve and myocardial contrast enhancement were predictive of functional recovery in hypokinetic segments following revascularization. Contrast echocardiography with intracoronary Albunex was used to identify myocardial hibernation by Nagueh et al[104] in patients with stable coronary artery disease and left ventricular dysfunction. These investigators reported myocardial contrast echocardiography, thallium-201 SPECT, and dobutamine stress echocardiography to be of comparable sensitivity in predicting functional recovery after revascularization, but specificity was highest with dobutamine stress echocardiography. With Intravenous Contrast Injections and Infusions

Until the last few years, radionuclide scintigraphy has been the diagnostic tool to address myocardial perfusion during stress testing. This method, especially when performed with 99m Tc rather than 201 Tl, provides high sensitivity in identifying patients with coronary artery disease. It is limited, however, by relatively poor spatial resolution and frequent attenuation artifacts. With intravenous perfluorocarbon contrast agents and nonlinear ultrasonographic techniques, detection of underperfused myocardial segments during stress echocardiography has become feasible (Fig. 8-14) . Using intravenous Optison and intermittent harmonic imaging, Kaul et al [105] described a 92% concordance between segmental perfusion scores by myocardial contrast echocardiography and 99m Tc-sestamibi SPECT at rest and during dipyridamole stress. Porter et al[52] likewise indicated a close correlation 171

Figure 8-14 (color plate.) Myocardial contrast produced from 0.3 mL

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intravenous injections of Optison at rest (left) and during dobutamine stress (right) echocardiography in three different patients with significant coronary artery disease in three different coronary artery territories. Ultrasonographic imaging is done with pulse inversion Doppler, and this results in bright myocardial opacification in normal regions at mechanical indexes of 0.2 or less. A, Inducible anteroseptal and apical defect; B, inducible inferior perfusion defect; C, inducible lateral wall contrast defect. All patients were found to have greater than 50% diameter narrowings at coronary angiography in the left anterior descending (A), right coronary artery (B), and left circumflex artery (C), respectively.

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between regional peak myocardial videointensity following intravenous PESDA and radionuclide tracer uptake during dipyridamole stress echocardiography performed with intermittent harmonic imaging. Most recently, Heinle et al[57] used an intravenous Optison infusion and harmonic power Doppler imaging at long pulsing intervals during adenosine stress testing to compare perfusion with 99m Tc-sestamibi SPECT in 123 patients with suspected coronary artery disease. There was an overall concordance between both techniques of 83%; concordance was higher in patients with no or multivessel coronary artery disease. Correlation was also dependent on which coronary territory was involved, with the best agreement occurring in the left anterior descending territory (81%). Agreement was not as good between the two techniques in the left circumflex (72%) or right coronary artery (76%) territories.[57] On a segmental basis, the highest concordance between techniques was in the midanterior septum (82%), whereas there was poor agreement in the basal lateral (51%) and posterolateral (59%) segments. This may be due to the fact that, even with continuous Figure 8-15 An example of an apical perfusion defect in the apical longaxis view (arrowheads) during dobutamine stress (bottom panels) using a continuous infusion of perfluorocarbon containing microbubbles. Under baseline conditions (top panels), no contrast defect was observed at incremental pulsing intervals. At peak dobutamine stress, an apical contrast defect was observed even at the longer 3000 msec pulsing interval. This patient had a totally occluded left anterior descending artery at angiography. DOB, dobutamine; PI, pulsing interval. (From Porter TR: Echocardiography 2000;17:92.)

infusion, assessment of the basal regions is often affected by attenuation. Nonetheless, use of a continuous infusion reduces attenuation artifacts and

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provides more homogeneous myocardial contrast opacification. It also may eventually allow us to clinically quantify myocardial blood flow (Fig. 815) . In patients with coronary artery disease, a noninvasive diagnostic option for the definition of occlusion degree would be particularly helpful. Animal stress echocardiographic studies involving continuous perfluorocarbon microbubble infusion and intermittent harmonic imaging have shown a strong correlation between the severity of a coronary stenosis and the severity of a replenishment contrast defect at peak dobutamine stress.[106] Low mechanical index imaging techniques have recently emerged as a much more practical method of detecting myocardial perfusion abnormalities during stress echocardiography.[58] Cwajg et al[59] used accelerated intermittent imaging and intravenous bolus injections of Optison and PESDA at rest and during dobutamine stress 173

Figure 8-16 (color plate.) An example of real-time myocardial contrast enhancement produced with an intravenous Optison injection (0.3 mL) in one patient at rest (top panels), during intermediate dose dobutamine at 70% predicted maximum heart rate (middle panels), and during peak infusion at more than 85% predicted maximum heart rate (bottom panels). Note that with low mechanical index pulse inversion Doppler echocardiography, myocardial contrast enhancement is seen throughout the cardiac cycle. Note that there was an inducible anteroseptal and apical perfusion defect during stress, which became evident at the intermediate dobutamine infusion stage. ED, end-diastole; ES, end-systole.

echocardiography in 45 patients with known or suspected coronary artery disease. In this study, the real-time assessment of perfusion improved the sensitivity of the test in detecting angiographically significant stenoses by more than 10%.[59] More recent phase II studies have demonstrated the incremental value of myocardial perfusion assessment using accelerated intermittent imaging during exercise testing. [107] With the advent of pulse inversion Doppler echocardiography, low mechanical index imaging during stress echocardiography has higher spatial resolution and improved signalto-noise ratio (Fig. 8-16) . Distribution of Transmural Myocardial Blood Flow Because of the high spatial resolution of ultrasonographic imaging, several investigators have demonstrated differences in the degree of

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echocardiographic contrast produced by an intracoronary or aortic root injection between the subendocardial and subepicardial layers of myocardium. Animal studies even demonstrated after an intracoronary injection of a monosaccharide-based contrast agent (SHU-454) that differences in the transmural distribution of contrast could be detected at different times in the cardiac cycle.[107] Lim et al[108] demonstrated with an intracoronary injection of hand-agitated contrast material in humans that there was a lower subendocardial contrast intensity during pacing in regions supplied by a critical coronary stenosis. Although these findings in humans are promising, subsequent animal studies have not been able to confirm that intracoronary or aortic root injections of ultrasonographic contrast agent can distinguish subendocardial from subepicardial blood flow.[90] These investigators have shown that transmural attenuation of the myocardium caused by the contrast agent creates a false impression of relative decreases in subendocardial contrast. In addition, there are other limitations involved in using ultrasonographic contrast to define transmural differences in ultrasonographic contrast, such as (1) the nonspecific scattering properties of microbubbles, (2) the signalto-noise problems that occur even with epicardial imaging in differentiating the subendocardium from subepicardium, and (3) interference from scattering of microbubbles within the arterioles and venules. These same investigators, however, have demonstrated that the quantitative assessment of myocardial blood flow that can be achieved with a continuous intravenous infusion of microbubbles may also be able to delineate transmural differences. [109] In an open chest canine study, only the endocardial-to-epicardial ratio of the product of the initial contrast replenishment slope and plateau myocardial signal intensity correlated with radiolabeled 174

microsphere measurements, whereas transmural measurements of myocardial blood volume did not.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Other Intravenous Applications of Microbubbles Improved Endocardial Border Delineation Several different intravenous ultrasonographic contrast agents have demonstrated their ability to improve the diagnostic value of echocardiographic examinations in patients with suboptimal imaging conditions. In routine ultrasonographic examinations of patients with poor echocardiographic windows, contrast enhancement of the left ventricular cavity provides better delineation of the endocardial border. Clinically, this could give more information regarding regional and global systolic function that could not be assessed with routine echocardiography. Tissue harmonic imaging by itself has significantly improved endocardial border, often eliminating the need for intravenous ultrasonographic contrast agents filled with room air.[110] During the last few years, studies have shown that intravenous perfluorocarbon-containing microbubbles, because of their consistent left ventricular opacification, have improved border definition in the left ventricle of patients with suboptimal tissue harmonic images (Fig. 8-17) . Figure 8-17 An example of how intravenous perfluorocarbon microbubbles can improve endocardial delineation at end-diastole (DIAS) and end-systole (SYS) when compared with harmonic imaging above in a technically difficult patient. With the addition of intravenous contrast, the previously poorly delineated borders are now well visualized throughout the cardiac cycle. AC, after contrast; BC, before contrast. (From Porter TR: Echocardiography 2000;17:92.)

Optison proved its superiority over Albunex in a multicenter study that included 200 patients with suboptimal baseline pictures.[111] In this trial, full ventricular opacification could be achieved in 87% of the patients using the maximum intravenous Optison dose (5 mL), but only in 36% with optimal Albunex dosing (0.22 mL/kg). In patients with an echocardiogram that was

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nondiagnostic because of poor images, the use of Optison resulted in diagnostic quality images in 74% of all cases, whereas the use of Albunex converted only 26% of poor-quality images to images of diagnostic value. Although the use of Optison increases the costs for routine transthoracic echocardiograms, substantial cost savings could still be made in the examination of patients with poor baseline harmonic image quality, because it would prevent the need for additional diagnostic studies in these situations. [112] Reilly et al[113] recently studied the effect of intravenous Optison injections in harmonic transthoracic echocardiography in the intensive care unit. Their results indicated a significant increase in interpreter confidence in evaluating myocardial segments that could not be analyzed without contrast application. Furthermore, the ability to estimate left ventricular ejection fraction was clearly improved with Optison. To accurately detect wall motion abnormalities during stress echocardiography, clear definition of endocardial borders is of particular importance. Several first-generation ultrasonographic contrast agents such as Albunex, 175

Levovist, and BY 963 have already been studied in pharmacologic and exercise stress tests, and all of the trials described better overall image quality at peak stress with these intravenous agents as compared with standard imaging.[114] [115] [116] [117] [118] [119] Contrast enhancement was especially helpful in interpretation of anterior and lateral wall segments.[119] Malhotra et al[120] most recently compared stress echocardiograms performed with both fundamental and harmonic imaging modalities with and without intravenous Optison contrast in 200 patients. They reported that the combination of harmonic ultrasonography with Optison resulted in the most consistent endocardial border delineation, which significantly exceeded the quality of either fundamental contrast imaging or tissue harmonic imaging alone. Interobserver agreement with Optison and harmonic imaging in this study was 95%. Unfortunately, in none of these studies has there been an analysis of whether improving endocardial border definition affects the sensitivity or specificity of the test when compared to radionuclide imaging or quantitative angiography. Contrast-induced homogeneous opacification of the left ventricular cavity

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could also assist physicians in detecting left ventricular thrombi or tumors [121] [122] and complications of acute myocardial infarction such as myocardial rupture and left ventricular pseudoaneurysm.[123] It has also been used during transesophageal echocardiography to delineate false and true lumen in patients with aortic dissection.[124] Doppler Enhancement Intravenous microbubbles affect Doppler recordings because the scatter from them is much greater than from red blood cells. Microbubbles therefore can increase the signal strength in a Doppler examination markedly, which may be helpful in patients with suboptimal imaging quality. Von Bibra et al[125] described a significant enhancement of spectral and color Doppler and an increase in the signal-to-noise ratio in the quantitative assessment of aortic stenosis, pulmonary venous flow, and mitral regurgitation by intravenous injection of Levovist. Transthoracic pulmonary venous flow velocities have been improved by intravenous contrast enhancement to the point that they are comparable to those obtained with transesophageal imaging. [126] Moreover, intravenous microbubble ultrasonographic contrast was successful in providing a clear spectral signal across stenotic aortic valves, in cases in which the echocardiogram would have been nondiagnostic without contrast enhancement.[127] The gradients determined using contrast-enhanced Doppler signals correlated well with catheterization calculations. [127] Okura et al[128] studied the effect of Albunex in 45 patients with prosthetic aortic valves. They found a significant improvement in transvalvular continuouswave Doppler signal intensity with intravenous Albunex, increasing the frequency of satisfactory Doppler signals from 64% to 93% of patients. In patients with congestive heart failure, Kuecherer et al[129] used intravenous ultrasonographic contrast during exercise to evaluate cardiac functional reserve. They reported close correlation between echocardiographic estimation of systolic pulmonary artery pressure and invasively measured values both at rest and during stress testing. Safety of Myocardial Contrast Echocardiography There are no investigations in large study populations concerning the safety of intra-aortic or intracoronary application of microbubbles. In smaller studies, there have been isolated reports of transient chest pain after intracoronary sonicated albumin.[28] In a study of 18 patients given injections of intracoronary Albunex (commercially available sonicated albumin), 1 mL injections had no effects on systolic or diastolic function.

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However, 2 mL injections did transiently alter diastolic function.[130] The effects of ultrasonographic contrast agents compare favorably with the effects of radiographic contrast agents that transiently affected both systolic and diastolic function. Stabilized gas-containing intravenous microbubbles contained by albumin or lipid shells disrupt during insonication and are also pressure sensitive. The gas that is emitted from the bubble is excreted via the lungs, whereas the components of the shell are metabolized by liver enzymes. Perfluorocarbon gases are not metabolized but only exhaled. The safety of intravenous contrast agents containing high molecular weight gases has been tested in both animals and humans. The results of these studies suggest that perfluorocarbon-exposed sonicated dextrose albumin,[12] Definity,[131] Optison,[132] SonoVue,[133] and NC100100[134] all produce no significant hemodynamic abnormalities or serious side effects. After repeated intravenous application of Albunex over several months in 12 patients, there was no evidence of an immune reaction, such as IgE or IgG antibodies, and there were no adverse effects on left and right heart hemodynamics.[135] Animal studies have demonstrated bioeffects resulting from the interaction between microbubbles, low-frequency ultrasound, and tissue. Although both hemolysis and platelet lysis have been described in animal studies, to date these effects have not been observed in the clinical setting.[136] [137] Therapeutic Application of Microbubbles and Ultrasound A number of studies indicate that ultrasound microbubbles not only enhance the diagnostic value of an echocardiographic examination, but may also be used for therapeutic purposes. Drug Delivery

The fact that microbubbles are destroyed by the ultrasound beam has led to the study of their potential role in depositing adherent drugs or genes to an "ultrasound-targeted" organ.[138] Skyba et al[139] studied the intravascular destruction of perfluorocarbon-containing microbubbles 176

and the bioeffects of this process in the isolated spinotrapezius muscle of rats. With just one sweep of a diagnostic ultrasound transducer (2.3 MHz), microbubble destruction was observed that caused local microvessel

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rupture. When the bubbles were mixed with colloidal particles, these particles were also "microinjected" into the interstitial space. The degree of microbubble destruction and resulting "drug delivery" was directly related to the mechanical index used.[140] Porter et al[141] demonstrated that perfluorocarbon-exposed sonicated dextrose albumin microbubbles bind large quantities of synthetic antisense oligonucleotides. These oligonucleotides are synthetic gene products that can be used to inhibit the translation of messenger RNA into proteins and enzymes that regulate pathologic processes such as neointimal hyperplasia following vascular injury. Their experiments indicated that external diagnostic ultrasound released the synthetic antisense into the insonified kidney if the antisense oligonucleotide was given intravenously bound to PESDA. In a recently published study, recombinant adenovirus containing β-galactosidase was attached to the surface of intravenously injected perfluorocarbon-containing albumin microbubbles and successfully targeted to the myocardium of rats by diagnostic ultrasound at a high mechanical index (1.5). Postmortem analysis showed β-galactosidase transgene expression in the myocardium after ultrasound antigene delivery, but no expression of the transgene in the control groups that had received Figure 8-18 (Figure Not Available) (color plate.) Echocardiographic delivery of microbubbles containing galactosidase (AdCMV-β-Gal). A, Short-axis view of rat heart reveals galactosidase staining 4 days after ultrasonic destruction of microbubbles carrying recombinant adenovirus containing β-galactosidase. B, Fast red stain of a 7 µm section from heart in A shows nuclear localization of galactosidase staining (× 20). C, Representative section from a control rat showing no galactosidase staining. D, Microscopic section from same control rat showing no galactosidase staining. (From Shohet RV, Chen S, Zhou Y-T, et al: Circulation 2000;101:1554, with permission.)

microbubbles alone, virus alone, or virus plus ultrasound (Fig. 8-18) (Figure Not Available) .[142] Targeted intramyocardial gene delivery has also been reported in vivo with lipid-encapsulated microbubbles. [143] Thrombolysis

Several investigators have examined the potential of high-energy ultrasound alone to dissolve thrombi in vitro as well as in an animal setting. Transcatheter ultrasound was able to reduce thrombus weight and possibly recanalize occluded femoral arteries.[144] Since this process involves cavitation, more recent investigations have focused on whether microbubbles could potentiate this phenomenon. When combined with intravenous perfluorocarbon microbubbles, low-

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intensity, high-frequency ultrasound significantly increased the thrombolytic effect of urokinase in vitro. Even more importantly, ultrasound plus perfluorocarbon-containing microbubbles alone proved to be equivalent to urokinase in degree of thrombus dissolution. Therefore, it appeared that ultrasound and microbubbles could produce a localized clot lysis similar to a fibrinolytic agent without a systemic lytic state.[145] Invasive clot dissolution with therapeutic ultrasound and PESDA alone has been successfully tested in animal experiments. In a study involving 10 rabbits, iliofemoral arteries received 177

Figure 8-19 (Figure Not Available) Case example of angiography of both iliofemoral arteries following thrombotic occlusion of the iliac arteries (A and B). The right iliac artery was treated with intravenous perfluorocarbon-exposed sonicated dextrose albumin (PESDA) and transcutaneous ultrasound, resulting in recanalization after 30 minutes of therapy (C). The control side, treated with PESDA alone, remained occluded (D). (From Birnbaum Y, Luo H, Nagai T, et al: Circulation 1998;97:130, with permission.)

transcutaneous ultrasound treatment on one side and no ultrasound treatment on the other after an acute artery thrombotic occlusion. PESDA was given intravenously. After ultrasound treatment, all arteries that had received PESDA and ultrasound were recanalized by angiography, but none of the arteries treated with PESDA alone were patent (Fig. 8-19) (Figure Not Available) . Ultrasound alone also was unable to recanalize any of the thrombosed vessels.[146] Although more investigation on this field is required, the combination of ultrasound and microbubbles may turn out to be a promising alternative to the established thrombolytic strategies because of its ability to localize treatment to just the desired area. Detecting Inflammation

According to several experimental studies, albumin microbubbles used for ultrasonographic contrast enhancement persist in the myocardium in regions undergoing ischemia followed by reperfusion. The reason for this prolonged persistence is not exactly known yet. There is evidence, however, that endothelial glycocalyx damage and the presence of inflammatory extracellular matrix increase microbubble adherence to vascular endothelium.[147] [148]

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Lindner et al[149] hypothesized that during the early inflammatory response after reperfusion, activated leukocytes adherent to the venular endothelial surface may bind microbubbles and therefore prolong their transit. Using tumor necrosis factor-α injection in an animal setting, they have shown that both lipid and albumin microbubbles attach to activated leukocytes. The binding of the albumin microbubbles was mediated by β2 -integrins while the interaction between leukocytes and lipid microbubbles involved the complement pathway.[149] In a subsequent investigation, the involved leukocytes were identified to be mostly neutrophils and monocytes. Lipid and albumin microbubbles were phagocytosed by these cells and remained acoustically active for up to 30 minutes. During this time, they responded to ultrasound and could be detected in vivo after microbubbles from the blood pool had already vanished (Fig. 8-20) (Figure Not Available) .[150]

These findings describe the potential of microbubbles to noninvasively assess inflammation and may even lead to a possibility for drug delivery to the affected organ system. Furthermore, since albumin-coated microbubbles adhere to sites where vascular endothelial damage occurs, 178

Figure 8-20 (Figure Not Available) Effects of single pulses of ultrasound (P1 through P4 ) at different peak negative acoustic pressures on phagocytosed albumin-coated microbubbles. Note that neutrophil cell membrane disruption and distortion occurred at higher peak negative pressures (- 1600 kPa). BL, baseline. (From Lindner JR, Dayton PA, Coggins MP, et al: Circulation 2000;102:531, with permission.)

this may be a method of targeting the delivery of drugs bound to the microbubble without ultrasound. For example, we have recently demonstrated that PESDA microbubbles can concentrate the delivery of the antisense to the c-myc protooncogene to balloon-injured sites in the coronary artery and thus prevent neointimal hyperplasia.[151]

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Summary The use of intravenous microbubbles for perfusion imaging is now a realtime reality. Future multicenter studies will demonstrate whether there is an incremental clinical benefit to examining myocardial perfusion during stress echocardiography and in acute coronary syndromes. Intravenous microbubbles also have a potential therapeutic role in the areas of targeted drug delivery, enhancing thrombolysis, and detecting inflammation.

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183

Chapter 9 - Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Roy W. Martin PhD

The purpose of this chapter is to provide insight into what happens when a beam of ultrasound is launched into the body. What are the factors that affect this interrogating energy? How does it interact with the tissue and return reflected information to us? What can contaminate this returned information? What influences the accuracy of the information, and how may we further use information that is present in the signal but has largely been ignored? The answers to these questions provide understanding of common problems encountered daily (such as imaging artifacts and concern about the accuracy of measurements we make from these images). Furthermore, they also provide understanding of methods that extend beyond conventional imaging, such as feature extraction, border detection, and tissue characterization. The thrust of this chapter is to provide insight into basic fundamentals and then to apply those fundamentals to aid in understanding some tissue characterization methods, the recent developments in harmonic imaging, and several measurement errors.

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Beam Patterns Ideally, we'd like to generate an infinitely narrow pencil beam of ultrasound that could be swept rapidly through the tissue, thereby interrogating all the regions of interest. Unfortunately, as we currently understand the physics of the problem, ultrasound energy doesn't allow this; instead of being narrow like laser beams, the beams are more like broad flashlight beams. Furthermore, the intensity is not uniform within and throughout the beam. This lack of a narrowness and uniformity leads to measurement errors and can contribute to artifacts. In addition, we would ideally like to be able to generate infinitely short pulses of ultrasound energy, but this is also only approximated in practice. Short pulses are easier to generate than narrow beams and therefore are not addressed in the chapter. Aperture The general term aperture refers to an opening through which radiation passes. In ultrasound transducers, aperture refers to the active surface of the transducer that emits or receives ultrasound waves. The behavior of these waves is similar to that of a plane wave passing through a hole that is the same size and shape as the active surface of the transducer; therefore, the use of the term has evolved. Several examples of commonly used apertures are shown in Figure 9-1 . With respect to the wavelength λ of the ultrasound, the size of the aperture of the ultrasound transducer is responsible for the overall beam pattern. The focusing and excitation patterns provide further modification to this general pattern. The wavelength of the sound is equal to the speed of sound c, in the media adjacent to the transducer divided by the ultrasound frequency f (i.e., λ = c/f). For example, because the average value of the speed of sound in tissue is 1540 m per second, then at 3 MHz, λ = 0.5 mm. Consider a circular aperture as shown in Figure 9-1A . If the radius of the aperture, a, is much less than the wavelength, the beam pattern is very

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broad, whereas if the aperture radius is much greater than the wavelength, the beam is narrower in the region referred to as the far field. In addition, other features of the beam patterns are influenced by the radius-towavelength size. A radius of approximately 10 times the wavelengths has been found to be a good compromise (i.e., a/λ = 10). The beam 184

Figure 9-1 Geometry of various apertures of transducers used in medical ultrasound. A, circular disc; B, square; C, rectangle; D, annular array; E, square array aperture; F, rectangular array aperture; G, annular aperture; H, small rectangular aperture. Note that D is composed of an assemblage of annular apertures such as G and that E and F are composed of sets of small rectangular apertures such as H.

patterns for three ultrasound frequencies at which this ratio is constantly maintained are shown in Figure 9-2 . [1] [2] The different patterns in the near field and far field of the transducer are seen in Figure 9-3A . Regions of increasing and decreasing pressure isocontours are present in the near field. This near-field effect is due to wavelets from various regions of the aperture arriving at different phases at several points in the near field. Consequently, these wavelets add and subtract depending on their relative Figure 9-2 Beam pattern (3 dB below the axial value) is shown for three circular apertures where a/λ = 9.7. The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). The ultrasound frequencies and radius of each aperture (from left to right) are 5, 3.5, and 2 MHz and 0.3, 0.43, and 0.75 cm, respectively. Note that the point along the z-direction where the beam is the most constricted for each aperture is known as its near-far field transition. Points closer to the aperture are in the near field, whereas further points are in the far field. (Data from Weyns A: Ultrasonics 1980;18:183–188.)

phase with respect to each other. In the far field, this phenomenon is not present because they are all of the same relative phase. In the transition region between the near field and the far field, the beam pattern becomes much narrower and there are no pressure fluctuations because of little difference in the phase of arriving wavelets. The distance at which this transition occurs (the extent of the near field) can be calculated easily for a

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disc transducer[3] [4] as near-field distance = a2 λ. In the far field the beam pattern increases progressively with distance because of the uniform spreading of the propagating energy. The excitation of the transducer with a short (instead of a continuous) tone burst reduces the complexity of the pattern in the near held (see Fig. 9-3B) . A common method of increasing the resolution in a portion of the imaging region is to introduce focusing into the transducer. The modification of a flat disc aperture to a curved aperture is illustrated in Figure 9-3C .[2] [5] The effect is like "pulling" the center of the flat aperture to the left, which also pulls the transition of the near field to far field to the left while decreasing the diameter of the beam in this region. A further effect is increasing beam divergence in the far field. The more the aperture is "pulled" to the left, the sharper the focusing becomes (i.e., the narrower the beam, the closer the focused region is to the transducer, and the greater the divergence of the beam in the far field) (Fig. 9-4) . Square and rectangular apertures ( see Fig. 9-1B and Fig. 9-1C , respectively) have beam patterns (Fig. 9-5) somewhat different from those of the disc-type of transducer (see Fig. 9-2) . First, symmetry is lost. The pattern is the same along the x-z–plane as the y-z–plane at the origin of the x-y–plane. However, at diagonal points, the pattern differs from the axial plane patterns. The rectangular aperture even differs at the x-z– to the y-z– planes. The near field, the distance to the transition, and the far fields all differ because the aperture distance to wavelength varies for these cases. The diagonal varies even further. Arrays The arrays that are commonly used have properties similar to those of the apertures discussed earlier. The structure of the arrays is illustrated in Figure 9-1 ( see Fig. 9-1D , an annular array; Fig. 9-1E , a square array; and Fig. 9-1F , a rectangular array). The annular array is composed of annular elements, such as the element illustrated in Figure 9-1G , and the square and rectangular arrays are composed of elements as illustrated in Figure 91H . The overall beam pattern considerations of an array are determined by the overall size of the array.[4] Therefore, if the radius-to-wavelength ratio of the annular array (see Fig. 9-1D) is the same as that of a solid disc (see Fig. 9-1A) , then the beam patterns are very similar (e.g., patterns such as those of Fig. 9-2 , Fig. 9-3A , and Fig. 9-3B ). A like consideration applies to the square and rectangular arrays ( see Fig. 9-1E versus Fig. 9-1B and

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Fig. 9-1F versus Fig. 9-1C , respectively). The individual elements of the arrays have their own beam patterns, but an assemblage of multiple array elements gives the overall aperture pattern. It is of interest to consider the miniature element in Figure 9-1H . The 185

Figure 9-3 The 3-dB isocontours for beam patterns along a plane passing through the axis of the transducers. On the left the edge view of the transducer on this plane is illustrated. A, Continuous wave pattern for a disc transducer. B, Beam pattern for the transducer in A but resulting from a very short tone burst of excitation (e.g., two cycles). C, Transducer surface that has been made curved (e.g., spherical curvature) showing how applying such a curvature changes the beam pattern from a flat disc (dotted pattern) to a more focused pattern of the curved surface disc. The arrows indicate the direction the pattern changes as a flat transducer becomes spherical. (Data from Weyns A: Ultrasonics 1980;18:183–188, 219–223.)

pattern of this rectangle element is similar to the pattern of Figure 9-1C except that the dimensions with respect to the wavelength are different. The vertical length of the array element (see Figure 9-1H) Figure 9-4 Beam pattern (3 dB below the axial value) for three circular apertures where a/λ = 9.7. The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). Right, for a disc transducer; center and left, for spherically focused transducers with the same aperture size as the disc. The radius of the spherical surface for the left pattern is much less than the radius for the center figure, thus increasing the focusing effect. (Data from Weyns A: Ultrasonics 1980;18:219–223; and Kossoff G: Ultrasound Med Biol 1979;5:359–365.)

is the same as the vertical length of Figure 9-1C ; therefore, the beam patterns in the vertical direction are the same. However, the horizontal width of the element (see Figure 9-1H) is very small in contrast to the horizontal width of the square or rectangle aperture of Figure 9-1B or Figure 9-1C . Therefore, in a horizontal plane the beam Figure 9-5 Beam pattern (3 dB below the axial value) for a square aperture (left) and a rectangular aperture (right). The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). For the rectangular aperture

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(right), the near-field to far-field transition distances are different along the x-axis versus the y-axis. Also, beam pattern spreading is different in the far field. (Data from Weyns A: Ultrasonics 1980;18:183–188.)

186

pattern transition of the near field to the far field occurs very close to the face of the element, and the far-field pattern diverges greatly and almost immediately in front of the face of the element. In fact, for a proper array, the element has a beam pattern that is so broad (approaching 180 degrees in angle) that its pattern overlaps with the patterns of all the other elements of the array. This overlap allows the array to have an overall pattern nearly identical to that of a solid aperture of the same size as the array. The real difference between an array and a single-element transducer is that each element in the array is connected to the electronic system, and therefore individual control of the timing associated with the transmission and reception of ultrasound is possible. For example, during transmission from an annular array, a beam of ultrasound energy is launched that focuses at a point similar to that discussed for a curved surface (see Fig. 9-3C) . This action is accomplished by exciting the outer element of the array first and then progressively exciting each annular element slightly later as one moves toward the center of the array. The real advantage is that the focus point can be electronically controlled by varying the respective time delays between elements. The greater the delay, the sharper the focus. During reception, by delaying the signals received by each element in a similar but inverse manner (across the array), one can achieve focusing comparable to transmission focusing. These signal delays are instituted before all the signals from each array element are combined to represent the A-line echo. However, the receiving situation is even more advantageous than transmission. Because the amount of delay imposed across the array can be varied continually as the signals are received, tracking the propagating wave is possible; that is, the receiving focus can move and remain pinpointed on the position of the transmitted burst of energy as it propagates away from the transducer. This action is called dynamic focusing and provides a narrower receiving beam over a much larger axial length than that which occurs without such focusing. It is worth noting that during the transmission of a burst or pulse of ultrasound, the focal point can be set only when the beam is launched. Therefore, only a fixed focal point can be used for transmission, but a dynamically tracking focus can be used

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during reception. Many systems use multiple transmissions, varying the focal point each time and using only the information received from each focal region, thereby blending the transmissions to make a composite received line. This approach, however, slows down the scanning rate, as each line requires several transmissions. This method is widely used in noncardiac scanning, in which a high imaging rate is not so important. Therefore, when multiple focusing positions, or zones, can be set (as is possible with some ultrasound machines), one must check that the frame rate is still fast enough for the desired purpose. Further electronic "tricks" can be employed to improve the beam pattern in modern ultrasound instruments. For example, rather than use the whole array when imaging near the transducer, one may use a smaller group of elements for that zone, which increases resolution in the near region. A further improvement is to use for each focusing zone the number of elements that gives the best resolution (e.g., a small group for the focusing zone nearest the transducer, a somewhat increased size for the next zone, and similar increasing sizes for each zone located farther from the transducer). Other improvement methods include apodization, tissue aberration correction, and synthetic apertures. A similar discussion to the annular array, regarding using delays across the array for focusing, also applies to square and rectangular arrays. However, the focusing pairs of elements are located an equal distance (but opposite) from the horizontal center line of the array, and they are not connected together as in the annular array. Furthermore, because each element can be controlled electronically in addition to focusing the array, one can also steer the beam to produce electronic scanning of a region. This electronic scanning is in contrast to the annular array, which must be mechanically swept to interrogate a region of tissue. Electronic scanning is accomplished by adding a linearly increasing delay to the elements, proceeding from one side of the array to the other. This action allows launching and receiving a beam at an angle with respect to the face of the array. The amount of delay used, or the slope of this linearly increasing delay across the array, determines the amount of the steering angle produced. Therefore, to perform a sector scan, one changes the slope of delay profile across the array between scan lines, proceeding to scan from one side of the sector to the other. A shortcoming of the square or rectangular arrays discussed is that electronic focusing occurs only in the horizontal direction ( see Fig. 9-

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1E and Fig. 9-1F ) because there is no electronic control in the vertical or elevational direction. In contrast, the annular array produces symmetric focusing around the axis, thereby usually producing markedly improved resolution. Consequently, there has been interest in designing rectangular arrays that have some or complete control of the beam pattern in the elevation direction as well. Two-dimensional (2D) or 11/n dimensional arrays are being employed for focusing in the elevational direction. (The 1/n implies that some amount of an array is distributed in the elevation direction, but it is less than a full assemblage of elements compared with the lateral direction.) The simplest designs have been referred to as 11/2 dimensional arrays, arrays in which a small division of the aperture has been made in the vertical direction (Fig. 9-6A) . It is not necessary to have separate transceivers for each vertical element here because it is possible to electrically wire together elements that are symmetrically displaced around a horizontal center line. For example, in Figure 9-6A , the vertically displaced elements associated with row 1 can be electrically connected together, as can elements labeled 2 in the figure. (Note: Only the individual elements in a column can be thus connected or the ability to sector scan would be lost.) By connecting elements in this manner, one can use phasing delays between numbers 1, 2, and the center element to produce focusing in the vertical direction at any of the horizontal steered angles, thereby improving the spatial resolution of the beam. In order to accomplish this, one needs only three times as many transceivers, even though the number of elements in the array has been increased five times. Of course, more than five elements can be used in a column 187

Figure 9-6 Two styles of array design offering added electronic beam control in comparison with the arrays of Figure 9-1 . A, So-called 11/2 dimension array offering electronic focusing in the vertical or elevational direction as well as full scanning control in the horizontal or lateral direction. B, Two-dimensional array offering complete three-dimensional beam scanning.

to provide even greater improvement, giving rise to the 1/n nomenclature. The complete 2D array of Figure 9-6B allows complete control of the beam in three-dimensional (3D) space if each element is connected to a

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transceiver and the delay control for each element is provided in the ultrasound system.[6] The problem is that achieving 3D resolution equivalent to current 2D imaging requires many elements and transceivers. For example, a 64-element array and a 3D scanning system equivalent to a 2D array would need 64 × 64 (or 4096) elements, as well as electric connecting wires, transceivers, and delay control elements. The fabrication and cost of such a system are formidable, but they may be less so in the future. A less complicated electronic system, using a 2D array, has been clinically tested for producing biplane images.[7] With this latter approach, the array elements are connected through a multiplexing method to a standard 2D scanning system in such a way that sector scanning can be performed in the horizontal plane; then the array is switched so scanning can occur in the vertical plane. Undoubtedly, numerous permutations of approaches between a full array and multiplexing of the array will emerge in the near future.

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Ultrasound Properties of Tissue There are four main acoustic or ultrasound properties of tissue: the velocity of propagation, acoustic impedance, attenuation, and the scattering of ultrasound. The first three of these are discussed in this section; the following section is dedicated to a more in-depth discussion of scattering. Velocity, impedance, and scattering are interrelated, and they all relate to the various constituents of different types of tissue as well. These parameters for most tissues have been measured,[8] [9] [10] but the published values vary greatly. This variation is due to differences in measurement methods, conditions of measurement (e.g., frequency, temperature), species tested, and tissue conditions (e.g., excised, fresh, fixed). Velocity of Propagation The velocity of propagation is fundamental to all ultrasound assessments. The commonly used average velocity of tissue at 37°C is 1540 m per second, which is used by most ultrasound machines for displaying calibration markers. Of course, individual tissues vary from this value, as illustrated in Table 9-1 . An approximate range of soft tissue variation for most tissue of usual concern with ultrasound is ±5%. The speed of sound also varies with the temperature of the tissue. Generally, most tissues have a small increase in speed as the temperature increases (a positive temperature coefficient); however, fat tissue has been found to have the opposite effect—a decrease in velocity occurs as temperature increases. [11] For in vitro experiments it is valuable to use water solutions that have the same speed of sound at room or body temperature that tissue has at body temperature. Speed regulation can be accomplished by varying the salinity of the water, as listed in Table 9-1 .[12] The speed of sound, c, in homogeneous media is given by the equation c = (β/ρ)1/2

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where β is the bulk modulus of the media and ρ is the density.[4] The stiffer a material, the greater its bulk modulus. It is generally believed that the bulk modulus varies more than density, and that it is therefore the primary factor accounting for the variation in velocity. Acoustic Impedance The second parameter, acoustic impedance, z, is related to velocity and density: z = ρc = ρ(β/ρ)1/2 = (βρ)1/2 Among other things, acoustic impedance is a useful parameter for assessing the amount of reflection and transmission that can occur at the boundary of two layers of tissue. The acoustic reflection coefficient Rc , which is defined as the ratio of reflected acoustic pressure pr to the incident acoustic

pressure pi on the boundary, is given as pr /pi = Rc = (z2 − z1 )/(z1 + z2 )

where z1 is the acoustic impedance of the first medium and z2 is the impedance of the second medium.[4]

The transmission coefficient Tc is defined as the ratio of the acoustic

pressure transmitted pt into the second medium with respect to the acoustic pressure incident on the boundary from the first medium[4] pt /pi = Tc = 1 + Rc

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TABLE 9-1 Impedance Velocity Density * (106 Temperature Other 3 Material (m/s) (kg/m ) kg/m-s) (°C) Conditions

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Air

343

Lung (bovine)

570 gv 360

Lung 640 gv (bovine) Lung 710 gv (bovine) Lung 830 gv (bovine) Lung 860 gv (bovine) Water 1482 [14] Water 1476 Water 1497 Water 1488 Water 1509 Water 1540

1.2

0.000415

20

0.21

22

430

0.28

22

540

0.38

22

640

0.53

22

720

0.62

22

998 [89] 1.48 [14, 89]

20 22 37 22 37 22

38

0% salinity [4] 0% salinity [4] 0.9% salinity [12] 0.9% salinity [12] 4.62% salinity [12] 3.10% salinity [12] 44% hematocrit [88] 40% hematocrit [88] Peritoneal, 1–7 MHz [16] Stomach, 5 MHz [11] Breast [14]

37

Orbital, 6–7 MHz

Water

1540

37

Blood

1556 [88] 1579 [88] 1580

23

Blood

Fat (bovine) Fat 1412 (canine) Fat 1435 (human) Fat 1462

1055 [89] 918

1.67 [88, 89] 1.45

Atmospheric pressure [4] 66% inflated, 0.55 MHz [89, 90] 60% inflated, 0.55 MHz [89] 49% inflated, 0.55 MHz [89] 64% inflated, 0.55 MHz [89] 32% inflated, 0.55 MHz [89] 0% salinity [14]

37 20 37

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(human) Liver (human) Liver (human) Liver (canine) Spleen (canine) Kidney (canine) Muscle (canine) Muscle (human)

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1584 [16] 1607 [16] 1596

1064 [89] 1064 [89]

1.69 [16]

20

[14] 1–7 MHz [16]

1.71 [16]

37

1–7 MHz [16]

37

5 MHz [11]

37

5 MHz [11]

37

5 MHz [11]

37

Skeletal, 5 MHz [11] Cardiac, perpendicular to fiber, 5 MHz [92] Cardiac, parallel to fiber, 5 MHz [92] Pig, age 5 mo, 15 MHz [91] Achilles, perpendicular to fiber, 5 MHz [30] Achilles, parallel to fiber, 5 MHz [30] Skull, outer table [93] Skull, inner table [93]

1601 1569 [11] 1593

1040 [89]

1.63 [11, 89]

1530

1052

1.61

18

Muscle 1555 (human)

1052

1.64

18

1094

1.87

25

1050

1.75

20

1050

2.12

20

1880

5.43–5.68

37

1910

4.56–5.52

37

*

*

Skin 1710 (porcine) Tendon 1670 (bovine) *

Tendon 2020 (bovine) *

Bone (human) Bone (human)

2890– 3020 2389– 2390

*Formalin fixed. gv, group velocity; [], reference number.

Attenuation

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The third parameter, attenuation, is defined as the loss in the amplitude of an acoustic signal as it propagates. This parameter is responsible for the decrease in the echo signal strength at greater imaging depths, and it is why time-varying gain compensation is used in almost all ultrasound machines. It has been observed that the amplitude of a wave decreases with distance in a logarithmic manner. This phenomenon was first observed with light and has been credited to Beer, Lambert, and/or Bourgher (not necessarily in that order). (Various texts and literature seem confused about whom to credit, and they refer to it as the Beer law, the Lambert law, or various combinations of their names [e.g., Beer-Lambert-Bourgher law].) The phenomenon can be described as follows: For a propagating acoustic pressure wave, if the pressure at point 1 is defined as p1 and the pressure at point 2 a further distance l (in centimeters) from the first point is defined as p2 , then the attenuation between the two points can be given by p2 = p1 e−αl where α is the attenuation coefficient defined in nepers per centimeter (Np/cm), or just cm-1 . Alternative units for the attenuation coefficient (αdB ) are decibels per

centimeter and directly relate acoustic pressure and distance to attenuation, p1 /p2 l = αdB . It is easily shown using logarithms that αdB (dB/cm) =

8.686α (Np/cm), which is a useful constant, because the attenuation coefficients are often given both ways. Finally, it is worth pointing out the relationship of attenuation with respect to intensity of ultrasound. The intensity I of an ultrasound wave has units of watts per centimeter squared and is defined as the average power of a wave per unit area (in centimeters squared). The intensity is related to the amplitude of the acoustic pressure p in most cases by the following equation: I = p2 /2z where z is the acoustic impedance as defined earlier. Therefore, for a propagating wave, the intensity at point 1, I1 , is related to the intensity at a point 2, I2 , located a distance l away by the following equation:

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I2 = I1 e−2αl The difference from the acoustic pressure equation is the 2 in the exponent.

189

The attenuation coefficient by itself does not separate out various mechanisms responsible for the loss of energy from the propagating wave. In order to provide further distinction, the attenuation coefficient has been defined to describe the scattering loss from the wave and the absorption of energy from the wave. The scattering directs energy in other directions, and the absorption describes the amount of energy in the wave turned into heat. The coefficient α is then defined as α = αs + αa , where αs is due to scattering and αa is due to absorption. One has to be careful in taking

coefficients from the literature because the distinction is not always made. Particularly in early work, the attenuation was called the absorption coefficient, because researchers did not realize that the scattering effect entered into their results. In fact, it is difficult to measure these effects in isolation. The next two important aspects of attenuation are that it is temperature- and frequency-dependent. Most tissues (not bone) have a negative temperature coefficient. [13] [14] Fat, as discussed later, has a high negative coefficient. All tissues have a strong frequency effect, with the attenuation coefficient varying directly with a power of frequency. For example, α = afb , where f is the frequency and a and b are constants. The power term b varies from 1 to as high as 4; the latter number is for αs , when scatters are much smaller than the wavelength (as discussed later in the scattering section). Most tissues have a coefficient b ranging between 1 and 2. The b (power of the exponent) attenuation factor for water is 2, because absorption is related to the viscosity of the water and the square of the velocity of particle motion. Absorption in tissue is believed to be related to the relaxation processes in the tissue,[15] but this is still not fully understood. The high dependence of the attenuation on frequency is why high-frequency transducers are not used to image deep in the body. The depth in the body at which one can image is inversely related to the ultrasound frequency used. This fact is emphasized by the expression of the attenuation coefficient as α/f in much of the literature. In considering the attenuation as a function of frequency,

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from the excellent compiled data,[9] [10] it is useful to fit a polynomial function to several of the tissues in which the simple expression (α = afb ) does not provide an adequate fit. The results of this equation and the simpler expression for attenuation for several tissues are given in Table 92 . Note: These fitted equations apply only in the specified frequency range designated; if applied out of that range they may provide erroneous results. TABLE 9-2 -- Approximate Ultrasound Attenuation Coefficients Material Air

Lung Water Blood

Fat

Liver Muscle Skin Bone

α(Np/cm) 1.86 × 10-13 f2

Comments Dry, 1 atmosphere

1.98 × 10-13 f2 + 6.36 × 10-7 f + 3.47 Canine, 1–5 MHz

Kinsler et al

8.1 × 10-15 f2 9.77 × 10-16 f2 + 1.09 × 10-9 f -6.22 × 10-15 f2 + 2.45 × 10-7 f 0.127

[4]

45% Goss et al[9] hematocrit, 2–50 MHz Pig back, 2– Gammell et 20 MHz al[13] Taniguchi et al[95] Goss et al[9]

1.3 × 10-7 f

[10]

Goss et al[9]

2.0 × 10-7 f 1.59 × 10-16 f2 + 2.55 × 10-8 f 0.0195 -4.01 × 10-19 f3 + 2.16 × 10-12 f2 4.12 × 10-7 f

Reference Tempest and Parbook[94] Goss et al[9]

[10]

2.0–10 MHz Goss et al[9] [10]

0.25–3.5 MHz

Goss et al[9] [10]

Fat seems to be a special tissue that is worth discussing briefly because it probably is responsible for the fuzziness of transcutaneous echocardiograms in many people. The reported measurements for fat are

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puzzling because of the dispersed range of attenuation values reported.[8] [9] [10] This variation may be partially caused by differences in measurement techniques. However, the attenuation of fat is known to exhibit a strong temperature dependence, and if the temperature at which the attenuation measurements were made is not reported it is difficult to make comparisons. For example, it has been shown that attenuation of excised mammalian fat samples at body temperature is much less than that taken at room temperature.[13] [16] Furthermore, the freshness of the specimen, the species and breed of the donor, and the region in the body from which the specimen is required may also play an important role in the value of attenuation measured. [13] Finally, because of the energy storage function of adipose tissue and the variation in lipid concentrations in adipocytes (adipose cells) in relationship to the degree of obesity,[17] the nutritional state of the donor could also affect the attenuation measurements obtained within a given species and region of the body. In general, the major fat tissue, white adipose tissue, is known to consist of cells 25 to 200 µ in diameter, composed of weight of 60% to 80% lipid, 5% to 30% water, and 2% to 3% protein. From 90% to 99% of the lipid is triglyceride. [18] These adipose cells are held in "grapelike" aggregates by connective tissue called lobules.[19] The cell sizes have been correlated with the degree of obesity (hypertrophic obesity). [17] In some tissue regions (hyperplastic obesity) the number of the cells correlates more strongly with obesity. For example, a general trend in male humans is hypertrophic obesity in the abdominal regions, whereas female humans show hyperplastic obesity in the subcutaneous femoral and gluteal fat depot regions.[20] The average size of adipocytes in pigs and sheep has been reported to be greater in the omental and the perirenal regions than in the subcutaneous region, whereas in humans the reverse has been found.[17] Cell diameters ranged from 25 to 180 µ in adult pigs ready for market.[17] As discussed later, the size of a scatter with relationship to the wavelength of the sound can affect the frequency dependence of the scattering. Therefore, the nutritional state and location of the fat may affect its attenuation properties. The other interesting constituents of tissue are water and collagen. Water and collagen tend to have opposite 190

effects on ultrasound attenuation. Water content generally reduces

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attenuation, whereas collagen increases attenuation.[21] [22] [23] [24] [25] Because water itself has a low attenuation in contrast to tissue, it is reasonable to expect that as the water content increases, the attenuation coefficient decreases. Fields and Dunn[26] in 1973 were the first to relate how the prominent differences in values of modulus between collagen and muscle may apply to the ultrasound echo properties of tissue. They pointed out that the low-frequency elasticity constant of collagenous fibers from tendon is about 1000 times greater than that of other tissues (e.g., 109 dyne/cm2 for collagenous fibers versus 105 to 107 dyne/cm2 for smooth muscle, [27] 2 × 108 dyne/cm2 for human calcaneal tendinous, and 5 × 104 dyne/cm2 for dog abdominal muscle).[28] From the above relationship of the bulk modulus β to acoustic impedance (z = [βρ]1/2 ) and velocity (c = [β/ρ]1/2 ), it is easily realized that tissue highly distributed with collagen may have sharp changes in z and c, which would produce high inhomogeneity in acoustic properties, thereby leading to a tissue with high scattering. An example of this is the highly collagenous tissue in the submucosa of the intestine. The submucosa produces much higher echogenicity than the muscle in the wall. [29] However, measurements of the modulus of fixed bovine flexor tendon at 5 MHz have revealed values of 45.1 × 109 dyne/cm2 in the direction of fiber orientation and 30.8 × 109 dyne/cm2 perpendicular to the fibers,[30] which were found to be only factors of 1.8 and 1.3 greater than the values in fixed human myocardium, with the fibers respectively oriented. One would expect higher ratios based on the low-frequency measurements of bulk modulus and the fact that only 1% (wet weight) of the myocardium is collagen, whereas 30% (wet weight) of the tendon is collagen. [30] The high modulus of the myocardium may be due in part to the fixation process, but it may also explain why the myocardium is both echogenic and attenuative. A high degree of scattering can produce a high attenuation coefficient, because attenuation is composed of both scattering and absorption. Goss and O'Brien[31] in 1979, using a 100-MHz acoustic microscope, measured the velocity of propagation in mouse tail tendons and found an average value of 1733 ± 56 m per second; this is in the range that Hoffmeister et al [30] found in 1994 for cross-fiber tendon velocity. Two other specific tissues, bone and lung tissue, also affect transcutaneous cardiac imaging. The attenuation of lung tissue has been found to vary with the degree of inflation,[32] [33] [34] and of course it is highly attenuative even with low inflation (see Table 9-2) . Both velocity and attenuation have been found to increase with increasing mineral content in bone.[35]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Scattering One of the most important events in ultrasound interrogation is the scattering of the propagating energy from its initial pathway as it encounters various structures. This event is important for several reasons, but foremost is that the scattered energy is detected in medical ultrasound imaging. Clearly, the more a region tends to scatter ultrasound, the more hyperechoic it is (all other things being equal). Therefore, understanding scattering is important in understanding what is actually measured, as well as in estimating what can be measured in a particular situation. The complexity of scattering is directly related to the complexity of the structure being investigated. Some of the initial understanding was provided by Lord Rayleigh[36] as early as 1877, but today research in scattering continues. Considerable insight into scattering can be obtained by first considering scattering from a single particle in a homogenous medium. As the mechanical properties of the particle with respect to the surrounding medium vary, so does the scattering. Further, the size of the particle with respect to the wavelength of the interrogating sound is very important. When the size of the particle is very large with respect to the wavelength, the particle reflects like a smooth surface. A second useful area for deliberation is scattering from a surface both smooth and rough, but this is not discussed here. Third, it is useful to consider tissue as a structure in which (1) the velocity of propagation varies some fractional amount with distance, and (2) each point in the tissue has identical acoustic properties over only a finite length (a correlation length). These three cases are simplifications of what occurs at all sites in the body, but they provide helpful insight for understanding the more complex situations. Some useful terms have grown out of the radar and sonar literature and have been applied to medical ultrasound in order to provide quantitative descriptions: Scattering cross σs = Ps /Ii with units of area (e.g., section

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σd (theta) = R2 Is (theta)/Ii

Backscattering cross σ = R2 I (180°)/I b s i section Backscattering coefficient

ηb = R2 Is (180°)/Ii V

cm2 ); with units of area per solid angle; with units of area per solid angle (e.g., cm2 /Sr); and with units of area per volume-solid angle or 1/length-solid angle (e.g., cm-1 Sr-1 )

where Ii is the ultrasound intensity incident on the particle; Ps is the average

power scattered from the particle; R is the radial distance from the particle to an observation point (where R is considered to be in the far field of the scatter); theta is the angle between the direction the sound is scattered and the direction the sound is propagating; Is (180 degrees) is the scattered intensity in the back direction (i.e., theta = 180 degrees); and V is a unit volume (e.g., cm3 ).

Each of these terms has a physical meaning. The scattering cross section σs describes the amount of cross-sectional area needed in the incident beam to contain as much power as is scattered by the object (i.e., power = area × intensity). The differential scattering cross section relates the incident intensity to the intensity scattered per unit solid angle in the direction described by the angle theta. The backscattering cross section relates the incident intensity to that scattered opposite to the direction the beam is 191

propagating (i.e., back, theta = 180 degrees). Most ultrasound instruments detect only backscattered signals, not those scattered at other angles. The radial distance R appears in the last two equations because we are relating two intensity terms, and we assume the scattered intensity is uniform over some small solid angle (consistent with the far-field approximation of an aperture). There is a directional or angular factor in the equations because scattering in a particular direction (e.g., the back direction) may be different from scattering in other directions; therefore, the units are area per solid

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angle, where the solid angle is defined in the units of steradians (Sr). Finally, these first two terms have worked well in radar and sonar, in which there are usually single objects in a homogenous medium producing the scattering. However, when one tries to apply these terms to tissue, a rather nonhomogeneous medium, the term backscattering coefficient ηb was

developed. This term relates the back directional scattering cross section σb to a volume or region rather than a single particle; hence ηb = σb per unit

volume, which takes on the expression related to Is (180 degrees)/Ii with the units of 1/length-solid angle (e.g., cm-1 Sr-1 ). Scattering from a Single Particle Scattering from a small fixed sphere in a fluid was first studied by Rayleigh. Small was defined as a sphere with a radius a where the circumference of the sphere, 2πa, divided by the wavelength λ is much less than 1 (i.e., ka = 2πa/λ <<1). In this equation, k is the wave constant = 2πf/c; f is the frequency of the wave; and c is the velocity of propagation. In the Rayleigh range, the differential scattering cross section has been shown for elastic spheres to be given by σd = 0.11 k4 a6 [{(κe + κ)/κ} + {3(ρe + ρ)/(2ρe + ρ)}cos (theta)]2 where, respectively, κ and ρ are the compressibility and density in the fluid, κe and ρe are the compressibility and density in the sphere, and theta is the

angle between the direction of the incident ultrasound energy and the direction of the scattered intensity, which for backscattering is 180 degrees. The red blood cell with a radius of about 4 µ is an example of a particle that is small compared with the wavelength for frequencies below 61 MHz (ka 1 at that frequency) and therefore falls into the Rayleigh scattering region. Therefore, the red blood cell can be approximated as an elastic sphere, and the equation for the scattering cross section in the Rayleigh region for elastic spheres can be applied in the back direction. The compressibility for plasma and a blood cell,[37] respectively, are κ and κe = 40.9 and 34.1 × 10−−12 cm2 /dyne, and the density ρ and ρe = 1.021 and

1.092 g/cm3 . Further, for backscattering, because cos (180 degrees) = −1, then σb = 6 × 10−−3 k4 a6 and k = 2πf/c (where f is the frequency and c is the velocity of propagation), the backscattering cross section is proportional to

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the fourth power of the frequency and the sixth power of the radius. Therefore, the scattering of blood is very dependent on frequency. The ratio of the backscattering cross section to the geometric cross section of the sphere (area of a circle of radius a) is given as σ/πa2 = 2.8(ka)4 This normalized relationship is plotted in Figure 9-7 on the left side of the graph. When ka → 1 there is often a resonance effect in which σ/πa2 oscillates above and below 1 as ka approaches, equals, and becomes greater than 1. For large scatters, the values of ka > 1, the value of σ/πa2 → 1 (if the sphere is infinitely stiff); that is, the scattering cross section becomes equal to the geometric cross section. Therefore, when ka << 1, the surface of the sphere appears as a flat surface with respect to wavelength, and the scattering becomes the same as reflection from a flat surface. For spheres with other values of compressibility, but large enough so the duration of the burst of ultrasound is over before the wave passes from the front of the particle to the back, σ/πa2 → [(z2 − z1 )/(z1 + z2 )]2 , where z1 is the acoustic impedance in the fluid media and z2 is the impedance of the particle. This

term is essentially the intensity reflection coefficient for an interface between two layers.[4] Therefore, there are three regions:

1. Rayleigh region, ka << 1, where σ/πa2 is proportional to the fourth power of frequency; that is, σ/πa2 = 2.8 (ka4 ) 2. Resonance region, ka 1, where σ/πa2 oscillates 3. Large scatter region, ka > 1, where σ/πa2 → the intensity reflection coefficient; further, when ka << 1, the scatter is so large it acts like a surface When ka 1 backscattering resonates, and the angular scattering around the sphere varies and is no longer uniform or isotropic. A particle that is a gas bubble in fluid is interesting for Figure 9-7 Scattering from a sphere in three regions of size with respect to wavelength. See text for discussion.

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192

a number of medical reasons (e.g., air emboli and/or ultrasound contrast agents). The isotropic (scattering in all directions equally) scattering cross section equation for a gas bubble in water is given by σs = 4πa2 /{[(fr /f)2 − 1]2 + (f/fr )2 δ2 } where f is frequency of sound, fr is bubble resonance

frequency, and δ is the damping coefficient for the bubble in the fluid.[37] This damping coefficient is related to the thermal properties of gas and fluid, the damping owing to scattering, and the viscosity of the fluid.[38] A value of δ = 0.15 is typical for air in water at 1 MHz. A plot of σs /πa2 , the ratio of scattering to the geometric cross section of a spherical bubble, is shown in Figure 9-8 , and the bubble size needed for resonating at various frequencies is shown in Figure 9-9 . Scattering from Multiple Particles When scatters are spaced in a medium at an adequate distance from each other, then the overall scattering cross section per unit volume (i.e., scattering coefficient) is given by the sum of the scattering cross sections of all the particles in the volume. If all scatters have the same scattering cross section, the number of scatters in the volume times the scattering cross section gives the scattering coefficient. However, when the scatters are located close together, the incident intensity on each scatter may be different because of shadowing from other scatters and/or intensity scattered onto it from other scatters. Further, the scattering arriving at some distant point from each scatter may also be different because of the effect just mentioned, and the scattering pathway from each particle may be altered by other particles in the way. When the particles are close enough for this action, multiple scattering effects occur. Shung et al[39] have studied this Figure 9-8 Isotropic scattering from an air bubble in blood. The vertical axis is the normalized scattering cross section. It is normalized by dividing the scattering cross section by the geometric cross section of the air bubble. The horizontal axis (f/fr ) is the ratio of the ultrasound frequency to the frequency at which the bubble will resonate.

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Figure 9-9 Approximate air bubble size at which resonance will occur for various frequencies in blood at body temperature.

effect with respect to scattering from blood at various hematocrits (e.g., porcine blood in laminar flow). Clearly, the higher the hematocrit, the greater the density of blood cells in a unit volume, and one would expect that scattering would linearly increase with the hematocrit if there were no multiple scattering effects. Yuan and Shung[40] described the observed findings with the following equation in terms of the backscattering coefficient: ηb = [σb Wo (1 − Wo )4 ] / [V(1 + 2Wo )2 ] where Wo is the hematocrit expressed as a fraction, V is the volume being studied, and σb is the backscattering cross section from a single cell. This

equation provides an excellent fit to the data in the 1993 report of Shung et al,[39] in which σb = 2.17 × 10−2 cm2 , V = 68 cm3 , and frequency = 7.5

MHz. The results are plotted in Figure 9-10 . The backscattering coefficient increases approximately linearly with hematocrit to a value of about 8%, then the rate of increase decreases until the scattering coefficient reaches a maximum at 13%; thereafter, it decreases with higher values of the hematocrit. When scatters are located closely together, the scattering is less than expected (based on a linear increase with the number of particles). Another interesting finding with blood is that the backscattering coefficient increases as the velocity of the blood decreases. For example, scattering from venous blood is greater than that from arterial blood, which is thought to be due to red blood cells clumping together at slower flow velocities, whereas at higher velocities the fluid shear tends to separate them. Considering that the backscattering cross section in the Rayleigh region is related to the sixth power of the radius of the scatter, clumping could increase the size of each scatter considerably, thereby increasing the scattering amplitude greatly because of this sixth power effect. This may be much more dominant than the fact that the number of individual scatters would 193

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Figure 9-10 The calculated backscattering coefficient for porcine blood in laminar flow for various hematocrit values. (Data calculated from an equation given by Yuan YW, Shung KK: J Acoust Soc Am 1988;84:52– 58; Data from Shung KK, Kuo IY, Cloutier G: Ultrasonic scattering properties of blood. In Roelandt H, Gussenhoven EJ, Bom N (eds): Intravascular Ultrasound. Boston, Kluwer Academic, 1993, pp 119–139.)

be reduced. In fact, reduction may also reduce some of the multiple scattering effect for normal hematocrits of 45%, thereby increasing scattering. The effect would be somewhat like moving to the left from 45% in Figure 9-10 . Because of this increased scattering, blood speckle movement can be observed with the higher-quality B-mode imaging equipment in venous blood but generally not in arterial blood. Finally, stagnant but unclotted blood becomes hyperechoic quickly after cell motion stops. However, on stirring it the blood becomes hypoechoic until the motion stops. Backscattering from Tissue Certain types of tissue, in some ways, acoustically can be considered to be a collection of scattering particles embedded in an acoustic conducting medium. A more meaningful model has been to consider the variation of the velocity of propagation through the tissue, and a term called the correlation length of the structure.[41] The average velocity variation µc is (<∆c>2 /∆c2 )1/2 , where c is the velocity of propagation and <∆c> is the time average change in the velocity as it propagates through a region of tissue. The maximal correlation length b is an expression of the spatial distance over which the acoustic properties of a region remain correlated (based on autocorrelation) with some initial starting point in the tissue. Basically, the acoustic properties are the same for a distance of about b from the starting point. For a region of tissue there is a distribution of correlation lengths. If one assumes a uniform distribution of correlation lengths in the tissue from zero to some maximal value bm , the following expression describes the backscattering coefficient for such tissue[41]

ηd = (3µ2 k/4π)[tan−1 (kbm ) + (1/9)tan−1 (3kbm ) − kbm /(1 + k2 bm 2 ) −

kbm /3(1 + 9k2 bm 2 )]

where k is the wave constant discussed earlier. The following constants

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were found to fit scattering data from dog heart muscle: the percentage root mean square of velocity variation µ = 4.94 and bm = 0.17 mm.[42] Applying

this equation and constant for various values of frequency produces the graph shown in Figure 9-11 . This has been compared over the frequency range of 3 to 7 MHz to measurements and was found to provide a good fit.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Tissue Characterization In general terms, ultrasound tissue characterization is an effort to use ultrasound to identify certain physiologic or pathologic conditions of tissue, or to try to classify various features or traits in specific regions of tissue that may be of diagnostic value. This identification has usually involved the application of some form of quantitative measurement and therefore goes beyond the usual imaging and Doppler processing and display. The general trend is to develop in vivo methods of measuring various acoustic parameters such as the velocity of propagation, acoustic impedance, acoustic attenuation, and scattering amplitude, then to apply the methods to normal and diseased tissue. This endeavor has a history starting in the 1970s and was spearheaded, in part, by a symposium titled Ultrasonic Tissue Characterization in 1976[43] the symposium has continued annually since. This annual Figure 9-11 Backscattering coefficient versus frequency for scattering from canine heart muscle using the equation given in the text. The kbm values for 30, 14.1, 5, and 2.5 MHz are, respectively, 2.1, 1, 0.35, and 0.18, and they are found to fit data from O'Donnell, Mimbs, and Miller. [42]

194

meeting has been a forum for presenting new areas of research into this broad field. The initial endeavor met with considerable enthusiasm, but when many of the approaches failed to demonstrate clinical use, the approaches lost their support. Some approaches failed because they were too complex to be implemented in a practical manner at the time; others failed because they were never taken to the point of adequate clinical testing; and some failed just because they seemed to provide no

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improvement in the "characterization" of the tissue tested. Many of the complexities are now more easily overcome with today's computing power and improvements in transducers. Nevertheless, these solutions often pose a Catch-22. To be clinically tested they need to be implemented into commercial machines, but the companies are reluctant to implement or explore such methodologies until the clinical demand or market has been demonstrated. Furthermore, the processing involves obtaining or controlling the ultrasound signals at "primitive" levels in the system, not easily performed by people who do not have the technical details of the specific ultrasound machine involved (i.e., nonmembers of the company making the machine). In spite of this problem, and because of the diligence of the investigators involved, some significant progress has been made related to echocardiography. Worthy of note is the application of various measures of myocardium ultrasound backscattering. These measures have been more readily applied to the in vivo case because they are more compatible with standard echocardiography interrogation. However, early work in the 1970s, for example, frequency and angular scattering effects,[44] backscattering coefficients versus frequency,[45] and attenuation measurement,[46] used excised tissue. In vitro work has continued to provide more basic information from which our understanding of the ultrasound tissue interaction has grown. In addition, early in vivo work involving the study of scattering from normal and ischemic hearts[47] helped fuel some of the work that has been widely reported. The term backscattering coefficient as defined earlier has continued and is continuing to be applied as a prominent measure of tissue characterization. Interested readers can find a comprehensive review of cardiac tissue characterization up to 1986 in a chapter provided by Skorton and Collins [48] in Greenleaf's book dedicated to tissue characterization using ultrasound. There are two troublesome problems in quantitative backscatter measurement. Both problems concern obtaining calibrated data related only to the region of interest. The first problem is the way the ultrasound machines are designed. They have been developed to provide the operator with numerous controls to produce the highest quality image. Adjustment of these controls may change the power transmitted, the gain of the amplifiers, the control curves in the time-varying gain, and the signal-togray level conversion (nonlinear compression). Consequently, unless all these controls are always set the same from patient to patient (which they

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rarely are), the amplitude of the echoes at the receiver are very difficult to quantify and compare from patient to patient. Finally, the frequency response and beam patterns of various transducers and instruments tend to be different, so they require calibration. A useful method of calibration has involved applying the transducer to some type of test phantom with a standard reflector (e.g., a large metal sphere) and recording echoes from it to represent reference data for comparison.[48] The more successful methods, in addition to this, have used information from a point in the imaging system where it has not been adjusted in the various manners mentioned earlier. Usually this is early in the instrument when the signals are still in the radio frequency form. Either the signal is tapped off at this point and linearly amplified, and brought out of the machine to a data acquisition system, or a special section in the instrument has been built to process these signals in a way that is needed just for tissue characterization (which is different from that used for image production). The second major problem is that the intervening tissue between the transducer and the site for measurement interferes with the signals in its passage, which poses formidable problems. This interference is in the form of attenuation, which is unknown not only in amplitude but also in its frequency dependence. The variation in the velocity of propagation through this intermediate region also can distort the beam (phase aberration) and affect measurements. Therefore, the most practical method has been comparing (when possible) adjacent regions of tissue of interest (e.g., suspected disease versus normal, blood versus wall, or changes in echoes from the proximal to the distal portion of the region) or comparing the same region at various time points (e.g., the changes during the cardiac cycle). These comparisons produce more relative measurements, but they offer more reliable approaches. Two measurements, spectral analysis and integrated backscatter, have been particularly studied, the latter extensively. Both methods involve making measurements of the radio frequency or uncontaminated rectified radio frequency signals obtained from a region in an image by setting a window of interrogation at a specific location in the tissue. Electronically, this means sampling and measuring the returning echoes during a specific time period. In spectral analysis, the signals are converted from the time domain to the frequency domain by using the Fourier transform, then the converted echoes are normalized by dividing by the amplitude of the similar frequency components acquired from signals from a calibration target. Comparison of the rate that the amplitude of the different

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frequencies changes over the spectrum has provided a relative measure of attenuation with frequency. Integrated backscatter has been more widely employed in cardiology. The method involves operating directly on the time domain signals. All the signals received during the set duration for interrogation are rectified in some way and integrated or added. This result is then normalized by dividing it by the similar measure (e.g., summation) from a reference target. Neither the spectral analysis nor the integrated backscatter approach by itself can compensate for the intervening tissue effect; therefore, these measurements need to be compared in some manner, as mentioned earlier. Comparison to scattering from blood in the cardiac chambers has been considered, and comparison of scattering from the myocardium to the pericardial interface has been successfully employed in diabetic patients.[49] Further, recording and analyzing the variation of 195

the amplitude of the integrated backscatter during the cardiac cycle have been highly useful. In fact, the cyclic variation of integrated backscatter has been found to provide useful diagnostic information. Overall backscatter has been found to be useful in depicting cardiomyopathy, [50] [51] [52] infarcts,[53] [54] [55] ischemia,[56] [57] [58] [59] [60] [61] and stunned myocardium.[62] [63] Infarcts that have become highly collagenous produce high backscatter and are more attenuative. Calcification produces even higher scattering and prominent shadowing beyond the calcification because of the high attenuation of the calcified tissue. The cyclic variation of integrated backscatter during the cardiac cycle has been found by Milunski et al[62] to be about 3.8 dB (0.65) in dogs, with the highest amplitude occurring during the cycle shortly after the QRS complex and minimum at end-systole. When ischemia was produced in these animals (15-minute occlusion),[62] the cyclic variation was reduced to 1.7 dB and wall thickening was reduced from 37% to 17%. Within 20 minutes of reperfusion, cyclic variation had recovered to baseline, whereas wall thickening only recovered to 23% in 2 hours. Based on the wall-thickening recovery rate and results of other occlusion experiments,[64] [65] the tissue was believed to be "stunned" and would have nearly recovered in 48 hours. The findings indicated that the recovery of the cyclic variation of integrated backscatter precedes the recovery of wall thickening after the myocardium has received an ischemia insult and then been reperfused. In a second report from the same group,[63] cyclic variations in integrated backscatter were studied in 21 patients within 24 hours of having symptoms, indicating acute

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myocardial infarction. Measurements from infarcted and normal regions of the heart were made. The average magnitudes of the cyclic variations were 0.8 dB in the infarct areas and 4.8 dB in normal areas. In 15 patients patency was later determined by coronary arteriography, then the patients were restudied with ultrasound within an average of 7.1 days after arteriography. In patients in which patency was documented, cyclic variation had increased from an average of 1.3 to 2.5 dB, whereas in patients without patency the cyclic variations had no recovery. Neither group had shown any significant wall-thickening recovery based on echocardiography at the time of the studies. This second study[63] tended to confirm the findings in animals.[62] In the Milunski et al studies,[62] [63] the normal variation found in the humans was about 1 dB greater than that in the dogs. Perhaps this result reflects a difference between dogs and humans, but it also may reflect the vigorous compensatory contractions that can occur in normal regions of the heart when a portion of the heart is infarcted, in contrast to when the entire heart is normal. We have observed this compensation effect using a regional ejection fraction measure when 3D imaging infarcted hearts. [66] Therefore, care should be taken when using other regions of diseased hearts for comparison. Further, numerous studies of cyclic variation by various investigators around the world have been sparked by the earlier and other findings. Not all investigations have found the same results, perhaps owing in part to differences in the study methods. Finally, considerable interest has been stimulated in trying to understand what exactly the ultrasound scattering mechanism is that is responsible for these findings; a few of these studies are discussed further later. Two related studies provide some insight into why there may be cyclic variations during the cardiac cycle. The orientation of myocardial fibers changes from the epicardium to the endocardium.[67] The scattering from the myocardium has been modeled as cylinder-shaped scatters, centered randomly, but angularly oriented and embedded in homogeneous medium. [68] The model demonstrated anisotropic backscattering, which varied with the orientation of the ultrasound impingement to the angle of alignment of the cylinders (maximal scattering when perpendicular), and their simulations could be fit to angular integrated backscattering measurements of others.[69] More recently, Rose et al[70] used ellipsoid shells with acoustic properties of collagen as elementary scatters in a homogeneous medium with the average properties of myocardium as a scattering model. The implications were that the myocytes are surrounded by collagen that forms

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the major scattering surface, whereas the rest of the tissue is fairly homogeneous. Based on the understanding of the dominant role that collagen plays in ultrasound scattering and the geometric arrangement of the collagen matrix of the myocardium,[71] this finding is reasonable. It also may explain why the myocardium is so echogenic. Again the model could be found to fit angular measurement data of others.[69] Therefore, as the myocytes shorten and expand with contraction, their orientation also may change with contraction, and this may produce a change in the backscattering. It doesn't, however, exactly explain why stunned but perfused myocardium might have cyclic variation whereas infarcted myocardium has little. Further studies of normal, stunned, and infarcted dog hearts were conducted with 5-MHz backscattering and 100-MHz scanning laser acoustic microscope measurements.[72] Ultrasound measurements were compared with myocardial water, lipid, and protein content measurements. The average attenuation at 100 MHz was significantly greater in normal (179 dB/cm) than in stunned (136 dB/cm) and infarcted (136 dB/cm) myocardium, and the velocity of propagation was significantly higher in normal and stunned myocardium (1597 and 1600 m per second, respectively) than in infarcted (1575 m per second) myocardium. The 5MHz backscatter was increased in the infarcted (-42.5 dB) compared with the normal and stunned (-47 dB) regions. These changes are interesting when compared with the tissue findings of significantly increased water content (81%) in infarcted regions, whereas the water content in normal and stunned regions is 73%. The protein content is lower in the infarcted regions (18.5%) than in the normal regions (21.5%), and an increase in lipid content is found in stunned (8.5%) compared with normal (5.5%) and infarcted (0.8%) regions. Perhaps most interesting is the increase in water content in the infarct areas. The reduction in attenuation and speed is consistent with the increase in water, based on the earlier discussions. Loss of intermyocyte collagen struts has been found with infarction, and this loss correlated with infarct expansion. [73] If backscattering from the myocardium is operating in the region of multiple scattering, an increase in spacing 196

between scatters may decrease the canceling effect of multiple scattering and thus increase the backscattered signal, but this is only speculation. The presence of fluid can increase the echogenicity in other muscle tissue, but it

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depends on the way the fluid collects.[74] Once again, insight has been gained into myocardium backscattering, but why cyclic variation may recover in stunned myocardium but not in infarcted myocardium remains a mystery.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Harmonic Imaging The new imaging formats referred to generally as harmonic imaging have improved the quality of images considerably. Interestingly, harmonic imaging has come about by serendipity. In trying to find methods of enhancing echo contrast images, researchers developed harmonic imaging and more recently pulse inversion imaging. It has been found by accident that these techniques improve images without the need to inject echo contrast. In seeking a reason for this improvement, we have learned that some of the former ways of thinking about ultrasound propagation imaging have not been entirely correct. The generally accepted concept was that ultrasound waves at acoustic levels used in diagnostics propagate in a completely linear manner. "Linear" in this setting implies that if one transmits at a certain frequency, the received energy returns only at the same frequency as that transmitted. One exception is Doppler shifts that might occur because of tissue or blood movement. However, Doppler frequency shifts in the human body are only fractional shifts in frequency from the fundamental, whereas harmonics involves frequencies two, three, or more times higher in frequency than the fundamental. In order to understand these frequency shifts, it is helpful to review what happens in a sound wave. An acoustic wave propagates away from an acoustic source of vibrating particles because particles adjacent to them must respond to the force by applying a countering force (Newton's third law of motion). In turn, these new stressed particles also must apply force to particles more distal but adjacent to them. Therefore, such a disturbance of vibrating particles couples through the media, particle by particle, continuing to attempt to satisfy the condition that in equilibrium the sum of all forces must be zero. This dynamic coupling action constitutes the propagation of a wave. The speed at which it propagates is related to the mass of the particles (i.e., the density of the media) and its "springlike characteristics" (i.e., bulk modulus). Further, the greater the velocity at which the particles originally

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vibrate, the greater the acoustic pressure in that region and the higher the intensity. As the wave propagates, one can consider the net velocity at which the particles move. This net velocity is the sum of both the particle velocity from the vibration and the speed at which the wave propagates. In a standard longitudinal wave, the particles vibrate along an axis that is in the same orientation as wave propagation. However, during the positive pressure (compressional part of the wave) the particles move in the same direction as the wave is propagating, but during the negative pressure (rarefactional part of the wave) they move in the opposite direction. The net effect is that the particles move slower during the rarefactional portion of the wave because the particle motion subtracts from the speed of propagation. In the compressional segment of the wave, particle velocity adds to the speed of propagation. These effects accumulate as the wave propagates along and have the tendency to distort a sine wave, with the compressional part becoming sharp at the front of the wave and the rarefactional part becoming retarded. The overall appearance tends toward a sawtooth-shaped wave rather than its original sinusoidal form. This distorted wave can be described as a wave composed of a certain amplitude of the fundamental frequency (f0 ) and various levels of higher harmonics (2f0 , 3f0 , 4f0 , and so on). The closer the distortion approaches the shape of a sawtooth wave, the higher the amplitude of the harmonics. On the other hand, if the wave remains a sine wave, there are no harmonics. A final key point is that the intensity or amplitude of the acoustic pressure is important. The higher the amplitude, the more rapid or closer to the transducer this nonlinear distortion occurs. This understanding of nonlinear propagation has principally been derived from propagation in water,[75] in which the attenuation is low. There have been no reports on experimental measurements in actual tissue (of which the author is aware); however, there have been several recent reports of nonlinear modeling, including tissue equivalent attenuation.[76] [77] [78] A major effect of tissue according to these models is that the increased attenuation with frequency tends to nullify the generation and propagation of higher harmonics to some extent. Therefore, the generation of sharp sawtooth waves appears unlikely. However, the wave can still be rich with harmonics as verified by the fact that harmonic imaging actually works. Considering earlier discussions, the reasons why images are now better are explained. First, the generation of harmonics requires the fundamental

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frequency to propagate some distance. This indicates that the various aberrations and possible reverberation effects that occur at the skin, fat, and muscle layers of the chest wall do not affect the harmonic waves because they develop deeper in the tissue. Therefore, the detrimental effects on the conventional image that occur as the result of aberration to the beam[79] owing to the chest wall is avoided, at least for the transmission portion of a transceiving process. Second, the higher the amplitude, the greater the tendency to produce these harmonics more rapidly and more extensively. Therefore, the generation of harmonics occurs more rapidly in the center of the beam of the wave at the fundamental frequency because the intensity there is higher. This action causes the harmonic beam to be narrower. As mentioned earlier in the chapter, for the same size aperture a higher frequency also produces a narrower beam pattern. The net result of these effects is that higher harmonics produces a beam pattern that is narrower than the beam formed at the fundamental frequency. This narrower beam leads to a higher resolution image. Finally, as indicated in Figure 9-7 , if the scatters fall in the Rayleigh region, the backscattering increases for the higher harmonics. Therefore, one anticipates increased backscattering from cardiac muscle (see Fig. 9-11) for 197

the higher harmonics. Similarly, backscattering from a nonperpendicular angle of encounter of the acoustic beam with a semirough scattering boundary may produce higher backscatter at the higher frequencies. These two effects also are most likely contributing factors to the improved images of the endocardium obtained by harmonic imaging. Having described the mechanisms for image improvement that harmonic imaging provides, there are still some design aspects of a conventional ultrasound imaging system that have to be overcome to obtain these advantages. These aspects include features that are needed for high range resolution. A wide bandwidth system is required to ensure the transmission and reception of very-short-duration excitation bursts. The shorter the duration, the wider the frequency spectral content of the excitation signal and the wider the bandwidth needed to transceive it. A wide bandwidth excitation signal also produces wide bandwidth harmonics. The difficulty arises because the lower frequency components of the harmonics tend to overlap into the frequency range needed for the higher frequency components of the fundamental excitation signal. This action degrades the advantage of the harmonic signals. Therefore, to receive only harmonics,

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special designs are needed. Careful shaping of the excitation signal and filtering of the received signal have been successfully employed.[80] An alternative is the use of pulse inversion methods,[76] which appear to automatically suppress the fundamental excitation signal and tend to allow recovery of only the harmonic. Although the advantages of harmonic imaging are becoming well recognized in echocardiography laboratories, there are limited formal studies of the advantages of harmonic imaging. Reports from symposia have provided some documentation. Improvements were found in visualization of the aortic valve in 70% of 40 patients with harmonic imaging, whereas visualization was possible in only 35% of the patients with normal imaging.[81] Left ventricular thrombi was looked for in 93 patients with myocardial infarction and only 7 were found with use of normal imaging, but two additional ones were found with use of harmonic imaging. [82] Harmonic imaging is now routinely used in the echocardiography laboratory at the University of Washington Medical Center because of the advantageous experience with its use. The only shortcoming our cardiac sonographers report is that valve leaflets tend to appear thicker with harmonic imaging than with normal imaging. This effect most likely arises from an artifact produced in the processing system, which is caused by the rapid movement of the valve leaflets. However, a more in-depth study is needed to clarify this observation and what the artifact mechanism actually is. Of final note, harmonic imaging is being found to provide better images in numerous other areas beyond echocardiography. This method is indeed an advancement in ultrasound imaging.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary The physics of ultrasound in terms of beam patterns, propagation, attenuation, and scattering is important in echocardiography. Some of the important aspects of these factors have been discussed in this chapter. This is by no means an exhaustive review, but it may stimulate the reader to more reading in this area and may provide some assistance in understanding this sometimes nonclinical literature. The spatial resolution, which consists of range resolution (related to the pulse duration), lateral resolution (related to the lateral beam width), and elevation resolution (related to the elevation beam width), is very important in the accuracy of length, area, and volume measurements. These factors are particularly important when the ultrasound beam impinges on boundaries obliquely. Evolving technical improvements in imaging, which improve resolution and reduce aberration effects of tissue (e.g., harmonic imaging), will provide more accuracy in quantitative measurement by reducing the effects that have been discussed. Continued technical improvement and discovery is certainly a hope for the future.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Measurement Errors Numerous errors can result when quantitative measurements are made using ultrasound. One area of difficulty is the variation in the speed of sound. Generally, most instruments use a value of 1540 m per second for the average speed of sound in tissue at 37°C. The calibration markings on the screen for distance are based on this value. Further, for phase arrays the delays used in the instrument to steer the beam to produce the scanning sector also use this value. As discussed earlier, the speed in different tissues varies to some extent. For example, if the distance across the aorta is measured as 2 cm based on the calibration on the screen using 1540 cm per second whereas the actual speed of sound in blood is 1579 cm per second, there would be an error of -2.5%. This is an error in making a onedimensional measure along the direction the ultrasound propagates. If the speed of sound is different from 1540 m per second, the angle of the phased array may be different, so lateral measurements in the image also can suffer some error because of speed-of-sound differences. Circular structures can become elliptic if there is a great difference in the speed of sound. Perhaps bigger mistakes can be made when investigators are performing in vitro studies using water or excised tissue at room temperature. The problem with water can be avoided by using a salinity of 4.62% (see Table 9-1) , in which the speed of sound is 1540 m per second. The speed of sound in excised, fixed tissue at room temperature also varies from body temperature speeds. Although the speed-of-sound errors can be quite important in many situations, the larger errors often may occur because the beam patterns are not ideal (i.e., infinitely narrow and pencil-like) and the duration of the interrogation pulse is not infinitely short. The earlier discussion explains imperfections of beam patterns, and later I discuss how these imperfections can cause errors in area and volume measurements. First, some of the errors that can occur from a finite duration of the interrogation pulse are illustrated in Figure 9-12 . The beam width is assumed to be very narrow.

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Two situations (a short and a long pulse) are shown in which the beam passes from a hypoechoic Figure 9-12 Diagram illustrating how the range resolution (related to the length of the interrogating pulse) can increase thickness of the ultrasound appearance of a hyperechoic layer. See text for explanation.

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to a hyperechoic layer, then back to a hypoechoic layer, again through a hyperechoic layer, and back to a hypoechoic layer. The two types of pulse are shown at different positions along the structure. They are shown just as they are entering the hyperechoic layers and just after the trailing edge of the pulse exits the hyperechoic layers. The resulting A-mode lines are illustrated. The key points here are that the beginning of the echo starts at the leading edge of the pulse, passing from a hypoechoic to a hyperechoic region, but the end of the echoes from the hyperechoic to hypoechoic passage do not end until the trailing edge clears the hyperechoic layer. The two pulse durations, when used for linear scanning of the two layers, then produce images as illustrated. With the long-duration pulse, the hyperechoic layers appear much thicker than they really are and the distance between the layers appears shorter than it really is (compare d2 on the figure with d1). Therefore, the pulse duration (which is of course related to the range resolution) if excessive may result in quite an error in layer thickness measurements. This has been a concern in measuring the layers of intestinal walls in gastroenterology,[83] measuring blood vessel walls, and measuring cardiac wall thickness. This consideration has brought up the topic of leading to leading boundary edge outlining and trailing to leading edge with correction methods.[84] [85] The next consideration is the effects of lateral beam width, which are illustrated in Figure 9-13 for narrow pulses and in Figure 9-14 for long pulses. The transducer is on the left with a beam pattern diverging to the right. Two situations are shown: (1) when the beam encounters boundaries fairly perpendicularly ( see Fig. 9-13A and Fig. 9-14A ) and (2) when the beam encounters boundaries obliquely ( see Fig. 9-13B and Fig. 9-14B ). In Figure 9-13A , the A-line echoes from a tubular structure (perhaps a shortaxis left ventricular view) are illustrated. Echo 1 arises from the proximal wall and echo 2 from the distal wall. Even with a short-duration pulse, echo

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4 is of longer Figure 9-13 Diagram illustrating how a short-duration pulse with a lateral beam pattern that is diverging and has a finite width can affect the measurement of wall thickness. The lateral beam width is related to the lateral resolution of the system. A, Beam tends to encounter the wall fairly perpendicularly. B, Beam encounters the wall at an oblique angle. See text for discussion. Figure 9-14 Diagram illustrating how a long-duration pulse with a lateral beam pattern that is diverging and has a finite width can affect the measurement of wall thickness. The lateral beam width is related to the lateral resolution of the system. A, Beam tends to encounter the wall fairly perpendicularly. B, Beam encounters the wall at an oblique angle. Note the increase in the wall echoes compared with those of Figure 9-13 . See text for a detailed discussion.

duration than echo 2 because a portion of the beam encounters the distal wall earlier than in Figure 9-13A (normal encounter). The effects of the longer pulse are shown in Figure 9-14 . Echoes 1 and 2 are of longer duration than those of echoes 1 and 2 in Figure 9-13A because of the effect illustrated in Figure 9-12 . In addition, echoes 3 and 4 are of longer duration than 3 and 4 in Figure 9-13B . If one is measuring the inside dimension or inside area of a chamber, the oblique encounter with a wide beam reduces the inside dimensions of the structure (compare d2 with d1 in Figure 9-13 ). This effect is even further aggravated by the long pulse (compare d2 in Figure 9-14 with d2 in Figure 9-13 ). This phenomenon can contribute to the underestimation of chamber or vessel area measurements with ultrasound. The final consideration is the effect of the beam width on the elevation direction. In Figure 9-15A a tubular structure is imaged so that the ultrasound imaging plane encounters the wall of the tubular structure perpendicularly. If the lateral beam width is extremely narrow and the pulse is very short, the image that is generated is similar to that illustrated in Figure 9-15C . The geometry of the imaged structure is faithfully reproduced. However, if the imaging plane encounters the wall at an oblique angle, because it has a certain beam width, it in essence images a thick oblique slice through the wall, like the slice illustrated in Figure 915B . Considering that echoes are generated as long as a portion of the beam is cutting tissue, the imaging of the structure shown in Figure 9-15B

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results in an ultrasound image as in Figure 9-15D (i.e., essentially an image with a reduced cross-sectional area of the inner chamber and increased area of the outer contour). In the real imaging situation, the lateral beam width and pulse duration also contaminate the image; therefore, the cross section of the inner cavity is reduced even more and the outer border area increased more than shown in Figure 9-15D . These effects may play important 199

Figure 9-15 Diagram illustrating how the elevation resolution (i.e., a finite beam width in the elevation direction) can affect the ultrasound image obtained from a tubular structure. A, Beam pattern encounters the wall in the elevation direction (direction out of the paper) at a fairly perpendicular angle. B, Beam encounters the wall in the elevation direction at an oblique angle. C, Type of image of the wall structure that is produced with perpendicular encounter as in A. D, Type of image of the wall structure that is produced with an oblique encounter as in B. Note the reduced inside area and enlarged outer area.

roles in causing underestimation of the inner area or volume (such as the volume of the left ventricle) of chambers or vessels. Much of the underestimation reported in the literature when measuring volumes (e.g., with 3D ultrasound) may arise from the oblique encounter with nonperfect beam patterns and pulses. Therefore, by orientating the imaging beam of the probe so that it encounters the organ walls as perpendicularly as possible, the best accuracy can be obtained. The method reported by Gopal et al[86] [87] in making 3D measurements of left ventricular volume is favorable from this viewpoint. It is also possible to correct for some of these artifacts by the way the contours are outlined. Perhaps, in some of the measurements in which underestimation was not reported, the outlining was performed in a manner that placed the border well into the echo boundary of the image. It is therefore very important to understand the various measurement artifacts that can arise and try to design measurement methods to minimize these effects.

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202

Chapter 10 - Three-Dimensional Echocardiography Approaches and Applications Florence H. Sheehan MD

Two-dimensional echocardiography provides visualization of many structures in the beating heart; however, interpretive skills are needed for the observer to mentally formulate the heart's complex three-dimensional anatomy. In three-dimensional echocardiography, the spatial location and orientation of each two-dimensional image plane is recorded with the image so that information from multiple images can be analyzed jointly. This permits multiplanar image data to be assembled into three-dimensional displays that facilitate the assessment and communication of anatomic relations. The three-dimensional format also enables the quantification of the size, shape, and function of cardiac structures with minimal geometric assumptions, a particular advantage when dealing with disease-distorted anatomy or complex shapes such as the right ventricle. Although threedimensional echocardiography was conceptualized in 1961, most of the advances were made during the past decade after fast and inexpensive computers became more readily available; Belohlavek et al[1] have reviewed the earlier work.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Modes of Three-Dimensional Echocardiography Three-dimensional echocardiography is often equated with volumetric imaging to obtain spatial visualization of cardiac anatomy[2] [3] (Fig. 10-1) . In this mode of three-dimensional echocardiography, spatially dense image data sets are acquired and processed to permit the shape of the structures to be appreciated visually using three-dimensional display formats such as surface rendering, which employs shading to indicate topology. The image data set can be opened at any cut-plane to provide a surgeon's eye view of the heart's interior. The third dimension can also be appreciated using stereoscopy or holography.[4] [5] In the surface modeling mode of three-dimensional echocardiography, the three-dimensional surface of the targeted structure is reconstructed based on tracings of its border from multiple image planes (Fig. 10-2) . All chambers and valves can be reconstructed, as well as intracardiac structures such as the papillary muscles and chordae tendineae for quantitative analysis of size, shape, function, and spatial relationships between structures. Surface modeling is the mode of three-dimensional echocardiography that provides superior accuracy in measuring ventricular volume and mass, and for accurate, reproducible measurement of a variety of cardiac descriptors. Volumetric imaging is primarily used to search visually for structural abnormalities such as congenital defects or deformed valves, although volumetric data sets can also be analyzed to measure volume or a defect's size. In both modes of three-dimensional echocardiography, quantification currently requires manual image analysis. Because both modes of three-dimensional imaging involve 203

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Figure 10-1 Volumetric imaging provides a realistic, "surgeon's eye" view of the heart. This study is of an in vitro heart imaged in a water bath. AML, anterior mitral leaflet; AoV, aortic valve; LV, left ventricle; LVOT, left ventricular outflow tract; PML, posterior mitral leaflet; RVOT, right ventricular outflow tract. (From Sheehan FH, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M, Fitzpatrick JM [eds]: Medical Image Processing and Analysis. Bellingham, Wash., SPIE Press, 2000, pp 609–674.)

the acquisition of image data continuously through the cardiac cycle, it is possible to prepare the data in time-varying format for visual review of the heart's dynamic function or for quantitative analysis of asynchronous events. As for visualization at end-diastole and end-systole, dynamic presentation is easily automated in volumetric mode.[6] For quantitation, however, the border tracing must be repeated at every time point, a daunting prospect until the accuracy and reliability of automated border detection suffices to be used clinically. Figure 10-2 Left ventricular endocardial surface of a normal subject at end-diastole, reconstructed using the piecewise smooth subdivision surface method from freehand transthoracic scanning.

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Image Acquisition The intended approach to data analysis determines the method for image acquisition. In general, imaging for surface reconstruction uses free hand scanning. In contrast, the tight format required for volumetric imaging has until recently mandated the acquisition of these data sets using a mechanical device at fixed spatial intervals. Because certain methods for surface reconstruction incorporate assumptions concerning the position and orientation of the image planes, the requirements for a particular analysis need to be met during acquisition. Violation of the assumptions introduces error into the analysis.[7] Tracking Systems Knowledge of the position (x, y, z) and orientation (ρ, phi, theta) of the ultrasound transducer permits assembly of the images and their derived data in three-dimensional space. There are a number of methods for tracking the transducer during scanning. These methods can be classified into mechanical, line of sight, and magnetic. Each technology has its own advantages and limitations. The oldest type of mechanical system employs a series of articulated arms with encoders at the joints (Fig. 10-3) . The scanhead is placed at one end of the system and the other end (the base) is rigidly mounted to a reference frame. Reading the encoders provides rotational information about the articulated arms attached to that joint. Knowing the length of the arms and the rotations yields the position and orientation of the transducer with respect to the base. The major limitations to using mechanical arms are bulk and intrusion into the measurement space. It is awkward for the sonographer to manipulate the arms to reach all required positions and orientations. Each degree of freedom in the arm's motion presents a potential source of error.[8]

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204

Figure 10-3 Schematic representation of an articulated arm for mechanical tracking of the ultrasound transducer. This arm has 6 degrees of freedom. (From Nikravesh PE, Skorton DJ, Chandran KB, et al: Ultrasonic Imaging 1984;6:48–59.) Figure 10-4 Mechanical tracking permits acquisition of images in parallel planes (A), angulated scans (B and C), or rotational scans (D) from the transesophageal window. (From Flachskampf FA, Franke A, Job FP, et al: Am J Cardiac Imaging 1995;9:141–147.)

205

Another mechanical approach is to rotate or angulate the transducer within a constant location while recording the angle (Fig. 10-4) . Rotational scans are generally performed at the apex around the long axis of the left ventricle but can also be acquired at parasternal, subcostal, suprasternal, or transesophageal windows for volumetric imaging, such as to assess congenital defects.[3] [9] [10] By acquiring a full 180-degree rotation and checking that the first and last images are mirror images, one can be assured that transducer position was maintained during image acquisition. Rotational scanning is the most common acquisition mode for volumetric imaging. Angulating the transducer from a fixed position produces a fanlike are of images and has been successfully performed in the transthoracic parasternal window for the left and right ventricles [11] and in the transesophageal approach.[12] [13] One major disadvantage of rotational and angulated scanning is that not all hearts fit within the image volume circumscribed by the rotated or angulated sector, so that the margins of dilated hearts even in children may be incompletely imaged.[14] If the left ventricle can be visualized completely within a parasternal rotation, experimental studies indicate that the accuracy of volume measurement is greater than with an apical scan, presumably because of the low incidence angle of the ultrasound beam to most of the myocardial wall.[15] A second disadvantage is that poorly visualized structures cannot be recovered by scanning elsewhere, because imaging is limited to one acoustic window. Third, the quality of the images often varies when the transducer is rotated mechanically about a fixed axis; in contrast, freehand scanning permits adjustment of the image plane to obtain optimal image quality.[16] A fourth disadvantage of rotational and angulated scans is the relatively limited

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spatial resolution in the far field where the image planes are more widely separated. For visualization of congenital defects, this problem is handled by centering the axis of rotation over the region of interest. Linear scanning, also called bread-loafing, parallel slicing, or pullback scanning when referring to transesophageal acquisition, generates images in parallel planes (see Fig. 10-4) . The narrow intercostal space limits a transthoracic interrogation of the entire ventricle.[2] However, partial scans still permit specific localized defects to be studied, for example, to examine congenital atrioventricular valve defects or to examine the success of a surgical correction.[17] Complete data sets can occasionally be obtained from the subcostal window.[17] A transesophageal echocardiography system was developed to obtain parallel image planes by straightening the esophagus[18] (Fig. 10-5) . Unfortunately, this maneuver displaces the transducer posteriorly away from the apex.[6] Owing to these acoustic window restrictions, linear scanning is more commonly used in abdominal imaging. Line of sight systems include ultrasonic and optical tracking systems. Ultrasonic tracking systems typically utilize a single sound wave source and three fixed, known sensors[19] [20] (Fig. 10-6) . The speed of sound through air allows the range between the source and sensors to be determined. Triangulation determines position. Multiple sound sources are required to determine orientation. Ultrasonic systems suffer from shadowing, ambient noise, Figure 10-5 Diagram of system for parallel tomographic image acquisition. After the transesophageal echocardiographic probe is positioned posterior to the heart, the carriage is straightened and the transducer is retracted with the use of a stepper motor to obtain closely spaced (1 mm) images. (From Wollschlaeger H, Zeiher AM, Geibel A, et al: Transesophageal echo computer tomography of the heart. In Roelandt JRTC, Sutherland GR, Iliceto S, Linker DT [eds]: Cardiac Ultrasound. London, Churchill Livingstone, 1993, pp 181– 185.)

and interference due to acoustic reflections. The accuracy depends on maintaining constant air temperature, which affects the velocity of sound by about 2% per 10°C. [21] Furthermore, the need to maintain a clear path between transmitter and sensor restricts the sonographer's movement, the device produces unpleasant sounds, and the size of the sensor impedes imaging. Optical systems are not temperature sensitive but do suffer not only from shadowing but also from high cost and inflexibility, the latter due to the need to keep the cameras in a known alignment. Therefore, they have

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not been applied to three-dimensional echocardiography. The magnetic field system generates three orthogonal fields whose strength and direction are detected by a small, light receiver mounted on the transducer [21] [22] [23] (Fig. 10-7) . Only magnetic field systems combine the following: (1) 206

Figure 10-6 Ultrasonographic transducer with three spark gaps (arrowhead) mounted. This configuration provides direct transmission of audible sound toward the localizing array of four microphones. (From Handschumacher MD, Lethor JP, Siu SC, et al: J Am Coll Cardiol 1993;21:743–753. Reprinted with permission from the American College of Cardiology.)

They are able to track the position and orientation of the scanhead during freehand scanning; (2) they allow acquisition of images from randomly oriented image planes; (3) they allow acquisition of images from multiple acoustic windows; and (4) they permit imaging within the body as well as transcutaneously. The disadvantages Figure 10-7 Schematic of three-dimensional echocardiographic image acquisition using a magnetic field system to track the position and orientation of the ultrasonographic transducer. (From Nguyen TV, Bolson EL, Zeppa M, et al: Am J Cardiol 1999;84:208–213. Reprinted with permission from Excerpta Medica Inc.)

are that sources of ferromagnetic interference such as hospital beds must be distanced from the field, and the system's safety for patients with pacemakers or implanted defibrillators is unknown. A novel ultrasonography machine has been developed that is capable of acquiring a pyramidal volume of image 207

Figure 10-8 Schematic of the image set acquired using a matrix array transducer. Demonstrated are two adjustable orthogonal B-scans perpendicular to the transducer and three adjustable C-scans parallel to the face of the transducer. (From Zwas DR, Takuma S, Mullis-Jansson

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S, et al: J Am Soc Echocardiogr 1999;12:285–289.)

data using a two-dimensional array transducer[24] (Fig. 10-8) . Because it obtains the entire image set from one cardiac cycle instead of assembling images acquired over multiple cardiac cycles, this "real-time" system eliminates the assumption, inherent in multiple beat analysis, that all of the component two-dimensional images fall on the same phase of the cardiac cycle and that the function, position, filling, and rhythm of the heart remain constant throughout imaging. The disadvantages are that images are acquired in a single acoustic window, enlarged hearts will not fit within the pyramid, a specialized ultrasonography machine must be purchased, and image quality is poorer than for three-dimensional echocardiography acquired using conventional ultrasonography machines.[25] In addition, the C-scan images, which are short-axis cross-sectional views parallel to the transducer face, have relatively poor lateral resolution. Consequently, volume and mass are underestimated and less accurate than measurements made from the B-scan images.[26] The speed of the three-dimensional acquisition enables scans to be obtained without sedation, even in infants.[27] One system provides real-time tracking of image plane position and orientation in addition to recording these parameters. The current image's location is indicated by a line of intersection with a previously acquired reference or "scout" image[20] (Fig. 10-9) . This technology helps to verify that the short-axis images are being acquired in nonintersecting image planes, a requirement of the polyhedral surface reconstruction method.[28] Use of a tracking system assumes that the patient will remain in the same position throughout imaging. To avoid inadvertent patient movement during image acquisition, it is important to explain the procedure in advance, coach the patient through the phases of the study, and carefully monitor the patient's position. Mechanical tracking also assumes system stability, but probe slippage can occur during a rotation or other manipulation.[29] Therefore, it is prudent to check the image data for possible misregistration, to obtain accurate quantitative analysis. To avoid using tracking systems, some investigators succeeded in producing three-dimensional reconstructions of the left ventricle based on freehand scans within a single acoustic window, by making assumptions concerning the location of the image planes. In one method, the alignment of short-axis contours along a parasternal long-axis contour is deduced from their vertical span and distance from the transducer.[30] Another approach is to assume the spatial location of the image planes based on the

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anatomy visible in the image. Fazzalari et al[31] located two orthogonal apical views by scanning anatomically, then rotated the transducer ±45 degrees away to record two additional views, which sufficed to reconstruct the left ventricle. Aakhus et al[32] located three standard apical views anatomically and then assigned to each its theoretical angular rotation. Though ingenious in their utilization of image data to substitute for tracking, these methods' assumption that the image planes were correctly positioned anatomically may not be correct.[33] Imaging Protocol One advantage of three-dimensional compared with two-dimensional echocardiography is that the quantitative analysis does not rely on the ability of the sonographer to acquire images positioned properly in certain standard views relative to the patient's cardiac anatomy. That is, when the reconstructions and measurements are derived from five or more image planes, the locations of those planes are not tightly prescribed. This is because the volume and function measurements are made from surface reconstructions rather than from geometric assumptions. There remain certain minimal requirements, however. The most important are visualization of the apex to define the long-axis length of the left ventricle, and adequate coverage of the ventricle. The protocol for image acquisition is dictated first by the tracking system and then by the reconstruction method. The least flexible are the mechanical systems that acquire a rotational or angulated scan from a fixed position within a single acoustic window or a linear scan from the esophagus. In contrast, articulated arms, acoustic locators, and magnetic field tracking systems permit freehand scanning. Freehand scanning has the potential for allowing the images to be acquired from whatever combination of acoustic windows and views provides optimal image quality for a given subject. The surface reconstruction program may limit this freedom, however. For example, the polyhedral surface reconstruction method requires nonintersecting short-axis views,[34] and the bicubic spline representation was designed for multiple long-axis views.[35] In contrast, the piecewise smooth subdivision surface method and methods based on spherical templates 208

Figure 10-9 Photograph of the line of intersection display. The long-

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axis view (center) is the reference image showing the "line of intersection" display identifying the location of the short-axis images obtained for volume computation. Below and to the sides are the individual short-axis cross sections from apex to base, with endocardial borders outlined. (From Sapin PM, Schroder KM, Gopal AS, et al: J Am Coll Cardiol 1994;24:1054. Reprinted with permission from the American College of Cardiology.)

accept intersecting short- and long-axis views.[36] [37] [38] Since patients vary in the image quality available at the parasternal versus apical windows, having the flexibility to acquire images at either or a combination of windows increases study yield and interpretability. Electrocardiographic and Respiratory Gating Because a three-dimensional image or surface reconstruction is assembled from the data of multiple cardiac cycles, it is necessary to segregate the acquired two-dimensional images according to phase in the cardiac cycle. This may be done manually, by selecting the image frames occurring at end-diastole and end-systole with the aid of the electrocardiogram (ECG), visually assessed chamber area, and closure of the mitral and aortic valves. Technology is available for triggering the acquisition of a cycle of images beginning at the R wave on the ECG in each plane; a volumetric set of image data can thus be accumulated at fractional or temporal intervals through the cardiac cycle. More sophisticated systems also filter out ectopic and premature beats. One should be aware that each ultrasonographic image requires a finite time interval for inscription. Thus, for example, the images showing the peak of the R wave on the ECG trace will cover variably overlapping time intervals around end-diastole, unless triggering is employed. This is unlikely to cause significant error, however, because end-diastole and end-systole are the periods of minimum change in chamber dimension. Analysis of contrast ventriculograms has shown that reducing the frame-rate from 30 to 15 frames per second did not increase error in measuring left ventricular volume or function.[39] On the other hand, reconstructions based on multiple cardiac cycles will be affected by the variable timing if the structure is moving rapidly, for example, a valve leaflet during opening. For fetal imaging in which no ECG is available for gating, retrospective cardiac gating can be performed using Fourier analysis of pixel intensity to reconstruct dynamic volumetric data sets.[40] Patient respiration alters the position of the heart within the chest. In freehand scanning, the patient is coached to breath-hold at end expiration without a Valsalva maneuver. Even heart failure patients are able to

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perform multiple 6-second breath-holds with brief rests in between.[41] In device-driven systems, the image acquisition may be gated to the respiratory cycle, such as by impedance measurement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Ventricles For quantitative analysis of ventricular size, shape, and function from threedimensional echocardiographic scans, it is necessary to extract the borders of the structure of interest from the images that have been acquired in multiple planes, reconstruct the structure from the borders, and make the desired measurements from the reconstructed surface. The advantage of this approach is that highly accurate representation of structures such as the left or right ventricle can be achieved from which its 209

Figure 10-10 (color plate.) System for image analysis. The twodimensional images are reviewed (right), and the borders of the target organ and associated anatomic landmarks are traced. Using position and orientation information from the tracking system, the x and y coordinates of each border are transformed into x, y, and z coordinates for display in a three-dimensional window (left) in which image and border registration can be verified. Here the red and green borders are traced from the left ventricular endocardium and epicardium, the blue and violet from the right ventricle, and the spheres from valve orifices, ventricular apices, and other anatomic landmarks. (From Sheehan FH, Bolson EL, McDonald JA, et al: Comput Cardiol 1998;25:649– 652. Copyright © 1998 IEEE.)

dimensions, shape, and function can be measured directly without geometric assumptions. The disadvantage is the labor required to trace the borders. Methods are being devised to alleviate the labor of tracing by automatically detecting heart borders from the images (see Chapter 7) . Also, a rapid analysis can be made from a small number of images by sacrificing some of the accuracy or information content (see "Measurement of Volume"). Border Tracing

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Human variability in border tracing has a greater impact on the accuracy and variability of quantitative analysis than error in image plane tracking or image timing relative to the ECG.[7] However, the multiplanar nature of three-dimensional echocardiography makes it possible to review tracings in their spatial as well as their temporal context. That is, border definition can be assisted not only by playing a cardiac cycle of images to track motion but also by using image information from adjacent or intersecting planes, or both, to compensate for poor image quality.[36] Another advantage of threedimensional imaging is the ability of some surfacing algorithms to handle partial borders rather than requiring a complete contour in each image plane.[36] [42] The missing information in one plane is provided in an intersecting plane or interpolated by the surfacing algorithm from nearby border data. A recommended design feature in the tracing software is handling the border as an overlay rather than replacing pixels in the image. [42] This allows the border display to be turned off while the original image is reviewed and then on again to verify that the tracer still agrees with the border location. A three-dimensional display format for reviewing traced borders facilitates the identification of discrepant borders (Fig. 10-10) . Based on their frequency and location, it is then easy to determine whether a single image was misinterpreted or a set of images was misregistered, such as due to patient movement.[42] The technological tool that will have the greatest impact on bringing threedimensional echocardiography into clinical practice is, of course, automated border detection. Numerous studies have already been performed to solve this problem, but none has yet succeeded. Current automation algorithms are reproducible but not accurate. For example, performing three-dimensional echocardiography with acoustic quantification by online integrated backscatter analysis produces smaller endocardial contours and volumes than by manual tracing.[43] Identification of the endocardial and epicardial contours can be aided using myocardial contrast enhancement.[44] Greater accuracy as well as reproducibility in measuring myocardial mass has been obtained in animal studies. It is important to employ a long-lasting contrast agent that persists into the myocardial phase to avoid attenuation from the chamber opacification and to obtain a time window long enough for the threedimensional echocardiographic scan. Doppler myocardial imaging can increase the yield and accuracy of three-

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dimensional echocardiography by using the frequency shift of the returning ultrasound signal in addition to its amplitude. Because the frequency shift is relatively independent of attenuation by chest wall structures, 210

Doppler myocardial imaging provides more complete endocardial boundary detection (80% to 85%) than gray scale images (67% to 71%; P < .05).[45] Surface Reconstruction Many methods have been developed for reconstructing the ventricular endocardial and epicardial surface from traced borders (Table 10-1) . The methods vary in (1) the assumptions or constraints placed on the input data, (2) geometric manipulations inherent in the reconstruction model, and (3) fidelity to cardiac anatomy. Given a series of ventricular contours in parallel planes, it is easy to extrapolate between the contours to produce an enclosed surface if desired for visualization. Such surfaces take a simple form with a single opening at the valve plane if produced from short-axis images alone, since long-axis views are needed to define both valves. Another approach for images acquired in an apical rotational scan is to intersect the traced borders with a series of parallel planes perpendicular to the long axis. The points where each plane intersects the traced borders are connected into a polygon or fitted to produce a curved contour[35] [46] [47] (Fig. 10-11) . Similar surfacing can be performed even if the images are not apical; for example, parallel planes can be intersected with borders from randomly oriented views.[48] The advantage here is the ability to utilize whatever combination of views provided optimal interrogation in a given patient. Instead of intersecting a set of traced borders with parallel planes, the borders can be intersected with a set of rotationally related planes to define the ventricular surface.[19] Borders traced from an angulated scan lend themselves to reconstruction using a cylindrical coordinate system.[11] The contour's area in each pair of adjacent image planes and the plane's angle of tilt are used to compute a wedge volume; the sum over all wedges is the chamber volume. It is computationally simpler to connect the points of intersection in each plane to form a polygon instead of fitting a curve to them,[49] but one risks underestimation of slice area and ventricular volume because, for example,

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the area of a dodecahedron is 4.5% less than the area of the circle circumscribing it.[7] A comparison of 12-, 24-, 48-, and 96-sided polygons revealed that 48 sides provides accurate representation of the shape and area of borders traced from photographs of short-axis slices of excised hearts.[50] The polyhedral surface reconstruction method operates on borders traced from short-axis images. Each traced border is divided into 180 points, and corresponding points on adjacent borders are connected to form a triangular tiled surface (Fig. 10-12) .[51] To enable the connections, the input image planes need not be parallel but must not intersect each other within the body of the ventricle. To check the short-axis images being acquired, Gopal et al initially record one or two parasternal long-axis images on which they display the locations of the short-axis images as lines of intersection. [20] The left ventricle is reconstructed from about eight or nine contours; the outflow tract is not delineated. This method has been Figure 10-11 Bicubic spine surface reconstruction. A, Left ventricular borders are traced from apical views. The algorithm compensates for skewed scan planes by stretching their borders lengthwise to match the longest long axis. The borders are then intersected with planes parallel to the mitral plane. B, Wire-frame representation of the reconstructed endocardial surface. (From Maehle J, Bjoernstad K, Aakhus S, et al: Echocardiography 1994;11:397–408.)

extensively validated in vitro and in vivo for left ventricular volume and mass[52] [53] [54] and can also be applied to the atria. Reconstruction can also be done based on a spherical coordinate system. In the method by Martin et al,[38] the x, y, and z coordinates of the manually traced borders are mapped into spherical coordinates before being fitted into a surface. These authors had developed a transesophageal echocardiography probe capable of recording images from both angulated and rotational sweeps.[55] Their approach was therefore designed to facilitate the handling of borders obtained from image planes with nontraditional orientations. An advantage of this method is that irregularly spaced and partial borders can be utilized. The method tends to round off all aspects of the ventricle, however, making it difficult to create sharp edges or orifices at the valves. A similar tendency to smooth out the valve planes is seen in a method based on deforming an initially spherical

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TABLE 10-1 -- Accuracy in Measuring Ventricular Volume and Fun Reconstruction Chamber Standard Subject Method Studies in Phantoms and Heart Models Phantom True Balloons Connect borders Phantom True Balloons Polyhedral surface Phantom True Balloons Polyhedral surface

Patient, Parameter N r

Phantom True Phantom True Phantom True

Phantom True

Phantom True

Phantom True Phantom True

Balloons Spheric template Balloons Spheric template LV Volumetric models scan; sum of slices Balloons Piecewise smooth subdivision surface Balloon Volumetric + pump scan; sum of slices

Balloon Polyhedral + pump surface Balloons Bicubic spline

Volume

8 0.

Volume

17 0.

Volume

30 0.

Volume

11 0.

Volume

10 0.

Volume

23 0.

Volume

6 1.

EDV

29 0.

ESV

0.

EF

0.

Volume

—

Volume

8

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Studies in in vitro Left Ventricles LV True Heart casts LV True Excised hearts LV True Excised hearts LV True Excised hearts LV

True

Heart casts Excised hearts Excised hearts Excised hearts Excised hearts

LV

True

LV

True

LV

True

LV

True

LV

True

Excised hearts

LV

True

Excised hearts

LV

True

Connect borders Connect borders Connect borders Connect borders; polar coordinates Polyhedral surface Spheric template Spheric template Spheric template Volumetric scan; sum of slices Piecewise smooth Subdivision surface Bicubic spline

Volume

5 0.

Volume

10 0.

Volume

11 0.

Volume

7 0.

Volume

15 0.

Volume

11 0.

Volume

28 0.

Volume

10 0.

Volume

14 0.

Volume

5 1.

Volume

Excised Volumetric Volume hearts scan; sum of slices LV True Excised Pyramidal scan; Volume hearts sum of slices Studies in Experimental Animals

11

7 0.

12 0.

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LV

Thermo

LV

Balloon in heart

LV

LV

LV

Balloon in heart

balloon in heart

Balloon in heart

Exptl Spherical animals coordinate system Exptl Spheric animals template

Exptl Spheric animals template

Exptl Spheric animals template

Exptl Spheric animals template

SV

57 0.

EDV

46 0.

ESV

38 0.

SV

38 0.

EF

38 0.

Volume

69 0.

SV

32 0.

EF

32 0.

EDV

19 0.

ESV

0.

SV

0.

EF

0.

Volume

84 0.

EDV

46 0.

ESV

38 0.

SV

38 0.

EF

38 0.

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LV LV

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Flow

Exptl animals Conductance Exptl catheter animals

Pyramidal scan; SV sum of slices Volumetric EDV scan; sum of slices ESV EF

LV LV

LV

LV

Balloon in heart Angio

Angio

Angio

Studies in Humans LV Doppler LV

Doppler

LV

MRI

Exptl Cylindrical animals Patients Sum of slices

Patients Connect borders; polar coordinates

Children Connect borders

Normal subjects Normal subjects Normal subjects

Spheric template Spheric template Polyhedral surface

Volume

14 0. 15 0.

0. 0. 11 0.

EDV

9 0.

ESV

7 0.

Volume

8 0.

SV

0.

EF

0.

Volume

26 0.

SV

0.

SV

19 0.

SV

14 0.

EDV

15 0.

ESV

0.

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LV

LV

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Angio

RNA

Normal Polyhedral subjects surface

Patients Polyhedral surface

EDV

39 0.

ESV

0.

EF

0.

EF

51 0.

0. LV

MRI

LV

Doppler

LV

MRI

Patients Polyhedral surface Patients Piecewise smooth subdivision surface Children Polyhedral surface

LV

Angio

Patients Polyhedral surface

LV

RNA

LV

MRI

Patients Volumetric scan; sum of slices Patients Volumetric and scan; sum of normal slices subjects

EDV

26 0.

ESV SV

0. 5 0.

EDV

12 0.

ESV EF EDV, ESV

0. 16 0.

EF

41 0.

EDV

46 0.

ESV

0.

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LV

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EF EDV

0. 24 0.

"

ESV

24 0.

"

EF

24 0.

SV

20 0.

EDV

50 0.

RNA,

ESV

0.

MRI

EF

0.

Angio

Patients Volumetric scan; sum of slices

Thermo LV

Angio,

Patients Bicubic spline

Right Ventricular Validation Studies RV True Heart Volumetric casts scan; sum of slices RV True Excised Volumetric hearts scan; sum of slices RV True Heart Replication and casts interpolation of three borders RV True Heart Piecewise casts smooth subdivision surface RV MRI Patients Volumetric scan; sum of slices

Volume

15 0.

Volume

14 0.

Volume

24 0.

Volume

10 0.

EDV

16 0.

ESV

0.

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RV

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MRI

Children Volumetric scan; sum of slices

EDV

13 0.

ESV

0.

EF

0.

2D, two-dimensional; Angio, ventricular angiography; EDV, end-diastoli volume; Exptl, experimental; LOA, limit of agreement (95%); LV, left vent subjects; R, Pearson correlation coefficient; RNA, radionuclide angiography standard error of the estimate; SV, stroke volume; Thermo, thermodilution.

214

Figure 10-12 Wire-frame reconstruction of a left ventricle using eight unequally spaced, nonintersecting short-axis image planes positioned with the line of intersection. (From Gopal AS, King DL: Threedimensional echocardiography. In Otto CM [ed]: Clinical Echocardiography. Philadelphia, WB Saunders, 1996, p 140.)

template along rays originating from the sphere's center to fit the traced data[36] (Fig. 10-13) . Nevertheless, this method has been flexible enough to reconstruct a variety of shapes, including excised ventricles and phantoms with localized protuberances, papillary muscle indentations, and aneurysms, and it accepts partial borders from images providing only limited visualization of the target chamber. It has yielded good accuracy in both left and right ventricular volume and mass measurement.[56] [57] [58] A method that measures ventricular volume accurately may not accurately represent the ventricle's three-dimensional shape, because there is an infinite number of shapes that contain a given volume. Most methods have been validated only for volume because no clinical applications Figure 10-13 Reconstruction using an initially spheric template. Left, Traced borders of human right ventricular cast with inflow region at upper left, apex below, and outflow at upper right. Right, Surface fitted to traced borders. (From Jiang L, Handschumacher MD, Hibberd MG, et al: J Am Soc Echocardiogr 1994;7:151–158.)

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beyond volume, ejection fraction, and mass were foreseen. However, regional ventricular function, stress, and shape can only be analyzed using methods that reconstruct the ventricle with spatial accuracy. Only one method has been shown to faithfully reproduce the threedimensional shape of the ventricle: the piecewise smooth subdivision surface reconstruction method.[37] [37] This method was developed to avoid the inherent limitations of other methods, which restricted their anatomical accuracy or application to different three-dimensional image acquisition techniques. A triangulated abstract mesh is designed as a model for each ventricle. Because it embodies knowledge about the expected shape of the targeted structure, the abstract mesh allows diversely shaped structures to be reconstructed, such as the left and right ventricles, atria, and papillary muscles. For example, parts of the mesh can be marked as sharp to handle valve and venous orifices and the junction of the right ventricular septal and free walls (Fig. 10-14) . Additional facets can be added to produce complex shapes. In fitting the abstract mesh to the manually traced borders, the locations of anatomic landmarks such as the apex, borders of the interventricular septum, or papillary muscle insertions can be retained for future reference (Fig. 10-15) . All four chambers of the heart can be reconstructed (Fig. 10-16) . Two methods have been developed to evaluate a three-dimensional surface's spatial fidelity to an anatomic specimen. Pirolo et al[59] made a solid biventricular model from photographs of a canine heart cut into parallel short-axis slices and showed that measurements of slice volume, slice area, slice perimeter, and other dimensions were similar in the photographs and model. Since the images were made after the heart had been sliced, this approach avoided the difficult problem of aligning the model to the specimen to ensure that the measurements were made at anatomically corresponding locations. To validate the piecewise smooth subdivision method, surface reconstructions 215

Figure 10-14 (color plate.) The piecewise smooth subdivision surface reconstruction method begins with a control mesh that embodies knowledge concerning the expected shape of the target organ. A, For the right ventricle, the control mesh indicates that there are sharp edges (indicated by yellow line segments) around the orifices of the pulmonary and tricuspid valves (filled with pink) and between the septal (blue) and free (green) walls. B, Final surface

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reconstruction of the same patient at end-diastole (wire mesh) and end-systole (blue). (From Sheehan FH, Bolson EL, McDonald AL: Comput Cardiol 2000;27:119–122. Copyright © 2000 IEEE.) Figure 10-15 (color plate.) In the piecewise smooth subdivision method, borders of anatomic landmarks can be carried through to the final surface reconstruction. A, Wire mesh display of borders traced of the left ventricular endocardium (black), mitral annulus (blue filled circles), aortic valve (green filled circles), and papillary muscles (red). B, On the fitted surface, the locations of the papillary muscle insertions are displayed in red.

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Figure 10-16 All four chambers can be reconstructed using the piecewise smooth subdivision method. The atrioventricular valves are fitted using a Fourier series approximation,[98] and the aortic and pulmonary valve orifices are fitted to a planar ellipse.

of animal hearts generated by three-dimensional echocardiography were aligned using anatomic landmarks to laser scans of plaster casts of those hearts; the small orthogonal distance between the two three-dimensional data sets proved this method's spatial fidelity[37] [37] (Fig. 10-17) . Measurement of Volume The advantage of three-dimensional echocardiography is its avoidance of geometric assumptions concerning the shape of the ventricle that are required to estimate volume from one or two two-dimensional views. This is the reason for the superior accuracy of three-dimensional echocardiography in volume determination, since the suitability of geometric assumptions is less for diseased hearts than for normally shaped hearts. The advantage is greater Figure 10-17 The piecewise smooth subdivision method produces reconstructions that accurately represent the three-dimensional surface of the target organ.[37] Left, laser scan of a plaster cast of a left ventricular endocardium; right, surface reconstruction.

for the right ventricle. One reason is that its complex shape is more difficult to model geometrically than that of the left ventricle. In addition, the

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paucity of clear anatomic landmarks makes it difficult to obtain reproducible views; the resulting ambiguity in image plane position increases the variability of volume measurements by two-dimensional echocardiographic methods. It is actually not necessary to reconstruct the endocardial surface to measure ventricular volume. Simpson's method is a computationally simplistic approach that can avoid assumptions regarding the ventricle's shape if the heart has been imaged in closely spaced parallel image planes. Then the area enclosed by the endocardial border traced in each plane is multiplied by the distance between the planes to obtain the volume of its corresponding "slice" of the ventricle. The volume of the ventricular chamber is then computed as the sum of the slice volumes. As in integral calculus, the accuracy of the volume measurement and of the threedimensional shape representation increases with the number of slices or image planes. Once the ventricular endocardium has been reconstructed, volume is measured directly from that surface without further assumptions. For example, to determine volume from a triangulated mesh surface, the volumes of tetrahedra defined by each surface triangle and a common origin are summed. Validation of the accuracy of ventricular volume measurement by threedimensional echocardiography is performed both in vitro and in vivo. The robustness of a reconstruction method can be assessed from its ability to handle not only a range of ventricular sizes but also a variety of shapes, as might be observed in diseased hearts. In vitro testing permits validation against the true value rather than against the modality that threedimensional echocardiography is supposedly replacing. In vitro models include phantoms such as balloons or fixed heart specimens. Experimental in vivo validation has been performed by positioning a balloon within the left ventricle for measuring volume over the cardiac cycle.[60] Clinical validation is by comparison with other imaging modalities such as magnetic resonance imaging, radionuclide ventriculography, contrast ventriculography, or computed tomography, or with flow measurements by Doppler or thermodilution. All clinical imaging modalities have their respective sources of error and variability, however. For example, magnetic resonance images smooth out trabeculae on the ventricular endocardium, thus shortening the border and diminishing the computed volume.[61] Therefore, it can be argued that comparing the novel—in this case three-

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dimensional echocardiography—with a more established imaging modality is actually an assessment of intermodality variability.[58] Because of the labor required to manually trace ventricular borders, it is advantageous to determine the minimum number of image planes that need to be analyzed and the effect of further data reduction on volume accuracy. Some investigators have found that volume or its derived parameters can be accurately determined from just three or four image planes.[15] [31] [32] [62] [63] [64] However, the standard error of the estimate when volume is measured from so few views is substantially larger than the 4 to 11 mL reported using borders from at least eight views.[30] , [51] [53] Buckey 217

et al[11] recommended at least six to eight planes, depending on the size of the ventricle. Their analysis was performed in vitro, however; a larger number of image planes may be needed clinically to compensate for poorer image quality. Tanabe et al[65] were able to obtain accurate volumes with only four to six axial images. Since this study was performed in small in vitro canine hearts, the results are comparable to a report that a 1 cm distance between serial parallel image planes suffices for the left ventricle. [66] In patients, left ventricular volumes measured from a three-dimensional image set acquired by rotational scanning and cut into 8-mm thick shortaxis paraplanes was comparable to volumes measured from 2.9-mm thick paraplanes, leading the authors to recommend the sparser data set for its speedier analysis.[67] However, because endocardial definition on paraplane images is poorer than on the original images used to synthesize them, the more complete volumetric data afforded by a dense rotational scan fails to provide superior accuracy over a simpler and faster freehand scan.[68] A theoretical analysis found that variability in left ventricular volume and mass determination by three-dimensional echocardiography decreases in proportion to the reciprocal square root of the number of slices.[69] In general, there is an inverse relationship between the knowledge inherent in the reconstruction method and the number of borders that must be traced. The spherical template method requires at least 8 to 12 images for accurate left ventricular volume determination but does not constrain the position or orientation of the images.[70] The polyhedral surface method utilizes fewer borders, eight or nine, but the reconstruction algorithm assumes nonintersecting short-axis image planes.[51] The piecewise smooth subdivision surface reconstruction method incorporates knowledge of the

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expected shape of the left ventricle via its abstract mesh.[37] It is thus able to provide accurate volume measurement and shape representation with as few as five randomly oriented left ventricular borders once the valve orifices have been defined.[71] Even this method cannot reconstruct the left ventricle from two borders, however. To proceed from such sparse data requires further shape assumptions such as relating the ventricle to an ellipsoid and produces only moderate accuracy (see Table 10-1) .[51] [53] Relatively little research has been performed to define the minimum amount of border data required to measure right ventricular volume accurately. Buckey et al[11] recommended at least six to eight planes for the right as well as the left ventricle, depending on the size of the ventricle. Janicki et al[66] recommend that more image data be acquired for the right ventricle because of its shorter longitudinal length and continually changing cross-sectional area. The smallest number of borders required uses just three standard, mutually orthogonal views (coronal, sagittal, and shortaxis), which are replicated and then interpolated.[72] Good accuracy is achieved by assuming that the shape of the coronal outline is constant over the anteroposterior extent of the ventricle. Measurement of Ventricular Mass The volume of a ventricle's myocardium is computed as the difference between its endocardial and epicardial volumes (Table 10-2) . Ventricular mass is determined by multiplying the myocardial volume by its specific gravity. Three-dimensional echocardiography has been shown in most studies to provide highly accurate and reproducible measurements of left ventricular mass; however, results for the right ventricle have been much poorer against both in vitro and in vivo standards. Reasons include incomplete visualization of the entire epicardium and greater obscurity of the myocardial-epicardial interface compared with the blood-tissue interface. The underestimation of right ventricular mass in one study was attributed to the surfacing method's tendency to round out sharp edges such as at the apex and distal outflow tract.[57] Measurement of Ventricular Function Nearly all validation studies have shown that measurement of ejection fraction by three-dimensional echocardiographic surface reconstructions more closely resembles the comparison standard than by two-dimensional techniques (see Table 10-1) . This is not unexpected, given the higher accuracy of three-dimensional echocardiography for volume measurement.

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Visual assessment of regional ventricular function can be performed from volumetric data sets using software to display each region dynamically. The image data can be cut to provide views that optimize endocardial definition and orientation. In one study, however, more segments could be visualized by standard two-dimensional echocardiography than from a real-time threedimensional echocardiographic scan. [73] Quantitative analysis of regional left ventricular function in three dimensions remains in its infancy, in part because most reconstruction algorithms fail to produce surfaces that are sufficiently faithful to the shape of the ventricular surface. Unlike volume, a measurement whose accuracy can be determined objectively, the analysis of regional function assumes knowledge of the pathway by which anatomic points on the left ventricular contour at end-diastole can be tracked to the same anatomic location at endsystole. For two-dimensional image analysis, attempts have been made to track endocardial "landmarks" or surgically implanted midwall markers. The wide discrepancy (90 degrees) between the trajectories for apical motion derived from these tracking studies acts to diminish confidence in their validity, however. The alternative is to use models of wall motion instead (for a wider discussion, see Chapter 5 ). The models developed to analyze wall motion from three-dimensional image sets are similar to those for two-dimensional images. An example is measuring wall motion radially toward a central origin or long axis.[7] [74] Because of the lack of objective evidence, such models are validated using empirical criteria such as sensitivity and specificity in distinguishing normal subjects from patients, just as was done for two-dimensional models. One study compared six reference systems and found greatest agreement with visual assessment when wall motion is measured toward the long axis.[75] More studies have been performed assessing regional function from the local change in wall thickness. Wall thickening more accurately reflects function 218

TABLE 10-2 -- Accuracy in Measuring Ventricular Mass by Three-Di Reconstruction Patients, Chamber Standard Subject Method N r SEE Re LV True Excised Polyhedral 11 0.995 2.91 Y =

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LV

True

LV

True

LV

True

LV

True

LV

True

LV

True

hearts surface Excised Piecewise hearts smooth subdivision surface Excised Volumetric hearts scan; sum of slices Excised Bicubic spline hearts Excised Volumetric hearts scan; sum of slices Excised Pyramidal scan; hearts sum of slices

Excised after scan LV True Excised after scan LV at risk Contrast Exptl animals LV

MRI

LV

MRI

LV

MRI

Volumetric scan; sum of slices Pyramidal scan; sum of slices

Volumetric scan; sum of slices Normal Polyhedral subjects surface Children Polyhedral surface Patients Volumetric scan; sum of slices

8.2 5 0.998 2.5 Y = +1

7 0.95 11.97 Y = - 2. 15 —

14 0.98

12 0.99

—

M diff 1.4 9.6 Y = +0 2.8 Y = +0

8 0.997 1.05 Y = 2.2 21 0.94

8.5 Y = +1

8 0.947 21

Y= +2

15 0.93

9.24 Y = +1 12 — — M diff 5.8 12 0.78 35.8 Y = 0.6

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LV

MRI

LV

MRI

RV

True

Patients Volumetric scan; sum of slices Patients Deformable shell

20 0.99

8.5 Y = 0.7

25 0.99

6.9 Y = +1

Excised Piecewise 10 0.996 4.5 Y = hearts smooth subdivision surface RV True Hearts Polyhedral 12 0.96 2.7 Y = +0 excised surface after scan RV MRI Patients Volumetric 16 0.65 — Y = scan; sum of +1 slices 1D, one-dimensional; 2D, two-dimensional; ED, end-diastolic; ES, end-sy left ventricle; MRI, magnetic resonance imaging; RMS, root mean square; S estimate. in hypertrophied hearts[76] and is independent of artifact caused by cardiac translation. The disadvantage is the need to trace and reconstruct the epicardium in addition to the endocardium. This doubling of work is not merely time consuming but also introduces additional opportunity for error. Imaging must be performed with the intent to quantify regional wall thickening, so care is needed to ensure that the epicardium is included in the scan sector throughout the cardiac cycle. Three-dimensional wall thickening analysis requires measurement of wall thickness orthogonal to the left ventricular wall. Analysis can been performed using twodimensional techniques on short-axis image planes located near the middle of the left ventricle. Accuracy is necessarily diminished in the more apical planes, however, where the oblique sectioning causes wall thickness to be overestimated. One method to measure regional wall thickness orthogonal to the left ventricular wall is to segment the myocardium into 64 elements and divide

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each element's volume by the mean distance between its endocardial and epicardial surfaces. [77] The centersurface method measures wall thickness along locally orthogonal vectors in the same way as in the centerline method for two-dimensional borders.[41] [78] [78] The vectors are normal to a three-dimensional medial surface constructed midway between the endocardial and epicardial surface reconstructions (Fig. 10-18) . Wall thickening is computed as the change in thickness normalized by the local end-diastolic wall thickness. To indicate the severity of an observed value's deviation from normal, thickening can be converted to units of standard deviations from the mean of the reference population, analogous to the approach used in two-dimensional measurement [78] [78] (Fig. 10-19) . Regional left ventricular function has also been evaluated from reconstructions of the endocardium and epicardium using finite element analysis. [79] More recently, a biomechanical model has been developed incorporating information about local fiber direction as well as material properties. The deformation of the myocardium was tracked between enddiastole and end-systole using curvature analysis.[80] The strain measurements predicted by this model have agreed well with sonomicrometer measurements in vivo.[81] Estimation of Infarct Size Infarct size is assessed from echocardiograms by measuring the amount of dysfunctional myocardium. The underlying assumption is that the extent of infarction correlates linearly with the extent of dyssynergy.[82] As in measuring ventricular volume, accuracy depends on the number of echocardiographic image planes analyzed and on the assumptions concerning the spatial location of the image planes and the geometry of left ventricular shape. Owing to limited visualization of the left ventricle, twodimensional echocardiographic approaches have quantified the proportion of infarcted myocardium, such as its 219

Figure 10-18 (color plate.) The centersurface method permits measurement of wall thickness orthogonal to the local myocardial wall. [158] Here the close and distant thirds of the left ventricle have been "cut away" to provide a tomographic view. A medial surface (green) is constructed midway between the endocardium (yellow) and the epicardium (blue). Chords are drawn perpendicular to the centersurface and extended

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to the endocardial and epicardial surfaces. The length of each chord is the local wall thickness.

circumferential extent in a short-axis view, rather than absolute infarct mass.[83] [84] [85] Such proportional measurements are unsuitable for serial studies because the fraction is affected by myocardial remodeling and thinning of the infarct region. Because of the more comprehensive assessment of the left ventricular surface, three-dimensional echocardiography yields absolute infarct size measurements that correlate closely with the true values in experimental animals.[86] [87] The principal difficulty with estimating infarct size from the extent of dyssynergy is deciding whether to include hypokinetic myocardium in the infarct region. Theoretically, including hypokinetic myocardium will overestimate infarct size because akinesis results from fibrosis of as little as 25% of the thickness of the myocardium.[88] If the infarct is transmural, then the infarct mass is truly equivalent to the mass of myocardium displaying akinesis or dyskinesis.[87] However, the transmurality of an infarction is difficult to determine ante mortem. When regional function is quantified rather than assessed visually, it is still necessary to select a threshold. In one clinical study, infarct mass by magnetic resonance imaging was associated with myocardium having absolute wall thickening greater than 2 mm.[89] The area of dysfunctional endocardium has been reported to correlate better with histopathologic infarct size than does the mass of dysfunctional myocardium, probably because of assumptions in the mass calculation.[86] Perhaps more importantly, three-dimensional measurements are also more consistent and less variable than two-dimensional.[86] The advantage here is that use of this metric as a clinical trial end point may reduce the number of patients needing to be enrolled. Following coronary occlusion, echocardiographic contrast material can be injected to define the size of the region at risk of infarction by its failure to show contrast enhancement.[90] [91] The contrast defect region corresponds to the infarct region in the absence of coronary reperfusion. Using volumerendering techniques, the size and location of the perfusion defect can be displayed within the framework of the reconstructed ventricle. Shape There has been relatively little progress in developing techniques for analyzing regional left ventricular shape from three-dimensional echocardiographic data. Most of the research has been conducted on

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magnetic resonance images despite the poor spatial resolution in the longitudinal axis. However, the methods developed for one modality are theoretically transferable to another modality. The most common approaches to shape analysis are geometry based. Regional curvature analysis has been applied for tracking endocardial displacement [80] and analyzing regional left ventricular strain. [81] The center-axis method measures distance radially from the long axis to the endocardial surface[92] (Fig. 10-20) . Its advantage is ease of computation; however, the results shift with the location of the long axis. The alignment method differs conceptually from previously described shape analysis methods because it directly compares the shape of a patient's heart with a reference heart after aligning them along regions of similar topography[93] (Fig. 10-21) . Shape differences are then Figure 10-19 (color plate.) Example of the visual presentation of regional left ventricular function in three dimensions. Here the wall thickening at each vertex has been converted into units of standard deviations from the mean of a normal reference population. Cool colors represent levels of hypokinesis; warm colors, hyperkinesis (color scale developed by S. Maza). Visualization as an overlay on the patient's three-dimensional surface facilitates appreciation of the location, extent, and severity of dysfunction.

220

Figure 10-20 A, The center axis method measures regional shape in terms of radial distance from a center axis to the endocardial surface. To normalize for heart size, the distance from the center axis to the reconstructed surface is divided by center axis length. The left ventricle is divided into 16 segments whose shape is calculated as the mean radial distance of the points lying within that segment to the center axis. B (color plate.), The severity of shape abnormality is displayed using a color scale allowing visual appreciation of the difference between a normal subject (NL74) and anterior and anterolateral dilation in a patient with idiopathic dilated cardiomyopathy (CM99). (From Munt BI, Leotta DF, Martin RW, et al: J Am Soc Echocardiogr 1998;11:761– 769.) Figure 10-21 (color plate.) The alignment method measures regional shape in terms of distance between the patient's heart and a reference such

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as normal average heart.[93] Here a normal end-diastolic left ventricular endocardial surface (mesh) has been deformed at the inferoapical wall (arrow) and aligned with its original, undeformed self (red surface) along regions of similar shape. The magnitude of shape abnormality can be quantified using the centersurface algorithm.

221

measured in terms of local orthogonal distance between them. Applications of regional shape analysis include assessing left ventricular remodeling following acute myocardial infarction,[93] [94] assessing regional stress,[95] and defining the pathophysiology of functional mitral regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Valves Three-dimensional echocardiography has contributed much more to the understanding of valvular heart disease than to the understanding of the ventricles. The ability to reconstruct the three-dimensional geometry of the valves, associated structures, and blood flow has not only provided mechanistic insight into the nature of disease processes but also totally altered our perception of normal cardiac anatomy. Owing to the dynamic nature of valvular function, which cannot be appreciated in the arrested heart, surgeons must rely on preoperative assessment based on imaging. For this reason, it has been a major focus of investigation to improve our knowledge of the structure-function relationship to better assist in surgical planning. Mitral Valve and Mitral Apparatus It was three-dimensional echocardiography that finally provided the tools for elucidating the saddle shape of the mitral annulus in humans.[96] Through three-dimensional reconstructions, this study demonstrated how the alignment of leaflet to annulus in the apical four-chamber view can give the artifactual appearance of mitral valve prolapse, resulting in false diagnosis by two-dimensional echocardiography. The underlying concept, that incomplete Figure 10-22 Schematic of the mitral annulus as reconstructed in three dimensions using Fourier series. The various dimensional parameters provide assessment of annular shape. (From Kaplan SR, Bashein B, Sheehan FH, et al: Am Heart J 2000;139:378–387.)

visualization of complex anatomical structures can lead to profound misunderstanding of their functionality, has stimulated the application of three-dimensional echocardiographic evaluation of numerous other cardiac

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pathologies to ensure that similar oversights are avoided. The most studied component of the mitral valve apparatus is the annulus. It can be visualized clearly from a rotational transesophageal scan and reconstructed by fitting a smooth spline curve or Fourier series approximation to the traced points.[97] [98] The area and eccentricity of the annular orifice are measured from its projection onto a least squares fitted plane. Annular height is measured relative to this plane. The accuracy of three-dimensional echocardiography for measuring these parameters has been validated in vitro.[98] Additional parameters of interest are its peak-topeak and valley-to-valley spans and annular motion, consisting of descent toward the left ventricular apex and tilting (Fig. 10-22) . Four-dimensional analysis of the annulus' shape change throughout the cardiac cycle is performed by reconstructing the annulus at multiple time points defined either from cardiac events or by normalization.[99] [100] [101] [102] The shape and dynamics of implanted annuloplasty rings can also be analyzed.[103] Ignoring the valve's three-dimensional shape, annular area can be estimated by planimetering its apparent orifice from short-axis paraplanes.[104] All components of the mitral apparatus can be reconstructed and analyzed quantitatively, not just the annulus. Leaflet reconstruction permitted analysis of leaflet-annular relations.[96] The left ventricle and left atrium can be reconstructed using surfacing methods.[105] The papillary muscles can be located and measured even though they are difficult to reconstruct because of their highly variable anatomy, and the chordae tendineae can be analyzed for position and orientation[105] (Fig. 10-23) . Such measurements are useful for evaluating functional mitral regurgitation.[42]

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Figure 10-23 (color plate.) Reconstructions of the left ventricular endocardium at end-diastole and the papillary muscles of a normal subject (left) and a patient with idiopathic dilated cardiomyopathy (right). The principal chordae tendineae proceeding from each papillary muscle head are displayed as pink or green line segments. The reconstructions enable visualization of the enlargement of the left ventricle, the outward displacement of the papillary muscle insertions, and the divergence of the chordae tendineae in the cardiomyopathy patient.

Aortic Valve

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There are several theoretical advantages of three-dimensional echocardiography for measurement of aortic valve area. First, direct planimetry of the valve's cross-sectional area or measurement of its radius from two-dimensional echocardiography is subject to error because of offaxis imaging of the valve, especially if shape is distorted due to congenitally bicuspid or degenerative stenosis. Second, calculation of valve area using the continuity equation method depends on proper positioning of the Doppler sample volume. Malpositioning of the image plane by as little as 10 degrees or 1.5 mm causes significant overestimation of valve area.[106] Three-dimensional echocardiography permits the orifice to be directly planimetered from a paraplane image that is correctly positioned anatomically in the true orifice, providing more consistent agreement with area determined by the Gorlin formula or the Doppler continuity equation than planimetry from two-dimensional images.[107] Regurgitant Flow The application of three-dimensional echocardiography for measurement of regurgitant flow rate using three-dimensional echocardiography promises an improved means for estimating effective orifice area and regurgitant volume, which are more reliable indicators of regurgitation severity. The increased accuracy that has been achieved can be attributed to avoidance of geometric assumptions inherent in the two-dimensional proximal isovelocity surface area (PISA) method. These assumptions are that the isovelocity surface is hemispheric in shape, the orifice is small and circular and lies on a flat surface, and the region adjacent to the flow convergence region is free of flow interference. To date, more research has been performed for assessment of mitral than aortic regurgitation. One reason is that the saddle shape of the mitral annulus and the variable leaflet topography violate the assumptions of the PISA method. There are several approaches for assessing valvular regurgitation that totally avoid using the PISA method. These methods are subject to pathophysiologic variations and imaging factors, however. One threedimensional approach is measurement of the regurgitant orifice area from a volumetric data set by direct planimetry from a cut plane providing a left atrial view of the orifice at its maximal area.[108] The authors validated it in vivo by demonstrating agreement between the three-dimensional and PISA measurements. Another approach is to analyze the dimensions of the regurgitant jet from multiplanar color Doppler images. For example, threedimensional Doppler measurement of proximal cross-sectional jet area

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correlated well with vena contracta area determined using laser flow visualization in vitro, although with 25% overestimation despite optimization of gray level threshold and color gain.[109] This error was attributed to poor lateral resolution of Doppler echocardiography, resulting in difficulty delineating the edge of the jet core from the adjacent entrainment flow. Jet volume agreed closely with mean and peak regurgitant flow, regurgitant fraction, and regurgitation stroke volume by electromagnetic flow meter in animal models of aortic regurgitation.[110] [111] Jet volume also agreed closely with angiographic grade of regurgitation in patients with eccentric as well as central jets, whereas two-dimensional jet area predicted regurgitation severity in central jets only.[112] One reason for the 223

greater accuracy of three-dimensional analysis is difficulty finding the plane displaying the maximum area of wall jets and eccentric jets from two-dimensional images. It is important to be aware that the relationship between jet volume and regurgitant flow-rate varies with Doppler angle, jet origin, jet-wall relationship (centric or eccentric), and orifice shape.[113] [114] It is possible to modify the PISA method to eliminate invalid assumptions. In vitro studies have shown that a number of factors affect the size and shape of the isovelocity surface. Its area varies with orifice shape, being larger for elongated split orifices than for circular or triangular orifices. Its shape is flattened near the orifice and eccentric for eccentric orifice shapes. One three-dimensional study described the shape of the flow convergence region as "complex and unpredictable" in its variety.[115] The varying local shape of the isovelocity surface away from hemispheric reflects the variations in leaflet and inlet geometry.[116] Simply reconstructing the actual three-dimensional isovelocity surface observed from Doppler data has been shown to enhance accuracy in measuring aortic regurgitation in an animal model.[117] The analysis of the regional shape of the three-dimensional reconstruction can be taken one step further, to compute the flow rate at each constituent of the Doppler isovelocity surface from its area and anglecorrected velocity (Fig. 10-24) . Integration over the entire surface generates a regurgitant flow measurement that correlates with true flow in vitro over a range of flow-rates and orifice shapes.[114] This is thus a Figure 10-24 (color plate.) Cut-away view of Doppler isovelocity

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surfaces in the flow convergence region (FCR), as measured at three velocity thresholds. The surfaces are flattened and elongated, reflecting the eccentric shape of the orifice (rectangular).[159]

geometry-independent method for quantifying regurgitant flow.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Processing Three-Dimensional Echocardiographic Data for Visual Assessment Visual assessment of image data has two forms. Volume rendering is a three-dimensional presentation of image data from closely positioned planes to obtain a realistic "surgeon's eye" view of the heart primarily for visual assessment. [118] For displaying the results of a quantitative analysis, three-dimensional surface reconstruction and graphics may be employed to facilitate appreciation of the anatomic location and extent of observed abnormalities. In volumetric mode, multiple images are acquired in close proximity and regular intervals and processed to create voxels, or three-dimensional image elements. Digital reformatting and image processing may be used to fill the space between image planes through interpolation to obtain a solid volume of voxel data, align the image data temporally, segment the tissue from the blood pool, and filter out noise and artifact. An algorithm assigns a binary value to each voxel to classify them as lying within versus outside the myocardium. The surface of the myocardium is generated by the computer from the boundary between voxel classes. The spatial dimension is displayed using volume rendering, a format that uses different gray levels 224

to indicate the depth of cardiac structures so that those lying "further" from the viewer are dimmer. Image processing tools are applied to give the sense of reality to the presentation, for example hiding distant regions that lie behind proximal regions. Lighting can also be arranged to illuminate "closer" features more brightly and cast shadows on surfaces behind them. The feeling of depth can be enhanced by computing pairs of images that are slightly rotated relative to each other and presenting one of these to each eye to create a stereoscopic display. Another tool allows the voxel set to be rotated and translated smoothly so that the viewer can peer into the heart

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from different perspectives. One advantage of volumetric imaging is the ability to compute twodimensional cross sections ("any-plane views") in planes that could not be acquired from standard precordial or transesophageal transducer positions. [3] [6] The quality of such synthetic images tends to be inferior, however, probably because of the interpolation required to fill in gaps between the original images. Most frequently, volumetric images are acquired using a mechanical device to obtain a closely spaced rotational scan. Techniques are being developed for interpolation between images acquired at high spatial frequencies from angulated freehand scans, however.[119] Recently, a method has been developed for spatial compounding of ultrasonographic images that combines information from multiple views while assigning higher weights to image data acquired at a near 0 incidence angle to the ultrasound beam. [120] Applied to scans of the shoulder, the method improved image quality in synthetic planes as demonstrated by reduction in the width of the border of the bone and lessened variability in intensity along the border. This kind of novel technology thus can enhance the information content of paraplane images while permitting combined volumetric analysis of multiple freehand scans. Prior to the ready availability of three-dimensional computer graphics and inexpensive computers, multiplanar image data were presented in various two-dimensional formats. One approach is to divide the left ventricle into four longitudinal quadrants that can be laid out "flat."[121] This permits assessment of endocardial surface area and area of infarcted myocardium based on regional dysfunction.[85] The left ventricle can also be presented as a bull's eye; however, regional areas are distorted, with particular exaggeration of the area of the base.[35] [47] This distortion can be avoided by mapping the multiplanar two-dimensional data onto a three-dimensional surface reconstruction of the ventricle (see Fig. 10-19) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Applications of Three-Dimensional Echocardiography Clinical Applications The avoidance of geometric assumptions in measuring ventricular volume is an important factor in the greater accuracy of three-dimensional as compared with two-dimensional echocardiographic techniques. This is even more evident when evaluating disease-distorted hearts. For example, the volume, mass, and ejection fraction of left ventricles compressed by pulmonary hypertension and in single ventricles of left ventricular morphology is more accurately determined by three-dimensional than by two-dimensional echocardiography (using magnetic resonance imaging as the standard).[122] [123] Similarly, the asymmetric crescent shape of the right ventricle poses problems for modeling from two-dimensional views but can be accurately represented using three-dimensional echocardiography, even in patients with congenitally distorted anatomy.[14] The anticipation is that three-dimensional echocardiographic techniques are useful for monitoring patients at risk of developing right ventricular dilation and heart failure. Similar methods can also be applied for measuring atrial volume.[124] Pericardial effusion volume is more accurately measured by threedimensional than by two-dimensional echocardiography. The reasons extend beyond the elimination of geometric assumptions concerning the shape of the ventricle and the spatial location and orientation of the image planes. In particular, three-dimensional echocardiography affords better visualization of all levels of the heart and is thus able to handle loculated effusions that may be asymmetrical in shape and unusual in location.[125] Another clinical application in which three-dimensional echocardiography has proven superior to two-dimensional is measurement of aneurysm volume.[126] [127] The avoidance of geometric assumptions and ability to accept and utilize nonstandard views combine to permit reconstruction of the aneurysm separate from the body of the left ventricle. This tool may be

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useful in planning surgical repair, estimating the size of the residual left ventricle, evaluating the stroke volume wasted by dyskinesis, and computing the expected functional benefit of surgery. Diagnosis The volumetric mode offers great potential for enhancing the diagnostic yield of an echocardiographic examination for several reasons. First, the possibility of cutting the image data in any plane reduces reliance on sonographer experience and skill and may even provide views that are difficult to acquire from traditional acoustic windows.[3] [6] That is, the size, shape, and motion of cardiac abnormalities can be displayed from any perspective. Even static views, when displayed from different perspectives, can assist in identifying structural abnormalities, visualizing their shape, and measuring their extent. The volume-rendered display assists experienced reviewers in diagnosing congenital, valvular, and structural pathologies, presumably by reducing the requirement for mental integration of the image data, so that sensitivity and specificity for discriminating normal from abnormal hearts is significantly enhanced compared with diagnosis from two-dimensional views.[128] Three-dimensional imaging has been estimated to provide improved spatial understanding of cardiac pathology over conventional transesophageal echocardiography in about one third of cases.[129] Transthoracic three-dimensional echocardiographic image sets provide information not seen in the two-dimensional study in the same proportion (one third) of adults with congenital heart disease. [130]

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One application is to assess the extension of abscesses into neighboring structures and to visualize mass lesions.[131] Another application is assessment of cardiac tumors to determine their shape, dimensions, origin, location, and involvement of valves prior to surgery.[132] Cutplane views provide a surgeon's eye preview of cardiac anatomy, for example, of the aortic valve from an aortotomy or of the mitral valve from above or below ("atriotomy" or "ventriculotomy" view).[133] It is speculated that such visualization may prove useful in surgical planning. For example, mitral valve abnormalities could be visualized as they would be seen intraoperatively for discussion with surgical consultants.[17] In patients with congenital anomalies, three-dimensional echocardiography provides additional diagnostic information on the mitral valve, aortoseptal

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continuity, atrial septum, and atrioventricular septal defects.[130] [134] Identifying small lesions or visualizing thin structures such as the aortic valve is beyond the resolution of the image, however.[130] To facilitate interpretation, cutting planes can be displayed dynamically to review the motion of valves or other segments of cardiac anatomy. Intrauterine sonography can provides prenatal assessment of anatomic and functional status regarding the myocardium, valves, and great vessels.[135] Therapy Planning and Assessment Volumetric imaging has been touted for therapeutic evaluation of atrial septal and other congenital defects because it can cut the image data to provide en face views that provide direct visualization of the defect in children and adults by the transesophageal or transthoracic approach.[133] , [136] These views provide information on the shape of the defect and its location relative to adjacent structures. However, measurement of its size and shape from en face views has variable accuracy.[134] [137] [138] [139] Clinical applications are presurgical planning and evaluation of the success of transcatheter closure of the defect.[138] Transesophageal three-dimensional echocardiography of ventricular septal defects can also be performed to quantify their location relative to ventricular apices and valve insertions, area, and circumference, for planning surgical or catheter repair.[140] Intraoperative transesophageal three-dimensional echocardiography of the valves provides the surgeon with information complementary to that yielded by routine two-dimensional echocardiography in the form of additional morphologic definition or interpretation of abnormalities seen on two-dimensional study.[141] In this study, the greatest contribution as well as the greatest error of three-dimensional echocardiography was in identifying leaflet fenestrations. Visualization of the valve leaflets during mitral balloon valvuloplasty can be performed from the esophageal window to monitor the process, guide and optimize commissural splitting, and minimize valvular regurgitation by arresting the procedure once minor leaflet tears appear. [142] The functionality of rigid mitral annuloplasty rings and their impact on outflow tract patency can be assessed using threedimensional imaging and reconstruction.[143] These studies were performed using magnetic resonance imaging, but three-dimensional echocardiography analytic tools are currently available and can be applied to assess the flexibility of mitral annuloplasty rings even when the absolute accuracy of annulus dimension is suboptimal.[96] [98] [144] Volumetric reconstruction has also been shown to assist in presurgical

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planning for right as well as left ventricular outflow obstruction by providing visualization of the morphology of the obstruction.[145] [146] Reconstruction of the left ventricular outflow tract by tracing its border from parallel short-axis paraplane images provides characterization of the anomalies specific to hypertrophic cardiomyopathy, identification of abnormal geometry that may prove useful in understanding the mechanism of obstruction, and assessment of the efficacy of surgery in remodeling the outflow tract.[147] Physiology and Pathophysiology Three-dimensional echocardiography has unparalleled potential for elucidating the mechanism of disease processes, owing to its high spatial and temporal resolution. For example, four-dimensional analysis of the annulus has permitted characterization of how the normal mitral valve achieves area reduction during systole through a combination of perimeter shortening and shape modulation.[101] [102] Such techniques permit measurement of the extent to which annular dynamics and static dimensions may be altered by disease processes such as ischemic heart disease or cardiomyopathy. Three-dimensional echocardiographic analysis of the components of the mitral apparatus has been instrumental in elucidating the cause of functional mitral regurgitation.[101] [148] [149] Serial Studies Measurements of ventricular volume, mass, and ejection fraction by threedimensional echocardiography are far more reproducible than by twodimensional echocardiography or by visual assessment (Table 10-3) . The clinical advantage of reproducible measures is sensitivity in detecting changes in a patient's condition. For example, patients with valvular lesions require close monitoring to select optimal timing for a surgical repair. Another important clinical application is the long-term monitoring of right ventricular volume and function following surgical repair of congenital defects such as Fallot's tetralogy in patients with residual pulmonary valve dysfunction or an intra-atrial baffle for transposition of the great arteries. With two-dimensional techniques, variability was introduced by estimating right ventricular volume from image planes whose anatomic position may have been difficult to reproduce from study to study. With threedimensional imaging, this source of error is eliminated. One analysis of interobserver variability reported that three-dimensional echocardiography has a 92% to 95% probability of detecting a change of 15

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mL in left ventricular end-diastolic volume, of 11 mL in end-systolic volume, 226

TABLE 10-3 -- Variability in Measuring Ventricular Volume and Fu Patients, Method Parameter N Interob Polyhedral Volume 17 4. Polyhedral Volume 30 2.65

Chamber Standard Subject Phantom True Balloon Phantom True Balloon; distortions Phantom True Balloon Spheric Volume template Phantom True Balloon Volumetric Volume with scan; sum pump of slices EF LV True Excised Spheric Volume hearts template LV True Excised Spheric Volume hearts template LV True Excised Bicubic Volume hearts spline LV True Excised Volumetric Volume hearts scan; sum of slices LV True Excised Pyramidal Volume hearts scan; sum of slices LV True In vivo Spheric Volume (balloon) template LV True In vivo Volumetric Volume (balloon) scan; sum of slices LV Balloon Exptl Cylindrical Volume

11

2

29

1

11

3 4

28

3

11

-1

7

13

12

0.8 ±

14

3

14

2.

11

6±

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in heart

animals

LV

Doppler

LV

MRI

Normal subjects Normal subjects

LV

Angio

Patients

LV

RNA

Patients

LV

MRI

Patients

LV

RNA

Patients

LV

MRI

Patients

LV

Angio

Patients

LV

MRI

Patients and normal subjects

Spheric SV template Polyhedral EDV

14

2

15

4.

ESV Polyhedral EDV

39

10

51

8 — 10

26

8

25

7 4 5

12

<

16

< < 1.9 ±

ESV EF Polyhedral EF surface Polyhedral EDV surface ESV EF Volumetric EF scan; sum of slices Polyhedral EDV surface ESV EF Polyhedral EDV surface ESV Volumetric EDV scan; sum of slices

46

6

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LV

LV

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Angio

Angio, RNA, MRI

Patients

Patients

ESV EF Volumetric Volume scan; sum of slices EF Bicubic EDV spline

24

3 3 3

10

3 6

ESV 3 EF 3 RV True Heart Volumetric Volume 15 4 casts scan; sum of slices RV MRI Patients Volumetric EDV 16 4 scan; sum of slices ESV RV MRI Children Volumetric EDV 13 1.4 ± scan; sum of slices Angio, ventricular angiography; EDV, end-diastolic volume; EF, ejection experimental; LV, left ventricle; MRI, magnetic resonance imaging; RNA, r standard deviation; SEE, standard error of the estimate; SEM, standard error and a change in ejection fraction of 2% when a rotational scan is performed at 16-degree increments.[150] Another observer variability study found that three-dimensional echocardiography can detect a smaller change in left ventricular volume (11 to 13 mL) with 95% confidence than twodimensional echocardiography, which can only detect change that exceeds 21 to 24 mL.[69] However, no difference in variability was found between two-dimensional and three-dimensional measurement of mass.[69] An advantage also accrues to clinical research, since fewer patients need be enrolled in a clinical trial to obtain statistical power to detect a treatment effect.[151] Aid to Clinical Image Acquisition

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227

Unlike other tomographic imaging modalities, standard ultrasonographic image acquisition is heavily dependent on the skill and experience of the sonographer. It is often difficult to obtain standard views of the right ventricle.[14] Studies have shown that even standard views of the left ventricle are difficult to acquire consistently in the prescribed location, even by experienced sonographers. [33] Consequently, referral centers frequently repeat studies rather than trusting a study from an outside hospital or clinic. The resulting worsening of medical costs and inefficiency can, however, by improved by three-dimensional technology. One approach is to assist the sonographer in locating anatomically correct image planes for the standard two-dimensional echocardiographic views. An image plane positioning error that foreshortens the long axis by 1 cm may underestimate left ventricular volume by 5%.[7] By tracking the transducer, a line of intersection can be displayed on the ultrasonographic image that indicates the current image plane's position in relation to a previously acquired scout image to provide visual guidance (Fig. 10-25) . Such a system has been shown to reduce interobserver variability to one third the level observed for unguided measurements.[152] Performing three-dimensional echocardiography, which does not require standard views, yielded more accurate and reproducible ejection fraction determinations by novice sonographers that approached the performance of experts using twodimensional echocardiography in accuracy and reproducibility of ejection fraction determination.[153] Experts were always more accurate than novices for either three-dimensional or two-dimensional measurement, but the three-dimensional technology allowed novices to acquire Figure 10-25 Visual guidance to facilitate ultrasonogram acquisition in the anatomically correct spatial planes. A and B, A line of intersection indicates the spatial location of the current image plane where it intersects with "scout" images previously acquired in orthogonal views. C and D, More guidance is provided when the spatial orientation as well as location of the current image plane (translucent image) are displayed relative to the scout images.

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data sets of diagnostic quality. It is speculated that three-dimensional

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echocardiography may permit echocardiography in regions lacking skilled sonographers, if combined with remote expert interpretation. Modeling Three-dimensional echocardiography offers the ability to reconstruct the chambers, valves, and other structures of the heart in the highest spatial and temporal resolution of any imaging modality. These data have many potential uses. For example, surgeons involved in designing a total artificial heart have sought improved annular definition for planning inflow and outflow ports of the device. [154] Reconstructions of the endocardium and epicardium are useful for finite element analysis of left ventricular stress and material properties. [155] Heart reconstructions can also be used to model the stress and fatigue of pacemaker leads in any combination of implantation configurations[105] [156] (Fig. 10-26) . Three-dimensional echocardiographic reconstructions of valve geometries seen in mitral stenosis have been used to generate models by stereolithography for analysis of the relationship between cardiac structure, pressure, and blood flow.[157]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Three-dimensional echocardiography has the potential to become a major clinical imaging modality because it Figure 10-26 Reconstruction of a normal right ventricle illustrating its use for measuring various internal dimensions, such as the distances spanning the apex and centroids of the tricuspid and pulmonary valves (white lines). (From Sheehan FH, McDonald AL, Bolson EL: Paper presented at 11th International Conference on Mechanics in Medical Biology, April 2–5, 2000, Maui, Hawaii.)

offers realistic visualization and accurate quantitation in combination with ultrasonography's traditional advantages of cost, portability, and freedom from ionizing radiation. These qualities already make three-dimensional echocardiography a valuable and productive tool for clinical research. Application of three-dimensional echocardiography to the clinical environment awaits the development of automated image analysis.

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Section 3 - Ischemic Heart Disease

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Chapter 11 - The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room Diagnosis, Triage, Treatment Decisions, Outcome Samuel Wang MD Kirsten E. Fleischmann MD, MPH

Background and Principles Several million patients in the United States each year present to emergency rooms with chest pain suggestive of acute coronary syndrome. However, a minority of these patients are ultimately diagnosed with myocardial ischemia or infarction.[1] [2] Conversely, approximately 5% of those with acute myocardial infarction are mistakenly discharged from the emergency room.[3] [4] A considerable body of evidence has accumulated since the 1980s supporting the hypothesis that early treatment of myocardial infarction improves the rate of coronary arterial patency, myocardial salvage, and patient survival.[5] [6] [7] [8] [9] Thus, it is clear that

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early diagnosis and treatment of acute chest pain have significant benefits for the individual patient, and for the society that finances the health care. The diagnosis of myocardial infarction is usually made on the basis of the patient's clinical history, electrocardiogram (ECG), and serum cardiac enzyme levels. Although these three methods in combination provide a relatively effective diagnostic approach, each has its own limitations. Patients presenting with "atypical chest pain" not infrequently rule in for myocardial infarction; on the other hand, patients presenting with symptoms typically associated with acute coronary syndrome may not, in fact, have myocardial ischemia or infarction. Although ST-segment changes on ECG provide a useful diagnostic tool for acute coronary syndrome, they may be absent in the initial ECG in a significant portion of patients who subsequently 236

meet the criteria for myocardial infarction. Pericarditis or prior myocardial infarction with aneurysm formation can cause ECG changes similar to those in acute myocardial infarction; the examination of subsequent ECGs in the former case and comparison with previous ECGs in the latter may help with differential diagnosis. The presence of pre-existing left bundle branch block (LBBB) results in baseline repolarization abnormalities that limit the utility of ECG in the diagnosis of acute myocardial infarction in these patients. Although a number of criteria have been proposed to discern indicators of acute myocardial infarction within the LBBB morphology,[10] these criteria have been found to be insensitive in the diagnosis of acute myocardial infarction.[11] Determination of serum cardiac enzyme levels constitutes a more sensitive and specific test.[12] However, serum cardiac enzyme levels may not be elevated until several hours after the onset of myocardial infarction; therefore, sole reliance on this method may delay starting appropriate treatment. Echocardiography can be a useful adjunct in the assessment of patients with chest pain. By evaluating global ventricular function as well as regional wall motion, echocardiography may allow the early diagnosis of myocardial ischemia and infarction, as well as determination of the coronary vascular territory involved. It is also useful in the differential diagnosis of acute chest pain by excluding such possibilities as aortic dissection, effusive pericarditis, and aortic stenosis among other conditions (Table 11-1) ; these topics are covered in greater detail in their respective

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chapters in this book. In the remainder of this chapter, we concentrate on the current and developing applications of echocardiography to the early diagnosis of acute coronary syndromes, as well as their advantages, limitations, and potential impact on patient management and outcome.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography and the Physiology of Acute Ischemia Acute ischemia results in a cascade of biochemical and physiologic changes in myocardial tissue.[13] When coronary flow is cut off, biochemical changes are quickly followed by abnormalities in diastolic and then systolic function. Moreover, these functional changes may precede development of classic electrocardiographic changes or even development of symptoms[14] and occur well before release of detectable amounts of enzyme markers such as creatine kinase and troponin. Thus, development of systolic regional wall motion abnormalities such as those TABLE 11-1 -- Goals of Echocardiography in Evaluation of Patients with Acute Chest Pain Diagnosis of acute coronary syndrome Determination of coronary vascular territory involved Assessment of the area of myocardium at risk Evaluation of global ventricular function Exclusion of other cardiac causes of chest pain Aortic dissection Pericarditis (with effusion) Aortic stenosis Hypertrophic cardiomyopathy detected by echocardiography occurs at a relatively early stage after onset of ischemia. This has led to considerable interest in the use of echocardiography to aid in the diagnosis and prognosis of acute coronary syndromes and in defining the coronary territory involved.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Aspects of Echocardiography in the Emergency Department Image Acquisition Echocardiographic examination of patients with chest pain in the emergency room should concentrate on the evaluation of biventricular function and global and regional left ventricular wall motion to look for evidence of cardiac ischemia or infarction. It should also screen for other possible nonischemic causes of chest pain such as aortic stenosis, hypertrophic cardiomyopathy, effusive pericarditis, and aortic dissection. The standard transthoracic two-dimensional echocardiographic views should be used for evaluation of all the left ventricular wall segments, including parasternal long-and short-axis, apical long-axis, and apical twoand four-chamber views (Fig. 11-1) . If adequate image quality cannot be achieved from the apex, subcostal four-chamber and short-axis views or parasternal short-axis views with the transducer moved more apically may be acquired instead. Off-axis or oblique views make interpretation of regional wall motion abnormalities more difficult and should be avoided. A well-trained and experienced sonographer or echocardiographer is essential in such a clinical setting. The sonographer should be trained to obtain the required images in an efficient manner, avoiding spending time on aspects of the examination not needed for immediate clinical use. Attention should be paid to proper patient positioning, use of appropriate transducers, and adjustment of machine settings. High-frequency transducers may improve the visualization of apical structures. In obese patients or those with chronic obstructive pulmonary disease, lowerfrequency (2.0 to 2.5 MHz) transducers and a subcostal window may be used to optimize the images. Colorization of two-dimensional echocardiographic images and, more recently, echo contrast have also been used to enhance visualization of the endocardial border.

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Optimization of endocardial border definition is of utmost importance. In addition to the standard techniques mentioned, newer imaging modalities such as second harmonic imaging and contrast echocardiography can be used for this purpose. Commercially available echocardiographic contrast agents contain air-filled microbubbles which are small enough to pass through the pulmonary circulation after intravenous administration. They opacify both ventricular cavities, allowing the border between myocardium and blood to be more easily identified (Fig. 11-2) . This technique is especially effective when combined with second harmonic imaging, which also improves the visualization of other cardiac structures.

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Figure 11-1 Still frames from the echocardiogram of a patient with acute chest pain, showing severe hypokinesis of the anterior, septal, and apical walls, in parasternal short-axis (A, diastole; B, systole) and apical fourchamber (C, diastole; D, systole) views.

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Figure 11-2 Improvement in left ventricular endocardial border delineation with the use of intravenous echocardiographic contrast and second harmonic imaging (A, without contrast; B, with echocardiographic contrast).

In an early study by Horowitz et al[15] on the use of echocardiography in patients with acute chest pain, adequate images were obtained in 81% of the patients. A large, multicenter study performed in Denmark in the early 1990s involving 7001 patients early after an acute myocardial infarction reported assessable echocardiograms in 93% of the patients.[16] With continual advances in echocardiographic technology since that time, one can expect to obtain adequate echocardiograms in an even larger proportion of patients. Stress Echocardiography Multiple studies have demonstrated the safety of stress testing if myocardial infarction and unstable angina are ruled out after several hours

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of observation. Echocardiographic imaging may be used in conjunction with exercise or pharmacologic stress to assess for ischemia, depending on the patient's ability to perform adequate exercise. For exercise stress, one of the standard treadmill exercise protocols, such as the Bruce or modified Bruce protocol, can be used. Because wall motion abnormalities associated with exercise may be ephemeral after treadmill exercise terminates, echocardiographic examination should start within a few seconds after exercise terminates. This helps avoid significant decrease in heart rate below the maximum achieved, which may have an impact on the sensitivity of the test. An alternative exercise method is the supine bicycle protocol. A patient in a supine position exercises on a specially designed bicycle mounted on the echocardiographic examination table. The amount of energy spent increases with each 3-minute exercise stage. In this approach, echocardiographic images can be acquired during exercise, thereby eliminating the delay seen with treadmill exercise between the cessation of exercise and the start of imaging. In addition, images can be recorded at low, medium, and peak levels of exercise stress for comparison in this protocol, whereas only preand poststress images are generally recorded for treadmill protocols. The supine bicycle exercise protocol is preferred if spectral Doppler echocardiographic measurement of tricuspid regurgitation velocity is required for estimation of pulmonary artery systolic pressure. For patients unable to achieve adequate levels of exercise, pharmacologic stress testing can be performed. The intravenous dobutamine protocol is most commonly used in the United States. After acquisition of baseline resting echocardiographic images, dobutamine infusion is generally started at 5 µg/kg/minute, and increased to 10, 20, 30, and 40 µg/kg/minute at each successive stage of 3-minute duration. The test is terminated if the patient develops evidence of cardiac ischemia, hypotension as a result of vasodilation or left ventricular outflow obstruction, significant arrhythmia, or other dobutamine-related side effects or if 85% of maximum predicted heart rate is achieved. In patients who do not achieve adequate heart rate with dobutamine infusion at 40 µg/kg/minute, such as those taking beta blockers, atropine may be administered intravenously with doses of 0.1 to 0.25 mg each, up to a total of 1 mg. Second harmonic imaging has also been found to improve endocardial border definition, diagnostic accuracy,

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and interobserver agreement for dobutamine stress echocardiography in patients with impaired image quality. In a study by Franke et al,[17] second harmonic imaging without use of echocardiographic contrast increased the sensitivity for the diagnosis of coronary artery disease in patients with poor image quality from 64% to 92% (P < .001). Specificity was 75% for both imaging modalities. Improvement in endocardial border delineation was most pronounced in all lateral and anterior segments. Image Interpretation The accurate interpretation of regional wall motion abnormalities requires an experienced echocardiographer. Using various views from the study, wall thickening and systolic endocardial motion are evaluated for all left ventricular myocardial segments. Each segment is classified as hyperkinetic, normal, hypokinetic, akinetic, or dyskinetic. The American Society of Echocardiography recommends a 16-segment model for evaluation of regional wall motion (Fig. 11-3) .[18] Each segment is assigned a score on the basis of visual inspection of its contractility: normal, 1; hypokinesis, 2; akinesis, 3; dyskinesis 4; and aneurysm, 5. A semiquantitative measure of the extent of regional wall motion abnormalities, known as the wall motion score index (WMSI), can be calculated by averaging wall motion scores for all visualized segments. A normal left ventricle has a WMSI of 1, while a ventricle with more significant left ventricular dysfunction would have a higher WMSI. WMSI has been found to relate to infarct size on clinicopathologic studies[19] and to perfusion defect size on single photon emission computed tomographic (SPECT) imaging.[20] A similar wall motion index using a 14-segment model has also been found to be a predictor of long-term survival in patients with chest pain.[21] The evaluation of stress-induced regional wall motion abnormalities in stress echocardiography requires careful comparison of rest and stress images, which is facilitated by digital acquisition and display of such images. ECG-gated digital acquisition allows video clips lasting one to several cardiac cycles to be captured and stored in memory. Thus, several clips can be acquired and the most satisfactory one for each view selected for repeated comparative display. Comparison of rest and stress images from each view is facilitated by the use of side-by-side quad-screen display of synchronized cineloops. Digital image acquisition and display in stress

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echocardiography have been found to have comparable diagnostic accuracy for coronary artery disease to videotape recording, and superior interobserver and intraobserver agreement.[22] [23] Mohler et al[24] compared digital echocardiographic images with videotape images in a prospective study involving 117 patients admitted to the emergency department with chest pain and found 94% overall agreement regarding regional wall motion and good correlation in WMSI determined using these two different technologies. The authors concluded that digital echocardiographic imaging provides an accurate summary of the complete examination, as well as relevant diagnostic data for assessment of Figure 11-3 A 16-segment model for evaluation of regional wall motion as recommended by the American Society of Echocardiography. A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; PL, posterolateral; PS, posteroseptal. (Adapted from Schiller NB, Shah PM, Crawford M, et al: J Am Soc Echocardiogr 1989;2:358–367.)

patients presenting with chest pain to the emergency department.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Clinical Applications Triage of Patients with Chest Pain in the Emergency Department A number of studies have assessed the use of two-dimensional transthoracic echocardiography or stress echocardiography in evaluating patients presenting with chest pain and suspected acute coronary syndrome. [15] [25] [26] [27] [28] [29] [30] [31] [32]

Horowitz et al[15] studied 80 patients who presented with acute chest discomfort to the emergency department and had no previous myocardial infarction, valvular heart 240

disease, cardiomyopathy, or significant pericardial effusion. Twodimensional echocardiography was performed within 8 hours of admission. Locations of regional wall motion abnormalities were described using a five-segment model, with septal, anterior, posterolateral, posterior, and apical segments. The echocardiograms were technically inadequate in 15 patients (19%) in this study performed in the early 1980s. Of the 33 patients with clinical evidence of myocardial infarction, 31 had regional wall motion abnormalities on the initial echocardiogram (sensitivity, 94%). The other 2 patients had uncomplicated nontransmural myocardial infarctions. In comparison, the initial ECG was diagnostic of acute myocardial infarction in 45%, and the initial creatine kinase-MB level was elevated in 52%. Of the 32 patients without clinical myocardial infarction, 27 had normal regional wall motion on the initial echocardiogram (i.e., specificity, 84%). It is noteworthy that none of the patients with normal regional wall motion on the initial echocardiogram had an in-hospital clinical complication. In the late 1980s, Sabia et al performed a prospective study using two-

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dimensional echocardiography in 180 consecutive patients who presented to the emergency department with symptoms suggestive of acute myocardial infarction.[27] [33] The echocardiographic findings were not utilized in actual patient management but in assessing the diagnostic accuracy and cost of an alternate management scenario. The echocardiograms were technically inadequate in 6%. Regional wall motion was assessed using a 12-segment model. Among the 30 patients with acute myocardial infarction, 9 had ST-segment elevation on ECG (sensitivity, 30%), 3 had normal ECGs, 8 had ECGs with LBBB, paced rhythm, or other baseline repolarization abnormalities that make the diagnosis of acute myocardial infarction impossible, and 10 had nonspecific ECG findings. Twenty-nine of these 30 patients with acute myocardial infarction had technically adequate echocardiographic studies. Twenty-seven had regional wall motion abnormalities (sensitivity, 90%). Among the 13 patients with in-hospital complications, all had regional wall motion abnormalities on the initial echocardiogram, whereas only 4 had ST-segment elevation on the initial ECG. Sabia et al proposed an alternate scenario for the management of patients who present to the emergency department with possible acute myocardial infarction.[33] Those with acute ST-segment elevation on ECG would be admitted to the coronary care unit. The others would undergo twodimensional echocardiography. If the study was technically inadequate, admission to the hospital would be decided using conventional criteria. For patients with technically adequate studies, those with regional wall motion abnormalities would be admitted to the hospital, and those with normal wall motion or with global dysfunction would be discharged. If this scenario is applied to the set of study patients, hospital admissions are reduced by 32% (coronary care unit admissions by 25%, and non-coronary care unit admissions by 41%), total hospital stay for all patients is reduced by 23%, and estimated total cost is 24% lower. Under this scenario, two patients with small acute myocardial infarctions and no complications would be sent home. In comparison, two patients with larger acute myocardial infarctions were sent home using the conventional criteria and one of them had a complication after acute myocardial infarction (complete heart block requiring permanent pacemaker). The authors concluded that two-dimensional echocardiography is superior to conventional criteria in the diagnosis of patients with suspected acute myocardial infarction in the prediction of in-hospital complications and in reducing hospital admissions and total cost. This conclusion would be strengthened by further prospective validation in a different cohort of patients.

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Use in Chest Pain Centers and Clinical Algorithms Specialized chest pain centers have been established to evaluate patients presenting with acute chest pain with published studies describing clinical outcome in patients treated according to a chest pain algorithm.[34] For example, Gibler and coworkers published results from their "Heart ER Program," a diagnostic and treatment program for patients with chest pain in an urban tertiary care emergency department.[35] Their initial evaluation algorithm is summarized in a flow diagram in Figure 11-4 . A total of 1010 patients with symptoms suggestive of acute coronary syndrome were enrolled over a 32-month period. Patients with known coronary artery disease, acute ST-segment elevation or depression of greater than 1 mm, hemodynamic instability, or clinical presentation consistent with unstable angina were directly admitted to the hospital. Other patients were entered into the 9-hour evaluation program during which creatine kinase-MB levels were checked on presentation and every 3 hours afterwards for three times and 12-lead ECG or ST-segment was continuously monitored. After the 9hour evaluation period, two-dimensional echocardiography and graded exercise testing were performed in the emergency department and used to reach discharge decisions. Of the 1010 patients, 829 (82.1%) were discharged from the emergency department, and 153 (15.1%) were admitted to the hospital for further evaluation. Among the 153 admitted patients, 52 (33.9%) were found to have a cardiac cause for their symptoms; 43 (28.1%) had acute coronary syndrome (12 with acute myocardial infarction, 31 with myocardial ischemia). The authors concluded that the "Heart ER Program" provides an effective approach for evaluation of low- to moderate-risk patients with possible acute coronary syndrome in the emergency department. Trippi et al[28] reported a clinical trial using dobutamine stress echocardiography for evaluation of patients presenting with chest pain to the emergency room to determine who can be safely discharged from the emergency department. The echocardiograms were digitized for electronic transmission according to their tele-echocardiography protocol. One hundred sixty-three patients with negative results on initial ECGs and blood studies who were recommended for hospital admission to rule out myocardial infarction or ischemia were evaluated. Rest echocardiography was performed in the emergency room and transmitted to an interpreting cardiologist. If the echocardiogram

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Figure 11-4 Chest pain evaluation algorithm used in the Heart ER Program by Gibler and coworkers. ECG, electrocardiographic; CAD, coronary artery disease; CK-MB, creatine kinase-MB; 2D, twodimensional. (Data from Gibler WB, Runyon JP, Levy RC, et al: Ann Emerg Med 1995;25:1–8.)

was normal, dobutamine stress echocardiography was performed by a trained nurse, with images again transmitted to the cardiologist. The test was completed within an average of 5.4 hours after presentation to the emergency room. Using clinical follow-up data and cardiac catheterization as the gold standard, the authors determined the sensitivity of the test to be 89.5%, the specificity 88.9%, and the negative predictive value 98.5%. In a later phase of the trial, patients with normal dobutamine stress echocardiography were released from the hospital; these constituted approximately 72% of the patients. Assessment of the Need for Urgent Coronary Angiography Coronary angiography is generally regarded as the gold standard in the diagnosis of coronary artery disease. In patients with a nondiagnostic ECG and a high pretest probability of coronary artery disease, clinicians can elect to have patients proceed directly to coronary angiography, possibly followed by percutaneous coronary interventions. This modality yields accurate information of coronary anatomy and may lead to prompt revascularization, which improves myocardial salvage and survival in patients with acute coronary artery occlusion. It does not directly provide information on the functional significance of the coronary artery stenoses, which can only be inferred from the location and severity of stenosis. Echocardiography can assist in the decision concerning the need for urgent coronary angiography. Normal global and regional wall motion may persuade the clinician to take a more conservative approach, with later stress testing to rule out significant coronary artery disease. The finding of a new wall motion abnormality, however, may prompt more urgent coronary angiography and intervention. Risk Stratification and Analysis of Long-Term Clinical Outcome Various diagnostic tests have been studied for their prognostic value in the treatment of patients with acute coronary syndrome. Savonitto et al [36]

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performed a retrospective analysis of the presenting ECGs of patients enrolled in the Global Utilization of Strategies To Open 242

Occluded Arteries in Acute Coronary Syndromes (GUSTO-IIb) study and found the 30-day incidence of death or myocardial reinfarction to be 5.5% in patients with T-wave inversion, 9.4% in patients with ST-segment elevation, 10.5% in patients with ST-segment depression, and 12.4% in patients with ST-segment elevation and depression (P < .001). Compared with those who had T-wave inversion only, the odds ratios (OR) of 30-day death or reinfarction remained higher for those with ST-segment elevation (OR, 1.68; 95% confidence interval [CI], 1.36–2.08), for those with STsegment depression (OR, 1.62; 95% CI, 1.32–1.98), and for those with STsegment elevation and depression (OR, 2.27; 95% CI, 1.80–2.86) after multivariate adjustment for other risk factors. Initial elevation in creatine kinase level is also associated with greater risk of death and reinfarction, as is elevation in serum troponin levels. [37] [38] [39] A number of studies have demonstrated the incremental utility of echocardiography, beyond clinical assessment and electrocardiography, in predicting clinical outcome of patients with acute chest pain.[40] [41] In a prospective study involving 466 visits to a large urban emergency department by patients with acute chest pain, Fleischmann et al[40] examined echocardiographic predictors of serious predischarge complications in patients with chest pain. Doppler echocardiograms were performed an average of 21 hours after presentation and used to assess global biventricular function, regional wall motion, and valvular disease. Regional wall motion was assessed using a wall motion index on the basis of a 14segment model. The composite complications end point included significant recurrent myocardial ischemia, heart failure, or arrhythmia. In univariate analysis, the following variables predicted complications: left ventricular function (OR, 2.9; 95% CI, 1.6–5.1), right ventricular function (OR, 2.7; 95% CI, 1.2–6.2), left ventricular end-diastolic dimension Figure 11-5 Kaplan-Meier survival curves for patients presenting with chest pain stratified by left ventricular function. LVD, left ventricular dysfunction. (From Fleischmann KE, Lee RT, Come PC, et al: Am J Cardiol 1997;80:1266–1272, with permission from Excerpta Medica Inc.)

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(OR, 1.6/cm; 95% CI, 1.1–2.3), left ventricular end-systolic dimension (OR, 1.4/cm; 95% CI, 1.1–1.9), and wall motion index (OR, 3.0; 95% CI, 1.8–4.8). In multivariate analysis, wall motion index remained an incremental predictor of subsequent complications beyond clinical and electrocardiographic variables. In a companion study involving 448 patients, the long-term survival of these patients was examined.[21] The follow-up period was 35.0 ± 12.1 months. In univariate Cox regression analysis, left ventricular function and size, wall motion index, right ventricular function, and aortic, mitral, and tricuspid regurgitation were significant predictors of total and cardiovascular mortality. In multivariate analysis involving a model adjusted for clinical and electrocardiographic data, the following were found to be independent predictors of mortality: moderate or severe left ventricular dysfunction (mortality rate ratio, 3.2; 95% CI, 1.8–5.8), and more than mild valvular regurgitation (mortality rate ratio, 2.0; 95% CI, 1.1–3.6). These two echocardiographic findings offer incremental prognostic value over clinical and ECG information alone in patients presenting with acute chest pain syndrome. Kaplan-Meier survival curves for these patients stratified by left ventricular function and by the grade of mitral regurgitation are shown in Figure 11-5 and Figure 11-6 , respectively. Chuah et al,[42] from the Mayo Clinic, examined the incremental utility of dobutamine stress echocardiography over clinical and rest echocardiographic variables in predicting outcome in a cohort of 860 patients with known or suspected coronary artery disease. The patient population in this study was not restricted to patients presenting to the emergency room with chest pain. Semiquantitative evaluation of regional wall motion was performed using the WMSI on the basis of the 16-segment model of the American Society of Echocardiography. The patients were followed for up to 52 months. End points consisted 243

Figure 11-6 Kaplan-Meier survival curves for patients presenting with chest pain stratified by grade of mitral regurgitation (MR) (on a 4+ scale). (From Fleischmann KE, Lee RT, Come PC, et al: Am J Cardiol 1997;80:1266–1272, with permission from Excerpta Medica Inc.)

of cardiac death and myocardial infarction. Seventy-two patients underwent

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coronary artery revascularization before any cardiac event during the follow-up period and were censored. Nonfatal myocardial infarction occurred in 36 patients, and cardiac death in 50 patients. Using a stepwise Cox multivariate regression model involving clinical and rest and stress echocardiographic data, the following were found to be independent predictors of cardiac events: a history of congestive heart failure (hazard ratio, 2.51; 95% CI, 1.54–4.07), the percentage of abnormal segments at peak stress (hazard ratio, 1.14; 95% CI, 1.05–1.23), and an abnormal left ventricular end-systolic volume response to stress (Hazard ratio, 1.98; 95% CI, 1.14–3.46). The model that incorporated clinical and stress echocardiographic data was found to be the best at predicting subsequent cardiac events. Evaluation of Other Causes of Chest Pain Although determination of global systolic function and regional wall motion is of paramount importance in the evaluation of patients presenting with acute chest pain to the emergency department, rapid screening for certain other causes of chest pain should not be neglected, especially in those patients whose presentation appears atypical for ischemic chest pain. Aortic dissection is potentially life-threatening and may be seen on transthoracic echocardiogram, although sensitivity is limited, precluding its use as a first-line imaging technique to exclude dissection. Evidence of an intimal flap may be seen in the aortic root and proximal ascending aorta on the parasternal long-axis view, in the aortic arch on the suprasternal view, and in the descending abdominal aorta on the subcostal view (Fig. 11-7) . The descending thoracic aorta cannot be adequately examined on a transthoracic study, however. In a series of 67 patients from the Mayo Clinic, the sensitivity of transthoracic echocardiogram was 79%, and the positive predictive value was 91%.[43] Transesophageal echocardiography Figure 11-7 Suprasternal view from a transthoracic echocardiogram demonstrating an aortic dissection involving the aortic arch and the ascending aorta.

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(TEE; especially multiplane) is a more sensitive and specific technique for

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examination of the thoracic aorta and should be performed if there is clinical suspicion of aortic dissection. Effusive pericarditis can be easily diagnosed, and the size of the pericardial effusion can be assessed on the transthoracic echocardiogram. The subcostal window is especially useful for this purpose even in patients in whom poor image quality is achieved on parasternal or apical views. The potential hemodynamic consequences of the pericardial effusion may be evaluated with examination of right heart chambers for collapse, Doppler echocardiography of mitral and tricuspid inflow velocities, and twodimensional examination of the inferior vena cava and its variation in size with inspiration. If pericardiocentesis is desired for diagnostic or therapeutic purposes, echocardiographic guidance can facilitate safe performance of the procedure. [44] [45] [46] [47] Rapid screening for aortic stenosis can be made with Doppler measurement of transaortic valvular flow velocity and two-dimensional examination of calcification and motion of the aortic valve leaflets. Similarly, assessment for echocardiographic evidence of hypertrophic obstructive cardiomyopathy can be made with measurement of septal thickness, detection of systolic anterior motion of the mitral valve leaflet, and Doppler echocardiographic measurement of a significant gradient in the left ventricular outflow tract.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Cost-Effectiveness Analysis Rapid advances in science and technology in the past century have improved the quality of health care and have also resulted in a great increase in health care costs. This development has generated increasing interest in applying the techniques of cost-effectiveness analysis to evaluate preventive, diagnostic, and therapeutic strategies in medicine. Table 11-2 lists key terms used in cost-effectiveness analysis. In formal cost-effectiveness analysis, cost is expressed in terms of monetary units, and effectiveness is expressed in units such as the number of lives saved, the years of life saved, the days of disability avoided, and so on. [48] To analyze difficult and complex clinical problems for which no clear consensus exists among experts, a clinical decision model may be constructed to outline explicitly various diagnostic or therapeutic options, and the possible clinical events and outcomes. Probabilities for various clinical events and outcomes can be estimated on the basis of the best available current evidence from the medical literature or, if this is not available, from the physicians' clinical judgment. Each possible outcome is assigned a cost and a utility. By convention, perfect health is assigned a utility value of 1, and death is assigned a value of 0. Various schemes have been devised to assign utility values to different degrees of disease or symptom severity. Thus, cost and health benefit can be calculated for the various options under consideration. The conclusions drawn from any type of clinical decision analysis can only be as accurate as the assumptions on which the model is based. In cases in which the TABLE 11-2 -- Key Terms in Cost-Effectiveness Analysis Cost: amount of resource required, usually expressed in monetary units. Effectiveness: health benefit achieved, commonly expressed in units such as the number of lives saved, the days of disability avoided, the years of

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life saved, and so on. Clinical decision model: a model of the clinical problem, usually constructed in the form of a decision tree, in which various diagnostic or therapeutic options are outlined, and the possible clinical events and outcomes are enumerated and assigned probabilities and utilities. This can be used to analyze the cost or health benefit of various options. Utility: the benefit associated with a specific outcome. By convention, perfect health is assigned a value of 1, and death is assigned a value of 0. Sensitivity analysis: an analysis in which certain parameters in the clinical decision model are systematically varied over reasonable ranges, so as to determine whether the results of the model are significantly affected. This is especially important if there is significant uncertainty or variability in the values of certain parameters. QALY: quality-adjusted life-year. Incremental cost-effectiveness: additional cost-effectiveness of a new strategy compared with the baseline strategy. parameters in the model can vary over a certain range or in which there is uncertainty regarding their values, it is critical to determine whether variation of parameter values over reasonable ranges significantly affects the results of the analysis. This process is referred to as sensitivity analysis. Given the results of a cost-effectiveness analysis, the decision about whether it is worthwhile to spend a certain additional amount to achieve an incremental benefit will depend on the society's values and socioeconomic conditions. In many analyses of health care delivery in the United States, the cost of renal dialysis (approximately $35,000 to $40,000 per patient per year in 1995) is often used as the benchmark for the cost that the American public is willing to bear to prolong life by 1 year. Data on the cost-effectiveness of echocardiography in patients presenting to the emergency department with acute chest pain are scarce. In more general cost-effectiveness analyses of diagnostic strategies for patients with chest pain, most studies have found the preferred initial strategy to be noninvasive testing for patients with low to intermediate pretest probability of coronary artery disease, and coronary angiography for those with high pretest probability. In a study by Kuntz et al,[49] exercise echocardiography cost $41,900 per quality-adjusted life-year (QALY) saved compared with exercise electrocardiography for 55-year-old men with atypical angina.

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Exercise SPECT cost $54,800 per QALY saved compared with exercise electrocardiography for these patients. The incremental cost-effectiveness ratio of routine coronary angiography compared with exercise echocardiography was $36,400 per QALY saved for 55-year-old men with typical angina. For 55-year-old men with nonspecific chest pain, the incremental cost-effectiveness ratio of exercise electrocardiography compared with no testing was $57,700 per QALY saved. The authors concluded that exercise electrocardiography or exercise echocardiography resulted in reasonable cost-effectiveness ratios for patients 245

at mild to moderate risk for coronary artery disease in terms of age, sex, and type of chest pain. Garber and Solomon analyzed the cost-effectiveness of five test strategies for patients with a history of chest pain and intermediate pretest probability (25% to 75%) of coronary artery disease.[50] These strategies involved a noninvasive test (treadmill exercise testing, planar nuclear imaging, SPECT, stress echocardiography, or positron emission tomography) followed by coronary angiography if the noninvasive test was positive. Using information from published literature on the sensitivity and specificity of each test, disease prevalence, and treatment efficacy, and basing cost calculations on Medicare payments, the authors developed a decision analytic model to assess the health outcomes and costs of the different strategies. They found that stress echocardiography improved health outcomes and reduced costs relative to exercise stress testing and planar nuclear imaging. The incremental cost-effectiveness ratio was $75,000 per QALY for SPECT relative to echocardiography, more than $640,000 per QALY for positron emission tomography relative to SPECT, and $94,000 per QALY for immediate coronary angiography relative to SPECT. The authors concluded that stress echocardiography, stress SPECT, and immediate coronary angiography are cost-effective alternatives to positron emission tomography and other strategies. Exercise treadmill testing for assessment of chest pain or risk stratification has been found to be cost-efficient even if greater expense is incurred when such tests are performed outside of regular laboratory hours. Krasuski et al [51] studied 195 patients scheduled for exercise stress testing during weekends or holidays for assessment of chest pain (75%) and other indications; the study population was not limited to chest pain patients from

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the emergency department. The authors found the approach to be safe and effective for risk stratification and to shorten hospital stay. Although a formal cost-effectiveness analysis was not performed in this study, this approach was found to result in cost savings even when the greater expenses associated with testing during weekends or holidays were taken into consideration. For a general discussion of cost-effectiveness analysis for noninvasive diagnostic testing for coronary artery disease, refer to the paper by Hunink et al.[52]

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Limitations Limitations in the Use of Regional Contractile Function to Evaluate Ischemia Evaluation of acute coronary syndrome with echocardiography has several limitations. Between episodes of cardiac ischemia, the patient's wall motion may be completely normal. Therefore, a normal resting echocardiogram performed in such a patient cannot rule out cardiac ischemia as the cause of the patient's symptoms. Stress testing should be considered after myocardial infarction is ruled out. The presence of pre-existing left ventricular dysfunction secondary to nonischemic cardiomyopathy or valvular heart disease makes the evaluation of new regional wall motion abnormalities more difficult and may cause the specificity of this technique to be lower for this population of patients. Image Quality The detection of regional wall motion abnormalities requires adequate visualization of endocardial borders. In patients with morbid obesity, chest wall deformity, chest trauma, or recent thoracic surgery, views with good image quality may be difficult to acquire, especially given the time constraints imposed by the need for rapid diagnosis and institution of therapy. The use of newer echocardiographic modalities, such as second harmonic imaging with echocardiographic contrast administration, may improve endocardial border delineation in such patients and make echocardiographic evaluation in the emergency department more practical. Personnel Availability Ready availability of sonographers to perform echocardiographic examinations and echocardiographers to interpret them is essential if

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echocardiography is to enjoy more widespread use in the evaluation of patients with chest pain in the emergency department. This is not a problem during usual working hours in most hospitals. However, it may not be economically practical to have the personnel physically "on call" in the hospital 24 hours a day for most community hospitals or even tertiary medical centers. Contacting sonographers and echocardiographers on call outside of the hospital inevitably causes a delay in the management of such patients. One approach to deal with this problem is to train emergency department personnel to perform echocardiograms. An obstacle to successful implementation of this approach is the difficulty in gaining and maintaining sufficient experience in performing echocardiographic studies in the context of the rotating shift system in most emergency departments. This logistical problem may be at least partially solved with the advent of digital tele-echocardiography systems. Acquired images can be transmitted over a high-speed network to an experienced echocardiographer outside the hospital for immediate interpretation. Future systems may incorporate the capability for greater real-time interaction between the off-site interpreting physician and the on-site sonographer to ensure the acquisition of all requisite images for any particular clinical situation.

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Future Developments Tele-echocardiography The accurate interpretation of stress echocardiographic images requires experienced echocardiographers, who may not be immediately available in the hospital during off-hours. Having an experienced echocardiographer available in the hospital 24 hours a day or to come into 246

the hospital when such cases occur may not be practical in many hospitals. In addition, the latter option may further delay definitive treatment. Electronic transmission of echocardiographic images has been used as part of telemedicine projects in a number of centers. In nonemergency settings, successful use has been reported in the difficult diagnostic cases requiring expert interpretation, such as patients with congenital heart disease.[53] [54] [55] In the clinical trial by Trippi et al[28] using dobutamine stress echocardiography to determine which patients presenting with chest pain to the emergency room may be safely discharged, the echocardiograms were digitized into a quad-screen systolic eight-frame cineloop format with resolution of 320 by 240 pixels, and transmitted to the interpreting physician over the standard telephone line using a proprietary "lossless" format developed before DICOM standards.[56] [57] The test was completed within an average of 5.4 hours after presentation to the emergency room. It was found to have very good sensitivity and specificity and could potentially result in significant cost savings, as discussed previously in the section on Clinical Applications. Rapid technologic developments since that time, including faster processor speed, availability of higher capacity random access memory, and faster network connections via the Internet or dedicated lines may result in more

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widespread use of this technology. Of course, the transmission of patientspecific data over publicly accessible networks will require proper encryption to ensure patient privacy. Myocardial Contrast Echocardiography The use of echocardiographic contrast with second harmonic imaging to evaluate myocardial perfusion is one of the most exciting developing areas of echocardiography. Ultrasonographic imaging for this purpose needs to be intermittent so as to minimize the destruction of micro-bubbles in the contrast agent. This technique, when perfected, has potential uses in the diagnosis of acute myocardial infarction, determination of ischemic and infarcted areas in conjunction with stress testing, evaluation of reperfusion status, detection of no reflow in the microvascular coronary circulation after restoration of flow in the epicardial coronary arteries, and evaluation of myocardial viability. Although promising, this echocardiographic technique needs to be further refined before its utility in the examination of patients with acute chest pain syndrome can be evaluated. Other Modalities Doppler tissue imaging[58] [59] [60] and color kinesis[61] [62] (Fig. 11-8) are two of the promising new imaging modalities, although further studies are needed to determine their utility in routine assessment of regional wall motion.

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Chest Pain Centers Centers dedicated to diagnostic evaluation of patients presenting with chest pain suggestive of acute coronary syndrome have been set up in a number of medical centers in the United States, with the goal of improving the efficiency of evaluation while preserving or improving outcomes.[2] [34] [63] Most chest pain centers are based within the emergency department or in an adjacent observation unit. Others are located in a part of an inpatient telemetry unit. Patients presenting to the emergency department with chest pain are first stratified into several risk groups on the basis of their history, physical examination, and initial 12-lead ECG. High-risk patients, including those with significant acute ST-segment changes, hemodynamic instability, and known history of coronary artery disease, are admitted directly, usually to the coronary care unit. Those with acute ST-segment elevation or new LBBB will receive reperfusion therapy with thrombolytic agents or cardiac catheterization. Patients with low to moderate pretest probability of acute coronary syndrome, who have no contraindications to diagnostic testing according to the chest pain center protocol and no serious comorbid conditions that may interfere with discharge from the emergency department, are evaluated further in the chest pain center. Other low- to moderate-risk patients may be admitted to a step-down telemetry unit for further evaluation. Patients with noncardiac chest pain are treated and triaged according to their diagnosis. Although individual protocols vary, patients in the chest pain center often undergo serial cardiac enzyme marker determinations (e.g., at 0, 3, and 6 hours after presentation). Serial 12-lead ECGs or continuous ST-segment monitoring is also performed. The monitoring period generally ranges from 6 to 12 hours, although an experience with immediate stress testing in lowrisk patients has also been reported. [64] [65] Patients who develop evidence of acute coronary syndrome during the period of monitoring are admitted. The

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rest will undergo further diagnostic testing after the monitoring period for diagnosis of coronary artery disease and for risk stratification. A number of studies address possible choices for diagnostic testing in emergency department patients presenting with chest pain.[27] [28] [35] , [41] [66] [67] [68] [69] Graded exercise ECG testing is often obtained for those patients who can exercise to an adequate level, have no contraindications to exercise testing, and have no baseline ECG abnormalities that may interfere with the interpretation of stress ECGs. Exercise or pharmacologic stress imaging can be utilized in other patients. The incremental value and costeffectiveness of imaging for patients being evaluated in chest pain centers who can exercise requires further study, as suggested by the American Heart Association.[70] Stress testing is usually supervised by an appropriately trained physician and performed in a dedicated area with resuscitative equipment available and should conform to American Heart Association guidelines for exercise ECG laboratories.[70] [71] As mentioned in an earlier section, accurate acquisition and interpretation of stress echocardiograms requires an experienced sonographer and echocardiographer. Thus, the chest pain center performing stress echocardiography will need a physician experienced in echocardiography to be available on call in or near the hospital, unless tele-echocardiography equipment is available to transmit images to the interpreting physician. Patients 247

Figure 11-8 (color plate.) Tissue Doppler imaging (TDI; top) and myocardial velocity gradient (MVG; bottom) images of the left ventricle in the parasternal short-axis view from a patient with left anterior descending coronary artery obstruction: at baseline (left), with low-dose (10 µg/kg/min) dobutamine (middle), and with high-dose (30 µg/kg/min) dobutamine (right). In the TDI images, the anteroseptal wall is color-coded blue because it is moving away from the transducer during systole. Similarly, the posterior wall is color-coded red because it is moving toward the transducer. MVG is derived from TDI, and it is defined as the slope of the regression line of the intramyocardial velocity profile across the myocardium. It reflects regional wall thickening and has been shown to be independent of the translational motion of the heart. In the MVG images, thickening of the myocardium is color-coded red, and thinning of the myocardium is color-coded blue. Calculated segmental MVGs are shown beside the corresponding segments. In this patient, MVG undergoes a dose-responsive increase in the posterior segment and no significant change in the anteroseptal segment supplied by the diseased coronary artery. (From Tsutsui H, Uematsu M, Shimizu H, et

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al: J Am Coll Cardiol 1998;31:89–93. Reprinted with permission from the American College of Cardiology.)

with positive stress tests will usually be admitted for further evaluation; those with negative evaluations will generally be discharged from the chest pain center with careful attention to adequate outpatient follow-up. An important part of the work of a successful chest pain center involves community outreach to increase public awareness of the importance of seeking prompt medical attention for chest pain. This will further improve the clinical outcome of patients presenting to the emergency department with acute coronary syndrome.

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Summary Transthoracic, transesophageal, and stress echocardiography may all be useful in the evaluation of patients with acute chest pain presenting to the emergency department. Echocardiography can aid in the diagnosis of cardiac ischemia and myocardial infarction, help assess for other important causes of chest pain, and provide incremental prognostic information on both short- and long-term outcomes. New developments to enhance imaging and endocardial border definition, digital acquisition of images, tele-echocardiography, and the possibility of perfusion-based imaging using echocardiographic contrast promise to increase its utility even further in the future.

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251

Chapter 12 - Echocardiography in the Coronary Care Unit Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Elyse Foster MD Zian H. Tseng MD

The earliest experimental models of myocardial infarction demonstrated that regional wall motion abnormalities ensue shortly after cessation of coronary flow.[1] When a coronary artery is ligated, the first abnormality is an impairment in relaxation of the affected wall. The diastolic abnormalities are followed within seconds by the development of systolic contraction abnormalities. These systolic abnormalities can be readily detected by conventional echocardiographic methods and form much of the basis for the echocardiographic evaluation of ischemia. Although segmental abnormalities in diastolic function are not readily measured by conventional echocardiography, the available information regarding global diastolic dysfunction has recently been found to have important prognostic significance.

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Historical Perspective The use of echocardiography in patients with myocardial infarction occurred with the introduction of the first echocardiographic imaging techniques. [2] [3] [4] [5] M-mode echocardiography, with its high frame rate, permitted precise assessment of the reduction in wall thickening, but it was limited by its narrow view of the left ventricle. For example, fractional shortening, measured from the ventricular dimensions at the level of the basal septum and posterior wall, inaccurately represented global left ventricular function in patients with mid and apical wall motion abnormalities. Two-dimensional (2D) sector scanning, developed in the late 1970s, provided the necessary tomographic views for a complete evaluation of regional ventricular function. This bedside imaging method was soon employed widely for the early identification of apical aneurysms and thrombus formation[6] , [7] in patients with anterior myocardial infarction. Two-dimensional quantitative techniques also were developed that could accurately measure left ventricular ejection fraction in the presence of regional wall motion abnormalities. The role of right ventricular infarction in low output syndromes was appreciated,[8] [9] [10] and the high prevalence of post-myocardial infarction pericardial effusions was recognized.

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The introduction of spectral and color Doppler echocardiography in the mid-1980s further enhanced the role of echocardiography by providing essential hemodynamic information. In addition, timely noninvasive diagnosis of complications of acute myocardial infarction, such as mitral regurgitation and ventricular septal defects, was possible. Newer methods, such as tissue Doppler imaging and mitral flow propagation velocities,[11] have enhanced our capacity to define left ventricular diastolic function

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Transesophageal echocardiography allows better definition of the anatomic alterations responsible for the complications of acute myocardial infarction (e.g., papillary muscle rupture). Finally, the advances in digital imaging techniques since the 1980s have enabled the dissemination of stress echocardiography, which has assumed a major role in evaluation of patients with ischemic heart disease, as discussed in Chapter 13 and Chapter 14 . The portability of echocardiography and the extent of hemodynamic and anatomic information it provides ensure its place in the coronary care unit (CCU). Although its ability to provide direct information regarding coronary anatomy and myocardial perfusion have been limited to date, there is continued progress in these areas.

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Applicable Modes of Echocardiography Transthoracic echocardiography (TTE) provides a rapid bedside assessment of wall motion and global left ventricular function, and it excludes the presence of complications.[12] [13] In the patient presenting with chest pain who has a nondiagnostic electrocardiogram, identification of a segmental wall motion abnormality assists in the determination of definitive therapy. In the patient with an established myocardial infarction, early noninvasive evaluation of ejection fraction indicates therapy with beta blockers, angiotensin converting enzyme inhibitors, or both. When recurrent pain complicates reperfusion therapy, electrocardiographic changes may be nonspecific. In this situation, echocardiography helps differentiate between recurrent ischemia and pericarditis. Importantly, the cause of hemodynamic instability in patients with myocardial infarction often can be established without invasive monitoring. In patients with severe hemodynamic compromise, TTE may be limited by mechanical ventilation and an inability to adequately position the patient. In this group, transesophageal echocardiography (TEE) has proven to be efficacious, especially in ruling out complications related to cardiac rupture.[14] [15] [16] [17] [18] [19] [20] [21] [22] Although large numbers of patients with acute myocardial infarction have not been studied, with careful sedation and close monitoring, TEE can be performed safely.[23] [24] [25] Stress echocardiography has assumed an increasingly important role in assessing the postinfarction patient for evidence of myocardial viability and for assessing the risk for recurrent ischemia. Dobutamine echocardiography, using low doses that do not significantly alter hemodynamics, has been shown to improve function in viable myocardial segments. Higher doses of dobutamine as well as exercise echocardiography can be used to detect residual ischemia, but they should be used with caution early after myocardial infarction.[26] Although one study showed no increase in cardiac enzymes after dobutamine stress, [27]

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there are isolated case reports of free wall rupture in association with highdose dobutamine stress testing within the first week following myocardial infarction.[28] [29] Contrast echocardiography remains investigational for the evaluation of myocardial perfusion. Only one intravenous left-sided contrast agent is commercially available in the United States. Although this agent crosses the pulmonary circulation and opacifies the left ventricular cavity, in the approved dose ranges it does not routinely offer adequate assessment of myocardial perfusion. In a study using an investigational agent, a comparison between single photon emission computed tomography (SPECT) and myocardial contrast echocardiography (MCE) revealed limited sensitivity and high specificity for MCE detection of moderate or severe perfusion defects. MCE also underestimated the extent of SPECT defects. [30] The accuracy of MCE was enhanced by the combination of MCE and wall motion assessment.[30] [31] Rapid technologic developments in this field are under way. Saline contrast may be indicated for enhancement of tricuspid regurgitant jets in order to estimate pulmonary artery pressures and to exclude a patent foramen ovale in patients with cerebral embolization or hypoxemia in the setting of right ventricular infarction.[32] [33]

Although three-dimensional (3D) echocardiography has proved to be an important research tool, it has not yet been widely adopted in the clinical setting. Studies in canine models suggest that accurate quantitation of infarct size with and without the use of myocardial contrast may be possible in the future.[34] [35]

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Advantages and Limitations of Echocardiography in the Coronary Care Unit The major advantages to echocardiography in the CCU include its portability, noninvasive nature, and the wealth of anatomic and hemodynamic information provided. TEE, a semi-invasive technique, has an extremely low complication rate even among the most seriously ill.[36] [37] The limitations of echocardiographic evaluation include the limited transthoracic windows often encountered in the acutely ill coronary care patient, frustrating identification of important complications. Newer technologies such as tissue harmonics have enhanced endocardial border definition even in the most difficult patients. Another limitation is the largely qualitative analysis of regional wall motion abnormalities; quantitative techniques are cumbersome, require manual tracing, and, for the most part, have not been widely employed in the clinical setting.[38] [39] Nevertheless, surface echocardiography remains a mainstay of noninvasive diagnosis in the CCU.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Pathophysiology and Echocardiographic Correlations Timing and Evolution of Infarction The effects of acute coronary ligation in animal models of experimental myocardial infarction have been studied by echocardiography, leading to several observations: 253

1. Acute coronary ligation results in diminished systolic wall thickening and outward motion of the affected myocardial segment (dyskinesis) with close correlation between echocardiography and sonomicrometry. [40] [41] [42] [43]

2. The degree of dyskinesis produced was directly related to the severity of the perfusion deficit.[40] 3. Interventions during ischemia that increase afterload worsen wall motion, whereas afterload-reducing and inotropic agents improve wall motion.[40] [44] 4. The extent of wall motion abnormalities correlates with infarct size to a variable degree. In one study the wall motion abnormalities present at 2 hours following coronary ligation tended to overestimate infarct size because function had improved over the subsequent 48 hours. Although in this dog model echocardiographic infarct size even as predicted by late (48 hours) wall motion abnormalities correlated poorly with pathologic infarct size,[45] subsequent studies demonstrated that the extent of regional contraction abnormalities on 2D echocardiography with early (20 minutes) or late (2 days) echocardiography after permanent coronary occlusion correlated well with infarct size.[46] Despite these seemingly disparate results, these early studies provided a

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basis for clinical studies using echocardiography to measure the beneficial effects of pharmacologic interventions on infarct size.[47] [48] [49] [50] [51] Reperfusion Therapy, Myocardial Stunning, and Infarct Size Experimental studies have demonstrated that approximately 30 minutes following an acute coronary occlusion, a wavefront of myocardial necrosis begins to proceed from endocardium to epicardium, resulting in a transmural myocardial infarction over a period of 4 to 6 hours.[52] This observation, coupled with the work of DeWood et al,[53] who demonstrated that an acute coronary thrombosis was responsible for most acute myocardial infarctions, led to what is probably the major therapeutic advance in cardiology: the use of thrombolytic therapy or primary angioplasty for acute myocardial infarction. The theoretical basis for the use of early reperfusion is grounded in the work of early investigators in this field who showed that timely restoration of coronary flow (i.e., coronary reperfusion) salvages myocardium. However, improvement in flow had variable immediate effects on wall motion abnormalities, with most animals showing improvement but others showing no improvement or even worsening.[40] After reperfusion there is no significant correlation between infarct size and extent of regional dyskinesis or area of systolic wall thinning by 2D echocardiography after reperfusion performed up to 10 days after reperfusion.[46] [54] Thus, echocardiographic wall motion abnormalities as a predictor of infarct extent appeared to be more accurate following permanent occlusion than after occlusion with reperfusion. There are several plausible explanations for the lack of correlation between infarct size and regional wall motion abnormalities in reperfused myocardium. Most often echocardiographic assessment results in an overestimation of infarct size. After restoration of flow, there may be persistent postischemic dysfunction in viable myocardial segments, known as myocardial stunning. The pathophysiologic basis for this phenomenon is covered in several excellent reviews.[55] [56] [57] Wall motion abnormalities 2 weeks after reperfusion correlate better with infarct size, [54] which suggests that return of function of stunned myocardium may be significantly delayed. The rate at which reperfusion occurs also affects function, and it may be relevant in terms of the type of therapy chosen in the acute postinfarction period. In a canine model of infarction, sudden complete reperfusion resulted in increased wall thickness and slow return of function over a 7-day period, which is consistent with cell swelling and reperfusion injury (albeit reversible). In contrast, staged partial reperfusion (followed

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by complete reperfusion) did not lead to an immediate increase in wall thickness, with functional recovery being seen as early as 30 minutes.[58] Thus, echocardiography early after a reperfused myocardial infarction (i.e., within 2 weeks) may overestimate the eventual area of necrosis because of stunning, reperfusion injury, or both. Infarct size also may be overestimated if the abnormal motion of infarcted myocardium impairs endocardial motion of adjacent normal myocardium owing to a "tethering" effect. [59] Alternately, the area of necrosis may be underestimated in the presence of a nontransmural infarction that subtends less than 25% of the wall thickness, with the salvaged normal subepicardial region resulting in overall normal segmental function.[60] In patients with old infarctions (>6 months), echocardiographic infarct size tends to underestimate the volume of necrosis when measured at autopsy.[61] In some cases, the ventricular remodeling process may be responsible for the change in the tendency from early (<2 weeks) overestimation to late (>6 months) underestimation of infarct size.[62] To identify postischemic ventricular dysfunction or "stunned myocardium," investigators have examined the effect of inotropic stimulation on the function of reperfused, noninfarcted myocardium and compared it with the effect on infarcted tissue. Serial 2D echocardiography during dopamine infusion demonstrates an increase in the contractility of the reperfused myocardium, with improvements in systolic wall thickening and fractional area change. This improvement in regional function is associated with an improvement in regional myocardial blood flow.[63] This study and others provided the experimental basis for the clinical use of dobutamine in detecting myocardial viability.[64] [65] [66] [67] [68] [69] Another echocardiographic method under investigation for determining myocardial viability is ultrasonic tissue characterization.[70] [71] [72] Nonischemic myocardium shows cyclic variation in the integrated backscatter, whereas in ischemic myocardium this variation is diminished or lost. MCE using sonicated iodinated contrast media identifies segments with persistent flow deficits despite reperfusion of the epicardial vessel. The areas of no reflow are believed to be due to microvascular damage and correspond to nonviable segments as identified by positron emission tomography and thallium scintigraphy.[73] MCE also can measure the extent of microvascular occlusion,

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which occurs after prolonged ischemia and prevents adequate reperfusion. [74]

Infarct Localization Infarcts are localized both with respect to the transmural extent of the infarction (i.e., subendocardial versus transmural) and to the anatomic location as related to the coronary distribution of the infarct related artery. Small nontransmural (i.e., subendocardial) myocardial infarctions may not be detected as an abnormality in contractile function. The transmural extent of infarction and regional systolic function is inversely related to fractional radial shortening in both acute (6 hours after occlusion) and subacute (72 hours after occlusion) infarctions.[60] [75] [76] Fractional shortening continues to deteriorate as the percent of total wall (transmurally) involved increases from 75% to 100%, contradicting the work of others who suggested the subepicardial third of the myocardium contributed little to systolic wall thickening.[77] The circumferential extent of the infarction and, to a lesser extent, its longitudinal extent (i.e., base to apex) correlate with the distribution of the affected coronary artery.[78] [79] The anterior, anterolateral, anteroseptal, and apical (anterior and septal) segments correspond roughly to the left anterior descending artery (LAD) distribution. The lateral wall and lateral apex are in the distribution of the left circumflex. The inferolateral wall is supplied by the posterior descending artery. In 80% of the population, the posterior descending artery arises from the right coronary artery (RCA) and supplies the inferolateral wall as well as the inferior free wall and inferior septum (right dominant). In the other 20% of patients, the posterior descending artery arises from the circumflex artery (left dominant system). The right ventricle is supplied by the RCA via its acute marginal branches. In general, infarctions in the LAD distribution tend to be more apically situated, whereas those in the RCA and the circumflex distribution are more basal in their location. Moreover, the extent of apical involvement and its distribution depends, to a degree, on the relative supply from the left anterior and posterior descending arteries. Of course, the presence of collaterals and previous bypass surgery alters the distribution of ischemia and infarction relative to the involved arterial supply. The most commonly accepted method for analyzing wall motion uses the 16-segment model recommended by the American Society of Echocardiography[38] (Fig. 12-

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1) , with the approximate and most common native coronary arterial distribution in relation to these segments depicted in Figure 12-2 . Experimental Models of Mitral Regurgitation Mitral regurgitation is common in the setting of acute myocardial infarction. Only recently have experimental studies elucidated the mechanism. These studies have demonstrated incomplete coaptation of the mitral valve leaflets owing to alteration of systolic left ventricular geometry Figure 12-1 The 16-segment model for segmental wall motion analysis recommended by the American Society of Echocardiography.[29] A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; L, lateral; PSAX, parasternal short axis; S, septal; SAX, short axis.

during ischemia.[80] [81] Infarction of a papillary muscle and the underlying ventricular myocardium results in incomplete leaflet coaptation owing to an increase in the distance from the point of mitral leaflet coaptation to the mitral annulus.[81] [82] Although the extent of the underlying wall motion abnormality may be small and left ventricular function may be globally preserved, papillary muscle ischemia alone is insufficient to cause mitral regurgitation. These studies are supported by the clinical observation that mitral regurgitation occurs in patients with ischemia or infarction of the inferolateral or posteromedial papillary muscle and a small area of underlying myocardium with otherwise well-preserved left ventricular function.[15] Incomplete leaflet coaptation also may occur as a result of severe global left ventricular dysfunction rather than localized papillary muscle dysfunction. [80] The proposed mechanisms contributing to malcoaptation of the leaflets in the setting of global ventricular dysfunction include a prolonged rate of rise of left ventricular pressure (i.e., Figure 12-2 Arterial distribution of blood flow superimposed on a parasternal short-axis view. LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery.

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decreased dP/dt), with less force exerted on the mitral leaflets; poor systolic approximation of the left ventricular walls; mitral annular dilation; and malalignment of the papillary muscles owing to increased left ventricular end-diastolic volume. More recent data from a canine model using 3D echo-cardiography suggest that functional mitral regurgitation associated with left ventricular systolic dysfunction occurs only in the presence of left ventricular dilation.[83] Hemodynamically significant mitral regurgitation relates strongly to the 3D geometry of the mitral valve attachments at the papillary muscle and annular in the presence of left ventricular dilation (i.e., postpericardiectomy). Likewise, in vitro modeling studies demonstrated an integrated mechanism of regurgitation in which an altered balance between abnormal leaflet tethering and decreased coapting forces results in mitral incompetence.[84] Thus, hemodynamically significant mitral regurgitation is seen both in patients with small inferior myocardial infarctions and posteromedial papillary muscle involvement and in patients with large anterior infarctions, left ventricular dilation, and globally reduced systolic function. Infarct Healing and Remodeling Echocardiographic studies have contributed significantly to the understanding of infarct healing and the ventricular remodeling that takes place in the hours and days following an acute myocardial infarction. The importance of these phenomena are recognized in relation to the beneficial effects of delayed reperfusion and afterload reduction with angiotensin converting enzyme inhibitors that reduce infarct expansion and ventricular dilation. The concept of infarct expansion originated with the observation that the infarcted segment of myocardium thins and stretches with an increase in the circumferential extent of the necrotic zone (Fig. 12-3) (Figure Not Available) . The clinical observation that infarct expansion is associated with higher mortality, both early (in-hospital) and late after myocardial infarction, [85] [86] , [72] led to the postulate that the change in the topography of the infarcted zone increases the hemodynamic burden on the remaining normal walls, Figure 12-3 (Figure Not Available) Concept of infarct expansion. In the initial phase of the infarction (left), there is regional dilation and thinning limited to the infarcted region. Over time, in addition to further expansion of the area of infarct, there may be

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compensatory dilation of the remaining ventricle (right). (Redrawn from Eaton LW, Weiss JL, Bulkley BH, et al: N Engl J Med 1979;300:57–62. Copyright 1979 Massachusetts Medical Society. All rights reserved.)

resulting in ventricular dilation and hypertrophy.[85] [87] [88] Both clinical and experimental data suggest the following: 1. Expansion of the endocardial segment occurs as early as 10 minutes after occlusion.[89] 2. Infarct thinning and expansion are progressive over a period of 7 days. [88]

3. A critical mass of infarction (approximately 20% of total left ventricular mass) was required for expansion.[90] 4. Infarct expansion in the dog is more likely after LAD than after left circumflex occlusion.[89] 5. Infarct expansion led to aneurysm formation.[88] 6. The segment lengths of normal myocardium increase in the presence of infarct expansion, leading to ventricular dilation.[91] 7. Microvascular obstruction in infarcted tissue plays a role in remodeling by reducing local myocardial function, which contributes to the dysfunction of adjacent noninfarcted myocardium.[92] The clinical significance of infarct expansion is further emphasized by the demonstration of the beneficial effects of a patent infarct-related artery. [87] Histologic studies in a rat model of infarction demonstrated that reperfusion too late to salvage myocardium (no reduction in infarct size or transmurality) inhibits infarct expansion[93] and was associated with increased scar thickness.[94] Echocardiographic studies in dogs showed that delayed reperfusion of an infarct (as late as 5 to 6 hours after occlusion) acutely decreases the degree of infarct thinning and ventricular dilation.[95] [96] Although delayed reperfusion may convert a bland infarct into a hemorrhagic infarct and may increase the risk of myocardial rupture slightly, many clinical studies support the concept that an open artery provides substantial benefit, possibly through decreased left ventricular dilation and aneurysm formation and, as a corollary, a decreased incidence of arrhythmias and a lower mortality.[87] [97] The time course of left ventricular remodeling following successful reperfusion in acute myocardial infarction is suggested by a 2D echocardiographic study that showed progressive infarct thinning for up to 1 month and left ventricular dilation for up to 14 days. The degree of remodeling as reflected in left ventricular volume was greatest in the patients with the largest infarcts (peak creatine kinase > 8000 U/L). Despite the progressive remodeling,

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wall motion score improved rapidly by 14 days, and it continued to improve gradually to 1 year. [98] Vasodilator therapy, theoretically through a reduction of left ventricular wall stress, influences post–myocardial infarction remodeling and improves prognosis. The salutary effects of treatment with angiotensin converting enzyme inhibitors, first shown in a rat model by Pfeffer et al,[99] [100] include attenuation of left ventricular dilation, improved left ventricular performance with a downward shift of the pressure-volume curve and higher ejection fraction, and improved long-term survival. These findings were subsequently confirmed in post–myocardial infarction patients with left ventricular dysfunction in the Survival and Ventricular Enlargement (SAVE) trial. Two canine studies using echocardiographic measurements have shown that nitrates and enalapril had similar beneficial effects on the remodeling process.[101] [102] The Carvedilol Heart Attack Pilot Study (CHAPS) demonstrated 256

attenuation of left ventricular remodeling with postinfarction administration of carvedilol. Echocardiography at baseline and after 3 months of treatment showed reduced left ventricular volumes and sphericity (long-axis–to– short-axis ratio).[103]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in the Diagnosis and Early Risk Stratification of Acute Myocardial Infarction Transferring the experience from the animal laboratory into the CCU, clinical investigators have confirmed the usefulness of echocardiography in diagnosis, localization, prognostic staging, and detecting of complications of myocardial infarction. Diagnostic Role of Echocardiography For an imaging modality to be useful in the diagnosis of myocardial infarction, it must be feasible in the majority of patients. Images of the left ventricle adequate for segmental analysis of wall motion can be obtained in greater than 90% of patients by skilled sonographers.[104] [105] [106] Tissue harmonic imaging and left-sided contrast agents have increased the percentage of patients in whom technically adequate images can be obtained.[107] [108] [109] In one study of segmental and global function in 70 critically ill patients, the number of uninterpretable segments fell from 5.4 with fundamental (standard) imaging to 4.4 with harmonic imaging and finally to 1.1 with a left-sided contrast agent. In addition, the usefulness of the modality is directly related to its sensitivity and specificity and to the prevalence of the disease in the population studied. The accuracy of an echocardiographic diagnosis of a myocardial infarction is dependent on echocardiography's ability to detect wall motion abnormalities in the involved segment. As shown in the animal laboratory, the severity of the wall motion abnormality depends on the transmural extent of the infarction and the circumferential limits depend on the arterial distribution and collateral blood supply. In considering the specificity of wall motion abnormalities for diagnosis of acute myocardial infarction, other causes of segmental dysfunction must be recognized. A false-positive diagnosis can often be avoided if wall

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thickening is examined in addition to endocardial motion. The inward motion of the endocardial surface may be delayed or paradoxical owing to abnormal conduction in the presence of Wolff-Parkinson-White syndrome, [110] a left bundle branch block,[111] or right ventricular pacing. [112] Paradoxical septal motion also is present in right ventricular volume overload and following open heart surgery.[113] [114] In these conditions, the systolic thickening of the septum or other involved segment (e.g., posterolateral wall in Wolff-Parkinson-White syndrome, type A) should be preserved.[115] Nonischemic causes of segmental dysfunction that result in reduced systolic thickening and endocardial motion include focal myocarditis[116] and idiopathic cardiomyopathy. Several studies that have examined the specificity of echocardiographic wall motion abnormalities for diagnosis of acute myocardial infarction are worth noting. Among 65 patients presenting to the emergency room with chest pain, there were 5 false-positive echocardiograms, demonstrating regional asynergy in patients without infarction for a specificity of 85%.[117] In a more recent study by Peels et al[118] of 43 patients with chest pain and normal or nondiagnostic electrocardiogram, the specificity of echocardiographic wall motion abnormalities was 78% for ischemia and only 53% for infarction. The apparent discrepancy between the two studies is probably due to differences in prevalence of disease in the population studied. Sabia et al[105] used echocardiography to study 202 patients presenting to the emergency room with acute shortness of breath or chest pain. Of the 140 patients who were ruled out for myocardial infarction, 60 had regional wall motion abnormalities detected by echocardiography. Of those patients, 52% (31 of 60) had had a prior infarction and 53% (32 of 60) were found to have evidence of coronary artery disease on subsequent testing. Although the development of electrocardiographic Q waves is usually associated with a transmural infarction, the absence of Q waves does not always signify a nontransmural or subendocardial infarction.[119] Non–Qwave infarctions are usually smaller, are associated with smaller enzyme leaks,[120] and more often are in the distribution of the left circumflex artery. [121] Two-dimensional echocardiographic evidence of a wall motion abnormality is present in 90% to 100% of patients with Q-wave infarctions [117] [122] [123] [124] compared with 75% to 85% in patients with non–Q-wave [104] [114] [117] [123] [124] [125] infarctions. , The most widely used scoring system for grading the severity of a wall

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motion abnormality is that recommended by the American Society of Echocardiography, in which normal = 1, hypokinesis = 2, akinesis = 3, dyskinesis = 4, and aneurysm = 5[38] (Table 12-1) . Unlike other published scales,[106] hyperkinesis is not distinguished from normal contraction. Weiss et al[124] demonstrated that the finding of akinesis or dyskinesis is most common in the setting of transmural infarction, with milder degrees of wall motion abnormalities (i.e., hypokinesis) most likely representing nontransmural infarction or ischemia. Localization of Infarction Clinical studies have documented the accuracy of echocardiography in identifying the site of coronary occlusion. Echocardiographic localization has significant advantages TABLE 12-1 -- Scoring System for Grading Wall Motion[38] Score 1 2 3 4 5

Wall Motion Normal Hypokinesis Akinesis Dyskinesis Aneurysmal

Endocardial Motion * Normal Reduced Absent Outward Diastolic deformity

Wall Thickening * Normal (>30%) Reduced (<30%) Absent Thinning Absent or thinning

*In systole.

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over electrocardiographic localization, particularly for apical and lateral wall myocardial infarctions. Pierard et al[126] correlated echocardiographic infarct location with the site of coronary obstruction by coronary angiography in 45 patients and by necropsy in 4 patients. They assigned specific segments to the major coronary branches and found the following sensitivities: basal anterior = first diagonal (LAD, 71%) basal anteroseptal = first septal perforator (LAD, 83 middle anterior = second diagonal (LAD, 100%)

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middle anteroseptal = second septal (LAD, 89%) basal posteroseptal = dominant RCA (89%) right ventricular anterolateral segment = right ventr ular marginal branch (83%)

Ogawa et al[127] analyzed the location of echocardiographic wall motion abnormalities, electrocardiographic Q wave, and angiographic site of coronary artery occlusion in 26 patients with single-vessel disease. Inferior Q waves (II, III, and aVF) were associated with mid-inferior wall motion abnormalities. Furthermore, extension to the inferior septum correlated with RCA disease, whereas extension to the inferolateral wall correlated with circumflex coronary disease. A tall R wave in V1 was associated with

posterolateral wall motion abnormalities and a coronary lesion of the proximal circumflex artery. Electrocardiographic evidence of lateral infarction (Q in lead I or aVL) correlated with wall motion abnormalities of the inferolateral and anterolateral walls and disease in the circumflex system involving a large obtuse marginal branch. Circumflex disease also was associated with the presence of a Q wave in V6 and dyssynergy of the lateral and inferior apical walls.[127]

These studies did not compare echocardiographic to electrocardiographic localization of infarction. However, a study by Otto et al[106] suggested that imaging may be more precise, with an 81% concordance between echocardiography and angiography compared with 76% for electrocardiography.[106] Thus, the use of echocardiography to identify the region of segmental dyssynergy in the patient presenting with a myocardial infarction is clinically accurate in determining the site of coronary occlusion (Table 12-2) . One caveat is that the presence of pre-existing wall motion abnormalities and surgical grafts or collateral circulation altering the distribution of flow must be taken into account. Right Ventricular Infarction Right ventricular infarction (Table 12-3) occurs in up to one third of patients with inferior wall infarction and is seen rarely in patients with anterior infarction. The right ventricle is predominantly supplied by acute marginal branches of the RCA that arise in the middle third of its anatomic course. Occlusion of the RCA proximal to the origin of these branches results in ischemia and usually infarction of the right ventricle. Much less frequently, the right ventricle receives blood supply from a dominant left circumflex artery. In addition, the anterior apex of the right ventricle may

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be supplied by the LAD "wrapping" around the apex of the heart. TABLE 12-2 -- Coronary Distribution Associated with Echocardiographic Segments Echocardiographic Segment Coronary Artery Supply * Base Anterior septum Proximal LAD Anterior Proximal LAD Anterolateral Proximal LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Mid Anterior septum Mid LAD Anterior Mid LAD Anterolateral Mid LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Apex Anterior Distal LAD Lateral Distal LAD Septum Distal LAD Inferior PDA (LAD) LAD, left anterior descending artery; LCx, left circumflex artery; PDA, posterior descending artery; RCA, right coronary artery. *Coronary distribution is variable in the presence of revascularization.

The hemodynamic consequences of right ventricular infarction were first recognized in the mid-1970s with several descriptions of the associated

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clinical syndrome appearing simultaneously in the literature.[128] [129] Using gated scintigraphy, detectable right ventricular dyssynergy was reported by other investigators shortly thereafter.[130] [131] In one of these reports, Sharpe et al[112] also described the M-mode echocardiographic finding of right ventricular infarction. In 6 patients, they found evidence of right ventricular enlargement and paradoxical septal motion correlating with the scintigraphic and hemodynamic findings. Isner and Roberts[132] reported the incidence of right ventricular infarction in 236 necropsy specimens of acute and chronic infarctions. In their series, none of the 97 patients with pathologic evidence of an isolated anterior wall myocardial infarction had right ventricular involvement. In contrast, the incidence of right ventricular involvement in patients with infarction involving the posterior wall was 24% (33 of 139). Specifically, all of the right ventricular infarcts, which were confined to the posterior portion of the right ventricular free wall, TABLE 12-3 -- Echocardiographic Signs of Right Ventricular Infarction PRIMARY Right ventricular dilation Segmental wall motion abnormality of the right ventricular free wall Decreased descent of the right ventricular base SECONDARY Paradoxical septal motion Tricuspid regurgitation Tricuspid papillary muscle rupture Pulmonary regurgitant jet pressure half-time ≤150 msec Dilated inferior vena cava Right-to-left interatrial septal bowing Right-to-left shunting across patent foramen ovale

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occurred in the 65 specimens with transmural infarction involving the posterior septum (33 of 65, or 50%). A subsequent pathologic study described that infarction of the right ventricular anterior free wall occasionally can be contiguous with an extensive anteroseptal infarction.[133] The diagnosis of right ventricular infarction should be suspected in a

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patient with evidence of jugular venous distention and clear lung fields in the setting of an inferior myocardial infarction. Although the electrocardiographic sign of ST segment elevation in V4R is both sensitive

and specific for the diagnosis,[134] it does not provide information as to the extent of involvement. The 2D echocardiographic signs of right ventricular infarction include right ventricular dilation, decreased right ventricular function, segmental wall motion abnormalities, and paradoxical septal motion (Fig. 12-4) .[135] Quantitative measurement of right ventricular ejection fraction by echocardiography is difficult because of the lack of an adequate geometric model for calculation of volumes; instead, fractional area change and descent of the right ventricular base are commonly used measures of right ventricular function. Right ventricular failure with high right atrial pressures results in bowing of the interatrial septum into the left atrium and dilation of the inferior vena cava with lack of inspiratory collapse.[136] Echocardiographic indicators of right ventricular function correlate with clinical status and prognosis. Goldberger et al[136] compared the echocardiographic characteristics in patients with hemodynamically significant infarction (jugular venous pressure [JVP] > 13 mm Hg; n = 9) with those without (JVP < 13; n = 15). There was no difference in the frequency of detectable wall motion abnormalities between the two groups (77% versus 66%). However, the group with higher estimated JVP had less descent of the base (.7 cm versus 1.3 cm); less inspiratory collapse of the inferior vena cava (22% versus 45%) and a greater right-to-left ventricular size ratio (1.1 versus 0.6). The pressure half-time of the pulmonary regurgitant jet reflects the compliance of the right ventricular Figure 12-4 Four-chamber view of an echocardiogram from a patient after an inferior infarction with right ventricular involvement. There is enlargement of the right ventricle (RV) and right atrium (RA). The left ventricle (LV) appears small and the interatrial septum is deviated from right to left, suggesting elevated right atrial and right ventricular enddiastolic pressures.

chamber. In a recent study, a short pressure half-time of the pulmonary regurgitant jet (<150 msec) in patients with right ventricular infarction was the only predictor of in-hospital events.[137] Thrombolytic therapy has been proved efficacious in right ventricular infarction, and echocardiographic features correlate with effective revascularization. In a recent study of 108 consecutive patients with a right ventricular infarction, there was a 78%

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correlation between Thrombolysis in Myocardial Infarction (TIMI) grade III perfusion in and normalization or improvement of right ventricular function by echocardiography.[138] Interatrial septal motion and interventricular septal motion normalized in all reperfused patients. The major complication rate and mortality were higher in patients with echocardiographic findings of right ventricular dysfunction persisting after thrombolytic therapy.[138] Two other complications associated with right ventricular infarction deserve mention. First, papillary muscle dysfunction associated with ischemia and right ventricular dilation may result in functional tricuspid regurgitation. Rarely, papillary muscle rupture may involve the tricuspid valve. Second, severe hypoxemia owing to right-to-left shunting across a patent foramen ovale has been reported with large right ventricular infarctions in association with elevated right atrial pressures. [139] Echocardiography for Prediction of Early Mortality Using echocardiography in the setting of acute myocardial infarction, clinical investigators have identified several important prognostic indices: (1) the extent of the wall motion abnormalities within the infarct zone; (2) the degree of infarct expansion and ventricular dilation; and (3) the presence of wall motion abnormalities outside the infarct zone (i.e., infarct extension). The importance of diastolic function as a prognostic indicator is discussed later. An echocardiographic wall motion score has been the most widely used measure of functional infarct size in clinical practice. The total score is derived by assigning a grade of 1 through 5 (see Table 12-1) to each myocardial segment that is adequately visualized. For a segment to be scored, the majority of the endocardium within that segment must be apparent, and wall thickening and endocardial motion should be examined. The scores for each segment are added and then divided by the number of segments graded for a total wall motion score. Several studies have demonstrated that a higher wall motion score index (12 to 24 hours after admission) is associated with a higher rate of in-hospital complications, including malignant arrhythmias, pump failure, and death.[104] [140] A higher wall motion score index also predicts a higher rate of complications, including free wall rupture, ventricular septal defect or papillary muscle rupture, and death from cardiogenic shock.[140] A higher wall motion score, signifying a more extensive infarction, also is predictive of late mortality. [140] [141] In reviewing the literature on this subject, it is important to

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recognize that many different scoring systems have been described, with consequent variability 259

in the absolute number of the wall motion score index associated with a poor prognosis. Infarct expansion is defined as an increase in the endocardial surface area of the infarcted zone owing to thinning and stretching secondary to necrosis and scar tissue formation. A landmark study in 1979 used serial 2D echocardiography to study 28 patients in the first 2 weeks after myocardial infarction. In eight patients, all with anterior infarctions, there was a progressive increase in the endocardial length of the infarcted segment and progressive ventricular dilation. In the group without infarct expansion (9 inferior myocardial infarction patients, 11 anterior myocardial infarction patients), there was little or no dilation. Although the number of patients in each group was too small from which to draw firm conclusions, the group with infarct expansion had a higher mortality rate (50%) compared with the group without expansion (0%). Other clinical studies have suggested that this mechanism contributes to congestive heart failure and poor functional status after infarction.[142] Later studies in the era of reperfusion confirm that infarct expansion is more common in anterior infarctions, but they suggest that most of the dilation is present by 3 hours.[143] Wall motion abnormalities remote from the infarction site may be present early in the course of the infarction or may develop in the presence of postinfarction angina, suggesting de novo ischemia. The echocardiographic finding of remote asynergy at or soon after clinical presentation is strong evidence of multivessel disease. Abnormal wall motion in a second (or even third) coronary distribution is possibly due to (1) previous infarction, (2) increased myocardial oxygen demands placed on the noninfarcted segment as a result of increased wall stress outstripping its oxygen supply, (3) a cessation in its collateral blood supply that originated from the newly occluded vessel, or (4) simultaneous infarctions in multiple coronary beds, the least likely cause.[144] Infarct extension results from the development of ischemia and infarction in a region remote from the original site after the initial event. Postinfarction angina with electrocardiographic changes distant from the acute infarct (i.e., "ischemia at a distance") is associated with a worse

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prognosis than ischemia within the infarct zone.[145] Although early observations were based on electrocardiographic evidence alone, more recent echocardiographic investigations show similar results.[125] [145] [146] Isaacsohn et al[146] performed echocardiography during 19 episodes of postinfarction ischemia. Echocardiographic extension was detected in seven of nine episodes with clinical evidence of extension (recurrent chest pain, new increase in creatinine kinase level, or new electrocardiographic changes). The in-hospital mortality rate was significantly greater in those with echocardiographic evidence of infarct extension (50% versus 12%) and was poorest in those with a high wall motion score.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Detecting Complications of Acute Myocardial Infarction The prognosis of myocardial infarction is directly related to the extent of necrosis (Table 12-4) . A large TABLE 12-4 -- Echocardiography in Complications of Myocardial Infarction HEMODYNAMIC STATES Hypovolemia Right ventricular infarction Globally reduced left ventricular contractility MECHANICAL COMPLICATIONS Papillary muscle rupture Ventricular septal rupture Free wall rupture and tamponade OTHER Left ventricular aneurysm Mural thrombus infarction encompassing greater than 40% of the heart is likely to result in severe pump failure. Transmural infarction is more likely to result in complications related to rupture, occurring in up to 3% of patients. Thus, in the hemodynamically unstable patient, it is critical to exclude rupture, a situation that is potentially amenable to surgery, before concluding that cardiogenic shock is on the basis of pump failure. In most cases, TTE (supplemented when necessary by TEE) is sufficient to exclude papillary muscle, free wall, and ventricular septal ruptures. Hemodynamic Classification of Myocardial Infarction Using Doppler Echocardiography

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A carefully performed Doppler echocardiographic study can provide sufficient information to determine a patient's hemodynamic category after infarction. A hemodynamic classification on the basis of these well-studied parameters is given in Table 12-5 . A simple method of estimating stroke volume is to measure the stroke distance, that is, the velocity time integral (VTI) of aortic flow by pulsed wave or continuous wave Doppler. Although continuous wave Doppler measurements are more reproducible, they can be used only in patients with normal semilunar valves; even a mild degree of stenosis increases the VTI. At a heart rate of 70 to 80 beats per minute, the normal stroke distance is 13 to 15 cm for the pulmonary artery and 18 to 20 cm for the aorta.[147] [148] Stroke distance varies inversely with heart rate, but it holds constant over a wide range of body surface areas.[149] This method eliminates the error in cardiac output measurements introduced by estimating the cross-sectional area of the orifice. Moreover, stroke distance measurements are simple to measure online. Recently, automated cardiac output measurements, based on the digital velocities from color flow mapping, have become available on some systems.[150] A more detailed discussion of Doppler measurements of cardiac output is found in Chapter 26 . Mitral inflow, measured at the tips of the leaflets in the four-chamber view, is informative with regard to diastolic function and left ventricular filling pressures.[151] Derived parameters of the time velocity curve include the ratio of peak early filling velocity to atrial filling velocity (E/A 260

TABLE 12-5 -- Hemodynamic Classification of Myocardial Infarction * by Echocardiography Hemodynamic Category LVEF Normal Nl Hyperdynamic Nl to incr Hypovolemia

Pulmonary LVOT Mitral Venous RVEF VTI E/A Flow Nl 20 A wave S > D † cm dom † Nl >20 A wave S > D † cm dom †

Variable Nl

<20

A wave S > D †

PASP (TR velocity) IV Nl N Nl to slight incr Nl to

N

Sm

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LV Failure Mild

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Mild decr Mod decr Severe decr Variable

Nl to decr Nl to decr Nl to decr Decr

cm

dom †

Mild decr Mod decr Sev decr Decr

E wave dom E wave dom E wave dom A wave dom †

decr

S>D

sp co

Mild incr Mod incr Mod incr Decr

N pl Severe S< D Incr N incr decr pl decr, decreased; D, diastolic; dom, dominant; E/A, ratio of early to late (a ventricular diastolic inflow velocity; incr, increased; IVC, inferior vena cava left ventricular ejection fraction; LVOT, left ventricular outflow tract; Mod, MR, mitral regurgitation; Nl, normal; PASP, pulmonary artery systolic pres right ventricular; RVEF, right ventricular ejection fraction; S, systolic; SFR flow reversal; TR, tricuspid regurgitation; VSD, ventricular septal defect; V velocity time integral; w/o, without. *As described by Pasternak, Braunwald, and Sobol.[162] †In the infarction age group. ‡Dependent on extent of LV infarction.

ratio), the deceleration time of early filling curve and the isovolemic relaxation time. Two distinct patterns of inflow reflect the two categories of diastolic dysfunction: impaired left ventricular relaxation and decreased left ventricular compliance. Impaired relaxation is characterized by a decreased E/A ratio and prolonged deceleration and isovolumic relaxation times; this pattern is encountered in chronic ischemic heart disease and hypertension and as a result of normal aging. The restrictive flow pattern noted under

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conditions of diminished left ventricular compliance demonstrates an increased E/A ratio and shortened isovolumic relaxation and deceleration times. This inflow pattern occurs in restrictive cardiomyopathies and in association with elevated filling pressures. An intermediate stage of diastolic function is present with "pseudonormalization" of the mitral filling pattern, usually associated with a moderate elevation of filling pressures. In a recent study of postinfarction patients with left ventricular ejection fraction less than 35%, a mitral deceleration time of less than 120 msec was highly predictive of a pulmonary capillary wedge pressure of greater than 20 mm Hg[152] (Fig. 12-5) . In a second study of patients with systolic dysfunction after infarction (ejection fraction >40%), there was an increased rate of adverse events in two years of follow-up in patients with higher mitral E/A ratios and shorter deceleration times.[153] This finding has been confirmed in subsequent studies[11] [154] [155] (Table 12-6) . Several new parameters of diastolic function have been studied in postinfarction patients. The deceleration time of the diastolic component of pulmonary venous flow has a better correlation with wedge pressure in post patients with myocardial infarction than does the mitral deceleration time. The sensitivity and specificity of a pulmonary venous deceleration time less than 160 msec in predicting greater than or equal to 18 mm Hg in pulmonary capillary Figure 12-5 Mitral inflow signal from a patient with a large anterior myocardial infarction. There is an increased E wave velocity and a shortened deceleration time. The deceleration time was measured between the two arrows as 80 msec. This measurement is evidence of elevated filling pressures and is a poor prognostic sign (see text).

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TABLE 12-6 -- The Role of Diastolic Functional Parameters in Prognosis After Myocardial Infarction Reference n Comment Pozzoli et 107 Patients with cardiac events had significantly higher E/A ratios and shorter mitral deceleration time al[153] Sakata et 206 Decreased A wave was associated with high in-hospital mortality and congestive heart failure al[154]

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Nijland et 95 1-yr survival rate: restrictive filling, 50%; nonrestrictive al[155] filling, 100% Moller et 110 Deceleration time < 140 msec was the most powerful predictor of cardiac death al[11] Total 518 wedge pressure were 97% and 96%, respectively, compared with 86% and 59%, respectively, for a mitral deceleration time of less than 130 msec.[156] The propagation velocity of mitral inflow measured on M-mode color Doppler echocardiography also has prognostic significance.[11] Technically adequate pulmonary venous flow tracings can be obtained in the majority of patients with surface echocardiography. The predominant pulmonary venous flow pattern is triphasic, with the initial systolic (S) forward flow in pulmonary veins occurring during atrial relaxation (xdescent), a second systolic phase coinciding with basal descent of the left ventricle, and forward flow during diastole (D) occurring in the conduit phase of ventricular filling while the mitral valve is open (y-descent). During atrial systole there is a low-velocity retrograde flow signal (A wave). In subjects older than 40 years of age with normal filling pressures, the peak velocities and VTIs are higher during systole than during diastole, and the duration of the pulmonary venous A wave is less than that of the mitral A wave. With high filling pressures, diastolic filling predominates and the A wave duration exceeds that of the mitral A wave.[110] [157] [158] In patients with acute myocardial infarction, a systolic fraction of pulmonary venous flow less than 45% was highly associated with a pulmonary capillary wedge pressure greater than 18 mm Hg.[150] Additionally, systolic flow reversal in the pulmonary veins is an important sign of hemodynamically significant mitral regurgitation.[159] Measurements of pulmonary artery systolic pressure using tricuspid regurgitant jets with or without contrast enhancement have been well validated in the literature,[160] and the size and respiratory dynamics of the inferior vena cava can be used to estimate right atrial pressure. [161] Combining these parameters with measurements (quantitative or qualitative) of left and right ventricular function and color flow Doppler interrogation for valvular abnormalities results in a comprehensive evaluation of the hemodynamic state after infarction as defined by

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Pasternak, Braunwald, and Sobel[162] using invasive data. A recent study found that a combination of automated Doppler cardiac output and pulmonary venous flow measurements was highly accurate in predicting the hemodynamic subset as measured invasively.[150] When the data are incomplete from a transthoracic examination, one should not hesitate to employ TEE given its established safety even in the critically ill patient. Of course, the hemodynamic information available from an echocardiographic examination is available only at a single point in time, and continued invasive monitoring may be necessary in patients with ongoing instability. Recurrent Ischemia After Infarction Although there have been few studies evaluating the usefulness of echocardiography in patients with recurrent ischemia after myocardial infarction, many clinicians rely on echocardiographic evaluation in this setting, given the sensitivity of this technique for detection of wall motion abnormalities. Worsening of wall motion after initial improvement suggests reocclusion of the infarct-related vessel. Wall motion abnormalities in regions remote from the area of infarction suggest multivessel disease.[146] In addition, alternative causes for chest pain after myocardial infarction (e.g., pericarditis) may be evident on echocardiographic examination. Postinfarction Pericarditis and Pericardial Effusion Postinfarction pericarditis most often occurs after a Q-wave infarction between 3 and 10 days following the myocardial infarction. Onset after 10 days is usually considered Dressler's syndrome. Chest pain caused by pericarditis typically is pleuritic and is accompanied by the auscultatory finding of a pericardial friction rub. Although a pericardial effusion is very common after infarction, it is not pathognomonic of pericarditis. Several investigators have reported on the incidence of pericardial effusion following infarction,[163] [164] [165] [166] [167] as summarized in Table 12-7 . In all the studies reviewed, pericardial effusion was associated with larger infarctions as measured by wall motion scores[163] [166] or degree of creatine kinase elevation.[164] [166] The TABLE 12-7 -- Incidence of Pericardial Effusion After Infarction Study Pierard et al[166] Galve et al[165]

No. of Patients 66 138

No. with Effusion (%) Comments 17 (26) Anterior > inferior 39 (28) Anterior > inferior

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Charlap et al

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172 30 (17)

Peaked on 3rd day Echo at 72 hr

[164]

Sugiura et al

185 44 (24)

Inferior MIs only; higher incidence with RV infarct Widimsky and 192 82 (43) Peaked 5th day; CHF or [167] Gregor death more common; no increase with thrombolysis or heparin CHF, congestive heart failure; MI, myocardial infarction; RV, right ventricular. [163]

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incidence of congestive heart failure and mortality is higher in those patients with effusions apparent on echocardiography.[167] In almost all cases the effusions are small and hemodynamically insignificant. Thus, the effusion did not cause the increase in morbidity and mortality but serves as yet another marker of a large infarction. Mitral Regurgitation Ischemic mitral regurgitation can be defined as valvular incompetence associated with myocardial ischemia or infarction in the absence of primary leaflet or chordal pathology (Fig. 12-6) . Acute mitral valve incompetence may occur in the setting of myocardial infarction owing to necrosis and rupture of papillary muscle tissue or incomplete coaptation of the mitral valve leaflets owing to distortion of ventricular architecture. Mitral regurgitation is common in the setting of acute myocardial infarction, with a reported incidence rate between 10% and 50%. Of almost 12,000 postinfarction patients catheterized at Duke University, 19% had evidence of mitral regurgitation by angiography.[168] [169] Hemodynamically significant mitral regurgitation occurs equally in anterior and inferior infarcts. Risk factors for significant postinfarction mitral regurgitation include advanced age, female gender, diabetes, and prior infarction.[170] [171] In patients with myocardial infarction, moderate to severe mitral regurgitation is associated with substantially reduced short- and long-term survival, with up to a 24% early and 54% 1-year mortality rate.[171] [142]

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Severe postinfarction mitral regurgitation also is an independent risk factor for coronary artery bypass surgery operative mortality. [168] Moreover, in patients presenting to the emergency room with chest pain, moderate or severe Figure 12-6 (color plate.) Mitral regurgitation in a patient with an inferior myocardial infarction and resultant inferobasal aneurysm. A, Diastolic deformity in this apical two-chamber view (arrow). B, Lack of thickening in this region during systole (arrow). C, Moderately severe mitral regurgitation (double arrow).

mitral regurgitation by echocardiography was associated with high risk for overall and cardiovascular mortality (risk ratio = 2.0).[172] Among these patients, only 60% had audible murmurs. The clinical recognition of mitral regurgitation in the setting of myocardial infarction may be confounded by several variables. Up to 50% of patients with hemodynamically significant mitral regurgitation do not have an audible murmur owing to rapid equalization of left ventricular and left atrial pressures (especially in a low output state) or because the murmur is obscured by lung sounds in a patient with pulmonary edema or mechanical ventilation.[171] In view of the adverse prognosis, early diagnosis is desirable to institute medical or surgical interventions that potentially improve outcome. Although some authors have advocated TTE in all patients admitted with myocardial infarction, this approach is probably not costeffective. However, echocardiography is mandatory in the postinfarction patient with a new systolic murmur, pulmonary edema, or sudden cardiac decompensation. In this situation, TTE is 100% sensitive in detecting mitral regurgitation and in distinguishing mitral regurgitation from ventricular septal defect.[173] Detection and grading of mitral regurgitation is accomplished with 2D, Mmode, color, and spectral Doppler techniques. Two-dimensional imaging detects abnormalities in the mitral valve apparatus, including flail leaflets or ruptured chordae. Although color flow parameters are those most often used, accurate grading of mitral regurgitation severity should encompass other echo-Doppler signs as well.[174] [175] In the patient with pulmonary edema, the unexpected findings of a small infarction, a hyperdynamic left ventricle, increased early mitral inflow velocity, or all three [176] should prompt a careful search for mitral regurgitation even when color flow Doppler mapping is unrevealing.

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263

Papillary muscle necrosis with rupture and a flail leaflet is a life-threatening complication of myocardial infarction that requires surgical intervention. The more frequent involvement of the posteromedial papillary muscle is thought to be due to its blood supply from a single coronary artery. Chordae to both leaflets arise from each of the papillary muscles so that in cases of "complete" rupture of the entire trunk of a papillary muscle, both leaflets are affected. In less severe cases, the rupture is "incomplete" and only a single head is torn. The 2D echocardiographic findings include prolapse of one or both leaflets, a flail leaflet, and liberation of a portion of the papillary muscle.[177] In some patients, the ruptured muscle may remain tethered to the chordae and chaotic motion is not present. Spectral and color flow Doppler imaging of the jet is usually easily accomplished with surface imaging, but an eccentric path of flow may complicate its identification. In our experience, TEE is superior in this regard,[36] supported by multiple case reports in the literature[16] [19] [21] (Fig. 12-7) . When only a single head of the papillary muscle is affected (incomplete rupture), medical stabilization often is possible. Initial treatment should include afterload reduction with diuretics, angiotensin converting inhibitors, nitroprusside, and (in cases of severe cardiac decompensation) inotropic support and intra-aortic balloon pump. When rupture is complete, involving the main trunk of the papillary muscle, the complication is uniformly fatal without immediate recognition and prompt repair.[177] [178] In the other forms of ischemic mitral regurgitation, reperfusion therapy with thrombolytics or angioplasty should be considered first-line therapy because reperfusion may improve regurgitant severity and patient prognosis. Coronary bypass in conjunction with mitral valve surgery should be considered in patients who show benefit from medical therapy or nonsurgical revascularization. Coronary bypass with mitral valve surgery is necessary in patients who develop circulatory collapse as a result of mitral regurgitation, despite the relatively high operative mortality in this patient group. In those patients who receive surgery for severe ischemic mitral regurgitation, there is evidence that early surgery, concomitant revascularization, and repair, rather than replacement, improve survival.[179] [180] In the recent SHOCK trial (SHould we use emergently revascularized Occluded Coronaries in cardiogenic shocK?), the survival rate in patients with

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Figure 12-7 (color plate.) Transesophageal echocardiogram of a patient with papillary muscle rupture after an acute inferior myocardial infarction. The papillary muscle rupture was incomplete and the head of the papillary muscle remained tethered to the mitral chordae. A, The triangular density representing the head of the papillary muscle (arrow) can be seen within the body of the left ventricle during systole. B, Associated severe mitral regurgitation with a prominent area of proximal isovelocity surface acceleration (double arrow).

acute severe mitral regurgitation who underwent surgery (40%) was higher than in those treated medically (71%, P < .003).[181] Ventricular Septal Rupture Ventricular septal defect owing to myocardial rupture complicates 1% to 3% of all acute myocardial infarctions and up to 5% of all fatal infarctions. In the GUSTO-1 trial (Global Utilization of Streptokinase and TPA for Occluded coronary arteries), the incidence of ventricular septal rupture was only 0.2% (84 of 41,021 enrolled patients), suggesting that thrombolytic therapy has reduced the incidence of rupture.[182] Ruptures occur only in the presence of transmural infarction and result from hemorrhage within the necrotic zone. Independent risk factors for the development of a ventricular septal defect are similar to those for papillary muscle rupture and include first infarction, advanced age (>65), hypertension, and female gender.[183] [184] There appears to be a higher incidence in patients without a history of prior angina and with infarcts in the distribution of a single vessel.[183] [184] [185] Thus, septal rupture appears to be more likely following abrupt occlusion of a single artery that vascularizes a territory for which there is little collateral flow.[184] Unlike papillary muscle rupture, ventricular septal rupture occurs with equal frequency among patients with anterior (LAD) and inferior (RCA) infarctions but less frequently in those with lateral (left circumflex artery) infarctions.[186] Conflicting evidence exists as to the effect of thrombolytic therapy on the development and outcome of postinfarction ventricular septal defect. Thrombolytic administration that is delayed more than 12 hours following the onset of chest pain may increase the incidence of ventricular septal rupture.[97] However, in most cases the slight increase in the risk of rupture is outweighed by the overall benefit of reperfusion therapy. In the GUSTO1 study, the onset of rupture was earlier on average (1 day) than that reported previously, suggesting that although thrombolytic therapy reduced the rate of rupture, it tended to occur earlier after thrombolysis.

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Ventricular septal defects usually present 3 to 6 days after infarction with recurrent chest pain, dyspnea, and sudden hypotension or shock. A new harsh pansystolic murmur is present in approximately 50% of patients. Bedside 264

echocardiography has been demonstrated to be highly sensitive and specific in the diagnosis of ventricular septal defect. The defect can be visualized by transthoracic 2D imaging in 40% to 70% of patients.[177] [187] The use of contrast and color flow Doppler imaging improves the sensitivity to 86% and 95%, respectively.[21] [97] [173] [177] When TTE is suboptimal, TEE is highly accurate with a reported 100% sensitivity and specificity, [188] [189] with improved delineation of the site of defect, the morphology, and presence of multiple defects[190] (Fig. 12-8) . The most common site for a ventricular septal rupture is the posteroapical septum. Visualization of the area of myocardial dropout is most often accomplished in the parasternal short-axis view just below the level of the papillary muscles or in the apical four-chamber view with slight posterior angulation of the probe. Anterior septal defects most often occur in the distal one third of the septum and are visualized in the apical four-chamber view with anterior angulation or in an apical short-axis view. Postmyocardial infarction ventricular septal defects may be multiple and often have a serpiginous course through the myocardium.[191] Associated echocardiographic findings include evidence of elevated right ventricular pressure including right ventricular dilation, decreased right ventricular systolic function, and paradoxical septal motion. Signs of increased right atrial pressure include right atrial dilation, bowing of the interatrial septum toward the left throughout the cardiac cycle, and plethora of the inferior vena cava. Color flow Doppler imaging is particularly useful in demonstrating the exact position of the defect; the width of the jet correlates with the size of the defect as measured at surgery.[191] Although the peak gradient across the ventricular septal defect measured with continuous wave Doppler allows an estimate of right ventricular systolic pressure, the measurement should be used with caution in patients with complex defects involving indirect tracts through the myocardium. [191] A recent study demonstrated a fair correlation between this Doppler estimate of right ventricular systolic pressure and that measured at catheterization (r = 0.71); the values were similar to those estimated from the tricuspid

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regurgitant jet. Echocardiography provides prognostic and diagnostic information in patients with ventricular septal rupture. Rupture Figure 12-8 (color plate.) Transesophageal echocardiogram showing a large ventricular septal defect (VSD) involving the posterior septum in a patient with a large inferior myocardial infarction and right ventricular extension. Left, The area of discontinuity can be visualized as a large, irregularly shaped area of myocardial dropout. Right, Color flow demonstrates left-to-right shunting across this ventricular septal defect. LV, left ventricle; RV, right ventricle.

of the posterior septum after inferior myocardial infarction is associated with a higher mortality rate, apparently related to the degree of associated right ventricular dysfunction.[186] [192] Moreover, posterior septal ruptures tend to be more complex and associated with remote myocardial involvement. In contrast, anterior septal defects more often have a direct course and involve a discrete myocardial region. Overall mortality is 95% to 100% without surgical intervention.[193] The strongest indicator of poor prognosis is the development of cardiogenic shock associated with as much as a 90% mortality rate.[192] Although early surgery appears to improve survival when cardiogenic shock is present, results in the recent SHOCK trial were disappointing. In the surgically treated group, the survival rate (19%) was only slightly better than that of the medically treated group (5%).[186] Right ventricular systolic pressure tended to be higher and right atrial pressure lower, among the survivors. When the patient can be stabilized medically, operative mortality may be improved when surgical repair is delayed until 6 weeks following the event.[184] In summary, the value of echocardiography in patients with suspected ventricular septal rupture is its ability to provide an accurate, timely diagnosis and important prognostic information that may assist in therapeutic decision making. Rupture of the Ventricular Free Wall and Pseudoaneurysm Free wall rupture occurs in approximately 3% of all acute myocardial infarctions,[194] and it is one of the leading causes of fatality (8% to 20%).[195] [196] [197] [198] [199] Risk factors for free wall rupture are similar to those for papillary muscle and ventricular septal rupture; however, this complication is more likely to occur in patients with a transmural myocardial infarction involving the posterolateral wall associated with a left circumflex occlusion

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or with a LAD occlusion.[201] Early successful reperfusion appears to decrease the risk of rupture. In one study of approximately 1300 patients, the overall incidence of cardiac rupture was lower in those receiving thrombolytic therapy (1.7%) than in those in the conventional therapy group (2.7%). Among

[200]

265

patients who receive thrombolytic therapy, patients older than 70 years of age and women had higher rates of rupture.[202] Moreover, patients in whom reperfusion was unsuccessful had a significantly higher rate of rupture than those who were successfully reperfused (5.9% versus 0.5%).[203] Conversely, late reperfusion appears to increase the risk of myocardial rupture though decreasing overall mortality.[97] [204] The use of nitrates in acute myocardial infarction may decrease the risk of rupture by as much as 30%.[205] The intensity of post-thrombolytic anticoagulation with heparin or hirudin does not appear to affect the rate of rupture. [202] Although ventricular free wall rupture usually presents clinically as an acute catastrophic event leading to rapid demise, several recent pathologic and clinical studies have suggested that many cases may involve subacute dissection and tearing of the myocardium before hemodynamic collapse.[194] [196] [200] [205] , Intramural hematoma or hemorrhage at the junction of the necrotic and the normal myocardium results in a small endocardial rent. The tear usually takes a circuitous pathway through the myocardium, ending in a small epicardial opening. Clinically, a prodrome of ongoing or recurrent chest pain (in the absence of an elevation in creatinine kinase), repetitive large volume emesis, unexplained agitation, hypotension or syncope may be associated with the initial small tear.[194] [196] [200] A small amount of hemorrhage into the pericardial space of blood may precede the final catastrophic event. Patients diagnosed during this subacute phase and taken promptly to surgery have a greater chance of survival. A second mechanism of rupture through the wall of an aneurysm has been described. [206]

Echocardiography has a high sensitivity for rupture[194] when the diagnosis is sought and all the echocardiographic findings are considered. The most frequent finding is pericardial effusion; the absence of pericardial effusion virtually excludes rupture. Increasing size of effusion and the presence of thrombus in the pericardial space significantly increases the specificity for rupture (>98%). [194] [204] , [207] An intrapericardial thrombus appears as an

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echo-dense mass; it may be mobile, undulating within the pericardial space or immobile, impinging on the cardiac chambers.[208] Direct visualization of the myocardial tear is possible with TTE in as many as 40% of patients.[201] Other echocardiographic findings include evidence of Figure 12-9 The difference between a true aneurysm (A) and a false aneurysm (B). Note that in the true aneurysm there is continuity of myocardium in the region of dilation, in contrast to the loss of this continuity in the pseudoaneurysm. (Modified from MacKenzie JW, Lemole GM: Tex Heart Inst J 1994;21:296–301.)

tamponade with right atrial and right ventricular diastolic collapse (40%), [201] respiratory variation of the tricuspid and mitral inflow pattern, and plethora of the inferior vena cava. Echocardiographic guidance of pericardiocentesis of the hemopericardium may be life saving in the patient with hemodynamic collapse before the patient can be transported to surgery. Patients at risk for rupture may be identified by evidence of infarct expansion with significant wall thinning at the infarct site. The mortality rate of free wall rupture in the absence of surgical intervention approaches 100%,[199] although recent series report as much as a 50% survival rate in patients who underwent pericardiocentesis and conservative medical management.[201] [209] The in-hospital mortality rate for those who undergo surgical repair is in the range of 40%.[193] [201] [204] Those who survive until hospital discharge appear to have a good long-term prognosis. Thus, early echocardiographic diagnosis with prompt surgical or percutaneous drainage is mandatory in patients who develop postinfarction myocardial rupture. A pseudoaneurysm is a myocardial rupture contained by pericardial adhesions resulting in a pouch that communicates with the left ventricular cavity. [177] A distinguishing echocardiographic feature is the narrow neck, compared with the broader "entrance" to the body of a true aneurysm, with a "neck" diameter-to-maximum diameter ratio less than 0.5. An echocardiographic study showed that this sign was only 60% sensitive in patients with post-myocardial infarction pseudoaneurysms.[210] The majority of post-myocardial infarction pseudoaneurysms were located in the inferoposterior or posterolateral regions (associated with right coronary or left circumflex coronary occlusions).[210] The walls of the pseudoaneurysm are composed of pericardium rather than

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the thin-walled myocardial scar of true aneurysm (Fig. 12-9A) . Occasionally a pseudoaneurysm may occur after rupture of the thin wall of a true aneurysm with the development of a "mixed" aneurysm (see Fig. 129B) . [211] Spectral and color Doppler imaging demonstrate characteristic flow in and out of the pericardial cavity at the site of the tear, as well as abnormal flow within the pseudoaneurysm. Respiratory variation of the peak systolic velocity has also been demonstrated.[212] A meta-analysis suggested that TEE has a higher diagnostic accuracy (>75%) than TTE (26%), although data 266

was available in only a small number of patients[213] (Fig. 12-10) . Surgical repair is the preferred treatment, although new reports have demonstrated that conservative medical treatment in certain high-risk patients is not associated with an increased risk of cardiac rupture.[210] [213] Infarct Expansion and Aneurysm Formation Infarct expansion is an increase in the circumferential extent of the area of infarction that results from stretching and thinning of the infarcted zone. Early clinical studies demonstrated that this phenomenon with a consequent increase in left ventricular volume and wall stress was associated with an adverse prognosis.[85] The importance of infarct expansion has been underscored by clinical trials using angiotensin converting enzyme inhibitors in patients with left ventricular dysfunction after myocardial infarction. In the SAVE trial (Survival and Ventricular Enlargement), which showed a 21% reduction in cardiovascular mortality with the use of captopril,[214] echocardiography demonstrated that ventricular enlargement and reduced fractional area change were independent risk factors for cardiac events. Patients treated with captopril had a lower incidence of ventricular enlargement, which was associated with the lower risk of events,[50] a finding that has been confirmed in subsequent studies.[141] [215] The final expression of infarct expansion is aneurysm formation. In the Coronary Artery Surgery Study (CASS) there was a 7.6% incidence of angiographically documented left ventricular aneurysms.[216] In a study by Visser et al,[218] the incidence of aneurysm was 22% (35 of 158), and most of those occurred in patients with anterior infarction. Formation of an aneurysm occurs only with transmural infarction with a full-thickness scar and, thus, is more frequent following a Q-wave than a non-Q-wave

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infarction. An aneurysm is more likely to complicate an infarct in the LAD distribution than in the right or circumflex arteries.[218] Spontaneous rupture of an acute aneurysm is rare (see "Rupture of the Ventricular Free Wall"), and late rupture virtually never occurs. Serial 2D echocardiographic studies show that aneurysmal dilation is present as early as 5 days after myocardial infarction (15 of 35, 43%, in the Visser study), and new aneurysms after 3 months are unlikely.[218] Despite the Figure 12-10 Transgastric views in transesophageal echocardiogram showing a large pseudoaneurysm involving the inferolateral wall. Left, short-axis view (horizontal plane); right, long-axis view (longitudinal plane).

beneficial clinical course attributed to delayed reperfusion with thrombolytic therapy, there has been no reduction in the frequency of ventricular aneurysms.[219] [220] The echocardiographic appearance of a ventricular aneurysm parallels the pathology. A true aneurysm is defined as a deformity of the thinned infarct segment that is apparent during diastole as well as during systole (see Fig. 12-6) and demonstrates a diastolic contour abnormality. In contrast, a dyskinetic myocardial segment deforms during systole, extending beyond the normal contour of the myocardium. The involved myocardial segment is scarred with thin walls (<7 mm) and increased echogenicity owing to the increased collagen content. [114] The wall of the aneurysm may eventually calcify. The most common location is the left ventricular apex, which is involved in approximately 90% of patients. Aneurysms may vary in size, and very small aneurysms may be difficult to visualize by echocardiography. Technically, the detection of an apical aneurysm is highly dependent on the skill of the operator. Routine employment of highfrequency transducers with a shallow focal point enhances near-field resolution and aids examination of the left ventricular apex. Left-sided contrast agents also may enable detection of small apical aneurysms. Using these methods, the sensitivity of TTE for detection of apical aneurysms should approach 100%. Occasionally, spontaneous echocardiographic contrast may be visible in large aneurysms. It should be noted that TEE may not provide adequate visualization of the left ventricular apex and, therefore, in our experience, is less sensitive than surface imaging.

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Echocardiographic recognition of a left ventricular aneurysm is clinically relevant for the following reasons: 1. The early formation of an aneurysm adversely affects early (inhospital) and late (1 year) mortality.[218] 2. Thrombi are frequently found within aneurysms. 3. Aneurysms and left ventricular thrombi are associated with systemic embolization. In patients with refractory heart failure and angina or recurrent embolic events, aneurysmectomy may be recommended occasionally. Functional measurements of the residual myocardium using quantitative 2D echocardiography is highly predictive of operative mortality and the clinical success of this procedure.[221] [222] A basal (residual) ejection fraction of greater than 40% was associated with a satisfactory result.[222] Left Ventricular Thrombus

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Studies in the early 1980s demonstrated a high sensitivity (90% to 95%) and high specificity (80% to 85%) for the echocardiographic identification of left ventricular thrombus.[223] [224] A prerequisite for thrombus formation is the presence of a segmental wall motion abnormality, most commonly in the left ventricular apex. The ultrasonic appearance of a mural thrombus is that of a mass distinct from the endocardium and protruding to a variable extent into the left ventricular cavity. Under ideal conditions, the surface of the thrombus can be distinguished clearly from the underlying endocardium and the mass can be visualized in two different imaging planes. The tissue characteristics of an acute thrombus are usually similar to that of the myocardium (Fig. 12-11) . A chronic thrombus may have increased reflectivity, demonstrate a layered appearance corresponding to the lines of Zahn, and contain areas of calcification (Fig. 12-12) . The base of attachment to the wall may be broad in the case of a sessile thrombus and narrow in a pedunculated thrombus. When multiple characteristics of the thrombus are analyzed, mobility of the thrombus is most closely associated (positive predictive value, 85%) with embolic events.[220] [225] In any given patient, the morphology may spontaneously change from sessile to pedunculated and vice versa; mobility may resolve spontaneously.[226] False-positive echocardiographic diagnoses are usually a result of

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pseudotendons (i.e., false chordae) spanning the left ventricular apex, coarse trabeculations associated with left ventricular hypertrophy, or nearfield artifacts (commonly present with low-frequency transducers). Highfrequency transducers with a short focus point can sometimes differentiate true thrombus from these other phenomena. Left-sided contrast agents may outline the contours of the thrombus, creating a filling defect[227] [228] with improved detection of thrombus. Thrombi most commonly develop in the presence of a large infarction during the hospitalization phase of a Figure 12-11 Acute thrombus in the posterior aspect of the apical septum. Note that the large mass is homogeneous in texture, without evidence of calcification.

Figure 12-12 Four-chamber view depicting a chronic thrombus within an apical aneurysm. The appearance of the thrombus is layered with areas of calcification. The layers correspond to the lines of Zahn.

myocardial infarction.[229] Like aneurysms, they are more likely following a myocardial infarction in the LAD (up to 33%) than in the RCA or left circumflex artery distribution (less than 1%).[230] [231] New data demonstrate that the best predictor of left ventricular thrombus formation after acute anterior myocardial infarction is a high initial end-systolic volume.[232] Anticoagulant therapy appears to decrease the risk of embolic events and enhances the resolution of thrombus, although spontaneous resolution also may occur.[229] [233] Patients with a left ventricular thrombus identified during the initial hospital stay have an increased long-term mortality rate (22%) compared with those without thrombi (7%). Left ventricular thrombi usually resolve during the first month after anterior myocardial infarction with routine thrombolytic and aspirin treatment, but appearance and resolution of thrombi can continue in a significant proportion of patients (12%).[234] In general, thrombolytic therapy appears to decrease the rate of mural thrombus development. In the Western Washington Randomized Trial of intracoronary streptokinase, the incidence of thrombus and emboli was similar in both treated and untreated groups,[219] but most other trials of

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intravenous thrombolytic agents have shown a reduction in the incidence of thrombi and emboli.[235] [236] [237] [238] Moreover, in the GISSI-2 trial there was no significant difference between the four treatment groups (recombinant tissue plasminogen activator ± heparin, streptokinase ± heparin), with an overall incidence of 28%.[239] The overall tendency for reperfusion therapy to decrease the size of the infarction is likely to lower the risk of thrombus formation. In addition, after thrombolysis, most patients receive an inhospital period of anticoagulation, which is known to decrease the rate of thrombosis and embolization[239] (Table 12-8) .

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TABLE 12-8 -- Effect of Thrombolytic Therapy on Incidence of Left Ventricular Thrombus in Anterior Wall Myocardial Infarction Study Eigler et al

No. of Patients Agent 22 SK

Mean Time Treated Untreated to Rx (hr) (%) (%) P <3 1/12 (8) 7/10 (70) <.005

[235]

Stratton et al

83 SK *

[219]

Natarajan et al[237] Lupi et al[236] Bhatnagar and al-Yusuf

45 SK 63 SK 118 r-TPA

4.7 7/45 6/38 (16) (16) <6 0/27 (0) 8/18 (44) ≤3 4/19 (22) <4 3/54 (5.5)

NS <.05

30/44 (54) <.05 8/44 (18) † <.05

[238]

NA 34/74 10/25 (40) NS (46) Domenicucci 222 SK, NA 26/97 71/125 <.005 [240] et al alteplase (27) (57) NA, not available; NS, not significant; r-TPA, recombinant tissue plasminogen activator; SK, streptokinase. Mooe et al

99 SK

[234]

*Intracoronary. †Received heparin.

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The decision to prescribe oral anticoagulation following hospital discharge is influenced by two additional considerations. Embolic events occur most likely in the first month after myocardial infarction and rarely occur in the absence of thrombus identified by echocardiography.[240] However, the risk of cerebral or systemic embolization after infarction is increased in patients with large apical aneurysms and poor systolic function independent of echocardiographically documented mural thrombus. Second, chronic mural thrombi, persistent for more than 3 months following a myocardial infarction, are very unlikely to embolize. Changes in the morphology of the thrombus with evidence of protrusion are most likely to predict late embolism (>3 months).[240] Thus, most physicians perform an echocardiogram during the acute phase of an anterior wall infarction to measure left ventricular function and to detect aneurysm, thrombus, or both. In the presence of a large apical aneurysm with or without a visible thrombus, oral anticoagulation is recommended in the absence of contraindications.[241]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Post-Myocardial Infarction Risk Stratification Echocardiography has an important role in the evaluation of a patient after discharge from the CCU. Echocardiography during low-dose dobutamine infusion is used to detect myocardial viability in segments that have persistent dysfunction following reperfusion.[64] Echocardiography during higher dose dobutamine infusion or with dynamic stress can be used to detect residual ischemia. Caution should be exercised in the first week after a transmural infarction because cases of myocardial rupture during highdose dobutamine infusion have been reported.[28] [29] Contrast echocardiography will have an important role with the development of reliable perfusion agents.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Early experimental models employing echocardiography for the detection and quantitation of ischemia and infarction helped investigators elucidate the pathophysiology. This work was directly transferable into the CCU and provided the basis for the clinical diagnostic and prognostic role of echocardiography. Advances in echocardiography, especially color flow Doppler imaging, increased the capabilities of echocardiography in detecting the occurrence of complications, such as ventricular septal defect and papillary muscle rupture. Future directions include the detection of flow deficits using myocardial contrast echocardiography and more accurate quantitation of infarct size using 3D techniques.

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275

Chapter 13 - Exercise Echocardiography Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Pamela A. Marcovitz MD

Stress echocardiography consists of a number of stress techniques used in conjunction with echocardiographic imaging. Exercise echocardiography is the most established of these techniques and has been increasing in popularity since the first paper was published on the use of twodimensional echocardiography with bicycle exercise in 1979.[1] Although the images were crude, they served to successfully demonstrate ischemia following cardiovascular stress and its resolution following coronary artery bypass grafting (Fig. 13-1) (Figure Not Available) . With technologic advances, including improvements in imaging and digitization, stress echocardiography has seen widespread acceptance as a first-line technique for the diagnosis of coronary disease. Recently, stress echocardiography has been increasingly used for prognostication in various patient subsets, including patients with chronic coronary disease, patients with recent revascularization, patients with recent myocardial infarction, and female patients. Despite recent advances, however, the principles of its use remain

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the same. In the presence of a significant coronary stenosis, an adequate level of physical exertion results in a transient mismatch between oxygen supply and demand, resulting in a wall motion abnormality within an area of myocardium supplied by a stenotic artery. The wall motion abnormality is detectable by echocardiography and serves as a marker of the degree and severity of ischemia. Future advancements may bring the ability to simultaneously track myocardial perfusion.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Rationale and Theoretical Basis for Ischemia Detection with Stress Echocardiography The rationale for the use of echocardiography to detect ischemia in conjunction with stress testing is that ultrasonography can visualize wall motion abnormalities that arise as the result of a transient mismatch between oxygen supply and demand, in turn resulting in ischemia.[2] [3] [4] [5] Regardless of the stress modality used to induce ischemia, the echocardiographic response to exercise will reflect the underlying state of the coronary arteries.[6] [7] [8] [9] In the absence of coronary artery disease, there will be inward motion (endocardial excursion of at least 5 mm) and increased wall thickening. These characterize the "normal hyperdynamic response" following exercise and signify normal underlying coronary arteries. Conversely, in myocardium subtended by a critical stenosis, a mismatch between oxygen supply and demand will develop during exercise, resulting in ventricular systolic dysfunction or dyssnergy, in a segment or segments of myocardium during cardiovascular stress. Dyssynergic responses may be classified by the degree of abnormality present: 1. Hypokinesia: less than normal (5 mm) degree of inward myocardial excursion and thickening 2. Akinesia: complete lack of inward motion and thickening 276

3. Dyskinesia: paradoxical outward motion and thinning of affected segment or segments. Figure 13-1 (Figure Not Available) Images from a 30-degree sector scanner demonstrating an exercise-induced apical abnormality prior to coronary artery bypass grafting (A) and normal apical wall motion after revascularization (B). (From Wann LS, Favis JV, Childress RH, et al: Circulation 1979;60:1300–1308. Reproduced with permission. Copyright 1979 American Heart Association.)

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The observation that abnormal wall motion reflects an underlying mismatch in supply and demand serves as the premise for the use of echocardiographic imaging in stress testing and occurs during a variety of states in which oxygen supply to the myocardium is reduced. Using a stylus attached directly to myocardium in an animal model, Tennant and Wiggers [10] were among the first to demonstrate that disruption of the coronary blood supply produces wall motion abnormality. Immediately after snare occlusion of a coronary artery, a reduction in wall thickening was observed, followed by normalization of wall motion along with release of the snare. This observation has since been validated with echocardiography in clinical settings in which arterial occlusion occurs, including balloon angioplasty and myocardial infarction.[11] [12] A variety of models have been studied to determine, in detail, the temporal and spatial sequence of events that occur during decreased regional blood flow of sufficient severity to create an imbalance in the myocardial oxygen supply-demand relationship. These models have included graded snare coronary occlusion in animals, balloon angioplasty, exercise, atrial pacing, and observation of spontaneous anginal episodes in humans.[13] [14] [15] [16] [17] [18] [19] In the early animal studies, a closely coupled relationship was noted between myocardial wall thickening and coronary flow, such that reductions in blood flow of 10% to 20% were found to impair regional (but not global) wall thickening within an ischemic zone. The observed reduction in wall thickening was found to be proportional to severity of flow reduction, with greater degrees of flow restriction causing greater severity in regional wall motion abnormalities.[16] , [20] Thus, whereas hypokinesis is noted following a threshold reduction in blood flow of around 10% to 20%, akinesis is observed with flow reduction of greater than 80%, and paradoxial motion, or dyskinesis, with transmural reductions in flow. These early studies also noted a tendency for decreased wall thickening to be more closely coupled with subendocardial rather than subepicardial flow and to extend into adjacent regions beyond welldemarcated zones of reduced flow, a phenomenon known as tethering.[3] [21] As the opportunities for echocardiographic monitoring grew, these observations in animals were extended to humans.[22] [23] [24] [25] Taken together, these studies form the basis for what we now regard as standard echocardiographic observations of ischemic myocardium. After acute, complete coronary occlusion, a series of predictable changes takes place in the myocardium, beginning with the development of diastolic and systolic dysfunction, followed by ST segment depression and angina. A

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wall motion abnormality is one of the initial events seen with the development of ischemia and precedes development of ST segment changes or angina by several minutes. This so-called ischemic cascade, which is known to occur after occlusion of a coronary artery, may occur in ischemic myocardium subtended by a critical stenosis whenever oxygen supply-demand mismatch occurs.[26] [27] [28] A similar temporal relationship between wall motion and electrocardiographic changes has been noted in multiple studies of patients undergoing balloon angioplasty.[12] [29] [30] [31] Hauser et al[31] noted that regional endocardial dysfunction was seen by echocardiography at 19 seconds, electrocardiographic changes occurred at 30 seconds, and chest pain occurred at 39 seconds after balloon inflation. In addition to clinical settings involving coronary occlusion, the "ischemic cascade" was found to occur in ischemic myocardium subtended by a severe stenosis subjected to cardiovascular stress. Examining changes following exercise-induced ischemia in the region of a coronary stenosis, Sugishita et al[28] noted that the average time to onset of wall motion abnormality was 30 seconds, versus 90 seconds for electrocardiographic changes. Clinically, the ability to detect exercise-induced regional wall motion abnormalities increases with the severity and number of coronary occlusions.[32] [33]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Diagnostic Approach Choosing the Optimal Form of Stress

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Exercise is one of a number of stress modalities performed in conjunction with echocardiographic imaging. An adequate level of stress is a prerequisite to performing exercise echocardiography. For the purposes of stress testing, clinically adequate exercise is usually defined as the ability to reach at least 85% of predicted heart rate, based on resting heart rate and age. For patients able to exercise maximally, exercise echocardiography provides a wealth of information regarding the overall level of fitness, functional capacity, and the clinical significance of an ischemic response, as well as the prognosis related to coronary disease. Given the additional diagnostic and prognostic information provided by exercise and hemodynamic parameters, exercise should be the stress method of choice whenever feasible. In the event that a patient cannot perform adequate exercise, other stressors are used (Table 13-1) . For patients unable to perform maximal exercise or to reach a target heart rate, pharmacologic methods of inducing stress are commonly used. These are discussed in greater detail in Chapter 14 , but briefly, currently available pharmacologic methods can be divided into one of two general categories: agents that simulate exercise and coronary vasodilators. [34] The first of these are sympathomimetic amines, are infused intravenously, and induce stress in similar fashion to exercise, that is, through increasing heart rate, blood pressure, and contractility. Of the exercise-simulating agents, dobutamine has emerged as the agent of choice in the United States, largely because of its availability and low cost. Dobutamine exerts its physiologic effects through beta agonist activity, increasing myocardial oxygen demand in a similar fashion to exercise. Unlike exercise, however, dobutamine is unable to provide information about level of fitness or electrocardiographic or

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hemodynamic response to exercise. In addition, TABLE 13-1 -- Stress Modalities Used with Echocardiographic Imaging Exercise Treadmill Supine bicycle Upright bicycle Lateral bicycle Pharmacologic stress Dobutamine Dobutamine-atropine Arbutamine (not currently available) Epinephrine Isoproterenol Dipyridamole Dipyridamole-dobutamine Adenosine Pacing Esophageal Atrial Other Hand grip Cold presser Mental stress Hyperventilation Postventricular beats dobutamine frequently does not cause an adequate rise in heart rate, and for this reason, atropine is often needed to increase myocardial oxygen demand.[35] [36] Despite these drawbacks, dobutamine can provide information about the presence or absence of coronary disease, which is valuable in patient management decisions and prognostication. Arbutamine, which is the only pharmacologic stress testing agent approved by the Food and Drug Administration, provides a more balanced heart rate and blood

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pressure response without the need for atropine.[37] [38] Because of cost, however, and because it did not provide a clear advantage over dobutamine, Arbutamine was withdrawn from the market. Isoproterenol, because it produces extreme tachycardia, is no longer used as a stress agent. Atrial pacing, sometimes employed via a transesophageal approach, is reliable but is cumbersome and uncomfortable for the patient and therefore rarely used. Vasodilators, such as dipyridamole and adenosine, create ischemia through the mechanism of coronary steal, or the selective dilation of nonstenotic coronary beds. Following administration of these agents, normal coronary beds dilate preferentially in relation to stenotic beds, in effect shunting flow away from stenotic beds and rendering them ischemic. Some experts believe, and the medical literature suggests, that echocardiography has a lesser sensitivity for the detection of coronary disease when vasodilators are used, as compared with exercise and dobutamine.[39] [40] [41] Nonetheless, dipyridamole continues to be used for the detection of coronary disease, chiefly outside the United States, where the cost of this agent is lower. The type of stress one chooses to apply in conjunction with echocardiography should be based on the patient's ability to exercise and the diagnostic information one wishes to gain from testing. For example, for the initial diagnosis of coronary artery disease in a patient whose chest pain is provoked by physical exertion, exercise would be preferred. For patients unable to exercise maximally because of arthritis, peripheral vascular disease, or general deconditioning, pharmacologic stressors are more appropriate. Rarely, chest pain may be believed to be provoked by vasospasm, and for those patients whose chest pain is suspected to be vasospastic, ergonovine or hyperventilation may be appropriate.[42] [43] The choice of stress should also be governed by the patient's familiarity with types of activities. In the United States, the most popular form of applied physical stress for the purposes of diagnostic testing for coronary disease remains treadmill exercise. Familiarity with walking may lead to achievement of higher cardiovascular workloads. In European countries, upright bicycle exercise is a more familiar activity and has assumed a prominent role. More recently, the supine bike, sometimes with lateral angling, is emerging in the United States as a popular technique for assessment of coronary artery disease. Supine bicycle exercise facilitates imaging whenever a continuous record of echocardiographic images is desired. In the diagnosis of coronary disease, bicycle exercise allows one to determine more precisely the level of exercise at which ischemia develops,

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which, as discussed later, may be advantageous in the serial assessment of patients. Bicycle exercise also facilitates assessment of the clinical significance of valvular 278

Figure 13-2 Stress echocardiography laboratory equipment set-up, beginning in the lower left-hand corner and moving clockwise: crash cart, frame grabber, echocardiography machine, bed with shelf above for pulse oximeter and automated blood pressure cuff, electrocardiographic monitoring machine, blood pressure (BP) cuff (manual), treadmill, intravenous (IV) infusion pump for pharmacologic stress echocardiography, and IV equipment. The room measures 15 × 18 feet and requires no more than two steps for the patient between treadmill and bed.

heart disease and pulmonary hypertension through assessment of Doppler jets at various workloads. Equipment, Methodology, and Personnel The equipment needed for exercise echocardiography partially depends on the type of stress applied in conjunction with echocardiography. In all cases, high-quality echocardiographic instrumentation with an integrated or free-standing digital frame grabber, an offline analysis system, and either a treadmill or bicycle (supine or upright) connected to a computerized 12lead electrocardiograph are required. The ergonomics of the stress echocardiography laboratory should facilitate moving from the imaging bed to the treadmill and back to the imaging bed immediately after exercise in as few steps as possible. Following the use of any standard treadmill protocol, the patient steps off the treadmill and onto the imaging bed. Extra steps spent between equipment may result in a critical loss of imaging time during the immediate postexercise period, leading to loss of sensitivity. Thus, the most critical period of time in performing exercise echocardiography is that spent between the termination of exercise and the start of imaging. A typical floor plan for a stress echocardiography laboratory that requires a minimum number of steps for both patient and technician-sonographer is shown in Figure 13-2 . The set-up shown in Figure 13-2 rarely requires multiple steps for the patient between the treadmill and imaging bed. Imaging should take place as quickly as possible, since it has been shown that information about ischemia, particularly single-vessel disease, will be lost as the heart rate returns to

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normal. Some experts believe that special imaging beds with lateral cut-outs for apical imaging facilitate image acquisition. Images are typically captured in four views for side-by-side comparison in a digital format. The parasternal long- and short-axis and apical four- and two-chamber views have traditionally been used, with the substitution of subcostal images, if necessary, for patients with chronic obstructive pulmonary disease or postbypass surgical bandages that interfere with imaging windows.[44] Modification of chest lead placement is sometimes necessary to 279

obtain the best imaging windows and rarely interferes with the integrity of the electrocardiographic response. The question of whether to perform a complete baseline study with Doppler imaging or to simply capture the minimum number of images required for stress imaging often arises. In our laboratory, the practice is to perform a complete baseline study unless one has recently been performed and there has been no interim change in the patient's clinical status. The personnel required to perform exercise echocardiography varies in different laboratories depending on local standards of practice, hospital regulations, and level of billing. In most cases, at least two people are required to carry out exercise echocardiography: a technician-sonographer to perform the imaging and a second technician to monitor the patient's hemodynamic, electrocardiographic, and symptomatic responses to exercise. Regardless of the type of exercise used (i.e., treadmill or bicycle), a sonographer records baseline images at rest, followed by images during or immediately after peak exercise, while a monitoring technician notes and records the hemodynamic and electrocardiographic responses to exercise. At the completion of exercise, the monitoring technician assists the patient in quickly stepping off the treadmill or upright bicycle and reassuming the left lateral decubitus position for postexercise and recovery images, which take place on an imaging table or bed. Alternatively, a nurse or a physician may monitor and assist the patient. One advantage to physician monitoring is that it allows for immediate image interpretation of poststress images. Some laboratories use registered nurses trained as sonographers for both imaging and monitoring functions, eliminating the need for two staff members. Depending on local standards of practice, some hospital laboratories require physician presence in all cases, either in the stress

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echocardiography room itself, or within the immediate area. In our hospital's echocardiography laboratory, all pharmacologic stress tests and high-risk patients referred for exercise tests are supervised directly by a physician. Outpatient clinic echocardiographic laboratories are growing in number. The equipment is the same as for hospital laboratories, but often one technician performs both monitoring and imaging functions, with a physician available within a few steps of the laboratory. The need for frequent hemodynamic monitoring will be facilitated by the use of an automated blood pressure cuff. Obviously, it is best not to perform exercise echocardiography on high-risk patients in this setting. The safety of exercise echocardiography is comparable to the safety of other stress testing modalities. A reported mortality rate of 1 in 10,000 patients with adverse events ranging from 4 to 9 in 10,000 are reported for stress electrocardiography, echocardiography, and nuclear scintigraphy.[45] [46] [47] [48] As with any form of stress testing, a crash cart should be kept within the vicinity of the testing area. Outpatients referred to hospital laboratories may not be well known to the staff performing the test, and for safety reasons, heart rate–lowering medications such as beta blockers and calcium channel blockers are sometimes continued. A question occasionally arises about whether to stop a patient's beta blocker prior to testing, since rapid decay of heart rate response after discontinuing exercise is largely responsible for loss of wall motion information. This may create the problem of achieving a submaximal test because of inadequate heart rate response. One potential solution in clinically stable patients is to decrease their beta blocker dose on the evening prior to testing to one-half dose, and to hold beta blockers on the morning of the test. This simple protocol often allows patients to minimize the antichronotropic effects of beta blockade while still retaining some measure of safety with a weaning protocol. Analysis of poststress images has been greatly facilitated by online digitization of images, which allows side-by-side comparison of views.[6] [49] [50] Prior to the development of digital images, the feasibility was lower— around 70%—for successful imaging in an unselected population owing to motion and respiratory artifact. With the advent of digital techniques, feasibility has risen to well over 90% in experienced laboratories. Frame grabbers for digital display allow selection of the optimal images out of multiple cardiac cycles, after all images are obtained. Thus, the technician

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is able to select images without lung interference after all imaging is completed. Asking the patient to perform a breathing maneuver for 2 to 5 seconds during acquisition is another technique that facilitates obtaining high-quality images devoid of respiratory artifact. This maneuver, which works best when practiced during baseline imaging, involves asking the patient to exhale completely or "take in a half breath" and hold his or her breath for a few seconds during the postexercise images. Following optimal image selection, which may be performed by the physician or an experienced sonographer, images are then displayed in side-by-side format with prestress and poststress images adjacent to each other for comparison, generally in right-to-left fashion (Fig. 13-3) . Side-by-side comparison of segments in a gated format facilitates recognition of more subtle abnormalities, raising diagnostic accuracy. Most digitization systems acquire loops of eight frames for each view, with 50 msec allowed for each frame. This time period allows for systolic frames, with a limited portion of diastole, to be captured by triggering image acquisition at the beginning of the R wave of the electrocardiogram. Eight frames are then displayed in a continuous loop format for playback. Imaging acquisition time should be of sufficient duration to digitize all four views but must be performed quickly enough to visualize transient wall motion abnormalities, lest important information be lost as ischemia quickly resolves. Approximately 10 to 20 seconds are needed for digital capture of each view. Ideally, all four views can be digitally captured in approximately 1 minute. In our laboratory, postexercise apical views are captured first to facilitate recording wall motion in distal coronary territories, which are most likely to display ischemic abnormalities. A videotaped recording is made for back-up, and review of these images is recommended to ensure that the captured images are representative of the videotape. Treadmill Exercise Echocardiographic Protocol The most popular form of stress used in exercise echocardiographic testing in the United States is treadmill 280

Figure 13-3 Quad-screen format depicting parasternal long-axis and shortaxis views. Diastolic frames (DIAS) and systolic frames (SYS) at baseline (PRE) and immediately after treadmill exercise (POST) are shown. The

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ventricular response is normal after exercise, with increased endocardial excursion and increased wall thickening in all visualized segments.

exercise, partly because of the familiarity of walking as a form of exercise and partly because of improved image quality over that of bicycle protocols. Analysis of images depends on the direct comparison of preexercise and postexercise images. Parasternal long-axis, short-axis, fourchamber, and two-chamber images are obtained at rest both on videotape and, as noted previously, on an eight-cell cine loop for display in a side-byside quad-screen format at 50 msec per frame. In our laboratory, a complete baseline study with Doppler examination is usually performed simultaneously. The patient is then asked to step onto the treadmill and to begin exercise on one of various standard protocols available. The Bruce protocol is the most commonly used protocol, but the modified Bruce or the Cornell protocol are options for patients who are not in optimal cardiovascular condition or who require a longer warm-up period. Once baseline images are obtained, treadmill exercise proceeds in usual fashion, limited by symptoms, significant electrocardiographic changes, or a predetermined maximal exercise capacity. After cessation of exercise, the patient steps off the treadmill and reassumes the left lateral decubitus position for 281

Figure 13-4 Wall motion score index incorporating a 16-segment model using the scoring system depicted at the top. Numbers 5 and 7 are arbitrarily assigned a score of 4 (indicating dyskinesis), whereas 6 (akinesis with scar) defaults to 3 (akinesis) for the purposes of calculating the wall motion score index. The report shows scores for pre-exercise and postexercise wall motion and demonstrates apical akinesis after treadmill exercise. The global wall motion score index is normal before exercise (1.0) and worsens (1.3) after exercise.

posttreadmill imaging within seconds. This requires a degree of patient agility, as well as considerable operator skill. As noted, because time delays may allow the decay of heart rate, and induced wall motion abnormalities may normalize quickly after exercise, any undue delays during the critical period between cessation of exercise and start of imaging may have the effect of lowering the overall accuracy of the test, particularly in areas of collateral flow, single-vessel disease, and moderately stenotic (50–70%) lesions.[51] Conversely, at higher workloads, greater degrees of ischemia

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occasionally ensue, and prolonged myocardial stunning may take place, with wall motion abnormalities persisting for several minutes after exercise.[1] [52] [53] [54] Because of the technical difficulties involved in the acquisition of images within a limited time frame, a learning curve exists for the experienced technician-sonographer of about 50 stress echocardiographic studies. This learning curve is clearly required prior to smooth performance and acquisition of images within the required 90second time period. Bicycle Exercise Echocardiographic Protocol Two bicycle protocols are currently in use: upright and supine. Although these are more widely used in Europe in conjunction with echocardiography, both have enjoyed an increase in popularity in the United States. In each of the bicycle protocols, imaging is performed at baseline, at peak exercise, and immediately after exercise. The upright bicycle protocol is shown in Table 13-2 . In the upright bicycle protocol, two-dimensional baseline images are recorded at rest in the parasternal long- and short-axis and apical four-chamber and two-chamber views in the left lateral decubitus position. The patient moves onto the upright bicycle, and the apical views are repeated at rest in the upright position. Using the same view facilitates comparison between rest and peak images. Exercise then begins with the patient pedaling, sometimes following a brief warm-up period, and proceeds in increments of 25 to 50 watts in 2- or 3minute stages. As the patient exercises, apical views can be recorded on tape throughout the examination. End points for bicycle exercise are the same as for treadmill imaging: predetermined age-related peak heart rate, the development of significant symptoms, or significant electrocardiographic changes. Just prior to stopping at peak exercise, the apical four-chamber and two-chamber views are recorded, and the patient resumes the left lateral decubitus position on an examining bed or table for immediate postexercise parasternal views, as well as repeat apical views. Digital TABLE 13-2 -- Upright Bicycle Protocol 1. Complete baseline study performed in left lateral decubitus position 2. Parasternal long-axis, short-axis, four-chamber, and two-chamber views recorded on tape and digitized 3. Patient assumes upright position on bicycle for apical rest views 4. Pedaling begins at 60 rpm, 25 watts, and increases by 25 watts every 2

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to 3 minutes 5. Peak exercise views obtained at the end of each stage 6. At completion of exercise, patient reassumes left lateral decubitus position for immediate postexercise and recovery images

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images are captured at the end of each stage, with each subsequent stage overriding the previous peak image. In this way, if a patient suddenly stops exercising early in any stage, the last image captured will be the peak exercise image. The exercise protocol itself may vary. One popular protocol is to have the patient begin pedaling at 60 rpm at 25 watts and to increase the resistance by 25 watts every 2 minutes while the patient continues to pedal at 60 rpm. Maximal exercise is then terminated at 250 watts or at 85% of the predicted maximal heart rate. Because many patients undergoing testing are older, their ability to pedal is highly variable, and tremendous latitude may be necessary in selecting workloads. Smaller increases in resistance are usually necessary in elderly individuals and patients unaccustomed to bicycle exercise. Also, variations in the imaging protocol are sometimes needed because of technical difficulty in obtaining apical views during exercise. One alternative to apical imaging is subcostal views.[44] This approach eliminates superimposition of the air-filled lung and may be more feasible for patients with chest wall deformities or chronic obstructive lung disease. Compared with the upright bicycle, supine bicycle exercise has a simpler protocol in that all imaging takes place with the patient on the bicycle, eliminating the need for an additional imaging table or bed for parasternal views. After acquisition of all four baseline views (parasternal long-axis, parasternal short-axis, four-chamber, and two-chamber) as described earlier, the patient begins pedaling in the supine position while apical views are obtained at each stage and recorded on videotape during exercise in similar fashion to the upright bicycle. At peak exercise, the images are digitized for viewing in quad-screen side-by-side format as previously described. In our laboratory, the four quadrants consist of pre-exercise images on the left and peak exercise images on the right, a display similar to that used in posttreadmill exercise. In addition, recovery images are

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recorded on videotape after the heart rate and blood pressure have returned to pre-exercise levels. Comparison of Stress Modalities As mentioned earlier, all forms of exercise have their relative advantages and disadvantages, and selection of stress modality should be based on individual patient characteristics, the patient's ability to exercise, and the information one wishes to obtain (Table 13-3) . With treadmill exercise, imaging at peak stress is technically difficult and, although a few reports have explored the feasibility of peak treadmill imaging, posttreadmill imaging TABLE 13-3 -- Comparison of Peak Bicycle and Posttreadmill Imaging Peak Bicycle Imaging Improved sensitivity Slightly decreased specificity Lower cardiovascular workloads More leg fatigue

Posttreadmill Imaging Less cumbersome protocol Improved image quality Higher cardiovascular workloads More familiar, better tolerated by most patients

remains the most widely applied technique. Advantages of treadmill exercise include patient familiarity as well as a lack of need for additional equipment, since most laboratories and hospitals are already equipped with a treadmill for routine exercise testing. In many cases, a digital frame grabber to digitize images at baseline and at peak exercise for side-by-side comparison is the only additional equipment required. One of the main disadvantages of the treadmill is that it relies on capture of images in "allor-none" fashion after exercise, providing a post-stress "snapshot" of the heart. Unlike with bicycle stress, which provides multiple views of the heart at various intermediate stages of stress, the exact stage of onset of ischemia cannot be detected with treadmill protocols. An advantage of bicycle exercise, therefore, is the ability to image at various levels of stress, allowing the time to onset of ischemia to be recorded and compared between serial studies, possibly providing additional prognostic information. Peak images, rather than posttreadmill images, also have the theoretical advantage of higher sensitivity, since wall motion abnormalities may revert to normal within seconds after exercise.[52] This advantage of bicycle exercise over treadmill exercise may be offset,

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however, by the fact that in the United States patients are usually more accepting of treadmill exercise and less limited by leg fatigue, since walking is a familiar activity. Exercising in the supine position requires that the weight of the legs be supported against gravity and may lead to earlier stopping because of leg discomfort and fatigue. In addition, supine exercise may lead to submaximal heart rate response and lower cardiovascular workloads, with the development of angina at a lower pressure rate product. [55] [56] Thus, maximal workloads attained in the supine position may actually be lower than those obtained in the upright position on the bicycle or the treadmill. Upright bicycle exercise theoretically produces higher workloads at equivalent levels of blood pressure and heart rate but provides a more cumbersome protocol. The major potential advantage of imaging performed at peak exercise rather than postexercise is that transient ischemia and its ensuing wall motion abnormalities may resolve quickly and be missed with posttreadmill testing, leading to a lower sensitivity for the detection of coronary artery disease. As noted, however, the higher workload achieved with treadmill exercise may offset the potential benefit of imaging during peak exercise. One study has directly compared the sensitivity and specificity of peak versus postexercise imaging using the same exercise modality in the same patients. Presti et al[52] used upright bicycle echocardiography to evaluate 104 consecutive patients referred for known or suspected coronary disease. Of these, 96 patients had echocardiograms suitable for wall motion analysis at rest, during peak bicycle exercise, and immediately after bicycle exercise (feasibility, 92%). The overall sensitivity of postexercise imaging for the detection of coronary disease was 70%, compared with 100% for peak exercise images. When the parasternal views were added, three additional patients demonstrated postexercise abnormalities. When the coronary anatomy of patients with false-negative studies was examined, it was found that the development of wall motion abnormalities 283

at only peak exercise was more likely to occur in patients with stenotic areas supplied by collateral flow. There have been few direct comparisons of different types of exercise in conjunction with echocardiography in the same patient population. Three studies have compared treadmill testing and bicycle exercise testing in conjunction with echocardiography. The earliest of these, by Applegate et

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al,[57] evaluated 21 patients after myocardial infarction using low-level, symptom-limited stress testing, with similar workloads achieved in each form of exercise. This study suggested that the delay in posttreadmill imaging did not significantly affect the sensitivity for detection of exerciseinduced ischemia in this postmyocardial infarction population. Two studies have compared posttreadmill with peak supine bicycle exercise in a stable population with coronary disease.[58] [59] One of these studies noted an advantage for peak stress bicycle imaging in the identification of coronary disease. Dagianti et al,[58] examining a small series of 10 male patients with coronary disease, noted 100% sensitivity for supine bicycle with only 60% for posttreadmill imaging. In a larger series of 74 patients, Badruddin et al [59] noted a sensitivity of 83% and specificity of 70% for supine bicycle and 75% and 90% for treadmill echocardiography, a difference that did not reach statistical significance. Taken together, these data may indicate a relatively small advantage in the detection of ischemia for selected patients who are able to perform bicycle exercise, particularly patients with singlevessel disease or collateral flow. Interpretation of Stress Echocardiograms Echocardiograms can be interpreted qualitatively, with a descriptive summary of the myocardial response to exercise, or quantitatively, providing a numeric description of wall motion (see Fig. 13-4) . For clinical purposes, a descriptive summary of wall motion response often provides enough information to aid the referring clinician in patient management. Regardless of the chosen scheme, a normal echocardiogram is one in which there is normal resting wall motion and a hyperdynamic response to exercise with symmetric wall thickening and equal excursion in all segments. The development of a wall motion abnormality either at peak exercise or immediately after exercise is sensitive and specific for ischemia and is evidence of underlying coronary disease. Using a qualitative approach, wall motion is often described as "normal," "ischemic," or "fixed," depending on the response to exercise (Table 13-4) . Ischemic segments are labeled as such if they appear normal or mildly hypokinetic at rest and worsen with exercise, whereas fixed areas are akinetic at rest and are unchanged or become dyskinetic with exercise, implying scarred myocardium due to transmural infarction. In most studies, new wall motion abnormalities may be detected when a coronary stenosis of greater than 50% exists, with increased likelihood for detection with stenoses of greater than 70%. Accordingly, using a visual estimate of 50%

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as a cut-off point would result in a lower sensitivity for detection of coronary disease than using 70%. Hypokinetic TABLE 13-4 -- Categorization of Exercise Echocardiographic Wall Motion Responses Wall Motion at Rest Normal Normal Abnormal excursion (thinned) Abnormal excursion (preserved thickness)

Wall Motion During Exercise Normal Abnormal: Worsening Fixed: No significant change New or worsening abnormality

Category Normal Ischemic Scar: Transmural infarction Hibernating

areas with full-thickness myocardium that worsen after exercise are likely to represent areas that are both viable and ischemic, the resting abnormality representing stunned or hibernating myocardium. Using qualitative terms such as these, one generally reports a description of wall motion and a diagnosis such as "inferior hypokinesis following exercise, consistent with inferior ischemia." Occasionally, lack of hyperdynamic response or frank hypokinesis will be noted in myocardium that is not supplied by a significant stenosis. This situation has been noted in aortic valve disease, in extreme elevations in blood pressure, and, in our experience, occasionally with occult myopathy. The most widely accepted quantitative approach is the wall motion score index recommended by the American Society of Echocardiography, which uses a scoring system from 1 to 4 depending on the degree of abnormality. [60] A grade of 1 is assigned to normal segments and 2 through 4 for hypokinetic, akinetic, or dyskinetic segments, respectively. Some laboratories also grade the lack of development of a hyperdynamic response as abnormal, assigning a grade of 0 to hyperkinetic regions. Grading lack of hyperdynamic response as abnormal results in higher sensitivity for the detection of coronary disease but may result in poorer specificity.[61] Using this wall motion scoring system, one then assigns a number to each of 16 segments and divides by the total number of segments for the calculation of a global wall motion score index (Fig. 13-5) . Alternatively, individual coronary territories can be assigned a "regional" wall motion score index. Either a global score or a regional score can then be used to assess responses to specific medical therapy or to cardiac

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interventions over time. With use of a regional wall motion score index, it is possible to predict the specific location of a coronary artery stenosis from the area of the wall motion abnormality and thus to provide important prognostic information regarding the nature of the underlying disease. A schematic representation of coronary blood supply in each segment using a 16-segment model is shown in Figure 13-5 . With this scheme, accurate distinction of anterior from posterior circulation is possible. Within the posterior circulation, separating left circumflex from right coronary artery territory is much more difficult because of individual variation in anatomy. In most situations, however, important diagnostic information is provided simply by separating the left anterior descending territory from the posterior circulation. Obviously, segments with normal resting ventricular 284

Figure 13-5 Diagram depicting how coronary artery territory is incorporated into the 16-segment model. Although some overlap is commonly seen, separation of anterior from posterior circulation is 80% to 90% accurate. Individual variation in coronary anatomy usually precludes accurate separation of right coronary from left circumflex territories. (Modified from Segar DS, Brown SE, Sawada SG, et al: J Am Coll Cardiol 1992;19:1199, with permission from the American College of Cardiology.)

function that augment during exercise indicate a patent coronary blood supply. Figure 13-3 depicts a normal hyperdynamic ventricular response after exercise, implying normal coronary arteries. As noted, normal resting ventricular function in a segment or segments that worsen during exercise indicates the presence of significant underlying coronary disease and ischemia. Figure 13-6 depicts an ischemic response following treadmill exercise. In this case, a 52-year-old woman with new-onset exertional discomfort demonstrated normal resting systolic function. After 6 minutes of exercise, a wall motion abnormality developed in the anterior septum, signifying left anterior descending artery ischemia (as seen in the postexercise systolic image). This patient was found to have a 75% stenosis of the left anterior descending artery. Abnormal resting ventricular function that worsens during or after exercise is sometimes a confusing picture and may represent one of a number of

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potential clinical possibilities. Areas of full-thickness myocardium that are hypokinetic at rest may represent areas of chronic repetitive stunning, chronically ischemic (hibernating) myocardium, or previous nontransmural myocardial infarction supplied by a critically stenosed artery. Regardless of the cause of resting hypokinesis, worsening after exercise is likely to represent an ischemic response. Segments that are bright, thin, and akinetic at rest and become dyskinetic after exercise are more likely to represent transmural infarction without significant ischemia. The patient depicted in Figure 13-7 is a 54-year-old man with chest discomfort who was able to exercise for 8 minutes on a Bruce protocol. The wall motion is normal at rest. Following treadmill exercise, an abnormality developed in the basal inferior segments (seen in the lower right-hand frame), and at catheterization the patient was found to have an 80% stenosis of the right coronary artery. One sees a break point in the myocardium (arrow) at the junction of the right coronary and left anterior descending artery territories, signifying left anterior descending artery patency juxtaposed against a stenosed right coronary artery. The patient in Figure 13-8 demonstrates abnormalities in the same myocardial segments of the basal inferior wall; however, in this case the myocardium is thinned and aneurysmal at rest, consistent with prior transmural infarction of the interior wall. Worsening 285

Figure 13-6 Exercise echocardiogram demonstrating anterior ischemia with dyskinesis of the anterior septum in parasternal long-axis view after exercise. The response suggests hemodynamically significant disease in the left anterior descending artery. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic.

in this case from akinesis to dyskinesis represents a fixed abnormality consistent with scar rather than ischemia. At catheterization, a total occlusion of the right coronary artery was found. As noted, myocardium that is hypokinetic at rest may represent stunning, hibernating, or a mixture of normal and infarcted myocardium. Accurately sorting out and interpreting the responses to exercise in these complex cases often requires integration of angiographic data derived from cardiac catheterization as well as the clinical

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Figure 13-7 Exercise echocardiogram demonstrating inferior ischemia. Diastolic (DIAS) and systolic (SYS) frames at baseline (PRE) and after exercise (POST) demonstrate normal resting wall motion with outward systolic motion (dyskinesis) of basal inferior segments after exercise. This patient had a critical stenosis of the right coronary artery. (See text for further explanation.)

history. Some of these complex responses and the possible relationship to the underlying clinical significance are shown in Table 13-5 . Advantages and Disadvantages of Exercise Echocardiography When compared with routine treadmill exercise, there are a number of advantages to performing exercise echocardiography, 286

Figure 13-8 Exercise echocardiogram demonstrating prior inferior wall myocardial infarction due to right coronary artery occlusion. The basal inferior segments are echogenic and akinetic at rest, suggesting scar. After exercise, the scarred region becomes dyskinetic, indicating "fixed" disease. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic.

as shown in Table 13-6 . Although routine treadmill testing remains the most prominent form of diagnostic testing for patients with known or suspected coronary disease in the United States, its sensitivity and specificity are limited in many patients in whom the ST segment response is unreliable or uninterpretable.[62] [63] [64] [65] Patients who have a high likelihood of false-positive, false-negative, or nondiagnostic electrocardiographic responses demonstrate improved accuracy for the detection of coronary TABLE 13-5 -- Clinical Interpretation of Complex Responses * Interpretation Normal Excursion Wall thickness CAD/No MI Excursion

At Rest

After Exercise

Normal Normal

Hyperdynamic

Normal

Hypokinetic, akinetic, or dyskinetic

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Wall thickness Normal CAD/Nontransmural MI Excursion Hypokinetic or akinetic

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Augmented, hypokinetic, akinetic, or dyskinetic (dependent on infarct artery patency)

Wall thickness Partial or full CAD/Transmural MI Excursion Akinetic Akinetic or dyskinetic Wall thickness Thinned CAD/Hibernating/Stunned Excursion Hypokinetic or Incompletely investigated May akinetic augment with mild exercise Wall thickness Partial or full CAD, coronary artery disease; MI, myocardial infarction. * Response depends on extent of residual stenosis.

disease with the addition of echocardiography.[6] These include women; patients with left bundle branch block; patients taking digoxin; patients with prior nontransmural myocardial infarction, Wolff-Parkinson-White syndrome, or mitral valve prolapse; patients with hyperventilation ST segment changes; and a large group of patients with nonspecific ST-T wave changes at rest. Echocardiographic imaging in conjunction with exercise stress testing has been shown to increase the diagnostic accuracy in patients such as these with resting electrocardiographic abnormalities, which some experts believe make up as much as 30% to 40% of patients presenting for exercise testing. A major advantage of exercise echocardiography is its versatility in the diagnosis of structural heart disease not related to coronary disease. Echocardiography has the ability to diagnose any and all forms of structural heart disease as a cause of angina or other cardiac symptoms. Thus, if exertional symptoms are due to valvular heart disease, pulmonary hypertension, diastolic dysfunction, or pericardial disease, the diagnosis can be made with exercise echocardiography. Figure 13-9 provides an example in which shortness of breath was suspected to be an anginal equivalent in a

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patient with multiple risk factors TABLE 13-6 -- Relative Advantages and Disadvantages of Stress Echocardiography Advantages Versatile (evaluates all structural abnormalities) Portable

Disadvantages Analyzed qualitatively Requires additional trained personnel Requires additional equipment Adds time to routine treadmill test

Minimal space requirements Increases sensitivity and specificity Evaluates wall thickening Low risk

287

Figure 13-9 Parasternal long-axis and short-axis views depicting a normal hyperdynamic response to exercise in a patient with severe left ventricular hypertrophy and resting repolarization changes on electrocardiogram. Systolic frames (SYS) are compared before (PRE) and after (POST) treadmill exercise. DIAS, diastolic.

for coronary disease. In this case, a patient with chronic renal disease, hypertension, and obvious left ventricular hypertrophy demonstrated baseline secondary ST segment changes and a positive electrocardiographic response to exercise, while the echocardiographic response clearly demonstrates a normal hyperdynamic response, with increased endocardial excursion and symmetric wall thickening in all segments. In some cases, the baseline study may provide clues to diagnosis and reveal a contraindication to stress testing, such as the finding of critical aortic stenosis or significant pericardial effusion. In our laboratory, a previously unsuspected but important cardiac diagnosis occasionally emerges from the resting echocardiographic study and engenders a reason to cancel the stress test. In this respect, exercise echocardiography provides a measure of safety unattainable by routine electrocardiographic monitoring or radionuclide imaging. Another advantage is that echocardiographic equipment can be transported to any area equipped with a treadmill or stationary bicycle, such

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as the hospital emergency department. Echocardiography is also the only bedside imaging technique that evaluates systolic wall thickening. There are some potential disadvantages to the addition of echocardiography to routine treadmill testing. First, it requires additional personnel and training. In most laboratories this requires two technicians, but one experienced technician may perform both the imaging and monitoring tasks, provided there is a physician in the immediate area (see Equipment, Methodology, and Personnel and also Fig. 13-2) . Another potential disadvantage to exercise echocardiography is the need for additional equipment, which in some cases is only a device for frame-grabbing digital images, since many outpatient clinics and hospitals are already equipped with echocardiographic instrumentation and a treadmill. Echocardiographic imaging also adds approximately 30 minutes to the time of the routine treadmill test. Also, although the results are reproducible, to date no highly quantifiable methods exist to evaluate wall motion or systolic thickening in the clinical setting.[64] Until an easily quantifiable system for wall motion evaluation exists, interpretation of stress echocardiograms remains largely qualitative. Given the overall accuracy reported, this has not proved a major disadvantage. Obviously, these potential disadvantages are a trade-off for increased diagnostic accuracy compared with treadmill testing. It is important to remember, however, that as with any form of imaging in conjunction with exercise testing, the sensitivity of stress echocardiography will be poor in patients who cannot reach an adequate level of cardiovascular stress. For those patients, pharmacologic stress echocardiography is a desirable alternative (see Chapter 14) . Patients who should undergo pharmacologic stress because of high rates of false-negative results due to inadequate exercise levels include patients with peripheral vascular disease, patients with orthopedic problems, elderly persons, and individuals who are deconditioned. For these and other unselected patient populations, the reported accuracy of dobutamine echocardiography for the diagnosis of known or suspected coronary disease has been excellent, around 85% to 95%. This is well within the range of competing nuclear imaging techniques.[7] [8]

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Clinical Applications of Exercise Echocardiography Accuracy in the Identification of Coronary Artery Disease Several studies have been published reflecting the overall accuracy of exercise echocardiography in the diagnosis 288

of coronary artery disease.[44] [51] [52] [55] , [61] [66] [67] [68] [69] [70] [71] [72] [73] [74] [75] [76] [77] [78] [79] In the first of these studies, published by Wann et al[1] [6] in 1979 at Indiana University, patients were studied with a 30-degree sector scanner during peak supine bicycle exercise. Despite primitive equipment, the overall sensitivity was 87% and the specificity was 100%, not unlike the sensitivities and specificities currently reported with state-of-the-art imaging equipment and digital acquisition techniques. The accuracy of various exercise stress echocardiographic techniques has been verified in numerous laboratories. Many early studies reported sensitivities in the range of 60% to 90%, whereas more recently, particularly with the advent of digital imaging methodologies, sensitivities have more consistently been in the higher end of this range. Table 13-7 compares the sensitivities and specificities of some of the larger reported studies. Many of the early studies focused on the ability of stress echocardiography to detect changes in global function, sometimes using radionuclide ventriculography as the gold standard.[69] [80] [81] [82] These studies demonstrated an increase in indices of global systolic function (such as ejection fraction or pressure/volume ratio) for normal subjects and depressed indices for patients with previous myocardial infarction. One of the first large studies demonstrating increased sensitivity and specificity with the addition of echocardiography to routine treadmill testing using arteriography as the gold standard was that of Armstrong et al,

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[6]

in which 95 patients underwent both posttreadmill exercise and cardiac catherization. Of the 59 patients in whom there was no evidence of prior infarction, 44 were found to have coronary disease at subsequent coronary arteriography. Exercise echocardiography was abnormal in 35 of these 44 patients, for an overall sensitivity of 80%. In contrast, the exercise electrocardiogram demonstrated ischemia in only 19 of these patients (sensitivity, 43%) and was normal in 13 patients (30%) and nondiagnostic in 12 patients (27%), demonstrating the ability of exercise echocardiography to identify coronary disease in patients with an ambiguous or inaccurate treadmill response. Conversely, exercise echocardiographic results were normal in 13 of 15 patients without coronary disease, for a specificity of 87%. In 36 patients with prior infarction, 35 had rest or exercise-induced wall motion abnormalities, or both, for a sensitivity of 97%. TABLE 13-7 -- Accuracy of Exercise Echocardiography

Study Limacher et al[69] Armstrong et al[6] Armstrong et al[32] Ryan et al

Patients, n Modality 73 Treadmill

Single Stenosis Vessel * Grade, Sensitivity, Disease, Sp % % % 50 91 64

95 Treadmill

50

88

—

123 Treadmill

50

88

81

64 Treadmill

50

78

76

[72]

Sawada et al[124] Crouse et al[61] Marwick et al[76] Hecht et al

57 Treadmill/upright bicycle 228 Treadmill

50

86

88

50

97

92

150 Treadmill

50

84

77

180 Supine bicycle

50

93

84

[50]

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Ryan et al

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309 Upright bicycle

50

91

86

150 Treadmill

50

91

—

80 Treadmill

50

89

76

[51]

Roger et al [67]

Marangelli et al[143]

* Definition of significant coronary artery disease.

Because the inclusion of patients with left ventricular wall motion abnormalities at rest falsely elevates the sensitivity of echocardiography for the detection of coronary disease (a fact that is also true for radionuclide imaging), a later study from the same laboratory examined the use of exercise echocardiography in 64 patients with normal wall motion at rest.[72] Twenty-four patients had no angiographic evidence of coronary artery disease, and all 24 had a negative exercise echocardiogram, for a specificity of 100%. Of 40 patients with coronary disease, 31 had a positive exercise echocardiogram (sensitivity, 78%). In a more current era, Marwick et al[76] reported an overall sensitivity of 84% and a specificity of 86% in 150 patients who underwent exercise echocardiography and coronary arteriography, with slightly higher sensitivity and slightly lower specificity when patients with nondiagnostic test results were excluded. Nondiagnostic test results stemming from an inability to reach a target heart rate in the setting of beta blocker use is a common problem in a clinical setting and appears to affect sensitivity more than specificity.[83] Sensitivities and specificities may vary between studies depending on the prevalence of disease in the population under study, the definition of significant disease, and the criteria used for a positive test. Clinical factors such as age, cardiac risk factors, and prior history of angina, all of which affect pretest likelihood of coronary disease, influence sensitivity and specificity, with sensitivities tending to be higher in populations with a higher pretest likelihood of disease. Sensitivity and specificity are also affected by the criteria used to define a positive test. Crouse et al[61] reported a high sensitivity of 97% and a relatively low specificity of 64% in a series of 228 patients undergoing treadmill echocardiography as a screening test. In this study, a normal test was defined as the presence of hypercontractility in addition to the absence of inducible wall motion abnormalities, adding to

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the sensitivity but detracting from the specificity of the results. Probably the biggest influence on specificity is that of posttest referral bias, which alludes to the fact that as a test becomes more accepted by the medical community, more patients with positive tests, and fewer of those with normal studies, are referred for coronary arteriography. Since only a small proportion of those with normal studies are given the opportunity to verify their test results, this 289

tends to lower specificity dramatically. Concomitantly, sensitivity is raised, since more patients with positive tests are referred for angiography. This point was illustrated in a study of 244 men and 96 women by Roger et al[80] that noted that bias in referral patterns for angiography may have a dramatic effect in lowering specificity. Accuracy of all types of stress testing is equally affected by biased referral for cardiac catherization or "verification bias," with lower sensitivities and higher specificities likely compared with those reported. To overcome posttest referral bias, in some studies a "normalcy" rate is calculated for subgroups thought to be at low risk for coronary artery disease within a population. This can then be used as a reasonable substitute for specificity. Thus, through clinical characteristics and demographic factors, subgroups likely to have a less than 5% pretest likelihood of significant coronary disease are identified, and these patients are then assumed to be free of significant coronary artery disease. The number of patients with a normal stress test within this group are identified. Normalcy is then calculated as the number of patients with a normal exercise test divided by the number of those at very low clinical risk for the disease. A few studies have reported normalcy rates when the catheterized population was skewed in the direction of patients with coronary disease. In a published series of 180 patients studied with supine bicycle and coronary arteriography, Hecht[50] reported an overall sensitivity of 93%, a specificity of 86%, and an overall accuracy of 92%. The normalcy rate for 42 patients who had a less than 5% pretest likelihood of significant coronary disease was 100%. Similarly, Marwick et al[36] have reported a normalcy rate of over 90% in 29 of 150 patients with normal results on an exercise echocardiogram and low pretest likelihood. Another influence on the accuracy of exercise echocardiography is the definition of significant disease, which is in part determined by the physiologic significance of a stenosis. This was illustrated in a study by

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Sheikh et al[33] who found that stenoses of greater than 75% diameter were more frequently associated with wall motion abnormalities during exercise echocardiography than stenoses of less than 25%. Stenoses in the range of 50% appeared to be evenly divided between positive and negative results when assessed by visual estimates of stenosis. Using quantitative angiographic methods, however, the authors were able to further stratify the ventricular responses into two subgroups. Those patients with wall motion abnormalities were associated with luminal stenoses of greater than 50%, whereas normal wall motion was associated with stenoses of less than 50%, suggesting that visual estimates may be unable to determine which stenoses in the moderate range are significant. This and other studies highlight the limitations inherent in using a diameter stenosis as visually determined to define significant disease.[73] [85] [86] Factors such as proximal location, presence of collateral flows, and plaque morphology have been shown to influence coronary flow, particularly in the setting of submaximal effort. Some recent studies have used intravascular ultrasonography rather than arteriography to define significant stenoses, and these studies further emphasize the limitations of "luminography" as a gold standard. An arteriogram being a two-dimensional representation of a three-dimensional artery may under- or overrepresent the degree of stenosis depending on the views selected. Factors such as bends or kinks in the vessel may cause some areas to falsely appear stenotic, whereas plaque irregularity may lead to underassessment of the functional significance of stenoses.[87] In clinical practice, functional assessment of a stenosis in relation to results of stress testing should always be undertaken along with integration of clinical factors with angiographic results. Currently, the overall accuracy of exercise echocardiography is in the range of 80% to 90%. A recent meta-analysis of 2637 patients reported in 24 articles noted an overall sensitivity of 85% and specificity of 77% for exercise echocardiography, examining only studies in a current era that reported results for all patients such that the calculation of sensitivity and specificity was possible with numbers of patients reported, along with coronary angiography used as the reference test.[88] Taken together, these studies illustrate the ability of exercise echocardiography to identify patients with angiographically significant disease and to provide an assessment of the physiologic significance of stenoses comparable to other stress imaging tests. Exercise Echocardiography After Angioplasty

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Because of its ability to target separate coronary artery distributions, exercise echocardiography may be an ideal tool for surveillance of patients after coronary interventions. Studies suggest that echocardiographic imaging can assess the initial outcome of angioplasty, atherectomy, and stenting, as well as provide valuable information regarding the presence of restenosis.[89] [90] [91] [92] [93] [94] [95] [96] [97] [98] [99] [100] One of the early studies demonstrating the ability of exercise echocardiography to provide a functional assessment in patients before and after angioplasty was that of Broderick et al[91] in which 36 patients were studied before and after coronary angioplasty. Thirty-one patients demonstrated ischemia with either an abnormal exercise test result (exercise-induced ST depression or angina) or an abnormal exercise echocardiogram (exercise-induced wall motion abnormalities). After successful angioplasty, 17 patients continued to demonstrate exerciseinduced ischemia by either electrocardiographic or echocardiographic criteria. Although 12 of these 17 patients continued to demonstrate exercise-induced wall motion abnormalities, most were improved compared with the studies prior to angioplasty. Exercise duration, workload, and METS (metabolic equivalents) increased after angioplasty, suggesting that some of the wall motion abnormalities after angioplasty might be explained by a greater ischemic burden. Since follow-up studies were performed 2 weeks or more after angioplasty and no patient had undergone repeat angiography, it is possible that some of these failures to demonstrate improvement represented early restenosis. A few other studies from high-volume laboratories have reported success in the use of exercise echocardiography to evaluate patients before and after angioplasty. Labovitz et al[94] noted new exercise-induced echocardiographic abnormalities in 12 of 17 patients prior to angioplasty and 290

in none of these patients after angioplasty. When 1 mm of ST segment depression was added to the criteria for ischemia, 16 of 17 patients demonstrated ischemia prior to angioplasty. Thus, using a combination of electrocardiographic and echocardiographic criteria increased the sensitivity for the detection of coronary artery disease from 71% to 94%. Both of these studies demonstrate improved accuracy with the addition of two-dimensional echocardiography to exercise testing in postprocedure

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assessment of the functional significance of coronary artery disease. In the study by Labovitz et al,[94] exercise ejection fraction also improved after angioplasty and was similar to that noted in age-matched normal control subjects. In our laboratory, if inducible wall motion abnormalities remain or recur after angioplasty at similar workloads as those noted prior to angioplasty, coronary arteriography is generally undertaken if the patient has symptoms or if a large coronary territory is in jeopardy. Figure 13-10 demonstrates the resting and posttreadmill systolic frames from a patient who had undergone angioplasty of the left anterior descending artery 3 months previously and who had developed atypical chest pain. Postexercise systolic images of the apical four-chamber view demonstrate an apical wall motion abnormality. At catheterization, the patient was found to have restenosis with a 90% luminal narrowing of the middle left anterior descending artery. Limited data have been published on the use of exercise echocardiography in the detection of restenosis, but these have been encouraging in suggesting a role for exercise echocardiography in the long-term follow-up of patients undergoing angioplasty. Hecht et al[93] used supine bicycle echocardiography to examine 80 patients an average of 6 months after angioplasty to determine whether this Figure 13-10 Systolic frames of apical four-chamber (A) and twochamber (B) views at rest (PRE) and after exercise (POST) demonstrating an apical abnormality in a patient with prior left anterior descending artery angioplasty. This patient was found to have restenosis at the site of previous percutaneous transluminal coronary angioplasty.

technique could detect restenosis. The overall sensitivity of supine bicycle exercise echocardiography was 87%, compared with 55% for electrocardiographic sensitivity. The specificity was 95% for exercise echocardiography, compared with 79% for exercise electrocardiography. Sensitivity was highest (91%) for the left anterior descending artery. The sensitivity of supine bicycle echocardiography for the detection of restenosis was surprisingly high, despite a low percentage of patients achieving 85% of predicted maximal heart rate, suggesting that the restenosis lesion was hemodynamically significant at a low cardiovascular workload. The fact that supine bicycle stress echocardiography utilizes peak exercise imaging may account for the higher sensitivities reported with this technique. In another study, Dagianti et al[101] demonstrated the

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usefulness of supine bicycle echocardiography shortly after balloon angioplasty to detect clinical restenosis at 6 months. Sixteen of 18 patients who subsequently went on to develop symptomatic restenosis documented angiographically had an early positive bicycle echocardiogram, suggesting that visual estimates may overestimate the early procedural success and that substrate for the restenosis lesion may begin early. Supine bicycle echocardiography was not successful in predicting asymptomatic angiographic restenosis, again pointing out that when performed in an asymptomatic population, percent diameter stenosis as determined by arteriography may not be an accurate reflection of the adequacy of flow. Chest pain is more closely linked to coronary flow reserve than is absolute stenosis diameter.[102] [103] Thus, patients who are asymptomatic despite angiographic evidence of restenosis may be better treated conservatively, particularly if they are able to engage in exercise without limitation. Few studies have compared radionuclide methods with 291

stress echocardiography for assessment of angioplasty results. One study compared single photon emission computed tomography (SPECT) thallium and exercise echocardiography before and after angioplasty. Fioretti et al[92] compared the results of exercise echocardiography with thallium-201 SPECT before and after angioplasty in 23 patients. Prior to angioplasty, the concordance rate between the two techniques was 78%. Nineteen patients were restudied with both techniques within 4 weeks after angioplasty. Echocardiography and SPECT were concordant in 17 of these 19 patients (89%), suggesting that exercise echocardiography is a feasible alternative to thallium-201 SPECT techniques for assessing patients who are undergoing angioplasty. These studies suggest that exercise echocardiography may have a role in serial assessment of patients undergoing coronary revascularization, both in the initial detection of functionally significant stenoses and in the assessment of the results of interventions. In contrast to these, an earlier study by Aboul-Enein et al[104] reported a sensitivity of only 67% using posttreadmill echocardiography to detect restenosis 6 months after successful coronary angioplasty. Looking at maximal predicted heart rate, pressure rate product, and exercise duration, the authors could find no significant differences between the 32 patients in whom exercise echocardiography correctly predicted restenosis and 16

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patients with false-negative results, suggesting a lack of functional significance of the angiographically determined stenosis. Differences in populations between this study and others with better sensitivity for restenosis detection may explain the lower sensitivity noted by these authors. Whereas the patients in the latter study underwent exercise echocardiography and coronary arteriography 6 months after angioplasty as part of a study protocol, regardless of symptoms, the patients in the study by Hecht et al,[93] for example, were evaluated because of recurrent chest pain, suggesting a higher pretest probability. Also, 38 of 48 (80%) of those found to have angiographic restenosis in the study by Aboul-Enein et al[104] had single-vessel disease, which is less likely to produce a positive test result. More recently, Mertes et al[95] examined the role of bicycle stress echocardiography utilizing peak exercise imaging in 86 patients approximately 6 months after nonsurgical revascularization, including angioplasty, stenting, and atherectomy. The overall sensitivity for peak bicycle stress echocardiography in the detection of significant coronary artery disease was 83%, and the specificity was 85%. This is compared with a sensitivity of 42% for stress electrocardiographic detection of significant coronary artery stenoses. In this study, stress echocardiography was also found to be useful for detecting progression of previously existing coronary stenoses that had not undergone revascularization. Interestingly, all patients with false-negative results in this study had failed to achieve the target heart rate at peak exercise. To circumvent the problem of suboptimal exercise, Hoffman et al [105] used transesophageal pacing echocardiography in the detection of restenosis in 60 patients approximately 5 months after successful angioplasty. The sensitivity of transesophageal pacing echocardiography for the detection of restenosis or progression of coronary disease in nondilated vessels was 84% and compared favorably with the 86% sensitivity for technetium-99m sestamibi-SPECT imaging. The sensitivity of electrocardiography in this study was 50%. Many centers have gone to the use of pharmacologic stress echocardiography after revascularization in patients who are unable to perform maximal exercise. Preliminary data suggest that dobutamine stress echocardiography is able to identify patients with significant coronary stenosis prior to angioplasty and to demonstrate improvement in wall motion abnormalities after successful angioplasty (see Chapter 14) .

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Exercise Echocardiography After Coronary Artery Bypass Grafting Although exercise echocardiography has become an accepted modality as a screening test in the initial evaluation of patients with suspected coronary artery disease, limited data exist regarding the use of exercise echocardiography to predict graft patency after coronary artery bypass grafting. Treadmill exercise testing has been the accepted modality for evaluation of patients after bypass surgery, but the high prevalence of resting electrocardiographic abnormalities in this group introduces a high rate of nondiagnostic electrocardiographic responses. For this reason, thallium SPECT imaging was recognized early on as a valuable adjunct in sorting out the nondiagnostic electrocardiographic responses in such patients.[106] It seems logical that if exercise echocardiography is able to accurately detect ischemic segments in territories deprived of blood supply via native vessels, segments supplied by stenotic grafts would be similarly detected. Although few in number, published studies using exercise echocardiography to detect graft patency have been extremely encouraging; these are summarized in Table 13-8 .[107] [108] [109] Sawada et al[107] used upright bicycle exercise echocardiography to assess bypass graft patency in 41 patients at a mean of 6 years after coronary artery bypass surgery. The presence of inducible ischemia was correlated with vessel stenoses, including obstructed bypass grafts, obstructed native vessels without prior revascularization, and diseased native vessels distal to anastomotic sites. In the 35 patients with graft stenosis, exercise echocardiography demonstrated ischemia in 33 patients, a sensitivity of 94%. Exercise echocardiography also correctly identified five of six patients without significant disease, with a specificity of 83%. Through the use of segmental wall motion analysis, accurate identification of the location of significant stenoses (i.e., anterior vs. posterior circulation) was possible. The sensitivity for detection of TABLE 13-8 -- Accuracy of Exercise Echocardiography After Coronary Artery Bypass Grafting (CABG) Study Sawada et al[107] Crouse et al[108] Kafka et al[109]

Patients, n 41 125 182

Years After CABG 6 7 3.6

Sensitivity, % 94 98 79

Specificity, % 83 92 82

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292

compromised arterial supply in the left anterior descending distribution was 89%, and in the posterior circulation it was 88%. Crouse et al[108] studied 125 patients a mean of 7 years after coronary artery bypass grafting and reported a sensitivity of 98% and a specificity of 92% for the detection of graft or native vessel stenoses of 50% or greater reduction in luminal diameter. More recently, Kafka et al[109] reported that exercise echocardiography was able to successfully detect both singlevessel disease and multivessel disease, with a sensitivity of 77% and 96%, respectively, in a population of 182 patients undergoing symptom-limited treadmill exercise, electrocardiography, and exercise echocardiography for routine follow-up. Patients in this study had undergone revascularization with coronary artery bypass grafting 3½ years previously. Despite a lower prevalence of disease in this series when compared to the series of Sawada et al[107] and Crouse et al, [108] the overall sensitivity and positive predictive value were high (85%) when compared with exercise electrocardiography, which had a positive predictive value of only 62%. The negative predictive value for the corresponding techniques was 81% and 52% for exercise electrocardiography and echocardiography, respectively. In summary, the results of exercise echocardiography compare favorably to results of studies using thallium SPECT in the detection of ischemia in the region of coronary artery bypass grafts. Echocardiography performed in conjunction with exercise electrocardiography has a high feasibility rate— greater than 90% in these reported series—and provides superior sensitivity and specificity than exercise electrocardiography alone. These studies illustrate the ability of exercise echocardiography to identify graft as well as native disease stenosis in a population in whom interpretation of electrocardiographic response is less than optimal. Exercise Echocardiography After Acute Myocardial Infarction Following successful reperfusion for acute myocardial infarction, accurate prognostic assessment is critical in directing expensive and limited invasive resources to those patients who will receive the greatest benefit. Two important determinants of prognosis are left ventricular systolic function and the severity of underlying coronary artery disease. Medical centers performing primary angioplasty may use the results of cardiac catheterization to provide risk assessment, but most clinicians have traditionally performed noninvasive testing to predict prognosis and guide

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future therapy. The practitioner has a choice of tests with which to accomplish this assessment. In the past, two tests have frequently been called upon to provide assessment of systolic function and ischemia: radionuclide ventriculography or echocardiography to determine systolic function and submaximal exercise testing for the assessment of ischemic burden. More recently, stress echocardiography has been used to provide data about both left ventricular function and the presence of residual ischemia to assess future risk of cardiac events. Future ischemic events appear to involve increasingly complex interactions between an ischemic milieu and inflammation, but stress echocardiography is a relatively inexpensive test that has been shown to correctly stratify patients into highand low-risk subgroups. Submaximal exercise testing can be safely performed after myocardial infarction and has been shown to provide useful prognostic information with regard to subsequent cardiac events.[110] [111] Treadmill testing, however, while able to identify some patients who are at high risk for subsequent cardiac events, has a sensitivity of only 50% to 70% for the prediction of subsequent coronary events.[112] [113] Thallium scintigraphy has been shown to improve the sensitivity for prediction of cardiac events after myocardial infarction.[114] More recently, two-dimensional echocardiography after low-level treadmill exercise has been shown to provide useful information for the purposes of risk stratification and prediction of subsequent cardiac events.[57] [115] [116] Most of the studies examining exercise echocardiography for postmyocardial infarction assessment were performed before the widespread use of reperfusion therapy and included as events the "soft" events of revascularization. Nonetheless, these studies demonstrate the ability of exercise echocardiography to identify a high-risk group, particularly when combined with clinical risk assessment. Jaarsma et al[115] studied a group of 43 patients with exercise echocardiography within 3 weeks of acute myocardial infarction. All patients were noted to have resting wall motion abnormalities. Images obtained immediately after exercise demonstrated new wall motion abnormalities, remote from the site of myocardial infarction, in 18 patients, 17 of whom were shown to have multivessel coronary artery disease. This is compared with only 5 of 25 patients without remote wall motion abnormality who were found at catheterization to have multivessel disease. The development of a new wall motion abnormality, remote from the site of myocardial infarction, predicted multivessel coronary disease with a

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sensitivity of 77% and a specificity of 95%. It also predicted a high-risk group for reinfarction or recurrent angina within 12 weeks, demonstrating the ability of exercise echocardiography to predict a higher risk group for cardiac events based on the identification of patients with multivessel disease. Transient remote ischemia during the first several hours of acute myocardial infarction has been attributed to a supply-demand imbalance in areas perfused by a critically stenosed vessel in noninfarcted segments of myocardium. Because remote ischemia signifies multivessel disease, these patients would presumably be at high risk for the development of subsequent events. Ryan et al[116] examined the predictive value of either remote or adjacent asynergy in 40 patients shortly after myocardial infarction using posttreadmill exercise echocardiography and found it to have an excellent predictive value for subsequent cardiac events. In a 6- to 10-month follow-up period, cardiac events occurred in 20 patients, 16 of whom had a positive exercise echocardiogram (80% sensitivity). A negative exercise echocardiogram was predictive of a good clinical outcome without subsequent cardiac events in 19 of 20 patients (specificity, 95%). In this group of postmyocardial infarction patients, treadmill characteristics were unable to identify high- and low-risk groups. Likewise, Applegate 293

et al[57] found that neither electrocardiographic nor clinical characteristics could identify a high-risk group in another study of 21 patients who underwent symptom-limited treadmill exercise shortly after acute myocardial infarction. In this study, multivariate logistic regression analysis was performed on several clinical, treadmill, and electrocardiographic characteristics. Wall motion abnormalities immediately after exercise and echocardiographically determined ejection fraction had the highest predictive value (P < .001) for the prediction of future cardiac events. In patients treated with thrombolysis, the ability to exclude significant multivessel disease may help to avoid cardiac catheterization and to direct expensive resources and higher risk technologies to those patients who are at higher risk for poor outcome. Quintana et al[117] examined exercise echocardiography within a week after myocardial infarction in 70 patients, about half of whom had received thrombolytic therapy. Exercise

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echocardiography correctly identified a high-risk group for cardiac events within 2 weeks after myocardial infarction. Twenty-two percent (6 of 27) of those with a positive exercise echocardiogram, versus only 5% (2 of 43) of those with negative studies, suffered an early cardiac event. At 4-year follow-up, the cumulative event-free survival rate was significantly better in patients with a negative exercise echocardiography. While the electrocardiographic response also identified patients in whom events were more likely to occur, exercise electrocardiography was unable to identify a low-risk group. These studies demonstrate the usefulness of twodimensional exercise echocardiography in helping to stratify patients into high- and low-risk groups after myocardial infarction and to predict a highrisk group for subsequent cardiac events on the basis of ischemia. An area of current active clinical investigation is the application of pharmacologic stress echocardiography to identify stunned and hibernating myocardium after myocardial infarction. The goal of these techniques is to determine potentially viable segments of myocardium that would be expected to recover function without revascularization after myocardial infarction, as opposed to those that are more likely to benefit from revascularization. Dobutamine echocardiography, discussed in Chapter 14 , has shown promise in the area of identification of stunned segments in the immediate post-infarction period and has been widely utilized for this purpose. Recruitment of myocardial segments with low-dose dobutamine shortly after acute myocardial infarction identifies segments that are likely to recover function without further intervention.[118] [119] Subsequent deterioration of some segments with higher doses of dobutamine (the socalled "biphasic" response) signify segments that may improve only after revascularization is performed. In theory, a low level of exercise could potentially be used to identify viable myocardium in analogous fashion to low levels of dobutamine infusion. A study by Hoffer et al[120] has investigated the utility of low-level bicycle exercise shortly after myocardial infarction to identify reversible dysfunction through augmentation of stunned segments. These authors noted improvement with low-level bicycle exercise in some akinetic segments within the infarction zone of patients with recent myocardial infarction, similar to the augmented response seen in viable segments with low-dose dobutamine infusion. Segments that improved with exercise were more likely to recover function at follow-up, signifying reversible dysfunction. Since multiple graded levels of exercise were not tested, it is unknown whether some segments that improve with low levels of exercise would demonstrate a biphasic response as well, with higher cardiac workloads. Whether

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echocardiographic monitoring during multiple graded levels of exercise could detect ischemic segments suitable for revascularization has not been investigated. Exercise Echocardiography in Women Despite the fact that cardiovascular disease is the number one killer of women in the United States, accounting for approximately 500,000 deaths annually, most studies involving noninvasive techniques to identify patients with coronary artery disease focused exclusively on men, until relatively recently. Because of a variety of social, economic, and medical beliefs, women were excluded from populations with coronary disease under study. Even in the current era, there are surprisingly few studies examining diagnostic and prognostic implications of noninvasive testing of women (Table 13-9) . One reason for the paucity of published data in the noninvasive assessment of coronary disease in women is the fact that stress testing is believed to be less accurate in women. Indeed, early studies of electrocardiographic stress testing in women usually displayed poorer sensitivity and specificity for the identification of significant coronary disease.[63] [121] [122] In retrospect, however, the majority of these studies were performed in women who, according to Bayesian theory, were of low pretest likelihood with lower disease prevalence than their male cohorts, a factor that adversely affects specificity. The low disease prevalence in populations under study contributed to the belief that women are less likely to suffer from coronary disease and less likely to need referral for invasive testing. As discussed previously, verification bias, or the tendency to avoid sending those with negative test results for cardiac catheterization, is also a major contributor to lower test specificity in women. Contributing to the lower sensitivity of stress testing in women is the fact that, in many early studies, women appear to have lower exercise capacity, achieving submaximal levels of cardiovascular stress more often, thereby rendering it less likely that ischemia would be provoked. In addition, hormonal and autonomic factors, inappropriate catecholamine release, syndrome X, and the presence of more comorbid diseases at the time TABLE 13-9 -- Studies Examining the Accuracy of Exercise Echocardiography in Women Study Sawada et al[124] Williams et al[125] Marwick et al[126]

Year 1989 1994 1995

Patients, n Sensitivity, % Specificity, % 57 86 86 70 88 84 161 80 81

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Roger et al[84]

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1997

96

79

37

294

of diagnosis, may further contribute to test inaccuracies in women. In an effort to increase the overall accuracy of stress testing in women, some practitioners have advocated the use of imaging techniques as an initial test. Recent studies have focused on the addition of echocardiographic imaging as a means to increase the accuracy of stress testing as an initial diagnostic test in women.[123] Recent studies have examined the echocardiographic responses to treadmill or bicycle exercise in women also undergoing diagnostic catheterization. [84] [124] [125] [126] Sawada et al[124] examined the diagnostic value of exercise echocardiography in 57 women with chest pain syndromes using coronary arteriography as the gold standard. Sensitivity and specificity for echocardiographic detection of coronary stenosis of 50% or greater were both 86%. Exercise echocardiography was particularly useful in sorting out patients with atypical chest pain with coronary disease (sensitivity, 84%) from those with a nondiagnostic exercise electrocardiogram who were free of coronary disease (specificity, 82%). Similarly, Williams et al[125] compared the accuracy of the exercise echocardiogram to the accuracy of 12-lead electrocardiography performed during maximal treadmill exercise in 70 women with a 53% pretest probability for coronary disease. Defining significant coronary disease as greater than 50% stenosis, exercise echocardiography had a sensitivity of 88% for the detection of coronary artery disease, compared with 57% for electrocardiographic analysis using ST depression of greater than 0.1 mV. The specificity of exercise echocardiography was 84%, compared with 51% for echocardiographic analysis. In both of these studies, the accuracy of exercise echocardiography significantly exceeded that of exercise electrocardiography and paralleled larger studies of predominantly male patients. [6] [51] , [61] [76] Marwick et al[126] investigated the use of exercise echocardiography in the detection of coronary disease in women and found it to have an overall accuracy of 81%, compared with overall accuracy of 64% for exercise electrocardiography. In addition, these authors examined the cost of exercise echocardiography and noted that it compared favorably with

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several potential diagnostic strategies in the work-up of cardiac symptoms in women. These authors sought to identify a diagnostic strategy that would balance the cost of diagnostic testing (defined as local Medicare reimbursement) with the lowest number of false-negative results and the fewest inappropriate referrals for cardiac catheterization. Compared with electrocardiography or echocardiography as an initial test (with and without Bayesian analysis) or angiography alone as the only diagnostic work-up, exercise echocardiography provided the best overall accuracy at the least cost. Data continue to accumulate that exercise echocardiography, because of preserved accuracy in patients with low to intermediate pretest likelihood of disease and because Medicare reimbursement rates are roughly half of those for radionuclide methods, may be the initial stress test of choice for women. The ultimate test of any noninvasive strategy may not be its ability to detect disease but its ability to predict future events. Recent studies have examined the ability of exercise echocardiography to predict prognosis in patients with known or suspected coronary artery disease.[127] [128] [129] Some of these studies focus on outcomes of women or include women as a major proportion of patients. One of the first of these studies was that of Sawada et al,[127] which encompassed 71 women among 148 patients who were followed for 28 ± 8 months after having a normal exercise echocardiogram. Cardiac events occurred in 2.8% (2 women) at 28 months without evidence of abnormality on exercise echocardiogram, demonstrating the ability of exercise echocardiography to identify a low-risk group for future events. Likewise, McCully et al[128] reported, in a large group of patients of whom about half were women, an excellent event-free survival rate for patients with normal treadmill echocardiograms who achieved an adequate level of cardiovascular stress (>5 METs for women). Another study examining prognosis in women reported that exercise-induced ischemia predicted cardiac events. In a multivariate analysis, Heupler et al[129] demonstrated incremental predictive value for exercise echocardiography in addition to clinical factors and exercise electrocardiography. Many of these studies have been performed in academic centers where referral of higher risk patients may falsely elevate the sensitivity of diagnostic testing and its ability to prognosticate. Exercise echocardiography has also been shown to correctly stratify women as to risk in a community setting. In a study of 1188 women with known or suspected coronary disease who underwent treadmill exercise echocardiography, the degree of ischemic wall motion abnormality was an

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important factor in identifying a very high risk group.[130] Patients with resting wall motion abnormalities in addition to exercise-induced ischemic abnormalities had the highest rate of cardiac death and myocardial infarction. These studies highlight the ability of echocardiography to risk-stratify patients into high-, intermediate-, and low-risk subsets based on echocardiographic response to exercise and to select patients who will most benefit from further invasive procedures. Further studies will need to be performed. Exercise Echocardiography in the Determination of Prognosis The acceptance of stress echocardiography as a diagnostic tool able to guide decision making for medical and interventional procedures has allowed for follow-up of patients with coronary disease. Published event rates for patients with myocardial infarction undergoing exercise echocardiography were discussed earlier and demonstrate a higher rate of cardiac events in patients with significant degrees of inducible ischemia after infarction. As with acute myocardial infarction, the major determinants of prognosis in chronic coronary artery disease are overall left ventricular function and the presence and severity of ischemia. Echocardiography, in its ability to evaluate both of these factors, makes an ideal tool for the determination of prognosis. Event rates for patients with chronic coronary disease with normal or abnormal test results have been examined with regard to "hard" cardiac events such as myocardial infarction and cardiac death as well as "soft" cardiac events such as revascularization. These findings demonstrate a more benign prognosis for patients with normal exercise echocardiograms, with higher event rates noted for those with inducible ischemia (Table 13-10) 295

TABLE 13-10 -- Exercise Echocardiography for Prognostic Assessment of Patients with Known or Suspected Coronary Artery Disease

Study Sawada et al[127]

Patients, n Follow-up, mos 148 28

Event Rates * Abnormal Normal SE SE — 1.7/.85 *

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Marwick et al[132] Krivokapich et al

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463 360

44 12

9/6.5 34/9

7/2 9/2

1325

23

—

2.5/<1

[131]

McCully et al[128]

* Percentage of events at 12 months, total/spontaneous. SE, stress echocardiography.

Two studies have noted low event rates of less than 1% per year in patients with normal resting function and no exercise-induced wall motion abnormality.[127] [128] Importantly, in both of these studies, a normal study finding is defined as one that is normal both at rest and with exercise. In some cases, higher event rates have been noted for patients with negative test results, and often these higher event rates were reported in studies that allowed patients with resting wall motion abnormalities to be included within the "negative" group. Krivokapich et al,[131] defining a negative test result as lack of ischemia with exercise, noted a higher event rate of 9% in patients with a negative exercise echocardiogram. In this study, soft events such as revascularization were also included as events, obviously having had an adverse affect on total event rate. When only myocardial infarction is examined, the event rate dropped to only 2%. Likewise, Marwick et al[132] noted in a group of 463 patients an event rate of 7% for patients with a negative exercise echocardiogram but when 15 of 20 patients with revascularization as the only event were excluded, the event rate was reduced to less than 2% per year for spontaneous events. These studies demonstrate that exercise echocardiography in patients undergoing stress testing for known or suspected coronary disease is able to effectively stratify patients as to future risk and to guide therapy for patients at higher risk. The presence of electrocardiographic ST depression appears to add prognostic information to the value of the echocardiographic response. For example, in the study of Marwick et al[132] , the rate of events including revascularization was highest in patients with both echocardiographic and electrocardiographic evidence of ischemia (event rate, 45%), with a lower event rate of 38% in patients without exercise-induced electrocardiographic changes. Likewise, Krivokapich et al[131] noted highest event rates for patients with both electrocardiographic and echocardiographic evidence of ischemia. In patients without echocardiographic evidence of ischemia,

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however, event rates were still higher in patients with a positive exercise electrocardiogram compared with a negative electrocardiogram. In both of these studies, although echocardiographic wall motion response appears to provide the greatest prognostic information, the electrocardiographic response appears to add prognostic value. Dobutamine echocardiography, discussed elsewhere, has provided the largest group of data for prognostication in patients referred for known or suspected coronary disease.[133] [134] In particular, dobutamine echocardiography appears to be able to accurately stratify risk in patients scheduled for vascular surgery, with published data encompassing more than 1500 patients.[135] Together, exercise and pharmacologic stress echocardiography is quickly gaining momentum as a test that can accurately and effectively stratify patient risk and guide therapeutic decisions. Cost-Effectiveness Issues The rising tide of health care costs, along with recent government budget cuts for reimbursement for many inpatient procedures, mandates that physicians be aware of the relative costs of procedures they order or perform on their patients. The cost of any procedure can be examined from a variety of viewpoints, including the cost to the patient—that is, insurance or Medicare reimbursement—the actual cost to the hospital or physician performing the test, and the cost of further diagnostic testing that the test result initiates. Cost-effectiveness examines cost versus healthcare outcome, usually expressed as a unit of effect on health care, such as survival or quality-assisted life-years. This is not meant to be a comprehensive discussion of cost analysis but a simple comparison of stress echocardiography with other testing strategies that provide similar information at similar risk to the patient. Several authors have addressed the issue of cost-effectiveness of stress testing as an initial strategy as compared with proceeding directly to invasive tests, and many of these assessments highlight the importance of determining pretest likelihood of disease prior to testing.[136] [137] [138] [139] If a high degree of likelihood exists that a patient has coronary disease, (greater than 75%), then the best initial strategy is likely to be proceeding directly to angiography, as suggested by Bayes' theorem. On the other hand, in case of very low pretest likelihood (i.e., less than 20%), perhaps no further testing is recommended. For patients with intermediate pretest likelihood of disease, the best initial strategy has been shown to be noninvasive testing

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followed by catheterization in patients with high likelihood of significant coronary disease based on results of noninvasive testing. In contrast, Shaw et al[136] examined the use of radionuclide imaging as an initial strategy in women and found that noninvasive testing was approximately $1000 less over a 2.5-year period as compared with proceeding directly to catheterization for patients with intermediate pretest likelihood of disease. Similarly, Marwick et al[126] examined multiple different strategies involving stress electrocardiography or echocardiography versus catheterization as an initial strategy, noting that exercise echocardiography led to the least number of false results, providing the greatest sensitivity and specificity for detection of coronary disease. False-positive test results were presumed 296

to lead to inappropriate angiography. Thus, although exercise electrocardiography was a less costly test from the standpoint of reimbursement, it was assumed to lead to a higher number of inappropriate catheterizations. Medicare fees and volumes for various stress testing techniques, which were published in 1996, compared professional and technical fees as well as relative value units (RVUs), which provide an estimate of relative cost.[140] Within the published guidelines of the American College of Cardiology and the American Heart Association for exercise testing, while treadmill testing alone was noted to be least costly (3.30 RVUs), performing this test in all cases would not necessarily result in lower cost of patient care, since test inaccuracies can be expected to lead to further unnecessary testing. Imaging adds considerably to the cost of reimbursement (5.3 times that of treadmill), as does echocardiography (2.3 times higher). However, as discussed previously, given the improved accuracy of exercise echocardiography, its relatively lower expense as an imaging modality when compared with radionuclide technology makes it an attractive alternative. In comparison with radionuclide techniques, echocardiography is likely to be reimbursed at roughly half the relative cost, based on Medicare reimbursement. In this light, few studies have examined nuclear techniques with echocardiography as a screening test. Garber et al[137] compared an initial strategy of arteriography with one of five noninvasive strategies, initially including echocardiography, nuclear techniques with SPECT, positron emission tomography, or treadmill electrocardiography. There were no significant differences in life expectancy based on the initial diagnostic test. The total cost of a strategy

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that used echocardiography was less than one that began with radionuclide based on a cost-effectiveness ratio. Because of improved sensitivity compared with treadmill testing, exercise echocardiography resulted in better outcome. Thus, echocardiography was a highly cost-effective alternative to treadmill or radionuclide imaging. Kuntz et al[138] examined the cost-effectiveness of noninvasive strategies with exercise treadmill electrocardiography, exercise echocardiography, or SPECT nuclear imaging versus arteriography in the initial diagnosis of coronary disease. These authors found that either exercise electrocardiography or exercise echocardiography resulted in "reasonable" cost-effectiveness ratios for patients with mild to moderate risk for coronary artery disease. Proceeding directly to arteriography was costeffective for patients with high pretest probability of coronary artery disease. Further studies of both cost and outcome will need to be performed in randomized fashion with longer term follow-up to determine whether exercise echocardiography will continue to assume a greater role in settings where HMO-driven decisions mandate the most information at the least cost.

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Exercise Echocardiography Compared with Other Imaging Modalities A number of studies have compared exercise echocardiography with the more well established radionuclide techniques for the diagnosis of coronary disease. An early study compared two-dimensional echocardiography with radionuclide angiography during left lateral decubitus bicycle ergometry.[44] This study noted a higher sensitivity, 91%, for radionuclide angiography versus 76% for exercise echocardiography using a bicycle protocol. The problem with this and many subsequent studies is that such comparisons take place in centers where one or the other of the techniques being compared is more widely utilized, and different levels of expertise exist for the competing technologies. An exception to this is the large study of 292 patients reported by Quinones et al[141] that analyzed all patients with both exercise echocardiography and SPECT thallium for the diagnosis of coronary disease. Sensitivity for single-vessel disease was quite low with both techniques (58% for echocardiography and 61% for thallium SPECT), and both techniques correctly identified three-vessel disease with a 94% sensitivity. Specificity was similar in both groups (88% for echocardiography and 81% for thallium SPECT). In a comparison of exercise echocardiography with technetium-99m MIBI-SPECT, Pozzoli et al[142] found a good correlation between perfusion and wall motion in 103 consecutive patients, with concordance in 84% of segments overall. Concordance was especially high (91%) in patients with previous myocardial infarction. These studies, while limited, demonstrate the ability of both techniques to detect patients with significant disease, providing similar clinical information about the functional significance of underlying coronary disease. The advantage of echocardiography lies in its ability to provide additional information about left ventricular function and underlying valvular disease without adding significantly to the time of the echocardiographic study. The accuracy of exercise echocardiography has also been compared to that

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of echocardiography with different forms of cardiovascular stress. Beleslin et al[40] compared exercise, dobutamine, and dipyridamole echocardiography in 136 consecutive patients with a high prevalence of coronary artery disease. The sensitivity of exercise echocardiography was 88%, compared with 82% for dobutamine echocardiography and 74% for dipyridamole echocardiography. Specificity for exercise, dobutamine, and dipyridamole echocardiography was 82%, 77%, and 94%, respectively. All three tests were noted to have acceptable diagnostic value, with a higher diagnostic accuracy for stress echocardiography in patients with singlevessel disease. Similarly, Marangelli et al[143] compared exercise, dipyridamole, and transesophageal atrial pacing in conjunction with echocardiography in 104 consecutive patients with normal resting wall motion who underwent coronary arteriography. The sensitivities for exercise, transesophageal atrial pacing, and dipyridamole were 89%, 83%, and 43%, respectively, suggesting that exercise and atrial pacing have similar sensitivities and may exceed the sensitivity of pharmacologic stress with vasodilators. In comparison with nonexercise forms of cardiovascular stress, the additional information gleaned from analysis of the hemodynamic response to exercise proves to be an invaluable adjunct in the clinical assessment of patients. If the patient is able to exercise, the additional clinical value gained in analyzing the physiologic exercise data adds 297

incrementally to the information learned from wall motion analysis alone.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Exercise echocardiography is an accurate technique for initial diagnosis of coronary disease and can provide prognostic information in many subgroups with known disease. Over the past decade, its acceptance by the medical community has grown and current applications have expanded to include diagnosis and prognosis in a wide range of patients, including women, for whom accuracy and cost appear better than other comparable techniques. Current clinical applications of exercise echocardiography include diagnosis of suspected coronary disease, guiding percutaneous intervention, surveillance of patients following coronary bypass surgery, and prediction of prognosis in chronic coronary disease as well as acute myocardial infarction. Accuracy of exercise echocardiography is now considered to be at parity with other noninvasive imaging techniques with a cost roughly half that of competing nuclear techniques. Its lower cost makes exercise echocardiography an attractive alternative as an initial diagnostic test and in follow-up of patients with coronary disease.

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301

Chapter 14 - Stress Echocardiography with Nonexercise Techniques Principles, Protocols, Interpretation, and Clinical Applications Thomas H. Marwick MD, PhD

302

TABLE 14-1 -- Indications for Nonexercise Stressors Unable to Exercise Inability to exercise maximally Diagnosis of coronary artery disease, decision making

Able to Exercise Specific indications Coronary spasm

Myocardial viability Risk stratification Developing indications Situations preventing exercise Onset of ischemia Angiography laboratory, operating room New technologies (TDI, CK, contrast) CK, color kinesis; TDI, tissue Doppler imaging.

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Background Indications for Nonexercise Stress Testing The performance of a maximal level of exercise is a critical determinant of the sensitivity of all stress modalities for the detection of coronary artery disease. Unfortunately, many patients—fully 30% to 40% at some tertiary centers (Fig. 14-1) (Figure Not Available) —either cannot exercise at all or cannot exercise maximally,[1] but these patients may still need to undergo stress testing for diagnostic, decision making, or prognostic purposes. The most common causes of limited exercise capacity are vascular disease (either peripheral or cerebrovascular) and orthopedic problems. Other situations warranting nonexercise stress testing include severe cardiopulmonary disease and general debility, especially among the elderly, in whom pharmacologic testing with both dobutamine and vasodilators has been shown to be well tolerated and reliable.[2] [3] [4] [5] Although the inability of a patient to exercise maximally constitutes the main indication for the use of nonexercise stressors, such stressors are less commonly indicated in other situations (Table 14-1) . The most important of these situations include circumstances in which the use of a pharmacologic agent may offer diagnostic dimensions that are not available from exercise stress, for example, the diagnosis of coronary spasm using ergonovine stress testing.[6] [7] A similar scenario involves patients early or late after myocardial infarction, after which left ventricular dysfunction may not be permanent. The diagnostic challenge in this situation is that whereas stunned myocardium improves spontaneously, the revascularization of hibernating Figure 14-1 (Figure Not Available) Proportion of patients undergoing exercise testing who are unable to exercise maximally. (From Marwick T: Acta Clin Belg 1992;47:1– 51.)

myocardium has implications for functional capacity and prognosis. As discussed later in the chapter, echocardiography can be used with dobutamine[8] or dipyridamole[9] [10] stress, or both,[11] for the identification of viable myocardium. Pharmacologic agents are more appropriate than exercise for stress testing in some environments, such as the cardiac catheterization laboratory or operating rooms. Finally, nonexercise methods have been used in

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preference to exercise echocardiography even in patients who are able to exercise because of their relative technical ease. The incremental nature of these stressors means that the time-course of ischemia can be identified; these data are not available using posttreadmill stress and are more difficult to obtain with bicycle exercise testing. Although the decision to use a nonexercise stress may not be justifiable with routine echocardiographic imaging at present, the facilitation of adjunctive techniques discussed subsequently—such as tissue Doppler, color kinesis, and contrast echocardiography (which may be less feasible during exercise than nonexercise stress)—could in the future justify the use of nonexercise techniques in patients who are able to exercise. Choice and Mechanism of Action of Nonexercise Stressors There are two general groups of nonexercise stress agents: those that induce ischemia by increasing myocardial work and oxygen consumption (exercise-simulating agents), and those that induce ischemia by influencing coronary perfusion and therefore myocardial oxygen supply (vasoactive agents). The latter include the coronary vasodilators dipyridamole and adenosine, which cause ischemia by provoking coronary steal, and ergonovine, which can be used to provoke coronary spasm. In addition to these stressors, nonpharmacologic approaches including hand-grip and the cold pressor test[12] [13] have been used. Hand-grip testing is often combined with dobutamine-atropine testing,[14] but the cold pressor test has not been widely adopted clinically because of limited efficacy and patient discomfort. Exercise-Simulating Agents

The exercise simulators include dobutamine and other sympathomimetic agents, pacing stress, and atropine 303

(usually used as an adjunct to the other approaches), all of which increase cardiac work and myocardial oxygen requirement. Thus, the induction of ischemia and regional dysfunction reflects the inability of the diseased coronary circulation to respond to this increased oxygen demand, a process that parallels the response to exercise. However, processes additional to classic "demand" ischemia may be active, and sympathomimetic agents may place an additional stress on the heart through effects on cardiac metabolism—an "oxygen-wasting" effect. In a group of patients with

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ischemic responses to both dobutamine and exercise, ischemia appeared at a significantly lower rate-pressure product during dobutamine than during exercise stress, consistent with the presence of a factor additive to that of cardiac work suggested experimentally.[15] [16] [17] Another contributor to this process might include concurrent "supply" ischemia due to reduction of coronary flow; certainly, sympathomimetic agents cause a dose-dependent reduction of subendocardial perfusion and maldistribution of coronary flow, in the face of mild coronary stenoses.[18] The latter component, together with regional flow heterogeneity based on tachycardia-induced coronary vasodilation, [19] is responsible for perfusion defects detected at myocardial perfusion imaging. Because increased cardiac workload and oxygen demand is the usual mechanism underlying ischemia in most ambulatory situations, the exercise-simulating agents are often considered to be a more physiologic means of stressing the heart, although "demand" ischemia may be combined with reduction in coronary supply due to vasospasm or coronary steal. Vasoactive Agents

The use of dipyridamole in combination with myocardial perfusion imaging is based on the induction of maximal coronary vasodilation in all territories. Flow heterogeneities (and therefore apparent perfusion defects) develop if a coronary stenosis limits the regional hyperemic response.[20] Of note, this process does not involve the provocation of ischemia in a functional or metabolic sense. In contrast, the development of regional wall motion abnormalities at stress echocardiography necessitates the induction of ischemia. The chief mechanism of vasodilator-induced ischemia is coronary steal,[20] which may be either "vertical" or "horizontal" through the left ventricular wall. The best known mechanism is horizontal steal, in which blood flows to nonstenosed from stenosed territory, owing to reduced collateral flow into the stenosed territory because of depressurization of vessels supplying the collaterals due to increased runoff. Vertical steal also occurs because of vasodilator-induced depressurization of the microcirculation, causing subendocardial vessels to collapse under the greater extravascular pressure in this region and "stealing" flow to the subepicardium from the subendocardium. Other mechanisms of vasodilator-induced ischemia, unrelated to coronary steal, include reduced coronary supply because of coronary spasm (which is the major effect of ergotamine), systemic hypotension, or collapse of the stenosis. Under conditions of maximal coronary hyperemia, driving pressure is the main determinant of

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myocardial perfusion because vasodilator reserve is exhausted. Hence, systemic hypotension may accentuate hypoperfusion due to coronary steal. Stenosis "collapse" may be provoked if profound microcirculatory vasodilation causes a reduction of lateral pressure induced by increased flow. Finally, myocardial oxygen demand may be increased in response to increased cardiac workload because of increased sympathetic activity secondary to angina. Agents Used to Identify Myocardial Viability

In the presence of dysfunctional but viable myocardium, regional function is enhanced by the inotropic effect of low-dose dobutamine, although this appears to require both recruitable perfusion and an increment in metabolism.[21] The mechanism of this is ill-defined but most likely pertains to enhanced calcium cycling. Viable myocardium supplied by a patent infarct-related vessel (generally corresponding to stunned myocardium) demonstrates a sustained improvement during the infusion, which then reverses after the test. Viable tissue supplied by a stenosed infarct-related artery (which may involve stunned or chronically ischemic— "hibernating"—tissue) is characterized by an initial improvement, occurring at low doses (<20 µg/kg/minute), or low heart rates, or both, followed by deterioration of regional function as the chronotropic effect becomes more prominent and myocardial work increases.[8] If the region is supplied by a critically stenosed artery, however, it may be possible for the territory to become ischemic before there is a noticeable enhancement of contractility. Moreover, the ability of the myocardium to thicken is determined by the amount of infarcted tissue within the segment.[22] Myocardial viability may also be inferred from the contractile response to dipyridamole. The mechanism of this is also putative but probably relates to myocardial congestion with interstitial fluid due to vasodilation. A socalled mini-Starling effect may be caused by this congestive process, producing additional tension on the myofibrils.[23]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Principles of Nonexercise Stress Techniques Pharmacology and Physiopathology of Nonexercise Stress Techniques Exercise-Simulating Agents

The exercise-simulating agents include dobutamine, dopamine, epinephrine, and isoproterenol. Of these, dobutamine has become the most commonly administered exercise-simulating agent, and the majority of published data on pharmacologic stress echocardiography have involved this agent. Arbutamine, a dobutamine isomer, was developed in the last decade but showed no substantial clinical merits compared with its parent compound, and distribution of the agent has been discontinued.[24] [25] Dopamine 304

stimulates alpha receptors and, if it extravasates, may cause localized limb ischemia due to vasoconstriction. Dopamine may also be a less effective precipitant of myocardial ischemia than is dobutamine.[26] Although other sympathomimetic agents have been used for stress testing,[27] epinephrine and isoproterenol are probably the more arrhythmogenic. This side effect is dose dependent, but its avoidance by conservative dosing may compromise the sensitivity of the test by limiting the amount of stress on the heart. Dobutamine is predominantly a beta-1 agonist, and normal areas become hyperkinetic in response to its inotropic effect. Myocardial segments supplied by a stenosed coronary artery may become akinetic or dyskinetic but more commonly are unable to augment their thickening and excursion, and the contrast between this response and the hyperkinetic function of normal segments facilitates the detection of zones with abnormal function. Vasodilation and chronotropy appear at higher doses, [26] usually at the 20 µg/kg/minute level of the routine dobutamine stress protocols, reflecting

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the stimulation of other receptors to a lesser degree. This chronotropic response appears to be the most important factor in terms of precipitating ischemia; most dobutamine stress protocols cause a mean heart rate increment of 40 to 50 beats per minute and mean peak heart rates of 110 to 120 beats per minute.[28] [29] [30] [31] [32] [33] [34] However, reflex bradycardia may occur in response to hypertension. The vasodilator effects of dobutamine may cause blood pressure to fall at peak doses, although blood pressure normally rises in response to the inotropic effect of the drug. Increases in myocardial oxygen demand due to increased cardiac work, as well as a weak vasodilator effect, lead to the development of coronary hyperemia in territories supplied by normal coronary arteries. Although this response is probably less than that induced by coronary vasodilators, the coronary hyperemic response to dobutamine stress permits its combination with perfusion scintigraphy.[34] [35] [36] [37] The detection of myocardial perfusion defects in the presence of coronary disease may be augmented by partial volume effects due to thinning of the ischemic wall. Vasoactive Agents

Most of the experience with pharmacologic stress echocardiography using vasoactive agents has been obtained with the coronary vasodilators dipyridamole and adenosine. The coronary vasodilators differ with respect to the onset and duration of their effects. Dipyridamole increases endogenous adenosine levels by reducing cellular reuptake and metabolism, and thereby acts indirectly.[20] This indirect mechanism causes some delay between the administration of this agent and the timing of peak vasodilation, the half-life of this effect being 6 hours. The indirect action of dipyridamole may account for interindividual variations in the magnitude of its effects. Adenosine acts directly on the vasculature, its vasodilator efficacy being equivalent to that of papaverine.[38] The potency and speed of onset of adenosine cause its side effects to be more intense but also more short-lived than those of dipyridamole. An increasing amount of literature describes the combination of ergonovine with echocardiography. This agent has a direct effect on the vessel; responsiveness to acetylcholine may be related to loss of nitric oxide production at the site of disease. Exercise Simulation Using Pacing Stress

Several nonpharmacologic approaches have been used for stress echocardiography, including "physiologic" stresses such as the cold pressor

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test, which are poorly tolerated. Pacing is an alternative means of increasing cardiac work without resorting to pharmacologic techniques. Pacing-induced tachycardia increases myocardial oxygen consumption and thereby causes myocardial ischemia in the setting of significant coronary stenoses.[39] [40] The reduction of subendocardial perfusion with pacing[40] may also contribute to the development of ischemia. Ventricular pacing is not favored, as it causes both abnormal regional contractility and abnormal perfusion, so that pacing stress techniques generally involve atrial stimulation, either transvenously or via the esophagus (only the latter having gained acceptance as a routine stress modality). Of these, direct atrial pacing has been used for other stress imaging tests, but it is invasive and therefore has not achieved acceptance. Of the transesophageal pacing approaches, the "pill" electrode has formerly been studied, but although this technique is effective, it has the disadvantage of causing significant discomfort. Attachment of pacing electrodes to transesophageal echocardiography probes has been reported in trials[41] [42] but has not moved into commercial production; perhaps miniaturized transnasal probes could make this feasible. The development of a small esophageal pacing catheter offers enhanced contact between the electrodes and the esophagus, which facilitates the test. In particular, the technique causes less discomfort than other pacing techniques because of the presence of smaller pacing thresholds.[43] Atrial pacing stress is more invasive than pharmacologic stress echocardiography but may be useful in patients in whom the pharmacologic approaches are contraindicated or associated with side effects. Moreover, this technique has additional attractions that might justify its use in preference to pharmacologic testing. These include the capacity to achieve a target heart rate in virtually all patients, the potential to immediately terminate the tachycardia if the patient develops complications (in contrast to pharmacologic methods, which require a period of time for the effects to dissipate), and the ability to perform measurements in the ischemic ventricle at a low heart rate (after cessation of pacing). The latter may be of particular value if Doppler indices of diastolic function are being assessed, as these are difficult to measure in the presence of tachycardia (which with dobutamine takes some time to resolve, by which time the ischemia may also have dissipated). Using atrial pacing stress, ischemic myocardium has been shown to have reduced ventricular compliance.[44] Sudden termination of stress during ischemia may also be of value in the combination of stress testing with color flow Doppler echocardiography, as the use of low frame-

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rates may pose a problem at high heart 305

rates. However, despite the benefits of transesophageal atrial pacing, its availability for many years,[45] and recent data showing correlation with dobutamine echocardiography despite a shorter test duration and better patient tolerance,[43] this technique has not become widely used because it remains somewhat invasive. Combined Approaches

Atropine reduces the depressant effect of vagal stimulation on heart rate and may be particularly useful when reflex reduction of the heart rate occurs in response to blood pressure elevation. The combination of atropine with dobutamine has been found to be useful in patients who fail to develop an adequate degree of tachycardia in response to dobutamine, the most common situation involving patients taking beta receptor antagonists.[46] [47] [48] An additional component of tachycardia (and therefore ischemia due to increased oxygen demand) can also be obtained by combining atropine with dipyridamole.[49] [50] [51] In both circumstances, the addition of atropine to other stressors has been associated with an increment in sensitivity. Indeed, there is a trend toward earlier use of atropine during the dobutamine protocol,[52] [53] especially in beta-blocked patients. However, although nondiagnostic results of a submaximal heart-rate response can be avoided by the use of atropine, this adjunct does not help the results of submaximal tests that reflect premature termination of pharmacologic stress due to side effects. The rationale for combining dobutamine and dipyridamole Figure 14-2 End-diastolic apical four-chamber image in fundamental (A) and harmonic (B) modes. The use of harmonic imaging substantially improves visibility of the lateral wall and distal structures.

reflects their action through different mechanisms. The sequence of drug administration can be used to produce a stepwise stress on the heart. The initial administration of dipyridamole permits detection of the most severe coronary stenoses due to the development of coronary steal. The subsequent incremental administration of dobutamine progressively increases oxygen demand, permitting the identification of progressively

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more moderate stenoses.[54] The combination has also been used to enhance the accuracy of detection of myocardial viability.[11] Although the combination of these techniques has afforded higher levels of sensitivity than the individual tests can provide, using the current methodology, this is obtained at the cost of an unacceptably long stress protocol.[54] Echocardiographic Approach to Nonexercise Stress Techniques Image Acquisition

The technical challenges of pharmacologic and pacing stress, although less extreme than those posed by exercise echocardiography (as the patient is neither moving nor hyperventilating), mandate the use of the best available echocardiography equipment. The development of harmonic imaging has made a substantial impact on endocardial visualization[55] [56] [57] (Fig. 14-2) and therefore the feasibility of stress echocardiography.[58] Although very few patients (<2%) have completely uninterpretable images, 306

failure to detect the endocardium in every myocardial segment is very common, and contrast is indicated if two to four segments are completely or partially obscured (Fig. 14-3) . Typically, transthoracic images are obtained in the four standard views (parasternal long- and short-axis and apical four- and two-chamber). Transesophageal echocardiography has been employed in combination with both pharmacologic[59] [60] [61] and pacing stress,[41] [42] [62] usually for patients with inadequate transthoracic images. During transesophageal imaging with pharmacologic stress, we approximate the standard imaging planes as closely as possible by recording transverse and longitudinal esophageal and transgastric short- and long-axis views. During pacing with electrodes attached to the transesophageal echocardiography probe, the need to stimulate the esophagus inhibits the ability to move the transducer, so that imaging is performed in the transgastric planes only. Although the constraints of a busy stress echocardiography schedule may preclude the performance of a detailed examination in every patient, a "screening" M-mode, pulsed wave (especially for left ventricular inflow), and color Doppler echocardiographic examination should be performed at the beginning of every study. Time should also be taken to optimize twodimensional echocardiographic images, gain settings (for endocardial

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detection), and image size (to obtain the best spatial resolution and framerate). During the stress, the patient is imaged continuously, and the images are stored on videotape. When the study is performed for the diagnosis of coronary disease, the digital quad-screen display is filled with a resting image, a low-dose image (10 µg/kg/minute dobutamine, 0.56 mg/kg dipyridamole, or a small heart rate increment with pacing), and two highdose images (40 µg/kg/minute dobutamine or 0.84 mg/kg dipyridamole with or without atropine), or a peak and early poststress image. When a resting wall motion abnormality is present, and the clinical question pertains to the possibility Figure 14-3 Use of myocardial contrast for left ventricular opacification during stress echocardiography. Compared with harmonic imaging (A), the post-contrast end-diastolic apical four-chamber image (B) shows significant improvement of lateral wall resolution.

of viable myocardium, we obtain two low-dose images (5 and 10 µg/kg/minute dobutamine) and one high-dose image. Image Processing

Both videotape and digital techniques are used for interpretation and archiving of stress echocardiograms. Because modern echocardiography systems are fully digital, digital image capture is an easy process that permits rapid acquisition. Moreover, digital image processing facilitates image display and interpretation by allowing a side-by-side display of resting, low-dose, and high-dose images, as well as the ability to review individual frames (the latter permitting an effective evaluation of the temporal sequence of contraction). Although the use of digital echocardiography enhances the accuracy of nonexercise echocardiography, however, all studies should be recorded on videotape as well as in digital format. This provides a back-up in case technical problems with the digital capture (especially triggering) or corruption of the archived data threaten loss of the study. Indeed, routine review of videotape has a significant impact on diagnosis, probably by permitting review of off-axis images and regions that are not adequately represented by saving a single cardiac cycle. [63]

Qualitative Interpretation

The interpretation of stress echocardiograms for clinical purposes is based on a qualitative evaluation of regional function at rest and stress.[64] Some

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standardization is obtained by scoring regional wall motion and thickening in a number of segments, the most widely used being a model based on that of the American Society of Echocardiography,[65] wherein the left ventricle is divided into 16 307

Figure 14-4 (Figure Not Available) Effect of a training period on the accuracy of interpretation of dipyridamole stress echocardiograms by learning and experienced groups of observers (shown at initial [Before] and follow-up [After] periods). (From Marwick T: Stress Echocardiography. Amsterdam, Kluwer Academic Publishers, 1994.)

segments (anterior, septal, lateral, and inferior at the apex, with these segments as well as anteroseptal and posterior segments at the base and midpapillary muscle level). Despite this standardization, however, the expertise of the physician interpreting the test is critical, and even accomplished echocardiographers require a significant learning period. In a study of echocardiographers learning dipyridamole stress echocardiography, Picano et al[66] reported that 100 supervised studies were required to bring the accuracy of "novices" to the level of "experts" (Fig. 14-4) (Figure Not Available) . The standard qualitative algorithm for interpretation of pharmacologic stress echocardiography is summarized in Table 14-2 . With the exception of the low-dose responses to dobutamine and dipyridamole, which denote myocardial viability (see later discussion), it may also be applied to pacing or other stressors. Regional wall motion at rest may be classified as normal, hypokinetic, akinetic, or dyskinetic. Severe hypokinesia may be difficult to distinguish from akinesia; a useful guide is based on endocardial excursion, with less than 2 mm identifying akinesia and less than 5 mm indicating hypokinesia. Regions that fail to thicken or that move only in late systole (after movement of the adjacent myocardium) may be moving passively and should be considered akinetic, irrespective of endocardial excursion. Segments with resting akinesis or dyskinesis are most likely composed of infarcted myocardium if the wall is TABLE 14-2 -- Interpretation of Myocardial Viability and Ischemia Using Dobutamine Echocardiography Resting

Peak/Poststress

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Function Normal Normal

Low-Dose Normal Normal (unless severe CAD)

Function Hyperkinetic Reduction vs. rest

Reduction vs. other segments Delayed contraction Viable, patent Hypo/akinetic Improvement Sustained IRA improvement Viable, Hypo/akinetic Improvement Reduction (c/w lowstenosed IRA dose) Infarction A/dyskinetic No change No change CAD, coronary artery disease; c/w, compared with; IRA, infarct-related artery. thinned and dense,[67] but in the absence of thinning are quite likely to consist of viable tissue. Indeed, hypokinetic segments are not identified as being infarcted, on the basis that residual contraction implies the presence of residual viability. Because the process of thinning and fibrosis takes some time after infarction, myocardium of normal thickness is commonly seen after recent or non-transmural infarction. Improvement of abnormal function in response to low doses of dobutamine (5 or 10 µg/kg/minute) or dipyridamole (0.28 or 0.56 mg/kg) suggests the presence of viable myocardium (Fig. 14-5) , although this finding is more reliable if the segment subsequently deteriorates, which indicates ischemia. The global left ventricular responses to dobutamine stress include an increase in cardiac output and reduction of left ventricular cavity size, although neither is as prominent with vasodilator stress. Left ventricular dilation implies multivessel or left main coronary artery disease, but this is less commonly seen with pharmacologic than exercise stress,[68] probably because of reduction of left ventricular loading. Together with an extreme inotropic response, this afterload reduction may produce cavity obliteration, and although this response is favorable prognostically (presumably reflecting a low probability of multivessel disease), it may impair sensitivity because endocardial excursion is reduced and small areas of wall motion are unrecognized.[69]

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The normal regional response of segments to maximal 308

Figure 14-5 End-diastolic and end-systolic freeze-frame images illustrating left ventricular enlargement at dobutamine echocardiography in a patient with left ventricular dysfunction and multivessel coronary artery disease. There is a resting wall motion abnormality in the apex, which is unchanged with stress. At peak stress, there is left ventricular enlargement with reduction of systolic motion and thickening of the lateral (and to a lesser degree the septal) wall.

inotropic stress is to increase endocardial excursion, speed of contraction, and degree of myocardial thickening. A deterioration of function from rest, or after an initial enhancement of function, indicates the development of ischemia with either dipyridamole or dobutamine (Fig. 14-6) . Variants of an overt deterioration include delayed contraction ("tardokinesis") and a reduction of myocardial thickening. Caution should be applied in the assessment of areas adjacent to zones of myocardial infarction, which may be tethered by the infarcted zone and hence fail to improve function with stress, or even appear dyskinetic if the infarct bulges during stress. Careful examination of wall thickening may assist in distinguishing peri-infarct ischemia and tethering. The diagnosis of ischemia in segments with abnormal resting function depends on the stress agent and is more difficult. At dobutamine echocardiography, if a segment shows akinesia or dyskinesia at rest, a further deterioration of function probably reflects increased loading rather than ischemia.[70] The most challenging interpretation is the diagnosis of ischemia in segments with resting hypokinesis. Segments demonstrating a stress-induced improvement are classified as normal, and those showing a deterioration (compared with either rest or low-dose) are identified as ischemic. However, differentiation between degrees of hypokinesia may be difficult, even with side-by-side cine-loop analysis. Some caution needs to be applied in the interpretation of regional variations in the degree of hyperkinesis, as these may occur in normal patients.[71] The diagnosis in hypokinetic regions that fail to improve function in response to stress is debated; if adjacent segments mount a hyperkinetic response, we characterize these as ischemic. The greatest limitations of the current application of stress

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echocardiography are concerns related to subjectivity and reproducibility. Although single-center studies 309

Figure 14-6 Apical two-chamber views illustrating the development of myocardial ischemia (reduced wall thickening) of the apex during dobutamine stress echocardiography. End-diastolic images are given on the left and systolic images on the right, with resting images above and peak dose below.

have suggested that the interobserver variation in interpretation is small,[72] interinstitution variability (although similar to that of other imaging techniques) is significant.[73] Interinstitution variability is particularly a problem in studies of poor image quality and in patients with mild ischemia. This discordance has been progressively reduced by definition of standard reading criteria[74] and more recently by the adoption of harmonic imaging.[75] The following reading guidelines are useful for controlling variation: minor degrees of hypokinesia are not identified as ischemia (especially if only apparent at peak and not at poststress readings); focal abnormalities that do not follow angiographic territories are ignored; abnormalities are corroborated whenever possible with another view; basal inferior and septal segments are not identified as abnormal in the absence of a neighboring abnormal segment; studies are read by multiple observers whenever possible; and reading is blinded to all other data. Finally, we find a standard sequence to be of value in the interpretation of stress echocardiograms (both exercise and nonexercise). We first review the video images of the resting examination, including M-mode and Doppler components. On beginning the review of the digital images, we first check that images are triggered correctly and the prestress, peak stress, and poststress views are comparable. We then briefly review the side-byside display to see if there are new wall motion abnormalities or obvious changes in cavity size (suggesting multivessel disease) or cavity shape. Segmental analysis is carried out by careful comparison of regional function in each of the 16 segments, comparing the same site at rest and at stress. Both wall motion and thickening are compared, using both cine-loop and frame-by-frame review of the digital images. If image quality is not good enough to permit the use of thickening criteria, the reader should focus on the first part of systole to minimize the contribution of rotational or translational movement. Finally, videotaped stress images are examined,

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to review nonstandard views 310

and to check on conclusions based on the digitized images. From review of digital and video data, the site, extent (number of abnormal segments), severity (segmental wall motion score), time of onset and offset of ischemia, and the effect of ischemia on global left ventricular function can be derived.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Aspects of Nonexercise Stress Techniques General Considerations The preparation for nonexercise stress testing does not deviate substantially from preparation for exercise stress testing. These tests should be performed in the fasting state, partly because nausea is a side effect with some agents (especially transesophageal pacing, dipyridamole, and adenosine), and also in case complications ensue, with attending risks of aspiration. For dipyridamole stress testing, coffee, tea, and cola drinks should be avoided for 12 hours before the examination, as xanthines antagonize the effects of dipyridamole on adenosine metabolism, as well as by direct competitive inhibition of adenosine activity. For diagnostic testing, patients should be instructed to stop anti-ischemic drugs on the day of the procedure, but medications may be continued if testing is being performed to assess the adequacy of therapy. During the preparatory stage of the test, intravenous access is secured, and electrocardiographic monitoring may be modified to remove electrodes from the echocardiographic windows. A minimum of two personnel (sonographer and physician) is mandatory for performance of these protocols, and many centers involve a nurse as well. Clinical and electrocardiographic monitoring during the tests parallels the monitoring undertaken during exercise stress testing. In addition to the usual resuscitation equipment, intravenous beta-adrenoreceptor blocking agents and nitrates should be available to treat severe ischemia, and for dipyridamole testing, aminophylline should be available for the treatment of severe ischemia, which occurs occasionally. Exercise-Simulating Agents Protocols for Administration of Sympathomimetic Agents

Dobutamine has been administered using various empirical dose regimens,

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but the relative plasma levels with these have not been studied, and none is clearly superior to the others. The most widely used is an incremental administration (Fig. 14-7) from 5 µg/kg/minute to 40 µg/kg/minute in 2- or 3-minute stages.[28] [29] [30] [31] [32] [33] [34] Variants include maximal doses of up to 50 µg/kg/minute and down to 20 µg/kg/minute; lower dose-rates administered over longer periods are able to attain hemodynamic effects similar to those obtained by the high-dose protocols.[33] New accelerated dobutamine protocols are currently being used to reduce the duration of the test, but whichever regimen is applied, a reasonable (i.e., 2- to 3-minute) period at peak heart rate is desirable, as ischemic wall motion abnormalities may take a short time to become apparent. If atropine is added to induce an increase in heart rate, the usual dose is 1 to 2 mg total in 0.25-mg increments. Arbutamine is no longer marketed, but other agents might be applied using a similar closed-loop computerized delivery system. The age and weight of the patient, target heart rate, and rate of heart rate augmentation (heart rate slope) were entered into the device. Based on the response to an initial dose, the microprocessor automatically increased the infusion rate to achieve the required rate of augmentation and eventually the desired peak. As the target rate was approached, the infusion was reduced and stopped. The device had a number of alarms to alert the supervising physician to responses that require attention, as well as safety features that permitted automatic shut-off of the system. Such a system could reduce the need for a nurse to increase the drug and monitor the hemodynamics. Hemodynamic Responses to Sympathomimetics

Dobutamine enhances left ventricular contractility at low doses, usually without the development of tachycardia. At doses greater than 20 µg/kg/minute, systolic blood pressure increases, and the heart rate augments to more than 100 beats per minute. Using a standard protocol without atropine, heart rate can be expected to increase to about 120 beats per minute in most patients, reflecting a heart rate increment of 40 to 50 beats per minute. In normotensive patients, the systolic blood pressure usually increases to about 170 mm Hg (an increment of 30 to 40 mm Hg), without a significant change of diastolic blood pressure. The systolic pressure response may be marked in hypertensive patients and blunted in patients with left ventricular dysfunction or multivessel coronary disease. The peak rate-pressure product increases to the range of 16,500 to 20,000. Although the development of ischemia at lower dobutamine doses and cardiac workloads indicates the presence of more extensive coronary

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disease, there is too much overlap for the hemodynamic response to be a reliable predictor of one-, two-, or three-vessel disease. The hemodynamic response to dobutamine shows significant variability between patients. Beta-adrenergic blockade may attenuate the physiologic responses to dobutamine through a process of competitive antagonism at the receptor level. Patients taking beta blockers have a significantly lower heart rate response (to a peak of 90 to 100 beats per minute), and a lower double-product (to levels of around 14,000), although this may be attenuated by use of atropine. The peak systolic blood pressure is less during dobutamine than exercise, although this difference is less than with heart rate.[29] Indeed, the cardiac stress imposed by dobutamine (even at maximal dobutamine dosage) is less than that obtainable with maximal exercise testing. In several head-to-head comparisons between 311

Figure 14-7 Standard incremental dobutamine protocol, starting at 5 µg/kg/min and going to 40 µg/kg/min with incremental atropine. Images and hemodynamics are obtained at the end of each stage.

dobutamine and exercise stress in the same patients, systolic blood pressure levels were comparable, but peak heart rate and double product were significantly greater during exercise than dobutamine stress.[33] [76] [77] [78] [79] [80] [81] These disparities have important implications for the relative sensitivity of dobutamine and exercise echocardiography (see later discussion). Side Effects of Stress Testing with Sympathomimetic Agents

Other than the development of myocardial ischemia, dose-limiting side effects experienced during dobutamine protocols generally reflect intense adrenergic stimulation. Consequently, dobutamine stress is contraindicated in patients with severe hypertension and serious arrhythmias. Serious side effects are rare during dobutamine stress testing. In more than 1000 dobutamine studies reported by Mertes et al,[82] no patients died or suffered myocardial infarction or sustained tachyarrhythmias. Similarly, in 650 studies with dobutamine and atropine reported by Poldermans et al,[83] no patients died or suffered myocardial infarction, and cardiac arrhythmias were most likely in patients with left ventricular dysfunction or pre-existing

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ventricular arrhythmias. In a multicenter study reported by Picano et al,[50] nine major cardiac events occurred in nearly 3000 studies (three due to ventricular tachycardia, two from ventricular fibrillation, two from myocardial infarction, one with severe ischemia, and one with hypotension). In this study, atropine psychosis was observed in five patients, but this finding has not been reported from other studies and this author has yet to see this complication in a personal experience of over 5000 studies, many of which have involved atropine usage. In our experience, serious side effects of dobutamine stress occurred in 3 per 1000 patients,[84] a similar result to that of a large German study.[85] Nonetheless, in case reports, fatalities have been reported from ventricular fibrillation and cardiac rupture.[86] Moreover, the safety of the test in patients at highest risk—those with severe left ventricular dysfunction—has been described only in small populations.[87] Nonetheless, considering that the sickest patients (those unable to exercise and those with questions of myocardial viability) undergo the test, this safety profile can be considered to be quite favorable and may in part reflect the detection of the extent and severity of ischemia by online echocardiographic imaging, permitting termination of the stress before serious problems arise. The most frequent serious but nonfatal complications are myocardial infarction and arrhythmias, although atrial fibrillation and sustained ventricular tachycardia are rare, and more common rhythm problems include atrial and ventricular extra systoles and nonsustained atrial and (less often) ventricular tachycardias. Other problems include palpitations (due to increased contractility), hypertension, anxiety (sometimes manifested as dyspnea or vagal reactions), tremor, and urinary urgency. Hypotension may arise from the vasodilator effect of high-dose dobutamine, the development of outflow tract obstruction, or the development of severe ischemia. [88] [89] [90] [91] Unlike hypotension during exercise testing, it does not denote the presence of serious coronary disease or left ventricular dysfunction. [92] All of the studies documenting the sensitivity and specificity of dobutamine stress echocardiography have documented these complications, but the recorded frequency of these side effects has varied from 5% if only serious, dose-limiting side effects are considered[28] to 82% if all side effects are included.[33] One source of variability relates to the definitions used to identify side effects. For example, in the initial experience with dobutamine stress testing, hypotension (which is usually asymptomatic) provoked termination of the test if the systolic blood pressure decreased by more than

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20 to 30 mm Hg or a greater than 15 mm Hg fall from baseline, whereas most centers now continue the infusion unless the systolic blood pressure falls to less than 100 mm Hg or the patient becomes symptomatic. Another source of variability relates to the type of stress protocol, the incidence being lower if the test is terminated for attainment of a target heart rate or when echocardiographic evidence of ischemia is seen[28] or if submaximal test responses are excluded.[29] Vasodilator Stress Protocols Stress Protocols

For dipyridamole stress, an intravenous line is inserted into a large proximal arm vein to minimize local discomfort from this strongly alkaline compound. Various dipyridamole administration regimens have been used, both intravenous and oral, although the absorption of the latter is variable and the approval of the intravenous form of 312

this agent by the Food and Drug Administration has removed the main reason for using this route. For myocardial perfusion imaging, the most commonly administered dose is 0.56 mg/kg IV,[93] but this infusion protocol has unsatisfactory levels of sensitivity when combined with stress echocardiography. The sensitivity of dipyridamole echocardiography can be significantly enhanced[94] [95] by an additional 2 minutes of infusion if the initial response is negative and no major side effects have appeared. Because the time of onset of ischemia correlates with the severity of coronary disease and prognosis (see later discussion), we record images every 2 minutes from the conclusion of the first dose until 18 minutes from the start of the study. Digitized images are saved at rest, before the start of the second dose (8 minutes), after the second dose (12 minutes, which is the most common time for the onset of ischemia), and at 16 minutes. Aminophylline (in aliquots of 50 to 75 mg IV) can be used to counteract the effects of dipyridamole if severe ischemia or side effects arise; the threshold for using this agent is influenced by the overall left ventricular function and the clinical state of the patient. Because dipyridamole acts via endogenous adenosine release, there is some delay between the time of its administration and the development of its effects. In contrast, because exogenous adenosine is able to act directly, it rapidly achieves steady state, and its biologic effects are of rapid onset.[38] It

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is therefore suitable for injection using an incremental dose schedule, with echocardiographic imaging at the end of each stage. Various dosing regimens have been used for echocardiographic studies, including a fixed dose of 0.14 or 0.17 mg/kg/minute and incremental protocols (3-minute stages starting at 0.10 mg/kg/minute, increasing to 0.14 and 0.18 mg/kg/minute).[96] [97] [98] [99] The use of aminophylline is rarely required for side effects, as these resolve within a minute of stopping the infusion. Hemodynamic Responses to Vasodilators

The mechanism of action of vasodilator agents is chiefly through the phenomenon of coronary steal. There is a small contribution of increasing oxygen demand from tachycardia,[23] which may be a response to angina and side effects rather than arising from the agents themselves. Similarly, blood pressure is usually little changed by these stressors, which may cause hypotension. The addition of atropine leads to an augmentation of heart rate and cardiac work, [49] [51] effectively combining reduced coronary supply with increased oxygen demand. Side Effects of Dipyridamole and Adenosine

The development of side effects during dipyridamole stress usually follows completion of the infusion and rarely precludes completion of the study. Side effects usually resolve spontaneously, but, if necessary, aminophylline can be used to reverse the effects of dipyridamole. Minor side effects, including flushing and headache (which reflect the systemic vasodilator effects of the compound), occur in about two thirds of patients studied with high-dose dipyridamole.[100] Severe or prolonged myocardial ischemia is infrequent but can be treated with nitrates or aminophylline. Serious side effects are very rare[50] [101] severe myocardial ischemia and infarction, bronchospasm, and complete heart block and even death have been reported. The frequency of these serious complications is probably less than with dobutamine, although ensuring that the comparison groups are matched for baseline risk is always difficult. Dipyridamole stress is contraindicated in patients with untreated atrioventricular block and bronchospastic disorders, although patients with chronic obstructive airway disease with no or minimal airway reactivity may undergo the test. Adenosine differs from dipyridamole stress only to the extent that the adenosine causing the physiologic effects is exogenous rather than endogenous. The side effect profile is therefore similar, and although the intensity and frequency of side effects with adenosine exceed those of

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dipyridamole, they are of shorter duration. Some form of side effect occurs in most patients undergoing adenosine stress.[102] In response to a high-dose protocol, [99] side effects prevented about one third of patients from achieving peak dose, a comparable frequency to that found with dobutamine. As the effect of adenosine is very transient, cessation of the infusion is usually the only treatment required for side effects. Vasoconstrictor Protocols An increasing amount of literature has developed regarding the use of ergonovine for the diagnosis of coronary spasm, especially in regions where this diagnosis is made in the absence of fixed coronary stenoses. In the West, however, this finding is considered unusual, with spasm being recorded in 4% of patients in whom it is suspected clinically, although the return may be increased significantly by focusing on smokers and patients with some coronary disease.[103] Although most practitioners feel more comfortable with the use of this agent in the angiography laboratory,[103] because spasm can be visualized directly and intracoronary nitrates infused to treat severe spasm, a significant evidence base attests to its safety when applied noninvasively in patients without significant stenoses.[104] [105] [106] Although most of the evidence base relates to patients in whom significant stenoses have been excluded, the test has been applied to some patient groups without previous angiography.[6] [7] The standard protocol involves repeated bolus doses of ergonovine maleate at 5-minute intervals up to a total cumulative dose of 0.35 mg, unless echocardiographic evidence of abnormal left ventricular wall motion is detected. Pacing Stress Stress Protocols

The use of transesophageal pacing requires topical pharyngeal anesthesia and mild sedation. The end points of the test are the same as those for other nonexercise stressors; 313

in the absence of these end points, pacing at peak heart rate is continued for 3 minutes. No protocol has been uniformly accepted. Although formerly we used an incremental protocol commencing at 100 beats per minute, with increases in 2-minute stages, we now take the heart rate to 85% of predicted maximum immediately, followed by 100% of predicted

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maximum. The benefit of a short protocol is that electrode movement and loss of capture are less likely. Atropine is often required to overcome Wenckebach's atrioventricular block. In our practice, we digitize resting, 100 beats per minute, peak, and post-pacing images and apply the usual guidelines for interpretation. Hemodynamic Responses

The hemodynamic response to pacing stress is more controllable than the response to pharmacologic agents. The heart rate is usually increased to 150 or 160 beats per minute, and systolic blood pressure is increased by only a small amount, giving a rate-pressure product of 15,000 to 20,000. In the case of atrial pacing using transesophageal imaging, the insertion of the transesophageal probe in an awake patient may itself provoke hemodynamic TABLE 14-3 -- Sensitivity and Specificity of Echocardiography with Dob 50 Patients)

Study Sawada et al

Significant Multivessel Myocard Dobutamine Stenosis Disease, n Infarctio n (% Al Patients, Protocol, Diameter, (% All N µ/kg/min % CAD) CAD) 103 30 >50 14 (40) 35 (43)

[28]

Cohen et al[29] Salustri et al

70 52

40 40

>70 >50

35 (69) 17 (46)

19 (37) 14 (38)

Marcovitz & 141 Armstrong[32] Mazeika et al 50

30

>50

47 (43)

—

20

>70

24 (67)

13 (36)

40 + atropine 40

>50

15 (32)

28 (60)

>50

74 (52)

0 (0)

66

40

>70

21 (42)

0 (0)

80

40

>50

33 (58)

15 (26)

[31]

[33]

McNeill et al

80

[46]

Marwick et al 217 [34]

Hoffmann et al[81] Previtali et al [78]

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Takeuchi et al 120

30

>50

37 (50)

62 (84)

40 + TEE 40 + TEE 40

>70 >70 >50

16 (76) 37 (60) 11 (9)

7 (33) 23 (37) 41 (34)

40 40 40 + dipyridamole 30 40 40

>50 >50 >50

21 (49) 16 (12) 16 (12)

9 (21) 38 (29) 38 (29)

>50 >50 >70

36 (55) 27 (67) 15 (60)

24 (37) 18 (41) 41 (39)

40 + atropine 40 + atropine 40 + atropine 40 + atropine 40 + atropine 40 + atropine

>50

42 (46)

25 (27)

>70

109 (74)

105 (71)

>50

34 (54)

0 (0)

>50

48 (40)

38 (30)

>50

122 (58)

>50

142 (61)

214 (70)

>50

113 (66)

55 (24)

>50 >50

— 15 (60)

>50

70 (64)

[214]

Prince et al[215] 81 Panza et al[59] 76 Beleslin et al 136 [79]

Senior et al[216] 61 Ostojic et al[54] 150 Ostojic et al[54] 55 Daoud et al[217] 76 54 Ho et al[218] Dagianti et al 60 [219]

Pingitore et al 110 [51]

Ling et al[220]

183

San Roman et al[221] Anthopoulos et al[222] Dionisopoulos et al[223] Elhendy et al

102 120 288 96 f

[224]

210 m Hennessy et al 219 [225]

Huang et al[226] 93 Lewis et al[227] 93 Nagel et al[228] 208

40 + atropine 40 Modified protocol 40 + atropine

—

— — 0 (0)

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Beleslin et al 168

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40

>50

0 (0)

40 (24)

[117]

SVD = single vessel disease, TEE = transesophageal echocardiography. changes and hence ischemia, so that "resting" transesophageal echocardiographic images may not be truly acquired at rest. Side Effects

Fewer side effects occur during transesophageal pacing than with pharmacologic stressors. The frequency of esophageal discomfort, gagging, or nausea is much lower with modern pacing electrodes. Angina may be provoked by stress but is usually self-limiting after cessation of pacing. Atrial flutter or fibrillation may also be precipitated. Esophageal injury is theoretically possible in response to high levels of stimulation over a prolonged period, but this has not been reported clinically.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/120.html/top

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Accuracy of Nonexercise Stress Echocardiography for Diagnosis of Coronary Artery Disease Dobutamine Stress Echocardiography The sensitivity and specificity of dobutamine echocardiography for the detection of coronary artery disease and results of recent studies are summarized in Table 14-3 . The 314

sensitivity for significant disease (defined as visually assessed stenoses of greater than 50% or greater than 70%) is variable between studies, with an interquartile range of 75% to 92%. The addition of atropine appears to enhance the sensitivity of the test, as does transesophageal imaging. The interquartile range for specificity ranged from 77% to 93%, which is comparable to that of exercise echocardiography. No single feature accounts for these false-positive results, although the most frequent site of false-positive results[107] is the basal inferior wall. Patients with apparent abnormalities in this segment should be identified as having coronary disease only if an adjacent segment (basal septal, mid-inferior, posterior) is also involved. One problem with assessments of sensitivity and specificity is that a 50% or 70% stenosis cutoff is arbitrary and does not take into account stenosis location or vessel size, both of which clearly influence the likelihood of an abnormal response. This concern has been addressed in several studies that have compared the results of dobutamine echocardiography with stenosis diameter at quantitative coronary angiography.[108] [109] [110] The angiographic cut-off value with the best predictive value for a positive dobutamine test was a luminal diameter of 1.07 mm, percent diameter stenosis of 52%, and percent area stenosis of 75%, of which minimal lumen diameter was found to have the best predictive value for a positive dobutamine stress test (odds

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ratio, 51; sensitivity, 94%; specificity, 75%).[108] Stenoses smaller than 1 mm in diameter can be identified with a sensitivity of 86%. [109] [110] The previous analyses were limited by comparison with the anatomic severity of stenosis, whereas a more physiologic comparison would be more meaningful. Myocardial fractional flow reserve is a functional index of coronary stenosis severity that takes into account collateral flow and is calculated as the ratio of mean hyperemic distal coronary to aortic pressure. The degree of dobutamine-induced dyssynergy correlates significantly better with myocardial fractional flow reserve than percent stenosis or minimal lumen diameter, and the sensitivity of dobutamine echocardiography is significantly lower for lesions in vessels smaller than 2.6 mm than for larger vessels.[109] Because the existence of a regional wall motion abnormality identifies the presence of coronary disease, dobutamine echocardiography demonstrates higher sensitivities in patients with myocardial infarction. In patients with single-vessel coronary disease, the sensitivity of dobutamine echocardiography (ranging from 40% to 70%) is lower than in patients with multivessel disease. As dobutamine produces a less potent stress on the heart than exercise (see earlier discussion), the results of dobutamine stress are probably more susceptible to external influences than are those of exercise echocardiography or myocardial perfusion scintigraphy. This may be pertinent to the extrapolation of results from clinical trials (in which patients were carefully supervised and tested under optimal conditions, off therapy), to routine clinical practice, in which patients are often tested on therapy and are more likely to have a "suboptimal" test result because of inability to complete the protocol or interference by beta-blocker therapy.[34] Stress Echocardiography Using Other Sympathomimetic Agents Combination of echocardiography with other agents, such as epinephrine and isoproterenol, offers moderate sensitivity in the diagnosis of coronary artery disease.[111] Failure to attain higher levels of sensitivity with these compounds has in part reflected limitations in the administered dose brought about by concerns about side effects. The sensitivity of arbutamine echocardiography for the identification of ischemia was 76%, and the sensitivity for identification of coronary disease was 84%. No specificity data were obtained, but in a group at low probability of coronary disease, the normalcy was 96%.[112] As in the case of dobutamine and exercise echocardiography, the sensitivity was lower in

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patients with less extensive disease and also in patients who were stressed submaximally. However, arbutamine stress echocardiography seems unlikely to be developed further for commercial reasons. Dipyridamole Stress Echocardiography Studies of more than 50 patients that address the accuracy of vasodilator stress echocardiography for the identification of coronary artery disease are summarized in Table 14-4 . The use of the low-dose (0.56 mg/kg) protocol is associated with lower sensitivities than those generally reported with the high-dose regimen, which range from 58% to 94%. The addition of atropine to dipyridamole appears to enhance the sensitivity of the test.[49] [113] In patients with single-vessel coronary disease, the sensitivity of dipyridamole echocardiography is in the range of 50%, and this has an important influence on the sensitivity of this test in comparison with dobutamine. Most studies show the specificity of the technique to be excellent. As in the case of dobutamine, the use of transesophageal imaging has enhanced the accuracy of dipyridamole stress echocardiography.[114] There appears to be more variation in the sensitivity of vasodilator stress echocardiography than for dobutamine and exercise echocardiography. The main variables that account for this heterogeneity are patient selection and the definition of "significant" disease. The use of greater than 70% diameter stenosis as a criterion of significant coronary disease has tended to enhance the sensitivity, as patients with milder stenoses (who would be more difficult to detect) are not included. Of more importance, however, are clinical factors, such as the prevalence of myocardial infarction and multivessel disease and the cessation of antianginal therapy[115] many of the more favorable results pertain to populations with a high percentage of patients with more severe coronary disease. As in the case of dobutamine stress, investigators have sought to address the accuracy of dipyridamole stress with physiologic rather than anatomic criteria of significant stenosis.[116] In 30 patients with isolated stenoses of the left anterior descending coronary artery, predictors of an abnormal dipyridamole echocardiogram were a stenotic flow reserve of less than 2.8, stenosis diameter greater than 59%, lumen diameter less than 1.35 mm, and coronary flow reserve less than 2.0, of which stenotic flow reserve was the only independent predictor of ischemia. This 315

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TABLE 14-4 -- Accuracy of Vasodilator (Dipyridamole and Exercise) Ech of More Than 50 Patients)

Patients, Study N Picano et al 66 [94]

Picano et al

93

[100]

Masini et al

83

[229]

Massa et al

52

[156]

Cohen et al

50

[230]

Picano et al

445

[231]

Simonetti et al[232] Zoghbi et al

51 73

[97]

Severi et al

429

[126]

Mazeika et al[233] Picano et al

55 130

[49]

Previtali et al[78] Marwick et al[99]

80 97

Multivessel Myocardia Definition Disease, n Infarction n (% All of CAD, (% ALL CAD) Agent Dose % CAD) Dipyridamole, >70 20 (40) 9 (18) 0.56 mg/kg 48 (67) 17 (24) Dipyridamole, >70 * 0.84 mg/kg Dipyridamole, >70 24 (62) 15 (38) * 0.84 mg/kg Dipyridamole, >70 12 (23) 9 (17) * 0.84 mg/kg Dipyridamole, >70 28 (78) 16 (44) 400 mg PO 119 (46) 0 (0) Dipyridamole, >50 * 0.84 mg/kg Dipyridamole, >70 0.84 mg/kg * >75 24 (44) 38 (70) Adenosine, 0.14 µg/kg/min * 114 (46) 0 Dipyridamole, >75 * 0.84 mg/kg 30 (75) 18 (45) Dipyridamole, >70 * 1.00 mg/kg Dipyridamole, >50 — — 0.84 mg/kg + atropine 33 (58) 15 (26) Dipyridamole, >50 * 0.84 mg/kg Adenosine, >50 28 (47) 0 (0) 0.18 µg/kg/min *

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Ostojic et al [54]

Marangelli et al[123] Beleslin et al[79] Dagianti et al[219] Tawa et al[98]

Djordevic et al[234] San Roman et al[221] Pingitore et al[51] Anthopoulos et al[222] Beleslin et al[117] HG, hand grip.

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150 Dipyridamole, 0.84 mg/kg * 60 Dipyridamole, 0.84 mg/kg * 136 Dipyridamole, 0.84 mg/kg * 60 Dipyridamole, 0.84 mg/kg * 67 Adenosine, 0.17 µg/kg/min + HG 58 Adenosine, 200 µg/kg/min * 102 Dipyridamole, 0.84 mg/kg * 110 Dipyridamole, 0.84 mg/kg + atropine 120 Adenosine, 0.14 µg/kg/min * 168 Dipyridamole, 0.84 mg/kg *

>50

16 (12)

38 (29)

>75

19 (54)

>50

11 (9)

41 (34)

>50

15 (60)

41 (39)

>50

7 (18)

22 (55)

>50

34 (54)

0 (0)

>50

48 (40)

38 (30)

>50

0 (0)

40 (24)

—

>50

* Low-dose positivity permits conclusion of study before stated "peak" dose.

study was interesting on two grounds: First, it implies that dipyridamole identifies fewer mild stenoses than dobutamine echocardiography, and second, it identified angiographic variables of stenosis severity to relate to dipyridamole echocardiographic results better than intracoronary Doppler variables. Other studies have confirmed that the optimal angiographic cutoff point for dipyridamole stress echocardiography is 60%, as compared with 58% for dobutamine and 54% for exercise echocardiography.[117]

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Vasodilator Stress with Adenosine Echocardiography The accuracy of adenosine stress echocardiography is also detailed in Table 14-4 . There is less of an evidence base for this test than for other pharmacologic approaches, and the published data show significant variations in accuracy. The most favorable results may be influenced by a high prevalence of multivessel coronary disease or prior infarction, the sensitivity being only 60% in patients with a normal electrocardiogram.[97] In patients without prior infarction, the sensitivity of this test was less than 60%.[99] The dose and duration of adenosine have an important influence on sensitivity, as does the coadministration of atropine. The accuracy of adenosine echocardiography has recently become the source of considerable interest because of the possibility of combining standard stress echocardiography and assessment of myocardial perfusion, either using contrast echocardiography or coronary flow reserve. Several studies have now shown that the intense coronary vasodilation induced by adenosine permits the comparison 316

of rest and hyperemic images using contrast echocardiography.[118] , [119] Although this comparison is certainly also feasible with dipyridamole,[120] adenosine may be superior. Similarly, coronary flow reserve may be measured at transthoracic or transesophageal echocardiography, using adenosine[121] as a vasodilator. The longer time course and less predictable peak flow with dipyridamole make this a less attractive agent, and if this is selected, high dose is certainly required. [122] Pacing Stress Echocardiography Table 14-5 details the accuracy of studies that have combined atrial pacing with echocardiography. Generally, very favorable results have been obtained with this stress, although the number of studies and patients within studies is still limited. The accuracy of both transesophageal imaging and pacing probably reflects the benefits of high-quality images as much as the role of pacing stress, as similar favorable findings have been obtained using transesophageal echocardiography with dobutamine and dipyridamole, as discussed earlier. The discrepancy between the reported accuracy in contrast with the limited application of the test is striking. Indeed, this became more prominent after

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a recent landmark study[43] found that transesophageal atrial pacing had a high level of feasibility, and safety, duration, and patient acceptance were more favorable than with dobutamine stress echocardiography. Moreover, the tests showed a high level of concordance in inducing regional wall motion abnormalities. Although the lack of clinical uptake for this modality may not appear to be readily understood, the following are important issues that influence our continued use of pharmacologic stress. First, the evidence base for diagnostic, management, and prognostic information using pharmacologic agents is substantially greater than with pacing stress. Second, the pacing test is unlikely to be useful for the detection of viable myocardium, and even when this is not needed from a clinical standpoint (e.g., the patient is not being evaluated for possible revascularization), the biphasic response has been shown to facilitate the distinction of ischemia in the setting of resting wall motion abnormalities. Third, although advances in pacing catheter technology have improved patient tolerance, as documented earlier, most patients and some TABLE 14-5 -- Sensitivity and Specificity of Atrial Pacing Stress Ech Definition Sensitivity: Patients, Feasibility, of CAD, Overall, % Sensi Study N Method % % (n) SVD, Iliceto et al 85 TTE 95 >75 91 (56) 80 (2 [45]

Lambertz 50 et al[42] Zabalgoitia 36 et al[235] Kamp et al 71

TEE

100

>50 93 (41)

85 (2

TEE

90

>70 90 (21)

100 (1

TEE

99

>50 83 (52)

69 (1

TEE

94

>70 86 (20)

—

31

TTE

—

75 92 (26)

—

80

TTE

77

>75 83 (35)

75 (1

65

TTE

69

TTE

[41]

Norris et al 32 [236]

Anselmi et al[237] Marangelli et al[123] Michael et al[238] Schroder

>50 87 52

>50 82 (69)

— 82 (6

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et al[239] SVD, single vessel disease; TEE, transesophageal echocardiography; TTE echocardiography. clinicians look upon the test as being excessively invasive. We believe the test will have several "niche" applications for situations in which dobutamine is unattractive: patients with hypertension or rhythm contraindications to dobutamine, potentially unstable patients (because the stress can be stopped suddenly), or patients with chronotropic incompetence of various causes. Comparison Between Nonexercise Stressors for the Diagnosis of Coronary Artery Disease Selection of the Optimal Pharmacologic Stress

It is clear from Table 14-3 and Table 14-4 that both dobutamine and vasodilator stress echocardiography are effective for the diagnosis of coronary artery disease. However, the relative efficacy of the stressors cannot be assessed by merely comparing the results of individual studies in the literature, because of variations in the study groups. The optimal study design should be based on a head-to-head comparison of the tests in the same patients, under the same conditions, as summarized in Table 14-6 . Such studies have generally demonstrated similar levels of feasibility with dobutamine and vasodilator stress. The sensitivity of dobutamine stress echocardiography has been shown to exceed that of vasodilator stress almost exclusively, although the two are close enough to be considered comparable in several studies. The main source of discrepancy appears to be patients with single-vessel coronary disease, among whom dobutamine appears to be superior to dipyridamole echocardiography. This difference parallels a significantly greater cardiac workload with dobutamine compared with vasodilator stress. As the contraindications to inotropes and vasodilators vary, the selection between them may be individualized; patients with hypertension or arrhythmias should undergo a vasodilator stress, and patients with bronchospasm or conduction disorders should be submitted to inotropic stress. However, in the majority of patients who do not have these contraindications, dobutamine appears to be the most sensitive agent for pharmacologic stress echocardiography, at least for diagnostic purposes.

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317

TABLE 14-6 -- Studies Comparing Sensitivity and Specificity of D Echocardiography Multivessel Myocardial Disease, n Infarction, Sensitivity: S (% All n (% All Dobutamine, Dip CAD) CAD) % 18 (72) — 76 56

CAD, Patients, n Study N (%) Martin et al 40 25 [240] (63) Salustri et al 46 18 18 (64) [152] (39) Marwick et 97 59 28 (47) [99] * al (61) 80 57 33 (58) Previtali et [78] (71) al Beleslin et 136 119 11 (9) [79] al (88) Ostojic et al 150 131 16 (12) [54] (87) Dagianti et 60 25 15 (60) [219] al (42) Anthopoulos 120 89 48 (40) [222] * et al (74) 102 63 34 (54) San Roman [221] (62) et al Loimaala et 60 44 18 (41) [205] al (73) Fragasso et 101 56 37 (65) [241] al (56) CAD, coronary artery disease.

15 (83)

79

82

0 (0)

85

58

15 (26)

79

60

41 (34)

82

74

38 (29)

75

71

41 (39)

72

52

38 (30)

87

66

0 (0)

77

77

0 (0)

93

95

0 (0)

88

61

* Adenosine used instead of dipyridamole.

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Selection of Pacing Rather than Other Nonexercise Stress

Few data are available to evaluate the relative status of pacing in relation to pharmacologic approaches to nonexercise stress testing. A recent comparison of pacing to dipyridamole stress echocardiography in 80 patients with suspected coronary disease and without prior infarction[123] showed the feasibility of the test was less with pacing stress than dipyridamole (77% versus 96%, P < .0001). In patients in whom pacing and dipyridamole testing were feasible, the respective sensitivities were 83% and 43% (P = .0005), and specificities were 76% and 92% (P = NS). Although these favorable results for pacing stress may reflect the inadequacies of dipyridamole echocardiography for diagnostic stress testing, a recent comparison with dobutamine stress echocardiography recently documented[43] that transesophageal atrial pacing showed safety, duration, and patient acceptance results more favorable than those achieved with dobutamine stress echocardiography, with a high level of concordance in inducing regional wall motion abnormalities.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Disease Significance Using Nonexercise Echocardiography In patients with known coronary artery disease, stress imaging procedures are often performed to facilitate clinical decision making, for example, regarding the referral of patients for coronary intervention. The location, extent, and severity of coronary disease can be important in this respect, and all can be determined using nonexercise echocardiography. The use of stress echocardiography for identification of the "culprit" coronary lesion is often constrained by the assumptions inherent in allocating territories of the heart to individual coronary vessels. The most ambiguous areas in this respect are the apex (usually assumed to be within the territory of the left anterior descending coronary artery) and the posterior wall (usually assumed to be supplied by the left circumflex artery). Because of the equivocal involvement of the right coronary or left circumflex vessels in the posterior territory, investigators have examined the ability to discern the presence of coronary disease in the anterior and posterior circulations. Although in the pre-harmonic imaging era the lateral wall was a source of false-negative results, the accuracy of dobutamine echocardiography in each territory appears to be equivalent (Fig. 14-8) . More severe disease in the vessel supplying an ischemic region generally correlates with a more severe wall motion disturbance. Likewise, multivessel disease usually corresponds to extensive areas of ischemia or the development of global ventricular dysfunction, or both, evidenced by poststress reduction of ejection fraction or increase of end-systolic volume, although these are much less common than with exercise, probably because of left ventricular unloading at peak stress. The presence of stenoses in multiple vessels is well known to be predictive of an adverse prognosis in patients with coronary artery disease. Consequently, the recognition of multivessel disease as such may be important in planning revascularization rather than medical therapy. The ability of dobutamine stress

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echocardiography to predict multivessel disease is greatest in patients with a history of previous myocardial infarction, under which circumstances its sensitivity for the correct identification of disease is 80% to 85% and its specificity is 88%.[28] [124] In contrast, the sensitivity for multivessel disease in patients without previous infarction is approximately 70%[28] and exceeds the levels reported in this situation using exercise echocardiography. A close correlation has been demonstrated between the extent of ischemia defined by dobutamine echocardiography and perfusion scintigraphy, although both underestimate the angiographic extent of disease as measured by the Gensini score,[34] a reflection of the difficulties of assessing the functional implications of disease extent on anatomic grounds. In addition to the "space coordinate" (i.e., extent of abnormal segments),[20] another physiologic indication of the extent of coronary disease is the "time coordinate" (i.e., ischemic threshold). Using dobutamine stress, multivessel disease may also be predicted if ischemia has an early onset (similar to the "ischemia-free" time at 318

Figure 14-8 Lateral wall ischemia. Freeze-frame images in the apical four-chamber view demonstrate normal thickening at rest (above), with reduced thickening at peak stress (arrows).

exercise testing), corresponding to its occurrence at a low dose or provocation at a low heart rate and rate-pressure product.[29] [125] Similarly, at dipyridamole stress, ischemia at "standard dose" (0.56 mg/kg) correlates with the presence of multivessel disease, [100] a lower ischemic threshold at exercise testing [126] as well as a worse prognosis (see later discussion). Nonetheless, patients with severe single-vessel disease may also demonstrate an early onset of ischemia, so that this relationship is only an approximate guide to lesion severity.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prognostic Evaluation Using Nonexercise Echocardiography Comparison of the results of nonexercise echocardiography with those of angiography validates the accuracy of these tests for diagnostic purposes and permits comparison with other noninvasive methodologies. The disadvantage of this approach, however, is that the angiographic criteria of stenotic significance are somewhat arbitrary and may not correlate with "physiologic" significance. A less artificial analysis is to use patient outcome to judge the efficacy of testing. Functional testing is commonly used for cardiac risk stratification in various groups of patients, such as those with chronic, stable angina or those who have had a myocardial infarction; for predicting complications at major noncardiac surgery; and in planning which patients should undergo coronary intervention. Prediction of Cardiac Events in Patients Undergoing Major Noncardiac Surgery Coronary artery disease is highly prevalent in patients with vascular disease elsewhere,[127] and cardiac events are the leading cause of perioperative complications at vascular surgery.[128] However, whereas coronary disease and 319

"soft" end points (postoperative unstable angina and heart failure) are frequent in patients with vascular disease, "hard" end points (death, myocardial infarction) occur in less than 10% of patients in the perioperative period, even in the absence of preoperative coronary intervention.[129] As the pretest probability of an event is low, Bayes' theorem would suggest that even if a noninvasive test were positive, the chance of an event would remain small. This explains the low predictive value of a positive test in many previous studies of stress testing in this setting. However, it is also important to remember that severe coronary

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disease is also the major contributor to late deaths after vascular surgery, and the screening of vascular patients for significant coronary disease is important for both perioperative and late risk stratification. The first step in preoperative risk stratification is clinical evaluation.[130] Patients with unstable coronary syndromes within the last 6 months constitute a high-risk group and, if surgery is mandatory, warrant careful functional testing to delineate the extent of jeopardized myocardium and possible intervention preoperatively. Those with previous bypass surgery (within 5 years) or coronary investigations (within 2 years) do not require reinvestigation in the absence of recurrent symptoms. The nature of the planned surgery is important; procedures carrying low cardiac risk such as ophthalmic or laparoscopic surgery should not provoke extensive risk evaluation, whereas vascular, major orthopedic, and major abdominal operations engender significant cardiac risk. Finally, the patient history has an important influence on risk, but the standard anesthetic risk scores[131] have limited applicability among vascular patients, who have greater cardiac risk than the general surgical populations from whom these risk scores were initially obtained. A simple score derived from the patient's age, presence of diabetes, angina, prior infarction, and congestive heart failure has been shown to identify low-risk patients, who do not need further investigation.[132] In a recent series of more than 4300 patients[133] undergoing high-risk surgery, history of ischemic heart disease, congestive heart failure or cerebrovascular disease, insulin treatment, and preoperative serum TABLE 14-7 -- Use of Stress Echocardiography to Predict Events in Patients Undergoing Vascular Surgery

Study Tischler et al[242] Sicari et al [243]

Rossi et al [244]

Predictive Value, % Patients, Events, POSITIVE NEGATIVE Stress N n TEST TEST Even Dipyridamole 109 8 78 99 MI, UAP, CHF Dipyridamole 121 9 25 98 Death MI, UAP Dipyridamole 110 10 100 Death MI,

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Pasquet et al Dipyridamole

129

9

30

97

Dobutamine

57

4

21

100

Dobutamine

60

13

29

93

Eichelberger Dobutamine et al[247] Langan et al Dobutamine

70

5

19

100

74

3

48

100

93

4

74

100

Poldermans Dobutamine et al[250] + atropine

131

15

43

100

Poldermans Dobutamine + atropine et al[251]

181

18

32

100

Poldermans Dobutamine + atropine et al[125]

300

27

38

100

Pellikka et al[252]

Dobutamine + atropine

80

8

29

98

Ballal et al

Dobutamine + atropine

233

8

all rvs

96

[136]

Lane et al [245]

Lalka et al [246]

[248]

DavilaDobutamine Roman et al + atropine [249]

[253]

UAP Death MI, UAP Death MI, CABG Death MI, UAP MI, UAP MI, AP, CABG MI, UAP, CABG Death MI, UAP, CHF Death MI, UAP, CHF MI, AP, LVF Death MI, UAP, CHF Death MI, UAP

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AP, angina pectoris; CABG, coronary artery bypass graft surgery; CHF, congestive heart failure; LVF, left ventricular failure; MI, myocardial infarction; UAP, unstable angina pectoris. creatinine level greater than 2.0 mg/dL were markers of risk; patients with none, one, two, or three or more of these factors had major cardiac complication rates of 0.4% to 0.5%, 0.9% to 1.3%, 4% to 7%, and 9% to 11%, respectively. It is important to keep in mind that patients with vascular disease are often inactive and are usually asymptomatic even in the presence of significant coronary disease. For patients at intermediate risk, stress imaging techniques with nonexercise stressors are required if screening is to be undertaken, as limitations of their exercise capacity render exercise testing approaches inadequate for the diagnosis of coronary artery disease, and the low sensitivity of pharmacologic stress electrocardiograms mandates the use of an imaging test. The relative availability and low cost of stress echocardiography, along with the potential for combining this approach with nonexercise stress, makes this an attractive technique for preoperative risk stratification. Table 14-7 shows that both dipyridamole and dobutamine stress echocardiography are effective for this purpose. The predictive value of a negative test is very high (usually greater than 90%), but as is the case with perfusion scintigraphy, the predictive value of a positive test is intermediate, varying from 20% to 70%. This value may be further stratified by paying attention to the ischemic threshold and the clinical risk factor status (Fig. 14-9) (Figure Not Available) . Clearly, the occurrence of cardiac events at the time of surgery does not only relate to the presence of coronary stenoses but is also modulated by medical treatment and anesthetic intervention. Only a handful of studies have compared stress echocardiography with single photon emission computed tomography (SPECT) for the prediction of perioperative cardiac events. From a meta-analysis of published work with dobutamine echocardiography and SPECT (mainly with dipyridamole stress), Shaw et al[134] concluded that the tests had comparable levels of accuracy but that cost features weighed in favor of echocardiography. A direct comparison by the group in Liege, Belgium showed the techniques to have similar prognostic value,[135] but another 320

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Figure 14-9 (Figure Not Available) Evaluation of risk in patients undergoing vascular surgery. Patients without clinical predictors of risk rarely have a positive dobutamine study (DSE), are unlikely to suffer events, and usually do not require testing. The presence of ischemia is predictive of events, especially if the patient has multiple clinical risk factors or a low ischemic threshold. MI, myocardial infarction; neg, negative; pos, positive; preop, preoperative. (From Poldermans D, et al: J Am Coll Cardiol 1995;26:648–653.)

comparison by a different Belgian group showed echocardiography to be significantly more specific than SPECT.[136] Prognostic Evaluation of Patients with Stable Coronary Disease Although the frequency of major cardiac events is low in stable chronic coronary disease (less than 1% per year), risk stratification is an important aspect of these patients because some have been shown to have a more favorable prognosis with intervention. The detection of left main or multivessel disease at coronary angiography is often used to identify subgroups likely to benefit from revascularization, but this procedure is too costly and invasive to be used for prognostic evaluation of all patients. As in the case of preoperative risk stratification, clinical data (including the severity of angina, prior infarction, heart failure, and diabetes) may identify high- and low-risk subgroups,[137] [138] and additional investigations are of most value in those at intermediate or greater risk. Exercise capacity and ST segment depression at exercise testing offer important prognostic information in patients who are able to exercise,[139] [140] and exercise SPECT [141] or exercise echocardiography have been shown to provide incremental data in some patients.[142] In those patients who are unable to exercise, pharmacologic stress echocardiography is a useful prognostic tool (Table 14-8) . The detection of ischemia at pharmacologic stress echocardiography has been shown to be an independent predictor of adverse outcomes, incremental to clinical and resting echocardiographic data. During dipyridamole stress, cardiac events occurred in 41% of patients with wall motion abnormalities occurring at low dose and 26% of those with high-dose responses (a reflection of the prognostic importance of ischemic threshold). Even in patients with known exercise electrocardiographic and coronary angiographic data,[143] ischemia at dipyridamole echocardiography was a better predictor of cardiac events (relative risk, 1.9) than either coronary stenoses or age (relative risks, 1.3 and 1.0, respectively). Similar data have been gathered during dobutamine stress testing (see Table 14-8) . The prognostic value of pharmacologic stress appears to be preserved within various subgroups, including

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hypertensive patients.[144] Few data have been gathered regarding comparisons between the stressors. Dobutamine and dipyridamole have been shown to offer effective and comparable efficacy of risk stratification in patients at low to moderate risk of cardiac events.[145] The prognostic content of stress echocardiography seems to be similar to that of SPECT.[146] The prognostic components of both tests include the presence, severity, and extent of induced ischemia. Perhaps the most important aspect of the prognostic literature is that a negative test portends extremely low risk, evidenced by an event rate of 1% or less per year. Prognostic Evaluation of Patients after Myocardial Infarction The frequency of cardiac events in the first year after myocardial infarction exceeds that in patients with chronic stable angina. Although clinical features such as age and the presence of heart failure should be used in the initial stratification of patients, the amount of infarcted and 321

TABLE 14-8 -- Use of Stress Echocardiography to Predict Events in Patie with Chronic Stable Coronary Disease Predictive Value, % Mean Patients, Follow- POSITIVE NEGATIVE TEST Comm Study Stress N up, mo TEST 51 24 68 77 High ri Mazeika et Dobutamine [254] al 77 10 50 87 Afridi et al Dobutamine [255]

Poldermans et al[256] Kamaran et al[257] Marcovitz et al[258] Schroder et

Dobutamine

430

17

26

87

Dobutamine

210

16

43

92

Dobutamine

291

15

10–17

99

Dobutamine

134

19

31

94

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al[259] Steinberg et al[260]

Pagina 7 di 8

Dobutamine

Senior et al Dobutamine

120

60

67

67 All eve

13 121

15

45

95 Hard events 88

860

52

14

96

13

—

1659

36

8–20

539

36

26

539

36

41

94

134

19

27

92

[261]

Chuah et al Dobutamine [262]

Davar et al Dobutamine

72 F

[263]

Poldermans Dobutamine et al[264] Picano et al Dipyridamole [144] (high dose) Dipyridamole (low dose) Schroder et Dipyridamole al[259]

100 Norma studies 96 Hard events 94

residual ischemic myocardium are major determinants of outcome that cannot be quantified clinically. Previously, the techniques used for this purpose included the exercise electrocardiogram, resting echocardiography, nuclear ventriculography, and thallium imaging. In a comparison of these alternatives,[147] the optimal approach for prediction of postinfarction complications was shown to be thallium imaging and nuclear ventriculography. Stress echocardiography, however, offers a means of replacing these two tests with one. Ischemia may be assessed as homozonal dyssynergy (peri-infarct ischemia) or heterozonal dyssynergy (multivessel disease), and infarction may be estimated from the resting wall motion score index. Exercise testing offers prognostically important adjunctive data on functional capacity. However, the majority of the postinfarction stress echocardiography literature (Table 14-9) concerns pharmacologic stress studies for three reasons: first, nonexercise studies are useful in patients who cannot exercise; second, they are useful for assessment of myocardial viability (see later discussion); finally, they provide an opportunity for

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obtaining a near-maximal stress reading early in the patient's admission, before many patients and physicians feel comfortable about performing maximal exercise stress testing. The last aspect is perhaps the most important, as early risk evaluation may identify at-risk patients before the occurrence of an event, permitting a reduction in hospital length of stay for low-risk patients and justifying angiography and possible intervention in those at higher risk. Both pharmacologic and atrial pacing stress tests have been used for risk assessment after myocardial infarction. All have proven to be effective for the detection of multivessel disease[124] [148] [149] and predictive for the subsequent development of cardiac events. Although atrial pacing is very safe (as the stress may be terminated instantly), it remains invasive and uncomfortable, and the pharmacologic techniques are best validated for this purpose. Moreover, the use of pharmacologic stress permits evaluation of myocardial viability, the detection of which has important implications for revascularization decisions. Table 14-9 summarizes the prognostic implications of positive and negative nonexercise stress echocardiography in patients after infarction. With dipyridamole stress echocardiography, the presence of ischemia and its time of onset are important predictors of cardiac events[150] in elderly patients, ischemia was an independent predictor of mortality.[151] An equivalent evidence base has been reported with dobutamine in the postinfarct period.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Therapy Using Nonexercise Echocardiography Medical Therapy In contrast to myocardial perfusion scintigraphy, the identification of ischemia with stress echocardiography is dependent on the development of ischemia. This is a disadvantage to the extent that antianginal therapy reduces the sensitivity of stress echocardiography, particularly when dipyridamole stress is used.[115] Patients on beta blockers account for most patients who fail to attain a heart rate greater than 85% of age-predicted maximum. With dobutamine echocardiography, the interaction between dobutamine and beta blockers involves competitive inhibition, and if enough dobutamine is administered, this effect may be overcome, leading several studies to suggest that concurrent drug therapy has no effect.[152] Atropine can be used to enhance the sensitivity of dobutamine stress testing, without reducing specificity or inducing serious side effects. The interaction between medical therapy and the development of ischemia may be of use in evaluating the adequacy of therapy.[153] [154] Although some data are being gathered with exercise echocardiography, the role of nonexercise stress remains largely unexplored. [155] In large part, this lack of data reflects the subjectivity of wall motion scoring, and use of stress echocardiography should become more feasible with a truly quantifiable approach. Follow-up after Coronary Interventions After angioplasty and bypass surgery, recurrent symptoms of chest discomfort may result because of restenosis 322

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TABLE 14-9 -- Application of Nonexercise Stressors to Post

Patients, FollowStudy Year N Timing Stress up, mo Outcomes Iliceto[44] 90 83 <3 wks Atrial Pacing 14 Reinfarction, angina Res * 95 69 3–5 Atrial Pacing 12.6 Cardiac death, days reinfarction, revascularizatio 217 Dipyridamole 24 Cardiac death Bolognese 92 [202]

Sclavo †

92

103 5–8 days

Dipyridamole 14.5

Picano[49] 93 Chiarella ‡ 94

925 10 days Dipyridamole 251 70 hrs Dipyridamole

Picano § 95 Neskovic 95

1080 10 days Dipyridamole 93 2–3 Dipyridamole wks

Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death

Cardiac death, reinfarction Cardiac death, reinfarction, angina 14 Cardiac death 13 days Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina 14 Reinfarction 16 Cardiac death Cardiac death,

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Sclavo ¶

Pagina 3 di 4

97

Lanzarini 96

60 3–4 days

Dipyridamole 15

41 8 days Dobutamine

7.5

[129]

Carlos £

97

214 2–7 days

Sicari[166]

97

778 12 days Dobutamine

9

Greco

97

178 12 days Dobutamine

17

Previtali

98

152 9 days Dobutamine

15

Dobutamine

>12

reinfarction Cardiac death, reinfarction, angina Cardiac death, reinfarction, angina, revascularizatio Reinfarction, angina, revascularizatio Cardiac death, reinfarction, angina, ventricular tachycardia, congestive hea failure Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death

[30]

Cardiac death, reinfarction Cardiac death, reinfarction,

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Picano[237] 98

Pagina 4 di 4

314 12 days Dobutamine

9

angina Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina

* Res et al: Am J Cardiol 1995;76:1112–1114 † Sclavo et al: Eur Heart J 1992;13:1348–1355 ‡ Chiarella et al: Eur Heart J 1994;15:842–850 § Picano et al: J Am Coll Cardiol 1995;26:908–913 Neskovic et al: Am Heart J 1995;129:31–39 ¶ Sclavo et al: G Ital Cardiol 1997;27:1000–1007 £ Carlos et al: Circulation 1997;95:1402–1410 Greco et al: J Am Coll Cardiol 1997;29:261–267

and graft closure, respectively. Because angioplasty is most often performed for single-vessel disease, routine exercise testing is usually considered to be insensitive for the diagnosis of restenosis, and exercise echocardiography or exercise myocardial perfusion imaging are often performed. Pharmacologic stress echocardiography performed before and after angioplasty has been shown to predict resolution of ischemia using dipyridamole[156] [157] and dobutamine stress.[158] [159] If the patient cannot exercise, pharmacologic stress echocardiography can be used effectively for the diagnosis of restenosis,[160] [161] the sensitivity being significantly greater than that of the stress electrocardiogram.[162] Similarly, after bypass surgery, stress imaging tests are usually obtained for diagnostic purposes (because the resting eletrocardiogram is often nondiagnostic). Exercise echocardiography has been shown to be accurate in this context, and if the patient cannot exercise, pacing or pharmacologic stresses can reasonably be used.[163] [164] The major application of echocardiography and perhaps stress echocardiography after revascularization, however, is to assess the improvement of dysfunctional but viable myocardium.[165]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Myocardial Viability Using Nonexercise Echocardiography Clinical Significance Left ventricular dysfunction after myocardial infarction is due not only to loss of myocardium but also to stunned and hibernating myocardium. Stunned myocardium shows spontaneous resolution of dysfunction,[166] but hibernating tissue requires myocardial revascularization to 323

resume normal function.[167] [168] Myocardial revascularization in patients with viable myocardium may be indicated to improve cardiac function or overall functional capacity, as well as to avoid subsequent cardiac events from this inherently unstable tissue. Thus, clinical decisions about whether to revascularize, which vessel to revascularize, and how to do it may be influenced by the detection of viable myocardium. In the following section, evaluation of the accuracy of various tests for the identification of viable myocardium is based on recovery of function after myocardial revascularization. This criterion is an imperfect gold standard, being influenced by the adequacy of revascularization, bypass graft closure, and restenosis, but it has the attraction of having direct clinical relevance. By this criterion, conventional techniques used for the detection of myocardial scar and viability (Q waves on the electrocardiogram, regional left ventricular dysfunction at ventriculography, and "fixed" perfusion defects at conventional scintigraphic procedures) have been found to be inaccurate. More accurate alternatives include position emission tomography and thallium scintigraphy using rest-redistribution or stressredistribution-reinjection protocols, both of which have a high negative predictive value.[169] A positive test result is less predictive of functional recovery, however, probably manifesting the sensitivity of these tests for

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small regions of viable myocardium that may not be able to contribute to regional function when revascularized. The use of dobutamine and dipyridamole stress echocardiography to detect viable myocardium has a large evidence base and is now part of standard practice. Use of Dobutamine Echocardiography for the Diagnosis of Viable Myocardium Administration of sympathomimetic agents (such as isoproterenol, dopamine, and dobutamine) has been shown to reverse postischemic left ventricular dysfunction.[170] [171] [172] [173] The typical response of viable myocardium is to increase thickening in response to low doses of dobutamine; in the presence of a stenosed infarct-related artery, function subsequently deteriorates as the tissue becomes ischemic. Indeed, there is a balance between the recovery of function and the development of ischemia, and, at least in theory, the development of ischemia may compromise the functional recovery of areas that are marginally perfused at rest. The highdose response (>20 µg/kg/minute) has been shown to be a less reliable predictor of recovery.[8] Although some investigators start at lower doses, or use only a low-dose protocol for the assessment of viability, and others use 5-minute rather than 3-minute increments, [174] there does not appear to be a clear benefit in favor of any of these alternatives. Dipyridamole has been shown to enhance both segmental shortening and load-independent indices of ventricular function in stunned myocardium.[175] The mechanism of this phenomenon is unclear, but a "local Frank-Starling response" (whereby augmentation of myocardial blood volume leads to increased sarcomere separation) appears to be the most likely explanation. Additionally, an indirect sympathomimetic response to dipyridamoleinduced ischemia may contribute to improvement of regional function, as may resolution of ischemia secondary to improvement of coronary perfusion. Dipyridamole appears to be an effective alternative in low-dose and "infra-low-dose" protocols[176] the choice of agent is dependent on local expertise and preference. The interpretive criteria are similar, irrespective of the stressor. Viable segments are characterized by reduced resting function, which augments in response to low-dose dobutamine (usually 7.5 to 10 µg/kg/minute). There is continued augmentation if there is a patent infarct-related artery or the tissue is well collateralized. In the presence of a stenosed infarct-related artery, an increasing proportion of segments become ischemic at dobutamine doses greater than 10 µg/kg/minute.[177] This initial

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improvement followed by deterioration in function constitutes the "biphasic response," which is strongly predictive of eventual functional recovery of the tissue.[177] A uniphasic response is less predictive of recovery, and a classic ischemic response is not very predictive of the recovery of resting function. Because the biphasic response is the most reliable finding (Fig. 14-10) , our preference is to induce ischemia whenever possible by proceeding to maximal stress (i.e., 40 µg/kg/minute dobutamine with or without atropine), rather than using a discreet "viability" or low-dose protocol. In patients with severe left ventricular dysfunction, this approach warrants caution, and early termination may be needed if ischemia is progressive or if other responses might induce instability. Finally, viability studies are the most difficult to interpret, and we commonly use both digital display, including doses of both 5 and 10 µg/kg/minute, and videotape for review of the study. The response of regional function to dobutamine is influenced by the extent of viable tissue, the degree of residual stenosis, the extent and magnitude of collateral vessels, the size of the risk area (which influences tethering), and the presence of drug therapy,[178] of which the extent of viable tissue and perfusion warrant further attention. The uniphasic response is an ambiguous signal that may be caused by part of the wall mounting a dobutamine response (i.e., admixture of scar and normal tissue) or all of the wall mounting a partial response (i.e., viable myocardium). The ability to discriminate the extent of subendocardial damage, with its implications for the likelihood of subsequent functional recovery, is poor. With respect to perfusion, augmentation of function is dependent on delivery of more substrate; thus, tissue supplied by more severe stenosis may become ischemic before it augments function. This may compromise the recognition of viability. The accuracy of dobutamine for prediction of regional functional recovery is summarized in Table 14-10 , although there is a large evidence base, most studies are relatively small and derive from expert centers. The overall sensitivity of dobutamine (approximately 80%) appears greater than that of dipyridamole stress (approximately 60%), although the specificity of the former is less (78% vs. 87%). Moreover, the nuclear approaches are more sensitive but less specific than these echocardiographic techniques.

324

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Figure 14-10 Apical four-chamber diastolic (right) and systolic (left) views at rest (top), with low-dose dobutamine (middle), and with peakdose dobutamine (below), illustrating a "biphasic" response to dobutamine stress (reduced systolic thickening at rest, increment with low dose, and deterioration at peak dose) in the lateral wall.

Prediction of Recovery of Global Function and Outcome Improvement of left ventricular function within individual segments is not usually the goal of revascularization, whereas improvements in ejection fraction, exercise capacity, and outcome are therapeutic goals. Recent work has sought to address the ability to predict these parameters. Stress echocardiography can be used to predict improvement of global left ventricular function after revascularization. Cornel et al[179] has reported an 89% sensitivity and 81% specificity for prediction of a significant (5%) improvement in ejection fraction, using a cut-off point of 4 of 16 viable (biphasic) segments at dobutamine echocardiography. Similarly, the global ventricular response to low-dose dobutamine is a strong predictor of global functional recovery.[180] Other factors clearly influence the likelihood of recovery, including an inverse relationship with the number of thinned and akinetic segments or ventricular volumes. [181] The revascularization of patients with adequate amounts of viable myocardium (usually >25% of left ventricular mass) is associated with improved functional class. The presence of viable myocardium may influence outcome in two ways. First, revascularized viable tissue may lead to improved function and thereby improved outcome.[182] Second, non-revascularized viable tissue may be unstable and act as a substrate for recurrent events,[183] including mortality.[184] These outcomes have not been reported in all series,[185] probably because of heterogeneity in populations studied and responses; for example, a uniphasic response early after infarction may be a benign finding.

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New Technologies that May Solve Limitations of Stress Echocardiography Image Quality Although perfect image quality is certainly not essential for a stress echocardiographic study to be interpretable, 325

TABLE 14-10 -- Sensitivity and Specificity of Dobutamine Echocardiogra for Identification of Myocardial Viability (Segmental Analysis) * Study Pierard †

Stress Dobutamine

Smart * [8]

Dobutamine

Previtali[30]

Dobutamine

Cigarroa ‡ Marzullo[275] Alfieri § Watada

Dobutamine Dobutamine Dobutamine Dobutamine

La Canna ¶ Dobutamine Dobutamine Charney[276] Perrone-Filardi Dobutamine

Patients, Sensitivity, Specificity, N % (n) % (n) Comm 17 83 (6) 73 (8/11) Early p MI 51 86 (22) 90 (26/29) Early p MI 42 79 (63) 70 Early p (109/158) MI 25 82 (11) 86 (12/14) 14 82 (49) 92 (24/26) 14 91 (93) 78 (25/32) 21 83 (66) 86 (43/50) Early p MI 33 87 (205) 82 (89/109) 17 71 (31) 93 (27) 18 88 (48) 87 (27/31)

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£

Afridi Arnese[70]

Dobutamine Dobutamine

20 74 (38) 38 74 (33)

Senior[110] Bolognese[202]

Dobutamine Dobutamine

45 87 (45) 30 89 (27)

73 (55/76) 95 (130/137) 82 (123) 91 (45)

Poli #

Dobutamine

51 72 (78)

68 (176)

Dipyridamole

51 51 (78)

82 (176)

40 40 36 73

40 79 (73)

94 (133) 94 (133) 63 (65) 86 (238/277) 83 (36)

53 69 (32) 86 (50) 30 89 (62) 18 68 (46)

100 (26) 57 (46) 82 (106) 83 (63)

Varga[10]

Dipyridamole Dobutamine Dobutamine Bax[283] Vanoverschelde Dobutamine

78 (40) 76 (40) 85 (27) 76 (167)

[285]

Perrone-Filardi Dobutamine

Early p MI Early p MI Early p MI

[282]

Furukawa[67] Cornel[87] Nagueh[279]

Dobutamine Dobutamine Dobutamine Dobutamine

Total

Dobutamine Dipyridamole

Akinet Hypok Biphas respon

726 81 78 (1065/1312) (1401/1796) 91 60 (71/118) 87 (269/309)

MI, myocardial infarction. * Average ejection fraction approximately 35%. † Pierard et al: J Am Coll Cardiol 1990;15:1021–1031 ‡ Cigarroa et al: Circulation 1993;88:430–436 § Alfieri et al: Eur J Cardiothoracic Surgery 1993;7:325–330 Watada et al: J Am Coll Cardiol 1994;24:624–630 ¶ La Canna et al: J Am Coll Cardiol 1994;23:617–626 £ Perrone-Filardi et al: Circulation 1995;91:2556–2565

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Afridi et al: Circulation 1995;91:663–670 # Poli et al: Heart 1996;75:240–246

it certainly favors concordance between observers[73] and facilitates an accurate diagnosis of disease extent and distinction of ischemia and scar. Major improvements in image quality obtained from harmonic imaging have translated into improvements in the accuracy of stress echocardiography.[58] Likewise, the use of contrast echocardiography may facilitate delineation of the endocardial border; the implications of this finding are addressed in another chapter. Quantitative Approaches to Interpretation As mentioned earlier, the current qualitative algorithm for interpretation of stress echocardiograms requires a significant level of expertise on the part of the observer. A less subjective means of interpretation would be attractive on the grounds of feasibility and reproducibility. Either semiquantitative or fully quantitative strategies of examining wall motion can be used to evaluate global and regional left ventricular function. Global indices (ejection fraction or end-systolic volume) are insensitive to milder degrees of ischemia and are not an answer to the shortcomings of qualitative interpretation. Wall motion scoring offers a semiquantitative regional approach, which may improve the reproducibility of observers, but this does not constitute a major deviation from the regional approach used by most experienced readers and does not measure function independent of the observer. True quantitation of regional function may be based on following either radial or longitudinal myocardial motion (see Chapter 5) . The simplest approach involves tracing of endocardial (and for some methods, epicardial) interfaces and their superimposition using a fixed or floating reference system and measurement of endocardial excursion or myocardial thickening. Historically, this approach has been limited by three major technical limitations, but recent developments have addressed some of these limitations. First, excellent border definition of both endocardium and epicardium (especially in the apical views) was obtainable in less than 50% of images, but harmonic imaging has improved image quality substantially, and contrast echocardiography may also be of value. Second, failure to

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compensate for rotational or translational cardiac movement may be associated with false-positive results, but correction for movement of the heart may also compromise sensitivity. A postprocessing approach (using color-enhanced digitized cine-loops) may be used to correct translational movement.[186] Third, the 326

process of tracing multiple systolic and diastolic frames is tedious, timeconsuming, and unattractive for clinical practice. However, recent developments in edge-tracking have led to automated programs for measuring endocardial excursion. Along similar lines, Perez has developed an online quantification of ventricular function during dobutamine echocardiography using acoustic quantification.[187] The feasibility and accuracy of this approach has now been documented in several studies[188] [189] (Fig. 14-11) (Figure Not Available) . Myocardial tissue Doppler may provide another means of quantifying regional function. A unique aspect of this approach is that it can be used to quantify motion in the longitudinal (base-apex) direction, which corresponds to the contribution of longitudinal subendocardial muscle fibers.[190] Tissue Doppler measurements can be obtained using color or pulsed wave modalities to gather peak velocity and timing parameters. Pulsed wave Doppler, although useful for resting imaging,[191] is less feasible during stress because of the need to acquire all values online within a limited time at peak stress. Tissue velocity profiles within each segment of a color myocardial Doppler image may be obtained by postprocessing, but this requires a high frame-rate (at least 80 to 100 frames per second) to ensure that true peak systolic velocity is captured (Fig. 14-12) . The development of ischemia causes a reduction of peak velocity and transmyocardial velocity gradient and a delay in the development of peak velocity, of which the first is the most reproducible. Peak velocity has been shown to correlate with wall motion interpretation[192] [193] and ischemia with dual isotope SPECT.[194] More recently, normal ranges at peak stress have been described, and these ranges have been applied to the identification of angiographically defined coronary disease, [195] providing comparable accuracy to an expert reader. This technique presents some unresolved problems; it appears to be more amenable to dobutamine than exercise stress, and further efforts are needed to remove the contribution of translational movement.

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Another quantitative approach that is independent of edge detection is the analysis of myocardial backscatter. Cyclic variation of backscatter has been shown to change during ischemia,[196] [197] but, until recently, backscatter analysis was strictly a research technique that was dependent Figure 14-11 (Figure Not Available) (color plate.) Color kinesis images with color coding showing sequential frames in systole and diastole in short-axis and apical fourchamber views. The graphics express regional fractional area change in each segment. (From Mor-Avi V et al: Circulation 1997;95:2087–2097.)

on the ability to export and process voluminous raw data from the echocardiography machine. Recent developments in computer technology, especially storage, have made this approach more feasible,[198] although whether it can be incorporated into clinical imaging remains to be seen. Stress Doppler Echocardiography Stress Doppler echocardiography has been used to examine systolic or diastolic blood flow alterations caused by ischemia. Unfortunately, because compensatory hyperkinesis of the nonischemic wall tends to preserve overall ventricular function, changes in stroke volume occur mainly in the presence of extensive ischemia,[199] and stress-induced alterations in global cardiac function are not specific for coronary disease. The development or worsening of mitral regurgitation on color flow mapping (which may explain the occurrence of dyspnea disproportionate to the severity of coronary disease) is another systolic parameter that may be predictive of ischemia during dobutamine stress testing,[33] but the frequency of this finding is low,[200] as vasodilation at peak dobutamine dose tends to reduce left ventricular cavity size and therefore regurgitation. Left ventricular relaxation is an active process that may be altered by the development of myocardial ischemia. These changes can be examined by transmitral flow measurements of the peak E and A wave velocities, E/A ratio, E wave deceleration time, diastolic time intervals, and flow-velocity integrals of passive and active flow.[201] Unfortunately, tachycardia causes the E and A waves to merge at higher heart rates. Nonetheless, reductions in passive left ventricular filling (probably reflecting impaired relaxation secondary to ischemia) have been correlated with ischemia during dobutamine stress echocardiography.[202] The same pattern has been recorded with other stressors that provoke ischemia without tachycardia, such as dipyridamole and pacing with cessation after the development of ischemia.[203] Unfortunately, however, the effects of ischemia (delayed

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relaxation) may be pseudonormalized by ischemia-induced increases in left atrial pressure (Fig. 14-13) . Tissue Doppler assessment may be of value in 327

Figure 14-12 (color plate.) Importance of high frame-rate to tissue Doppler velocity. Doppler velocity profiles are shown in the same segment at different frame-rates. A high frame-rate (>100 frames per second [f/s]) is necessary to obtain the true peak velocity as well as timing variables.

examining regional diastolic function with less influence from left atrial pressure. [204] Changes of diastolic function in response to stress are not specific for ischemia, however, and may be induced by left ventricular hypertrophy, for example.

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Alternatives to Nonexercise Stress Echocardiography Exercise Stress Echocardiography Nonexercise stress approaches are invaluable in patients who are unable to exercise maximally. Attempts to use exercise stress in such patients are attended by suboptimal sensitivity, and this is true also of isometric exercise. [205] Pharmacologic stressors have also been used in patients who are able to exercise, among whom the results of Figure 14-13 Development of a pseudonormal pattern, probably due to ischemia-induced increment in left atrial pressure. This patient with resting left ventricular dysfunction developed extensive ischemia by wall motion assessment. However, there is an increment of E wave velocity and shortening of the deceleration time, rather than development of a delayed relaxation pattern.

exercise and pharmacologic techniques can be compared. Table 14-11 summarizes several studies that compared exercise and nonexercise stress echocardiography on a "head-to-head" basis. Most studies have shown no significant differences in sensitivity or specificity between exercise and nonexercise stress echocardiography. Some of these comparisons have suggested that the nonexercise technique has greater feasibility, although this may be colored by greater expertise in pharmacologic than in exercise echocardiography at some centers. However, several of these comparisons have involved designs that do not replicate the usual clinical scenario, such as exclusion of patients with technically difficult studies, as well as cessation of antianginal therapy before the test. The latter may have an important influence on this analysis; in one comparison of dobutamine and exercise echocardiography, the sensitivity of dobutamine stress was significantly less than that obtained with bicycle exercise in patients who

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were treated with beta receptor blockers, or who failed to complete the dobutamine protocol because of the development of side effects. Interestingly, among the patients with coronary disease in whom both tests were positive, the extent of ischemia was reliably greater with exercise than with dobutamine, reflecting the greater cardiac workload imposed by exercise. This more extensive ischemia may lead the observer to be more confident in the results of exercise than dobutamine stress testing, despite the image quality being better with dobutamine. The advantages of pharmacologic approaches are feasibility, better image quality, and ability to image the heart during stepwise increments of stress as well as at peak stress. These are balanced by a number of considerations that favor the use of exercise stress in those who can perform it. Exercise stress testing provides a greater level of stress on the heart, renders electrocardiographic data useful (the results of which are less useful with pharmacologic stressors), and gives results regarding functional capacity and data about stress that are readily extrapolated to everyday life. Exercise also offers important prognostic 328

TABLE 14-11 -- Sensitivity and Specific

Study Picano et al[265]

Myocardial CAD Multivessel, Infarction, Patients, CAD, Diameter, n (% all n (% all N n % CAD) CAD) EXERCI 55 34 >70 18 (53) 6 (18) 76

Hoffman et al[81]

66

50 >70

21 (42)

0 (0)

80

Cohen et al[76]

52

37 >70

21 (57)

11 (30)

78

136

119 >50

11 (9)

41 (34)

80

Beleslin et al[79]

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Marangelli et al[123]

60

35 >75

19 (54)

—

89

Marwick et al[77]

86

56 >50

34 (61)

0 (0)

88

Dagianti et al[219]

60

25 >70

15 (60)

0 (0)

76

Rallidis et 85 85 >70 [266] al CAD, coronary artery disease.

40 (47)

42 (49)

77

329

data. Based on these considerations, exercise echocardiography appears to offer more data than the nonexercise approaches, and we limit the use of exercise-simulating techniques to patients who are unable to perform maximal exercise. However, the new techniques that are adjunctive to stress echocardiography (for example, contrast, tissue Doppler, and acoustic quantification echocardiography) are more easily performed in the stationary patient and may lead to an increase in the number of nonexercise studies in the future. Stress Electrocardiography In the current medical-economic climate, much attention is being paid to using less expensive diagnostic and therapeutic methodologies. Because stress electrocardiography is substantially less expensive than stress imaging tests, it might be considered as an alternative to stress echocardiography. In this respect, it is important to differentiate between the stress electrocardiographic component of the pharmacologic tests and

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the exercise electrocardiogram. The latter is an option only if the patient can exercise maximally, and in this situation, both dobutamine and dipyridamole stress echocardiography are as sensitive as or more sensitive than the exercise electrocardiography. Nonetheless, the discussion suggests that if the patient can exercise, the choice should be between the exercise echocardiogram and the exercise electrocardiogram. If the use of nonexercise stress is restricted to patients who cannot exercise, there is little to recommend the use of the pharmacologic stress electrocardiogram, which has poor sensitivity for the diagnosis of coronary artery disease, even if the standard exercise electrocardiographic criteria are altered for use with nonexercise approaches. Although this test should not be performed in isolation, the presence and characteristics of ischemic electrocardiographic changes add useful information about the severity and prognostic implications of an abnormal stress echocardiogram.[206] TABLE 14-12 -- Comparison of Pharmacologic Stress Echocardiography Coronary Arte Patients, Study N Stress 25 Adenosine Nguyen et [267] al Amanullah 40 Adenosine [268] et al Marwick 97 Adenosine [99] et al Marwick 217 Dobutamine [99] et al Forster et 21 Dobutamine [269] al Gunalp et 19 Dobutamine [270] al 61 Dobutamine Senior et [216] al Ho et al[271] 54 Dobutamine Huang et 93 Dobutamine

Sensitivity, % NUC ECHOCARDIOGRAPHY IMA 60 90

Dose 0.14 mg/kg/min 0.14 74 mg/kg/min 0.18 58 mg/kg/min 40 µg 72

94 86 76

40 µg + atropine 30 µg

75

83

70

90

40 µg

93

95

40 µg 40 µg

93 93

98 90

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al[126] Santoro et al[272] San Roman et al[273] Perin et al [274]

Simonetti et al[232] Santoro et al[272] San Roman et al[273]

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60 Dobutamine 40 µg

61

91

102 Dobutamine 40 µg + atropine

78

87

25 Dipyridamole 0.56 mg/kg 35 Dipyridamole 0.84 mg/kg 60 Dipyridamole 0.84 mg/kg 102 Dipyridamole 0.84 mg/kg

58

95

86

91

55

97

81

87

Pharmacologic Stress Echocardiography versus Perfusion Scintigraphy Thallium (or technetium MIBI) imaging has the advantage of being the most widely used imaging technique for the noninvasive diagnosis of coronary artery disease and is technically easier to perform and interpret than is stress echocardiography. However, nuclear imaging has disadvantages pertaining to specificity, cost, and inconvenience to the patient. As there is a substantial variation in the reported accuracy of both stress echocardiography and nuclear imaging, based on variations in the population studied, the relative accuracies of each test can only be addressed by direct comparison in the same patient population. The relative abilities of the tests to deal with the diagnosis of coronary disease, identification of viable myocardium, and prognostic assessment are discussed separately. Bearing in mind the preceding discussion regarding the selection of patients for nonexercise stress, this discussion is confined to patients who are for some reason unable to exercise. Diagnosis of Coronary Artery Disease

Several studies focusing on the comparison of stress echocardiography and scintigraphy using dipyridamole, adenosine, dobutamine, or atrial pacing stress for the diagnosis of coronary disease have been published (Table 14-

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12) . The concordance rates between scintigraphy and echocardiography for the presence or absence of disease range from 80% to 90% in most studies. There are several pertinent points in the interpretation of this literature. First, it is important to have a reference standard (coronary angiography) to judge which test is "wrong" if the results are discordant, despite the inherent selection bias that this design produces toward studying patients with more severe disease, as well as the imperfections of using angiography as the arbiter of disease. Second, because both techniques may be technically demanding and require 330

considerable interpretive skill, studies coming from centers with expertise in one or the other are unlikely to be meaningful. The corollary of this observation is that for the choice even to be considered routine practice, high-quality nuclear and echocardiographic laboratories should be available; if a center has expertise in only one methodology, the alternative should not be considered. Simply put, good scintigraphy is always better than poor stress echocardiography and good stress echocardiography is always better than poor scintigraphy. Using dobutamine or pacing stress, the sensitivities of both tests for the identification of coronary artery disease are comparable, with most studies showing slightly greater sensitivity with scintigraphy (see Table 14-12) . This difference is most evident in patients with single-vessel disease,[207] a finding that might be expected from the identification of flow heterogeneity with perfusion imaging, which is an earlier event in the ischemic cascade than regional dysfunction, identified by echocardiography. For the same reason, antianginal therapy influences the results of echocardiography because it prevents the development of ischemia[115] but does not influence the results of perfusion scintigraphy.[208] On the other hand, the better spatial resolution of echocardiography and the ability to categorize wall motion independently in each segment (contrasting with the relative flow comparisons used in myocardial perfusion imaging) may compensate for its requirement of ischemia. Thus, the similarities in the sensitivity of echocardiography and scintigraphy reflect the balance between the underlying physiology of the tests and their imaging characteristics. In contrast, studies with adenosine and dipyridamole have shown vasodilator stress echocardiography to be significantly less sensitive than perfusion scintigraphy.[209] This

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Figure 14-14 (Figure Not Available) Prognostic content of single photon emission computed tomography (201 TI SPECT) and stress echocardiography scans. The correlation with outcome of the extent of perfusion defect (PDS) and wall motion abnormality (WMS) appears comparable in this exercise stress study. (From Olmos LI, et al: Circulation 1998;98:2679–2686.)

difference is most marked in patients with single vessel coronary disease and reflects failure to develop coronary steal in the absence of extensive coronary disease. This difference in sensitivity is less prominent in patients with multivessel disease. With either dobutamine or vasodilator stress, the specificities of stress echocardiography and perfusion scintigraphy are also comparable, with most series showing a small benefit for echocardiography. Whereas the high sensitivity of myocardial perfusion imaging with SPECT may have been gained at the cost of a sacrifice in specificity, two important sources of false-positive results are patients with left bundle branch block and patients with left ventricular hypertrophy. The influence of left bundle branch block has been investigated in a small number of patients,[210] among whom stress echocardiography produced more favorable results for specificity, although insufficient numbers of patients have been studied to reliably address sensitivity. Patients with hypertension and left ventricular hypertrophy are prone to false-positive SPECT results, probably owing to small vessel disease. Stress echocardiography, especially with dobutamine stress, appears to offer greater levels of accuracy.[211] Prognostic Assessment

Stress myocardial perfusion scintigraphy is widely used for risk stratification of patients undergoing vascular surgery, patients with chronic coronary disease, and patients who have had a myocardial infarction. Unfortunately, although a substantial amount of literature regarding the individual predictive abilities of echocardiography and 331

TABLE 14-13 -- Comparison of Nuclear and Stress Echocardiographic T (Evidenced by Improvement of Regional Left Ventric Sensitivity, % Dobutamine

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DOBUTAMINE Thallium Protocol, THALLIUM SPECT ECHOCARDIOGRA Study Technique µg/kg/min Low-dose, 86 82 Marzullo et al Rest[275] redistribution 10 Low-dose, 95 71 Charney et al Rest[276] redistribution 10 Kostopoulos et RestLow-dose, 90 87 [277] al redistribution 10 Qureshi et al[278] RestHigh-dose, 90 74 redistribution 40 Nagueh et al[279] RestHigh-dose, 91 68 redistribution 40 Low-dose, 92 87 Senior et al[280] Stress (dobutamine)- 10 rest/NTG Arnese et al[281] Stress Low-dose, 89 74 (dobutamine) 10 reinjection Low-dose, 100 79 Perrone-Filardi Stress [282] (dobutamine) 10 et al reinjection Stress Low-dose, 93 85 Bax et al[283] (dobutamine) 10 reinjection Low-dose, 100 94 Haque et al[284] Stress (exercise) 20 reinjection Vanoverschelde Stress High-dose, 72 88 [285] et al (exercise) 40 reinjection High-dose, 87 95 Elsasser et al[286] Stress (dobutamine) 40 reinjection SPECT, single photon emission computed tomography. * Average ejection fraction 38%.

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perfusion imaging is available, comparative data are sparse. In patients undergoing surgery for vascular disease, dipyridamole stress thallium imaging has been shown to have a negative predictive value of more than 90% in most studies.[130] The occurrence of unexpected cardiac events in some patients is probably due to intracoronary thrombus formation on nonsignificant stenoses (which do not cause abnormal perfusion results). The predictive value of ischemia at scintigraphy ranges from 30% to 50%, this result being attributable to positive perfusion studies in the context of mild (prognostically benign) coronary disease and falsepositive results. Overall, these results are comparable to those of pharmacologic stress echocardiography (see Table 14-7) . There are few comparative studies between stress echocardiography and SPECT. The group of Pierard[135] compared the ability of dobutamine stress echocardiography and dobutamine technetium-99m sestamibi SPECT to predict postoperative cardiac events in 156 patients, among whom the adverse event rate was 5.6%. Both tests were characterized by a high negative predictive value (96% for echocardiography; 97% for SPECT). Postoperative cardiac events were predicted by previous cardiac symptoms, a Detsky score of 15 or greater (RR, 3.0), a positive dobutamine echocardiogram (RR, 3.7), and a positive dobutamine SPECT scan (RR, 7.4). In contrast, work by Pasquet et al[212] suggests that the specificity of stress echocardiography exceeded that of SPECT for the prediction of subsequent events. In patients with chronic stable coronary disease and after myocardial infarction, the relative prognostic roles of stress echocardiography and myocardial perfusion scintigraphy appear comparable (Fig. 14-14) (Figure Not Available) . Ischemia may be difficult to identify within segments having abnormal resting function, and this is a source of discrepancy from the findings of perfusion scintigraphy. Because the territory is supplied by the infarct-related artery, the analysis of sensitivity and specificity does not permit discrimination of which test is correct. Preliminary data comparing dipyridamole stress echocardiography and MIBI-SPECT in patients after recent myocardial infarction have shown the finding of ischemia at echocardiography (and not at scintigraphy) to be predictive of subsequent hard events.[213] Diagnosis of Viable Myocardium

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Positron emission tomography, thallium reinjection techniques, and dobutamine echocardiography have all been shown to reliably identify viable myocardium. A significant evidence base has been accumulated regarding the comparison of these variables (Table 14-13) . In one of the initial studies of patients after thrombolysis, dobutamine responsiveness and spontaneous improvement at follow-up were detected in stunned myocardium (normal flow with reduced function), and no dobutamine response correlated with failure to improve at follow-up was seen in infarcted tissue (reduced flow and reduced fluorodeoxyglucose activity). Hibernating tissue (reduced flow with preserved fluorodeoxyglucose activity) was responsive to dobutamine but failed to improve at follow-up, although not all patients in this category underwent myocardial revascularization. The majority of the comparative studies show SPECT techniques to be more sensitive but of lower specificity for the prediction of functional recovery.

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Consequences of Special Characteristics In addition to the effects noted earlier, there are other differences in intravascular ultrasound owing to the use of high frequencies and size constraints. The strength of backscattered ultrasound relative to the incident ultrasound strength is called the backscattering coefficient. This coefficient is determined not only by the composition of the tissue but also by the frequency of the ultrasound. The backscattering coefficient increases with higher frequencies for virtually all tissues, but the rate of increase is different for each tissue, depending on the microscopic structure.[4] In particular, the strength of the backscattered signal from fibrous tissue increases at a rate greater than that of the other tissues in the arterial wall.[5] A fibrous plaque may have strong echogenicity compared with other tissues at 10 MHz, but it still may be less than calcified tissue. At 30 MHz, however, the strength of the signal from fibrous tissue may be equal to or even greater than that from calcified tissue (Fig. 15-7) . Strong echo alone cannot be used to identify the presence TABLE 15-2 -- Comparison of Characteristics of Systems Type of System Electronic Cable, direct Cable, mirror Motor, direct

Resolution Good Very good Very good Very good

Nonuniform Rotation No Yes Yes No

Ring Down Yes Yes No Yes

Figure 15-7 Calcified and fibrous tissue can have very similar echo intensities. This clinical intracoronary image shows an area of dense fibrosis with some calcification. The area of fibrosis extends from 10 to 4 o'clock, but the area from 11 to 1 o'clock, which has the brightest echo

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intensity, also has the least shadowing. This finding indicates that there is calcification in the plaque in all areas except 11 to 1 o'clock. Note the "halo" surrounding the catheter, owing to ring-down artifact.

of calcium in the wall of the vessel, because fibrous tissue may mimic this. Calcified tissue can be distinguished by the additional presence of "shadowing," a profound weakening of signal strength distal to the calcified tissue, owing to the intense attenuation caused by the calcification. Fibrous tissue does not cause this same degree of attenuation, regardless of the intensity of the backscattered signal. Thus, if we see a very bright echo without shadowing, we should suspect that it is fibrous tissue, whereas a bright structure with shadowing should be identified as calcification. It should be noted, however, that the actual classifications are not so clearcut. Fibrous tissue may have microscopic calcifications, which also cause shadowing. Size constraints lead to other practical issues as well. Intravascular ultrasound catheters need a guidewire for placement, and of the several different types that have been developed, the simplest and least flexible is a fixed guidewire at the tip of the catheter. This type of guidewire does not interfere with the imaging function, but it cannot be used for the exchange of catheters over it. A much more adaptable approach is a removable guidewire, but this approach poses the problem of where to place the guide in the already tight constraints of space at the tip of the catheter. For catheters with electronic beam steering, the center of the catheter is free for use by a guidewire because there is no motor or drive cable. For mechanical systems, there is a space problem, which can be solved in one of two ways. The first solution is to have a channel on the outside of the imaging portion of the catheter through which the guidewire can pass. This approach leaves the imaging portion relatively unchanged, but the guidewire is present in the imaging field, causing a bright echo. The second solution is to use the same channel for the guidewire and an imaging core consisting of the transducer and drive cable, alternately withdrawing one to 345

allow passage of the other. This approach has the advantage of a concentric design with no echo from an adjacent guidewire. Because the imaging core

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and the guidewire do not have to occupy the tip at the same time, the tip size can be much smaller. For this reason, this design enables the use of the smallest catheters now available. One final consideration is the need to prepare the catheter. All the mechanical designs must be flushed with fluid before use to provide sound transmission from the transducer to the blood; the presence of even microscopic bubbles can adversely affect image quality. The various designs also differ in how easy they are to flush, depending on the size of the catheter and the size of the flushing channel. This consideration is not applicable with electronically steered systems, because the blood itself provides the contact with the transducer.

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340

Chapter 15 - Principles of Intravascular Ultrasound David T. Linker MD

Intravascular ultrasound is a relatively new technique for imaging a vascular structure from a catheter placed within that structure.[1] The basic physical principles are the same as those for other ultrasound techniques, but the physical constraints and characteristics of a catheter-based imaging technique lead to solutions different from those normally employed in other forms of ultrasound examination. This chapter examines the ways in which the constraints and characteristics of intravascular ultrasound dictate certain forms of design solutions and their consequences on the resultant capabilities of the systems used. The practical consequences for clinical application and future development are also outlined.

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Special Ultrasound Characteristics The principles governing all types of ultrasound imaging are the same, whether the transducers are outside the body, as in transthoracic ultrasound, or within the body, as in transesophageal or intravascular ultrasound. The major differences are transducer size, the distance to the structure being imaged, and the intervening tissues (Table 15-1) . For intravascular ultrasound, these parameters are significantly different. The transducer itself must be very small so that it can be placed inside a catheter, which is inside the arteries or veins. Typical catheter sizes range from less than 1 up to 2.6 mm in diameter. The distance to the structures being imaged is very short, and there is an enveloping layer of fluid (blood) surrounding the transducer at all times. This homogeneous layer of fluid TABLE 15-1 -- Comparison of Intravascular Ultrasound with Other Ultrasound Techniques Technique Transthoracic Transesophageal Intravascular

Transducer Size (cm) >2 <1.2 <0.26

Depth (cm) ˜3–20 ˜2–20 ˜0.05–4

Intervening Tissues Skin, fat, muscle Esophagus, atrium Blood

is also the main tissue between the transducer and the structures of interest. In transthoracic echocardiography there is little constraint on the size of the transducer, other than convenience and the size of the interspace between ribs. The distance between the transducer and the structures of interest can be much larger, up to tens of centimeters. The intervening tissues are very heterogeneous, including skin, subcutaneous tissues, fat, and muscle. The connection between the transducer and the body must be improved by use of ultrasound gel.

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Transesophageal echocardiography has some of the constraints of intravascular ultrasound but not all. The transducer must be small but not as small as that for intravascular ultrasound. Typical sizes are 10 to 12 mm in diameter. The distances to the structures imaged are short, but they still range from 2 to 20 cm. The contact is through a structure with both fluid and air, and therefore variable, and the structures through which sound must pass are almost the same as for transthoracic ultrasound, except for the skin. In summary, the special characteristics of intravascular ultrasound are a very small transducer size, a very short distance from the transducer to the tissues being imaged, and a relatively homogeneous medium between the transducer and the structure being imaged. To understand the consequences of these characteristics and constraints, we must review some details of the physics of ultrasound imaging. Resolution/Attenuation Most imaging transducers are used both for transmission and for reception of the ultrasound energy. For transmission there is a spatial pattern of signal strength, and for reception there is a spatial pattern of sensitivity. These patterns are often similar in form, and taken together they are referred to as the beam pattern of the transducer. A narrow beam leads to improvement of lateral resolution of the image, whereas a wider beam yields lower resolution. This beam pattern is primarily determined by the shape of the transducer and its frequency. The 341

pattern is similar to the diffraction pattern resulting from light traveling through a single small slit. This "single-slit diffraction," which is covered in basic optics, results in a bright central band and less bright alternating bands on either side of the main band, because of interference. A similar pattern results with a single ultrasound transducer: a single main "lobe" of sensitivity and smaller side lobes, owing to interference. For a transducer of given shape and size, the width of the main lobe becomes narrower if the frequency of the transducer is increased, thereby improving lateral resolution. If the frequency is lowered, the main lobe becomes wider, degrading lateral resolution. Increasing the diameter of the transducer creates a narrower main lobe and improves resolution, whereas decreasing the diameter increases the width of the main lobe. These two

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effects of frequency and diameter are closely related. In fact, for two transducers of different size but the same shape, the product of the frequency of emitted sound and the transducer diameter determines the beam pattern (Fig. 15-1) . If we reduce the transducer size and wish to maintain the same lateral resolution, we must increase the frequency proportionately. The main constraint on increasing frequency in diagnostic ultrasound is poor tissue penetration because of attenuation (reduction of the signal strength). Attenuation is increased with higher frequencies and with higher depth. Attenuation also is a function of the tissues through which the sound passes, and it is increased by varying tissue composition, so a uniform tissue such as blood reduces attenuation significantly. Because large distances increase attenuation, the short distance in intravascular ultrasound is also an advantage. Because of these factors, higher frequencies can be used for intravascular ultrasound: up to 40 MHz in some coronary instruments used clinically today, and 20 to 30 MHz for peripheral vascular studies, without encountering prohibitive attenuation of the ultrasound signal strength. The frequency of the transmitted ultrasound can be increased to match the smaller transducer size, improving lateral resolution. Resolution in the direction Figure 15-1 Simulated beam profiles for four transducer size and frequency combinations. Each profile has a central main lobe and may have side lobes as well. Each profile represents the result obtained with a given frequency-diameter product, with the other variables held constant. Moving from A to B represents reduction of the frequency or the transducer diameter by half. Each additional step is another halving of the frequency-diameter product, so that A represents a frequency-diameter product eight times higher than D.

of the beam (axial) is also increased, because shorter pulse lengths can be used at higher frequencies. Short Imaging Distance The other effect of very short distances is that imaging is performed very close to the surface of the transducer itself. Imaging close to the transducer face can be unfavorable because of two physical effects: ring-down and near-field artifact. When the transducer is electrically excited to generate the pulse of sound, it "rings" for a short time, much like a bell. This vibration generates electric

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signals similar to, but much stronger than, the signals generated by returning ultrasound. As a result, if we use the same transducer for transmission and reception of the ultrasound signal, which is the case in most systems, the received signal is buried in the ring-down signal (Fig. 152) . This signal creates a limit on the shortest distance from the transducer within which we can generate a useful image. This period of ringing can be shortened by damping the transducer, which has an effect similar to placing a gloved hand on the ringing bell. The problem with this approach is that it reduces both the transmitted ultrasound energy and the sensitivity to received ultrasound signals. Increasing the frequency of the transducer also reduces the ringing time, but it can never completely eliminate it. The other effect is near-field distortion. If the source of the reflected ultrasound is a long distance from the transducer, each wavefront arrives at roughly the same time across the entire face of the transducer, and the resultant signal is the sum of all the received signal (Fig. 15-3) . If the source of the reflected ultrasound is a very short distance in front of the transducer, there is interference of the wavefronts across the face of the transducer, causing loss of signal and distortions in the image. The distance at which this occurs is a function of the frequency and diameter of the transducer. The range of distances that are affected is much larger than that affected by ring down. These two effects combine to make imaging close to the transducer undesirable. Beam Steering To create a two-dimensional image, ultrasonic pulses must be transmitted and received in various directions. There are two fundamental ways of doing this, and the constraints of size and the length of the catheter affect how these methods can be used. The first method is mechanical motion of the transducer element (or elements) to point it (or them) in the different directions. This method can use a rocking motion, as is used in most mechanical ultrasound systems today, or a rotary motion, which was more common in earlier transthoracic systems. Rocking motion is difficult to reproduce at the end of a long catheter, so it has not been used so far for intravascular ultrasound. Rotation of the element is a uniform motion and therefore easier to produce. All mechanical systems used for intravascular ultrasound so far use this technique.

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342

Figure 15-2 Transducer ring down is demonstrated using an actual signal from a clinical 30-MHz intravascular ultrasound probe. The region labeled Ringing shows the signal caused by excitation of the transducer to create the ultrasound pulse. The area labeled Catheter shows returning ultrasound signals, in this case very strong signals from the housing of the catheter. The areas labeled Blood and Tissue show the returning signal from blood and adventitia, respectively.

The most direct way to cause the rotary motion of the transducer would be to use a small motor at the tip of the catheter (Fig. 15-4) , but it has been difficult to develop such a small motor with sufficient power. In spite of this, one group has made such a catheter for use in larger vessels. The more common method of causing the transducer to rotate is to have the drive motor outside the body and to use a flexible cable to transmit the torque to the transducer end of the catheter. With this sort of design a significant problem is nonuniformity of rotation of the transducer end of the catheter, because the position is measured at the motor end of the catheter. If the drive cable binds, either through a manufacturing defect or because of sharp bends in the catheter, there is a hesitation of rotation of the distal, transducer end, whereas the proximal, motor end continues to turn.[2] When this Figure 15-3 The cause of near-field artifacts is the difference in timing of arrival of wavefronts across the transducer. If the echo source is far away from the transducer face (left), the wavefronts arrive roughly at the same time all across the transducer face. If the echo source is close to the transducer (right), different parts of the transducer receive different phases of the wavefronts, possibly even parts of other wavefronts. The result is decreased and variable signal strength, causing distortion.

happens, several pulses are transmitted in the same direction but are displayed as if they are in different directions, causing a blur in the image (Fig. 15-5) . When the rotation is finally resumed, the speed is much faster than Figure 15-4 Schematic examples of three different types of catheter construction. Cable mirror and motor direct are examples of mechanically steered designs, using a flexible cable or a micromotor to cause rotation. One uses a mirror to direct the beam in differing

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directions, reducing near-field and ring-down artifacts, whereas the other uses a transducer pointed directly outward. Either of these can use a micromotor or a drive cable to provide torque. The electronically steered catheter has no moving parts and a large number of smaller transducers mounted on the surface. Only a few transducers are shown here, for clarity.

343

Figure 15-5 Illustration of how nonuniform rotation causes distortion of images from a mechanical system. Beams are sent out and received in uniformly spaced directions to create an image. If the transducer is delayed in its rotation because of a mechanical problem, the motor continues to turn and pulses continue to be sent out, but they will go in the same, or almost the same, direction (beams 1 to 5, left). When the transducer starts to rotate again, it rotates much faster, skipping some regions (beams 6 to 10). The display, however, distributes the beams equally, causing distortion (right).

normal and the image is compressed. This process can occur at one part of the image or at several (Fig. 15-6) . The construction of the transducer end can also vary. There are two fundamental types of transducer orientation. The simplest to understand is the one with the transducer pointed directly out of the catheter toward the vessel wall. The actual direction of the transducer is usually slightly forward, so that internal reflections within the catheter cause less of a problem. This design has the advantage of simplicity, but there are difficulties stemming from the proximity of the transducer to the structures being imaged. Because the same transducer is used to generate and receive the signals, and there is a very short distance from the transducer to the outside of the catheter, ring down causes a bright halo near the transducer, although this is often blanked out on the screen. Near-field distortion can also be a problem close to the transducer. These two artifacts can be troublesome if the structures of interest are adjacent to the catheter, as they can be in small vessels or in tight stenoses. Figure 15-6 Clinical examples of nonuniform rotation distortion on intracoronary images. A, There is distortion due to nonuniform rotation in one region, similar to what is illustrated in Figure 15-5 . Note that the "smeared" portion from 3 to 4 o'clock represents when the transducer was not rotating fast enough, whereas the compressed region from 5 to 6 o'clock represents when the transducer was rotating too fast. A clue to this artifact is the size of the speckle, which

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becomes larger when the transducer is rotating too slowly and smaller when it is rotating too fast. B, Demonstration of what happens when the rotation of the transducer is slowed in several different directions as it rotates, at about 12, 2, 4, 7, and 10 o'clock.

The alternative transducer orientation deals with the problems of near-field artifact and ring down directly by increasing the effective distance between the transducer and the outside of the catheter. This increase in distance is achieved by directing the transducer toward an internal rotating mirror, which then directs the ultrasound outward. Although slightly more complex, this type of design results in less or no ring-down effect at the surface of the catheter and reduced near-field distortion. The other technique for steering the beam is based on electronic combination of the signals from multiple small transducers. These signals can be arranged in a linear phased array, with all the elements potentially contributing to the image formation, or a curvilinear array, in which only some of the elements are used at one time. Because an intravascular device images in all directions, a linear phased array would not be able to steer the beam in all those directions, so the curvilinear array is the one that has been applied. As a result of the constraint of size, it is difficult or 344

impossible for each of the elements of the array to be wired separately, as is the case in the usual array system. Specialized electronics at the tip of the catheter are necessary in order to switch sequentially between the individual transducer elements; therefore, elements cannot be used simultaneously, and several sequentially acquired signals from adjacent transducers must be added together electronically after they have been received in order to create the "beam" signal. This technique is called synthesized aperture, because the equivalent of a simultaneous signal from the entire transducer (aperture) is created (synthesized) by adding the individual signals together. As a result of the need to send the beams out sequentially, the frame rate of image generation is reduced. Also, because the array is curved, some of the elements at the sides of the beam direction contribute little to the imaging, resulting in a smaller effective transducer diameter, reducing effective resolution.[3] Electronic systems share some, but not all, of the problems of mechanical

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systems. The transducer elements are on the surface of the catheter, so they are even closer than in the direct, rotating transducer designs, which means that the ring-down effect and near-field distortion are even more problematic for these systems than for mechanical systems. Because there are no moving parts, however, there is no problem with nonuniform rotation, and the images are stable no matter how much the catheter is bent (Table 15-2) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Practical Issues Unless we understand the limitations and variations of generation of the intravascular ultrasound image, we may misinterpret what is seen. What we see is primarily generated by the differences in acoustic properties between different tissues rather than the absolute value of those properties. An example of this is the media of the artery, which we can see quite clearly as an echolucent zone if there is intimal thickening, but which disappears completely if the intima is of normal thickness. It is reasonable to ask why the intima is not always visible. The answer to this is not clear, but there are two hypotheses. The first is that the intima must exceed a certain thickness, similar to the resolution limit, before it becomes visible. Once it exceeds this resolution limit, it is clearly visible. The problem with this explanation is that a plane reflector should be visible, even if it is smaller than the resolution limit, because the latter refers to resolving two sources of reflection, not one. An alternative explanation is that the normal intima has acoustic properties that are close to those of blood and media, and therefore are not visible, whereas thickened and abnormal intima has different properties and is visible. An issue discussed previously in this chapter is that of Figure 15-8 Altered appearance of calcification using different imaging systems. The clinical intracoronary image (A) shows intense shadowing owing to calcium from 2 to 3 o'clock, imaged with a mechanical system. B, Much less intense shadowing is visualized when using an electronically steered system, from 9 to 11 o'clock.

the relative intensity of echoes from structures and their relationship to the frequency of ultrasound. Although calcium may have a much stronger echo than fibrous tissue at the frequencies of ultrasound used for transthoracic and transesophageal imaging, the relationship may be reversed at the

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frequencies used for intravascular ultrasound. Thus, the brightness of the generated echo may not be sufficient to identify calcium, and other findings, such as the presence of shadowing, should be used (see Fig. 157) . The appearance of pathologic structures can also be influenced by the type of ultrasound instrument used and the settings of the instrument. These factors influence the range of gray values that can be accurately represented, and they can in some cases completely alter the appearance. Shadowing caused by calcification can be less apparent with curvilinear array systems than with systems that use a mechanically rotating transducer (Fig. 15-8) , for reasons that are not entirely clear. If we use the same criteria to-diagnose calcification in both situations, we may misinterpret the images. Similarly, the ability to see thickened media or lipid-rich plaque may be altered by the instrument gain settings and the type of instrument. Numerous distortions in the image can occur.[6] The most obvious cause, mentioned earlier, is nonuniform rotation with a mechanical catheter system. The visual distortions may be obvious or may be mistaken for abnormalities of the vessel contour and, therefore, pathology. These distortions may also affect any measurements that can be performed, so interpretation of vessel and lesion size should be made with great caution in the presence of such artifacts. The degree of distortion is greater the more eccentric the position of the catheter, so if the catheter is concentric with the vessel and the disease is also concentric, cautious interpretation may be possible. Another source of alterations in measurement is angulation of the catheter relative to the vessel. This type of problem is more difficult than problems of angulation with other forms of ultrasonic examination in which the operator has both direct control and awareness of the orientation of the transducer. In intravascular ultrasound the transducer moves freely within the vessel. It is not possible to determine the orientation of the vessel relative to the catheter from the images themselves, nor from 346

manipulation of the catheter. Angulation of the catheter relative to the wall can introduce geometric distortion owing to the oblique plane of imaging.[7] This distortion can lead to misinterpretation of the wall pathology or the dimensions of the vessel or lesion. In general, however, the actual

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magnitude of these distortions is minimal. As an example, a 10-degree angulation can cause less than a 2% increase in luminal area; 20-degree angulation causes about a 6% change. Quantitative evaluation of lesions is also affected by the imaging medium surrounding the catheter because the distances on ultrasound examination are determined by time-of-flight of the ultrasound, which in turn is determined by the speed of ultrasound in the intervening medium.[7] The speed of ultrasound in solids and liquids is predominantly governed by the specific gravity and compressibility, the former being the main variable in liquids. In blood, the main variable determinants of specific gravity are protein content and red cell content. Both change specific gravity, and as a result the time-of-flight of the ultrasound pulse, and the calculated measurements change (see Chapter 9) . This change can be as much as a 5% difference in the clinical range of proteins and red cell counts.[8]

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Future Directions The clinical application of intravascular ultrasound depends in large part on being able to identify clinical situations in which the information obtainable with the technique would lead to better or more specific treatment. So far, the best example of this is using intravascular ultrasound to assess the placement of vascular stents. Such observation has demonstrated that many stents that appear to be properly placed on the basis of angiographic images show poor apposition to the arterial wall on intravascular ultrasound images.[9] [10] The use of additional balloon inflations to improve the ultrasound appearance has reduced the incidence of subacute thrombosis of the stents, even though the patients received less intense anticoagulation than is otherwise customary.[11] As a result, the use of intravascular ultrasound has become routine whenever there is any question about stent placement. In addition, intravascular ultrasound is frequently used to help evaluate lesions with difficult or hard to interpret angiographic appearance. It seems likely that more specialized intravascular ultrasound probes will be developed. Smaller size is one possible direction, and there are already reports of imaging guidewires.[12] Combination with interventional devices is an obvious direction of development and combined imaging/balloon catheters[13] and imaging/atherectomy catheters [14] have already been produced. Other possibilities likely to be developed include forwardlooking devices, which have already been reported by two groups.[15] [16] [17] [18] Also, the advantages of ultrasound guidance of lasers[18] [19] [20] [21] [22] have spurred interest in combined laser/imaging catheters. Another general trend is toward increasing transducer frequencies, which result in improved resolution, both in the lateral and in the axial directions. In addition to the formidable technologic difficulties of dealing with higher frequencies, there is the physical difficulty of increased backscatter from

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blood. Increased backscatter results from the marked increase in relative backscatter from blood at higher frequencies compared with all other tissues, which translates into decreased contrast between blood and arterial tissues. Because of this, there have been studies using signal processing techniques to reduce the relative intensity of the blood signal relative to tissue, thereby improving contrast at higher frequencies.[23] [24] Although it is possible to correlate the visual appearance of plaque on the intercoronary ultrasound image with histology,[25] [26] there have been numerous attempts to improve discrimination and reproducibility by automating this process of discrimination. The two general approaches have been to base the processing on the images as they are presented to the viewer, or to use the raw ultrasound signal before it is processed into an image. The former example has the advantage of being easier to implement, requiring only a video digitizer, which is currently easily available. Analyzing the raw signal is much more complicated, requiring modification of the ultrasound instrument as well as specialized digitization hardware to sample the signal at the high frequencies observed. Nonetheless, reasonable results have been achieved using both techniques. An automated analysis of digitized images correlated well with both histology and visual analysis.[27] In another study, the normalized backscatter power and slope were examined in a limited number of samples, and they showed some discrimination of different tissue types.[28] A limiting factor of all of these studies is the need for a standard, because the characteristics of different instruments as well as different catheters can vary, requiring some measurement to normalize the results. For studies based on video digitization, this measurement is normally based on something that is easily visible in the image, and most frequently this has been the adventitia. Because the only parameter being measured is brightness of the ultrasound image, the results are normalized to the brightness of adventitia. For raw ultrasound signal studies, the benchmark has been the reflection from a perfect reflector, which is either a steel or plastic block. This method is clearly impractical in the clinical setting because it requires very careful measurements with micromanipulators to position the reflector. A recently proposed alternative is to use backscatter from the flowing blood within the artery as a standard.[29] In addition to being readily available, the results are less variable than the backscatter from adventitia. Overall, although there have been some intriguing results to date regarding automated analysis for tissue identification, as well as improved tissue identification, the ultimate limits of discrimination of

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intravascular ultrasound are still unclear, and unambiguous identification may be possible only in very limited situations.

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349

Chapter 16 - Intravascular Ultrasound Histologic Correlation and Clinical Applications Katsuhiro Kitamura MD Paul G. Yock MD Peter J. Fitzgerald MD, PhD

More than 10 years have passed since intravascular ultrasound (IVUS) was introduced into the clinical setting, bringing about a new era for the assessment and treatment of vascular pathology. Moreover, it has provided a method to directly examine atherosclerosis and other vascular disease processes. The ability to image the vascular wall as well as its lumen has changed the focus of the assessment of vascular disease by clinicians. Although pathologists have long recognized that measurement of lumen dimensions often poorly reflects the extent and importance of arterial disease,[1] [2] [3] IVUS has the ability in vivo to measure both lumen and vessel size.[4] [5] This information brought forth by IVUS has also brought new insights into coronary interventions by direct examination of their effects on atherosclerotic plaque and the vascular wall. With increasing experience and continuing advances in image quality and catheter design, IVUS has become the standard for the assessment of vascular disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Background Angiography: A Shadow of the Truth The introduction of coronary angiography to assess coronary atherosclerosis by Sones in 1958[6] focused attention on the vascular lumen; however, several investigators[7] [8] [9] [10] [11] have subsequently demonstrated that a particular coronary lesion involved in an acute coronary syndrome is not related to its angiographic severity. Pathologic reports have shown that the underlying mechanism of coronary occlusion is thrombus formation precipitated by the rupture of a lipid-laden atherosclerotic plaque, rather than the progression of a previously severe coronary stenosis.[12] [13] [14] [15] [16] [17] [18] Furthermore, it has become apparent that narrowing of vascular lumen is a late event in the development of atherosclerosis. Glagov et al[19] demonstrated that vessels compensate for the development of atherosclerosis by increasing their cross-sectional area to accommodate the plaque burden. Luminal narrowing does not occur until this compensatory mechanism fails. On average, angiographically apparent atherosclerosis occurs only when greater than 40% of the vessel area is occupied by plaque.[20] Thus, angiography, which generates a silhouette of the vessel lumen and no direct information about the vascular wall composition, underestimates the severity[21] and extent[22] of atherosclerosis and offers little information about the characteristics of obstructive plaque. Although angiography provides a road map, IVUS may provide a clinically applicable means to augment the road map by imaging the arterial wall as well as its lumen in vivo. The History of Intravascular Ultrasound The development of IVUS has been made possible by the advances in computerization and electronics and, in particular, the miniaturization of ultrasound transducers. Although catheter-based ultrasound was shown to be feasible in 1956 by Ciezynski, these initial attempts to

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350

develop IVUS systems were aimed at measuring the dimensions of cardiac chambers. [23] The first real-time, two-dimensional intracardiac images were produced by Bom et al[24] using a 5.6-MHz, 32-element phased array transducer mounted on a 3.2-mm catheter, but the development and widespread clinical application of transcutaneous echocardiography overshadowed the progress in intravascular cardiac imaging. It was not until catheters were further miniaturized that the assessment of atherosclerotic plaque became practical.[25] [26] [27] [28] [29] The first real-time, two-dimensional images from human peripheral vessels were recorded in 1988,[30] followed by the first in vivo imaging of human coronary vessels in 1989.[31] [32] Since that time, advances in catheter design and image quality have allowed the introduction of ultrasound catheters less than 1 mm in diameter that are capable of accurately assessing lumen and vessel dimensions as well as plaque morphology. In 1990, three-dimensional IVUS reconstruction was first described by Burrell et al,[33] and it has dramatically progressed by advances of catheters, pullback devices, and sophisticated computer algorithms.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Basic Principles Catheter Design Two basic approaches to catheter design have been developed. The first approach involves the use of a single piezoelectric crystal with mechanical rotation of the ultrasound beam to achieve circumferential imaging. The second approach involves a solid-state, multielement transducer (Fig. 161) . These catheters are delivered into the vascular lumen over a guidewire to enable their safe delivery to the region of interest. Both systems are fundamentally different and have their own unique strengths and weaknesses. A mechanical catheter has a flexible drive cable, traveling the whole length of the catheter, which rotates its single transducer on the distal tip at a speed of 1600 to 1800 rpm. Because the maximum delivery of acoustic power is larger than a solid-state system, the penetration Figure 16-1 Diagram of the two basic IVUS imaging catheter configurations.

and resolution of the surrounding tissue becomes larger, resulting in better image quality. One problem associated with this type of catheter is nonuniform rotational distortion, which is characterized by portions of stretched or compacted images and is caused by kinking or compression of the ultrasound catheter. This artifact is problematic in vessel curvature of greater than 40 degrees and may cause absolute errors for diameter and area measurement by more than 20%.[35] Solid type catheters have 64 multiple imaging elements, arranged cylindrically at the distal tip, which visualize cross-sectional images perpendicular to catheter axis. This type of catheter does not experience

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nonuniform rotational distortion, which is an important advantage In addition, the over-the-wire design makes the catheter relatively easy to use and manipulate in the coronary arteries. The multielement design, however, produces ring down. This artifact, seen as a bright ring surrounding the catheter, is generated by continued vibration of the piezoelectric crystals after cessation of the activating electrical impulse. Although this artifact can be electronically subtracted out by eliminating all early signals detected by the catheter, this masking may prevent the detection of structures close to the catheter surface. With respect to image quality, transducers, made from small parts of elements have relatively weak acoustic power, leading to an ambiguous image. The size of both types of catheters has continually decreased to diameters less than 1 mm, which allows for compatibility with 6-F guiding catheter platforms. Imaging frequencies have also increased, now greater than 40 MHz, providing substantially higher resolution for delineating subtle plaque variations in the vessel. Typical ultrasound images are shown in Figure 16-2 . It can be easily recognized that a higher frequency catheter can provide higher resolution at the expense of increased signal strength in blood and decreased signal penetration in tissue.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Image Interpretation The Normal Artery The ultrasound appearance of an organ or tissue depends on the acoustic properties of its components, specifically the degree of acoustic impedance difference between its layers. From the ultrasound point of view, normal arteries are mainly composed of collagen and elastin, which are highly echo reflective, and smooth muscle cells, which are relatively sonolucent. The arterial adventitia, which is mainly composed of collagen and elastin, is highly echo reflective, producing bright signals on IVUS. The media of arteries varies according to the respective anatomic location. Large central arteries, such as the aorta and iliac arteries, have an elastic media, which is also highly echo reflective, making the differentiation of media, adventitia, and intima indistinct, especially when the adventitial collagen is densely packed.[36] [37] [38] Typically in elastic arteries, the media is as bright as the surrounding tissue.[28] However, medium size arteries, such as the coronary 351

Figure 16-2 Ultrasound images obtained by 30-MHz (A), 40-MHz (B), and 50-MHz (C) catheters. Higher frequency catheters can provide improved resolution, but signal strength of blood increases as signal penetration decreases.

and femoral arteries, have a muscular, echolucent media. The detection of arterial intima depends on its thickness.[39] [40] In normal peripheral muscular arteries, reflections from the intima produce a bright inner layer, which helps to produce a distinctive three-layered appearance[41] [42] (Fig. 16-3) . Siegel et al[43] studied the precise origin of this three-layered

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appearance. These researchers confirmed that the innermost bright layer is produced by the intima and internal elastic lamina, the echolucent middle layer is produced by the media, and the bright outermost layer arises from the adventitia and external elastic membrane. However, in coronary arteries, the intimal thickness may not be sufficient to generate a distinct reflective layer. Fitzgerald et al[39] demonstrated that vessels with a threelayered appearance have a significantly thicker intimal layer than those without ultrasound layering. An intimal thickness of at least 178 µm was required before layering was seen with a 30-MHz transducer. Thus, Figure 16-3 Ultrasound image of mild coronary disease, illustrating the typical three-layered appearance. This appearance is a result of the acoustic difference between the layers of the artery: intima, media, and adventitia.

in truly normal coronary arteries without intimal thickening, a layered appearance is not seen. Because the "normal" appearance of coronary arteries was first described in patients with diffuse intimal thickening, a three-layered appearance was considered to be normal. Assessment of Atherosclerosis Atherosclerosis is a diffuse vascular disease process initially characterized by intimal thickening. In the early phases, lipid and macrophages accumulate within the intima, then, as the disease progresses, collagen is added by vascular smooth muscle cells.[44] [45] [46] As the production of collagen and accumulation of lipid continues, calcium may also be deposited and the media may thin.[47] The amount of lipid, collagen, and calcium within individual plaques varies widely. Plaque composition is related to the clinical course of coronary atherosclerosis. Fibrous 352

plaques tend to be stable and slowly progressive, with a clinical presentation of stable angina. Lipid rich plaques are less stable and may rupture, producing an acute, unstable ischemic syndrome.[12] [13] [14] [48] , [49] IVUS allows the quantification of the extent of atherosclerosis and an assessment of the composition of the plaque. In muscular arteries the echolucent media provides a separation between the thickened intima and the adventitia, which allows the cross-sectional area of the plaque to be

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clearly delineated. The plaque area should be measured using a leading edge technique, outlining the blood-intima and media-adventitia boundaries. The media-adventitia border is selected because this boundary corresponds to a true anatomic boundary compared with the outline of the plaque, which does not always correspond to the plaque-media boundary. Signal attenuation at the outline of a plaque may produce dropout in the image, masking the true plaque-media boundary. A large plaque burden may also be associated with thinning of the media, making the separation of plaque from adventitia difficult. [28] [47] , [50] However, this boundary is usually apparent in adjacent proximal or distal cross sections. Regions of calcification within the plaque are highly echo reflective. Calcification generates bright echoes (more intense than the surrounding adventitia) associated with acoustic shadowing and reverberations (Fig. 164) .[29] , [51] [52] This acoustic shadowing obscures the media-adventitia border and makes the assessment of the plaque burden difficult, especially when the calcification is extensive and superficial.[28] The reliability of ultrasound in detecting plaque calcification is pretty high. In a histologic comparison study, Di Mario et al[51] reported that calcium deposits were detected by IVUS with 97% accuracy. In vivo studies have also confirmed that IVUS often detects calcification not visible by angiography.[53] [54] Mintz et al[55] reported that calcification was present in 48% of target lesions by fluoroscopy and 76% of lesions by IVUS (P < .001) in patients with coronary interventions. Calcification was more likely to be visible by ultrasound only if it occupied less than 90 degrees of the vessel circumference and/or was less than 5 mm in length. These researchers also reported that calcium was detected in 72% of target lesions in 1442 patients and lesions with an ultrasound plaque burden greater than 0.75 or an angiographic Figure 16-4 Examples of calcified plaques. Deep and superficial calcium with acoustic shadows (A and B) and circumferential calcification with reverberations ("napkin-ring" appearance, C) are shown.

diameter stenosis greater than 0.25 had a prevalence of calcium of at least 65%. [56] Fibrous plaque is also echo reflective, although less so than calcium. It produces relatively bright echoes, often of a similar intensity to the adventitia.[28] [29] [42] [51] However, the intensity of echoes from fibrous plaque is variable. This variation may, in part, reflect machine gain settings, but it

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is also likely to be related to the collagen content of the plaque. Dense fibrous plaque can produce echoes that are brighter than the adventitia and can even cause acoustic shadowing, but they cannot produce the reverberations typical of calcification. Lipid is a poor reflector of ultrasound. Therefore, predominantly lipid-rich plaques, fibrofatty or fatty plaques, are often echolucent and less intense than the surrounding adventitia. Lipid pools can also be detected within plaques as echolucent regions without internal structure.[28] [29] The accuracy of IVUS in detecting lipid plaque has been reported to be as high as 78%.[29] In practice, however, echolucent regions must be cautiously interpreted. Artificial echolucency can be produced by ultrasound systems with limited dynamic range. When the dynamic range of the system is low, weak signals are not displayed, creating an image that mimics "lipid lakes" within plaque. The detection of thrombus is also difficult by IVUS because of the acoustic properties of thrombus, which are weakly echo reflective, variable, and often similar to blood or soft atherosclerotic plaque. At 20 to 30 MHz, blood has a fine, variably speckled appearance. This backscatter from blood is often valuable in the interpretation of IVUS images, allowing the discrimination of the inner plaque margin. The echogenicity of blood in vivo is mainly determined by the flow rate. At low flow rates, red blood cells aggregate, increasing the strength of the backscatter. Regions of slow blood flow, such as around dissections or within aneurysms, produce a brighter ultrasound image. The ultrasound appearance of thrombus varies with its composition. Platelet-rich thrombi have a very low echogenicity (similar to saline in vitro), whereas thrombi rich in red blood cells have a much greater echogenicity and demonstrate a uniformly speckled appearance.[57] [58] The echolucency of platelet-rich thrombi may explain the frequent failure of IVUS to detect thrombus in patients 353

Figure 16-5 An example of in-stent thrombus. A large amount of homogeneous echo patterns is observed inside stent struts (arrows).

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with unstable angina.[59] [60] In vivo, thrombus often has a diffuse, illdefined, homogeneous appearance (Fig. 16-5) . The sensitivity for detecting thrombus by IVUS has been reported between 36% and 80%.[60] [61] [62] Validation of Intravascular Ultrasound Measurements Numerous in vitro studies have validated IVUS measurements using histology as the gold standard.[25] [27] [28] [29] , [63] [64] Nishimura et al[65] reported an excellent (r = 0.98) correlation between lumen area measured by IVUS and histologic measurements in 130 fresh arterial segments. In vitro measurement of atherosclerotic plaque thickness has also been shown to be accurate (r = 0.91), [27] although in some studies plaque thickness was consistently smaller by histology, possibly owing to tissue shrinkage during processing. [28] IVUS measurements have been compared with angiographic measurements in a variety of studies. Nissen et al[66] reported, using normal human arteries, high correlation of diameter measurements between ultrasound and angiography (r = 0.98). The correlation between angiography and IVUS in diseased vessels, however, is not as close, especially when the lesion is eccentric.[67] [68] Following balloon angioplasty, the correlation between ultrasound lumen area and histology is good (r = 0.88),[69] but the correlation between angiography and IVUS is poor (r = 0.26),[5] [54] [70] , [71] These differences reflect the limitations of angiography in quantifying the complex, irregular lumen, which is typical following balloon angioplasty.[72] Many studies have also compared ultrasound assessment of lesion severity by cross-sectional area with traditional quantitative angiography.[54] [66] [73] [74] [75] [76] Nissen et al[67] reported that the cross-sectional lumen area by ultrasound has only a moderate correlation (r = 0.63) with the angiographic lumen area, which was supported by Tobis et al.[54] The reason for lack of correlation is because lesion severity by IVUS is calculated as a ratio of lumen area to vessel area, whereas for quantitative angiography it is based on the minimal lumen diameter within the lesion and the reference segment. Angiographically normal segments are often diagnosed as diseased by ultrasound. [22] Typically, reference segment plaque occupies 35% to 40% of the vessel cross-sectional area. The ultrasound assessment of lesion severity is affected by the remodeling phenomenon[77] [78] [79] therefore, the vessel size at the lesion may not be representative of the nondiseased vessel size. Lesion Morphology

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In addition to these issues of quantification, IVUS and angiography also provide different views of plaque morphology. Fitzgerald et al[76] compared lesion eccentricity by ultrasound with that by angiography. They found 77% of plaques were judged to be eccentric by ultrasound, but only 33% were eccentric by angiography. Additionally, many of the angiographically eccentric plaques were found to be concentric by ultrasound. The accuracy of the detection of morphologic features of plaque remains less certain. Histologic studies have demonstrated that IVUS can detect endothelial tears. Van der Lugt et al[80] reported that the sensitivity of IVUS in detecting morphologic features for each vascular specimen was high for dissection and media rupture (79% and 76%, respectively), but it was low for plaque rupture (37%). The ability of ultrasound to detect spontaneous plaque ruptures, which are often microscopic, is poor.[81] Ge et al[82] performed IVUS on patients with angina and compared groups with disrupted and nondisrupted plaques by IVUS findings. They found that disrupted plaque was related to unstable angina and concluded that IVUS can identify plaque rupture and vulnerable plaques. Yamagishi et al[11] reported that large eccentric plaques, containing an echolucent zone by IVUS, can be at increased risk for instability even though the lumen area is preserved at the time of initial study. They also showed that among 12 coronary sites with an acute occlusion at follow-up, 10 sites contained the echolucent zones. Inter- and Intraobserver Variability of Intravascular Ultrasound Measurements The limited image quality of early IVUS systems often made the interpretation of in vivo images difficult. Despite these limitations, early reports indicated that the inter- and intraobserver correlation of measurements was greater than 95%.[29] [64] [83] In one study, Blessing et al[84] assessed the inter- and intraobserver variability in 100 Palmaz-Schatz stent cases. The result showed that interobserver correlation ranged from 0.92 to 0.97 and intraobserver correlation ranged from 0.94 to 0.97 for measuring reference and minimal stent areas. These studies have clearly shown that the IVUS analysis of selected frames is highly reproducible. However, the variability introduced by selection of frames to be analyzed 354

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is another problem. Pathology reports indicated that lesion morphologic characteristics were typically constant only over a region 100 to 200 µm in length.[81] The characterization of a plaque may depend on which section is analyzed, and it is common practice to assess a lesion at the minimal lumen area, which may not be representative of the plaque as a whole within the target segment.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Applications of Intravascular Ultrasound Safety Clinical use of IVUS has been emphasized as a safe procedure, [54] [64] , [67] [85] [86] [87] but the studies cited involved only a small number of patients. Coronary artery spasm was reported to occur, but only rarely was it found to be severe.[88] Hausmann et al[89] reported safety information from 2207 patients undergoing IVUS, including 505 cardiac transplant recipients. In 3.9% of patients, complications occurred that might have been related to the performance of the ultrasound. Sixty-three patients (2.9%) had coronary artery spasm during performance of the ultrasound, which did not lead to further complications. Major procedural complications were more frequent in patients with unstable angina or acute myocardial infarction (2.1%) compared with stable patients (0.8%, P < .01) and more frequently in association with coronary interventions (1.9%) than for other indications (0%, P < .001). Bocksch et al[90] reported that IVUS imaging was done in 103 patients with acute myocardial infarction and showed a remarkable abrupt closure rate of 3.9%. These studies are not comparable because patient characteristics were so different from those of Hausmann's report, but Bocksch emphasized that IVUS should be performed by experienced investigators. Batkoff and Linker[86] reported safety data from 718 IVUS cases. Eight (1.1%) complications occurred, including spasm, vessel dissections, and guidewire entrapment, but no cases resulted in critical outcomes. No differences in frequency of complications among participating institutions were reported (P = .232). In order to perform IVUS safely, it is important to ensure adequate anticoagulation during the procedure. It is our practice to administer 5000 to 10,000 U of IV heparin before performing an IVUS interrogation as well as nitroglycerin before IVUS to standardize measurements.

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Detection of Angiographically Silent Disease One of the most basic insights derived from IVUS is the ubiquitous nature of coronary atherosclerosis. Patients with angiographic "discrete" stenoses were found to have significant plaque burden throughout the coronary tree by IVUS. In fact, Mintz et al[22] reported that reference segment crosssectional narrowing was 51% ± 13%, and only 6.8% of angiographically "normal" reference segments were normal by IVUS. Hausmann et al[91] found that patients with familial hypercholesterolemia had extensive coronary plaques by IVUS, even if angiography showed only minimal narrowing (Fig. 16-6) . This undetected plaque is not visible by angiography because the lumen size is preserved by arterial remodeling, despite significant intimal thickening. [19] [77] [78] [79] [92] , [93] However, such plaques may be of clinical significance. Vasospastic angina and acute coronary syndromes can occur in patients with coronary arteries that are normal by angiography.[11] [94] IVUS also aids in the assessment of lesions that are not well displayed by angiography and may change therapeutic strategy.[95] [96] Angiographic interpretation of lesions may be difficult because of overlapping branches or extreme vessel tortuosity. Bruchhauser et al[96] reviewed cases with ambiguous angiographic appearances using IVUS and, as a result, changed therapy in 21 of 31 patients, thereby eliminating interventions in 19 patients, with excellent clinical results. The accurate assessment of ostial lesions may also be difficult by angiography. Ge et al[97] reported finding plaques in 31 of 92 angiographically "normal" left main coronary arteries. In this study, the average diameter stenosis was 19.3%, with an area stenosis greater than 50% detected in four patients. Assessing the severity of ostial right and ostial left anterior descending lesions is often difficult by angiography; however, IVUS can offer another venue for interrogation and may assist in more careful assessment of these clinical situations. Guidance of Coronary Interventions One of the most widely investigated and applied uses of IVUS is to guide percutaneous coronary interventions. In addition to balloon angioplasty, a variety of new interventional devices, including stents and directional and rotational coronary atherectomy, are currently available to treat coronary stenoses. IVUS has provided new insights into the mechanisms of action of these devices. These insights have led to more appropriate device selection based on the ultrasound appearance of lesions. Additionally, IVUS has

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influenced the way in which operators gauge procedural success. Balloon Angioplasty

Andreas Gruentzig[98] speculated that balloon angioplasty compresses atherosclerotic plaque, thus increasing lumen diameter. Early pathologic reports from fatalities following percutaneous transluminal coronary angioplasty (PTCA) reported extensive plaque dissection.[99] It was not until the introduction of IVUS, however, that the mechanism of successful balloon angioplasty could be investigated directly in living patients. Ultrasound studies have demonstrated that lumen area doubled after angioplasty. Three basic mechanisms of this lumen enlargement have been described, including tearing of the plaque, stretching of the vessel wall, and a redistribution of plaque at the treatment site.[69] [100] [101] [102] [103] [104] [105] [106] [107] [108]

The efficiency of PTCA seems to depend on a controlled 355

Figure 16-6 Typical example of angiographically silent disease. The angiogram shows no evidence of disease, but at A, B, and C, corresponding IVUS images show mild intimal thickness.

disruption of the plaque. Dissections typically occur at the thinnest region of the plaque, at the junction of the plaque and normal vessel wall, or between the media and adventitia.[106] [109] [110] The GUIDE I study[76] found that plaque fracture or dissection was detected by ultrasound in 49% of lesions imaged following PTCA. The study by van der Lugt et al[110] showed that dissections were detected in 63% of whole cases and were generally seen at the thinnest region of the plaque on both histologic sections (92%) and IVUS cross sections (93%). Angiography clearly underestimates the frequency of dissection following PTCA.[111] [112] Typical IVUS images after balloon angioplasty are presented in Figure 16-7 . Dissections appear to be of therapeutic importance. Botas et al[104] demonstrated that vessel distensibility and compliance were returned to normal by balloon angioplasty. Schroeder et al[111] suggested that substantial coronary dissections after PTCA, which do not diminish antegrade blood flow, do not lead to an increase in acute or long-term events. A significant portion of luminal gain may be within these plaque fractures.[113]

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Dissections after PTCA vary in severity from limited intimal surface tears to full-thickness dissections, extending into the adventitia. The site of these dissections can often be predicted by ultrasound. In an in vitro and in vivo study, van der Lugt et al [110] reported that plaque fracture after angioplasty occurred at the thinnest region of the plaque, regardless of the preinterventional plaque characteristics. Fitzgerald et al[114] showed the close association between lesion calcification and dissection in vivo. Additionally, in this study, calcified lesions had larger dissection flaps. Direct ultrasound data also suggest that stretching and compression or displacement of plaque are important mechanisms of balloon angioplasty. Vessel area has been reported to increase following balloon angioplasty. [101] [102] [115] , Marsico et al[115] reported that a 2.4-mm2 increase in lumen area of coronary arteries following balloon angioplasty was associated with a 1.6-mm2 increase in total vessel area. It has been suggested that plaque area reduction is a result of plaque compression; however, atherosclerotic plaque is relatively incompressible. A possible explanation is that plaque is redistributed to each side of the lesion rather than physically compressed by balloon angioplasty. Baptista et al[108] indicated that plaque compression or redistribution accounted for 57% of the lumen enlargement following coronary balloon angioplasty. The precise mechanism of balloon angioplasty in a particular case depends on the mechanical properties of individual plaques[101] and may explain the variation in effects seen in various studies.[102] [105] [116] , [117] Stents

IVUS has made a significant contribution to the safe and effective deployment of coronary stents. Two types of stents are currently available, demonstrating distinctive ultrasound appearances. For stents with a slottedtube 356

Figure 16-7 Ultrasound images of dissection after balloon angioplasty.

design (e.g., Palmaz-Schatz, Multilink), the images show distinct points corresponding to the struts of the stent encountered in cross section by the beam (Fig. 16-8A) . Coil stents (e.g., Gianturco-Roubin, Wiktor) are

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composed of stainless steel wire arranged in a sinusoidal coil. The image of the stent shows a combination of points and short arcs, derived from the struts at any given cross section within the stent being either orthogonal or oblique to the imaging plane (see Fig. 16-8B) . The use of IVUS to guide stent deployment was pioneered by Colombo et al.[120] A major clinical problem with the use of stents was the 3% to 6% incidence of subacute stent thrombosis or hemorrhagic complications from the use of anticoagulants. Colombo's group recognized that most stentrelated complications were due to inadequate deployment despite an angiographically satisfactory appearance.[36] [118] [119] This work led to the routine use of high-pressure inflation (greater than 12 atm) for stent deployment, which has lowered the rate of subacute thrombosis to approximately 1%.[120] The Multicenter Ultrasound Stenting in Coronaries (MUSIC) study[121] demonstrated that IVUS-guided stent deployment could be safely performed with aspirin alone. In this study, the rate of subacute thrombosis at 1 month was only 1.3% and Figure 16-8 Ultrasound images of different stent echo signatures. A, A typical cross-sectional view of the slotted-tube design. B, A view from coil design stent. Variation of its echo patterns comes from the struts at any given cross section within the stent being either orthogonal (solid arrow) or oblique (open arrow) to the imaging plane.

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the 6-month restenosis rate was 9.7%. Despite the use of high-pressure deployment, ultrasound still shows, in a significant portion of cases, that the struts are not as well expanded as the angiogram suggests. In the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study,[122] 36% of the IVUS-guided group received additional PTCA because of insufficient stent expansion by IVUS, resulting in an increased minimal stent area from 6.25 to 7.14 mm.2 Figure 16-9 illustrates successful stent delivery following high-pressure deployment by angiography, but the stent is not yet well expanded by ultrasound. Several randomized trials have been published to assess whether complete expansion with IVUS guidance can produce a clinical benefit after stenting. The CRUISE study compared angiography-guided with IVUS-guided stenting.[122] There were significant differences between groups for poststent

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minimal stent area (7.78 versus 7.06 mm2 ; P < .001) and 9-month target vessel revascularization (8.5% versus 15.3%; P < .05). The RESIST (REStenosis after Ivus guided STenting) study[123] compared stent deployment with and without additional ballooning according to IVUS criteria. The group with IVUS guidance had significantly larger minimal stent area at 6-month follow-up (4.47 versus 5.36 mm2 ; P < .03), but the rate of restenosis was almost the same between the two groups (29% versus 23%). Although final results have not been published, the AVID trial [124] [125] compared angiography-guided stenting with IVUS-guided stenting. There was a significant difference between both groups regarding final minimal stent area (7.54 versus 6.94 mm2 ; P < .01) and 12-month target lesion revascularization (7.9% versus 14.6%; P < .04) for vessels less than 3.25 mm by angiography. Lower 12-month target lesion revascularization rates were seen in vessels with a distal reference diameter of 2.5 mm by angiography and in vessels with greater than 70% preprocedure stenosis by angiography, saphenous vein grafts. Directional Coronary Atherectomy

IVUS has also provided insights into the mechanism of directional coronary atherectomy (DCA). Based on Figure 16-9 Angiogram after stent deployment in the mid right coronary artery shows an acceptable result (A), but the initial IVUS image (B) reveals underexpansion. IVUS image after further dilation with bigger ballon (C) demonstrates substantial improvement in minimal stent area.

angiographic studies alone, it has been unclear how much of the beneficial effect of directional atherectomy is due to plaque removal and how much is due to lesion dilation by the atherectomy catheter (Fig. 16-10) . Ultrasound has revealed that about 40% of increased lumen area is due to vessel wall stretching and more than 60% is due to plaque removal.[115] [116] [126] , [127] Lesion morphology influences the outcome of directional atherectomy. Softer, more echolucent plaques are more effectively treated with directional atherectomy than fibrocalcific plaque.[128] Popma et al[129] found that the residual plaque area was greater in calcified than noncalcified lesions, especially in lesions with an arc of calcium that extended for more than 90 degrees of the lesion circumference. The current cutting capabilities of the DCA device depend on not only the presence of calcium in a lesion but also the location of the calcium relative to the lumen. A superficial rim of calcium at the lumen border generally prevents any tissue removal.

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Ultrasound has significant potential to optimize the performance of directional atherectomy. The angiographic appearance of a lesion reveals little about the volume or distribution of atherosclerotic plaque. Several studies have reported the retrieval of media and adventitia by atherectomy, [130] [131] which may lead to increased rates of intimal proliferation.[131] IVUS provides detailed information about the orientation of plaque and the residual plaque burden. The CAVEAT study failed to show any restenosis benefit for DCA versus PTCA,[132] but additional studies have compared IVUS-guided atherectomy and PTCA. The Optimal Atherectomy Restenosis Study (OARS) [133] was a prospective, four-center registry demonstrating that IVUS-guided DCA resulted in high rates of procedural success, with 2.5% in-hospital major complication. The rates of restenosis and target lesion revascularization at 6 months were 29% and 18%, respectively.[134] The Adjunctive Balloon Angioplasty After Coronary Arthrectomy Study (ABACAS) was another multicenter trial[135] that showed that IVUS-guided DCA followed by balloon angioplasty resulted in lower residual plaque mass compared with DCA alone (42.6% versus 45.6%; P < .001), with 358

Figure 16-10 Images of IVUS-guided directional coronary atherectomy (DCA). The lumen area is increased following serial atherectomy without dissections.

low complication rate (2.7% versus 3.6%; P = ns). Moussa et al[136] have reported that stenting after DCA (81% cases were IVUS guided) produced a lower restenosis rate (11% at 6 months) and target lesion revascularization rate (7% at 18 months). DESIRE is a multicenter randomized trial that compared stenting with or without DCA under IVUS guidance. [137] It showed that the acute lumen gain was greater in patients who underwent stenting after DCA compared with those who underwent stenting alone (7.2 versus 5.7 mm2 ; P = .02), resulting in a larger minimal luminal area after the procedure (8.6 versus 7.2 mm2 ; P = .03).[137] Followup data are forthcoming. Radiation Therapy

Recently, intracoronary radiation has emerged as a potential antiproliferative therapy to prevent restenosis after angioplasty or stenting.

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Many animal models and clinical trials have revealed that lowdose ionizing radiation reduces the incidence of neointimal formation and positive vessel remodeling.[141] [142] [138] [139] [140]

IVUS can play a valuable role to elucidate the response following intracoronary radiation therapy. Sabate et al[143] demonstrated in 21 patients, investigated by three-dimensional IVUS analysis and treated with PTCA followed by radiation therapy, that both the mean external elastic membrane volume and plaque volume increased significantly, but the luminal volume remained unchanged in the β-irradiated segments. IVUS also has clarified several important mechanisms of findings specific to radiation therapy. Edge effect, which is not specific to radiation therapy, is a phenomenon of restenosis at the stent margins. Albiero et al[144] [145] reported in a study of 32 P radioactive β-emitting stents that the incidence of edge effect was 42%, and it remained unchanged even after deployment of radioactive stents with a higher activity level (12 to 21 µCi). The mechanisms of edge effect are now hypothesized to be due to the combination of low-dose radiation and injuries in the segments adjacent to the irradiated site.[143] [144] The edge effect for catheter-based radiation therapy has been described as geographic miss,[146] causing neointimal growth of non- or poorly irradiated adjacent segments. It is the most important issue for preventing edge phenomenon. Intracoronary radiation may also prevent normal healing processes after balloon injury, called unhealed dissection, although nearly all angiographic dissections heal within 6 months after nonradiated angioplasty.[52] Kay et al [147] reported, based on the data from the BERT 1.5 study, that 16 dissections were recognized among 22 cases by IVUS after intervention, and at 6 months follow-up 8 unhealed dissections were seen by IVUS. No relationship between the existence of unhealed dissection and prescribed radiation dose was found. Meerkin et al[148] found 7 of 16 dissections partially healed but still remained at follow-up, yet there was no correlation with poor outcomes. Another important finding by IVUS is late stent malapposition. This phenomenon was first reported by Kozuma et al[149] after new stent deployment followed by 32 P β-radiation. They speculated that positive vessel remodeling and inhibition of neointimal formation by radiation were the primary mechanism. IVUS is the only method currently available to elucidate this specific phenomenon.

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Three-Dimensional Reconstruction

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Although coronary angiography provides the longitudinal information of the vessel lumen shape, conventional two-dimensional IVUS cannot provide such information, which has been a big limitation. Also, the lumen and vessel parameters are measured manually, which is very time consuming and suffers from high inter- and intraob-server variability.[150] Three-dimensional IVUS, however, combines wall and lumen characteristics of single planes with the longitudinal extension of the vessel, providing quantitative analysis of the coronary vessel morphology in an objective and reproducible manner through automated contour detection techniques. The three-dimensional reconstruction of a vessel from twodimensional images may provide a greater appreciation of the distribution of plaque and other morphologic features. In order to reconstruct a three-dimensional image from a series of twodimensional pictures, information is required about the longitudinal relationship of the images. This information is usually provided by performing a pullback at a known speed (0.5 or 1.0 mm per second) and assuming that in each time interval the transducer moves a known distance. The video image signal is digitized and each pixel is assigned a unique position in a three-dimensional grid with the x- and y-axis derived from the two-dimensional image and the z-axis derived from the timing sequence of the frame. Such three-dimensional pixels are known as voxels. To perform three-dimensional reconstruction with IVUS, several corrections must be made. For cyclic changes in vascular dimensions that create image artifacts (sawtoothed appearance), an ECG-gated threedimensional IVUS system has been developed.[151] [152] The other corrections include catheter movement during cardiac contraction and respiratory movement, curved path of the transducer, and axial IVUS image rotation. Slager et Figure 16-11 A longitudinal three-dimensional reconstruction of the left anterior descending artery (LAD) from a series of cross-sectional images during pullback at 0.5 mm per second. A fibrofatty plaque and superficial calcium are seen in the mid-LAD (arrowheads). The trajectory of the intravascular ultrasound pullback is assumed to be straight (center dark bank). IM,

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intermediate branch; LCx, left circumflex coronary artery; LM, left main coronary artery.

al[153] developed a new technique for correcting these artifacts. They investigated the feasibility of a new three-dimensional reconstruction model by fusion of angiography and IVUS (ANGUS). This system can reconstruct the three-dimensional contour of lumen and vessel along a spatial trajectory of IVUS pullback by combining the data of biplane angiography. High correlation for geometric measurements (r = 0.84 to 0.97) was observed between three-dimensional and biplane angiographic images by this system. Figure 16-11 illustrates a longitudinal view of a pullback from distal left anterior descending to left main coronary artery. The spatial relationship among plaque, calcification, and vessel wall can be easily recognized. In addition, computer-assisted automated vessel quantification is possible from these three-dimensional images. Several algorithms have been developed to trace automatically.[154] [155] Three-dimensional IVUS has been used for the creation of dose-volume histograms for interventional radiation therapy for restenosis[156] [157] [158] and to control intimal hyperplasia after PTCA followed by brachytherapy.[143] [159] In addition, it may serve as a valuable tool in the assessment of the regression and progression of arteriosclerosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions Tissue Characterization By IVUS, several in vitro and in vivo studies have tried to identify plaque components in coronary artery lesions with visual analysis of the gray scale images or quantitative videodensitometry analysis.[160] [161] [162] These gray scale IVUS images, however, cannot accurately distinguish among plaque components (fibrous tissue, fibrofatty tissue, and various stages of thrombus).

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Analysis of the unprocessed backscattered radiofrequency ultrasound signal has been conducted, which may convey more specific information relating to the intrinsic architecture of the plaque substance and permit a more reliable means for intravascular plaque characterization.[163] The internal backscatter from plaque, whether assessed by its peak amplitude or frequency, combined with time averaging methods, has been shown to distinguish plaque types.[164] Vulnerable plaque with lipid pool beneath thin fibrous cap, responsible for acute coronary syndromes and myocardial infarction, generally cannot be identified by the current level of image quality.[51] Several investigators have reported the usefulness of frequency or backscatter analysis in detecting vulnerable plaque.[165] [166] Komiyama et al[165] reported on in vitro study in which radiofrequency signal analysis could detect plaques with lipid core with higher sensitivity and specificity compared with gray scale analysis. Ultrasound frequency and backscatter analysis may be useful to detect plaques at risk of spontaneous rupture or complication with percutaneous

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interventions and also provide information for atherosclerotic plaque and thrombus characterization as well as transplant vasculopathy.[167] [168] Sonotherapy IVUS has been used for therapeutic purposes. Several investigators have reported biomechanical effects of ultrasound for prohibiting migration and adhesion of smooth muscle cells,[169] [170] which can be applied for the prevention of neointimal hyperplasia after coronary intervention. A system for intracoronary sonotherapy treatment (URX, PharmaSonics Inc.) has been developed, and favorable effects on neointimal hyperplasia in vivo have been reported using a porcine stent injury model.[171] This system is composed of ultrasonic transducers, generating a peak intensity of 100 W/cm2 at a center frequency of 700 kHz. At 7 days, smooth muscle cell proliferation assessed by bromodeoxyuridine histology preparation was significantly reduced in the sonotherapy group compared with the sham group (24.1% versus 31.2%; P < .05). The catheters have been further miniaturized for coronary use and investigated (Fig. 16-12) . Post et al[172] found, also in a porcine model, that sonotherapy significantly decreased the intimal hyperplasia after stenting compared with the control group. In this study, sonotherapy was associated with slight increase in mild vessel wall injury, but endothelialization was complete at 180 days. Intracoronary sonotherapy may be a good modality to inhibit restenosis, and it may also offer treatment advantages when compared with intracoronary brachytherapy. The sonotherapy system does not require the use of radioisotopes, thus negating the need for shielding and oncologists' support, thereby facilitating procedural "ease of use." Ultrasound has been reported to enhance drug delivery as well as gene transfection, suggesting that sonotherapy may be augmented further with a pharmacologic approach.[173] [174] [175] Therapeutic catheter-based sonotherapy Figure 16-12 (color plate.) A schematic view of a sonotherapy catheter (URX IST, PharmaSonics Inc.). This catheter is compatible with an 8F guiding catheter and peak intensity of 100 W/cm2 at a center frequency of 1 MHz with 5 minutes dwell time.

is currently under clinical investigation as a tool to prevent restenosis.

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Drug-Eluting Stent Because coronary stent use has become widespread for reducing restenosis after intervention, stents have been proposed as means for local drug delivery. Recently, several drugs with antiproliferative properties have been reported to reduce intimal hyperplasia after balloon angioplasty or stent implantation. Rapamycin, an immuno-suppressive agent with antiproliferative properties, has been reported to inhibit intimal thickening after balloon angioplasty in animal study[176] or after stent implantation in clinical study.[177] Paclitaxel, a microtubule-stabilizing compound with potent antitumor activity, has also been reported to prevent intimal hyperplasia after intervention.[178] [179] These drugs showed dramatic neointimal inhibition in long-term and short-term findings, but excessive or too-fast drug elution provoked incomplete intimal coverage over the stent struts. Although the optimal dose and the elution rate of the drug have yet to be determined, incomplete apposition (which has been observed in 6% to 30%[180] [181] ) may prevent effective tissue drug delivery and increase the risk of strut thrombosis by retarding endothelialization. IVUS can detect incomplete apposition easily and maximize drug delivery to the arterial wall.

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Summary IVUS provides a new window for viewing the vascular system. It allows the characterization and quantification 361

of the vascular wall as well as its lumen. This advantage has provided a new understanding of the pathology of atherosclerosis and provided insights into the mechanisms and outcomes of percutaneous coronary interventions. Because IVUS, unlike angiography, can detect stent underexpansion, additional PTCA to optimize stent deployment may translate into better long-term clinical results. Moreover, for brachytherapy, IVUS can provide precise information about mechanisms and appropriate dosing for therapy. IVUS is now being investigated to detect vulnerable plaques (tissue characterization), thereby contributing to "lesion-specific" therapy. In view of IVUS as a therapeutic modality, the use of sonotherapy is just beginning. The unique information provided by IVUS promises to lead to continuing advances in the understanding and treatment of vascular disease.

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Section 4 - Valvular Heart Disease

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Chapter 17 - Quantitation of Valvular Regurgitation Beyond Color Flow Mapping Sheila K. Heinle MD

Echocardiography is an essential tool in the diagnosis and management of patients with valvular regurgitation. Cardiac chamber size and function are assessed by two-dimensional echocardiography, and severity of regurgitation is semiquantitatively assessed by Doppler color flow mapping of jet area as mild, moderate, or severe. However, more precise quantitation of valvular regurgitation may be necessary for early detection of hemodynamically significant valvular regurgitation before development of left ventricular dysfunction.[1] [2] Furthermore, since valve repair is associated with low mortality rates, some investigators now suggest that minimally symptomatic patients in whom significant valvular regurgitation is identified be considered as candidates for valve repair procedures.[3]

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Limitations of Doppler Color Flow Mapping Doppler color flow mapping provides real time visualization of regurgitant flow signals. Although Doppler color flow images are derived from autocorrelation techniques that provide mathematical estimates of mean velocities along each scan line, this technique is most commonly applied qualitatively to assess the presence and spatial distribution of the flow disturbance due to valvular regurgitation. Numerous studies have demonstrated concordance in results of color flow mapping and other methods for evaluating regurgitant severity of aortic or mitral regurgitation. For mitral regurgitation, initial studies compared depth of jet penetration into the left atrium[4] 368

and maximal jet area with angiographic severity. Improved correlation was observed when mitral regurgitant jet area was corrected for left atrial area.[5] In patients with aortic insufficiency, measurement of the aortic regurgitant jet height relative to the left ventricular outflow tract height was a better predictor of angiographic grade than the maximal length and area of the regurgitant jet.[6] Criteria based on regurgitant jet size also have been proposed to assess the severity of tricuspid and pulmonic regurgitation.[7] Although maximal jet area correlates well with the semiquantitative angiographic grade of severity, however, only limited correlation is observed with quantitative measures of regurgitant volume (r = 0.55) and fraction (r = 0.62).[8] In addition, maximal jet area is not predictive of hemodynamic abnormalities such as an elevated pulmonary wedge pressure or reduced forward stroke volume. This lack of correlation is related to several factors, including jet geometry, physiologic variability, and instrument settings.[9] In any image plane, regurgitant jet area depends on the geometry and

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direction of the jet.[10] Doppler color flow mapping of free regurgitant jets that are unbounded by surrounding structures may lead to overestimation of severity due to entrainment of adjacent fluid by the high-velocity jet.[11] In contrast, the area of an eccentric jet is only 40% of the area of a free jet with the same regurgitant fraction.[10] Eccentric jets are influenced by adjacent constraining surfaces,[12] so that area measurements correlate poorly with regurgitant volume.[13] It also is important to note that the color flow map of a regurgitant jet represents the spatial distribution of velocities and is not a direct measure of volume flow rate.[14] Although color Doppler jet area increases with regurgitant volume, this relationship is not linear because it is highly influenced by driving pressure,[15] compliance of the receiving chamber,[16] and the size and shape of the regurgitant orifice.[17] Further, evaluation of regurgitant jet area depends on the echocardiographic approach, transducer frequency, and other instrument parameters. Specific factors influencing regurgitant jet size include ultrasonographic system variability, gain settings, pulse repetition frequency, transducer frequency, and tissue priority algorithm. [18] Thus, estimates of regurgitant severity often are greater when measured by transesophageal compared with transthoracic echocardiography. [9] In addition, measurements of color Doppler jet area are subject to substantial intraobserver[19] and day-to-day[20] variability. A superimposed change in loading conditions or hemodynamics between examinations further confounds evaluation of color Doppler jet area.[21] For example, acute severe mitral regurgitation may be underestimated by color Doppler imaging because of increased heart rate, decreased systemic blood pressure, and a rapid rise in pressure in the noncompliant left atrium.[22] Thus, despite the clinical utility of color Doppler flow mapping for evaluation of patients with known or suspected valvular regurgitation, this qualitative measure of regurgitant severity is not ideal. Efforts to derive more quantitative and clinically applicable measures of regurgitant severity are ongoing.

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Volumetric Methods Regurgitant fraction can be calculated from the difference between flow rates determined at two separate intracardiac sites using the continuity equation. Total stroke volume is measured as antegrade flow across the regurgitant valve, whereas net forward stroke volume is measured as antegrade flow across a competent valve.[23] The combined use of twodimensional echocardiography with conventional pulsed-wave Doppler and continuous wave Doppler allows the estimate of volumetric flow across any of the cardiac valves using the following equation: SV = CSA × TVI (1) where SV is stroke volume, CSA is cross-sectional area of the annulus, and TVI is time velocity integral measured as the area under the Doppler spectral velocity curve. Volumetric quantification of intracardiac flow using the continuity equation is based on the following assumptions: a constant cross-sectional valve area, a flat velocity profile, and a circular flow area. Although mitral and tricuspid annuli are nearly circular, optimal accuracy requires consideration of their elliptical shape by modifying the equation for stroke volume using an elliptical cross-sectional area: CSA = π(D1 ·D2 )/4 (2) where D1 and D2 are annular diameters measured in two orthogonal views.

When the cross-sectional area is presumed to be circular, for example, in the left ventricular outflow tract, cross-sectional area is calculated as [24]

CSA = πr2 (3)

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To quantitate mitral regurgitant volume (RV), net forward stroke volume (SV) is measured from the aortic annulus and subtracted from the total stroke volume measured at the mitral annulus, as follows: RV = Total SV − Forward SV (4) Total stroke volume can also be obtained by subtracting end-systolic from end-diastolic volume obtained by two-dimensional echocardiography.[25] Regurgitant fraction (RF) is then calculated from the ratio of regurgitant volume to total stroke volume: RF = RV/Total SV (5) Good correlation has been observed between volumetric and angiographic regurgitant fractions for isolated mitral or aortic regurgitation (r = 0.91).[26] Although correlation with angiographic grading is poor, the limitations of using qualitative angiography as a reference standard for assessing the severity of valvular regurgitation have been well documented. [27] The volumetric method is usually applied to left-sided regurgitant lesions, although it is theoretically possible to substitute flow across a competent pulmonary or tricuspid valve for aortic flow in patients with concomitant aortic insufficiency.

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Figure 17-1 Two-dimensional echocardiogram (left) and Doppler spectral velocity envelope (right) demonstrating proper positioning of the Doppler sample volume at the mitral annulus for accurate time-velocity integral measurement to calculate stroke volume. (Courtesy of Brad Roberts, RDCS.)

Although the volumetric method has been validated in a large series of patients with valvular regurgitation, overestimation of mitral regurgitation is a potential limitation of this approach.[28] Improper positioning of the Doppler sample volume may result in overestimation of the mitral timevelocity integral because of the increase in velocity from the annulus to the tip of the leaflets.[29] However, this potential limitation can be avoided by meticulous positioning of the sample volume at the level of the mitral annulus so that diameter and flow velocity are measured at the same anatomic site (Fig. 17-1) . [28] Aortic flow may be underestimated if there is a nonparallel intercept angle between the ultrasound beam and the direction

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of blood flow.[30] Again, this limitation is minimized by careful patient positioning and use of multiple ultrasonographic windows with meticulous adjustment of transducer position to obtain the highest velocity signal. Perhaps the most common source of error in Doppler flow calculations is inaccuracy in the measurement of mitral or aortic annulus cross-sectional area. [31] Because the two-dimensional echocardiographic diameters are squared in order to calculate an elliptical or circular cross-sectional area, small errors in diameter measurement result in large errors in crosssectional area. Moreover, the assumption of a constant maximal flow area using the pulsed Doppler volumetric method does not acknowledge the temporal changes in flow area during the cardiac cycle and contributes to overestimation of regurgitant flow. Errors in diameter measurement can be minimized by using an ultrasonographic window that provides a perpendicular intercept angle between the anatomic structure and the ultrasound beam, by careful attention to gain and other instrument settings, and by averaging several beats. When combined, these potential sources of error may contribute to reported regurgitant fractions up to 20% in normal subjects.[26]

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Indirect Markers of Regurgitation Severity Although indirect markers of regurgitation severity do not provide quantitative estimates of regurgitant volume, they provide valuable information regarding the hemodynamic impact of the regurgitant lesion on atrial pressure and left ventricular end-diastolic pressure.[32] Mitral Regurgitation Pulmonary Venous Patterns

Pulsed Doppler sampling of the pulmonary vein results in a spectral envelope that consists of three distinct waves. A systolic antegrade wave followed by a smaller diastolic antegrade wave represent pulmonary venous inflow during ventricular systole and diastole, respectively. Following the electrocardiographic P wave, there is a small negative wave that represents atrial reversal during atrial contraction. With increasing mitral regurgitation severity, the systolic phase of pulmonary inflow progressively decreases, with eventual reversal of flow in systole when severe mitral regurgitation is present (Fig. 17-2) . [33] Several studies have examined the value of reversal of systolic pulmonary venous flow as a marker of severe mitral regurgitation (Fig. 17-3) .[33] [34] There is an inverse correlation between the ratio of systolic to diastolic pulmonary venous flow velocity time integrals and the mitral regurgitant fraction in patients with normal left ventricular systolic function (ejection fraction > 45%).[35] In patients with left ventricular systolic dysfunction, a normal pulmonary venous systolic flow pattern indicates a small (<0.3 cm2 ) regurgitant orifice area.[34] Conversely, pulmonary vein systolic flow reversal predicts a large (>0.3 cm2 ) regurgitant orifice, consistent with severe regurgitation. However, blunted systolic flow is much less predictive, as it may be associated with a broad spectrum of regurgitant severity, ranging from trivial to severe regurgitation (Fig. 17-4) .

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To optimize the sensitivity of pulmonary venous systolic flow reversal as an indirect marker of mitral regurgitation severity, it is important to sample both right and left pulmonary veins, since jet direction can influence the pulmonary venous flow pattern.[36] Discordant flow patterns have been observed in the right and left pulmonary veins, with systolic flow reversal demonstrated more 370

Figure 17-2 Summary of the relationship between left atrial pressure hemodynamic and pulmonary venous flow Doppler profiles in 2+, 3+, and 4+ mitral regurgitation (MR). As MR increases, the v wave and v-y descent increase, and the a wave and x-y descent decrease, which is coincident with decreased pulmonary venous systolic (S) flow, increased diastolic (D) flow, and reversed systolic flow (RSF) in 4+ MR. AR, atrial reversed flow velocity. (From Klein AL, Stewart WJ, Bartlett J, et al: J Am Coll Cardiol 1992;20:1345–1352. Reprinted with permission from the American College of Cardiology.) Figure 17-3 Reversal of systolic flow by pulsed Doppler sampling of the pulmonary vein during transesophageal echocardiography in a patient with severe mitral regurgitation.

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Figure 17-4 Regurgitant orifice area and regurgitant stroke volume in three different pulmonary venous flow patterns. Open triangles, normal flow; open circles, blunted flow; solid circles, reversed patterns. Dashed lines indicate regurgitant orifice area of 0.3 cm2 . (From Pu M, Griffin BP, Vandervoort PM, et al: J Am Soc Echocardiogr 1999;12:736–743.)

often in the right pulmonary vein.[33] [34] Other limitations of this indirect method include the influence of other factors on pulmonary venous flow pattern, in addition to left ventricular systolic and diastolic function, including atrial fibrillation, mitral stenosis, ventricular loading conditions, left atrial compliance, and left atrial contractile function.[37] [38] In an effort to account for these other factors, it has been proposed that the systolic component of the pulmonary inflow pattern be expressed as a percentage of

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the total (systolic and diastolic) velocity time integral and then corrected for left atrial filling volume measured from single-plane transthoracic echocardiography. This approach correlated well with Doppler-derived regurgitant fraction[39] however, it remains unclear whether this combined method can be used reliably in patients with acute severe mitral regurgitation, patients with eccentric jets, or patients in atrial fibrillation. Peak E Wave Velocity

Early diastolic mitral inflow is represented by the E wave velocity, which is directly related to the pressure gradient between the left atrium and the left ventricle at the time of mitral valve opening. The added regurgitant volume in mitral regurgitation increases the initial atrial-to-ventricular pressure gradient, thus increasing the peak E wave velocity.[40] A recent retrospective study showed a modest positive predictive value (75%) for an E velocity greater than 1.2 m per second for identifying patients with severe chronic mitral regurgitation. This relationship was independent of other variables such as heart rate, age, and restrictive left ventricular diastolic function.[41] However, increased mitral inflow velocity has also been observed in patients with severe aortic regurgitation.[42] Moreover, the predictive value of this marker has not been tested in patients with acute mitral regurgitation. Therefore, although peak E wave velocity may be a simple screening method for hemodynamically significant mitral regurgitation, it should be not used in isolation to judge regurgitant severity. Aortic Regurgitation Pressure Half-Time

The pressure half-time index represents the time for the peak gradient across the aortic valve in diastole to decay to half of its initial value. Doppler velocity and catheterization pressure half-times have been demonstrated to be linearly related (r = 0.91), with Doppler pressure halftime inversely related to the angiographic grade of aortic regurgitation.[43] Patients with severe aortic regurgitation have a shortened pressure half-time because of the rapid rate of decline in aortic diastolic pressure and rise in left ventricular diastolic pressure, resulting in rapid equalization of aortic and left ventricular pressures (Fig. 17-5) . A Doppler pressure half-time of 400 msec separates mild (1+, 2+) from significant (3+, 4+) aortic regurgitation by angiographic grading with a specificity of 92% and positive predictive value of 90%.[43] Aortic regurgitant severity may be overestimated, however, if the left ventricular end-diastolic pressure is

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elevated because of depressed left ventricular systolic function resulting in a significant overlap in pressure half-times between patients with mild, moderate, and severe regurgitation.[43] In addition, other factors such as stroke volume, aortic and left ventricular compliance, and systemic vascular resistance influence the pressure half-time.[44] Pressure half-time is most useful as an additional method to classify and monitor progression of chronic aortic regurgitation when color flow Doppler methods are discrepant. [45] Deceleration Slope

With increased severity of aortic regurgitation, the diastolic aortic pressure falls rapidly while left ventricular filling pressure rises rapidly, resulting in a steeper deceleration slope on a continuous wave Doppler echocardiogram. Although deceleration slope and pressure half-time both are measured from the continuous wave Doppler curve, deceleration slope is not dependent on the initial pressure gradient. Deceleration slope has been reported to be a better index of regurgitant severity than pressure halftime, demonstrating a close correlation with angiographic grade of regurgitation even in patients with associated aortic stenosis, mitral valve disease, or low cardiac output.[46] A deceleration slope greater than 3 m/sec2 suggests severe aortic regurgitation. Unfortunately, a deceleration slope less than 3 m/sec2 can be seen with mild, moderate, or severe regurgitation. [46] [47] Left ventricular compliance influences the reliability of deceleration slope as an index of aortic regurgitant severity, since a steep slope can be observed in a patient with only mild aortic 372

Figure 17-5 (color plate.) Color Doppler image (A) and continuous wave Doppler image (B) demonstrate severe aortic regurgitation with a pressure half-time of 49 msec and deceleration slope of 18 m per second2 resulting from rapid equalization of pressure between the aorta and left ventricle. (Courtesy of Brad Roberts, RDCS.)

regurgitation but a stiff left ventricle. As with pressure half-time, deceleration slope is influenced by systemic vascular resistance.[44] Thus, pressure half-time and deceleration slope are unreliable methods to assess changes in aortic regurgitation severity in response to vasodilators. However, these approaches may be helpful in assessing whether aortic regurgitation is chronic and well-compensated (flat slope), as compared

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with the steep slope in patients with acute, decompensated regurgitation. Diastolic Flow Reversal

Severe aortic regurgitation is associated with diastolic reversal of flow in the aorta (Fig. 17-6) [48] as well as Figure 17-6 Diastolic flow reversal demonstrated by pulsed Doppler interrogation of the descending aorta in the same patient shown in Figure 17-5 with severe aortic regurgitation. (Courtesy of Brad Roberts, RDCS.)

systolic augmentation of flow within the central aorta.[49] Pandiastolic reversal of flow in the superior abdominal aorta using pulsed Doppler echocardiography from a subcostal window is highly specific and sensitive for predicting severe aortic regurgitation.[50] It is possible to calculate aortic regurgitant fraction from the ratio of reversed to forward flow in the aortic arch using M-mode measurements to account for the systolic and diastolic changes in aortic diameter.[49] However, diastolic flow reversal in the aorta is directly related to aortic compliance, as well as to regurgitant volume. Abnormal diastolic flow patterns can be observed in subjects with abnormal compliance in the proximal aorta or in patients with left to right shunt from the aorta 373

(such as a patent ductus arteriosus).[49] Compared with the ascending aorta, pulsed Doppler interrogation of the descending aorta has been reported to more reliably reflect severity of aortic regurgitation, owing, in part, to the more uniform velocity profiles more distally in the aorta.[51] Other Indirect Markers

High left ventricular diastolic pressure associated with severe acute aortic regurgitation results in echocardiographic findings such as premature closure of the mitral valve or diastolic mitral regurgitation.[52] However, these markers of severe aortic regurgitation are poorly sensitive, being present in fewer than half of the patients with this condition.[42] [52] Increased E/A ratio was reported to be more sensitive for severe symptomatic aortic regurgitation, with greater sensitivity than pressure half-time, M-mode, or color flow mapping for predicting regurgitant severity. [42] [52]

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Tricuspid Regurgitation A reliable marker of severe tricuspid regurgitation is systolic reversal of flow in the hepatic veins and venae cavae (Fig. 17-7) .[53] Another index of severe tricuspid regurgitation is an associated annular diameter greater than 34 mm or greater than 21 mm/m.[28] Intracardiac Pressure Gradients Continuous wave Doppler echocardiography can be utilized to measure instantaneous and mean pressure gradients to assess the hemodynamic effects of regurgitant valvular lesions by using the modified Bernoulli equation. Left atrial pressure can be derived from the mitral regurgitant Doppler signal by subtracting the peak gradient from systolic blood pressure.[54] Similarly, left ventricular end-diastolic pressure can be calculated from the diastolic blood pressure and the aortic regurgitant enddiastolic pressure gradient.[47] [55] However, Doppler consistently overestimates left ventricular end-diastolic pressure because of suboptimal angulation of the interrogating ultrasound beam, resulting in underestimation of the peak velocity and gradient. [47] Therefore, the main limitation of this technique is suboptimal angulation and the inability to obtain a complete high-quality Doppler spectral envelope. When there is a rapid rise in left atrial pressure (V wave), the mitral regurgitant jet may appear asymmetric and cut off in late systole (Fig. 17-8) . Although right ventricular systolic pressure can be estimated from continuous wave Doppler interrogation of flow across a regurgitant tricuspid valve, [54] it is of little value in assessing the severity of tricuspid regurgitation, since increased regurgitant severity results in increased right atrial pressure and decreased peak tricuspid velocity and pressure gradient.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Proximal Flow Convergence Region Principle of Conservation of Mass Accelerating laminar flow patterns have been observed proximal to stenotic, regurgitant, and shunt orifices by Doppler color flow mapping by transthoracic and transesophageal echocardiography.[56] [57] [58] [59] [60] Regurgitant flow rate can be calculated from these laminar flow patterns based on the conservation of mass, which assumes that fluid converges uniformly and radially toward a restrictive orifice, forming a series of concentric isovelocity layers. These isovelocity surfaces are hemispheric for orifices that are small relative to the region of acceleration.[61] Compared to the turbulent downstream jet, this more predictable pattern of flow in the proximal flow convergence region makes quantitation of regurgitant severity possible. By Doppler color flow mapping, the radius (r) of the isovelocity surface is measured as the distance from the orifice to the point of color aliasing (Fig. 17-9) . Instantaneous flow rate can be calculated as the product of the aliasing velocity VA at any of these hemispheric contours times the surface area (2πr2 ) of that shell: Peak flow rate = VA (2πr2 ) (6) This calculation is based on the conservation of mass, which assumes that the accelerating flow through each isovelocity surface equals flow through the regurgitant orifice, since all flow through the isovelocity surface must pass through the orifice.[57] It is also assumed that the isovelocity hemispheric shells in the proximal flow convergence region demonstrate increasing velocity and decreasing surface area as the regurgitant orifice is approached. Each shell is associated with a particular velocity relative to its surface area. In theory, the proximal isovelocity surface area (PISA) derived from this zone of accelerating laminar flow is less dependent on

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instrument[62] and hemodynamic factors that influence the spatial extent of the regurgitant jet in the receiving chamber. Furthermore, unlike the volumetric method, the PISA method has the practical advantage of being independent of other associated regurgitant lesions. Initial in vitro and animal studies have demonstrated the validity of the hemispheric assumption for proximal isovelocity surfaces of small planar orifices relative to the acceleration zone.[57] [59] [63] There have been several clinical studies in patients with mitral or tricuspid regurgitation validating the PISA method using two-dimensional and quantitative Doppler techniques[64] [65] or color Doppler flow mapping.[66] The cause of mitral regurgitation did not affect the correlation of proximal flow acceleration estimates with angiography and quantitative Doppler calculations.[67] The PISA method was less useful in patients with aortic regurgitation in whom the Doppler beam angle exceeded 30 degrees.[66] By multiplane transesophageal echocardiography, comparison of flow rate calculations from the proximal convergence zone with angiographic grades of mitral regurgitation revealed that the proximal flow convergence method better distinguished severe from mild regurgitation than color Doppler area 374

Figure 17-7 (color plate.) Systolic flow reversal in the hepatic veins demonstrated by M-mode (A) and pulsed Doppler images (B) in a patient with severe tricuspid regurgitation. (Courtesy of Brad Roberts, RDCS.)

375

Figure 17-8 Continuous wave Doppler with V wave cut-off sign in severe mitral regurgitation (A) with simultaneous hemodynamic tracings (B) demonstrating the pressure relationship that causes the alteration in the deceleration slope of the time-velocity signal (arrows). Note the dark signal intensity of the Doppler signal. In the same patient, increased E wave velocity in A is additional evidence for severe mitral regurgitation. (Courtesy of Rick Nishimura, MD.)

and ratio of systolic to diastolic pulmonary venous flow velocities.[68]

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Technical Considerations The accuracy of the proximal flow convergence method is highly dependent on precise measurement of the PISA Figure 17-9 (color plate.) Color Doppler image of a patient with severe tricuspid regurgitation illustrating the proximal flow convergence zone with the hemispheric blue-to-yellow aliasing contour (blue-yellow interface or Nyquist limit) on the ventricular side of the tricuspid leaflets. (Courtesy of Brad Roberts, RDCS.)

radius, which requires high-resolution imaging and zoom magnification.[63] Furthermore, the proximal flow convergence region is not optimally visualized in all patients with regurgitant lesions, particularly in those with mild regurgitation. [66] [67] , [69] [70] Regurgitant Flow Rate and Aliasing Velocity

Adequate visualization of proximal flow acceleration thus depends on the severity of regurgitation and the aliasing velocity. Patients with very mild mitral regurgitation (regurgitant flow rate less than 20 m per second or regurgitant stroke volume less than 4.5 mL) do not have a visible proximal acceleration zone at the typical Nyquist velocity (VN ) of 49 to 58 cm per

second.[67] Because flow rate is underestimated unless the Nyquist velocity is much less than the orifice velocity, the hemispheric assumption for calculating regurgitant flow rate cannot be used with larger Nyquist velocities.[61] In in vitro models, the measured radius is always higher at lower aliasing velocities for a given flow rate (Fig. 17-10) . [69] Thus, the hemispheric model is most accurate with larger volume flow rates or with lower aliasing velocities. To improve accuracy, the aliasing velocity can be optimized to better define the hemispheric contour. [71] [72] Regurgitant flow rate is systematically overestimated furthest from the orifice and underestimated closest to the orifice because of progressive flattening of the flow convergence region (Fig. 17-11) . Therefore, the hemielliptical model may more accurately reflect flow rates closer to the orifice.[69] In the hemielliptical PISA method, radii from the orifice to the aliasing boundary are measured from long-axis (minor) and short-axis (major) views. This method correlates well with actual volume flow rates under

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376

Figure 17-10 (color plate.) In this patient with severe mitral regurgitation, the radius of the proximal flow convergence zone appears larger at a lower aliasing velocity of 22 cm per second (A) compared with an aliasing velocity of 33 cm per second (B). (Courtesy of Brad Roberts, RDCS.)

both constant and pulsatile flow conditions. When a flattened proximal convergence zone exists near the orifice, with a major-to-minor axis ratio greater than 2.0, the hemispheric model underestimates the actual volume flow rate by more than 50%. [69] Based on in vitro models, correction factors have been proposed to adjust for errors in flow rates calculated by the PISA method. [61] Orifice Size and Shape

The initial assumption that fluid converges toward an orifice in concentric hemispheric shells applies to an infinitesimally small orifice but cannot be applied to the finite orifice size of regurgitant orifices. In vitro models have demonstrated that the velocity distribution is independent of orifice size if measured at least two orifice diameters from the orifice, in situations in which the hemispheric assumption is valid.[61] In the clinical setting, a discrete Figure 17-11 Diagram of flow converging toward a finite orifice (bottom) showing the streamlines (dotted lines) and the consecutive isovelocity contours (solid lines), illustrating progressive contour flattening as the orifice is approached. (From Vandervoort PM, Thoreau DH, Rivera JM, et al: J Am Coll Cardiol 1993;22:535–541. Reprinted with permission from the American College of Cardiology.)

circular regurgitant orifice is rarely seen. Moreover, irregular or multiple orifices may make application of the PISA method more difficult. It has been proposed, however, that the PISA method can be consistently applied with irregular or multiple orifices if the measurements are obtained at greater distances (at least two orifice diameters) from the orifice.[59] [63] These studies conclude that measurements obtained far from the regurgitant orifice eliminate the influence of orifice size and shape. Other studies have demonstrated that orifice shape does not influence the accuracy of flow rate calculations if the aliasing velocity is small (<5%) relative to the orifice velocity.[61]

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Surrounding Geometry

In the setting of nonplanar surrounding geometry, the isovelocity shells cannot develop as full hemispheres and are effectively truncated as the orifice is approached.[56] [73] Distortion of the flow field is most pronounced when the constraining wall is positioned close to the regurgitant orifice, resulting in overestimation of the calculated flow rates. This situation can be observed with regurgitation caused by a posterior mitral leaflet flail (Fig. 17-12) . [74] Therefore, in the setting of mitral valve prolapse or flail, the following correction factor adjusts the calculated flow rate for the proximal flow convergence angle (α) (Fig. 17-13) : 2π(α/180) (7) Effective Regurgitant Orifice Area Experimental[75] [76] and clinical studies[77] have indicated that the effective regurgitant orifice area (EROA) provides unique quantitative information about the severity of regurgitation and is less influenced by hemodynamic variables than regurgitant volume and fraction.[75] [78] EROA 377

Figure 17-12 (color plate.) Posterior mitral leaflet flail (left) is demonstrated on transesophageal echocardiography with proximal flow convergence and a severe eccentric jet of regurgitation by color Doppler imaging (right) (see also color plate).

was initially calculated by the PISA method in an in vitro model using the following equation: EROA = (2πr2 VA )/VO = Q/VO (8) where VA is the velocity at a distance r from the orifice and VO is the orifice

velocity obtained by continuous wave Doppler.[79] Thus, in vitro and animal models demonstrated that EROA calculated by the PISA method demonstrated good correlation to actual EROA and to regurgitant stroke volume and fraction (Fig. 17-14) .[79] [80] Alternatively, if mitral regurgitant velocity is assumed to be about 5 m per second and the Nyquist limit is set to 40 cm per second, this equation can be simplified to

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EROA = r2 /2 (9) By comparison to angiographic grades of mitral regurgitation, grade I was associated with an EROA of less Figure 17-13 (color plate.) Flail posterior leaflet by transesophageal echocardiography demonstrating proximal flow convergence with wall constraint because of the proximity of the posterior wall. To adjust for the predictable overestimation caused by this geometric distortion, regurgitant flow rate and orifice area are adjusted by α/180. LA, left atrium; LV, left ventricle. (From Breburda CS, Griffin BP, Pu M, et al: J Am Coll Cardiol 1998;32:432–437. Reprinted with permission from the American College of Cardiology.)

than 10 mm2 and grade III with an EROA of greater than 25 mm2 . [79] In subsequent clinical studies, EROA measured by the PISA method correlated well with EROA measured by quantitative Doppler and twodimensional echocardiographic methods for tricuspid,[81] mitral,[82] and aortic regurgitation.[83] Limitations of EROA calculation by the PISA method include underestimation of aortic EROA in patients with an obtuse (>220-degree) proximal flow convergence angle [83] and overestimation in patients with mitral valve prolapse.[82] Overestimation of EROA in patients with mitral valve prolapse can be explained in part by dynamic changes in the effective orifice area.[84] [85] The PISA method provides instantaneous measurement of regurgitant flow and EROA and thus may not accurately reflect the overall severity of mitral regurgitation over the entire cardiac Figure 17-14 Line plot showing the correlation between effective regurgitant orifice area calculated by the proximal flow convergence method (y-axis) and the Doppler echocardiographic method (x-axis) in the clinical setting of mitral regurgitation. (From Vandervoort PM, Rivera JM, Mele D, et al: Circulation 1993;88:1150–1156.)

378

Figure 17-15 Typical examples of the types of dynamic changes in the

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regurgitant orifice area obtained by the electromagnetically determined flow method (EM). The regurgitant orifice size usually increases to maximal size in early to mid-systole (arrow) and decreases in late systole. (From Shiota T, Jones M, Teien DE, et al: J Am Coll Cardiol 1995;26:528–536. Reprinted with permission from the American College of Cardiology.)

cycle. Furthermore, the dynamic changes in EROA do not necessarily parallel the changes in regurgitant volume.[84] In late systole, despite continued increase in EROA, there is a decrease in the ventriculoatrial gradient and regurgitant velocity.[53] Experimental and clinical data further support the observation that the mitral regurgitant orifice changes dynamically during systole (Fig. 17-15) .[80] [86] Furthermore, the temporal variation in mitral regurgitant orifice area during systole varies according to the underlying cause.[86] Thus the PISA method of calculating EROA has the potential advantage of identifying the dynamic changes in regurgitant orifice area during the cardiac cycle. Changes in EROA are measured sequentially during the cardiac cycle by color M-mode echocardiography from the zenith of the isovelocity hemisphere.[80] [85] [86] The clinical implications of these data are that the EROA is not completely independent of hemodynamic variables and its changes may explain the beneficial effects of vasodilator therapy on functional mitral regurgitation.[77] In contrast, the existence of dynamic changes in aortic regurgitant orifice area is controversial.[87] [88] Dynamic changes have also been observed in the tricuspid regurgitant orifice area using the proximal flow convergence method.[89] Regurgitant Volume Although the calculation of regurgitant flow rate by the PISA method is relatively simple, requiring only the measurement of the isovelocity radius and aliasing velocity in a single view, it estimates peak, but not mean, flow rate. The measurement of regurgitant volume (RV) may be more accurate and clinically useful because the inclusion of the time velocity integral (TVI) by continuous wave Doppler may better reflect regurgitant jet dynamics during the cardiac cycle[64] [90] [91] RV = EROA × TVI (10) When regurgitant volume and flow rate by the PISA method are compared with angiographic grading of mitral regurgitation, PISA-derived regurgitant volume is better than flow rate at distinguishing 4+ mitral regurgitation from the other regurgitant grades.[71]

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In addition to the technical considerations that affect the validity of the hemispheric assumption of the PISA method, there are a number of limitations of this method for estimating regurgitant volume and flow rate. Since the PISA method relies on color Doppler to identify the region of proximal flow convergence, it is limited by technical factors that influence the accuracy of color Doppler flow mapping. Of these factors, the angle between the Doppler beam and direction of blood flow is most critical. The angle of the central PISA radius and the ultrasound beam must approach zero for optimal accuracy.[66] Other technical factors to be optimized include wall filter settings, interrogation depth, pulse-repetition frequency, and spatial beam expansion.[92] Furthermore, translational motion of the valve annulus affects the apparent PISA velocity, with overestimation with movement in the same direction[93] and underestimation with movement away from the PISA velocity shift.[94] Moreover, when the entire flow crossing the aliasing boundary does not pass through the restrictive orifice, as in ventricular septal defects,[93] the conservation of mass principle is not strictly applicable. Although attempts have been made to standardize the PISA method to calculate regurgitant flow, the optimal instrument settings for aliasing velocity and its corresponding radius remain unclear.[72] [91] [95] Furthermore, the accuracy of the PISA method is highly dependent on precise measurement of the radius from the orifice. Theoretically, the higher frequency imaging of transesophageal echocardiography provides improved spatial resolution and lower color aliasing velocity, which should improve the accuracy of the radius measurement.[96] Although attempts have been made to better define the radius by high-resolution imaging with zoom magnification, the exact position of the regurgitant orifice may still remain elusive.[70] [97] Errors in measurement of the PISA radius could result in significant errors in the estimation of volume flow. Vandervoort et al[97] propose an automated algorithm to locate the regurgitant orifice from a computer-simulated flow field, but this approach is not widely available.

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Vena Contracta Width Experimental and Clinical Validation The vena contracta width is defined as the narrowest diameter of regurgitant flow immediately downstream from the flow convergence region (Fig. 17-16) . Although, like proximal jet size, it is relatively unaffected by flow rate and driving pressure,[21] [98] vena contracta width is not identical to proximal jet size, since vena contracta width requires measurement of the diameter at the narrowest portion of regurgitant flow between the flow convergence region and the downstream turbulent jet.[99] Furthermore, the vena contracta width more directly reflects 379

Figure 17-16 (color plate.) Transesophageal imaging in the long-axis view demonstrates the vena contracta width as the narrowest extent of regurgitant flow immediately downstream from the flow convergence region in this patient with severe mitral regurgitation.

changes in the size of the regurgitant orifice.[100] Unlike proximal jet width, vena contracta width remains accurate in the presence of eccentric jets (Fig. 17-17) . [99] [101] [102] [103] [104] [105] The feasibility of measuring the vena contracta is 92% to 97% in patients with mitral regurgitation with minimal inter-observer variability.[100] [104] [106] Multiplane transesophageal echocardiography was shown to be more accurate than single plane imaging.[106] [107] Thus, the vena contracta method has been proposed to be a simple yet accurate method of assessing mitral regurgitant severity intraoperatively.[107] [108] Furthermore, vena contracta width is more predictive of the severity of mitral regurgitation than color Doppler jet area, left atrial size, and pulmonary venous flow.[104] Since mitral regurgitation worsens in the anteroposterior

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Figure 17-17 Linear regression plot showing good correlation between vena contracta width in the parasternal long-axis view and regurgitant volume (left) and regurgitant orifice area (right). Solid circles represent eccentric mitral regurgitation jets; open circles central jets. (From Hall SA, Brickner ME, Willett DL, et al: Circulation 1997;95:636–642.)

direction of the mitral valve orifice, accurate measurement of the vena contracta is obtained from long-axis views by transthoracic and transesophageal echocardiography. [100] [104] , [106] For mitral regurgitation, a vena contracta width of 5 mm or greater identifies severe mitral regurgitation, and a vena contracta width of 3 mm or less identifies mild mitral regurgitation.[104] In clinical and animal studies of aortic regurgitation, the vena contracta width correlates well with quantitative Doppler and electromagnetic flowmeter measurements, [103] [105] so that a vena contracta width of 6 mm or greater predicts severe aortic regurgitation, whereas mild aortic regurgitation is identified by vena contracta width of less than 5 mm.[105] EROA is estimated from the vena contracta width (VCW) by the following equation: EROA = π(VCW/2)2 (11) The estimated EROA and regurgitant volume flow correlated well with reference measurements by electromagnetic flowmeter (Fig. 17-18) .[103] A vena contracta width of 6.5 mm or greater predicts severe tricuspid regurgitation and correlates with EROA significantly better than visual estimates of jet area, which are influenced by right atrial pressure.[99] Clinical Considerations Accurate measurement of the vena contracta width is critically dependent on imaging with optimized axial resolution. Imaging views with poor lateral resolution result in artifactual widening of the flow signal and overestimation of regurgitant lesion severity. Precise imaging of the vena contracta requires smaller sector angles, high frame-rates, high resolution, appropriate color and tissue priority, and zoom mode magnification. However, the vena contracta width may be difficult to measure with poor acoustic windows, orifice movement, or rapid divergence of the jet beyond the orifice. Vena contracta width is not a direct measurement of regurgitant orifice area and is actually smaller than the anatomic orifice by a factor 380

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Figure 17-18 Correlation between peak regurgitant flow rates calculated by color Doppler vena contracta and electromagnetic flow meter methods. (From Ishii M, Jones M, Shiota T, et al: Circulation 1997;96:2009–2015.)

of 0.8 (coefficient of contraction). There is considerable overlap of actual regurgitant orifice areas in the intermediate mitral regurgitant vena contracta width range between 3 and 5 mm.[104] Therefore, regurgitant lesions in the intermediate vena contracta range may require additional methods of quantitation to more fully assess regurgitant severity.[109] In addition, the vena contracta width as a single measurement does not reflect dynamic changes in the regurgitant orifice during the cardiac cycle. In the presence of an irregular regurgitant orifice, multiple vena contracta width measurements in more than one plane may be necessary to improve accuracy.[103] [106] [109] , [110] Three-dimensional imaging of the vena contracta area accurately measures mitral regurgitant orifice by transesophageal echocardiography intraoperatively and may become the approach of choice as three-dimensional methods become clinically feasible.[108] The value of vena contracta width in the presence of multiple or diffuse regurgitant jets or atrial fibrillation is not known.

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Conservation of Momentum Theoretical Background Based on experimental studies of fluid dynamics of turbulent jet flow, the velocity distribution of the jet in the receiving chamber is best characterized by its momentum, which combines several factors such as flow rate, driving pressure, orifice velocity, and orifice area.[111] In the absence of a pressure gradient within the receiving chamber because of an adjacent wall or counterflow from another orifice, momentum should remain constant within the turbulent jet.[112] The principle of momentum conservation states that the momentum measured anywhere in the downstream jet is the same as the momentum of the jet at its orifice: Momentumorifice = Momentumjet (12) At the orifice, momentum is calculated by the product of jet velocity (Vo ) and flow rate (Q):

Momentumorifice = Vo Q (13) Thus, the regurgitant orifice flow rate (Q) can be calculated from jet momentum (M) measured anywhere along the extent of the jet, divided by orifice velocity (Vo ), measured by continuous wave Doppler[113] Q = M/Vo (14) Methods for Quantitation of Momentum In an in vitro model, when jets are formed through 0.005 to 0.5 cm2 orifices at a driving pressure of 1 to 81 mm Hg, the velocity distribution

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downstream conforms to a gaussian (bell-shaped) profile with the centerline velocity decaying inversely with distance from the orifice.[113] Jet momentum (M) flux can be calculated across the transverse plane of the jet by integrating flow velocity (v) across the area (A) of the jet in that plane: M = ∫A v2 dA (15) For an axisymmetric jet (circular cross section), momentum can be calculated from a single velocity profile across the jet: M = 2 π∫0 ∞v2 rdr (16) where r is the radial distance from the jet centerline to a point at which each velocity is measured. Thus, orifice flow rate can be accurately calculated by dividing momentum by the orifice velocity using equation 14. Effective regurgitant orifice areas then can be calculated by dividing momentum by the square of the orifice velocity: EROA = M/Vo 2 (17) An alternative approach, based on data from an in vitro pulsatile model, is to measure only the centerline velocity (Vc ), which is inversely proportional to the distance (x) from the orifice[114]

Vc (x) = 7.8√M/x (18) Then flow rate (Q) can be calculated by recording a single centerline velocity (Vc ) at a distance x from the orifice as well as orifice velocity

(Vo ):

Q = Vc 2 x2 /60.8Vo (19) The flow convergence centerline velocity/distance methods correlated well with reference methods in small

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381

clinical[115] and animal[116] studies that quantitated mitral and aortic regurgitation. The proposed benefit of the centerline velocity method over the PISA method is that the use of several data points instead of a single velocity data point improves accuracy.[116] Clinical Practice In spite of experimental validation and proposed theoretical advantages of using jet momentum or centerline velocity methods to quantitate valvular regurgitation, these methods are rarely used in the clinical setting for several reasons. First, since it has been reported that free jets are observed in only 60% to 70% of patients with mitral regurgitation,[10] the critical assumption of a free axisymmetric jet may not apply to a significant number of patients with eccentric jets in whom momentum is not conserved because of jet impingement on an adjacent wall or interference from pulmonary venous counterflow. It has been demonstrated that eccentrically directed jets are significantly underestimated by the momentum quantification method.[117] Moreover, application of the centerline velocity profile method requires accurate resolution of velocities within the turbulent jet, which is difficult because aliasing due to high velocities is often seen with mitral regurgitation. The considerable variation in the instantaneous velocity and position of the jet axis during the cardiac cycle requires data averaging using the simplified centerline velocity equation. Finally, the applicability of these methods is not known with varying size and compliance of the receiving chamber. Thus, these practical considerations limit the routine use of these momentum-based methods of quantification in the clinical setting.

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Amplitude-Weighted Mean Velocity Amplitude-weighted mean velocity is a nonvolumetric method for calculating the ratio of flow in shunt and regurgitant lesions based on the theory that the amplitude of the recorded Doppler signal is proportional to the number of erythrocytes contributing to the backscattered signal. This approach assumes a hematocrit within the normal range.[118] The amplitudeweighted mean velocity is calculated as the sum of the individual velocities of the erythrocytes within the continuous wave Doppler spectrum multiplied by their respective signal amplitudes.[118] Therefore, the basis of this approach is that each velocity is weighted according to the strength of its signal. Applying this concept over the cardiac cycle, the flow volume during a given time interval is proportional to the time integral of the average weighted mean velocity. Therefore, regurgitant fraction (RF) can be calculated as follows:

where the amplitude-weighted mean flow (AWMF) is measured at the regurgitant valve (regurg. valve) and at a competent reference valve (ref. valve). [119] The advantages of this method are that measurement of valvular surface areas is not necessary and its accuracy is not impaired in the presence of mitral valve prolapse. Regurgitant fraction calculated by the amplitudeweighted mean velocity method has been shown to correlate with ventriculographic[118] [120] and quantitative Doppler and two-dimensional echocardiographic findings.[119] There are technical considerations that limit the amplitude-weighted mean velocity method for calculation of regurgitant severity, however. These include the requirements that the continuous wave Doppler beam be of adequate width to include the entire area of the regurgitant signal (for example, the entire mitral annulus). In addition, the beam must be directed

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properly to avoid inclusion of adjacent flows, and the transducer must be maintained in the same position throughout the recording period to avoid translational motion from one valve to another. Furthermore, determination of the amplitude-weighted mean velocity varies with instrument gain settings and the effect of depth on signal strength. Thus, the ratio of amplitude-weighted mean velocity from the mitral valves to that from the aortic valves may not yield a value of 1.0, even in the absence of valvular regurgitation.[119] In addition to requiring a normal hematocrit, this method is applicable only in the setting of isolated regurgitant lesions, since separation of erythrocytes from blood plasma may falsely elevate the signal amplitude recorded from stenotic lesions.[118] Because the amplitude-weighted mean velocity is dimensionless, its measurement does not represent a physiologic variable and does not allow calculation of regurgitant volume or regurgitant orifice area. Thus, amplitude-weighted mean velocity may best be used as an adjunctive tool to quantitate valvular regurgitation. Finally, the requirement of special software limits the use of this approach in the clinical setting.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Three-Dimensional Echocardiography Three-dimensional echocardiography is an evolving technique that has been applied for the assessment of intracardiac anatomy,[121] [122] for quantification of intracardiac volumes, [123] and to better characterize mitral valve morphology by multiplane transesophageal echocardiography.[124] Initial three-dimensional reconstruction of color Doppler flow mapping for shunts and valvular regurgitant jets could only be visualized in gray scale and did not include quantitative information or comparison with actual flow rates.[125] [126] However, more recent in vitro studies have demonstrated that regurgitant flow may be accurately quantitated by three-dimensional reconstruction for bioprosthetic valves[127] and for varying native valve orifice shapes and jet morphologies.[110] In a preliminary clinical study, three-dimensional reconstruction has also been shown to accurately quantitate mitral regurgitant orifice area compared with the proximal flow convergence method intraoperatively in patients undergoing mitral valve repair.[108] Although early attempts to obtain color-coded images from threedimensional reconstruction required manual digitization of Doppler flow signals,[125] more recent studies 382

have demonstrated three-dimensional reconstruction of Doppler signals in original color coding by using direct digital data, which allows separate visualization of intracardiac flow and cardiac structures.[128] [129] These threedimensional images reveal the complex geometry of eccentric regurgitant jets in patients with mitral valve prolapse and demonstrate how misleading two-dimensional visual assessment or planimetry of regurgitant jets can be ( Fig. 17-19 and Fig. 17-20 ).[128] , [129] Since recent three-dimensional volumes are measured by an automated segmentation and voxel count procedure, they are independent of manual planimetry or subjective

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estimation. The technical and hemodynamic factors that influence color Doppler flow imaging also influence three-dimensional Doppler images.[129] However, the main limitation of three-dimensional echocardiography is the need for stable positioning of the transducer during image acquisition or a method to continuously track transducer position relative to cardiac structures. Another limitation is that three-dimensional reconstruction is time consuming, and the presence of irregular heart rhythms such as atrial fibrillation can significantly prolong the process. Furthermore, the timerelated changes of three-dimensional jet Figure 17-19 (color plate.) A, Transesophageal color Doppler images in a patient with a mitral regurgitant jet recorded at different rotational angles (0 and 90 degrees). B, Three-dimensional reconstruction of the central regurgitant jet in a patient with atrioventricular septal defect. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

areas and volumes have not yet been characterized. Some of these limitations will be overcome in the future with the advent of real-time three-dimensional echocardiography.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Implications The quantitation of valvular regurgitation is important, not only for the early detection of hemodynamically significant lesions but also for monitoring of therapeutic success. It has been suggested that not all patients respond favorably to vasodilator therapy, and quantitative methods can thus assist in differentiating patients by their response to therapeutic interventions.[130] [131] [132] However, the quantitative assessment of valvular regurgitation is a far more complex issue than the measurement of such variables as regurgitant volume, regurgitant fraction, and regurgitant orifice area. In addition to the anatomy of the regurgitant lesion, its hemodynamic impact should also be taken into account, since symptoms are not necessarily related to regurgitant severity.[32] [133] A semiquantitative index has been proposed that incorporates variables reflecting 383

Figure 17-20 (color plate.) A, Transesophageal color Doppler images show a wall-impinging mitral regurgitant jet at different angles (0 and 90 degrees). None of these conventional views is able to visualize the regurgitant jet entirely. B, Three-dimensional Doppler reconstructions show that the regurgitant jet resembles a spoon. The lower panel shows the convex face of this spoon jet. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

384

TABLE 17-1 -- Calculation of the Mitral Regurgitant Index Characteristic Jet penetration

Score Description 0 No jet

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1 2

PISA

CW jet

3 0 1 2 3 0 1 2 3

Pulmonary artery pressure Pulmonary venous flow

0 1 2 3 0

Central jet that does not impinge on lateral wall in any view Eccentric jet that extends to the pulmonary vein Eccentric jet that encircles the atrium No PISA visualized PISA ≤0.5 cm radius PISA 0.5–1.0 cm PISA ≥1.0 cm No jet detected Incomplete jet envelope Complete envelope, jet density 20%–50% of mitral inflow Complete envelope, jet density 50%–70% of mitral inflow <25 mm Hg 25–30 mm Hg 31–45 mm Hg >45 mm Hg Systolic flow exceeds diastolic flow by ≥50%

1 Systolic flow exceeds diastolic flow by <50% 2 Diastolic flow > systolic flow 3 Systolic flow reversal Left atrial 0 None enlargement 1 Mild 2 Moderate 3 Severe The mitral regurgitant index = total score/number of variables CW, continuous wave Doppler ultrasonography; PISA, proximal isovelocity surface area. From Thomas L, Foster E, Hoffman JIE, et al: J Am Coll Cardiol

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1999;33:2016–2022. the hemodynamic impact as well as characteristics of the regurgitant jet (Table 17-1) .[133] The same regurgitant volume may be associated with changing valve structure and varying degrees of chamber dilation and function. Furthermore, echocardiographic signs of severe chronic regurgitation may not be applicable in the acute setting. Although volumetric and proximal isovelocity surface area methods have been validated both clinically and experimentally, these methods are rarely applied in routine clinical practice because they are time consuming and highly dependent on operator experience. Indirect TABLE 17-2 -- Proposed Doppler Criteria for Identifying Severe Valvular Regurgitation by the Transesophageal Approach Mitral Regurgitation Jet area/left atrium area >40% Regurgitant fraction >40% Vena contracta width >5.5 mm Systolic pulmonary vein flow reversal Present Aortic Regurgitation Vena contracta width >12 mm Pressure half-time of regurgitant flow <350 msec End-diastolic flow velocity in the descending aorta >18 cm/sec Modified from Tribouilloy C, Shen WF, Leborgne L, et al: Éur Heart J 1996;17:272–280.

TABLE 17-3 -- Summary of Echocardiographic Methods to Quantify Valvular Regurgitation Method Doppler color flow mapping

Volumetric Doppler

Limitations Jet area represents velocity not volume and is influenced by driving pressure, receiving chamber compliance, regurgitant orifice size, and instrument factors. Underestimation of severity occurs with eccentric jets. Accurate in experienced hands, yet time consuming. Greatest measurement of mitral or

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aortic cross-sectional area. Requires competent valve to measure forward stroke volume. Pulmonary venous In addition to severe MR, systolic-to-diastolic flow pulmonary flow ratio may be influenced by other variables, such as LV function, LA compliance, atrial fibrillation, mitral stenosis, loading conditions, sampling of left vs. right pulmonary vein. AR pressure half-time Both markers are less reliable when systemic and deceleration slope vascular resistance is altered or in the presence of LV dysfunction with significant overlap of values for varying degrees of AR severity. Aortic diastolic flow Related to regurgitant volume and aortic reversal compliance. Proximal flow Relies on hemispheric geometric assumptions. convergence Requires selection of optimal aliasing velocity and identification of the orifice for precise measurement of the radius. Overestimation of flow is observed with eccentric jets. Vena contracta width Simple and accurate but requires optimal axial resolution and imaging plane for clear definition. Limited with rapidly divergent jets and overlap in lesion severity between 3–5 mm. Momentum Measures flow rate and ROA from a single velocity profile across an axisymmetric jet. Validated in vitro but rarely used clinically. Not applicable to eccentric jets. Amplitude-weighted Nonvolumetric method for calculating ratio of flow mean velocity based on the amplitude of the Doppler signal. Requires special software. Three-dimensional Reveals the complex geometry of regurgitant echocardiography lesions. Requires stable positioning of transducer and patient during image acquisition, which may be time consuming. AR, aortic regurgitation; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; ROA, regurgitation orifice area.

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markers are affected by other variables and should not be used in isolation to determine regurgitant severity (Table 17-2) . Although there are many proposed echocardiographic methods to quantify valvular regurgitation (Table 17-3) , the main limitation has been the lack of a true gold standard for comparison.[27] [134] The challenge to future investigations in this area is to develop a better gold standard for quantifying valvular regurgitation by extracting more reproducible yet accurate spatial, temporal, and velocity information from color Doppler imaging.

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389

Chapter 18 - The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation David J. Meier MD Carolyn K. Landolfo MD Mark R. Starling MD

The optimal timing of surgical intervention in patients with chronic mitral and aortic regurgitation remains controversial and challenging. Historically, mitral and aortic regurgitation have been considered hemodynamically equivalent as conditions of left ventricular (LV) volume overload.[1] Although mitral regurgitation is a condition of primary LV volume overload, aortic regurgitation generates both a pressure and a volume overload on the left ventricle. In both conditions, preload is elevated because of excess volume, resulting in the development of eccentric hypertrophy. In aortic regurgitation, however, afterload is also increased secondary to LV pressure overload, resulting in the development of concomitant concentric hypertrophy. These fundamental hemodynamic differences are responsible for the observed differences between mitral and aortic regurgitation in the natural history of the disease processes, mechanisms for LV systolic dysfunction, response to surgery, and the appropriate timing of surgical intervention.

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After a long asymptomatic period, often lasting several years, prolonged mitral or aortic regurgitation inevitably leads to LV pump dysfunction, which is characterized by decreased LV ejection fraction and contractile dysfunction. [2] [3] [4] [5] [6] [7] [8] In assessing LV pump performance in valvular regurgitation, it is important to distinguish between ejection performance and contractile performance of the left ventricle. Left ventricular ejection performance, commonly measured by indices such as ejection fraction and percent fractional shortening, refers to the global pumping capability of the left ventricle. Because LV ejection phase indices are affected by multiple variables, such as contractility, heart rate, preload, and afterload, an abnormal LV ejection fraction does not necessarily imply abnormal contractility. Likewise, LV ejection fraction may be normal, despite significant underlying contractile dysfunction. Left ventricular contractility, on the other hand, refers specifically to the performance of the contractile apparatus of the left ventricle, independent of loading conditions. Although both mitral and aortic regurgitation eventually lead to LV pump dysfunction, the mechanisms underlying decreased LV pump performance differ between the two conditions. Wisenbaugh et al[9] evaluated the hemodynamic characteristics of patients with severe aortic regurgitation (n = 9) and severe mitral regurgitation (n = 8) and compared the findings to those of normal subjects (n = 7) (Fig. 18-1) . Despite a similar volume of regurgitation between the patients with aortic and mitral regurgitation, afterload (end-systolic stress) was found to be significantly increased above control in patients with aortic regurgitation, but not in patients with mitral regurgitation. Conversely, LV contractile dysfunction, measured by the ratio of end-systolic stress to end-systolic volume index, was found to be more depressed in patients with mitral regurgitation than in patients with aortic regurgitation, despite comparable reductions in LV ejection fraction. These data suggest that the mechanism for decreased LV pump performance in aortic regurgitation is afterload excess, in contrast to mitral regurgitation, in which LV contractile dysfunction is the primary mechanism. Because 390

Figure 18-1 The relationship between left ventricular ejection fraction (EF) and end-systolic stress, constructed from the data of Wisenbaugh et al,[9] is illustrated for normal subjects and patients with mitral (MR) or aortic (AR) regurgitation. End-systolic stress or afterload is increased only in the AR group. (From Devlin WH, Starling MR: Cardiol Rev 1994;3:16–28.)

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of the favorable loading conditions in mitral regurgitation, however, ejection phase indices of LV systolic performance often remain normal, thereby masking the severity of LV contractile dysfunction. Although afterload excess is the primary mechanism for LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to decreased LV pump performance, but typically as a late manifestation of severe, prolonged regurgitation.[11] These hemodynamic differences between mitral and aortic regurgitation have very important clinical implications, both in terms of disease progression and in response to corrective surgery. Because afterload excess is responsible for the early decline in LV pump performance in aortic regurgitation, the decrease in afterload that follows aortic valve replacement favors improvement in LV systolic performance, even when preoperative LV ejection phase indices are depressed.[12] [13] [14] [15] [16] [17] Later in the course of the disease, however, significant contractile dysfunction also develops, resulting in progressive and potentially irreversible LV failure. In contrast, contractile dysfunction develops relatively early in the natural history of mitral regurgitation, but it may be masked by the favorable preoperative loading conditions and the compensatory activation of the sympathetic nervous system with resultant beta-adrenergic stimulation.[18] [19] [20] [21] [22] [23] [24] Postoperatively, as loading conditions change with elimination of the regurgitant leak into the low-resistance left atrium, this underlying contractile dysfunction becomes unmasked, resulting in a decreased in LV ejection fraction.[5] [6] [7] [16] [25] [26] [27] [28] [29] Patients with mitral regurgitation who have even a mildly depressed LV ejection fraction preoperatively often have severe contractile dysfunction and are, therefore, at risk for significant LV systolic dysfunction, congestive heart failure, and death in the postoperative period.[4] [5] [6] [7] [8] However, in patients with occult contractile dysfunction marked by a mildly elevated end-systolic dimension in the presence of a normal LV ejection fraction, recovery of contractile function often does occur postoperatively.[30] Thus, these data highlight the clinical imperative in mitral regurgitation to identify early, occult, but potentially reversible contractile dysfunction to optimize the long-term results of mitral valve surgery. This is important because there appear to be two populations of patients: those in whom contractility improves and those in whom contractility does not improve following mitral valve surgery.

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Therefore, because reduced LV ejection fraction reflects more severe contractile dysfunction in mitral compared with aortic regurgitation, a greater degree of preoperative LV pump dysfunction is tolerated without adverse clinical outcome in aortic regurgitation, provided that the duration of LV pump dysfunction is brief. Prolonged LV pump dysfunction reflects severe contractile dysfunction in both mitral and aortic regurgitation and is associated with an adverse postoperative outcome. The ability to identify contractile dysfunction and correct the regurgitant lesion before contractile dysfunction becomes irreversible is critical to the timing of surgical intervention for both regurgitant valve lesions. Although contractile dysfunction is the mechanism for the early decrease in LV ejection fraction in mitral regurgitation, the type of operation performed also significantly affects the degree of postoperative LV pump dysfunction. [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] LV ejection fraction almost always declines after conventional mitral valve replacement with removal of the submitral apparatus, even when preoperative indices of LV pump performance are normal.[31] [32] [33] [36] [37] This decline of LV ejection fraction has been attributed to an alteration in LV geometry resulting from transection of the chordae tendineae and removal of the papillary muscles. Conversely, LV ejection fraction is not decreased to the same extent after mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] , [40] Therefore, because mitral valve reconstruction preserves LV pump performance and can be performed with a low operative morality rate and low risk for thromboembolism and endocarditis, earlier surgical intervention has been advocated in all patients in whom valve repair is feasible, particularly those with reduced LV pump performance. [42] The major challenge in the management of patients with valvular regurgitation is the ability to identify contractile dysfunction and to correct the regurgitant lesion before irreversible contractile dysfunction develops. The purpose of this chapter is to present the echocardiographic parameters that can be used to guide timing of surgical intervention in aortic and mitral regurgitation. Because LV contractility dysfunction is the most important determinant of survival and postoperative outcome in valvular regurgitation, the primary goal guiding the timing of surgical intervention is assumed to be preservation of contractility. Unfortunately, many noninvasive variables currently used to guide surgical intervention identify patients likely to do poorly after surgery, but they do not pinpoint the onset of occult, reversible contractile dysfunction when timely operative

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intervention would be warranted. [11] [18] , [26] [28] The proposed algorithms presented in this chapter for the evaluation of patients with valvular regurgitation incorporate clinical, hemodynamic, and echocardiographic variables into rational guidelines for 391

appropriate timing of surgical intervention directed toward the long-term preservation of contractility.

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Pathophysiologic Mechanisms Although LV volume overload is the primary hemodynamic abnormality in mitral regurgitation, both pressure and volume overload exist in aortic regurgitation. [1] Significant elevations in preload caused by increased regurgitant volume in both mitral and aortic regurgitation lead to the development of eccentric hypertrophy, characterized by LV enlargement and increased myocardial mass.[2] [3] [20] The degree of hypertrophy is commensurate with the degree of LV dilation, maintaining the ratio of LV mass to end-diastolic volume within the normal range. In addition to eccentric hypertrophy, increased systolic wall stress (afterload) in aortic regurgitation also leads to the development of concentric hypertrophy.[1] [9] The differences in the compensatory mechanisms of the left ventricle to pure volume overload in mitral regurgitation and both pressure and volume overload in aortic regurgitation account for the observed difference in disease progression, changes in LV pump performance, and response to operation. Mitral Regurgitation Acute Mitral Regurgitation.

The pathophysiologic mechanisms underlying mitral regurgitation have been well reviewed by Carabello.[43] [44] Left ventricular ejection fraction increases in acute mitral regurgitation as a result of increased preload and decreased afterload. In acute mitral regurgitation, the left ventricle compensates for the sudden increase in volume by increasing sarcomere diastolic length (preload). Left ventricular end-diastolic volume increases, leading to augmentation of LV stroke work by the Frank-Starling mechanism. In addition to increased preload, systolic ejection of blood through the incompetent mitral valve into the low-impedance left atrium lowers systolic wall stress (afterload). Decreased afterload, in turn, augments ventricular emptying, resulting in reduced end-systolic volume,

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increased total stroke volume, and increased ejection fraction. In acute mitral regurgitation, therefore, the left ventricle compensates for the volume overload by emptying more completely. Chronic Compensated Mitral Regurgitation.

The transition from the acute to the chronic state of mitral regurgitation is characterized by LV enlargement and compensatory eccentric hypertrophy, resulting in an increase in LV end-diastolic volume and mass. The increase in LV end-diastolic volume enables augmentation of total stroke volume, helping to return forward stroke volume toward the normal range. With the development of eccentric hypertrophy, the radius of the left ventricle increases without a significant change in wall thickness, increasing wall stress into the normal range, in accordance with the law of Laplace. As wall stress increases into the normal range, LV emptying decreases and endsystolic volume increases. In the compensated phase, therefore, the increase in LV end-diastolic volume produced by increased preload and the increase in end-systolic volume result in an ejection fraction that is within the normal range, but less than that of the acute stage. Chronic Decompensated Mitral Regurgitation.

As a result of these compensatory mechanisms and the stimulation of the sympathetic nervous system, patients with chronic mitral regurgitation may remain asymptomatic for long periods of time and LV ejection phase indices may remain normal, despite underlying contractile dysfunction. Eventually, contractility declines beyond the compensatory capabilities of the left ventricle and the sympathetic nervous system.[24] With LV decompensation, ejection fraction decreases because of an increase in endsystolic volume. Left ventricular end-diastolic pressure increases, resulting in further eccentric hypertrophy and LV dilation. With progressive increases in the radius of the left ventricle, wall stress increases above normal, resulting in a significant increase in end-systolic volume. A vicious cycle thus evolves, leading to a progressive decline in LV pump performance. Response to Operation.

In compensated mitral regurgitation, correction of the regurgitant lesion results in a decrease of LV end-diastolic volume and end-diastolic dimension into the normal range. Although postoperative end-systolic stress remains normal, LV ejection fraction decreases in nearly all patients

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after mitral valve replacement with removal of the submitral apparatus.[45] Left ventricular ejection fraction generally remains unchanged in patients with compensated mitral regurgitation who undergo mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] [34] , [40] In decompensated mitral regurgitation, there is marked preoperative LV enlargement, elevation in end-systolic wall stress, and decreased fiber shortening. [45] Postoperatively, the left ventricle remains persistently dilated, end-systolic wall stress increases, and ejection fraction declines significantly. Interestingly, in children and young adults, the early postoperative course of LV systolic dysfunction is similar to that in adults, but the long-term occurrence of LV systolic dysfunction is significantly different. In a recent study by Krishnan et al,[46] long-term postoperative LV systolic dysfunction was found to be rare, but it occasionally occurred. Better clinical postoperative results were associated with a shorter duration of mitral regurgitation. Aortic Regurgitation Acute Aortic Regurgitation.

In acute aortic regurgitation, because the normal LV chamber cannot acutely adapt to the large regurgitant volume, forward stroke volume is reduced, resulting in significant elevation in LV end-diastolic pressure.[47] Prolonged regurgitation eventually leads to the development of LV dilation and eccentric hypertrophy.[20] Chronic Compensated Aortic Regurgitation.

In the transition from acute to chronic compensated aortic regurgitation, LV dilation and eccentric hypertrophy accommodate a larger end-diastolic volume. [20] [48] The increased LV end-diastolic volume, in turn, allows for 392

increases in both total and forward stroke volume, thereby returning LV filling pressures to normal. These compensatory mechanisms maintain LV ejection fraction and end-systolic volume within the normal range. In addition, vascular adaptation, as measured by total arterial elastance, has been found to occur in response to chronic aortic regurgitation. This LV-

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arterial coupling occurs in a heterogeneous pattern. In some patients it decreases, thereby maximizing LV work and performance, whereas in others it increases, causing "double loading" of the left ventricle and progressive pump dysfunction. [49] Concentric hypertrophy also develops in aortic regurgitation in response to pressure overload.[1] [9] [20] Unlike mitral regurgitation, in which the excess volume is unloaded into the low-impedance left atrium, in aortic regurgitation, the forward and regurgitant volume must be pumped into the higher pressure arterial system, resulting in an increase in end-systolic pressure and wall stress.[50] In accordance with the Laplace relationship, an increased end-systolic wall stress results in concentric hypertrophy, leading to an increase in wall thickness, returning the ratio of cavity radius to wall thickness to within the normal range. Chronic Decompensated Aortic Regurgitation.

The transition to decompensated aortic regurgitation is characterized by progressive LV dilation and deterioration in LV pump performance resulting from intrinsic contractile dysfunction.[2] [51] At this stage, the left ventricle has reached its limit of compensation and can no longer increase wall thickness to compensate for increases in preload. The ratio of cavity dimension to wall thickness increases, resulting in elevated end-systolic wall stress and afterload mismatch. Total and forward stroke volumes decrease and end-systolic volume increases, resulting in a decline in ejection fraction and elevation in left-sided filling pressures. Response to Operation.

In chronic compensated aortic regurgitation, valve replacement results in a reduction in end-diastolic volume and regression of LV hypertrophy. [16] [17] , [52] [53] [54] [55] [56] [57] Afterload also decreases, resulting in improved LV pump performance, even if LV ejection fraction was reduced preoperatively. In chronic decompensated aortic regurgitation, there is marked LV enlargement, significant elevation in end-systolic wall stress, and decreased LV pump performance.[59] [60] Despite successful valve replacement, LV dilation and hypertrophy persist, end-systolic wall stress remains elevated, and systolic performance remains depressed, indicating the development of irreversible contractile dysfunction.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Function in Valvular Regurgitation Although the pathophysiologic mechanisms differ between the two regurgitant valve lesions, LV pump performance is the most important determinant of survival and postoperative outcome in both mitral and aortic regurgitation. As a result, most of the variables used to predict outcome in valvular regurgitation relate to LV ejection phase indices. How, then, is LV systolic performance best evaluated in chronic valvular regurgitation? Ejection Phase Indices. Left ventricular pump performance is often gauged by indices such as ejection fraction and percentage of fractional shortening. These LV ejection phase indices can be altered dramatically, however, by changes in loading conditions, heart rate, and contractility.[18] Alteration in any one of these factors can change LV ejection fraction without necessarily implicating abnormal contractility as the mechanism.[22] Likewise, LV ejection fraction can remain normal, despite markedly impaired contractility. [26] [28] Because mitral and aortic regurgitation are states of altered load, LV ejection phase indices may not accurately assess contractility in these conditions. End-Systolic Indices. To overcome the limitations of LV ejection phase indices in the assessment of contractile state in valvular regurgitation, investigators have alternatively used load-independent variables.[18] [21] [22] [23] [46] Because preload is elevated in valvular regurgitation, preload-independent variables, particularly the end-systolic indices, are commonly employed to assess contractility in mitral and aortic regurgitation.[19] [61] [62] [63] [64] [65] [66] [67] [68] [69] The endsystolic indices have been classified according to those that measure afterload, including end-systolic stress and end-systolic pressure; and those that indicate LV size, including end-systolic volume and end-systolic

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dimension. The ratio of end-systolic stress (or end-systolic pressure) to endsystolic volume (or end-systolic dimension) are preload-independent indices of contractility that also correct for afterload. The basic principle underlying the use of these indices of contractility is that for a given afterload, a ventricle that can shorten to a smaller end-systolic volume has greater contractility than a ventricle with a larger end-systolic volume. End-Diastolic Indices. End-diastolic indices, including end-diastolic dimension and end-diastolic wall stress (the product of end-diastolic pressure and dimension divided by the wall thickness) have also been used to evaluate LV performance in valvular regurgitaton. [59] [66] Left ventricular end-diastolic dimension increases in valvular regurgitation in response to volume overload. In mitral regurgitation, end-diastolic dimension increases without significant changes in wall thickness, whereas in aortic regurgitation both end-diastolic dimension and wall thickness increase. Progressive increases in enddiastolic dimension and end-diastolic wall stress are suggestive of decompensation in both conditions of valvular regurgitation. Pressure-Volume Relationship. The slope of the LV end-systolic pressure-volume relationship has also been used as a load-independent measure of contractility.[11] [20] [21] , [26] [69] [70] [71] Unfortunately, determination of this slope requires measurement of endsystolic volume at different levels of afterload, typically using pharmacologic stress during cardiac catheterization. In most clinical settings, therefore, the pressure-volume relationship cannot be used as a routine tool for serial assessment of contractility in valvular regurgitation. Importantly, however, it can be used to provide insights into the occurrence of contractile dysfunction that can be translated into better use of ejection phase indices to determine the appropriate timing of surgical intervention, particularly in mitral regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Chronic Mitral Regurgitation 393

Traditionally, surgery for chronic mitral regurgitation has been delayed until the onset of symptoms. Unfortunately, by the time symptoms have developed, severe irreversible contractile dysfunction may already be present. Contractile dysfunction typically develops during the asymptomatic period when ejection phase indices of LV pump performance remain within the normal range. Because survival is reduced in patients with mitral regurgitation who have irreversible contractile dysfunction, current management strategies have been directed toward the timing of surgery to prevent progression to irreversible contractile dysfunction. Advances in detection of occult contractile dysfunction, better knowledge of the preoperative predictors of surgical outcome, reduction in mortality for mitral valve replacement using chordal-sparing techniques, and advances in mitral valve repair are leading to earlier surgical intervention in this population of patients. Etiology The mitral valve apparatus consists of the annulus, the anterior and posterior leaflets, the chordae tendineae, and the papillary muscles. Mitral regurgitation develops from alterations in one or more components of the mitral apparatus. [72] Causes of chronic mitral regurgitation are listed in Table 18-1 .[73] The most common causes of pure isolated mitral regurgitation include myxomatous degeneration (62%) (Fig. 18-2) , ischemia-related papillary muscle dysfunction (30%), infectious endocarditis (5%), and rheumatic disease (3%).[72] Changing Etiology of Mitral Regurgitation.

The spectrum of surgical mitral valve disease has changed significantly

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since the 1970s, with a decline in surgical referral for rheumatic valvular disease and an increase for myxomatous degenerative disease.[74] [75] [76] [77] In one review, TABLE 18-1 -- Causes of Chronic Mitral Regurgitation Mechanism Condition Inflammatory Rheumatic heart disease Systemic lupus erythematosus Takayasu's arteritis Scleroderma Degenerative Myxomatous degeneration of mitral valve leatlets Mitral valve annular calcification Marfan's syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Infectious Bacterial endocarditis Structural Ruptured chordae tendineae Rupture or dysfunction of the papillary muscles Dilation of the mitral valve annulus Hypertrophic cardiomyopathy Paravalvular prosthetic leak Congenital Mitral valve clefts or fenestrations Parachute mitral valve abnormality Adapted from Haffajec CI: Chronic mitral regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown. 1987, pp 111–119. Figure 18-2 (color plate.) Transesophageal echocardiogram in the longitudinal plane (two-chamber view) from a patient with myxomatous degenerative mitral valve disease who presented with a 3-month history of dyspnea. Demonstrated is mitral valve prolapse (A) with a flail posterior leaflet secondary to a ruptured chordae tendineae, resulting in severe mitral regurgitation (B).

rheumatic valvulitis accounted for 46% of all surgically treated cases of

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mitral regurgitation from 1970 through 1974, but only 15% from 1985 through 1989. Conversely, myxomatous degenerative disease accounted for only 37% of cases in the earlier years, but it represented 60% of cases in the latter years.[75] Changes in the etiology of mitral regurgitation have been paralleled by changes in surgical therapy for the disease. The number of valves being repaired has steadily increased, particularly in centers experienced in valve reconstruction. At the Cleveland Clinic, 80% of patients referred for correction of mitral regurgitation in 1988 underwent valve repair (see Chapter 19) .[74] Because of the potential for valve repair, the specific anatomic defect responsible for mitral regurgitation, defined by twodimensional and transesophageal echocardiography, has become an integral part of the evaluation of patients with mitral regurgitation. The potential to repair myxomatous degenerative valves has been further stratified according to the specific anatomic defect. Because operative mortality and overall complication rates are lower with mitral valve repair procedures,[72] [77] the ability to repair a valve favors earlier surgical intervention to prevent development of occult contractile dysfunction. Natural History Importance of Left Ventricular Pump Performance.

394

The natural history of mitral regurgitation is variable and depends on multiple factors, including the volume of regurgitation, LV pump performance, contractile state, and the underlying etiology of the disease.[3] [78] [79] The most important determinant of survival, however, is LV contractile state. Chronic mitral regurgitation represents a state of volume overload in which elevated preload and compensatory eccentric hypertrophy maintain overall LV ejection fraction within the normal range for extended periods of time.[43] [44] In addition, recent evidence suggests that LV pump performance in chronic mitral regurgitation is also maintained by activation of the sympathetic nervous system. Nagatsu and colleagues[24] used a canine model to show that indices of LV ejection and contractile performance could be maintained in the normal or near-normal range by beta-adrenergic stimulation in surgically created chronic mitral regurgitation, despite the

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presence of significant underlying contractile dysfunction.[49] This implied that by the time contractile dysfunction is detected in the absence of betaadrenergic blockade, severe contractile dysfunction is already present. In human subjects, Mehta and colleagues[80] [81] found that the sympathetic nervous system was activated in proportion to the increase in LV endsystolic volume and the reduction in ejection fraction, rather than the severity of mitral regurgitation (Fig. 18-3) . Activation of the sympathetic nervous system was found to increase and was clearly evident at echocardiographic LV end-systolic dimensions of 40 mm or more. Despite the initial compensatory function of beta-adrenergic stimulation in mitral regurgitation, chronic stimulation may have adverse effects on LV contractility. Canine models of surgically created mitral regurgitation have shown that sustained beta-adrenergic blockade resulted in Figure 18-3 The relationship between the extravascular norepinephrine release rates (NE2 ) and echocardiographically determined left ventricular end-systolic dimension (ESD) is shown. Note that sympathetic tone is markedly elevated in mitral regurgitation patients with a left ventricular ESD of greater than 40 mm. (From Mehta RH, Supiano MA, Oral H, et al: Am J Cardiol 2000;86:1193–1197.)

improved LV pump performance. This effect was associated with an improvement in cardiocyte contractility secondary to an increased number of contractile elements in isolated cardiocytes.[82] These compensatory mechanisms allow patients to remain asymptomatic for many years. Eventually, a transition phase ensues, during which time insidious contractile dysfunction begins to develop. During this transition phase, however, patients generally remain asymptomatic or are just beginning to develop mild symptoms of fatigue. The development of atrial fibrillation often heralds the onset of this decompensation.[83] [84] By the time patients become overtly symptomatic, with exhaustion, decreased exercise tolerance, and congestive heart failure, severe irreversible contractile dysfunction may have already developed.[3] , [78] It is important to understand that, despite significant and potentially irreversible contractile dysfunction, LV ejection fraction may be reduced to only 40% to 50%. [26] [28] Right heart failure, characterized by congestive hepatomegaly, ascites, and peripheral edema, may develop late in the course of the disease.[77] [85] Medical versus Surgical Therapy.

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Overall survival in chronic mitral regurgitation appears to be improved with surgical therapy in patients with normal or reduced LV pump performance. Because the natural history of severe mitral regurgitation has been significantly altered by surgical advances, only a few studies exist that directly compare medical with surgical therapy[86] [87] [88] [89] (Table 18-2) . Rapaport[86] studied the natural history of 70 patients with mitral regurgitation treated medically over a 5- and 10-year period. The survival rate at 5 and 10 years was reported to be 80% and 60%, respectively, for patients with isolated mitral regurgitation. Hammermeister et al[87] reported much lower 5- and 9- to 10-year survival rates for 36 medically treated patients at 55% and 22%, respectively. Survival was significantly improved in the 61 patients who underwent mitral valve replacement, with 5- and 9to 10-year survival rates of 72% and 63%, respectively. Delahaye et al[89] also reviewed the outcomes of 216 patients with chronic mitral regurgitation. Actuarial survival at 8 years for the surgical group (n = 116) was 74%, compared with 33% for the medical group (n = 54). For mixed mitral regurgitation and stenosis, survival with medical therapy has ranged from 45% to 65% at 5 years and 27% to 32% at 9 to 10 years. Surgery also improves mortality in this subset of patients, with survival rates reported at 61% to 84% at 5 years and 75% at 9 to 10 years. Although survival is reduced in patients with impaired LV pump performance, overall mortality is improved with surgery compared with medical therapy. [87] Therefore, surgery should not be withheld in patients with chronic mitral regurgitation on the basis of reduced LV ejection fraction. Mitral Valve Replacement Importance of Preservation of the Submitral Apparatus.

Left ventricular ejection fraction frequently decreases after surgical correction of chronic mitral regurgitation, 395

TABLE 18-2 -- Survival in Chronic Mitral Regurgitation: Comparison Surgical Therapy Medical Therapy

Sur

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PATIENTS, Study Condition n MR 70 Rapaport[86] MR/MS 102 Hammermeister MR 36 [87] et al MR/MS 22 99 Munoz et al[88] MR/MS Delahaye et al MR 54

9- TO 10YEAR 5-YEAR SURVIVAL, SURVIVAL, PATIENTS, % % n 80 60 65 32 55 22 61 63 45 33

27

45 45 116

[89]

MR, mitral regurgitation; MS, mitral stenosis. even if preoperative indices of LV pump performance are normal.[16] [25] [29] Traditionally, it was believed that afterload (end-systolic wall stress) was decreased in mitral regurgitation by systolic "unloading" into the lowimpedance left atrium. Correction of mitral regurgitation with elimination of the low-resistance leak into the left atrium was thought to acutely increase afterload, resulting in the decrease in LV ejection fraction observed postoperatively.[29] It is now known that for the majority of patients with severe mitral regurgitation, afterload is normal before surgical correction. Furthermore, changes in afterload are not solely responsible for the observed decrease in LV pump performance after surgical correction of mitral regurgitation. Rather, primary contractile dysfunction, resulting from chronic volume overload, and alterations in LV geometry secondary to removal of the submitral apparatus during conventional mitral valve replacement are also responsible for the post-operative decline in LV pump performance. Conventional mitral valve replacement with transection of the chordae tendineae and removal of the subvalvular apparatus almost always results in a postoperative decline Figure 18-4 Preoperative (PRE) and postoperative (POST) left ventricular (LV) ejection fractions depicted for patients undergoing mitral valve replacement with transection (open squares) and preservation (solid circles) of the chordae tendineae. Data for individual

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patients are represented by smaller symbols; mean ± SEM is represented by larger symbols. Mitral valve replacement with transection of the chordae tendineae resulted in a decrease in LV ejection fraction, but mitral valve replacement with chordal preservation did not. (From Rozich JD, Carabello BA, Usher BW, et al: Circulation 1992;86:1718–1726.)

in global and regional LV ejection fraction, even when preoperative indices of LV pump performance are normal.[90] LV ejection fraction decreases immediately after removal of the subvalvular apparatus[34] and persists over the long term after excision.[89] For the majority of patients, however, this decline in LV ejection fraction does not occur with mitral valve reconstruction[34] [91] [92] or mitral valve replacement with preservation of the chordae tendineae and papillary muscles [31] [33] , [40] (Fig. 18-4) . In addition to preservation of LV systolic performance, postoperative survival and exercise capacity have been shown to improve in patients who undergo mitral valve replacement with chordal preservation.[37] The mechanisms for preservation of LV pump performance after mitral valve replacement with chordal preservation have been defined by Rozich et al[40] using two-dimensional echocardiography. Disruption of the functional components of the submitral apparatus during conventional mitral valve replacement disturbs the continuity between the mitral annulus and LV wall through the leaflets, chordae tendineae, and papillary muscles, resulting in significant increases in end-systolic volume and 396

end-systolic stress. In addition, the ratio of the LV major axis to minor axis dimension decreases significantly, suggesting a loss of LV geometry with assumption of a more spherical shape.[33] [40] [45] Mitral valve replacement with chordal preservation maintains LV systolic performance by preserving LV geometry, resulting in a smaller LV cavity and a decrease in endsystolic wall stress.[35] Although the decline in LV pump performance after conventional mitral valve replacement can be attributed, at least in part, to disruption of LV geometry after removal of the submitral apparatus, underlying contractile dysfunction secondary to long-standing volume overload is still the major determinant of postoperative LV pump dysfunction. Left ventricular pump performance declines postoperatively in patients with significant preoperative LV enlargement, despite mitral valve replacement with preservation of the submitral apparatus. Wisenbaugh et al[93] demonstrated

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that patients with an end-systolic diameter of greater than 50 mm had a poor long-term outcome after mitral valve replacement, despite chordal preservation. Similar data have been reported by Enriquez-Sarano et al[5] for patients undergoing mitral valve reconstruction, with a decline in postoperative LV ejection fraction demonstrated for patients with a preoperative LV ejection fraction of less than 60%. These data confirm the fact that occult contractile dysfunction secondary to long-standing volume overload is an important mechanism for the observed postoperative decline in LV ejection fraction after correction of mitral regurgitation. Mitral Valve Reconstruction Left Ventricular Systolic Performance.

The long-term success of mitral valve reconstruction for mitral regurgitation has been reported in numerous series.[37] [77] [79] , [91] , [94] [95] [96] [97] [98] [99] [100] [101] [102] [103] [104] [105] [106] [107] [108] In addition to preservation of LV geometry, mitral valve reconstruction has been shown to confer additional operative and long-term survival advantages over mitral valve replacement for chronic mitral regurgitation. The reduction in LV pump performance that has been observed after conventional mitral valve replacement has not been observed with mitral valve reconstruction, provided that the preoperative contractile state remains intact (Table 18-3) . TABLE 18-3 -- Preoperative and Postoperative Ejection Fraction: A Comparison of Mitral Valve Repair and Mitral Valve Replacement with Chordal Transection and Preservation

Study Duran et al[91] David et al[33] David et al[31] Goldman et al[34] Hennein et al[37] Sakai et al[92]

Repair, % PREOP POSTOP 47 54 63 63 44 65

49 68

Replacement with Chordal Transection, % PREOP POSTOP 54 47 62 51 55 48 64 40 46 31 64 57

Replacement with Chordal Preservation, % PREOP POSTOP 64 53

65 52

50

54

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Rozich et al[40] 60 63 54 69 Enriquez-Sarano et al[5] Preop, preoperative; Postop, postoperative.

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36 49

63

61

Mortality.

Operative mortality and long-term survival rates are also better after mitral valve repair compared with mitral valve replacement (Table 18-4) . Mitral valve reconstruction has been compared to replacement in several studies. The first large retrospective study was reported by Duran et al [91] in 1980 for 562 patients undergoing mitral valve surgery predominantly for rheumatic heart disease. Operative mortality for the 255 patients undergoing mitral valve repair was 1.9% compared with 11.4% for the 307 patients in the replacement group. Survival at 2 years was better for the repair group (98.3%) than for the replacement group (92.9%), largely due to the differences in operative mortality. Only one prospective trial exists comparing mitral valve reconstruction with replacement. Perier[110] studied 400 patients with mitral regurgitation predominantly of rheumatic origin. Patients were divided into four groups of 100 patients each, with one group undergoing mitral valve repair and the remaining three groups treated with valve replacement using different prostheses. The 7-year survival rate was 82% for the repair group versus 56%, 61%, and 60% for the three replacement groups. Yacoub et al[108] reported long-term results for mitral valve reconstruction versus replacement for the "floppy mitral valve syndrome." Survival rates at 5 and 10 years were 91% and 81%, respectively, for the repair group, versus 81% and 39% for the replacement group. In addition to preservation of LV pump performance, therefore, mitral valve reconstruction also confers a survival advantage over mitral valve replacement. Thromboembolism.

In addition to the decreased operative mortality and increased long-term survival associated with mitral valve repair, the thromboembolic and hemorrhagic complications associated with mitral valve reconstruction are also significantly decreased compared with mitral valve replacement. Several studies have reported that approximately 95% of patients are free from thomboembolic complications at 5 to 10 years after surgery.[111] In contrast, 10% to 35% of patients with mechanical prostheses have thromboembolic events within 5 to 10 years of surgery.[112]

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Hemorrhage.

Because only a minority of patients who undergo valve reconstruction are maintained on chronic anticoagulation therapy, the incidence of significant bleeding complications is also extremely small,[101] [111] in contrast 397

TABLE 18-4 -- Operative Mortality and Long-Term Survival: Mitral Valve Repair versus Replacement Operative Mortality

Long-Term Survival YEARS AFTER

REPAIR, REPLACEMENT, REPAIR, REPLACEMENT, n (%) n (%) OPERATION % % Study Duran et 255 1.8 307 11.4 4 96 81 [91] al 86 3.1 46 7.0 5 91 62 Yacoub [108] et al Oliveira 82 4.9 101 5.0 6 88 68 [106] et al Adebo 21 0 44 6.8 5 85 78 and Ross [96]

100 2.0 100(SE)

13

100(BS) 100(BP) 131 6.1 106

12 12 7.5

7

82

5

92

60(BS) 56(BP) 72

222

4.0

5

76

56

Angell et 112 5.4 72 al[95] 75 4.0 63 Cohn et [97] al

18.1

5/10

90/75

55/40

3.0

3

94

85

Perier et al[110]

Orszulak et al[107] Sand et al

48 0

61(SE)

[94]

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Galloway 280 2.0 169(ME) et al[101] 975(BP) Craver et 65 1.5 65 al[99] Kawachi 43 2.3 48 [103] et al Enriquez- 151 1.3 175 * * Sarano et al[7]

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6.6

5

76

72(ME)

8.5 4.6

4

84

69(BP) 82

8.3

5/8

91/91

82/75

5.7

9

79; EF > 60

71; EF > 60

48; EF < 60 68

50; EF < 60

Enriquez- 44 † 6.8 39 † 30.8 10 52 Sarano et al[5] BP, bioprosthesis; BS, Björk-Shiley; EF, ejection fraction; ME, mechanical; SE, Starr-Edwards. *Age ≤ 75 years. †Age > 75 years.

to relatively frequent episodes of bleeding after valve replacement.[112] Endocarditis.

The risk of endocarditis is also decreased after mitral valve repair compared with replacement. In the series of Duran et al,[91] infectious endocarditis occurred at a rate of 0.4% per year after repair and at 2.2% per year after replacement. Late endocarditis after mitral valve reconstruction is negligible, in contrast to the 3% to 6% incidence after mitral valve replacement. [111] Predictors of Postoperative Outcome and Survival As previously stated, patients with mitral chronic regurgitation who have reduced LV pump performance prior to surgery are at risk for a suboptimal postoperative outcome, characterized by persistent LV systolic dysfunction, congestive heart failure, and death. Presumably, operation in such patients

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is being performed late in the hemodynamic course at a time when severe, irreversible contractile dysfunction has already developed. So, should surgery be performed "prophylactically" in all asymptomatic patients to prevent occult contractile dysfunction? The optimal time for surgery is at the onset of LV contractile dysfunction, justifying the surgical risk, but early enough in the course to be reversible. If it were possible to pinpoint this critical moment in the natural history of chronic mitral regurgitation, then it would be simple to plan the timing of surgery in these patients. Unfortunately, no variable that can be routinely measured in the clinical setting is able to define the precise onset of reversible contractile dysfunction in chronic mitral regurgitation. Several markers, however, have been identified that predict a poor outcome after mitral valve surgery. These variables, in conjunction with those that have recently been identified to predict an optimal outcome, can be used to provide a rational framework for the timing of surgery in this valve disease for the purpose of preservation of contractility. Table 18-5 summarizes the preoperative clinical, hemodynamic, angiographic, and echocardiographic parameters that have been used to predict postoperative outcome in patients with mitral regurgitation. Clinical Predictors.

Among 177 surgically treated patients with mitral valve disease, Hammermeister et al[87] found age to be the only independent predictor of survival after mitral valve replacement. Patients older than 61 years had a 5-year survival rate of 40%, compared with 74% in patients 41 to 60 years old and 87% in patients younger than 40 years. In a study by Phillips et al,[8] patient age was also found to predict survival. Patients younger than 60 years at the time of surgery had a 5-year survival rate of 91%, compared with 72% for those 61 years old or older. In several studies by EnriquezSarano and colleagues,[5] [7] age was also found to be an important predictor of operative morality in patients undergoing mitral valve surgery. Operative mortality in elderly patients (older than 75 years) was 30.8% for valve replacement and 6.8% for valve repair versus 5.7% for valve replacement and 1.3% for valve repair in patients younger than 75 years of age. In addition to age, Enriquez-Sarano and colleagues[5] [6] [7] also found the following clinical variables to be predictive of overall survival, operative mortality, and postoperative LV ejection fraction in patients undergoing mitral valve replacement or reconstruction: creatinine (no level specified), New York Heart Association (NYHA) functional class greater than II, atrial

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fibrillation, and concomitant coronary artery disease. Recently, in a study of 576 consecutive postoperative survivors, Dujardin et al[113] found that preoperative LV ejection fraction (<60%) and concomitant 398

TABLE 18-5 -- Surgery for Mitral Valve Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Clinical Age

Value

NYHA functional class Atrial fibrillation Coronary artery disease Hemodynamic Mean pulmonary artery pressure Cardiac index LV end-diastolic pressure Catheterization LV ejection fraction End-systolic volume index

ES stress

> 60 years > 75 years > Class II

8 5 5–7, 114, 116 5–7 5–7

> 20 mm Hg

4

< 2.0 L/m/m2 > 12 mm Hg

116

≥ 30 mL/m2

116 8 19 4

≥ 50 mL/m2

62

≥ 60 mL/m2

64

< 50%

< 2.6 dyne × 103 /cm2

ES volume index Echocardiography LV ejection fraction

References

mL/m2 < 50% < 60% < 63%

6 7 25

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Fractional shortening End-diastolic dimension End-systolic dimension

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< 31% > 70 mm > 50 mm > 45 mm ≥ 40 mm

69 25 25, 93 6, 7 30 69

End-systolic dimension > 2.6 cm/m2 index End-systolic stress index > 195 mm Hg 69 Doppler-derived LV dP/dt < 1343 mm Hg/sec 118 Radionuclide Right ventricular ejection < 30% 119 fraction ES, end systolic; LV, left ventricular; NYHA, New York Heart Association.

coronary artery disease were each positively associated with postoperative mortality and congestive heart failure. Ramanthan et al[114] likewise found NYHA functional class to be an important predictor of survival in medically treated patients with mitral regurgitation followed for a 4-year period, with mortality rates of 53% and 44% for class III and class IV patients, respectively. Similarly, in a recent study of 478 patients with organic mitral regurgitation corrected surgically, Tribouilloy et al[115] found preoperative functional class III/IV symptoms to be independently associated with decreased immediate and long-term postoperative survival. The excess mortality associated with NYHA class III/IV as compared to class I/II was demonstrated regardless of LV ejection fraction (Fig. 18-5) . These researchers concluded that surgical intervention should be considered when no or minimal symptoms are present in low operative risk patients. Salomon et al[116] retrospectively analyzed multiple patient-related risk factors to determine survival after mitral valve replacement in 897 patients, 240 with mitral stenosis, 352 with mitral regurgitation, and 305 with mixed stenosis and regurgitation. In addition to patient age of less than 60 years, preoperative NYHA class of III or lower, cardiac index of 2.0 or greater, and LV end-diastolic pressure of 12 or less were also found to predict improved perioperative as well as long-term survival. Similarly, Crawford et al[4] found that a mean preoperative pulmonary artery pressure of 20 mm Hg or greater predicted a reduced LV ejection fraction after

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mitral valve replacement. Left Ventricular Ejection Fraction.

Although it does not identify asymptomatic patients with early contractile dysfunction, LV ejection fraction has been used extensively to predict outcome after surgery. As mentioned earlier, Dujardin et al[113] found, in a study of 576 consecutive postoperative survivors of mitral valve surgery, that Figure 18-5 Overall survival is compared between patients in New York Heart Association (NYHA) class I/II and those in class III/IV who had a preoperative left ventricular ejection fraction (EF) of 60% or greater (A) or less than 60% (B). (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1995;91:1022–1028.)

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Figure 18-6 Postoperative survival following mitral valve surgery on organic mitral regurgitation based on patients' preoperative left ventricular ejection fraction is shown. (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1994;90:830–837.)

LV ejection fraction of 60% or greater was associated with improved survival (adjusted risk ratio 0.49) and reduced incidence of congestive heart failure (adjusted risk ratio 0.30). In a study by Enriquez-Sarano et al[7] of 409 patients with isolated mitral regurgitation undergoing mitral valve surgery, preoperative LV ejection fraction was found to be the most important predictor of long-term survival. Survival at 10 years was 72% for patients with a mean preoperative LV ejection fraction of 60% or greater, 53% for patients with an ejection fraction in the range of 50% to 60%, but only 32% percent for those with an ejection fraction of less than 50% (Fig. 18-6) . Enriquez-Sarano et al[6] also reviewed the echocardiographic predictors of postoperative LV pump performance in 266 patients undergoing mitral valve replacement for mitral regurgitation. Independent predictors of postoperative LV pump dysfunction (defined as an ejection fraction of less than 50%) included a preoperative LV ejection fraction of less than 50% or an end-systolic dimension of greater than 45 mm. Postoperative LV pump

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dysfunction (ejection fraction of less than 50%) was associated with an increased mortality rate evidenced by an 8-year survival rate of 38% in patients with decreased postoperative LV ejection fraction, compared with 69% for patients with a postoperative LV ejection fraction of greater than 50%. In a study of 150 patients undergoing mitral valve replacement for isolated mitral regurgitation, Phillips et al[8] also demonstrated the value of preoperative LV ejection fraction in predicting long-term survival. Fiveyear survival rates for patients with a preoperative LV ejection fraction of 50% or greater, 40% to 49%, and less than 40% were 89%, 71%, and 38%, respectively. These data suggest that by the time LV ejection fraction had decreased to below the lower limits of normal, severe contractile dysfunction had already developed, and recovery was unlikely after surgery. Reduced LV ejection fraction, therefore, identifies patients who are likely to do poorly after surgery, but a normal LV ejection fraction does not distinguish between patients with normal contractility and those with occult early contractile dysfunction, who might benefit from prompt surgical intervention. Crawford et al[4] studied 48 patients with mitral regurgitation and 23 patients with mixed mitral stenosis and regurgitation to determine the role of LV size, pump performance, and clinical status in predicting survival and LV pump performance after mitral valve replacement. Mortality and increased NYHA functional class due to congestive heart failure were significantly higher in patients with mitral regurgitation and a postoperative LV ejection fraction of less than 50% and in patients with mixed stenosis and regurgitation and postoperative LV enlargement, defined by an enddiastolic volume index of greater than 101 mL/m2 . The strongest predictor of postoperative LV ejection fraction was the preoperative ejection fraction. Preoperative predictors of postoperative LV enlargement included an endsystolic volume index of greater than 50 mL/m2 and a mean pulmonary artery pressure of greater than 20 mm Hg. Similarly, Starling[30] studied 15 patients with chronic mitral regurgitation with micromanometer LV pressures and radionuclide angiograms for LV volumes over a range of loading conditions before and 1 year after successful mitral valve surgery. This study demonstrated that LV contractile impairment is reversible in many patients with chronic mitral regurgitation and that the best predictors of this reversibility include a normal preoperative LV ejection fraction and less LV dilation as manifest

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by end-systolic volume (Fig. 18-7) . Thus, following mitral valve surgery for chronic mitral regurgitation, LV contractility improved in those patients with an average preoperative LV ejection fraction of 0.63 ± 0.09 and an end-systolic volume index of 44 ± 12 mL/m2 , whereas it remained abnormal in those patients with an LV ejection fraction of 0.49 ± 0.12 and an end-systolic volume index of 89 ± 28 mL/m2 . This implies that early surgical intervention can preserve LV contractility and portend an excellent long-term outcome in some patients with mitral regurgitation.

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Figure 18-7 The left ventricular (LV) end-systolic pressure-volume relationship (Ees ) both before and after successful mitral valve surgery uncorrected (A) and corrected (B) for LV size is shown. A substantial increase in contractility occurs on the postoperative study compared with the preoperative study in the majority of patients, although a small group of patients shows either a decline or no change in this contractile index. *P < .05. (From Starling MR: Circulation 1995;92:811–818.)

The percentage of fractional shortening has also been used to assess LV pump performance in mitral regurgitation. Zile et al[69] found that a preoperative fractional shortening of less than 31% predicted postoperative congestive heart failure and death after mitral valve replacement in patients with mitral regurgitation. Despite the fact that survival is decreased in patients with reduced LV pump performance, patients with a decreased LV ejection fraction have improved survival with surgery over medical therapy.[87] The 5-year survival rate in patients with a reduced LV ejection fraction (31% to 50%) was 82% with valve repair or replacement, compared with 45% for the medically treated group. The 10-year survival rate was 82% for the repair group, 74% for the replacement group, and less than 20% for medically treated patients. Therefore, despite reduced overall survival in patients with mitral regurgitation and impaired LV pump performance, mitral valve surgery, particularly valve repair, should not be withheld in this subset of patients, as survival is significantly worse with medical therapy alone. End-Systolic Dimension.

Using two-dimensional echocardiography, Schuler et al[25] demonstrated the

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importance of the preoperative LV end-systolic dimension as a predictor of postoperative LV pump dysfunction in 16 patients with mitral regurgitation who underwent conventional mitral valve replacement. Group I consisted of those patients with a normal preoperative LV ejection fraction and mild LV enlargement; group II included those patients with a low normal LV ejection fraction and moderate LV enlargement. Postoperatively, at a mean follow-up of 15 months, group I patients demonstrated a significant decrease in mean echocardiographic LV end-diastolic and end-systolic dimension, a slight decline in LV ejection fraction, and regression of LV hypertrophy. In contrast, group II patients had no significant decrease in LV end-diastolic dimension, an increase in end-systolic dimension, and a marked reduction in LV ejection fraction. A preoperative LV end-diastolic dimension of greater than 70 mm, end-systolic dimension of greater than 50 mm, and LV ejection fraction of less than 55% identified the majority of patients with postoperative LV pump dysfunction and lack of regression of LV hypertrophy. Wisenbaugh et al[93] evaluated the outcome of 66 patients after mitral valve replacement with preservation of the submitral apparatus. At a mean follow-up period of 24 months, postoperative death or severe heart failure were predicted by a preoperative echocardiographic end-systolic dimension of 50 mm or greater. A preoperative LV end-systolic dimension of less than 40 mm identified all patients with an excellent postoperative outcome. The importance of echocardiographic end-systolic dimension in predicting adverse postoperative outcome has also been reported by Enriquez-Sarano and associates[6] [7] for an end-systolic dimension of greater than 45 mm and by Zile et al[69] for an end-systolic dimension index of greater than 26 mm/m2 . Similarly, in a recent study by Flemming et al,[117] 27 patients were evaluated with micromanometer LV pressures, radionuclide angiography, and echocardiographic parameters prior to and at 3 and 12 months after mitral valve surgery. They found that the most predictive echocardiographic indicator of early occult LV contractile dysfunction was an end-systolic dimension of 40 mm or more (Fig. 18-8) . This index was also able to predict a unique response to mitral valve surgery that was characterized by a short-term fall in LV pump performance, but a long-term recovery to normal LV pump performance, possibly because of a recovery of LV contractile function. They concluded that this measure may be useful to separate those with and without early occult LV contractile dysfunction and normal LV pump performance and to identify those patients who may

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benefit from early mitral valve surgery with or without mild symptoms to preserve LV systolic performance. End-Systolic Volume.

Borow et al[19] have evaluated the 401

Figure 18-8 Receiver operator characteristic curves were generated using sensitivity and 100-minus specificity for echocardiographic left ventricular (LV) end-systolic dimension (ESD), fractional shortening (FS), and end-diastolic dimension (EDD) to identify contractile dysfunction in mitral regurgitation (MR) patients with a normal LV ejection fraction. An LV ESD of 40 mm or greater was optimal for identifying patients with MR and a normal LV ejection fraction and early occult contractile dysfunction. (From Flemming MA, Oral H, Rothman ED, et al: Am Heart J 2000;140:476–482.)

role of the preoperative end-systolic volume index as a predictor of postoperative LV pump performance and survival in chronic mitral regurgitation. Abnormal postoperative LV pump performance was predicted by a preoperative end-systolic volume index of greater than 60 mL/m2 . Furthermore, a preoperative end-systolic volume index of greater than 90 mL/m2 predicted increased postoperative mortality. Specifically, four of five patients with an end-systolic volume index of greater than 60 mL/m2 died in the perioperative period, whereas no patients with an endsystolic volume index of less than 60 mL/m2 died of cardiac failure. All patients with an end-systolic volume index of less than 60 mL/m2 achieved NYHA class I or II postoperatively. In the study by Crawford et al,[4] an end-systolic volume index of 50 mL/m2 or greater was similarly found to predict postoperative LV pump dysfunction. End-Systolic Wall Stress.

In addition to an echocardiographic LV end-systolic dimension index of greater than 26 mm/m2 and percentage fractional shortening of less than 31%, Zile et al[57] have also demonstrated that an echocardiographic LV end-systolic wall stress index of greater than 195 mm Hg can be used to predict postoperative congestive heart failure and death after mitral valve replacement for chronic mitral regurgitation.

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End-Systolic Wall Stress/End-Systolic Volume Index.

Variables predictive of reversible LV contractile dysfunction have been identified in mitral regurgitation, but such measurements have required complex invasive hemodynamic protocols. In a study of 21 patients with mitral regurgitation, Carabello et al[64] found that the ratio of end-systolic wall stress to end-systolic volume, a preload-independent index of contractility, was the best predictor of outcome after mitral valve replacement for mitral regurgitation. The end-systolic wall stress to endsystolic volume index was 5.6 in normal subjects, 3.3 in patients with a favorable postoperative outcome (NYHA class II or lower), and 2.2 in patients with an unfavorable postoperative outcome, including NYHA class III or IV symptoms or death. The fact that the absolute value of the ratio of LV end-systolic wall stress to end-systolic volume index was lower in patients with a favorable postoperative outcome than in normal subjects suggests that preoperative contractility was abnormal in this subset of patients with mitral regurgitation, but to an extent that did not adversely affect postoperative outcome. A significant decrease in the LV end-systolic wall stress to end-systolic volume index, on the other hand, appeared to identify a patient group with severe, irreversible contractile dysfunction. The LV end-systolic wall stress to end-systolic volume index may, therefore, be useful in identifying patients with early contractile dysfunction in whom timely operative intervention would be warranted. In a subsequent study, Carabello et al [62] further demonstrated that an endsystolic wall stress to end-systolic volume index ratio of 2.6 or less predicted poor surgical outcome, defined as postoperative death or NYHA class III or IV symptoms. Pressure-Volume Relationship.

Starling et al[26] have demonstrated that the slope of the end-systolic pressure-volume relationship (chamber elastance), a load-independent measure of contractility, can be used to identify occult reversible contractile dysfunction in patients with mitral regurgitation who have a normal LV ejection fraction. Patients with a normal preoperative LV ejection fraction but impaired contractility (reduced elastance) had an initial decline in ejection fraction in the immediate postoperative period, but it improved within 1 year of surgery. In contrast, patients who had both impaired contractility and a reduced ejection fraction preoperatively had persistent postoperative LV pump dysfunction. These data suggested that the combination of abnormal elastance and normal ejection fraction can identify a patient group in whom contractile dysfunction is present but still

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reversible. In this particular group of patients, prompt surgical intervention is indicated to avoid progression to irreversible dysfunction. Unfortunately, because measurements of elastance require complex hemodynamic protocols, elastance cannot be used as a routine tool for serial assessment of patients with mitral regurgitation. However, the information gained using elastance has helped to interpret the clinical data used to determine the appropriate timing for surgical intervention in patients with mitral regurgitation. In a preliminary analysis of patients with mitral regurgitation and normal LV ejection fraction, patients with impaired contractility could be separated from those with normal contractility on the basis of echocardiographic indices of LV size and performance.[117] An LV end-systolic dimension of greater than 40 mm approximated a reasonable separation of these patients and may, therefore, represent a reasonable surrogate for the elastance concept in patients with mitral regurgitation. Doppler-Derived dP/dt.

The spectral velocity pattern of mitral regurgitation obtained by continuous wave Doppler echocardiography can also be used to assess LV systolic performance in mitral regurgitation. The spectral velocity curve represents the instantaneous pressure difference between the left ventricle and the left atrium. When systolic performance is reduced, the rate of rise of LV 402

Figure 18-9 Spectral Doppler signal of mitral regurgitation from a patient with depressed left ventricular function, demonstrating a slow rate of acceleration to peak regurgitant velocity, reflecting a low dP/dt. The dP/dt is estimated from the time interval (dt) required for the mitral regurgitant velocity to rise from 1 to 3 m per second. In this case, the dP/dt measured 800 mm Hg per second.

pressure is decreased, resulting in a concomitant decrease in the rate of increase in the velocity of mitral regurgitation. The slope of the mitral regurgitant velocity curve, designated as dP/dt, is decreased when LV systolic performance is decreased (Fig. 18-9) . Pai et al [118] studied the Doppler-derived index of the rate of LV pressure rise (dP/dt) in 25 patients with mitral regurgitation before and 6.5 weeks after mitral valve surgery. The LV dP/dt was found to be the best independent predictor of postoperative LV ejection fraction. A preoperative dP/dt of 1343 mm Hg

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per second or less predicted a postoperative ejection fraction of 50% or less. Right Ventricular Ejection Fraction.

Hochreiter et al[119] assessed the prognostic importance of right ventricular ejection fraction in 35 medically treated and 21 surgically treated patients with chronic mitral regurgitation. Patients with a right ventricular ejection fraction of 30% or less had a markedly reduced 4-year survival rate (18%) when treated medically compared with those treated surgically (84%). Left Atrial Size.

Reed et al[120] studied the role of left atrial size in predicting postoperative outcome in 176 symptomatic patients who underwent mitral valve replacement with a mean follow-up of 3.8 years. An abnormal left atrial size index (defined as the product of the major and minor atrial dimensions measured in the apical four-chamber view) was found to predict postoperative death. The left atrial size index, however, predicted mortality independent of LV systolic performance only in patients with a supernormal LV ejection fraction (>75%). Since patients with an LV ejection fraction in this range have an excellent prognosis, regardless of the left atrial size, this index appears to offer no additional prognostic information to LV systolic performance. Timing of Surgery Before discussing a rational approach to the proper timing of surgical intervention for chronic mitral regurgitation, the following key points should be emphasized: 1. Chronic severe mitral regurgitation leads to a progressive decline in LV pump performance. 2. Patients may remain asymptomatic with a normal LV ejection fraction for extended periods of time. 3. Occult contractile dysfunction generally develops at a time when patients remain asymptomatic and LV ejection fraction remains normal, and it may be reversible after surgical intervention. 4. Patients with normal LV ejection fraction and occult reversible contractile dysfunction who undergo mitral valve replacement or reconstruction have a favorable long-term prognosis. 5. Patients with LV pump dysfunction and irreversible contractile dysfunction are at risk for postoperative LV systolic dysfunction,

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6.

7. 8. 9.

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death, and congestive heart failure. Although reduced LV pump performance is associated with an overall decrease in long-term survival for patients with mitral regurgitation, survival is improved with surgical therapy compared with medical therapy. Compared with conventional mitral valve replacement, mitral valve reconstruction preserves LV pump performance and reduces mortality and comorbid complications. If feasible, mitral valve reconstruction should be the procedure of choice in patients with reduced preoperative LV pump performance. Long-term postoperative LV pump dysfunction due to mitral regurgitation in children and young adults is rare, but it does occur. However, a shorter duration is associated with improved postoperative results.

Since long-term survival in chronic mitral regurgitation is dependent on the contractile state of the left ventricle, the primary goal of surgical intervention should conceptually be to preserve contractility. All symptomatic patients with mitral regurgitation should be referred promptly for valve repair or replacement. It is often difficult for clinicians to justify referral of asymptomatic patients for surgical procedures that have a finite risk for death, even when the risk is small. The immediate operative and postoperative risks, on the one hand, must be balanced by the risk for progression to severe, irreversible contractile dysfunction and, thus, reduced long-term survival. Table 18-6 presents a proposed algorithm for the timing of surgery in patients with chronic mitral regurgitation, based on a system in which points are assigned to the different clinical variables that normally play a role in the decision-making process. The major components of the decision analysis, depicted in part A of the algorithm, include clinical and hemodynamic parameters, LV size and pump performance, and the feasibility of valve repair. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were selected on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. The ability to repair a valve should be determined based on the anatomic and pathologic defects of the valve as defined by transesophageal echocardiography. The feasibility of valve repair, based on the echocardiographic findings, should then be determined in consultation with a surgeon experienced in valve reconstruction. In general, symptomatic patients with congestive heart

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TABLE 18-6 -- Proposed Algorithm for Timing of Surgery in Patients with Mitral Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size EJECTION * FRACTION, END-SYSTOLIC Feasibility of Valve Clinical DIMENSION, mm Repair Points Symptoms % 0 None > 60 < 40 None 1 I/II 50–60 40–45 Possible 2 III/IV < 50 > 45 Definite Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; recommend clinical and echocardiographic followup at 12 months 2 Borderline; recommend clinical and echocardiographic follow-up at 6 months ≥ 3 Proceed with surgery Part C: Although not essential for decision analysis, additional predictors of adverse outcome, all of which can be measured by twodimensional echocardiography, can also be used to support decisions. Additional Predictors of Adverse Outcome in Aortic Regurgitation † Value Fractional shortening < 31% End-systolic volume index > 30 mL/m2 End-systolic stress index End-diastolic dimension Doppler dP/dt of mitral regurgitant jet Right ventricular ejection fraction

> 195 mm Hg > 70 mm < 1343 mm Hg/sec < 30%

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*Add one point for age > 60 and coronary artery disease; add three points for history of atrial arrhythmias. †Add two points for each predictor present.

failure, decreased exercise tolerance, or atrial arrhythmias should be referred for surgery, regardless of the status of the left ventricle, particularly when mitral valve reconstruction can be performed. Asymptomatic patients with an LV ejection fraction in the low-normal range (<55%) or LV dilation with an end-systolic dimension of greater than 40 mm are likely to have contractile dysfunction and should, therefore, be referred for surgery. Asymptomatic patients with a high-normal LV ejection fraction (>60%) and small (<40 mm) end-systolic dimension can be followed clinically with serial echocardiography every 6 to 12 months for evidence of reduced exercise tolerance, declining LV ejection fraction, or increased end-systolic dimension. Any change from baseline may indicate the onset of contractile dysfunction, and patients should be referred for prompt surgical intervention. Parenthetically, symptoms in patients with chronic mitral regurgitation are sometimes subtle and difficult to elicit. They are normally fatigue, not dyspnea. Based on the outcome data, patients with early symptoms should also undergo surgery even if they do not meet these LV size and performance criteria. Recently, the natural history of chronic mitral regurgitation and its surgical correction were evaluated in children and young adults.[121] Although the early postoperative course of LV pump dysfunction in children parallels the course in adults, children usually demonstrate a late improvement in LV systolic performance. Thus, early surgical intervention in children without symptoms or LV pump dysfunction is not necessary for most children. However, the duration of mitral regurgitation is correlated with outcome; and for those children who will inevitably require mitral valve repair, operative intervention should be entertained prior to the onset of heart failure. Included in the algorithm in Table 18-6 are additional parameters that identify patients at high risk for contractile dysfunction and, therefore, can be used to strengthen decisions for surgical intervention. Although some of these predictors were validated using nonechocardiographic techniques, all parameters included in this part of the algorithm can be measured using two-dimensional echocardiography. Because more detailed measurements

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and computations are required, most are not included as part of a routine echocardiographic report. These variables are not requisite components of the algorithm and should be considered adjunctive to decision making. Two case studies illustrate how this algorithm can be applied in the clinical setting. The first patient was a 32-year-old aerobics instructor referred for an evaluation of an asymptomatic murmur. Transesophageal echocardiography revealed mitral valve prolapse with a flail posterior leaflet and severe mitral regurgitation. The LV ejection fraction measured 65%, and the end-systolic dimension measured 38 mm. Using step A of the algorithm, this patient would be given a total of 2 points, based on the high feasibility of mitral valve repair. Given the normal LV end-systolic dimension and the high-normal ejection fraction, the possibility of occult contractile dysfunction in this patient was thought to be very small; therefore, surgery was deferred in this patient with follow-up performed 404

every 6 months. At 1-year follow-up, although the patient remained asymptomatic, the LV ejection fraction had decreased to 60% and the endsystolic dimension had increased to 42 mm, suggesting the onset of early contractile dysfunction. This patient was then referred for successful mitral valve reconstruction. The second patient was a 50-year-old woman with a history of rheumatic heart disease who presented with atrial fibrillation. Echocardiography revealed an LV ejection fraction of 55%, mild mitral stenosis with mild leaflet thickening, and severe mitral regurgitation. According to the proposed algorithm, the development of atrial fibrillation and the LV ejection fraction of 55% resulted in a total of 3 points, justifying operative intervention. Mitral valve repair in this particular case of rheumatic mitral regurgitation was considered possible but not definite; hence, this patient was referred for possible valve repair to be followed by valve replacement if reconstruction was unsuccessful.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Chronic Aortic Regurgitation Despite significant volume and pressure overload on the left ventricle, patients with aortic regurgitation typically remain asymptomatic for extended periods of time.[122] Symptoms of dyspnea, orthopnea, nocturnal angina, and syncope develop relatively late in the course of the disease. Aortic valve replacement has clearly been shown to prolong survival and improve functional class in patients with severe symptoms.[12] [123] [124] The optimal timing for valve replacement in asymptomatic or minimally symptomatic patients, however, is less concrete. Progression to contractile dysfunction may precede symptom onset; therefore, if symptom onset is used as the sole guide for surgical intervention, a small subset of patients will be at risk for LV dilation and pump dysfunction and, thus, congestive heart failure and death in the postoperative Figure 18-10 The relationship between left ventricular (LV) ejection fraction and total vascular load is shown in aortic regurgitation (AR) patients with normal LV contractility (solid circles) and depressed contractility (open circles). There was a significant difference between the slopes of these two relationships, indicating that in patients with AR and contractile dysfunction, the sensitivity of LV ejection fraction to total vascular load was greater than in patients with preserved contractility. (From Devlin WH, Petrusha J, Briesmiester K, et al: Circulation 1999;99:1027–1033.)

period.[14] Fortunately, in contrast to mitral regurgitation, LV pump performance often improves postoperatively in patients with aortic regurgitation, even if depressed preoperatively.[1] [17] [125] , [126] Because afterload excess is primarily responsible for the initial decline in LV pump performance in aortic regurgitation, the decrease in afterload after aortic valve replacement favors postoperative improvements in LV systolic performance in the majority of patients. Although developing relatively late in the natural history of the disease, contractile dysfunction also contributes to LV pump dysfunction in aortic regurgitation and is associated with an

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increased risk for postoperative morbidity and mortality. It is also apparent from one recent study[49] that LV loading conditions have a greater effect on LV pump performance in patients with contractile dysfunction compared with those with preserved LV contractility (Fig. 18-10) . So, should prophylactic aortic valve replacement be performed to preserve LV contractility? The benefits of preserving contractility, on the one hand, must be weighed against the immediate operative risks and the potential for bleeding, thromboembolism, and endocarditis associated with prosthetic valves.[127] [128] Ideally, to justify the surgical risk, the appropriate timing of surgery in patients with aortic regurgitation is at the onset of LV pump dysfunction, yet early enough to avoid the development of irreversible contractile dysfunction. Etiology Aortic regurgitation results from primary pathologic abnormality of the aortic valve leaflets (Fig. 18-11) or of the wall of the aortic root, or a combination of both abnormalities. [129] [130] Aortic root disease accounts for approximately one third of all patients with isolated aortic regurgitation, who ultimately undergo valve replacement. The 405

Figure 18-11 (color plate.) Transesophageal echocardiogram in the longitudinal plane (long-axis view) from a patient who presented with dyspnea on exertion several years after having been treated for aortic valve endocarditis. Demonstrated are focally thickened aortic valve leaflets with prolapse of the leaflets into the left ventricular outflow tract (A), resulting in severe aortic regurgitation (B).

etiology of aortic regurgitation, grouped by the mechanism of regurgitation, is given in Table 18-7 . Natural History of Medically Treated Patients The clinical history of patients with chronic aortic regurgitation is characterized by a long asymptomatic phase, often lasting several decades, followed by a symptomatic phase with a relatively rapid progressive deterioration in clinical status.[86] [131] [132] [133] All patients with aortic regurgitation have reduced survival with medical therapy, with approximately 75% of patients alive at 5 years and 50% alive at 10 years after the initial diagnosis has been made.[79]

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Asymptomatic Patients.

Asymptomatic patients with normal LV pump performance have an excellent long-term prognosis.[61] In a study of 77 asymptomatic patients with a normal LV ejection fraction, 90% of patients remained asymptomatic at 3 years; 81% at 5 years; and 75% at 7 years (Fig. 18-12) . The percentage of patients requiring aortic valve replacement was less than 4% per year. Data suggest that vasodilator therapy with nifedipine reduces LV dilation and hypertrophy in asymptomatic patients with aortic regurgitation who have normal LV TABLE 18-7 -- Mechanisms and Etiology of Aortic Regurgitation Mechanism Inflammatory

Structural

Destructive

Congenital

Condition Rheumatic fever Syphilis Systemic lupus erythematosus Ankylosing spondylitis Reiter's syndrome Behçet's syndrome Takayasu's arteritis Methysergide therapy Unicuspid, bicuspid, quadricuspid valves Annular dilation from aortic aneurysm Sinus of Valsalva aneurysm Fenestrated valve Infectious endocarditis Trauma Aortic dissection Marfan's syndrome Ventricular septal defect Pseudoxanthoma elasticum Osteogenesis imperfecta Mucopolysaccharidoses Ehlers-Danlos syndrome

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Abnormal loading conditions

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Hypertension

Renal failure Adapted from Alpert JS: Chronic aortic regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown, 1987, pp 283–318. systolic performance.[133] [134] [135] [136] [137] [138] [139] [140] Furthermore, these beneficial hemodynamic effects have significantly delayed the need for aortic valve replacement in this subset of patients. Because afterload excess is the primary hemodynamic abnormality leading to LV pump dysfunction in chronic aortic regurgitation, the beneficial unloading effects of nifedipine can be anticipated in this setting. Figure 18-12 The clinical course of 77 asymptomatic patients with chronic aortic regurgitation and normal left ventricular (LV) function is presented from the time of initial diagnosis. Clinical end points include onset of symptoms or development of LV pump dysfunction. (From Bonow RO, Rosing DR, McIntosh CL, et al: Circulation 1981;68:509–517.)

406

In contrast to the excellent long-term prognosis of asymptomatic patients with normal LV pump performance, approximately 66% of asymptomatic patients with impaired LV function are likely to require surgery within 2 to 3 years.[13] [129] [130] Symptomatic Patients.

Severely symptomatic patients with aortic regurgitation have a poor prognosis with medical therapy.[141] [142] [143] Only 4% of patients with NYHA class III or IV symptoms of congestive heart failure are alive at 10 years. Similarly, patients with both symptomatic congestive heart failure and LV pump dysfunction generally die within 2 years without surgical intervention. Patients with right-sided congestive heart failure have a particularly poor prognosis, with less than 10% of patients alive at 4 years. [144]

Natural History of Surgically Treated Patients

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Survival.

Although there have been no randomized trials directly comparing medical therapy with surgery, surgical intervention appears to improve survival and functional class in patients with symptomatic aortic regurgitation. Rapaport [86] reported 5- and 10-year survival rates of 75% and 50%, respectively, for medically treated patients with aortic regurgitation. Operative and inhospital mortality rates for symptomatic patients with chronic aortic regurgitation have ranged from 4% to 10%.[12] [124] [144] [145] Increased operative mortality after aortic valve replacement for aortic regurgitation is associated with advanced functional class (class III or higher), creatinine level greater than 3.0 mg/dL, and atrial fibrillation.[146] [147] Long-term survival after aortic valve replacement for aortic regurgitation is displayed in Table 18-8 . The observed variability in survival with surgery predominantly reflects the year of surgery, improvements in surgical technique in the later years, especially with regard to myocardial preservation using cardioplegic arrest, differences in patient populations, and the presence of concomitant coronary artery disease. Five-year survival rates after aortic valve replacement from studies published in the mid1980s have ranged from 82% to 83%.[12] [68] [148] The 10-year survival rate reported in only one of these studies was 65%.[148] Clinical Improvement.

Aortic valve replacement results in significant relief of symptoms in the majority of TABLE 18-8 -- Survival After Aortic Valve Replacement for Aortic Regurgitation Study Hirshfeld et al[147] Roberts et al[154] Forman et al[123] Clark et al[150] Greves et al[124] Acar et al[144] Louagie et al[148] Bonow et al[12]

Patients, n 3-YEAR 88 55 26 76 90 79 17 61 36 85 126 85 114 90 80 90

Survival Rate, % 5-YEAR 8- TO 10-YEAR. 48 48 65 58 — — — — 85 — 70 49 82 65 83 —

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62

88

83

—

patients.[12] [143] Whereas 70% to 80% of patients will have improvement in functional class, approximately 40% of patients will become completely asymptomatic. In contrast to the situation for chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation demonstrate clinical improvement, despite NYHA class III or IV symptoms of congestive heart failure and a decreased LV ejection fraction.[149] Left Ventricular Pump Performance.

Left ventricular pump performance typically improves after aortic valve replacement with correction of the volume and pressure overload.[14] [58] [150] , [151] Patients with normal preoperative LV ejection fraction generally have normal postoperative LV pump performance and an excellent long-term prognosis.[12] [14] [151] Unlike patients with chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation who have a decreased preoperative LV ejection fraction often demonstrate significant improvements in LV pump performance after correction of the volume and pressure overload.[12] [15] [17] [58] , [63] [151] There is, however, a smaller subset of patients who have persistent LV systolic dysfunction postoperatively, suggesting the presence of irreversible contractile dysfunction.[12] [14] [15] [60] This group of patients has an extremely poor prognosis, with death often occurring from progressive congestive heart failure. Predictors of Outcome and Survival Clinical Predictors.

Several clinical factors, the majority of which indirectly reflect longstanding volume and pressure overload on the left ventricle, have prognostic significance in chronic aortic regurgitation (Table 18-9) . Heart volume, indicated by the cardiothoracic ratio on the chest radiograph, has been shown to predict long-term survival.[126] [144] [152] In one study, patients with a cardiothoracic ratio of 0.58 or greater had a 5-year survival rate of only 48%, compared with 90% for patients with a ratio of less than 0.58. Earlier studies from the 1970s suggested that an age older than 65 years,[144] [153] electrocardiographic evidence of marked LV hypertrophy,[154] [155] NYHA class III or IV,[126] [154] and elevated systolic blood pressure (>140 mm Hg) or decreased diastolic pressure (<40 mm Hg)[156] identified patients at increased risk for postoperative death. In a recent study by Klodas et al [157] comparing postoperative survival in functional class I or II patients with

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functional class III or IV patients, preoperative 407

TABLE 18-9 -- Surgery for Aortic Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Clinical Age Cardiothoracic ratio NYHA functional class Poor exercise tolerance Prolonged LV dysfunction Electrocardiographic evidence of LV hypertrophy Hemodynamic LV end-diastolic pressure Cardiac index Catheterization LV ejection fraction End-systolic volume index Peak systolic pressure/End-systolic volume index Echocardiography Percentage fractional shortening

End-systolic dimension

Value > 65 years ≥ 0.58 ≥ Class III < 8 METs > 18 mo > 18 mo

> 20 mm Hg < 2.5 L/m/m2 < 50% ≤ 45% ≥ 60 mL/m2 ≤110 mL/m2 ≥ 1.72 mm Hg/mL/m2 < 25% < 28% < 29% > 50 mm

References 144, 153 126, 144, 152 126, 153 14, 158 15 147, 156

144 123, 124 123 124 19 62, 168 169

60 66 155 66

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> 55 mm > 60 mm End-systolic dimension index

> 2.6 cm/m2 End-systolic wall stress > 235 mm Hg End-systolic dimension > 80 mm > 72 mm End-diastolic dimension (R) ≥ 3.2 End-diastolic wall thickness (th) ≥ 4.0 LV, left ventricular; NYHA, New York Heart Association.

60 63 59 66 59, 60 66 66 59

functional class III or IV symptoms were found to be independent risk factors for increased early and long-term postoperative mortality, suggesting that the onset of symptoms should warrant a rapid consideration of surgery. This is particularly true for women. Hemodynamic Predictors.

Hemodynamic predictors of adverse postoperative outcome have also been used to stratify patients prior to aortic valve replacement. The 2-year survival rate in patients with a reduced cardiac index ( 2.5 L/m/m2 ) has been reported to be 72%, compared with 94% for those with a normal index.[144] In two other studies,[123] [124] survival rates at 3 and 5 years in patients with a cardiac index of 2.5 L/m/m2 or less were reported to be 63% and 66%, respectively. Elevated LV end-diastolic pressure of 20 mm Hg or greater has also been associated with increased mortality after aortic valve replacement.[144] Indices of Left Ventricular Systolic Performance in Symptomatic Patients Ejection Phase Indices!

Left ventricular pump performance has been shown to be the most important determinant of survival in symptomatic patients with aortic regurgitation. [123] [124] , [153] Forman et al[123] found preoperative LV ejection fraction to be the most important determinant of survival in 90 patients with chronic aortic regurgitation who underwent valve replacement. Patients with an ejection fraction of less than 50% had a poor 3-year survival rate (64%) when compared with those with an LV ejection fraction of 50% or greater (91%). Greves et al[124] similarly demonstrated an adverse outcome

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in patients with a reduced LV ejection fraction secondary to aortic regurgitation, reporting a 5-year survival rate of 54% in patients with an ejection fraction of 45% or less, compared with 87% for those with an ejection fraction of greater than 45%. Duration of Left Ventricular Systolic Dysfunction.

In addition to decreased LV pump performance as an important predictor of adverse outcome in chronic aortic regurgitation, Bonow et al[15] have also demonstrated the impact of the duration of preoperative LV pump dysfunction in determining survival (Fig. 18-13) . Despite comparable reductions in LV fractional shortening and similar exercise tolerance, patients with prolonged LV systolic dysfunction (≥18 months) had a survival rate of only 45%, compared with 100% for patients with a more brief (<14 months) duration of LV pump dysfunction. Percentage of Fractional Shortening.

Percentage of fractional shortening, an ejection phase index of LV systolic performance derived using two-dimensional or M-mode echocardiography, has also been used to predict postoperative death and LV systolic dysfunction in symptomatic patients with aortic regurgitation. Cunha et al [155] found that the postoperative 5-year survival rate was 100% in patients with a fractional shortening of greater than 35 percent, compared with a rate of 91% for a fractional shortening in the range of 31% to 35%, and a rate of 78% for a fractional shortening of 30% or less. In a study conducted by the National Institutes of Health,[14] a fractional shortening of less than 29% was associated with a 3-year survival rate of 62%, compared with 91% for a fractional shortening of 29% or greater. Similar data have been reported for a fractional shortening of less than 25%[60] and of 28% or less. [66]

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Figure 18-13 Survival in aortic regurgitation after aortic valve replacement as a function of the duration of left ventricular (LV) dysfunction, demonstrating significantly reduced survival in patients with prolonged (>18 months) LV pump dysfunction. (From Bonow RO, Picone Al, McIntosh CL, et al: Circulation 1985;72:1244–1256.) Exercise Capacity.

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Preoperative exercise capacity has been shown to provide additional prognostic information to LV pump performance in aortic regurgitaton.[14] [158] Poor exercise tolerance (defined by the National Institutes of Health protocol, equivalent to approximately 8 metabolic equivalents [METs]) also predicts survival in symptomatic patients with aortic regurgitation. The 3year survival rate in patients with preserved exercise capacity was 100%, compared with 52% for patients with reduced exercise tolerance. Exercise capacity further stratifies patients with concomitant LV pump dysfunction into low- and high-risk groups. Decreased exercise tolerance in patients with a decreased fractional shortening (<29%) identified a patient subgroup at significantly higher risk for postoperative LV pump dysfunction and death secondary to congestive heart failure (Fig. 18-14) . Survival at 3.5 years was 32% in this particular subgroup of patients. In addition to exercise capacity, the LV ejection fraction response to exercise has been used to evaluate functional reserve in symptomatic patients with aortic regurgitation.[47] [159] [160] [161] [162] [163] [164] [165] [166] [167] The majority of symptomatic patients with aortic regurgitation have an abnormal LV ejection fraction response to exercise; however, no specific level of reduced exercise performance has clearly been shown to predict survival or LV pump dysfunction in this patient population. Hence, the LV ejection fraction response to exercise in symptomatic patients provides no prognostic information in addition to resting LV ejection fraction and exercise capacity in determining outcome in chronic aortic regurgitation. The difficulty in assigning a specific cut-off level for exercise performance in aortic regurgitation relates to the fact that ejection phase indices of LV systolic performance are highly dependent on heart rate, preload, afterload, and contractility, all of which are altered during exercise.[18] End-Systolic Dimension.

Henry et al[58] prospectively studied 50 patients with symptomatic aortic regurgitation prior to aortic valve replacement to define echocardiographic predictors of adverse postoperative outcome. Left ventricular end-systolic dimension of greater than 55 mm predicted postoperative congestive heart failure and death after aortic valve replacement. The survival rate at 3.5 years was 83% for patients with an end-systolic dimension of less than 55 mm, but only 42% for an end-systolic dimension of greater than 55 mm. Left ventricular end-systolic dimension of greater than 55 mm and a percentage fractional shortening of less than 25% identified a patient group at high risk for adverse outcome, with death occurring in 9 of 13 patients (69%) (Fig. 18-15) . More recently, Carabello et al[63] showed that

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symptomatic patients with impaired LV pump performance and an endsystolic dimension of less than 60 mm have an excellent long-term survival and experience improvement in LV ejection fraction after aortic valve replacement. In patients 409

Figure 18-14 Survival in symptomatic patients with aortic regurgitation and reduced preoperative echocardiographic left ventricular (LV) fractional shortening (<29%) presented as a function of the preoperative exercise capacity. Patients able to complete 22.5 minutes of the National Institutes of Health protocol had significantly improved survival compared with patients with impaired exercise capacity, despite similar reductions in LV function. (From Bonow RO, Rosing DR, Kent KM, et al: Am J Cardiol 1982;50:325– 336.)

with a reduced LV ejection fraction preoperatively, an end-systolic dimension of less than 60 mm correlated with a postoperative ejection fraction of 55%. End-Systolic Volume Index.

Borow et al[19] studied 41 symptomatic patients with mitral or aortic regurgitation and found that a normal preoperative LV end-systolic volume index predicted normal postoperative LV pump performance and improvement in symptoms to NYHA functional class I or II. For the subset of patients with chronic aortic regurgitation, an end-systolic volume index of 90 mL/m2 or greater identified patients at higher risk for postoperative death and persistent LV pump dysfunction. Similar findings were reported by Carabello et al[62] Figure 18-15 The relationship between preoperative echocardiographic left ventricular (LV) fractional shortening and end-systolic dimension in determining prognosis in symptomatic patients after aortic valve replacement for chronic aortic regurgitation is illustrated. The 97% confidence intervals for normal subjects are indicated by the elliptical area. The highrisk area defined by an LV end-systolic dimension of greater than 55 mm and fractional shortening of less than 25% identifies patients at risk for postoperative death. (From Henry WL, Bonow RO, Borer JS, et al: Circulation 1980;61:471–483.)

for an end-systolic volume index of greater than 110 mL/m2 and by Taniguchi et al[168] for an end-systolic volume index of greater than 200

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mL/m2 . In these two studies, the greater degree of preoperative LV pump dysfunction tolerated without adversely affecting outcome has been attributed to improved surgical techniques in more recent years, particularly with regard to myocardial preservation during cardiopulmonary bypass. End-Diastolic Dimension.

Echocardiographic LV end-diastolic dimension has also been used to determine prognosis in aortic regurgitation, but it is less sensitive than endsystolic dimension in predicting postoperative outcome. A preoperative end-diastolic dimension of greater than 80 mm has been shown to identify a subset of patients with severe preoperative LV enlargement at risk for persistent postoperative LV dilation and congestive heart failure.[59] [60] Although it is less useful as a preoperative predictor, a postoperative enddiastolic dimension of greater than 70 mm identified patients at significant risk for postoperative death from congestive heart failure.[60] End-Diastolic Radius–to–Wall Thickness Ratio.

The end-diastolic radius–to–wall thickness ratio, measured by twodimensional echocardiography, has also been used to predict outcome in aortic regurgitation. The ratio of LV dimension reflected in radius (r) to wall thickness (th) at end-diastole is linearly related to the ratio of LV volume to mass and has been used to determine the degree to which mass is appropriate for a given volume. In patients with chronic aortic regurgitation, the degree of LV dilation may exceed the limit of compensatory LV hypertrophy, resulting in significant LV dilation and pump dysfunction and an increase in the r/th ratio. Gaasch et al,[59] in 12 patients with chronic aortic regurgitation who underwent aortic valve replacement, found that a r/th ratio of 4.0 or greater identified all four patients who showed no reduction in LV dimension or mass postoperatively. Similarly, Kumpuris et al [66] demonstrated that a r/th ratio of 3.2 or greater predicted persistent postoperative LV dilation. Pressure-Volume Relationship.

410

The slope of the LV end-systolic pressure-volume relationship is a loadindependent measurement of contractility that is commonly employed to assess contractile state in valvular regurgitation. Starling et al[11] have used the slope of the pressure-volume relationship and the circumferential stress-

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shortening relationship (the ratio of end-systolic stress to ejection fraction) in patients with aortic regurgitation to differentiate reversible from irreversible LV pump dysfunction. As noted previously, although afterload excess is responsible for the early decline in LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to pump failure, but late in the course of the disease. Starling et al[11] demonstrated that the severity of preoperative contractile dysfunction determined recovery of LV ejection fraction. LV pump performance recovered postoperatively in the group of patients with less severe contractile dysfunction, in whom afterload excess predominated, but failed to recover in patients with more severe contractile dysfunction. Unfortunately, measurements of the slope of the end-systolic pressure-volume relationship and circumferential stressshortening relationship require complex, invasive, hemodynamic protocols; therefore, these indices cannot be routinely applied in most clinical settings. However, assessment of contractility using these techniques is important in that it provides the framework for timing of surgery using noninvasive modalities. To simplify the measurement of the end-systolic pressure-volume relationship, the ratio of the peak systolic pressure to end-systolic volume generated from a single point at rest has also been used to demonstrate abnormal contractility in patients with aortic regurgitation.[70] [169] Pirwitz et al[169] found the ratio of peak systolic pressure to end-systolic volume to be the strongest predictor of postoperative outcome in 27 patients with aortic regurgitation and LV dilation with an end-diastolic volume of greater than 60 mL/m2 . A ratio of 1.72 mm Hg/mL/m2 or greater identified all patients with postoperative functional class I or II, whereas a ratio of less than 1.72 identified 31% of patients in class III and 8% (n = 1) of patients who died. Indices of Systolic Left Ventricular Performance in Asymptomatic Patients Ejection Phase Indices.

As previously noted, asymptomatic patients with normal LV pump performance have an excellent long-term survival rate, and less than 4% of patients per year require aortic valve replacement.[61] Asymptomatic patients with impaired LV ejection fractions, on the other hand, have a considerably more aggressive clinical course and should be referred for elective aortic valve replacement to avoid progression to irreversible contractile dysfunction. Several investigators have evaluated the LV ejection fraction response

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during exercise as a way of predicting the onset of resting LV pump dysfunction in asymptomatic patients with aortic regurgitation.[160] [166] [170] Using radionuclide angiographic techniques, Borer et al[160] evaluated 22 asymptomatic patients with aortic regurgitation to assess LV ejection fraction reserve during exercise. Of the 21 patients (95%) with a normal resting LV ejection fraction, 9 patients (43%) had an abnormal LV ejection fraction response to exercise. The authors concluded that exercise-induced LV systolic dysfunction may precede the development of symptoms and abnormal resting LV pump performance and, therefore, may be used to follow patients for clinical deterioration. Although a decrease in LV ejection fraction with exercise may precede the onset of resting LV pump dysfunction in patients with aortic regurgitation, an abnormal exercise response does not necessarily portend a poor surgical or adverse postoperative outcome. End-Systolic Dimension.

To predict the subset of asymptomatic patients with aortic regurgitation likely to develop symptoms or require aortic valve replacement, Henry et al [142] studied 37 asymptomatic patients with serial echocardiograms for a mean of 34 months. The need for subsequent operative intervention was best predicted by the preoperative LV end-systolic dimension.[59] Eighty percent of patients with an end-systolic dimension of greater than 55 mm required surgery within the follow-up period, compared with 20% of patients with an end-systolic dimension of less than 55 mm. Left ventricular end-systolic dimension has also been used to predict asymptomatic patients likely to require aortic valve replacement. No patient with an LV end-systolic dimension of 40 mm or less required aortic valve replacement at 4 years, whereas 65% of patients with an end-systolic dimension of greater than 50 mm required surgery within the follow-up period. Pressure-Volume Relationship.

The slope of the LV end-systolic pressure-volume relationship has also been used to demonstrate abnormal contractility in asymptomatic patients with aortic regurgitation.[70] [71] [167] [171] Schuler et al[71] studied 14 asymptomatic patients with chronic aortic regurgitation and found that the slope of the end-systolic pressure-volume relationship could be used to identify contractile dysfunction in patients with preserved exercise tolerance and a normal LV ejection fraction.

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Timing of Surgery in Chronic Aortic Regurgitation In considering the timing for surgical intervention in these patients, several facts should be re-emphasized: 1. Chronic aortic regurgitation leads to a progressive decline in LV pump performance secondary to afterload excess. 2. Subclinical LV contractile dysfunction may develop when the LV ejection fraction remains normal, although unlike in patients with mitral regurgitation, LV ejection fraction in aortic regurgitation generally improves after valve replacement. 3. Asymptomatic patients with a normal LV ejection fraction have an excellent long-term prognosis with medical therapy. 4. Asymptomatic patients with normal LV pump performance should be treated with afterload reduction to delay the progression of LV dilation and the need for aortic valve replacement. 5. Valve replacement in symptomatic or asymptomatic patients with mild or moderately depressed LV pump 411

performance improves survival over medically treated patients with aortic regurgitation. 6. Severe preoperative contractile dysfunction is associated with persistent LV dilation and pump dysfunction, often resulting in postoperative congestive heart failure and death. 7. NYHA functional class III and IV symptoms are independently associated with increased early and long-term postoperative death. TABLE 18-10 -- Proposed Algorithm for Timing of Surgery in Patients with Aortic Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size Clinical END-SYSTOLIC Exercise EJECTION * Points Symptoms FRACTION, % DIMENSION, mm Capacity † 0 None > 60 < 45 Preserved 1 I/II 50–60 45–55 2 III/IV < 50 > 55 Decreased

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Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; clinical and echocardiographic follow-up at 12 mo 2 Borderline; recommend clinical and echocardiographic follow-up at 6 mo ≥ 3 Proceed with surgery Part C: Although not a requisite part of the algorithm, these additional predictors of adverse outcome can also be used in decision analysis. These variables marked with a double-dagger (‡) can be measured by two-dimensional echocardiography. Additional Predictors of Adverse Outcome in Aortic Regurgitation ‡ Value Percentage fractional shortening < 29% End-systolic volume index > 60 mL/m2 End-systolic wall stress End-diastolic dimension End-diastolic dimension (radius) (R)/End-diastolic wall thickness (th)

> 235 mm Hg > 80 mm ≥ 3.2

*Add one point for age > 65; cardiothoracic ratio 0.58; LV hypertrophy on electrocardiogram. †Preserved = ability to complete at least 8 METs on graded exercise treadmill testing or stable exercise performance; Decreased = inability to complete 8 METs on graded exercise treadmill testing or a decline in exercise performance from an established baseline. ‡Add two points for each additional predictor present.

In aortic regurgitation, the timing of surgery in both asymptomatic and symptomatic patients is relatively straightforward. In general, the majority of symptomatic patients have improved survival, functional class, and LV pump performance with aortic valve replacement; therefore, they should be referred promptly for aortic valve replacement, regardless of the status of LV ejection fraction. Asymptomatic patients with impaired LV pump

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performance have a rapidly progressive course and are likely to develop symptoms and require aortic valve replacement within 2 to 3 years. These patients should be referred for elective aortic valve replacement. Asymptomatic patients who have normal exercise tolerance and preserved LV pump performance can be treated medically and followed closely with serial noninvasive assessments of LV ejection fraction. Left ventricular end-systolic dimension and exercise capacity are parameters that can be used to serially assess asymptomatic patients with aortic regurgitation for the development of LV pump dysfunction. A poor or decreasing exercise tolerance, defined as the inability to complete approximately 8 METs on a graded exercise treadmill test or any decline in LV pump performance from a previously established baseline, may signal the onset of LV decompensation. Similarly, patients who develop a progressive increase in end-systolic dimension likely have contractile dysfunction and, therefore, should be referred for surgery. Given that functional class III and IV symptoms are independent predictors of early and long-term postoperative mortality, patients with class II symptoms should be referred for surgical correction before class III or IV symptoms develop. Table 18-10 presents guidelines in the form of an algorithm for timing of surgery in patients with chronic aortic regurgitation based on a system in which points are assigned to different clinical variables. The major components (part A) of this algorithm include hemodynamic variables, including LV ejection fraction, LV size, and exercise capacity. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were chosen on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. Included in this algorithm (part B) are additional parameters, all of which can be measured using two-dimensional echocardiography, that identify patients at high risk for contractile dysfunction. These parameters may, therefore, be used to confirm a decision to proceed with surgery, but they are not considered requisite components of the algorithm. These variables should be considered only supplemental to the decision-making process. The use of this algorithm to gauge the appropriate 412

timing of surgical intervention in aortic regurgitation is illustrated in the following case study. The patient was a 45-year-old construction worker

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with severe aortic regurgitation secondary to a bicuspid aortic valve. At the time of initial evaluation, the patient was able to complete stage III of a Bruce protocol without symptoms. Echocardiographic LV end-systolic dimension measured 45 mm, and the LV ejection fraction measured 55%. According to the algorithm, the patient would be assigned two points, justifying medical therapy with serial clinical and echocardiographic follow-up. The patient was treated with a vasodilator and followed every 6 months for 1 year, and then yearly thereafter. At 5 years after the initial diagnosis, although the patient remained asymptomatic, echocardiography revealed an increase in the LV end-systolic dimension to 55 mm and a decrease in the LV ejection fraction to 48%, resulting in a total of 3 points. The patient was then referred for successful aortic valve replacement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary After a long asymptomatic period, often lasting several years, severe, chronic mitral and aortic regurgitation eventually lead to reduced LV pump performance. In aortic regurgitation, decreased LV ejection performance is predominantly caused by afterload excess until late in the course of the disease, when contractile dysfunction supervenes. In contrast, contractile dysfunction occurs early in the course of mitral regurgitation, but it is masked by the favorable preoperative loading conditions. For both conditions, the development of irreversible contractile dysfunction is associated with increased risk for postoperative LV pump dysfunction and death from congestive heart failure. To justify the risk of surgery, the ideal timing for surgical intervention in patients with valvular regurgitation is, therefore, at the onset of contractile dysfunction, yet early enough to prevent the development of irreversible contractile dysfunction. Two-dimensional echocardiography, in conjunction with a thorough history and physical examination, provides an accurate, reproducible, and costeffective methodology for the serial screening for the development of contractile dysfunction in patients with valvular regurgitation. In this chapter, all of the major predictors of clinical outcome in valvular regurgitation, including those validated from nonechocardiographic methodologies, have been integrated to create the pathophysiologic framework necessary to develop algorithms for timing of surgical intervention using echocardiographic tools. The proposed algorithms for timing of surgery in patients with chronic mitral and aortic regurgitation guide operative intervention to preserve contractility and thereby improve long-term postoperative outcome and minimize unnecessary risk.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

417

Chapter 19 - Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Brian P. Griffin MD William J. Stewart MD

The advent of transesophageal echocardiography (TEE) and innovations in ultrasound technology have led to progressive improvement in the outcomes of valve surgery, especially mitral valve repair. Echocardiography has been used extensively in the operating room since the early 1980s. It is an essential element of every valve reconstruction operation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Indications for Intraoperative Echocardiography Intraoperative echocardiography has both diagnostic and monitoring functions that are useful in mitral valve repair and other valve-sparing operations. The diagnostic functions are used before cardiopulmonary bypass (prepump) to determine the mechanism and severity of the mitral valvular dysfunction, identify lesions of other valves, and refine the surgical mission. The diagnostic functions are used after cardiopulmonary bypass (postpump) to determine the success of the surgical mission. Intraoperative echocardiography is essential in performing valve repair, aortic homograft, and pulmonary autograft implantation.[1] In addition to its use in valve surgery, the diagnostic function of intraoperative echocardiography also is used in the surgical management of congenital heart disease, [2] [3] hypertrophic cardiomyopathy,[4] [5] reconstruction of the ascending aorta,[6] [7] and many other surgeries (Table 19-1) . [8] The monitoring function of intraoperative echocardiography is used to determine the hemodynamic status of the patient before and after surgery, for assessing intravascular volume, and ventricular contractility. Perioperative monitoring of left ventricular function is important in patients with impaired contractility who are undergoing any kind of cardiac surgery, including myocardial revascularization, [9] [10] and in those with significant cardiac disease undergoing high-risk noncardiac surgery such as reconstructive surgery of the descending thoracic and abdominal aorta[11] [12] [13] (see Chapter 3) . Intraoperative echocardiography also is used to help position intravascular and intracardiac catheters,[14] , [15] including those used for retrograde cardioplegia via the coronary sinus. When postpump echocardiography detects intracardiac air, [16] [17] this can be cleared by further venting of the cardiac chambers to prevent embolization to the coronary blood vessels[18] 418

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TABLE 19-1 -- Indications for Intraoperative Echocardiography Mitral Disease Assess feasibility and success of mitral repair for mitral regurgitation. Assess feasibility and success of commissurotomy for mitral stenosis. Determine need for mitral surgery in patients undergoing revascularization or aortic surgery. Assess presence of disease of other valves or other cardiac structures. Aortic Disease Assess feasibility and success of aortic valve repair. Assess size of prosthesis. Assess feasibility and success of homograft implantation or Ross procedure. Tricuspid Disease Assess need for and feasibility and success of tricuspid repair. Prosthetic Function Determine presence and site of paravalvular leak. Assess perivalvular tissue for abscesses or infection. Assess site and presence of pannus or thrombus. Revascularization Assess regional wall motion and global left ventricular function before and after revascularization. Determine sequence of graft placement. Detect and assess complications of infarction (ventricular septal defect, mitral regurgitation). Surgery on Aorta Assess size and extent of aneurysm. Determine the mechanism and severity of associated aortic regurgitation. Determine presence and complications of aortic dissection. Determine presence and extent of aortic atheroma. Transplantation/Devices

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Assess left ventricular function and suture lines postoperatively. Assess appropriate sizing, function, and hemodynamic changes with ventricular assist devices. Congenital Heart Surgery Determine connections (ventriculoarterial, atrioventricular). Assess systemic and nonsystemic ventricular size and function. Assess anatomy of shunts and valvular anatomy. Monitoring Assess ventricular volume and function. Monitor drug effects on ventricular function. Diagnose presence and location of ischemia. or the brain.[19] In patients who are difficult to wean off cardiopulmonary bypass or who remain hypotensive in the early postoperative period, echocardiography is a useful diagnostic and monitoring tool.[20] [21] More recent indications for intraoperative echocardiography include use in patient selection and monitoring for alternative surgical approaches such as the use of smaller incisions, port access techniques for cannulation, and offpump coronary artery grafting without cardiopulmonary bypass. [22] [23] The most frequent indication for intraoperative echocardiography is the postpump assessment of valve reconstruction surgery to determine whether the desired surgical result has been obtained. The availability of online feedback concerning the adequacy of the surgical result has allowed surgeons to become more innovative in repair techniques. Immediately after valve repair and before the chest is closed, the echocardiographer can determine whether the repair is adequate or if there is residual regurgitation or other complications present, requiring further repair or prosthetic implantation. Making this determination before the chest is closed allows the surgeon to perform further surgical procedures during a second run of cardiopulmonary bypass (a "second pump run") to optimize the surgical outcome. This second pump run eliminates the need for another surgical procedure at a later time, which would require another thoracotomy and create an increased mortality risk for the patient. In one study, 11% of patients undergoing valve surgery had inadequate results based on postpump echocardiographic imaging and required further surgery.[24] In our experience, intraoperative echocardiographic findings require a second pump run in 6% of cases.[1]

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It is axiomatic that all elective patients undergoing cardiac surgery have a full diagnostic work-up and a definite surgical plan before arriving in the operating room. Despite this, there are findings on the prepump echocardiogram that alter management by refining the preoperative diagnosis and the surgical mission. In our unpublished series of 436 consecutive prepump echocardiograms in patients with various valve problems, the surgical procedure was changed in 40 cases (9.2%). In a series of 154 consecutive patients undergoing valvular surgery, 29 patients (19%) had significant new findings by prepump intraoperative echocardiography. These findings changed the operative plan in 14 patients (9%). The changes were more common in mitral than aortic operations. The most frequent additional finding in this study was an increase in the severity of the valvular regurgitation compared with preoperative studies.[24] Even in patients in whom no major change in plan occurred, the prepump echocardiogram provided an updated understanding of the specific valvular anatomy and the mechanism of dysfunction, which helped to refine the surgical technique. These changes result from the improvement in resolution of TEE over preoperative transthoracic echocardiography (TTE) or cardiac catheterization and from changes in hemodynamic conditions or ischemia between the time of preoperative testing and the time of surgery. A 1999 study of 1918 consecutive cases in which intraoperative echocardiography was used showed a very low prevalence (2.5%) of discordant findings by echocardiography compared with operative findings. In only 0.3% of patients were the discrepancies sufficiently severe to warrant a change in the operative procedure. [25]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technique of Intraoperative Echocardiography Intraoperative echocardiography may be performed from either the transesophageal or epicardial imaging windows (Table 19-2) . Transesophageal Echocardiography TEE is the most widely used technique for intraoperative echocardiography. Figure 19-1 illustrates the experience with intraoperative echocardiography at the Cleveland Clinic Foundation from 1984 through 1999. TEE became available in 1987 and progressively supplanted the epicardial route for most studies. Compared with epicardial echocardiography, TEE has the advantage of allowing image acquisition without interfering with the surgical field or procedure. Immediately after induction 419

TABLE 19-2 -- Relative Advantages of Epicardial and Transesophageal Approaches to Intraoperative Echocardiography INDICATIONS

TRANSDUCER ADVANTAGES

Epicardial LVOT gradients; HOCM; congenital, aortic atheroma; TEE impossible or nondiagnostic 3.5–7.5 MHz transthoracic (standard TTE) sector scan Excellent images, especially of LVOT and septum; rapid imaging in emergency

Transesophageal All others

3.5–7.5 MHz transesophageal Does not interfere with sterile field; continuous imaging possible

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DISADVANTAGES Requires plastic covers for May be difficult to sterile preparation of probe; intubate esophagus once patient is draped; interferes with operative field and procedure; imaging occasionally impossible to obtain images (e.g., due to of posterior structures hiatal hernia, air), imaging difficult with prosthetic of anterior structures shadowing; may interfere difficult with hemodynamics; requires >1 person HOCM, hypertrophic obstructive cardiomyopathy; LVOT, left ventricular outflow tract; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. of anesthesia and endotracheal intubation, the TEE probe is inserted and left in place throughout the operation. Although the technique of intraoperative TEE is similar to its use in the echocardiography laboratory, there are additional potential pitfalls. First, it is occasionally difficult to pass the probe, particularly if the patient has been draped and the ether screen has been positioned. Usually, Figure 19-1 Cleveland Clinic Foundation experience with intraoperative echocardiography from 1984 to 1999. The total number of intraoperative echocardiograms per year is shown (bars).

this problem can be overcome using a laryngoscope and direct vision. Inadequate imaging occurs with the transesophageal approach for a number of reasons. Anatomic causes include a hiatal hernia or the presence of an echodense structure such as a mechanical valve prosthesis can cause shadowing of other cardiac structures. With all TEE studies, there is a "blind spot" approximately 2 to 4 cm in size in the middle portion of the ascending aorta caused by interposition of the trachea between the esophagus and the ascending aorta. Interference from electrical apparatus such as electrocautery leads to distortion of two-dimensional imaging and renders spectral and color Doppler signals impossible to interpret. Fortunately, imaging may be resumed once the electrocautery is discontinued. Another potential cause of ultrasonic probe dysfunction in the operating room is the thermistor in the transesophageal probe, which can sense an elevated esophageal temperature and cause the probe to stop

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functioning. This safety feature, designed to minimize the risk of esophageal damage from excess heat buildup in a malfunctioning probe, may deactivate the TEE transducer while the heart is being rewarmed after surgery. Newer probes have a mechanism whereby the probe temperature can be reset to take into account the patient's temperature. Finally, while the heart is on cardiopulmonary bypass, the absence of cardiac motion causes suboptimal images until the heart is filled with blood again and starts to eject during rewarming. Epicardial Echocardiography In epicardial imaging, images of the heart are acquired by placing a standard transthoracic transducer directly on the epicardium. Sterility is maintained using a double plastic sleeve. Intervening air is eliminated by using sterile acoustic gel inside the layers of plastic and by moistening the epicardial surface. An acoustic standoff such as a sterile bag or glove filled with saline is sometimes used if the structures of interest are superficial, in the first centimeter of depth below the probe. Epicardial echocardiography often provides better image quality than TEE of structures such as the ascending aorta, aortic arch, and left ventricular outflow tract, and it is especially accurate in measuring the outflow tract velocities. We use an epicardial approach when images obtained by TEE are inadequate during an open-chest procedure. Similarly, TTE can be used when needed during closed-chest procedures, including most types of noncardiac surgery. In addition, epicardial imaging is needed in infants who are too small for the available TEE probes. In the experience at the Cleveland Clinic Foundation, progressively fewer procedures are performed using an epicardial imaging window. The major current indication for an epicardial approach is in the evaluation of the ascending aorta of patients with suspected ascending atheroma, on the basis of clinical suspicion, calcification on chest x-ray study, or palpation by the surgeon. Identification of the severity and location of atheroma helps the surgical team optimize the location and methods of cannulation, 420

including the use of an alternative cannulation site such as the subclavian artery. In 1987 we described the following four standard imaging windows (Fig. 19-2) to be useful for epicardial imaging:[26]

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1. Parasternal equivalent. The transducer is placed on the most anterior portion of the heart, the right ventricular outflow tract. Image planes are similar to those for transthoracic imaging from the left parasternal imaging window. Both long-axis and short-axis views are obtained. The heart is scanned in the short axis from base to apex. By imaging more medially, the tricuspid valve and right ventricle also may be imaged. 2. Aorta-pulmonary sulcus. The transducer is placed in the sulcus between the pulmonary artery and ascending aorta, with the long side of the transducer against the left side of the ascending aorta. This view provides excellent images of the left ventricular outflow tract, aorta, aortic valve, mitral valve, and left atrium. 3. Subcostal equivalent. The transducer is at the most inferior portion of the thoracotomy incision against the most inferior portion of the right ventricular free wall. The four-chamber view is used to evaluate all four chambers, mitral and tricuspid valves, pulmonary artery, and the systemic veins. Angling medially allows imaging of the venae cavae, atria, and atrial septum. Angling superiorly visualizes the right ventricular outflow tract. Angling laterally brings in the left ventricular apex. 4. Aorta-superior vena cava position. The long side of the transducer is placed against the right side of the ascending aorta, pointing inferiorly and to the left, to image the left ventricular outflow tract and the aortic and mitral valves. This view is the best way to determine left ventricular outflow gradients with the continuous wave Doppler beam parallel to flow. The left atrium is also well seen from this view. Figure 19-2 The four standard positions for epicardial transducer placement. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

The epicardial window allows excellent imaging of intracardiac structures such as the cardiac valves and myocardium. High-velocity jets may be measured by continuous wave Doppler either with an imaging transducer or a stand-alone, nonimaging transducer. The epicardial window also has some disadvantages: 1. It enters the operative field and interrupts the operation itself. For this

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reason, a more limited time is available for imaging. 2. Imaging of structures in the near field may be difficult unless a good acoustic standoff is achieved. 3. Most surgeons and individuals that are accustomed to scrubbing for surgery are not adept at image acquisition with a hand-held transducer or echocardiographic anatomy, which requires a substantial learning curve. 4. If the probe is applied too heavily against the heart, it may cause arrhythmias or transiently interfere with cardiac filling. Equipment Ideally, an ultrasound machine devoted solely to intraoperative echocardiography should be available. In addition to interfacing with transesophageal and transthoracic transducers, the machine should be capable of recording M-mode and two-dimensional imaging and all Doppler modalities. A facility should be available near the operating room for cleaning and disinfecting the probes. Transthoracic probes from 3.0 to 7.5 MHz may be useful for different purposes, depending on the objectives of the study, using the lower frequency for general cardiac imaging and the higher frequency for infant congenital cases and aortic atheroma investigation. A stand-alone continuous wave Doppler probe should also be available. Sterile sleeves and acoustic gel should be available for epicardial imaging. The ultrasonic machine should have a capability for cineloop display and retrieval to compare prepump with postpump images. Videotapes or digital storage media should be available for archival of each study, an important consideration for medical-legal purposes. Cables should be available to input the electrocardiographic signal from the operating room monitoring system into the ultrasound machine. Many institutions have the capability of transmitting images from the operating room to a remote site such as the echocardiography laboratory in order to allow oversight or second opinions to be obtained in selected cases. Increasingly, digital storage of images is possible, which allows rapid retrieval to demonstrate findings to the surgical personnel and facilitates comparison of the preoperative and postoperative images.[27] Personnel Intraoperative echocardiography is a highly demanding technical field requiring specialized personnel skilled in transesophageal and epicardial imaging. This field requires

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421

familiarity with the phases of cardiac surgery and their effects on hemodynamics as manifested by echo and Doppler studies. The American Society of Echocardiography suggests that those learning TEE be in the phase of developing level 3 experience, which is equivalent to experience in performing at least 300 echocardiographic studies. In busy operating rooms in which a large volume of intraoperative studies are being undertaken, an echo technologist or other ancillary support person, working under the aegis of the echocardiographer, can facilitate and improve the efficiency of acquiring multiple studies, some of which may be needed simultaneously. Intraoperative Echocardiography Examination Intraoperative echocardiography should be performed in a standard comprehensive manner so that the acquisition of critical information is not omitted. It is important to do a complete TEE study, using imaging planes that allow good views of each intracardiac valve and chamber as well as the great vessels.[28] The entire prepump examination should be recorded on videotape or digitally to provide a durable record of the examination, especially as a reference for postpump studies and for medical-legal purposes. In cases in which comparison with postpump findings is likely, storing key images in a cineloop facilitates rapid comparison at the end of the operation. In diagnostic (as opposed to monitoring) studies, the structure of interest to the primary surgical mission should first be examined thoroughly in multiple planes, using imaging and Doppler modalities. If the echo study must thereafter be abbreviated because of pressing demands of the surgical agenda or the need to limit anesthetic and cross-clamp time, the primary concern, the raison d'être of the echo study, has at least been addressed. Other structures of interest should then be examined, including long- and short-axis views of all four chambers, all four valves, and the great vessels. The entire aorta should be examined in all cases. We also advocate a routine intravenous contrast injection to look for intracardiac shunting. The number of times the probe is passed through the gastroesophageal junction should be minimized, as should all unnecessary manipulation of the probe, to reduce the risk of mucosal trauma, esophageal tears, and pharyngeal trauma that are reported in a very small percentage of cases.[29] Once the prepump study is completed, a written report of the examination detailing significant findings should be made. Although ultrasound has not

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been demonstrated to cause any significant damage to cardiac structures during prolonged examinations,[29] it is advisable to put the machine on freeze so that no ultrasound energy is transmitted when imaging is not required. After cessation of cardiopulmonary bypass, a second comprehensive examination should be carried out and a second or updated report generated. The intraoperative examination has several aspects that are different from a TEE or TTE study in the outpatient echocardiography laboratory: 1. The echocardiogram is performed simultaneously with the operation; therefore, the room conditions, including the lighting and the space for the machine, may be suboptimal. For example, radiofrequency interference from other machines may mar the quality of images for long periods. 2. The hemodynamic milieu may change quickly, and the echocardiographic appearance may differ from images acquired outside the operating room. Changes in hemodynamics, such as intravascular volume, preload, and afterload, substantially affect the severity of valvular lesions. If necessary, the hemodynamic situation may be manipulated to match "street conditions" in order to determine the true or potential severity of a valvular lesion. 3. The surgeon who requests the intraoperative study may request online interpretation. Care must be maintained to make only diagnoses and conclusions that have been verified by examination from multiple imaging planes under appropriate imaging and hemodynamic conditions.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prepump Intraoperative Echocardiography in Patients Undergoing Valve Repair for Mitral Regurgitation The prepump echocardiogram assessment of mitral regurgitation (Table 193) usually merely confirms findings made previously by preoperative echocardiography or cardiac catheterization. TEE, however, often can improve on the accuracy and resolution of preoperative TTE because of improved resolution of the component structures, the mitral valve and the regurgitant jet. There are four main goals of intraoperative echocardiography in mitral valve disease: 1. To assess the severity of mitral regurgitation and determine the need for mitral valve surgery. 2. To assess the mechanism of mitral regurgitation and determine if a repair rather than prosthetic replacement is feasible and to determine the technique of repair. 3. To determine the presence of other significant valvular 422

disease that may require surgical attention, such as tricuspid regurgitation or aortic valve disease. 4. To assess left and right ventricular function in order to be able to compare with the postpump study. TABLE 19-3 -- Intraoperative Assessment of Repair and Reconstructive Valve Operations Prepump Assess severity of stenosis/regurgitation. Assess mechanism of regurgitation and potential reparability of valve.

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Measure dimensions of annulus, chambers, valves. Assess whether lesions other than the primary lesion require surgery. Determine biventricular function. Postpump Assess severity and mechanism of residual regurgitation/stenosis. Detect systolic anterior motion of the mitral valve and left ventricular outflow obstruction. Determine change in severity of other valve lesions. Assess biventricular function. Detect iatrogenic complications. Severity of Mitral Regurgitation The severity of mitral regurgitation is assessed by intraoperative echocardiography in the same manner as the use of echocardiography for other applications in other parts of the hospital (see Chapter 1) .[30] [31] [32] [33] [34] Several have indicated that the intraoperative assessment of mitral regurgitation agrees with the preoperative assessment by contrast ventriculography or TTE.[35] [36] In patients with ischemic mitral regurgitation, agreement between preoperative studies and the intraoperative assessment is less, possibly because of changes in hemodynamics or the degree of ischemia. One study of patients with ischemic mitral regurgitation showed that in 11% of patients the preoperative and intraoperative assessments of mitral regurgitation severity differed by more than one grade, with discordance occurring in both directions.[37] Discordance was more common in patients with clinical instability or those who received thrombolysis. It is important to remember that mitral regurgitation is dynamic and is affected by loading conditions. Reduction of afterload or intravascular volume at the time of the operation may reduce the true severity of the regurgitation. When less mitral regurgitation is found than expected, the intravascular blood volume should be expanded and systemic vascular resistance increased transiently using repeated boluses of IV phenylephrine. The velocity of mitral regurgitation, and therefore display of its jet by color Doppler, depends on the pressure difference between the left atrium and left ventricle, which is higher with hypertension. The size of the jet in the left atrium is also very sensitive to changes in color gain (directly proportional) and pulse repetition frequency (inversely proportional) (see Chapter 17) .

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The transesophageal imaging window has advantages over epicardial imaging in the assessment of mitral regurgitation. A mitral prosthesis or severe mitral calcification causes acoustic shadowing of the regurgitant jet when the transducer is placed anteriorly, such as in epicardial imaging or TTE. Excellent agreement, however, has been reported between the epicardial and transesophageal approaches in assessing mitral regurgitation. [38]

Semiquantitation of mitral regurgitation on a scale from 0 to 4+[30] [31] is determined based on a weighted average of several criteria: 1. The size of the left atrial flow disturbance, based on the depth of penetration and area of the regurgitant jet in the left atrial cavity assessed in multiple imaging planes; a multiplane probe facilitates this process, especially in eccentric jets. 2. The geometry of the jet; eccentric jets tends to have a higher regurgitant volume than free jets of the same area.[32] 3. The size of the proximal convergence zone, also called the proximal isovelocity surface area (PISA) technique. More severe regurgitation is associated with a larger radius of the proximal flow convergence.[33] Flow convergence can be used to calculate regurgitant flow, orifice area, and volume (see later). 4. The width of the proximal portion of the regurgitant jet on the left atrial side of the orifice is also useful and may be less load sensitive than mapping of the regurgitant jet in the atrium.[39] 5. The pulmonary venous pulsed Doppler tracing. Severe mitral regurgitation often leads to systolic reversal of flow in the pulmonary veins,[34] which is 69% sensitive and 98% specific in predicting a regurgitant orifice area of greater than 0.3 cm2 .[40] Blunting of pulmonary vein flow is somewhat reliable in predicting severe mitral regurgitation for patients in normal rhythm with normal left ventricular function but is unreliable in patients with severe left ventricular dysfunction or atrial fibrillation. A normal pulmonary vein flow pattern is useful in excluding severe mitral regurgitation and predicting a regurgitant orifice area of less than 0.3 cm2 . Importantly, in patients in which the right and left pulmonary vein flow pattern is discordant (23% of patients), the more abnormal pattern is most predictive of mitral regurgitation severity. 6. Quantification of mitral regurgitant volume (RV) from the difference between Doppler echocardiography measurements of antegrade flow through the mitral and the aortic valves. Regurgitant fraction (RF) is

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the proportion of total mitral flow (MF) that is regurgitant: RF (%) = RV/MF Mitral and aortic valve flow can be assessed by the product of annular cross-sectional area derived from echo and velocity derived from pulsed Doppler measurements at the same site. Mitral cross-sectional area is derived from two orthogonal diameters of the annulus, which is elliptic in shape.[41] This method has not been used routinely because of the timeconsuming nature of the measurements required and the ease and general reliability of semiquantitative techniques (see Chapter 17) . Other methods of assessing the severity of mitral regurgitation in the operating room include surgical palpation of the left atrium for the thrill of a mitral regurgitant jet, evaluation of the size of v waves on the left atrial pressure tracing, fluid filling of the arrested left ventricle, and contrast echocardiography. These methods lack sensitivity and are not as reliable or as convenient as color flow Doppler techniques.[36] [42] [43] The size of the regurgitant orifice area can be derived from Doppler echocardiography techniques in the operating room,[44] using either the antegrade flow difference method or the flow convergence method. The maximum regurgitant orifice area is calculated by dividing regurgitant flow rate by the maximum mitral regurgitant flow velocity (Vmax ) obtained from continuous wave Doppler. The regurgitant orifice area is greater than 0.4 cm2 in severe mitral regurgitation and greater than 0.25 cm2 in moderately severe mitral regurgitation. The flow convergence, or PISA, technique analyzes flow proximal (on the left ventricular side) to the regurgitant orifice, assuming a hemispheric shape.[44] [45] In this area, blood accelerates predictably as it moves toward the 423

regurgitant orifice and forms a series of concentric shells of decreasing area and increasing velocity that are depicted clearly as easily measured hemispheres on the color image because of the color aliasing of the accelerating flow. Because the surface area of a hemiellipse can be calculated from 2πr2 for blood flow moving at velocity v and at a radius r from the regurgitant orifice (Fig. 19-3) , flow rate Q can be calculated as

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follows: Q = 2πr2 v The PISA method provides excellent estimation of regurgitant flow when the flow convergence is centrally located, well away from the walls; however, this method overestimates regurgitant flow when the proximal flow is constrained by the left ventricular wall. Use of appropriate correction factors can compensate for this problem.[46] Automated analysis of digital velocity maps in the echocardiographic machine is feasible and has the potential to further simplify this technique.[47] The PISA method of determining the regurgitant orifice area (ROA) may be simplified without significant loss of accuracy. If the aliasing velocity of the color Doppler is set to approximately 40 cm per second and the mitral regurgitation by continuous wave Doppler (Vmax ) is assumed to be 5 m per second (500 cm per second), then the formula becomes

ROA = (2πr2 v)/Vmax ROA

[2(3.14)(r2 )(40 cm/s)]/(500 cm/s)

ROA

250 r2 /500

ROA

r2 /2

This method has particular merit in the operating room where rapid quantification is often helpful. Mechanism of Mitral Regurgitation Assessment of the cause (Fig. 19-4) and mechanism (Fig. 19-5) of mitral regurgitation is of great importance Figure 19-3 (color plate.) Proximal convergence zone of a patient with severe mitral regurgitation. The hemisphere produced by flow at an aliasing velocity of 51 cm per second is shown (arrow). The radius of the hemisphere is 1 cm.

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Figure 19-4 Feasibility of mitral repair by etiology of valve disease at the Cleveland Clinic Foundation. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

in determining the suitability of the mitral valve for repair. Mitral valve repair is most likely in patients with mitral regurgitation due to myxomatous degeneration and is least likely in patients with regurgitation due to endocarditis. Repair is now successful in greater than 90% of all patients with myxomatous disease. The probability of repair, however, is affected by the mechanism of regurgitation, especially whether the posterior leaflet, the anterior leaflet, or both leaflets are involved. Repair is most likely with posterior prolapse or flail, whereas bileaflet involvement and isolated anterior leaflet prolapse reduce the likelihood of successful repair substantially.[48] An Organized Approach to Imaging the Mitral Valve

To adequately assess the pathophysiologic mechanism responsible for mitral regurgitation, it is essential to perform Figure 19-5 Feasibility of mitral valve repair by mechanism of regurgitation in myxomatous mitral valve disease. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

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a thorough examination of the mitral valve and mitral apparatus and to determine the origin and geometry of the regurgitant jet. The long-axis imaging planes are best for determining which mitral leaflet is involved. Long-axis views of the mitral valve are obtained by imaging from midesophageal TEE planes. Figure 19-6 shows the "multiplane protractor" with all of the multiplane angles superimposed on the mitral valve. Most basilar long-axis views around the entire multiplane sweep allow portions of both leaflets to be examined individually. At approximately 50 to 60 degrees in most patients, the imaging plane parallel to a line between the commissures, is very useful for determining which portion of the anterior or posterior leaflet is involved. Imaging at a multiplane angle of about 135 degrees cuts perpendicular to this intercommissural line.

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The short-axis views also are useful for determining which portion of the anterior or posterior leaflet is involved. These views may be obtained from either the transgastric short-axis view or the epicardial parasternal shortaxis equivalent view.[49] The posterior leaflet has three divisions or scallops: the medial, middle, and lateral. The anterior leaflet is not segmented but has a central portion known as the bare area between the insertions of the chordae from the anterolateral and posteromedial papillary muscles. In a similar way the posterior leaflet is also supported, about half each by chordae from the anterolateral and posteromedial papillary muscles. The papillary muscles lie below each mitral commissure. The papillary muscles and chordae usually are well visualized from the transgastric long-axis views of the left ventricle using biplane or multiplane probes.[50] In assessing the mitral valve and in providing the results to the surgeon, giving an accurate localization of the abnormality is important. A prospective study of 50 patients used a segmental approach to the mitral valve, breaking each leaflet into three segments, and found that TEE was 96% accurate for localization compared with surgical findings.[51] Other Figure 19-6 The short-axis view of the mitral valve in systole from a transverse transgastric view. The medial and lateral commissures (COMM) and the positions of the medial (MED), middle (MID), and lateral (LAT) scallops of the posterior leaflet are shown. ANT, anterior. (From Stewart WJ; Griffin B, Thomas JD: Am J Cardiol Imaging 1995;9:121–128.) Figure 19-7 Transgastric short-axis view of the mitral valve in a patient with severe prolapse of the middle scallop of the posterior leaflet (arrow). ANT, anterior leaflet.

researchers have shown that localization of the defect to the posterior leaflet by TEE is 78% sensitive and 92% specific in myxomatous disease, with accuracy being least when the medial rather than the lateral or middle scallop is involved.[52] Assessment of the mechanism of mitral regurgitation is performed by analyzing the motion of the valve leaflets with twodimensional echocardiography (Fig. 19-7) and the direction of the regurgitant jet with color flow imaging [53] (Table 19-4) . Three types of leaflet motion (Fig. 19-8) may be associated with mitral regurgitation: (1) excessive motion, as seen with prolapse or flail valve caused by chordal rupture or elongation, (2) restricted motion, as seen in rheumatic disease and papillary muscle infarction, and (3) normal motion, as seen with leaflet perforation and ventricular-annular dilation.

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Intraoperative echocardiography has been shown to be highly sensitive and specific in determining the mechanism of mitral regurgitation in patients undergoing mitral TABLE 19-4 -- Determination of the Mechanism of Mitral Regurgitation from Analysis of Jet Direction and Leaflet Mobility Jet Direction Anterior Posterior

Leaflet Motion RESTRICTIVE NORMAL

EXCESSIVE Prolapse/flail of posterior leaflet Prolapse/flail of anterior leaflet

Restriction of posterior > anterior leaflet Equal restriction of both leaflets

Central

Prolapse/flail of both leaflets

Commissural

Rupture of commissural chordae or papillary muscle

Eccentric origin

Apical tethering from LV dilation Apical tethering from LV dilation, annular dilation

Leaflet perforation or cleft

LV, left ventricular.

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Figure 19-8 Morphology and echocardiographic appearance of normal, excessive, and restricted motion of the mitral valve, each of which can cause mitral regurgitation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

valve surgery. In a study of 286 patients undergoing mitral valve surgery in whom the echocardiography mechanism was correlated with the surgical findings, echocardiography was highly accurate (86%) in determining the mechanism of mitral regurgitation.[53] Echocardiography was least accurate in ascertaining the mechanism of mitral regurgitation in patients with

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leaflet perforation, bileaflet prolapse, or ventricular-annular dilation. Excessive Leaflet Motion.

Excessive leaflet motion occurs with elongation or disruption of any portion of the mitral valve or of the mitral apparatus, including the papillary muscles and chordae. Myxomatous disease, endocarditis, and papillary muscle infarction all can lead to this abnormality. With excessive leaflet motion, the regurgitant jet is directed away from the affected leaflet. Thus, prolapse or flail of the posterior leaflet leads to an anteriorly directed jet (Fig. 19-9) . In bileaflet prolapse, the excessive motion is often asymmetric, and the jet direction is away from the more severely affected leaflet. When the amount of prolapse or flail is completely balanced between both leaflets, a central jet direction occurs. If the chordae to the commissures are ruptured, then a jet originating at the commissures is seen in the transgastric short-axis view. Jets originating at the commissure also are seen in infarction of a papillary muscle, most commonly the posteromedial one.[54] Excess motion with overwhelming mitral regurgitation results when the head of a papillary muscle ruptures in an acute myocardial infarct. This type of rupture may be differentiated from acute chordal rupture by detecting a mass attached to the flail leaflet that is a portion of the muscle and by the appropriate clinical setting (Fig. 19-10) . Precise delineation of which portion of the valve has excess motion is important in planning the surgical repair. Rupture of the posterior chordae is the most common abnormality and is repaired by quadrilateral resection of the posterior leaflet (Fig. 19-11) . Elongation of the chordae is repaired by chordal transfer or by implantation of artificial chordae. Papillary muscle elongation or disruption may be repaired by reimplantation, supporting, or shortening the affected muscle.[48] Postoperative prognosis is best in those with excessive leaflet motion. Restricted Leaflet Motion.

This pattern is seen most commonly in rheumatic disease, but it also can occur in regurgitation from ischemic heart disease, the chronic phase of lupus, or acquired valvular disease caused by certain drugs such as ergot derivatives and anorexigenic drugs such as the fen-phen combination (fenfluramine and phentermine). In rheumatic, lupus, and drug-induced diseases, the leaflets are thickened. If both leaflets are equally affected by the pathologic process, the jet direction is central. More commonly in rheumatic disease, the posterior leaflet is more severely affected than the

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anterior leaflet, and the relatively normal anterior leaflet "over-rides" the restricted posterior leaflet. The direction of the regurgitant jet in this situation is posterior, toward the affected leaflet. The surgical approach to this condition includes débridement of the valve tissue and chordae, commissurotomy, and annuloplasty. This type of repair is more technically demanding and is less often successful. In ischemic heart disease, the posterior leaflet is typically restricted in motion owing to apical displacement of the posteromedial papillary muscle. The displacement results from ischemia or infarction of this papillary muscle or the muscle to which it is attached and which is usually in the perfusion territory of the right or circumflex coronary artery. The leaflets themselves are normal and are not thickened but fail to coapt adequately (Fig. 19-12) . In extreme cases the leaflets may not touch at all. The surgical approach to this problem usually involves placement of an annuloplasty ring to reduce the size of the mitral annulus and coronary revascularization. Use of a figureof-eight or Alfieri stitch either alone or in combination with annuloplasty ring also has been used. The Alfieri 426

Figure 19-9 (color plate.) Posterior leaflet prolapse (A) with severe mitral regurgitation (B) before mitral valve repair and no mitral regurgitation after successful mitral valve repair (C).

stitch effectively converts the mitral valve into a doubleorifice valve by attaching the leaflets at their midpoint. Surgical treatment of ischemic regurgitation with restricted leaflet motion is less successful in that residual regurgitation is often more significant than after myxomatous valve repair. Figure 19-10 Papillary muscle rupture with resulting severe mitral regurgitation. The rupture portion of muscle is seen prolapsing into the left atrium (arrow). Normal Leaflet Motion.

Perforation of the valve leaflet causing mitral regurgitation occurs most commonly because of endocarditis or because of a congenital cleft in the valve. Occasionally it is iatrogenic, after attempted repair. The jet origin is eccentric, arising from the midportion of the leaflets rather than from the coaptation line. The

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Figure 19-11 Quadrilateral resection of the posterior leaflet of the mitral valve with annular ring implantation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

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Figure 19-12 Ischemic mitral regurgitation with restricted posterior leaflet motion and posteriorly directed jet of mitral regurgitation.

prejet flow acceleration also may be seen away from the coaptation line, along the affected leaflet. Leaflet perforation may be repaired in some instances by suture closure or with pericardial patch.[55] Normal leaflet motion is commonly seen in patients with mitral regurgitation secondary to left ventricular dilation of any cause, such as disease of other valves, dilated cardiomyopathy, or severe ischemic cardiomyopathy. We have previously termed this category ventricularannular dilation. Ventricular enlargement causes displacement of the mitral coaptation point toward the apex with resultant impaired coaptation. Annular dilation is seen in these patients, but it occurs in proportion to left ventricular dilation, in contrast to myxomatous or rheumatic mitral regurgitation patients whose annulus size is often abnormally large. Annuloplasty with ring insertion is commonly used in the surgical management of these patients. An Alfieri stitch to support the valve also has been used instead of or in addition to the annuloplasty. There has been an upsurge in interest in the surgical management of severe mitral regurgitation in patients with dilated cardiomyopathy. Excellent functional improvement with a relatively low operative mortality has been reported even in selected patients with severe mitral regurgitation and severe left ventricular dysfunction. One study of 248 patients undergoing mitral valve surgery showed that TEE was greater than 90% accurate for definition of the mechanism of regurgitation, localizing the origin of regurgitation, and in detecting a flail segment. TEE was 88% accurate in detecting ruptured chordae. The TEE findings of valve function were highly predictive not only of valve reparability but also of long-term survival, which were independent of age,

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gender, ejection fraction, and coronary artery disease. [56] Other Valve Disease and Biventricular Function During Mitral Repair The severity of aortic and tricuspid valvular disease is assessed by intraoperative TEE using color flow mapping to determine the severity of the dysfunction and the necessity of valve surgery. These decisions should be made preoperatively, but diagnostic information should be refined intraoperatively, as mentioned earlier. Intraoperative diagnosis is particularly important in patients with active endocarditis. Significant tricuspid or aortic regurgitation usually requires operative intervention; however, intraoperative echocardiography tends to underestimate the degree of tricuspid regurgitation because of optimization of the hemodynamics that usually results in a reduction of right-sided pressures and volume. Because the preoperative echocardiogram is generally performed under ambulatory conditions, it is a better guide to decision making with regard to tricuspid valve repair, as opposed to the intraoperative findings alone. Regional and global left ventricular function is best assessed using TEE from long- and short-axis transgastric views and various midesophageal long-axis views. The long- and short-axis views from any epicardial imaging window also show the left and right ventricle well. Right ventricular function is assessed by TEE in the midesophageal 45-degree view at the level of the short axis of the aortic valve, from the midesophageal transverse four-chamber view, or from a longitudinal transgastric view rotated clockwise to obtain a long-axis image of the right ventricle.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Determining the Need for Mitral Valve Surgery in Patients Undergoing Cardiac Surgery for Other Reasons Intraoperative echocardiography increasingly is used to determine the need for a mitral valve operation in patients undergoing aortic valve surgery or revascularization procedures; this is especially true in the assessment of patients in whom the severity of the mitral regurgitation preoperatively is significantly different by cardiac catheterization and echocardiography, when the severity of mitral regurgitation over time is variable (such as in ischemic heart disease), and when the mitral regurgitation is of moderate severity. The following questions must be considered when determining the need for mitral valve surgery in addition to the primary surgery: 1. How severe is the mitral regurgitation? 2. Is there a primary abnormality of the mitral valve (such as a torn chord or prolapse)? 3. Will the mitral regurgitation change as a consequence of the primary operation? 4. Is the valve repairable or is prosthetic replacement necessary? 5. What is the additional risk imposed by the additional mitral valve procedure? The final decision on surgery is made by the surgeon; however, when the surgical objectives are changed in the operating room, telephone consultation with the referring cardiologist is advisable. In many patients, especially those in whom the regurgitation is secondary to ischemia or left ventricular dilation, 428

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the severity of the regurgitation may be variable. Sometimes, the severity of regurgitation detected at the time of operation is different from that recorded preoperatively. Frequently the difference in severity is due to a true physiologic change. Compared with ambulatory conditions, the loading conditions during surgery often entail a lower intravascular volume and less peripheral vasoconstriction, both of which may reduce the severity of valvular regurgitation and reduce stenotic valve gradients. On other occasions this discrepancy reflects the superior ability of esophageal and epicardial echocardiography to visualize mitral regurgitation. When approaching patients whose regurgitation is 2+ or less, we often purposely increase the afterload with multiple boluses of 100 µg of phenylephrine to determine the severity of regurgitation at a mean arterial pressure that is transiently as high as 120 mm Hg. Patients with 3+ or more mitral regurgitation at rest, or during this afterload stress test, are generally considered candidates for a mitral valve operation. The threshold for surgery on the mitral valve also is affected by other factors, including whether there is a primary structural abnormality of the valve. If the valve appears to be repairable, the threshold for surgery is lower, given the relatively low morbidity and mortality associated with repair as compared with valve replacement, whereas the threshold for surgery is higher in patients with valves that are not reparable. In patients undergoing surgery for aortic stenosis, improvement in the severity of the mitral regurgitation can be expected postoperatively. Therefore, the threshold for concomitant mitral surgery is higher.[57] [58] A postpump assessment of the mitral regurgitation is made regardless of whether a surgical intervention on the mitral valve has been performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Postpump Intraoperative Echocardiography in Mitral Repair The most significant indication for intraoperative echocardiography in mitral valve repair (see Table 19-3) is to determine the competency of the repair immediately after cardiopulmonary bypass. If the repair is inadequate, further repair or replacement can be performed immediately during the same thoracotomy. Timing Return of the patient to normal loading conditions is necessary to make valid assessments of valvular performance. It is also best to make valvular assessments after ventricular function has reached its postoperative plateau. The most appropriate time to image after repair is when the patient is off cardiopulmonary bypass, the intravascular volume is replete, and the loading conditions are similar to those in the ambulatory state. Imaging can be initiated after the aortic cross clamp is off and when the left ventricle is at least partially filled, but abnormal findings at this time may result from abnormal left ventricle geometry. The surgeon should not act on these findings unless they are subsequently confirmed by further imaging after the cessation of cardiopulmonary bypass. Intraoperative Findings In most cases, with an experienced surgeon, mitral valve repair leads to a competent mitral valve with mild or no residual mitral regurgitation; however, there are potential complications of mitral valve repair that are readily recognized by postpump intraoperative echocardiography. Many of these complications may not be apparent clinically or may take longer to accurately diagnose without echocardiography. If left untreated, these complications may interfere with the long-term success of the procedure and require early reoperation. Complications seen after mitral valve repair by intraoperative echocardiography are shown in Table 19-5 .

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Incomplete Mitral Repair Significant residual mitral regurgitation is the most common postpump problem detected by intraoperative echocardiography. The incidence of this complication varies with the cause of the valvular regurgitation, the complexity of the repair, the experience of the surgeon, and the threshold of the operative team to accept a suboptimal result. Frequently, if the echocardiographer can define the mechanism of the residual regurgitation, further repair of the valve leads to an improved result with reduction or elimination of mitral regurgitation. In some patients, TABLE 19-5 -- Management of Abnormal Findings on Doppler Echocardiography after Mitral Valve Repair Complication Residual mitral regurgitation

Management Define mechanism. If ≤1 +, accept. If 2 +, give phenylephrine to recheck MR with increased afterload; if >2 +, further surgery is required. Systolic anterior motion with Assess LVOT gradient and MR. LVOT obstruction Increase ventricular volume, stop positive inotropes, and increase afterload. If these measures are not successful, further surgery is needed to revise repair. Dehisced ring or leaflet perforation Another pump run is needed to fix annuloplasty. Residual mitral stenosis Quantify severity. If mean gradient >5 mm Hg or area < 1.5 cm2 , consider further surgery. Significant tricuspid regurgitation If 3 + or more, consider further repair. Regional left ventricular Assess intracardiac air; if not resolved dysfunction after further time on pump, consider coronary bypass. Global (right or left) ventricular Assess volume status, afterload, and dysfunction response to medications. LVOT, left ventricular outflow tract; MR, mitral regurgitation.

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429

further repair is impossible or fails, and the patient requires another pump run to implant a prosthesis. Moderate (2+) or more mitral regurgitation, either at rest or following afterload challenge with phenylephrine as previously described, is generally considered excessive after mitral repair and is an indication for a further surgical procedure. If the regurgitation is mild (1+) or less, then the result is usually accepted, though individual surgeons vary in their willingness to accept even mild grades of regurgitation. The severity of mitral regurgitation detected by immediate postpump intraoperative echocardiography correlates well with angiographic or TTE and TEE estimates of severity obtained later.[59] [60] Rarely, changes in the early postoperative period such as chordal rupture, suture dehiscence, or early postoperative endocarditis may cause acute worsening of the mitral regurgitation. Thus, intraoperative echocardiography is a reliable measure of the severity of mitral regurgitation and the need for further intervention. Other considerations in deciding whether residual mitral regurgitation should be accepted or subjected to another surgical procedure include the mechanism of the mitral regurgitation, the overall condition of the patient, and left ventricular function. Postpump determination of the mechanism of the residual mitral regurgitation helps the surgeon to determine whether a further reparative procedure could lessen the regurgitation and yet conserve the valve. More mitral regurgitation than is usually desirable might be accepted when other surgical procedures such as aortic valve replacement or coronary artery bypass grafting also have been accomplished, particularly in elderly patients or those with significant left ventricular dysfunction. For example, in patients with extensive mitral annular calcification, mitral prosthetic insertion may be technically more difficult and more hazardous for the patient than accepting a 2+ or even 3+ mitral regurgitation.[61] In one study of 100 patients undergoing mitral valve repair, 8% needed a second pump run, and 3% had persistent mitral regurgitation that was greater than 2+. Further repair in all three patients led to an improvement in regurgitation. [35] In another study of 309 patients undergoing mitral valve repair, 26 (8%) had immediate failure and required further cardiopulmonary bypass. Ten of those patients (3.2%) had excessive residual regurgitation. Two of the 10 patients subsequently had mitral prosthetic implantation, and eight had further repair. The further repair

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included chordal shortening in three patients, annuloplasty in four patients, and both procedures in one patient. Residual mitral regurgitation after the second repair was mild or absent in all patients. In this study, inadequate repair was associated with a degenerative cause of the mitral regurgitation and with the absence of an annuloplasty ring implantation at the time of initial repair.[62] In another study, residual mitral regurgitation caused by inadequate repair was seen in 4% of patients immediately postpump. In this study, need for reoperation because of inadequate repair or systolic anterior motion of the mitral valve was more common in patients with anterior mitral leaflet or bileaflet prolapse, as opposed to those with posterior prolapse.[63] Impact on Clinical Outcome The severity of residual mitral regurgitation after mitral valve repair is important for prognosis, as shown by several studies. In one of these studies, moderate or greater mitral regurgitation was associated with a higher incidence of congestive heart failure, repeat valve surgery, or postoperative death.[37] In a study of ischemic mitral regurgitation, residual regurgitation by postpump intraoperative echocardiography was a strong predictor of survival after mitral valve repair.[24] Residual mitral regurgitation in ischemic heart disease, however, correlates more with the degree of permanent contractile impairment rather than the technical success of the repair procedure. In another study, two patients with 3+ mitral regurgitation as determined by postpump intraoperative echocardiography who did not undergo a further pump run at the time of initial surgery required reoperation within 5 days because of hemodynamic instability and the inability to wean off mechanical ventilation.[35] Patients who undergo a second pump run for an initially inadequate repair have an in-hospital complication rate that is similar to that of patients who require a single pump run.[64] In one study, residual mitral regurgitation of 1+ or 2+ did not increase hospital complications when compared with trivial or no regurgitation postoperatively. There was a trend for patients with 1+ or 2+ mitral regurgitation, however, to need more reoperations in late follow-up than those with trivial or no mitral regurgitation.[65]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Other Complications of Mitral Valve Repair Systolic Anterior Motion of the Mitral Valve Significant left ventricular outflow obstruction caused by systolic anterior movement of the mitral valve (SAM) has long been recognized as a complication of mitral valve repair.[66] [67] This abnormality simulates that seen in hypertrophic cardiomyopathy, even though septal hypertrophy is absent. Similar to outflow obstruction in hypertrophic cardiomyopathy, SAM after mitral repair is dynamic and exacerbated by reducing the size of the ventricular chamber or augmenting the contractile state. SAM may cause pressure gradients of 100 mm Hg or more, severe hypotension, severe mitral regurgitation, and inability to wean the patient from cardiopulmonary bypass. Fortunately, this series of complications is readily recognized and quantified by an experienced echocardiographer on the postpump echocardiogram study (Fig. 19-13) . SAM has been reported in 2% to 9% of patients undergoing mitral valve repair.[35] [63] [68] Several mechanisms have been proposed to explain SAM following mitral valve repair. These mechanisms include anterior displacement of the posterior ventricular wall, anterior displacement of the posterior mitral leaflet, and narrowing of the angle between the mitral and aortic valves.[69] It is clear that SAM occurs primarily in patients 430

Figure 19-13 (color plate.) Series of images indicating the presence of systolic anterior motion at the end of the first pump run (A, arrow) leading to severe mitral regurgitation (B) and outflow obstruction (C). The maximal velocity measured in the outflow tract was 4.6 m per second, giving a pressure gradient of 85 mm Hg.

with degenerative mitral valve disease, those with large mitral leaflets, and

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in the presence of a hyperdynamic small ventricle.[63] SAM is usually seen only after annuloplasty ring insertion, but it has been reported after a suture annuloplasty.[63] It is seen more commonly with stiff than flexible annuloplasty rings.[63] [68] One quantitative study has shown that SAM is associated with anterior displacement of the mitral coaptation line. The anterior displacement is reduced or disappears after successful revision of the repair and elimination of SAM.[69] More recently, the ratio of the length of the anterior and posterior leaflet in the coapted state and the distance from the coaptation point to the septum were shown to be predictors of systolic anterior motion on preoperative TEE. The smaller the ratio between anterior and posterior leaflet and the narrower the distance between the coaptation point and the septum, the greater the likelihood of SAM.[70] When severe, SAM is easily recognized and may involve both leaflets. The left ventricular outflow gradient and the severity of mitral regurgitation are important indicators of the hemodynamic severity. The deep transgastric imaging window with the heart in an orientation similar to a transthoracic apical five-chamber image provides the best transesophageal window for assessing the left ventricular outflow tract gradient with continuous wave Doppler. When this examination cannot be reliably performed with the transesophageal approach, an epicardial study may be needed. The initial management of this condition should be to increase intracardiac volume by fluid repletion and to stop any positive inotropic agents that are being administered.[63] Systemic afterload can be supported by a pure alpha agonist (phenylephrine), avoiding any beta agonists. If these measures are inadequate to reduce the severity of SAM, another pump run to improve the SAM is indicated. Further procedures to improve SAM include (1) a sliding posterior leaflet advancement (sliding plasty), which reduces the anteriorposterior height of the posterior leaflet; (2) insertion of an annuloplasty of larger size; and (3) removal of the annuloplasty ring. Sliding annuloplasty is currently used as a component of the primary operative procedure on patients who are considered at risk for developing SAM and has significantly reduced the incidence of this complication in those patients in whom it has been used.[71] [72] If SAM persist despite these maneuvers, the final recourse is mitral prosthetic implantation. Patients in whom SAM is discovered by TTE days or longer after mitral valve repair, obviously a subset selected to have milder obstruction by successful weaning from bypass and extubation, may be treated medically with

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negative inotropic agents. Some patients show a late reduction in the left ventricular outflow gradient, but this may remain inducible by amyl nitrite. [73]

Suture Dehiscence

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Occasionally, suture dehiscence leads to significant mitral regurgitation immediately after mitral valve repair. This complication occurred in 2% of operations in one series.[62] Dehiscence of a suture at the site of the leaflet resection in the posterior leaflet simulates a posterior leaflet perforation and is easily repaired on a second pump run. Another rare complication of mitral valve repair that can be detected by intraoperative echocardiography is partial dehiscence of the annuloplasty ring. The annuloplasty ring shows increased mobility and regurgitation originates outside the ring (Fig. 1914) . Left Ventricular Systolic Dysfunction Some reduction in left ventricular function often is detected after mitral valve repair.[74] [75] When dysfunction occurs, it is most often global and may reflect the unmasking of left ventricular dysfunction present preoperatively that had been concealed by the effects of increased ventricular preload and decreased afterload. In a minority of instances, a regional wall motion abnormality is detected, despite normal coronary vasculature preoperatively. This abnormality is usually caused by passage of air into a coronary vessel, and it can cause transient wall motion abnormalities and occasionally permanent infarction.[18] Because of its anterior position, air is more likely to travel to the right coronary artery in a supine patient, causing inferior wall motion abnormalities. Air within the left ventricular cavity is readily detected by echocardiography because it is echodense. The presence of large amounts of air on echocardiography is an indication for increased surgical venting of the left ventricle to prevent coronary embolization. In minimally invasive operations in which small hemisternotomy incisions are used, surgical venting may be difficult or impossible. In this situation, resumption of cardiopulmonary bypass may be necessary for a period of time in order to allow slow resolution of the air. Fortunately, most instances of air embolization of the coronary vessels resolve without significant long-term

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ventricular dysfunction. A rare complication of mitral valve repair or of any mitral operation is the inadvertent entrapment of the circumflex artery in the annulus sutures, which causes a wall motion abnormality in the Figure 19-14 (color plate.) Ring dehiscence leading to severe mitral regurgitation. The dehisced portion of the ring is shown (arrow).

basilar posterolateral wall that may also be detected echocardiographically. Tricuspid Regurgitation Generally, tricuspid regurgitation that is treated with a ring annuloplasty at the time of mitral surgery should be rechecked on the postpump intraoperative echocardiogram.[76] The success of the tricuspid surgery should be checked only after the intravascular volume status has been normalized. [77] Occasionally, tricuspid regurgitation that did not appear to be significant preoperatively may appear to be more severe on the postpump study and require a further pump run for tricuspid repair. Mitral Stenosis In performing a mitral valve repair in a nonrheumatic valve, the surgeon may remove a significant portion of the leaflet or perform an annuloplasty that reduces the size of the mitral annular orifice. Despite these anatomic derangements, it is unusual to have any significant stenosis in degenerative or ischemic mitral valve repair. The annulus area is 5 to 10 cm2 , varying with the size of the annuloplasty ring inserted. In contrast, residual stenosis of mild degree is common after rheumatic mitral valve repair because of the thickened leaflets and fusion of subvalvular chordae and commissures. The mitral valve gradient should be measured using continuous wave Doppler after every mitral valve repair. A mean gradient in excess of 5 mm Hg should arouse suspicion of some degree of stenosis of the valve.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Mitral Valve Repair Involving Commissurotomy Although balloon valvuloplasty is a common method of treating selected patients with mitral stenosis, mitral repair with open commissurotomy still has a place, especially in patients with moderate amounts of valve calcification or thickening, those with multivalvular disease, or those with combined stenosis and significant regurgitation. Before surgery, intraoperative echocardiography is used to determine the severity of stenosis as a reference to assess the success of surgery. The severity of mitral stenosis is determined by measuring the transmitral pressure gradient and the pressure half-time with continuous wave Doppler.[78] [79] An epicardial approach using a para-sternal short-axis equivalent view may be used to obtain views suitable for planimetry of the mitral orifice if needed, but most TEE short-axis views of the mitral valve from the transgastric short-axis view are not of sufficient quality. The mechanism of the stenosis, whether valvular or subvalvular, should also be determined. A splitability score generated in a manner similar to the transthoracic method used for percutaneous mitral valvuloplasty may help to determine the degree of valvular fibrosis and calcification and whether a valve-sparing procedure is feasible.[80] Because 432

the surgeon can débride the valve under direct vision, open commissurotomy is sometimes possible even with a moderately high splitability score of 9 to 11, when a balloon valvuloplasty is not as likely to be effective or durable (see Chapter 20) . The presence of mitral regurgitation is also determined, and its mechanism, usually restricted leaflet motion, is determined. It is important also to detect left atrial and appendage thrombus preoperatively so that the surgeon can remove it. Postpump mitral valve gradient and area and mitral regurgitation are assessed. The presence of residual mitral regurgitation of 2+ or greater, or a

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mitral valve area of less than 1.5 cm2 is an indication for a further pump run, either to improve the repair or to implant a prosthesis. Frequently, when the patient has a large atrium or atrial fibrillation, the surgeon attempts to ligate the left atrial appendage in an effort to reduce the embolic risk. One study with TEE Doppler has demonstrated that these ligation attempts may be incomplete in up to one third of patients and in these instances blood still may enter and leave the appendage.[81] Patients with incomplete ligation remain susceptible to left atrial appendage thrombus formation and even thromboembolism. It has not been demonstrated that TEE evaluation of the competency of the ligation at the time of surgery improves the outcome.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions The acquisition and storage of digital images is available on many of the current echocardiographic machines and opens up new vistas for intraoperative echocardiography. This storage method preserves image quality better than does videotape. Retrieval of digital images also is more facile, but it depends on how and where the data is stored. Comparing previously performed studies directly with the current study provides a more reliable detection of change. Digital storage and retrieval of previously performed studies may reduce the need for prepump intraoperative studies, or at least shorten their duration. Appropriate training of additional personnel is changing intraoperative echocardiography for the better. Cardiac anesthesiologists are quickly learning the requisite skills, which could reduce the need for dedicated cardiology support to the cardiac operating rooms except to consult when specific problems arise. Online consultation is increasingly feasible with the availability of digital archival and retrieval of images on a common server. Additionally, training of cardiac surgeons in epivascular imaging of the aorta has the potential to reduce the involvement of other echocardiographers directly in image acquisition. New technology is constantly becoming available both in terms of the echocardiographic machines themselves and in terms of the available transducers. Image quality has improved remarkably, from faster computers and parallel processing circuitry. New technology including Doppler myocardial imaging, harmonic imaging, and contrast analysis software provides improved physiologic analysis. On the other end of the spectrum, smaller hand-held machines having many of the capabilities of bigger machines will soon become available in cardiac operating rooms, although they likely will need to be supplemented by more sophisticated technology for cases with significant diagnostic needs. As yet, these smaller machines have not had transesophageal capability, nor has their use in the operating

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room been reported. Newer transducers that are currently being evaluated include transnasal probes.[82] These smaller transducers, inserted through the nasopharynx, lessen the risk to teeth and the interference with the endotracheal tube. Currently, these probes are not available with multiplane capabilities. They are therefore at a disadvantage compared with standard multiplane TEE probes. Three-dimensional echocardiography has tremendous potential in any analysis of complex cardiac morphology, including the assessment of lesions in which repair or reconstruction is being considered[83] (see Chapter 10) . The complex three-dimensional geometry of some valvular and congenital lesions is easier to display and understand using three-dimensional echocardiography.[84] , [85] Threedimensional reconstruction may allow more appropriate selection of patients, help determine the most appropriate surgical procedure, and potentially allow the surgeon to map out the reconstruction ahead of time in three-dimensional computer space. Recently, the feasibility of intraoperative three-dimensional TEE has been shown, with acquisition time less than 3 minutes and reconstruction possible in greater than 90% of patients. Three-dimensional data yielded incremental information to TEE in up to 25% of patients but only led to a change in the operative plan in one of 60 patients studied.[86] Three-dimensional imaging for reconstruction of some structures has already been accomplished, including the regurgitant orifice area in patients with severe mitral valve prolapse.[87] Although realtime three-dimensional echocardiographic acquisition hardware is now a reality, transesophageal applications are not currently available and the exigencies imposed by the data acquisition render the image quality inferior to current two-dimensional echocardiographic images. Real-time acquisition of three-dimensional data has the potential to further expand echocardiographic abilities intraoperatively by allowing rapid changes in volume and structure to be quantified online and in allowing multiple slices of structure to be generated at a later time from one stored data set.

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Chapter 20 - Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Cheryl L. Reid MD

Historical Background and Technique of Mitral Balloon Commissurotomy Mitral stenosis in the adult occurs most commonly as the late result of rheumatic fever. Rarely, mitral stenosis may be caused by congenital or mitral annular calcification, particularly in the elderly patient. The natural history of rheumatic mitral stenosis is progressive symptomatic deterioration owing to reduction in the mitral valve orifice area. In the 10 to 20 years following an initial bout of rheumatic fever, the effective mitral valve area decreases because of fusion of the commissures, thickening and calcification of the mitral leaflets, and fibrosis and retraction of the chordae tendineae. The normal mitral valve area of 4.0 to 5.0 cm2 gradually decreases to 2.0 cm2 or less, at which time symptoms begin to develop usually with moderate to severe exercise. When the mitral valve area is reduced to 1.5 cm2 or less, symptoms may become severe and complications may develop.

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Mechanical intervention for the treatment of mitral stenosis, either open or closed mitral commissurotomy, has evolved in the past 40 years. Surgery, which has been shown to be highly effective, is usually performed for the relief of symptoms. Surgical replacement of the mitral valve may be necessary in patients with rigid, calcified mitral valves or severe mitral regurgitation in whom results with commissurotomy are suboptimal. Early experience with surgical commissurotomy showed that M-mode echocardiography could be helpful in selecting patients who would have a successful surgical mitral commissurotomy. It is important to identify patients who will have a successful commissurotomy because of the wellrecognized complications of valve prostheses, including thromboembolism, endocarditis, and higher operative mortality. The percutaneous approach to dilate a stenotic mitral valve was first reported by Inoue et al[1] in 1984, with subsequent evolution of catheter design and technique since the initial description. Simply stated, the technique consists of the percutaneous insertion of a dilating balloon into the right atrium. Using a trans-septal approach, the balloon catheters are then positioned across the stenotic mitral orifice and inflated at high pressures (1 to 2 atm). The desired result from inflation of the balloons is splitting 436

Figure 20-1 Technique of double-balloon valvuloplasty of the mitral valve. Top left, Two trans-septal sheaths from the right femoral vein are advanced to the left atrium (LA). Top center, Two end-hole balloon wedge catheters are positioned in the apex of the left ventricle (LV). Top right, Two curved exchange guidewires are inserted through the balloon catheters, which are then withdrawn. Bottom left, Two dilation balloon catheters are placed across the mitral valve orifice and into the LV apex. Bottom center, Two dilating balloon catheters are then fully inflated. Bottom right, Valve dilation balloons are removed. AO, aorta; IVC, inferior vena cava; RA, right atrium. (From McKay CR, Kawanishi DT, Rahimtoola SH: JAMA 1987;257:1753–1761, with permission. Copyright © 1987 American Medical Association.)

of the fused mitral commissures with resultant increases in the mitral valve orifice area. The procedure can be performed using either the doubleballoon or Inoue technique (Fig. 20-1) . In the double-balloon technique, two balloons are positioned side by side across the mitral valve orifice and then simultaneously inflated to achieve the desired result. The Inoue technique uses a unique self-seating single balloon that sequentially inflates

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from the distal to proximal end of the balloon. In recent years, the technical complexity and potential for serious complications (specifically, cardiac rupture inherent with the double-balloon technique) have largely lead to the abandonment of the double-balloon technique in favor of the Inoue technique. Early results of the procedure showed that the increase in mitral valve area is comparable to that obtained with surgical mitral commissurotomy.[2] [3] [4] Mitral balloon commissurotomy is now considered the procedure of choice for the treatment of symptomatic mitral stenosis in selected patients. Twodimensional Doppler echocardiography has played a major role in the evolution of mitral balloon commissurotomy, guiding our understanding of the mechanism by which the mitral valve area is increased. It is essential for the evaluation and selection of patients before the procedure and for the assessment of complications following the procedure. Hemodynamic measurement of the severity of the mitral stenosis and associated valve disease before the procedure, immediate hemodynamic changes during the procedure, and long-term follow-up can be reliably estimated with Doppler echocardiography (Table 20-1) .

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Evaluation of the Patient Before Mitral Balloon Commissurotomy Mechanisms of Increase in Mitral Valve Area Studies performed by two-dimensional echocardiography have shown that the primary mechanism for the increase in mitral valve area following mitral balloon commissurotomy is splitting of the fused commissures (Fig. 20-2) .[5] Tears of either the anterior or posterior mitral valve leaflet rarely occur and usually result in moderate to severe mitral regurgitation. In contrast to open, surgical commissurotomy in which the fused and retracted chordae can be manually separated, it is unclear that mitral balloon commissurotomy has a significant effect in dilating the subvalvular apparatus. Fortunately, the subvalvular region is rarely the primary orifice in patients with mitral stenosis.

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TABLE 20-1 -- Role of Two-Dimensional Doppler Echocardiography in the Evaluation of Patients Undergoing Mitral Balloon Commissurotomy Initial studies Severity of valve disease Mitral valve gradient Mitral valve area Mitral regurgitation Initial valve morphology Left atrial thrombus During mitral balloon commissurotomy

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Balloon position or trans-septal catheterization Changes in valve area or gradient Changes in mitral regurgitation Complications (rupture, atrial septal defect, etc.) Immediate results Changes in valve function Complications Long-term results Restenosis Mitral regurgitation Atrial septal defects Pulmonary artery pressure Ventricular size and function Other valve disease Mitral Valve Morphology The pathologic processes of rheumatic heart disease include (1) fusion of the commissures, (2) thickening and calcification of the valve leaflets, and (3) fusion and shortening of the chordae tendineae. These processes result in varying degrees of involvement of the mitral apparatus. Given that the mechanism of the increase in mitral valve area by surgical or percutaneous techniques is splitting of the commissures, it is expected that the morphology of the mitral valve apparatus will influence the results of the procedure. Experience with both surgical mitral commissurotomy and mitral balloon commissurotomy has confirmed this expectation. The characteristic feature of rheumatic mitral stenosis on two-dimensional echocardiography is doming of the body of the mitral valve leaflets during diastole caused by the fused commissures. As blood flows from the left Figure 20-2 Two-dimensional echocardiogram in the parasternal shortaxis view at the level of the mitral valve during early diastole. A, Before double-balloon catheter balloon valvuloplasty the transverse diameter was 20 mm. Calcification of the posterior commissure was present. B, After catheter balloon valvuloplasty the transverse diameter increased to 27 mm. The increase in

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transverse diameter suggests that the split occurred at the commissures. Figure 20-3 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis. The mitral valve is mobile with doming of the anterior leaflet. Minimal valve thickening and no subvalvular disease is noted. Right, Transesophageal echocardiogram in the midesophagus fourchamber transverse view from the same patient. The mitral valve morphology in this patient is ideal for mitral balloon commissurotomy and excellent results would be expected. LA, left atrium.

atrium to the left ventricle through the narrowed mitral orifice, the body of the leaflets balloon apically. The mobility of the leaflets (amplitude of doming) reflects the degree of calcification of the leaflets and commissural fusion. Both qualitative and semiquantitative criteria have been proposed for evaluation of leaflet morphology. [6] [7] In patients in whom the transthoracic echocardiogram is inadequate, transesophageal echocardiography can provide a similar analysis of the mitral valve morphology, although nonstandard image planes may complicate interpretation ( Fig. 20-3 and Fig. 20-4 ). [8] [9] In addition, subvalvular thickening and calcification may be underestimated on transesophageal imaging because of masking of the subvalvular region from thickening and calcification in the mitral valve leaflets. To some extent, these limitations can be avoided by use of biplane or multiplane transesophageal echocardiography with imaging of the subvalvular region in the transgastric longitudinal imaging plane. Total echocardiographic scoring systems based on leaflet morphology have been proposed as a guide to the selection of patients for mitral balloon commissurotomy. Although studies using these methods have been shown Figure 20-4 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis undergoing evaluation for mitral balloon commissurotomy. The mitral valve is heavily calcified with decreased excursion of the mitral leaflets during diastole. Right, Transesophageal echocardiogram in the midesophagus transverse view, which again shows a heavily calcified immobile mitral valve. The assessment of the morphologic features of the mitral valve are similar between the transthoracic and transesophageal echocardiographic examinations. The increase in mitral valve area from mitral balloon commissurotomy in this patient would be expected to be minimal. LA, left atrium.

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Figure 20-5 The anatomic features of the mitral valve in relationship to the resultant mean mitral valve area immediately after catheter balloon valvuloplasty are shown for the presence or absence of calcification, subvalvular disease, and pliable or rigid mitral valves. The mean mitral valve area was greater in the groups with pliable mitral valves without calcification or subvalvular disease.

to correlate with the immediate results, the wide scatter of the data makes their value questionable in an individual patient for predicting the hemodynamic results of the procedure ( Fig. 20-5 and Fig. 20-6 ). These criteria should be used, therefore, only as a guide to the severity of the individual morphologic variables of the mitral valve. Table 20-2 is a summary from the literature of the morphologic features of the mitral valve and the criteria used in assessment before mitral balloon commissurotomy. The single best echocardiographic morphologic variable that predicts the results of mitral balloon commissurotomy is leaflet mobility, which reflects the extent of commissural fusion and calcification of the mitral leaflets.[10] In the studies of the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry and Reid et al,[6] [10] leaflet mobility was the only independent echocardiographic variable to predict the results of mitral balloon commissurotomy (Table 20-3) . The presence of calcification and the involvement of one or both commissures assessed in the twodimensional echocardiography parasternal short-axis view may also be helpful in predicting the success of commissural Figure 20-6 Total morphology score by echocardiography versus mitral valve area (MVA) measured by cardiac catheterization after mitral balloon commissurotomy (MBC). There is significant (P < .001) but weak negative correlation (r = -0.24).

splitting by the balloon dilation (see Fig. 20-2) .[11] In asymmetric involvement of the commissures, in which one commissure is heavily fibrosed or calcified, splitting occurs in the opposite commissure. If both commissures are equally fused without marked calcification, both commissures are expected to split. In one study, if at least one commissure split, 89% of patients had a good hemodynamic result.[11] The presence of severe subvalvular fibrosis and calcification may also result in suboptimal results from mitral balloon commissurotomy because it is unclear that balloon dilation is able to split chordal fusion. Isolated subvalvular disease,

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however, rarely occurs and is usually associated with extensive fibrosis and calcification of the commissures and valve leaflets. The best hemodynamic result based on echocardiographic evaluation is expected in a patient with a highly mobile mitral valve without evidence of calcification or severe subvalvular disease (see Fig. 20-3) . In this group of patients, a mean resultant mitral valve area greater than 2.0 cm2 is predicted.[6] Mitral valve morphology, however, should not be used alone in the selection of patients to undergo mitral balloon commissurotomy. In occasional patients, satisfactory hemodynamic and clinical improvement can occur with more severe mitral valve disease. Other variables that have been shown to influence the results of the procedure and should be considered in the selection of patients include evidence of long-standing disease such as a low cardiac output, baseline mitral valve area, and left atrial size and technical factors such as the balloon diameter used in the dilation. Assessment of Left Atrial Size and Left Atrial Thrombi As a result of chronic pressure overload, the response of the left atrium is progressive enlargement. With long-standing mitral stenosis, an extremely large or "giant" left atrium (>6.5 cm anteroposterior diameter) may result. The 439

TABLE 20-2 -- Two-Dimensional Echocardiographic Assessment of Mitral Valve Morphology Predicted Results SUBOPTIMAL Variable OPTIMAL Leaflet Highly mobile with restriction Minimal forward motion of motion of only leaflet tips and H/L leaflets in diastole or H/L ratio ≥ 0.45 ratio ≤ 0.25 Leaflet Leaflets < 4–5 mm or Leaflets > 8.0 mm thick or a thickening MV/PWAo ratio of 1.5–2.0 MV/PWAo ratio ≥ 5.0 Subvalvular Thin, faintly visible chordae Thickening and shortening disease tendineae with only minimal of chordae to papillary thickening below valve muscle; areas with echo

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density greater than endocardium Commissural Homogeneous density of both Both commissures heavily calcium commissures calcified H, height of doming of mitral valve; L, length of dome of mitral valve; MV, mitral valve; PWAo, posterior wall of aorta. Data from Reid CL, Chandraratna PAN, Kawanishi DT, et al: Circulation 1989;80:515–524; and Abascal VM, Wilkins GT, Choong CY, et al: J Am Coll Cardiol 1988;2:257–263. enlarged left atrium can compress the inferior vena cava, resulting in increased Doppler flow velocities and an increased incidence of hepatomegaly.[12] Other well-recognized complications associated with an enlarged left atrium include the development of atrial fibrillation and blood stasis within the enlarged left atrium with thrombus formation. Left atrial thrombi occur in approximately 25% of patients with mitral stenosis and are seen even in patients in normal sinus rhythm. [13] In the majority of cases, the thrombi are confined to the body of the left atrial appendage, but they may also protrude into the body of the left atrium or attach to the left atrial wall or interatrial septum (Fig. 20-7) . In patients undergoing mitral balloon commissurotomy, the size of the left atrium has been noted to have a significant influence on outcome.[14] In patients with large left atria (>6 cm), technical difficulties may be encountered in performing the trans-septal puncture and crossing the mitral valve orifice. Enlarged left atria also are more frequently associated with a suboptimal increase in the resultant mitral valve area, perhaps because of technical difficulties or as an index of more severe and chronic disease. Conversely, smaller left atria are more frequently associated with the development of an atrial septal defect after mitral balloon commissurotomy. In such patients, shorter balloon sizes should be used or care taken during the procedure to prevent slippage of the balloon catheter against the interatrial septum. Systemic embolization has been reported in 0 to 4% TABLE 20-3 -- Predictors of Mitral Valve Area Variable NHLBI-BVR[10]

R2 0.31

P value <.001

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Pre-MBC MVA <.001 Cardiac output .004 Leaflet mobility .01 Left atrial size .01 Balloon diameter .02 0.65 .0001 REID et al[6] Leaflet motion .0001 EBDA .03 Cardiac output .002 EBDA, effective balloon dilating area; MBC, mitral balloon commissurotomy; MVA, mitral valve area; NHLBI-BVR, National Heart Lung, and Blood Institute Balloon Valvuloplasty Registry. of patients undergoing mitral balloon commissurotomy.[15] Because the dilating balloon catheters must traverse the left atrium to be positioned across the stenotic mitral orifice, the risk of embolization is increased if a left atrial thrombus is present. Transesophageal echocardiography has been shown to be more sensitive than transthoracic echocardiography in the identification of left atrial thrombi, especially for imaging of the left atrial appendage where most thrombi occur. Furthermore, by transthoracic echocardiography the left atrium lies in the far field of the ultrasound beam, thus the image quality is suboptimal. In contrast, the left atrium is the structure closest to the ultrasound beam by transesophageal echocardiography and thrombi therefore can be accurately located and characterized by size and shape. Identification of left atrial thrombi is especially important in patients who are undergoing mitral balloon commissurotomy because of the risk of systemic embolization.[16] Although some of these episodes are undoubtedly from left atrial thrombi, other sources also must be considered, such as atherosclerotic debris and catheter thrombi.[17] The role of transesophageal echocardiography in patients before mitral balloon commissurotomy is controversial. Although mitral valve morphology and hemodynamic Figure 20-7 Transesophageal echocardiograms from two patients undergoing evaluation for thrombi before mitral balloon

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commissurotomy. Recordings were made at the midesophagus in a four-chamber view. Left, The interatrial septum through which the dilating balloon catheter is inserted is thin and without evidence of clot. Right, The interatrial septum is markedly thickened with evidence of a layer clot along the left atrial side of the septum (arrows). LA, left atrium; RA, right atrium.

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assessment of the severity of the mitral valve disease can be reliably predicted in most patients by transthoracic echocardiography, only transesophageal echocardiography can accurately exclude the presence of a left atrial thrombus. Obviously, if a left atrial thrombus is detected by transthoracic echocardiography, then a transesophageal echocardiogram is not usually necessary. Although the presence of a left atrial thrombus is not an absolute contraindication for mitral balloon commissurotomy, it should only be considered in patients that are at high risk for surgical commissurotomy. In such patients, monitoring by transesophageal echocardiography during the mitral balloon commissurotomy can be used to help guide the placement of the balloon catheters to avoid the thrombus. [18] A layered thrombus along the interatrial septum is a particularly high risk because of the trans-septal puncture. If no contraindication to anticoagulant therapy is present, it is prudent to treat the patient with anticoagulants for 1 to 3 months before the mitral balloon commissurotomy because some thrombi may resolve with anticoagulant therapy. Transesophageal echocardiography should then be performed in close temporal relationship to the mitral balloon commissurotomy. If a left atrial thrombus is present, anticoagulant therapy may be continued if the patient is clinically stable to attempt to resolve the thrombus or the patient should be referred for surgical mitral commissurotomy. Although anecdotal cases of patients having successful mitral balloon commissurotomy with thrombi confined to the atrial appendage have been noted, the procedure should be considered in patients only after thorough consideration of the risks and potential benefits.

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Hemodynamic Assessment of the Patient Undergoing Mitral Balloon Commissurotomy Hemodynamic assessment of the severity of mitral valve disease in the patient undergoing mitral balloon commissurotomy can be measured reliably by Doppler and two-dimensional echocardiography. The severity of the stenosis can be quantitated by measurement of the mitral valve area and gradient and the presence, and the severity of mitral regurgitation can be assessed by two-dimensional echocardiography in combination with spectral and color Doppler data. TABLE 20-4 -- Comparison of Mitral Valve Areas by Doppler Echocardiography with Gorlin-Formula Mitral Valve Areas Before and After Mitral Balloon Commissurotomy

Author Reid et al[6]

Method T½ 2D echo Abascal et al T½

MVA, Mean ± SD (cm2 ) r Value AFTER BEFORE AFTER BEFORE 1.0 ± 0.2 1.9 ± 0.4 0.73 0.42 1.0 ± 0.2 2.2 ± 0.4 0.71 0.34 0.9 ± 0.2 1.5 ± 0.4 0.75 0.46

[7]

2D echo 0.9 ± 0.3 1.8 ± 0.4 0.81 0.75 Nakatani et al Continuity 0.9 ± 0.3 1.6 ± 0.4 0.77 0.86 [27] equation 0.8 ± 0.2 2.4 ± 0.6 0.81 0.84 Chen et al[30] T½ MVA, mitral valve area; SD, standard deviation; T½, pressure half-time; 2D echo, two-dimensional echocardiography.

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Mitral Stenosis Severity Pressure Gradients

The mean diastolic mitral valve gradient is measured from Doppler flow velocity tracings based on the modified Bernoulli equation. In patients undergoing mitral balloon commissurotomy, Doppler gradients are accurate as shown by simultaneous measurement of mitral valve gradient before and after mitral balloon commissurotomy in comparison to cardiac catheterderived gradients (r = 0.70 and 0.89, respectively). [19] Pressure gradients across stenotic valves depend on the volume flow rate and orifice size. Thus, the pressure gradient varies depending on the hemodynamic state of the patient. If the volume flow rate increases, such as with exercise, the gradient increases. Conversely, if the patient is dehydrated, the gradient may be low. Because of this flow rate dependency, calculation of mitral valve area is essential. Mitral Valve Area Two-Dimensional Echocardiographic Planimetry of Mitral Valve Orifice.

Two-dimensional echocardiography or Doppler echocardiography is used for determination of the mitral valve area in patients with mitral stenosis. By two-dimensional echocardiography, the mitral valve orifice can be directly planimetered when visualized in the parasternal short-axis view. * Careful scanning by two-dimensional echocardiography of the mitral valve apparatus must be performed to identify the smallest or most restrictive orifice. The gain settings of the machine must be adjusted to prevent "blooming" because of the presence of calcification. The accuracy of this method in patients before mitral balloon commissurotomy has been confirmed in several studies with r values of two-dimensional echocardiography compared to cardiac catheterization ranging from 0.71 to 0.81 (Table 20-4) . The mitral valve area estimated by two-dimensional echocardiographic planimetry of the mitral valve orifice before mitral balloon commissurotomy, in reported series, ranges from 0.9 to 1.0 cm2 , with a resultant increase immediately following the procedure to 1.8 to 2.2 cm2 .[6] [7] After mitral *See Otto CM (ed): Textbook of Clinical Echocardiography, 2nd ed. Philadelphia, WB Saunders, 2000, pp 229–264. 441

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balloon commissurotomy, the correlation ranges from an r value of 0.51 to 0.75.[19] [20] [21] [22] Similar to patients after surgical commissurotomy, in patients following mitral balloon commissurotomy the orifice becomes more irregular and technically difficult to planimeter, especially if calcium is present. Because of the accuracy of this technique, two-dimensional echocardiography measurement of the mitral valve area should be performed in all patients undergoing mitral balloon commissurotomy in whom it is technically feasible. Doppler Pressure Half-Time Mitral Valve Area.

Doppler spectral tracings are used to estimate mitral valve area based on the pressure half-time method described by Hatle et al.[23] The pressure halftime (T1/2 ) is defined as the rate at which the initial mitral valve gradient declines to one half of the initial value, with mitral valve area (MVA) calculated as: MVA = 220/T1/2 (Fig. 20-8) . Although several clinical studies have validated the accuracy of this method, there are limitations to the technique, some of which are unique to patients undergoing mitral commissurotomy. Factors that influence the accuracy of the Doppler pressure half-time method are both technical and hemodynamic. The accuracy of Doppler flow velocity tracings for hemodynamic measurements depends on the Doppler beam being parallel to the direction of blood flow. In patients with mitral stenosis, Doppler flow velocity recordings typically are made in the apical four-chamber view with the Doppler beam directed through the center of the mitral stenotic jet. Adequate tracings can be recorded in most patients with the aid of Doppler color flow to identify the stenotic jet even in patients for whom two-dimensional echocardiography is inadequate. In the rare patient in whom transthoracic flow velocity tracings cannot be obtained, transesophageal echocardiography can be performed to obtain the flow velocity tracings from a high esophageal position in a four-chamber view. Another technical limitation to the Doppler pressure half-time method is difficulty in identifying the diastolic deceleration slope. In some patients, the diastolic flow is Figure 20-8 Doppler transmitral flow velocity from a patient with mitral stenosis. The pressure half-time (T1/2 ) is the time required for the

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initial gradient to decrease to one half. This point is identified on the diastolic slope of the transmitral flow tracing. Figure 20-9 Transmitral Doppler flow velocity tracing from a patient with nonlinear flow (arrow). In this circumstance the mid-diastolic flow, which is more linear, should be extrapolated back to obtain the maximal initial velocity (dashed line).

nonlinear (Fig. 20-9) . If linear flow cannot be obtained by careful angulation and placement of the Doppler beam, the mid-diastolic flow, which is more linear, should be used and the slope extrapolated back to obtain the initial maximum velocity.[24] In patients with rapid heart rates who are in sinus rhythm the A wave may be superimposed on the diastolic slope, making identification impossible. Similarly, rapid atrial fibrillation and atrial flutter may preclude identification of the early diastolic slope. Hemodynamic considerations in the application of the Doppler pressure half-time method include the effects of coexisting valve disease. When aortic regurgitation is present, the increased diastolic filling may result in a more rapid rise of the left ventricular end-diastolic pressure. As a result, the pressure half-time may be shorter than expected for the valve area; therefore, the severity of the mitral stenosis may be underestimated.[25] The severity of the aortic regurgitation can be assessed by color Doppler flow and, if mild or moderate, the pressure half-time method may be applied. If the aortic regurgitation is severe or acute (which is unusual in mitral stenosis patients), the limitation of the pressure half-time method should be recognized and an alternative method applied for estimation of the mitral valve area. One of the major limitations of the Doppler pressure half-time method is calculation of the mitral valve area when hemodynamics are changing rapidly. With the advent of mitral balloon commissurotomy, it was recognized early that calculation of the mitral valve area immediately following mitral balloon commissurotomy might be inaccurate.[5] The Doppler pressure half-time method assumes that the left atrial and left ventricular compliances are stable (Fig. 20-10) .[26] This assumption is not valid following relief of the mitral stenosis by balloon dilation because there are rapid changes in the left atrial pressure and left ventricular filling with consequent changing compliances of both the left atrium and left ventricle. The mitral valve

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Figure 20-10 Left atrial (LA) and left ventricular (LV) compliance curves showing the relative changes in LV and LA pressures and volumes before and after percutaneous mitral valvuloplasty (PMV). The LA pressurevolume relationship (top) shifts to the left after PMV because of reduced LA size and pressure, whereas the LV pressure-volume relationship (bottom) shifts to the right because of increased diastolic ventricular filling. Despite these significant shifts in individual chamber compliance, the net compliance remains almost constant before and after valvuloplasty. (From Thomas JD, Wilkins GT, Choong CY, et al: Circulation 1988;78:980–993.)

area by the pressure half-time method also varies directly with the square root of the initial pressure gradient across the mitral valve, further complicating post-mitral balloon commissurotomy data as pressures rapidly fall. It should be noted, however, that the widely accepted catheter-derived mitral valve area based on the Gorlin formula also may be inaccurate following mitral balloon commissurotomy because of significant mitral regurgitation and the presence of an atrial septal defect leading to inaccurate measurement of transmitral volume flow.[27] In patients before mitral balloon commissurotomy, the noninvasive estimation of mitral valve area correlates well with invasive estimates (see Table 20-4) , with a standard error of the estimate ranging from 0.15 to 0.11 cm2 (r = 0.71-0.81) for Doppler pressure half-time method, 0.22 cm2 (r = 0.77) for the continuity equation method, and 0.17 cm2 (r = 0.71-0.81) for the twodimensional echocardiographic planimetry method.[19] [20] [21] [22] [23] [27] Immediately following mitral balloon commissurotomy, however, the Doppler pressure half-time method correlates less well with invasive data or with two-dimensional echocardiographic planimetry of valve area (see Table 20-4) . This inaccuracy is multifactorial and includes the rapid hemodynamic changes and the development of an atrial septal defect in many patients post mitral balloon commissurotomy.[28] In this setting, the pressure half-time method may overestimate the mitral valve area and depends on the magnitude of the shunt. In one study, occlusion of the atrial septal defect in patients after mitral balloon commissurotomy decreased the difference in the mitral valve area calculated by hemodynamic measurements and by the Doppler pressure half-time method.[29] This difference was due largely to a decrease in the mitral valve area calculated by the Gorlin formula when the atrial septal defect was occluded.

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The accuracy of the Doppler pressure half-time method has been shown to improve with time from the procedure. At 24 to 48 hours, hemodynamic equilibrium may be reached and the Doppler pressure half-time accuracy improves.[27] Furthermore, the mitral valve area calculated by the continuity equation decreases slightly at 24 hours probably because of a loss of "stretch" of the mitral valve. Because of these many considerations, caution should be taken in estimating the noninvasive mitral valve area immediately following mitral balloon commissurotomy. Doppler Continuity Equation Mitral Valve Area.

The calculation of mitral valve area by the continuity equation is based on the law of conservation of mass. The mitral valve area is calculated as MVA = (AVA [or PVA] × TVIa [or TVIp ])/TVIm where MVA is mitral valve area, AVA (PVA) is aortic (pulmonary) valve area measured from two-dimensional echocardiography, TVIa (TVIp ) is time velocity integral of the aortic (pulmonary) flow, and TVIm is time velocity integral of transmitral flow. One advantage of the continuity equation is that it is theoretically independent of transvalvular gradient and compliance. The continuity equation method, however, is much more difficult to perform. In addition, application of the continuity equation requires that the flow across the stenotic valve and another valve must be equal, based on the conservation of mass. In patients with associated mitral regurgitation, particularly if greater than mild, the stroke volume across the valves is different. Similarly, if greater than mild aortic regurgitation is present, pulmonary flow should be used. If the continuity equation is used to calculate the mitral valve area in the presence of mitral stenosis and an atrial septal defect, the transaortic Doppler flow should be used to avoid the effect of shunt flow volume. Other limitations of the technique include difficulty in measuring accurate pulmonary and aortic diameters. Regardless of the technical difficulty, studies have shown the method to be accurate in the calculation of mitral valve area with a correlation of r = 0.81 before mitral balloon commissurotomy and r = 0.84 after mitral balloon commissurotomy.[30] Stress Doppler Echocardiography

The clinical decision on interventional therapy for the relief of mitral stenosis must take into consideration the patient's symptoms in addition to the severity of the stenosis based on area and gradient. In some patients, symptoms of mitral stenosis caused by the elevated left atrial pressure and

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pulmonary congestion may be present 443

only during exercise. The transmitral gradient is dependent on flow volume and, thus, the severity of the mitral stenosis is underestimated in patients with low cardiac output at rest. Exercise hemodynamics have been used in patients with mitral stenosis to determine whether the mitral stenosis limits the transmitral flow and contributes to the patient's symptoms.[31] [32] Stress testing in patients with mitral stenosis is performed during supine bicycle or pharmacologic stress, which allows recording of the Doppler flow velocity. The calculation of mitral valve area by Doppler methods is controversial and the reliability of the pressure half-time in this setting is questionable.[32] [33] Calculation of the mitral valve area by the continuity equation in this setting is technically difficult. The severity of the mitral stenosis still can be reliably assessed by measurement of the transmitral gradient and pulmonary artery systolic pressure and assessment of the patient's symptoms. Studies have shown that mitral flow dynamics are improved in patients who have undergone mitral balloon commissurotomy with a decrease in the transmitral gradient and heart rate at maximal stress. [34] [35]

Associated Lesions Mitral Regurgitation

Mitral regurgitation, in varying degrees of severity, is commonly associated with mitral stenosis. The severity of associated mitral regurgitation can be assessed using standard Doppler echocardiography techniques (see Chapter 17) . Because most patients undergoing mitral balloon commissurotomy have transesophageal echocardiography, the variability in assessing the severity of mitral regurgitation by transesophageal and transthoracic echocardiography should be recognized. Because of the closer proximity of the transesophageal probe to the flow, shallower depth setting, decreased attenuation of the Doppler signals, and higher transducer frequency, the flow disturbance by the mitral regurgitation appears larger by transesophageal echocardiography.[36] [37] [38] Thus, there is a tendency to overestimate the severity of the mitral regurgitation when assessed by transesophageal echocardiography. Caution must be taken in estimating the severity of the mitral regurgitation in association with mitral stenosis.

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Patients with severe mitral regurgitation associated with mitral stenosis are not considered candidates for either balloon or surgical commissurotomy. In patients with moderate mitral regurgitation (grade 2+), commissurotomy should only be undertaken based on the patient's symptoms and the degree of mitral stenosis. Mild mitral regurgitation is not considered a contraindication to mitral balloon commissurotomy. In patients with associated mild or moderate mitral regurgitation, however, left atrial size is greater, which may cause more technical difficulties during the procedure. Pulmonary Hypertension

In patients with severe, long-standing mitral stenosis, the elevated left atrial pressure results in pulmonary hypertension and elevated pulmonary vascular resistance. Initially, the increase in pulmonary artery pressure is "passive" because of the increased resistance to the pulmonary venous drainage within the left atrium. With chronic elevation of the left atrial pressure, the pulmonary hypertension becomes "reactive" with an increase in the pulmonary vascular resistance.[39] Secondary effects of pulmonary hypertension include the development of right ventricular hypertrophy, right ventricular enlargement and dysfunction, and tricuspid regurgitation because of annular dilation. Estimation of the degree of pulmonary hypertension can be made based on the velocity of the tricuspid regurgitant jet.[40] The simplified Bernoulli equation applied to the peak tricuspid regurgitant jet velocity can be used to calculate the right ventricular peak systolic pressure when added to the estimate of right atrial pressure. In patients without right ventricular outflow tract obstruction, the right ventricular systolic pressure reflects pulmonary artery systolic pressure. Pulmonary vascular resistance, however, cannot be determined directly with Doppler echocardiography techniques. The severity of the pulmonary hypertension and pulmonary vascular resistance shows a significant relationship to the mitral valve area (Fig. 20-11) . Because of the wide variation in pulmonary pressures observed with a any given degree of mitral obstruction, however, specific predictors of pulmonary hypertension cannot be identified based solely on the severity of the mitral stenosis.[39] In patients in whom the pulmonary hypertension is out of proportion to the severity of the mitral stenosis, other possibilities, such as coexisting pulmonary disease, should be considered. In patients undergoing mitral balloon commissurotomy, there is a significant decrease in the pulmonary artery pressure as estimated by Doppler echocardiography immediately following mitral balloon

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commissurotomy despite the presence of severe pre-existing pulmonary hypertension.[40] Following mitral balloon commissurotomy, there is an immediate decrease of approximately 10 mm Hg in pulmonary artery pressure. The decrease in pulmonary hypertension following mitral balloon commissurotomy, however, cannot be predicted based on baseline characteristics. [39] Despite the initial improvement in pulmonary artery pressures, Doppler estimate of right-sided pressures should be followed closely for evidence of persistently elevated or increasing pressures.[41] Associated Other Valve Disease

Rheumatic heart disease affects not only the mitral valve but also the aortic valve and to a lesser incidence the tricuspid valve. The severity of these lesions can be assessed using standard Doppler echocardiography techniques. Patients that have significant stenosis of the aortic or tricuspid valve can be considered for concurrent dilation with the mitral valve. The symptomatic improvement in patients with aortic stenosis, however, may be limited because of the less than favorable results with balloon aortic valvuloplasty. Associated aortic regurgitation of mild or moderate severity does not significantly affect the hemodynamic and 444

Figure 20-11 Mitral valve area at catheterization on x-axis versus pulmonary vascular resistance on y-axis with inverse curve fit. (From Otto CM, Davis KB, Reid CL, et al: Am J Cardiol 1993;71:876. Reprinted with permission from Excerpta Medica Inc.)

symptomatic improvement obtained with mitral balloon commissurotomy. [42] The severity of the tricuspid regurgitation can be semiquantitated, similar to mitral regurgitation, based on the size of the regurgitant jet. Increasing severity of tricuspid regurgitation is directly related to the severity of the mitral stenosis. Patients with severe tricuspid regurgitation have a less favorable long-term result from mitral balloon commissurotomy than patients with mild or moderate regurgitation. [43] Ventricular Function The presence of mitral stenosis results in a chronic restriction in left ventricular diastolic filling. Left ventricular volumes are reduced in patients

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with isolated mitral stenosis compared with normal patients.[44] Left ventricular systolic function is normal. Increased left ventricular diastolic volumes suggests the presence of concomitant mitral or aortic regurgitation. Following successful mitral balloon commissurotomy, left ventricular end-diastolic volume and mass increase without significant change in end-systolic volume or ejection fraction. [45] Right ventricular end-diastolic volumes are increased in patients with severe mitral stenosis. Right ventricular volumes and function in patients with mitral stenosis are affected by the increased afterload because of pulmonary hypertension and the presence and severity of associated tricuspid regurgitation. Successful mitral balloon commissurotomy significantly improves but does not normalize right ventricular function.[46]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Role of Doppler Echocardiography in Predicting Results and Complications of Mitral Balloon Commissurotomy Patient Selection Doppler echocardiography plays a major role in the selection and evaluation of patients to undergo mitral balloon commissurotomy (see Table 20-1) . In patients with symptomatic mitral stenosis (mitral valve area < 1.5 cm2 ), the ideal candidate for mitral balloon commissurotomy based on the Doppler echocardiographic examination is one in whom the mitral valve is highly mobile without significant calcification of the leaflets or subvalvular apparatus. The presence of mitral regurgitation of greater than 2+ severity and a large left atrial thrombus within the left atrium or attached to the interatrial septum is considered a contraindication to mitral balloon commissurotomy. Immediate and long-term results are less successful in patients with evidence of long-standing disease such as large left atrium (>6 cm) or low cardiac output, although results vary in individual patients. The presence of significant other valvular disease such as critical aortic stenosis or severe aortic or tricuspid regurgitation and coronary artery disease may warrant consideration for surgical referral. The decision to perform mitral balloon commissurotomy in patients considered to be high risk for surgery because of other medical diseases, suboptimal mitral valve morphology, or a left atrial thrombus must be based on consideration of the risk-to-benefit ratio and the patient's desire. During Mitral Balloon Commissurotomy Doppler echocardiography plays a major role not only in the selection and evaluation of patients before mitral balloon commissurotomy but also is a useful adjunct during the procedure (see Table 20-1) . Doppler echocardiography equipment should therefore be available during the procedure to assess the immediate results and potential complications.

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Imaging by two-dimensional echocardiography of the interatrial septum can be performed to confirm and aid in the proper location of the transseptal catheter in difficult circumstances. Variability in the location of the interatrial septum may occur because of aortic root dilation, right atrial dilation, or cardiac deformity owing to scoliosis, 445

and in these settings, fluoroscopy may be misleading. Echocardiography can be useful in this setting by visualization of the interatrial septum and confirming by contrast saline injection the location of the needle within the left atrium once the trans-septal puncture is performed.[15] The identification of the needle tip may be difficult if it is out of the imaging plane, but it can be assessed indirectly by the "tenting" of the interatrial septum. Following the trans-septal puncture, two-dimensional echocardiography can aid in positioning the catheters across the stenotic mitral orifice. This positioning is important if the double-balloon technique is used. The Inoue balloon technique involves a unique self-seating design, which makes positioning of the balloon catheter easier. Echocardiography is helpful to prevent inadvertent inflation within the left atrium, which may result in an atrial septal defect if it butts against the interatrial septum. In patients with left atrial thrombi considered high risk for surgical commissurotomy, transesophageal echocardiography may be beneficial in preventing inadvertent migration of the catheter into the left atrial appendage. Two-dimensional echocardiography can also be used during the procedure to assess the affects of sequential balloon dilation. The transmitral gradient and changes in mitral regurgitation can be rapidly assessed to determine the need for further inflations. If the mitral regurgitation increases by one or more grades the procedure should be terminated. The success of mitral balloon commissurotomy has been shown to be related to the mitral anulus–to–balloon diameter ratio.[47] The mitral anulus by two-dimensional echocardiography can be measured to aid in selecting the appropriate balloon sizes. The increase in mitral valve is directly related to the mitral anulus–to–balloon diameter ratio. If the balloon diameter is too large, however, excessive tearing of the commissures or mitral leaflets may occur resulting in significant mitral regurgitation. In patients undergoing doubleballoon dilation, a ratio of the sum of diameters of the two dilating balloons to mitral anulus of ≥1.1 is associated with a significant increase in mitral regurgitation without further increase in mitral valve area.

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Complications of Mitral Balloon Commissurotomy Complications that may occur with mitral balloon commissurotomy are those known to be associated with invasive procedures, including death, myocardial infarction, stroke, bleeding, and heart failure. In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry, the incidence of serious complications was 12% and inhospital deaths 1%.[48] The reported complications of mitral balloon commissurotomy that can be detected by Doppler echocardiography are shown in Table 20-5 . Doppler echocardiography provides a rapid method for the early detection of complications and a noninvasive technique for serial evaluation. Atrial Septal Defects

The creation of an atrial septal defect in patients undergoing mitral balloon commissurotomy results from the TABLE 20-5 -- Complications of Mitral Balloon Commissurotomy Detected by 2D Doppler Echocardiography Event Thrombus (systemic embolization) Cardiac perforation (tamponade) Left-to-right shunt (atrial level) Valve related Acute mitral regurgitation (requiring early surgery) Increase in MR

Incidence (%) 2 4 10 3 12 36

Inadequate result (MVA < 1.5 cm2 ; ≥ 2 + increase MR) Restenosis ? MR, mitral regurgitation; MVA, mitral valve area. Data from National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry Participants: Circulation 1992;85:448–461, 2014– 2024. trans-septal approach. The reported incidence of atrial septal defects depends on the method of detection. By oximetry immediately following mitral balloon commissurotomy, the reported incidence ranges from 7% to 33% depending on the type of balloons used and diagnostic criteria.[3] [49] [50]

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Transesophageal echocardiography is the most sensitive method for detection of left-to-right shunting after mitral balloon commissurotomy and defects have been reported in 87% of patients examined within 24 hours of the procedure.[52] Transthoracic echocardiography detects left-to-right shunting in about half of the patients immediately following mitral balloon commissurotomy.[53] [51]

The detection of left-to-right shunting after mitral balloon commissurotomy requires a thorough evaluation of the interatrial septum in any patient who has undergone mitral balloon commissurotomy. The optimal view of detecting defects of the interatrial septum is obtained from the subcostal approach (Fig. 20-12) . In this position, the cardiac flow is parallel to the ultrasound beam, which is optimal for detection by color Doppler. The characteristic Doppler flow pattern is a continuous or late systolicholodiastolic left-to-right flow caused by the high pressure gradient between the right and left atrium in patients with mitral stenosis. The size of the defects range from 0.3 to 1.5 cm in diameter. By color Doppler, a jet width less than 0.5 cm is not likely to be detected by oximetry. Atrial septal defects greater than 1.0 cm are associated with significant right heart oxygen stop-ups. Shunt flow volumes calculated by Doppler echocardiographic methods range from 0.08 to 4.87 L per minute. The highest incidence of atrial septal defects is reported immediately after mitral balloon commissurotomy. Defects that are less than 0.7 cm in diameter usually close within 6 months.[54] Factors that have been associated with the development of atrial septal defects after mitral balloon commissurotomy include smaller increases in mitral valve area, the presence of mitral valve calcification, and smaller left atria. Atrial septal defects have also been reported to be initially detected during follow-up. Persistence of an atrial septal defect during follow-up is associated with larger sizes, a decrease in mitral valve area, and an increase in the mitral valve gradient. Clinically, significant problems are not associated with small atrial 446

Figure 20-12 (color plate.) Two-dimensional echocardiogram in the subcostal view from a patient after mitral balloon commissurotomy. Color Doppler flow mapping shows flow from the left to right atrium through a large atrial septal defect. The defect created by the dilating balloons measured 0.9 cm in diameter. RA, right atrium; LA, left atrium.

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septal defects. The effect on the right heart hemodynamics of large atrial septal defects with or without restenosis of the mitral valve remains to be determined. Mitral Regurgitation

Mitral regurgitation is a frequent complication of mitral balloon commissurotomy (Fig. 20-13) . The presence and severity of the mitral regurgitation should be carefully Figure 20-13 (color plate.) Transthoracic and transesophageal echocardiograms from a patient who had undergone mitral balloon commissurotomy (MBC). A, Transthoracic apical four-chamber view before MBC, which by color Doppler flow mapping shows a small blue jet in the left atrium during systole (arrow) consistent with mild mitral regurgitation. B, Same echocardiographic view obtained during the procedure following the first balloon inflation. The Doppler flow mapping shows turbulent flow into the left atrium. The mitral regurgitant jet is directed along the lateral wall and wraps around, almost completely filling the left atrium. C, Transesophageal echocardiogram from the midesophagus longitudinal view, which shows both the anterior and posterior leaflets of the mitral valve are flail with ruptured chordal attachments. LA, left atrium; LV, left ventricle.

evaluated by Doppler echocardiography using standard techniques before mitral balloon commissurotomy so that any change in severity can be recognized and evaluated immediately. Creation of new or an increase in pre-existing mitral regurgitation has been reported in 19% to 85% of patients undergoing mitral balloon commissurotomy.[5] [55] [56] [57] [58] [59] In most patients, however, the increase in mitral regurgitation is mild. An increase of greater than 2 grades in mitral regurgitation occurs in only 3% to 10% of patients. [48] [55] [56] [57] [58] [59] In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry early surgery for mitral valve replacement owing to severe mitral regurgitation occurred in 2% of patients.[55] This rate is comparable to results of surgical mitral commissurotomy. Although some patients who develop severe mitral regurgitation require urgent surgery for mitral valve replacement, others may tolerate the mitral regurgitation acutely. The mechanisms in the development of mild increases in mitral regurgitation differs significantly compared with the mechanisms of severe mitral regurgitation.[58] [59] [60] [61] [62] Echocardiographic studies of patients who develop mild increases in mitral regurgitation have shown that the

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regurgitant jet originates from the split commissures. Severe mitral regurgitation following mitral balloon commissurotomy, however, results from tearing of the valve leaflets or rupture of the chordal attachments. In one study of patients having balloon commissurotomy with the Inoue technique, the incidence of severe mitral regurgitation was 7.5%.[59] The most common cause was rupture of the chordae tendinae to the anterior or posterior leaflet in 43% of cases. A heavily calcified posterior leaflet resulted in tearing of the leaflet in 30%. Other variables that have been associated with the development of severe mitral regurgitation include severe calcification of both commissures and extensive subvalvular disease. [60] Splitting of the commissures, which most commonly is associated with mild increases in mitral regurgitation, can, if "excessive," result in severe regurgitation owing to incomplete coaptation of the valve leaflets during systole.

447

Unfortunately, the development of severe mitral regurgitation in patients undergoing mitral balloon commissurotomy cannot be reliably predicted from baseline characteristics, valve morphology, or technical factors during the mitral balloon commissurotomy procedure. The incidence of severe mitral regurgitation is not significantly different between patients undergoing double-balloon or Inoue techniques.[48] [56] [57] [58] [59] [60] [61] [62] [63] Similarly, stepwise inflation with the Inoue balloon technique has not reduced the frequency of severe mitral regurgitation. Indeed, inadvertent inflation of the Inoue balloon within the subvalvular apparatus, which may occur because of the unique design of the balloon catheter, can result in rupture of the chordal attachments or tear of the leaflets. Care must be taken in the positioning of the catheter before inflation. In one study, calcification of the posterior leaflet of the mitral valve resulted in a tear of the leaflet in the region of the calcification.[62] After each sequential balloon inflation, Doppler echocardiography should be performed to evaluate changes in mitral regurgitation. Two-dimensional echocardiography in the parasternal short-axis view permits evaluation of commissural splitting to assess the need for subsequent balloon inflations. Cardiac Perforation

Perforation of a cardiac chamber can occur during mitral balloon commissurotomy and is a major cause of death in these patients (see Table 20-5) . Atrial perforation can occur during the trans-septal catheterization

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and left ventricular perforation during the balloon inflations. The incidence of cardiac perforation is directly related, in part, to the dilation technique. In the Balloon Valvuloplasty Registry of patients undergoing mitral balloon commissurotomy with either a single- or double-balloon technique, the incidence of perforation was 4%. Perforation was the most common cause of death during the procedure, usually left ventricular perforation, and the most frequent indication for emergency cardiac surgery.[48] Cardiac perforation with the Inoue technique is much less common (<2%).[56] [61] [62] Left ventricular perforation occurs in the relatively thin apex owing to the positioning of the catheters and guidewires used in the technique. Manipulation of the catheters can then result in puncture of the apex. Perforation of the left ventricle usually results TABLE 20-6 -- Follow-up by Doppler Echocardiography of Patients Undergoing Mitral Balloon Commissurotomy Mean F/U No. of Author Method Patients 2D 235 Vahanian et al[63] Desideri et al[65] T½ 57 T½ 33 Georgeson et al

MVA (cm2 )

Mo RANGE BEFORE AFTER 18 1–48 1.1 2.0 19 9–33 1.0 2.2 17 1–38 1.1 2.0

F/U 1.9 1.9 1.7

[41]

Park et al[67] Hernandez et al

2D T½ 2D T½

59(I) * 13 61(D) † 561 39

— —

1.1 0.9 0.9 1.0

1.9 1.8 1.9 1.8

1.7 1.6 1.7 1.7

[70]

F/U, follow-up; MVA, mitral valve area; T½, pressure half-time; 2D, two-dimensional valve area. *Inoue balloon technique. †Double-balloon technique.

in abrupt hemodynamic collapse. Prompt recognition of this complication is essential. The role of echocardiography in the early diagnosis of this devastating complication is the most commanding reason for availability of echocardiographic equipment during the procedure. Echocardiography can

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identify the presence of cardiac tamponade caused by the perforation and guide the pericardiocentesis required to stabilize the patient. Although the incidence of left ventricular perforation has been reduced with the Inoue technique, the risk of perforation of the atria is common to both procedures. This risk is due to the need for trans-septal catheterization to position the balloons across the mitral orifice. Perforation of the atria, however, usually has less devastating consequences and can frequently be treated with pericardiocentesis or careful observation.

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Long-term Outcome The reported follow-up of patients who have undergone mitral balloon commissurotomy for mitral stenosis have ranged from 6 to 69 months.[40] [41] [57] [64] [65] [66] [67] [68] [69] [70] [71] , Early improvement in functional status occurs in approximately 90% of patients with the majority being in New York Heart Association functional class I or II. Sustained clinical improvement in functional status has been shown to be predicted by baseline characteristics.[64] [65] [67] [68] [69] [70] [71] [72] Patients with noncalcified valves by echocardiography and an excellent result from the mitral balloon commissurotomy (mitral valve area > 2.0 cm2 , < 2 + mitral regurgitation) have an event-free survival rate of 79% at 5 years.[67] Noninvasive testing with Doppler echocardiography eliminates the need for repeat cardiac catheterization in the hemodynamic evaluation of these patients during long-term follow-up. In the limited reported studies, the mitral valve area by Doppler echocardiography has shown a small decrease in valve area but remains significantly greater than that measured before the procedure (Table 20-6) . Restenosis (loss of 50% of the initial increase and a valve area of < 1.5 cm2 ) occurs in 6% to 21% at a mean follow-up of 19 to 22 months depending on the type of valve anatomy.[64] [66] Clinical and echocardiographic variables that have been shown to predict a poor long-term result are shown in Table 20-7 . The strongest predictor of the long-term 448

TABLE 20-7 -- Baseline Variables Associated with Poor Long-term Results Following Mitral Balloon Commissurotomy Clinical

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Advanced Age Higher NYHA Previous commissurotomy Hemodynamics Lower initial valve area Presence of MR Poor valve morphology or calcification Severe tricuspid regurgitation Higher pulmonary artery pressure Immediate Hemodynamic Results

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64, 67, 69 43, 67, 69 43, 63 63 43, 64, 68 43, 64, 65, 66, 67, 69, 70, 71 43 67 67, 69

Poor initial result (MVA ≤ 1.5 cm2 ) 43, 63, 65, 67, 70 Severe MR (> 2T) 63, 70, 71 Procedural EBDA 67, 68 EBDA, effective balloon dilating area; MR, mitral regurgitation; NYHA, New York Heart Association functional class. results, as with the immediate results of mitral balloon commissurotomy, is the degree of valve deformity. Patients with severe calcification of the mitral valve have both a poorer immediate result and long-term outcome than patients with more favorable valve anatomy. Other predictors of an adverse outcome include a lower initial valve area, the presence of mitral regurgitation or severe tricuspid regurgitation, and a higher pulmonary artery pressure. Increases in mitral regurgitation, which are common following mitral balloon commissurotomy, are generally well tolerated during follow-up. Although patients who develop severe mitral regurgitation usually require valve replacement during short-term follow-up, the changes in the mild to moderate mitral regurgitation are variable. The degree of mitral regurgitation by color Doppler echocardiography in reported series remains unchanged in 46% to 60%, decreases in 30%, and increases in 20% to 10% of patients.[64] [66] Multivariate analyses, however, have shown that the

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presence of mitral regurgitation both before and after mitral balloon commissurotomy is associated with a lower event-free survival.[65] [68] Thus, patients with either pre-existing or new mitral regurgitation should be followed closely after mitral balloon commissurotomy with clinical and echocardiographic evaluation for the development of symptoms or changes in valve function. The long-term effects of atrial septal defects is yet undetermined. Small defects close in about two thirds of patients during follow-up, and small defects that persist are generally well tolerated. Factors that are associated with the persistence of an atrial septal defect are a pulmonary-to-systemic shunt ratio of greater than 1.5, elevated right and left atrial pressures, smaller mitral valve area following mitral balloon commissurotomy, and evidence of restenosis.[66] These findings are not unexpected because elevation of left atrial pressures either caused by a poor initial result or restenosis would favor shunting through the atrial septal defect and perhaps prevent healing of the atrial septum. The long-term effects of the right ventricular volume overload is unknown. If the patient requires mitral valve surgery during follow-up, the atrial septum should be carefully examined and any defect surgically closed. Difficult management problems, however, occur in patients who have a successful mitral valve dilation but in whom a significant atrial septal defect results. Unfortunately, the hemodynamic burden of mitral stenosis in these patients is exchanged for an iatrogenic Lutembacher's syndrome. Importantly, these patients should be closely evaluated by Doppler echocardiography during follow-up to evaluate the atrial septal defect and evidence of developing right ventricular volume overload or restenosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Limitations and Alternate Approaches The technique of mitral balloon commissurotomy has proved that sustained clinical and hemodynamic improvement occurs in most patients treated for symptomatic mitral stenosis. The immediate results are equal to those obtained with surgical commissurotomy. The technique is not, however, without its limitations. Suboptimal results and complications occur in a number of patients regardless of whether the double-balloon or Inoue technique is used. Doppler echocardiography has been invaluable in the evaluation of patients and the technique as mitral balloon commissurotomy has evolved. Patients with mitral stenosis who require intervention can be identified and the results predicted by careful Doppler echocardiographic evaluation. Before intervention, patients with mitral stenosis can be evaluated reliably by the pressure gradient, valve area, severity of valvular regurgitation, and indirect evidence such as chamber size and intracardiac pressures. Thus, the majority of patients with isolated mitral stenosis do not require more invasive testing with cardiac catheterization. In older patients, in whom the presence of coronary artery disease is a consideration, coronary angiography should be performed. Furthermore, cardiac catheterization, either as the initial evaluation or in patients in whom restenosis is suspected, should be reserved for those patients in whom there is a discrepancy between the physical or clinical signs and the Doppler echocardiographic examination. The choice of mitral balloon commissurotomy or surgical commissurotomy in patients identified who require intervention depends on a number of factors. Presently, mitral balloon commissurotomy should be considered the procedure of choice in patients with isolated mitral stenosis with favorable mitral valve anatomy because it is cost-effective and safe. In other patients, mitral balloon commissurotomy may be required if the patient refuses surgery or the medical condition makes surgery high risk. In

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patients with less favorable valve anatomy, the decision for mitral balloon commissurotomy or surgical commissurotomy must be made based on the consideration of risks and benefit of each procedure. Mitral balloon commissurotomy, however, should only be considered a palliative procedure, which may delay the time in which surgical 449

intervention may be required for mitral valve replacement.

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Future Directions Although the immediate and current follow-up of patients undergoing mitral balloon commissurotomy is favorable and comparable to surgical commissurotomy, several issues remain. Potential long-term questions remain unresolved. For example, does the presence of persistent small atrial defects significantly alter the clinical course of patients? In order to answer this question and others, continued follow-up of patients who have undergone mitral balloon commissurotomy is required. Further refinements in the technique and in the development of balloon catheters also may be expected; however, whether these changes will result in significant improvement in the expected outcome depends on careful patient selection. The development of intracardiac echocardiography also may be of benefit in the guidance of the procedure.[73] Regardless of these considerations, mitral balloon commissurotomy has become a proven technique and will continue to play a major role in the treatment of patients with symptomatic mitral stenosis.

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451

Chapter 21 - Clinical Decision Making in Endocarditis Nelson B. Schiller MD

Infection of the endocardium walls or lining layer of the heart—whether on valve leaflets or chordae, congenital defects, chamber walls, paraprosthetic tissue, or the attachment of implanted shunts or conduits—is known as infective endocarditis. The major milestones in our understanding of infective endocarditis include availability of diagnostic blood culture techniques in the first decades of the 20th century; reversal of its invariably fatal course with antibiotics; palliation of potentially fatal valvular complications with surgery; and, most recently, immediate and accurate diagnosis of its anatomic and hemodynamic manifestations with echocardiography. Although no technique in isolation can always establish this diagnosis, echocardiography has a very high sensitivity for detection of valvular vegetations and complications of infective endocarditis. Thus, echocardiography is the only imaging modality that has a significant role in the clinical diagnosis and treatment of infective endocarditis. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the clinical application of echocardiography (Table 21-1) indicate that echocardiography is an essential technique in the diagnosis and treatment of endocarditis and is mandatory in nearly all patients with this disease. [1] This chapter discusses the use of echocardiography in infective endocarditis

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with emphasis on both clinical applications and utility in research studies. The weaknesses and pitfalls of the technique are discussed, particularly how these factors might cause the performance of echocardiography in practice to fall short of published data.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Basic Principles Underlying a discussion of the use of echocardiography in patients with suspected infective endocarditis must be an attempt to come to terms with a clinical definition of the diagnostic criteria of the syndrome. First, should the diagnostic criteria include echocardiography? The studies that initially evaluated the role of echocardiography in the diagnosis of infective endocarditis could not, of course, use an echocardiographic definition of this disease. Instead, TABLE 21-1 -- ACC/AHA Guidelines for Use of Echocardiography in Patients with Infective Endocarditis CLASS I (Evidence or general agreement that echocardiography is definitely indicated) Detection and characterization of valvular lesions, their hemodynamic severity, and/or ventricular compensation * Detection of vegetations and characterizations of lesions in patients with congenital heart disease suspected of having infective endocarditis Detection of associated abnormalities (e.g., abscesses, shunts) * Re-evaluation studies in complex endocarditis (e.g., virulent organism, severe hemodynamic lesion, aortic valve involvement, persistent fever or bacteremia, clinical change, or symptomatic deterioration) Evaluation of patients with high clinical suspicion of culture-negative endocarditis * CLASS IIA (Conflicting data, but the weight of evidence/opinion is in favor of the usefulness of echocardiography) Evaluation of bacteremia without a known source * Risk stratification in established endocarditis * CLASS IIB (Conflicting data, but efficacy is less well established) Routine re-evaluation in uncomplicated endocarditis during antibiotic

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therapy CLASS III (Not indicated) Evaluation of fever and nonpathologic murmur without evidence of bacteremia Modified from Cheitlin MD, Alpert JS, Armstrong WF, et al: J Am Coll Cardiol 1997;29:862–879. *Transesophageal echocardiography (TEE) may provide incremental value in addition to information obtained by transthoracic echocardiography. The role of TEE in firstline examination awaits further study.

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TABLE 21-2 -- Clinical Definition of Infective Endocarditis Definite Direct evidence based on histology from surgery or autopsy or bacteriology by Gram stain or culture of valvular vegetation or arterial embolus Probable A. Persistently positive blood cultures plus one of the following: 1. New regurgitant murmur or 2. Predisposing heart disease and vascular/immunologic phenomena (e.g., splinter hemorrhages, Osler's nodes, glomerulonephritis) B. Negative or intermittently positive blood cultures (<2 of 2 or 3 of 3 or 70% positive if more than four obtained) plus all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena Possible A. Persistently positive blood cultures plus one of the following: 1. Predisposing heart disease or

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2. Vascular phenomena B. Negative or intermittently positive blood cultures with all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena C. For Streptococcus viridans cases only: At least two positive cultures without an extracardiac source and fever Rejected A. Infective endocarditis unlikely and alternative diagnosis apparent B. Infective endocarditis possibility warrants antibiotic therapy C. Culture-negative infective endocarditis diagnosed but excluded by autopsy Modified from Von Reyn CF, Levy BS, Arbeit RD, et al: Ann Intern Med 1981;94(part 1):505–518. most studies adopted or modified the criteria of Von Reyn et al[2] (Table 212) . These somewhat complex criteria have been useful in developing the literature that has established echocardiography as a required part of the clinical work-up, but they now have been replaced by criteria incorporating echocardiographic findings. New criteria ( Table 21-3 and Table 21-4 ) that incorporate echocardiographic findings in the diagnostic criteria for endocarditis have been developed by the Duke Endocarditis Service and have been prospectively tested at several centers.[3] [4] [5] [6] [7] [8] [9] [10] [11] In the initial Duke study, each of 405 retrospectively reviewed suspected cases was classified as definite/probable, possible, or rejected using both the old (nonechocardiographic) and new (echocardiographic) criteria. Only 51% of the pathologically definite cases were detected using the older Von Reyn criteria compared with 80% using the newer Duke criteria. Confirming these findings, in a small prospective study of 63 patients admitted to a nonreferral hospital with a diagnosis of suspected endocarditis,[4] [5] the detection rate for pathologically confirmed cases increased from 50% to 100% when echocardiographic data were used for diagnosis. In this study, all patients had both transthoracic

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echocardiography (TTE) and transesophageal echocardiography (TEE). In the 17 cases with echocardiographic evidence of a vegetation, TABLE 21-3 -- Definitions of Terminology in Duke Criteria for Endocarditis Major Criteria I. Positive blood culture for infective endocarditis Typical microorganism for infective endocarditis from two separate blood cultures (Streptococcus viridans, Streptococcus bovis, HACEK group, community-acquired Staphylococcus aureus or enterococci) in the absence of a primary focus or Persistently positive blood cultures of an infective endocarditis consistent organism recovered from a. Cultures drawn at least 12 hours apart or b. The majority of four cultures spanning more than an hour II. Evidence of endocardial involvement Echocardiogram positive for infective endocarditis by 1. Oscillating mass on valve or apparatus or in jet pathway or on implanted material in absence of alternative explanation or 2. Abscess or 3. New prosthetic dehiscence or III. New valve regurgitation (increase or change in pre-existing murmur not sufficient) Minor Criteria I. Predisposition: predisposing heart condition or intravenous drug history II. Fever ≥ 38°C III. Vascular phenomena: major arterial emboli, septic pulmonary embolism/infarction, mycotic aneurysm (with and without hemorrhage), conjunctival hemorrhage, and Janeway lesions IV. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor V. Microbiologic evidence: positive blood culture but not meeting major criteria (excludes coagulase-negative staphylococci and organisms not causing infective endocarditis) or serologic evidence of infective

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endocarditis organism VI. Echocardiogram consistent with but not meeting major criteria for endocarditis Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. the process was detected only by TEE in 7 cases (41%) (Table 21-5) . In the past 5 years, the Duke criteria have received extensive confirmation. [6] [7] [8] [9] [10] [11] Some studies have suggested ways of improving the criteria while confirming that they TABLE 21-4 -- Duke Criteria for Endocarditis Using Definitions in Table 21-3 I. Definite infective endocarditis Pathologic criteria Microorganisms: demonstrated by culture or histology in a vegetation (in situ or embolized) or in an intracardiac abscess Pathologic lesions: vegetation or intracardiac abscess confirmed active by histology Clinical criteria using definitions in Table 21-3 2 major criteria or 1 major and three minor or 5 minor II. Possible infective endocarditis Findings consistent with but falling short of I Definite but not III Rejected III. Rejected Firm alternative diagnosis for manifestations Resolution of manifestations with 4 days or less of antibiotics No surgical or pathologic evidence with 4 days or less of antibiotics Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209.

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TABLE 21-5 -- Clinical versus Echocardiographic-Based Criteria: Results of Two Trials Retrospective Duke Trial * Clinical criteria identified 51% of pathologically definite infective endocarditis Echocardiographic/clinical criteria identified 80% Prospective Harbor/UCLA Trial † Clinical criteria identified 50% Echocardiographic/clinical criteria identified 100% (41% by TEE only) *Data from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. †Data from Bayer AS, Ward JI, Gintzon LE, Shapiro SM: Am J Med 1994;96:211– 219; Bayer AS: Clin Infect Dis 1996;23:303–304.

are the preferred systematic diagnostic approach. One suggestion is to eliminate minor criterion status for a nondiagnostic echocardiogram[12] based on the widespread use of TEE. Another suggestion is to consider a positive Staphylococcus aureus blood culture or Q fever seropositivity as major criteria. However, regardless of possible modifications of the Duke criteria, these studies provide compelling evidence for the inclusion of echocardiography as an integral element in the diagnosis of infective endocarditis. The remainder of this chapter concentrates on the details of the echocardiographic approach to the patient with infective endocarditis by discussing the strengths and weaknesses of each component of the echocardiographic examination as it relates to the detection and analysis of vegetations and complications and the estimation of prognosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Vegetations The first goal of the echocardiographic examination is identification, characterization, and localization of valvular vegetations. For many reasons, the process is one of integrating circumstantial findings and epiphenomena, and, through indirect (albeit compelling) evidence, reaching a reasonable conclusion that a given echocardiographic set of observations has identified the pathologic hallmark of endocarditis, the vegetation. Once a vegetation has been identified, criteria can be applied to judge clinical prognosis. This diagnostic process first depends on a solid knowledge of the normal appearance of cardiac structures seen in a variety of technically mediated circumstances. These circumstances include the choice of transducer frequency, variations among commercial ultrasound instruments, the unique technical characteristics of each patient, the settings of the instrument, variations in technique among technicians, and the duration and intensity of the examination as influenced by the level of pretest and intratest index of suspicion regarding the likelihood of disease (Table 21-6) . Qualitative and Technical Factors Transducer Frequency

Lower frequency transducers (i.e., nominal center line frequency of approximately 2.5 MHz) are the type most commonly employed in adult patients because they combine superior penetration with optimal color flow and spectral Doppler sensitivity. Although the images obtained at lower frequencies are easier to acquire, they are lower in resolution than those obtained at higher frequencies, particularly in the middle and far fields of the image where beam spread causes image degradation. From the precordial window, the mitral valve lies in the middle field, and from the apical window, it lies in the far field. At these distances, a normal valve examined with low frequency insonation tends to take on an irregular or

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lumpy appearance. If present, small vegetations tend to be obscured and normal irregularities magnified. For these reasons, sequential use of both a lower frequency and higher frequency transducer is recommended for routine examinations in order to develop familiarity with the normal appearance of cardiac structures generated under both circumstances and to promote recognition of genuine pathologic changes. Harmonic imaging has become widely available and will soon become the standard modality for most examinations. In this technique, insonation is accomplished by transmission at a standard frequency, but with detection of the reflected signal at its harmonic frequency (one-half the transmitted value). For example, if 3.5 MHz is used for transmission, the received signal is analyzed at 1.75 MHz. The technique provides greater sensitivity for the low-level signals arising from the endocardium, allowing better evaluation of regional ventricular wall motion. Tradeoffs for this beneficial increase in contrast resolution include accentuation of normal leaflet irregularities and homogenation of valve texture; both tend to reduce specificity for identifying a mass as vegetation. The chordal attachment points are particularly likely to take the appearance of small lumps. At the time of this writing, the technique is not available with TEE because it has not been possible to adapt it to the higher frequencies at which TEE examinations are conducted. It is, therefore, not uncommon to perform a TEE examination at 7 MHz in a patient with a "lumpy" mitral valve on transthoracic harmonic imaging but find that the valve is absolutely normal in appearance on TEE. Commercial Instruments and Instrument Setting Variation

Dynamic range options, pre- and postprocessing algorithms among instruments, and changes in these settings within instruments alter the appearance of valves. Depth settings, probe frequency, deployment of electronic focusing, and sector width have differing influences on the frame rate at which the image is displayed. At greater TABLE 21-6 -- Technical Factors Affecting Detection of Valvular Vegetations Transducer frequency (particularly low-frequency imaging) Instrument characteristics and settings (especially harmonic imaging) Patient characteristics Pretest expectations and probability

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depth settings (e.g., 20 cm), slower frame rates, especially in the far field, may obscure the characteristic rapid vibrations of many vegetations. Some devices offer "B color" tagging of tissue images. This method expands the dynamic range of the display and may influence the appearance of valve pathology. The highly reflective nature of calcific degeneration may be easier to differentiate from the tissue or thrombus-like appearance of vegetations when using this type of image postprocessing. Patient Physical Characteristics

Obesity, hyperinflated lungs, narrow interspaces, valvular and annular calcification, and valve prostheses impede the transmission of ultrasound between the transducer and the heart. A tall patient may have greater distance from the apical impulse location to the mitral valve. All of these factors can obscure a vegetation that might have been seen under other circumstances. TEE is less sensitive to these constraints and nearly always provides an excellent examination. The difference between TTE and TEE must be considered when analyzing the endocarditis literature or when choosing the ideal imaging modality for a given patient. Pretest Expectations

The physician or sonographer begins each examination with some notion about what is being sought in each patient. If there is strong suspicion of endocarditis, it is only natural to scrutinize the valves with augmented intensity using a complete array of probes and processing algorithms. Under such circumstances, maximal "performance" of the technique may be approached. However, as sensitivity rises, specificity must fall pari passu. Under the magnification of increased surveillance, small, normally unseen irregularities, anatomic variants, and artifacts may be mistaken for vegetations. When only transthoracic imaging was available, considerable time and care was taken to visualize the valve structures in patients with suspected endocarditis with reported sensitivities for detection of valvular vegetations much higher than in subsequent studies comparing TEE with TTE. The lower sensitivities in these studies may possibly be due to a shifting of attention to the TEE arm of the study. Nonetheless, these lower sensitivities are probably more representative of what may be expected in daily clinical practice.

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M-mode Echocardiography M-mode echocardiography was the first ultrasound imaging modality widely applied in endocarditis. With M-mode imaging, the smallest size of vegetation that can be detected is estimated to be about 5 mm.[13] Although the role of M-mode imaging is less important when two-dimensional imaging is used, the M-mode approach remains useful in specific situations. M-mode echocardiography offers high sampling rates and fine resolution when compared with two-dimensional imaging (>1000 Hz vs. two-dimensional echocardiography at 30 to 60 Hz). M-mode imaging not only allows recognition of vegetations that prolapse (by location) but also can detect their characteristic tissue level images and typical vibrations. These vibrations occur as the prolapsing mass, composed of platelets, thrombus, bacteria, inflammatory cells, and disrupted valve tissue, is caught in the regurgitant jet. Although it is normal for the aortic valve to vibrate slightly during systole, diastolic vibrations almost certainly indicate that the mass is a vegetation, a torn leaflet, or both (Fig. 21-1A) (Figure Not Available) . Similarly, systolic vibrations of the mitral leaflet are highly suggestive of a vegetation, ruptured valve, or both (see Fig. 21-1B) (Figure Not Available) . In seeking to confirm a mass as a vegetation, it is useful to employ these specific but insensitive signs,[14] but when doing so, to remember that in modern ultrasound equipment their sensitivity has been diluted by lowered resolution and the limited frame rate of the video display in comparison with a single crystal probe combined with a strip chart recorder. Two-Dimensional Echocardiographic Imaging of Vegetations In a meta-analysis of 16 early studies (641 patients) O'Brien and Geiser[15] reported a mean sensitivity of 79% for two-dimensional echocardiography in the detection of vegetations in infective endocarditis. M-mode imaging sensitivity from the same series was only 52%. In one of the first reports of two-dimensional echocardiography in definite (autopsy/surgery) cases of infective endocarditis, Gilbert et al[14] noted good agreement between the location and identity of large vegetations and pathologic findings but encountered difficulties when comparing exact ultrasound measurements to pathologic reality. More importantly, this study found that "several" small vegetations of less than 3 mm in maximum dimension were undetectable by two-dimensional echocardiography. This lower size limit on vegetation detection continues to be a current problem in the use of TTE. In the decade since the Gilbert et al study, the sensitivity

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of TTE has dropped despite major improvements in ultrasound equipment (Table 21-7) . For example, on review of 7 studies performed between 1989 and 1994[16] [17] [18] [19] [20] [21] [22] [31] the mean sensitivity for TTE was 62%, whereas for TEE it was 92%. As stated, the reason for the decrease in TTE sensitivity is probably a combination of more rigorous and less biased case selection in the contemporary studies and less intense scrutiny of the patient with TTE than with TEE. TABLE 21-7 -- Two-Dimensional Echocardiography versus M-mode Echocardiography versus TEE: Sensitivity for Detecting Vegetations Meta-Analysis of 16 Early Studies M-mode, 52% Two-dimensional echocardiography, 79% Meta-Analysis of 7 More Recent Studies Two-dimensional echocardiography, 62% Transesophageal echocardiography, 92%

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Figure 21-1 (Figure Not Available) A, M-mode image of a disrupted aortic valve showing coarse systolic vibrations (arrowheads) specific for vegetation, disruption, or both. Very fine systolic vibrations are normally seen and can be barely discerned. B, M-mode image of an infected mitral valve showing increased thickness and systolic vibrations specific for vegetation, disruption, or both.

The accuracy of the measurement of structures in echocardiographic images is limited by resolution. Because TTE underestimates the size and complexity of large vegetations and fails altogether to detect small vegetations (<3 mm in diameter), it is reasonable to conclude that if knowledge of the size and behavior of vegetations is predictive of prognosis and useful in guiding therapy, TTE underachieves as a prognostic and therapeutic guide. Furthermore, in a review of the literature of infective endocarditis, none of the studies stated the carrier frequency of the transthoracic transducer. From this omission, it may be inferred that there is considerable variation in performance of TTE within and among studies, weakening the use of size criteria in clinical practice. In a comprehensive published study of the prognostic value of the

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morphologic details of TTE images of vegetations, Sanfilippo et al[23] retrospectively studied 204 patients who met clinical criteria of infective endocarditis. Documented clinical events were correlated with echocardiographic vegetation characteristics. The events or complications were as follows: 1. Failure of febrile illness to respond to an appropriate course of antibiotics so that a change in treatment was required 2. Congestive heart failure on or after admission 3. Pulmonary, systemic, or peripheral embolization 4. Surgery 5. Death Valvular vegetations were defined as "a discrete mass of echogenic material adherent at some point to a leaflet surface and distinct in character from the remainder of the leaflet." Separate classifications were made for nonspecific thickening ("diffuse irregularities"), aortic valve disease, mitral valve disease, mitral prolapse, prosthetic valve, and no evidence of vegetations. If a mass was identified as a vegetation (Table 21-8) , it was analyzed according to four properties: Size: Two largest orthogonal diameters perpendicular and orthogonal to the leaflet (Fig. 21-2) (Figure Not Available) Mobility: Grade 1, fixed; grade 2, fixed base, free edge; grade 3, pedunculation; grade 4, prolapsing (Fig. 21-3) (Figure Not Available) Density: Grade 1, calcified; grade 2, partially calcified; grade 3, more dense than myocardium but not calcified; grade 4, equivalent to myocardium Extent: Grade 1, single; grade 2, multiple on a single leaflet; grade 3, multiple leaflets; grade 4, extending to extra valvular structures The overall incidence of complications was 55%, with equivalent rates for native and prosthetic valves and for clinical endocarditis in nonspecifically thickened valves. Unexpectedly TABLE 21-8 -- Five Characteristics Allowing a Valve Mass to Be Designated a Vegetation Texture

Gray scale and reflectance of myocardium

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Location Characteristic motion Shape Accompanying abnormalities

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Upstream side of valve in path of jet Chaotic and orbiting Lobulated and amorphous Abscess and pseudoaneurysm Fistulas Prosthetic dehiscence Paravalvular leak: significant pre-existing or new regurgitation

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Figure 21-2 (Figure Not Available) Vegetation size is measured in two axes or diameters. D1 is the maximum size of the vegetation perpendicular to the leaflet; D2 is the maximum extent of the vegetation parallel to the leaflet surface. The larger of the two dimensions was used for analysis. Ao, aorta; LA, left atrium; LV, left ventricle. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191– 1199. Reprinted with permission from the American College of Cardiology.)

high rates of complications were found for tricuspid endocarditis (77%) and studies with no abnormality (27%). There tended to be more complications with higher grades of mobility and lesion extent. Vegetation consistency did not predict complications except that those with calcified vegetations had no clinical complications (Fig. 21-4) (Figure Not Available) . Size was perhaps the most powerful predictor of complications. The probability of sustaining a complication was 10% in 6-mm vegetations, 50% in 11-mm vegetations, and almost 100% at 16-mm vegetations in maximum dimension (Fig. 21-5) (Figure Not Available) . Sanfilippo et al also proposed a "score" for risk, calculated as the sum of the scores for size, mobility, and extent (each grades 1 to 4). The highest possible score Figure 21-3 (Figure Not Available) A vegetation mobility grading scheme is illustrated (see text). (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) Figure 21-4 (Figure Not Available) Complication rates by the extent of a graded vegetation abnormality: mobility, extent, and consistency. The numerator above each

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subgroup refers to the number of patients with a given complication, and the denominator refers to the total number in that subgroup. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

for any valve is 12. As Figure 21-6 (Figure Not Available) (mitral) and Figure 21-7 (Figure Not Available) (aortic) show, a high score is always present in patients with complications (i.e., high sensitivity), but only half or less of those with high scores actually develop complications (i.e., low specificity). There is a trend for aortic valve endocarditis to have a higher complication rate, but the statistical significance is not clear from this study. These figures are reproduced here because they may prove useful in clinical decision making; however, their "exportability" to TEE findings is uncertain. Because a given vegetation on TEE is likely to appear larger, a higher score may be required for a given level of risk when using the newer modality. Seeking to improve on this study, De Castro et al[24] examined 57 patients with large (>10 mm) vegetations and no previous embolic events at the time of the study using both TTE and multiplane TEE. In the course of the Figure 21-5 (Figure Not Available) Complications relative to vegetation size. Note that this graph is not limited to any one complication such as peripheral embolization but plots all complications relative to size. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

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Figure 21-6 (Figure Not Available) Mitral valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

study, 44% sustained clinically apparent embolic events. Although this study confirmed that large vegetations define a high-risk population, within this group, no single characteristic of vegetation location, mobility, or appearance predicted embolization. Millaire et al[25] used advanced imaging techniques (e.g., magnetic resonance imaging, computed tomography, and other modalities) in 102 patients meeting the Duke criteria for infective endocarditis. Combining the

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results of imaging with a 21-month follow-up, the investigators found that 51% had imaging evidence of embolization and that many were clinically inapparent. There was a trend toward higher mortality in those with emboli (20% versus 12%), but the trend did not reach statistical significance. From these data it was concluded that demonstrable embolization is far more common than previously thought; therefore, a study seeking to predict events by vegetation characteristics needs to use advanced imaging as a reference standard. There is no evidence that such a study has been performed, and the question of the capability of echocardiography to predict outcome remains unsettled. Transesophageal Echocardiography When two-dimensional imaging supplanted M-mode echocardiography as the imaging mode of choice, some published cases still suggested suboptimal sensitivity even with two-dimensional echocardiography.[26] These suspicions were shown to be well founded when TEE was applied to the study of patients with suspected endocarditis.[27] It was not until almost a decade later, however, when a number of studies addressed the marked differences in sensitivity between TTE and TEE[19] ( Fig. 21-8 , Fig. 21-9 , Fig. 21-10 ). The role of TEE in endocarditis is a direct result of its high sensitivity in detecting the defining manifestation of Figure 21-7 (Figure Not Available) Aortic valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

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Figure 21-8 Discrepancy between TTE and TEE. Left, Apical fourchamber view showing only subtle changes in the posterior leaflet of the mitral valve (arrow). Right, TEE shows a flail, thickened valve with evidence of a vegetation at the tip of the posterior leaflet (pML). The anterior leaflet (aML) has normal thickness and is normally positioned. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Figure 21-9 Four small vegetations (small arrows) arrayed along the

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anterior mitral leaflet. By transthoracic echocardiography, only one of these (large arrow) was suspected.

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Figure 21-10 A, Four-chamber TEE view taken in the transverse plane. Small solitary vegetation (Veg, arrow) is seen at the coaptation of the anterior and posterior mitral leaflets (aML, pML) but was not apparent on transthoracic echocardiography. Note the gray texture of the mass, which closely resembles myocardium. This appearance is typical of a vegetation. Ao, aorta. B, Larger vegetation detected by TTE but found to be 3 mm larger by TEE. C, Transverse plane view of the base of the heart from TEE. The left atrial (la) appendage (laa) is occupied by an irregular mass whose shape, location, and motion are typical of thrombus (thr). Note that the gray texture of the mass is indistinguishable from that of vegetation. Thus, vegetations and thrombi are identified by circumstantial rather than direct evidence.

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TABLE 21-9 -- Reported Sensitivity and Specificity of TEE for Native Valve Endocarditis TTE (%)

TEE (%)

Sample Size (n) SENSITIVITY/SPECIFICITY SENSITIVITY/SPECIFICITY Shively et al 66 44/98 94/100 [19] (1991) Pedersen et 24 50/— 100/— [31] al (1991) 61 Birmingham et al (1992) [28]

Aortic Mitral Sochowski and Chan

25/— 50/— 105 —/—

88/— 100/— 91/—

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(1993)[21] 64 60/91 87/91 Shapiro et al [30] (1994) TOTAL 256 46/95 93/96 TTE, transthoracic echocardiography; TEE, transesophageal echocardiography. the disease, valve vegetations. The comparison of the sensitivity of TTE to that of TEE is an important issue because if the two methods are similar in this regard, the less invasive and less expensive modality will be used. Five studies that address the differences in sensitivity between TTE and TEE in detecting vegetations[19] [28] [29] [30] are presented in Table 21-9 . Generally, patients reported in these studies are considered to have vegetations when a valve abnormality (mass) has the characteristics that allow it to be identified as a vegetation with a "high degree of certainty."[23] These characteristics include the texture of the mass, its location, characteristic motion, shape, and accompanying abnormalities. In general, experienced readers recognize a vegetation as having a gray scale and a low level of reflectance similar to myocardium (Fig. 21-11) . Vegetations are usually positioned on the upstream side of the valve (e.g., on the atrial side of the mitral valve and on the ventricular side of the aortic valve) and concentrated at the point where a regurgitant or stenotic jet impinges on the valve or wall. The mass is usually lobulated, amorphous, and mobile. The mobility Figure 21-11 TEE image of a bulky vegetation involving the atrial surface of the mitral valve and the annulus. Note the amorphous shape and gray texture, which resembles myocardium. This patient also had moderate to severe mitral regurgitation. LA, left atrium.

may be chaotic, appear to orbit around the valve, or have fine vibrations imparted by the jet of abnormal flow. Abnormalities that accompany vegetations include periannular abscesses (solid or cystic), fistula formation, and severe regurgitation (Fig. 21-12) . In prosthetic endocarditis, paravalvular leaks, valve dehiscence, and occasional obstruction are seen (Fig. 21-13) . Vegetations also characteristically prolapse into the upstream chamber: mitral vegetations into the atrium in systole, aortic vegetations into the left ventricular outflow

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tract during diastole. As stated, they tend to flank the regurgitant jet or form on a jet target. Characteristics that identify an abnormal mass as being unlikely to be a vegetation include high reflectivity, bistable appearance (white not gray), fibrillar appearance with narrow base of attachment (Fig. 21-14) , and lack of associated regurgitation (Table 21-10) . These characteristics are used by experienced readers regardless of whether a transthoracic or transesophageal window is used. Their appearance on TEE, however, is considerably more vivid, and the resolution for very small vegetations is higher. The superior sensitivity of TEE is clearly and consistently documented by the studies listed in Table 21-9 , in which the differences between modalities were strongly significant statistically. From these findings and from the study of Lowry et al[32] it can be concluded that a transesophageal echocardiogram with a negative result makes the probability of endocarditis very low; it does not, however, eliminate the possibility, and the physician must always temper interpretations with clinical judgment. For example, it may be appropriate to repeat an initial TEE examination with a negative result after 1 to 2 weeks if the clinical suspicion and disease course continue to suggest endocarditis. As the sensitivity of a test increases, specificity is likely to decrease. Falsepositive findings in TEE arise because small, previously invisible irregularities and degenerative processes are clearly seen in magnified format. A two-center study, in which this researcher participated as an "expert" blinded reader, compared TTE with TEE in infective endocarditis. Although no false positives occurred, some minor irregularities were encountered.[19] For example, tiny mobile strands on either valve are frequently encountered. These strands probably represent a normal degenerative process and are known as Lambl's excrescences. Strands, possibly from the same source, can arise on the sewing ring of prosthetic valves. Occasionally, a suture end can be visualized and might be mistaken for a pathologic finding. Redundant chordae or false tendons in the left ventricle as well as Chiari's remnant on the TABLE 21-10 -- Characteristics of a Mass Not Likely to Be a Vegetation Texture Location Shape

Reflectance of calcium/pericardium (appears white) Outflow tract attachment, downstream surface of valve Stringy or hairlike strands with narrow

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attachment Lack of accompanying No regurgitation abnormalities

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Figure 21-12 Endocarditis of the mitral and aortic valves leading to abscess (Ab)/pseudoaneurysm, aortic and mitral vegetations (veg), severe aortic insufficiency (AI), and fistula formation (not shown) between the aorta (Ao) and left atrium (LA). A, Contiguous vegetations on both aortic and mitral leaflets. B, Thick-walled, expansile abscess of the aortic root. C (color plate.), Broad jet of aortic insufficiency filling the outflow tract. D (see color plate), Width and timing of jet seen in C documented by color M-mode echocardiography. Wide jets that occupy more than 65% of the left ventricular outflow tract are indicative of severe regurgitation. LVOT, left ventricular outflow tract; RA, right atrium.

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Figure 21-13 (color plate.) Prosthetic dehiscence due to endocarditis. Note that the ring of this mechanical prosthesis is displaced from its expected plane and separated from the posterior aortic (Ao) root (top). Bottom, Color flow documents that the site of aortic insufficiency (AI) is paraprosthetic.

right side may pose as vegetative masses. All of the masses mentioned in this paragraph have a tendency to be highly reflective in appearance with the approximate echodensity of pericardium or aortic root.

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Prosthetic Valve Endocarditis Prosthetic valve endocarditis is a special case (Table 21-11) . The materials used to construct these devices usually do not allow passage of ultrasound and, as a result, these valves shadow or obscure structures lying between the valve and the transducer. For example, it is usually impossible to image the atrial side of the mitral prosthesis or the arterial side of the aortic prosthesis from an apical TABLE 21-11 -- Prosthetic Valve Endocarditis: A Special Case Both transesophageal echocardiography and transthoracic echocardiography must be used to circumvent shadowing— Ventricular side of mitral valve: Transthoracic echocardiography Atrial side of mitral valve: Transesophageal echocardiography Two or three prostheses: Shadow one another

TABLE 21-12 -- Prosthetic Valve Endocarditis: Comparison of TEE to TTE Sensitivity

Daniel et al (1993)[33] Zabalgoitia et al (1993)[35] Bioprostheses Abscess

TEE TTE Sample Size Sensitivity Sensitivity (n) (%) (%) 33 82 36 44 4

86 100

44 25

TTE approach. TEE solves this problem in mitral prostheses and improves it in aortic prostheses. When both mitral and aortic devices are present, however, shadowing from the mitral device tends to obscure the region of

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the aortic prosthesis. Multiplanar TEE probes allow improved imaging in this situation, but some areas may remain obscured; therefore, a combination of TTE and TEE imaging may be needed for complete visualization of the valvular structures. Tricuspid and pulmonic devices pose similar problems, but they are effectively evaluated by TEE. Daniel et al[33] reported on 33 cases of prosthetic endocarditis studied with both TEE and TTE and found sensitivities of 82% and 36%, respectively. Alton et al[34] reported similar findings but with smaller numbers. In a study of TEE in 44 patients with bioprosthetic valves who were going to surgery, Zabalgoitia et al[35] found that TTE had a sensitivity of 44%, whereas TEE had a sensitivity of 86% (Table 21-12) . In abscess identification, TEE was 100% sensitive, whereas TTE was only 25% sensitive (Fig. 21-15) . Figure 21-14 Ruptured chordae tendineae (rct) of the posterior mitral leaflet. This prolapsing mass is thin and brighter in appearance than a vegetation (similar to the aortic root and anterior leaflet). Although this condition was associated with severe mitral regurgitation, there were no other clinical features of endocarditis.

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Figure 21-15 Large posterior abscess in a bioprosthesis. A, TEE image of a thick-walled abscess with an abscess cavity or pseudoaneurysm posterior to the aortic root and protruding into the left atrium. The arrow points to the collapsed cavity during diastole. Note that the cavity is contiguous with the posterior stent of the aortic prosthesis. B, Systolic expansion of the cavity (arrow). Note the anterior shadowing of structures that lie beyond the prosthesis. C, Transthoracic echocardiography in the same patient showing little more than the sewing ring (sr) of the prosthesis and a vague outline of the aortic ring (short arrow). The large gulf in resolution between these two modalities is illustrated here. a, anterior; p, posterior.

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Prediction of Clinical Outcome Once a native valve vegetation is identified, the attending physician is obligated to estimate the risk that the process poses to the patient's recovery or survival and to decide on an appropriate therapeutic plan. Unexpectedly, the bacteriology of the responsible organism was not found to be of prognostic importance in the Sanfilippo et al[23] or Mugge et al[16] studies. Prognostic estimations and decisions, however, can be made by a careful analysis of the clinical and TEE presentation. There are interesting and provocative studies that the clinician can use in making these decisions.[16] [36] [37] [38]

Using TTE to predict embolic events, researchers at Duke[38] looked at the site, size, mobility, shape, and attachment of vegetations. They found high interobserver agreement on the presence and location of vegetations but less agreement on the size, mobility, and shape. A vegetation size of greater than 10 mm was associated with an embolic rate of greater than 50%, whereas a vegetation size of less than 10 mm was associated with an embolic rate of 42%. In contrast to the study by Sanfilippo et al,[23] these researchers found that characteristics of vegetations from TTE were not helpful in predicting complications. In applying TEE to the same question, Mugge et al[16] concurred with the lack of correlation between site, mobility, shape, and attachment of the vegetation and prediction of embolic events. Mugge et al, however, probably owing to the increased sensitivity of TEE imaging, found a stronger association between vegetation size and embolic events than did researchers of the Duke study, particularly if the vegetation was present on the mitral valve. A vegetation size of greater than 10 mm was associated with an embolic rate of 46%, whereas vegetation size less than 10 mm was associated with only a 20% risk (P < .001). These observations are not comparable to the TTE study of Sanfilippo et al,[23] in which all complications were related to vegetation characteristics: the use of

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vegetation characteristics to predict specific complications such as systemic embolism was not examined. Also, if all studies had employed TEE and surveillance imaging for subclinical embolic events, perhaps a better correlation between size and outcome would have been demonstrated. In one of the most interesting and useful studies, Rohmann et al[36] performed serial TEE in 83 patients and found that if a vegetation size increased or remained static during 4 to 8 weeks of therapy, prognosis was much worse than if vegetation size decreased with therapy. These differences were striking and included incidence of valve replacement (45% versus 2%), embolic events (45% versus 17%), abscess formation (13% versus 2%), and mortality (10% versus 0%) (all P < .05). These data suggest that it may be logical to temporize by performing serial studies in patients who have not experienced complications and who present with large vegetations that tempt early surgical intervention. They also dispel somewhat the concern that a shrinking vegetation is tantamount to embolization of a fragmenting mass. When indicated, it is appropriate to repeat the TEE after 7 days of antibiotic therapy and compare the size of the vegetations. Although this time scale is considerably shorter than the 4 464

TABLE 21-13 -- TEE Vegetations and Outcome Size Mugge et al (1989) >10 mm: 46% emboli [16]

Heinle et al (1994) [38]

>10 mm: >50% emboli

Temporal Behavior Rohmann et al (1991)[36] Serial TEE at 4–8 wk: Static or enlarged vegetation Valve replacement 45% Embolic events 45% Abscess formation 13%

<10 mm: 20% <10 mm: 40%

(P < .001) (P = ns)

Smaller vegetation 2% 17% 2%

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Death

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10%

0%

(P < .05 for all)

to 6 weeks in the Rohmann et al study, dramatic decreases in vegetation size may be seen after only 1 week of treatment. A prospective study is needed to determine the shortest time interval required between the first observation at the beginning of treatment and the second observation to reliably establish a patient as a responder or nonresponder to antibiotic therapy (Table 21-13) . It is also important to consider the implications of a TEE examination that fails to show vegetations in a patient with suspected infective endocarditis (Table 21-14) ; Shively et al[19] found a negative predictive value of 98% for a TEE study with a negative result in patients with suspected endocarditis. Sochowski and Chan,[21] however, using monoplane TEE, found 65 of 105 patients with suspected infective endocarditis with a negative finding on initial examination. Of these, 56 patients never developed definite endocarditis, but in five patients, infective endocarditis was eventually documented. In three of these five, repeat TEE demonstrated new vegetations. The most common type of patient with infective endocarditis in whom initial TEE fails to detect a vegetation is one with an aortic prosthesis. Although a false-negative TEE examination occurs in only 5% or less of patients with infective endocarditis, all negative studies impose an obligation on the physician to follow patients until a sustained afebrile status is confirmed. Under some circumstances it may be permissible to withhold antibiotics while monitoring for signs of infective endocarditis.

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Intracardiac Complications of Endocarditis In the process of bacterial infiltration and proliferation in valve tissue, the integrity of the leaflet may be destroyed. This TABLE 21-14 -- Implications of an Initial TEE with a Negative Result Shively et al (1991)[19] 98% negative predictive value Sochowski and Chan 65 of 105 suspected cases had a negative result on initial examination (1993)[21] 56 never developed infective endocarditis 5 eventually developed disease (3 showed vegetations on repeat examination) Aortic prosthetic endocarditis was most likely to be negative destruction leads to regurgitation of varying severity. Etiology makes little difference in the echocardiographic features of severe mitral regurgitation. There is a distinct feature of valves in infective endocarditis, however, that merits consideration; that is, it is very difficult to differentiate a disrupted, prolapsing, and flail segment of leaflet from a mobile prolapsing vegetation. Both have the same motion during the cardiac cycle and the same visual tissue characteristics, and both may be simultaneously present in the same location. Measuring a flail leaflet that has been mistaken for a vegetation may lead to miscalculation of risk level, or worse, an incorrect diagnosis of endocarditis. TEE substantially improves the likelihood of distinguishing leaflet from vegetation; this ability probably contributes to its advantages as a prognostic and diagnostic tool. Beyond this feature, the principles that govern the Doppler and two-dimensional evaluation of the severity of valvular regurgitation remain the same and are discussed thoroughly elsewhere in this book. When the endocardial infectious process spreads beyond the valve leaflets

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or endocardium it invades the continuous basal myocardium and tissue of the fibrous cardiac skeleton. Early in this process, the contagion produces cellulitis. If tissue necrosis and white cell activity continue, the central portion of this process undergoes pyogenesis and forms an abscess cavity ( Table 21-15 ; see also Fig. 21-12 , Fig. 21-15 , and Fig. 21-16 ). Because the abscess wall is under considerable pressure, the weakened necrotic tissue may disrupt, resulting in communication with a ventricle, atrium, or great vessel (Fig. 21-16) . In the setting of this fistulous communication the abscess cavity can also be viewed as a pseudoaneurysm,[39] particularly if it involves the aortic wall directly. Examples of fistulous communications include aorta to left atrium (associated with a new continuous murmur) and left ventricle to right atrium. If the abscess extends into the septum, the conduction system may be interrupted or slowed and a right bundle branch block with first-degree A-V block may ensue. [40] In a landmark study of the effectiveness of TEE in detecting abscesses in endocarditis, Daniel et al[20] studied 118 cases and found evidence of abscess formation in 37%. The mortality rate among those with abscess was 23% versus 14% for those without. The sensitivity and specificity of TTE imaging was 28% and 99%, respectively, whereas TEE imaging had a sensitivity and specificity of 87% and 95%, respectively, for detection of paravalvular 465

TABLE 21-15 -- TEE Myocardial Abscess Leung et al (1994) [20]

Sample Size Abscess Formation Detection by TTE Sensitivity Specificity Detection by TEE Sensitivity Specificity

Daniel et al (1991) n = 118 44 (37%)

[41]

n = 34 (all aortic) 11 (32%)

28% 99%

36% 100%

87% 95%

100% 100%

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Mortality With abscess Without abscess Staphylococcus aureus With abscess Without abscess Site of Infection Native aortic root Para-aortic prosthesis

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23% * 14% * p = NS

5/11 (45%)

52% † 16% † p <.001 14/44 (32%) 12/44 (27%)

*P = ns. †P < .001.

abscess. Karalis et al[40] found a similar disparity in sensitivity between TTE and TEE. From these data it is also evident that abscess-related lesions are relatively common in endocarditis (especially when the infecting organism is S. aureus) and patients with a demonstrable abscess on echocardiography represent a subgroup that is at high risk for death. In one study the mortality rate was as high as 45% when an abscess was detected.[41] Because of proximity to the transducer, TTE is most effective in detecting an anterior abscess at the aortic septal junction and least effective in detecting those that lie more posteriorly. Its overall adequacy is insufficient for detection of abscesses because its Figure 21-16 (color plate.) Aortic root abscess in communication with the aortic root. In this case of aortic endocarditis, there is a large vegetation on a partly destroyed aortic valve (AV) and a root abscess (Ab). Note that color flow imaging demonstrates both severe aortic regurgitation (right, large arrow) and flow into the abscess cavity (arrowheads). LA, left atrium; RVOT, right ventricular outflow tract; SVC, superior vena cava.

sensitivity is far too low and the extent of the lesion is unlikely to be fully

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Right-Sided Infective Endocarditis Vegetations of the tricuspid valve are commonly encountered in populations of intravenous drug users. Most reported series use TTE to study this group of patients. Hecht and Berger[42] collected 132 instances of right-sided infective endocarditis in 121 intravenous drug users. S. aureus was the organism in 82% (108 of 132). The tricuspid valve was the site in 127 patients, the pulmonic valve in 4 patients, and both valves in 1 patient. In 80% the vegetation was 1 cm or greater in diameter. There was a strongly significant association between vegetation size greater than 2 cm and mortality rate (33% in those with a vegetation > 2 cm vs. 1.3% in those with a vegetation < 2 cm; P > .001). San Roman et al[43] studied 48 intravenous drug users suspected of having infective endocarditis with both TEE and TTE. Both techniques were equally sensitive and specific, each identifying the same 22 vegetations. In no instance did TEE find a vegetation that was overlooked by TTE. In 63%, however, the vegetation was better characterized by TEE. From this study San Roman concluded that TEE did not confer sufficient advantage to justify its routine use in intravenous drug users with suspected right-sided endocarditis. This study met with criticism because it was mostly conducted with monoplane equipment. In my own experience, the use of multiplane TEE in these cases has increased the yield of pulmonic vegetations[44] ( Fig. 21-17 and Fig. 2118 ). Another concern is the possibility of left-sided involvement in patients with right-sided vegetations. If the duration of medical therapy would be affected by the presence of left-sided vegetations, TEE may be needed. It remains to be seen whether further experience will justify an expanded role for TEE in right-sided endocarditis. For the moment, the issue remains unsettled.

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Figure 21-17 (color plate.) Four-chamber view from TEE in a patient with a tricuspid valve vegetation. The color flow image of tricuspid regurgitation (arrow) obscures the vegetation. Note that the interatrial septum is bulging abnormally from right to left, confirming the severity of the regurgitant lesion. Figure 21-18 Transverse (left) and longitudinal (right) plane images of a pulmonic valve vegetation (Veg). The use of multiplane TEE was probably responsible for the identification of this vegetation, because it was very difficult to appreciate in the transverse plane. LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract.

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TABLE 21-16 -- Key Points in Echocardiographic Evaluations of Patients with Endocarditis 1. Echocardiography has a central role in diagnosis and management of infective endocarditis 2. All patients with infective endocarditis should undergo serial TTE 3. Most if not all patients with infective endocarditis should undergo TEE at least once 4. Technical factors are paramount 5. Experienced operators and readers are essential 6. High-frequency probes and biplanar/multiplane TEE are required

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Summary In summary (Table 21-16) , echocardiography has an unassailable place in the diagnostic evaluation and management of infective endocarditis. TTE and TEE are complementary from the point of view of comprehensively evaluating hemodynamics and anatomy. TEE is superior to surface imaging by dint of its greater sensitivity in detecting native valve vegetations, prosthetic valve vegetations, paravalvular abscesses, and other pyogenic complications. A negative finding on a TEE study makes endocarditis unlikely, and a large vegetation that fails to shrink during therapy connotes a poor prognosis. Based on these considerations and clinical experience, it is an established medical fact that all patients with infective endocarditis should undergo TTE, and it is the firm opinion of most experts that these patients should also have at least one TEE examination.

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469

Chapter 22 - Aortic Stenosis Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making David M. Shavelle MD Catherine M. Otto MD

Evaluation of Stenosis Severity The echocardiographic evaluation of the patient with valvular aortic stenosis focuses on quantitation of stenosis severity and assessment of the left ventricular response to chronic pressure overload. However, complete evaluation also includes quantitation of coexisting aortic and mitral regurgitation, estimation of pulmonary artery pressures, assessment of left ventricular diastolic function, measurement of the degree and extent of aortic root dilation, and evaluation of any other coexisting cardiac abnormalities. Evaluation for concurrent coronary artery disease may require additional diagnostic procedures. The basic clinical echocardiogram includes measurement of maximum aortic jet velocity and calculation of continuity equation aortic valve area, as detailed in the Textbook of Clinical Echocardiography. [1] Although echocardiographic measures of stenosis severity have been well validated, it still is the responsibility of each echocardiographer to be aware of the

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theoretical basis of these techniques and potential pitfalls in their clinical application. In some clinical situations, other measures of stenosis severity may be helpful in patient management. In addition, a more detailed assessment of stenosis severity may be important for understanding the natural history of this disease and for assessment of interventions to slow or reverse disease progression. Pressure Gradient versus Jet Velocity The velocity of blood flow through the narrowed aortic orifice is related to the pressure difference across the valve as described by the Bernoulli equation. For valvular aortic stenosis, the simplified Bernoulli equation, ∆P = 4v2 , which ignores the effects of acceleration and viscous losses, has proven to be remarkably accurate as compared with simultaneous invasive pressure gradient measurements. The relationship between Doppler velocity and manometric pressure measurements has been evaluated in in vitro models of a stenotic valve, in animal models of valvular and nonvalvular stenosis, and in patients with clinical disease.[2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] In these studies, simultaneous measurements show a close correlation between Doppler and 470

invasive maximum instantaneous and mean pressure gradients over a wide range of stenosis severity. In addition, the Doppler technique accurately measures changes in pressure gradient with changes in flow rate.[11] [13] [15] Of course, nonsimultaneous recordings of Doppler and manometric data correlate less well, since interval physiologic changes in transaortic volume flow rate and heart rate may result in interval changes in the transaortic gradient. Some clinicians may be confused by the use of Doppler velocity and maximum gradient measurements if the differences between maximum instantaneous, peak-to-peak, and mean systolic gradients are not appreciated. The Doppler maximum velocity corresponds to the maximum instantaneous pressure gradient across the valve (Fig. 22-1) . The "peak-topeak" gradient measured manometrically—the difference between peak left ventricular and peak aortic pressures—does not correspond to a specific Doppler measurement, since these two pressure peaks are not simultaneous and thus this "pressure difference" does not actually occur at any time point in the cardiac cycle. In a physiologic sense, the "peak-to-peak" gradient does not truly exist. Clarity in the echocardiographic report prevents any

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potential confusion on the part of the referring physician in regard to differentiating between the maximum Doppler gradient and the "peak-topeak" catheter gradient. Measurement of Doppler mean gradients is more comparable to the mean gradient measured in the catheterization laboratory because both represent the average pressure difference across the valve during the systolic ejection period. Of note, maximum and mean transaortic pressure gradients (∆P) are linearly related when measured either by Doppler or manometric techniques. The regression Figure 22-1 Relationship of pressures to Doppler velocities in normal and aortic stenosis. Note that the maximum pressure gradient (doubleheaded arrow) corresponds to the maximum Doppler velocity in both situations, but the timing of the left ventricular (LV) to aortic (Ao) pressure gradient is quite different when valve obstruction is present.

equations described for this relationship[16] [17] [18] include the following: Mean ∆P = (max ∆P/1.45) − 2.2 mm Hg and Mean ∆P = 2.4(Vmax )2 where Vmax is maximum aortic jet velocity. These two equations, derived

from separate patient populations, give similar results. It is important to recognize that these equations apply only to native aortic valve stenosis because the close correlation between maximum and mean gradient is dependent on a similar shape of the velocity curve (or pressure difference) with respect to time among the patient population. Given this linear relationship between maximum and mean pressure gradients, it becomes clear that there is little additional information content provided by gradient calculations versus simply reporting the Doppler aortic jet velocity alone. Since maximum and mean gradients are linearly related, and since maximum gradient is related to maximum velocity as stated in the simplified Bernoulli relationship, a given maximum velocity consistently corresponds to a given maximum and mean gradient. For example, a maximum jet velocity of 4 m per second corresponds to a

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maximum gradient of 64 mm Hg and a mean gradient of 38 mm Hg. Similarly, a maximum jet velocity of 5 m per second corresponds to a maximum gradient of 100 mm Hg and a mean gradient of 60 mm Hg. These close relationships between maximum jet velocity, maximum gradient, and mean gradient explain why maximum jet velocity data alone are so useful in clinical decision making in adults with valvular aortic stenosis. The technical aspects of recording aortic jet velocities in patients with valvular aortic stenosis cannot be overemphasized (Fig. 22-2) . The utility of Doppler data in patient management clearly is dependent on accurate data recording. Since the direction of the aortic jet is unpredictable and often eccentric, careful examination from multiple acoustic windows is needed for detection of the highest velocity signal. Use of a small, dedicated continuous wave Doppler transducer, careful patient positioning with an apical "cut-out" in the examination bed, and operator experience all are critical factors in obtaining accurate data. ( See Chapter 9 of the Textbook of Clinical Echocardiography for further details on data acquisition.) Even with an experienced operator and attention to technical details, there is some degree of measurement variability, as for any clinical measurement. In the absence of interval physiologic changes, the coefficient of variability for recording and measuring aortic jet velocity is 3%,[19] so that a change in jet velocity greater than 0.2 m per second and a change in mean gradient greater than 4 mm Hg are outside the range of measurement variability. Another physiologic issue that needs to be considered in the Doppler assessment of pressure gradients in patients with aortic stenosis is the phenomenon of distal pressure recovery.[20] [21] [22] [23] [24] [25] The fluid dynamics of valvular aortic stenosis [26] are characterized by a laminar highvelocity jet in the 471

Figure 22-2 One of the technical pitfalls in recording aortic jet velocities is correct recognition of the velocity signal. In this patient, three high-velocity systolic signals were obtained from an apical transducer position. The aortic stenosis jet (A) is distinguished by a shorter ejection time than either mitral (B) or tricuspid (C) regurgitation. Other factors helpful in identifying the signal include

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the accompanying diastolic flow signal and the shape of the velocity curve. When identification is problematic, use of two-dimensional and color-flow guided continuous wave Doppler echocardiography may be helpful.

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narrowed orifice with the narrowest segment of the flow stream (the vena contracta) occurring downstream from the anatomic valve orifice. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure ("pressure recovery") such that when aortic pressure in measured in the distal ascending aorta, the left ventricular to aortic pressure difference is less than if aortic pressure is measured in the vena contracta. No doubt pressure recovery accounts for some of the discrepancies between Doppler and invasive data reported in the literature. Clinically, however, the observed magnitude of pressure recovery is only 5 to 10 mm Hg, an effect that is unlikely to affect clinical decision making. The magnitude of pressure recovery is greater with a larger valve area and with a smaller aortic root. Thus, patients with severe aortic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and a small or normal aortic root dimension. In any case, the phenomenon of pressure recovery supports the use of Doppler data in evaluation of aortic stenosis patients. Since the maximum aortic jet velocity reflects the pressure difference between the left ventricle and the vena contracta, pressure recovery is a "problem" only in comparing the Doppler data with manometric data measured downstream from the vena contracta. In effect, the Doppler velocity measures the physiologic variable of most importance; it is the manometric data that must be interpreted with caution. The major potential limitation of Doppler velocity data in evaluation of patients with valvular aortic stenosis is that velocities (and pressure gradients) are volume flow rate dependent. When coexisting aortic regurgitation results in a high transaortic volume flow rate, aortic jet velocity may be high even if the degree of valve narrowing is only moderate. Conversely, when transaortic volume flow rate is reduced because of left ventricular systolic dysfunction or coexisting mitral regurgitation, jet velocity may be only moderately elevated despite severe valve narrowing. In an individual patient with aortic stenosis, aortic jet velocity varies with volume flow rate. For example, jet velocity increases with exercise as transaortic volume flow rate increases. Thus, comparisons of stenosis severity at different time points in an individual patient may be

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confounded by interval changes in transaortic volume flow rate. In each of these clinical situations, calculation of valve area, which takes the transaortic volume flow rate into account, is needed. Continuity versus Gorlin Formula Valve Areas: Assumptions and Accuracy Aortic valve areas have traditionally been calculated from invasive hemodynamic data using the formula of Gorlin and Gorlin.[27] Gorlin valve area calculations have provided accurate and important data for clinical decision making since the initial publication of the formula in 1951. More recently, however, Doppler echocardiography has allowed noninvasive calculation of valve area using the continuity equation.[19] [28] [29] [30] [31] [32] Since Gorlin valve areas have been used as the standard of reference for validation of continuity equation valve areas, it is important to review the derivation of these equations to understand the differences between these two approaches (Fig. 22-3) . Aortic valve area (AVA) is calculated using the formula of Gorlin and Gorlin as AVA = (cardiac output) / (C × SEP × ∆Pmean ) where mean ∆P is measured manometrically, SEP is systolic ejection period, and C is a constant. As for any clinical measurement, careful data acquisition is important. Accurate pressure gradient measurements depend on careful attention to frequency response, damping, and catheter positioning. The use of a double-lumen catheter or, alternatively, two separate catheters (with measurements obtained in the left ventricle and in the aorta), as opposed to measurement of the femoral artery pressure as a surrogate of the aortic pressure, provides more accurate results. Cardiac output should reflect transaortic volume flow rate. Although a Fick or thermodilution output can be used for isolated aortic stenosis, when aortic regurgitation is present, an angiographic cardiac output measurement is more appropriate. When both mitral and aortic regurgitation are present, accurate invasive determination of the transaortic volume flow rate in the clinical setting is not possible. The constant in the Gorlin formula, which has been empirically derived, attempts to account for several factors. The Gorlin constant incorporates (1) the coefficient of contraction, which reflects the difference between the

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anatomic valve area and the area of the vena contracta, (2) the coefficient of velocity, which relates to the conversion of potential to kinetic energy, (3) measurement of pressure in mm Hg, and (4) an empirical "correction" factor. Both in vitro and in vivo studies suggest that the Gorlin constant may vary with changes in volume flow rate, orifice shape, and stenosis severity.[33] [34] [35] [36] [37] Despite potential limitations of Gorlin valve areas, alternative reference standards for quantitation of aortic stenosis severity remain problematic. Unlike rheumatic mitral stenosis, in which commissural fusion results in a fixed anatomic orifice that can be measured directly at surgery, calcific aortic valve stenosis is characterized by stiff leaflets that open to a variable degree depending on the force applied by the surgeon's finger. This limits attempts at direct measurement of aortic valve area. Doppler continuity equation valve area calculations provide the advantages of noninvasive data collection and absence of an empirical constant.[3] [13] [28] [29] [31] [38] [39] , , Continuity equation aortic valve area (AVA) can be calculated using either velocity time integrals or maximum velocities (V) as follows: AVA = (VLVOT × CSALVOT ) / VAS-JET where left ventricular

outflow tract (LVOT) diameter is measured from a two-dimensional parasternal long-axis view, parallel and adjacent to the aortic valve plane, for calculation of a circular cross-sectional area (CSA); LVOT flow velocity is measured from an apical approach using pulsed Doppler ultrasonography; and the aortic stenosis jet (AS-JET) velocity is measured with continuous wave 473

Figure 22-3 Comparison of valve areas by the continuity equation (A) and the Gorlin formula (B).

Doppler echocardiography from the echocardiographic window that yields the highest velocity signal (Fig. 22-4) . Continuity equation valve area calculations assume accurate recording of the maximum aortic jet velocity, as discussed earlier for pressure gradients. However, the largest source of variability in continuity equation valve area calculations is in the measurement of the outflow tract diameter. The mean coefficient of interobserver and intraobserver measurement variability is 5% to 8%,

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resulting in a measurement variability for valve area of 0.15 cm2 for a valve area of 1.0 cm2 . In an individual patient, outflow tract diameter remains relatively constant over time, such that a change in valve area greater than 0.1 cm2 most likely represents an actual interval change. Continuity equation valve area calculations depend on accurate measurement of transaortic volume flow rate. In theory, volume flow rate could be measured at any one of several intracardiac sites (pulmonary artery, mitral annulus, left ventricular outflow tract). However, when there is coexisting aortic regurgitation (which is present to some degree in more than 80% of adults with valvular aortic stenosis), volume flow measured across other valves does not equal the volume flow rate across the aortic valve.[19] From a technical standpoint, flow measurements just proximal to the stenotic aortic valve are feasible in nearly all adult patients, whereas volume flow rate calculations at other intracardiac sites often are limited by image quality. Thus, in practice, the left ventricular outflow tract is used for measurement of transaortic volume flow rate in nearly all cases. Volume flow measurement proximal to the stenotic aortic valve assumes that (1) the cross-sectional area of flow is circular in systole and flow fills the anatomic cross-sectional area, (2) the pattern of blood flow is laminar with uniform parallel stream lines of flow, (3) cross-sectional area and flow velocity are measured at the same site, and (4) the spatial flow velocity profile is relatively "flat" during ventricular ejection; that is, flow velocities are the same in the center and at the edges of the flow stream. The assumptions of a circular cross-sectional area with flow filling the anatomic area have been corroborated by careful short-axis two-dimensional and color flow imaging in animal models and in patients with valvular obstruction.[5] Laminar flow is confirmed by recording a narrow band of velocities throughout ejection on the pulsed Doppler spectral tracing. The circular cross-sectional area of the outflow tract is calculated from a two-dimensional parasternal long-axis measurement of mid-systolic diameter, immediately adjacent and parallel to the aortic valve plane. Since the outflow tract is perpendicular to the ultrasound beam from this view, axial resolution provides a more accurate diameter measurement than the use of apical views. Flow velocity is measured from an apical approach, because Doppler measurements are most accurate when the ultrasound beam is parallel to the direction of blood flow. To ensure that the diameter and flow measurements are recorded from the same anatomic site, it is important that both measurements be made as close to the aortic valve as

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possible. On the two-dimensional image, the valve leaflet insertions provide an accurate and reproducible landmark, and on the Doppler recordings, the aortic valve closing click ensures that the sample volume is adjacent to the aortic valve. Although a region of flow acceleration occurs on the left ventricular side of the stenotic aortic valve, this area is spatially small and is easily avoided by recognition of spectral broadening on the Doppler velocity recording. In theory, the spatial flow profile in the outflow tract should be relatively flat because of the tapering of the 474

Figure 22-4 Continuity equation valve area is calculated based on a parasternal left ventricular outflow tract diameter (2.6 cm) for calculation of a circular cross-sectional area (A), placement of a sample volume immediately proximal to the aortic valve in an anteriorly angulated apical four-chamber view (B) with pulsed Doppler recording of laminar flow proximal to the aortic valve with a maximum velocity of 0.9 m per second (C). The highest velocity aortic signal (4.9 m per second) was obtained from an apical approach using continuous wave Doppler (D) in this patient. In this example, the continuity equation valve area is 1.0 cm2 . Ao, aorta; LA, left atrium; LV, left ventricle; SV, sample volume.

outflow tract and acceleration of blood during systole, both of which result in blunt flow profiles at the entrance to large vessels (Fig. 22-5) . Direct examination of the spatial flow profile in the left ventricular outflow tract proximal to the stenotic aortic valve initially was performed with conventional pulsed Doppler by carefully recording flow at sequential sites across the two-dimensional image in both apical long-axis and anteriorly angulated four-chamber views of the outflow tract.[19] [40] A more recent study, using color flow imaging to map the spatial flow profile, showed variable skewing in the spatial flow profile, most often with highest velocities along the septum, in 10 patients with aortic stenosis both before and after aortic valve replacement[41] (Fig. 22-6) . In another study, patients with predominant aortic stenosis were found to have relatively flat flow profiles, whereas normal subjects and patients with aortic regurgitation had skewed velocity profiles, with the highest velocities occurring anteroseptally[42] (Fig. 22-7) . In practical terms, even when the flow profile is somewhat skewed, if the recorded flow velocity is a reasonable approximation of the spatial and temporal flow velocity in the outflow

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tract, then a reasonably accurate volume flow rate will be calculated. It is likely that in most patients, when the Doppler sample volume is positioned near the center of the outflow tract in two orthogonal views, the recorded flow velocity approximates the spatial mean velocity across the outflow tract. Rather than examining the assumptions underlying the Doppler approach to volume flow rate calculations, a more pragmatic approach to validation of the accuracy of transaortic volume flow measurements is to compare 475

Figure 22-5 (color plate.) An apical long-axis view (in the same patient as shown in Fig. 22-4) shows relatively laminar flow in the left ventricular (LV) outflow tract proximal to the stenotic valve (arrow) with a flow disturbance in the ascending aorta (Ao) corresponding to the high-velocity jet and post-jet flow disturbance.

Doppler data with an established standard of reference. This has been difficult in clinical studies because most patients with aortic stenosis have coexisting aortic and mitral regurgitation. Although the degree of regurgitation may not be hemodynamically "significant," when regurgitation is present, neither the forward (Fick or thermodilution) nor the total (angiographic) cardiac output will accurately represent the volume flow rate across the aortic valve. In the research setting, transaortic volume flow rate can be measured directly, with an electromagnetic or transit time flow meter (Fig. 22-8 (Figure Not Available) and Fig. 22-9 (Figure Not Available) ). In both acute and chronic models of valvular aortic stenosis, Doppler transaortic volume flow rates have been shown to be accurate (Table 22-15, 15 ) with a standard error of TABLE 22-1 -- In Vivo Studies of Simultaneous Invasive and Doppler Vo Measurements from Left Ventricular Outflow Tract at Aortic Annulus in Su Aortic Stenosis and Subjects Without Aortic Stenosis Patients, Standard of Study Model N Reference Burwash Chronic 75 Transit time[15] et al valvular flow AS

Cardiac Output Strok RANGE SEE, RA r L/MIN L/MIN r m 0.86 0.9– 0.50 0.86 9 6.2

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(closedand openchest dogs) altered volume flow rate Otto et al Acute 52 Electromagnetic 0.90 0.9– 0.25 0.88 5 [38] valvular flow 3.2 AS (openchest dogs) altered volume flow rate Stewart Normal 33 Roller pump 0.98 0.5– 0.30 NA N ‡ et al (open5.0 chest dogs) altered volume flow rate Lewis et Patients 35 Thermodilution 0.91 2.1– 0.63 0.95 24 † al (no AS) 9.5 Labowitz Patients 31 Thermodilution 0.90 1.6– 0.95 NA N * et al (no AS) 8.4 AS, aortic stenosis; NA, not available; SEE, standard error of the estimate. ‡Stewart et al: J Am Coll Cardiol 1985;6:653. †Lewis et al: Circulation 1984;70:425. *Labowitz et al: Am Heart J 1985;109:327.

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Figure 22-6 Three-dimensional plot of velocity distribution in left ventricular outflow tract close to the level of aortic annulus. Velocity is plotted against position in the left ventricular outflow tract diameter and against time. There are 20msec intervals along the time axis and approximately 2 mm between each observation along the diameter axis. (From Wiseth R, Samseth S, Rossvoll O, et al: J Am Soc Echocardiogr 1993;6:279–285.)

the estimate of 2 to 4 mL for stroke volume and 0.25 to 0.5 L per minute for cardiac output over a wide range of flow rates (Fig. 22-9 (Figure Not Available) and Fig. 22-10 ). In comparing Gorlin and continuity equation valve areas, it is important to bear in mind that although they both describe stenosis severity, they measure different parameters. The Gorlin formula examines the hydraulic load and calculates an anatomic orifice area, whereas the continuity equation describes the physiologic flow area of the vena contracta.[43] [44] Thus, it is neither expected nor essential that these two measurements be identical to each other. In terms of clinical decision making, the precision, reproducibility, and ability to predict patient outcome of these measures are more important than agreement or disagreement between the two approaches. As Gorlin and Gorlin note, "We need not be frustrated when valve areas derived by two different methods are not the same. Rather, we should, like the princes of Serendip, seize upon the difference for what it reveals about the anatomy of the valve orifice as opposed to the physiology of the total obstructing valve tract under active pressure and flow conditions."[45]

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Figure 22-7 (color plate.) The two photos show the color Doppler registrations from a patient with aortic regurgitation: A, three-chamber view; B, five-chamber view. In the left ventricular outflow tract, a line, drawn along the transverse axis from the posterior to the anterior wall in the threechamber view and from the septal to the lateral wall in the five-chamber view, shows the location (x) from where velocity information (v) is obtained. The lower panels show, from top to bottom, the uncorrected and the angle-corrected velocity profile along the two transverse axes as they appear on the computer screen. Below them, the time- (and angle-) corrected spatial velocity profiles from the beginning of the color Doppler sweep are shown. A, anterior wall; AO, aorta; L, lateral wall; LA, left atrium; LV, left ventricle; P, posterior wall; RA, right atrium; RV, right ventricle; S, septal wall. (From Sjöberg BJ, Ask P, Loyd D, Wranne B, et al: J Am Soc Echocardiogr

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1994;7:276–285.)

Other Measures of Stenosis Severity Continuity equation valve areas provide an accurate, reproducible, and useful measure of stenosis severity in patients with valvular aortic stenosis when data are recorded carefully with attention to technical details of data acquisition. However, other measures of stenosis severity may be needed in individual patients if the results of clinical and diagnostic evaluation are discrepant. In these situations, it may be helpful to utilize Gorlin formula valve areas derived from invasive data, other noninvasive measures of stenosis severity, or continuity equation valve areas calculated under conditions of altered transaortic volume flow rate. Even within the physiologic range, the degree of aortic valve opening appears to depend on the interaction between the force applied to the valve leaflets (as reflected in the transaortic volume flow rate) and the stiffness and rigidity of the valve leaflets. Changes in valve area of 20% to 30% can be observed for a 50% change in volume flow rate.[46] [47] [48] [49] [50] [51] [52] This potential flow dependence is of most concern in patients with coexisting left ventricular systolic dysfunction in whom separating the effect of reduced left ventricular force from the effect of leaflet stiffness on the degree of valve opening remains difficult. This clinical dilemma has led to a search for a flow-independent measure of stenosis severity. Several alternative measures of stenosis severity have been proposed, including two-dimensional valve area on transesophageal imaging,[52] [53] left ventricular stroke work loss,[48] [54] valve resistance,[50] [55] [56] [57] changes in aortic valve area during the cardiac cycle,[58] three-dimensional valve area, [59] and scoring of valve calcium.[60] [61] On transthoracic imaging, planimetry of the aortic orifice is limited by image quality. In addition, the anatomy of the stellate stenotic orifice is complex in three dimensions (Fig. 22-11) , so that it is not always possible to obtain a planar image of the valve orifice. Similar considerations apply to the higher quality images obtained on 477

Figure 22-8 (Figure Not Available) Simultaneous volume flow and pressure data in a canine model of aortic stenosis. The electrocardiographic (ECG) recording is displayed on top, instantaneous volume flow rate in the middle, and left ventricular (LV) and aortic (Ao) pressures at the bottom. The recordings on the left demonstrate

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the hemodynamics at one flow rate. The recordings on the right display the hemodynamics at a larger volume flow rate during dobutamine infusion. Pmax , maximum instantaneous pressure gradient; Pmean , mean pressure gradient; SV, stroke volume. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.) Figure 22-9 (Figure Not Available) Typical Doppler echocardiographic recordings made in one subject at two different volume flow rates. The left ventricular outflow tract (LVOT) velocity profile and velocity time integrals (VTI) (A) and aortic stenosis (AS JET) velocity (Vmax ) and velocity time integral (VTI) (C) are displayed at one flow rate. Increases in LVOT velocity (B) and AS JET velocities (D) were observed in the same subject with a dobutamine-induced increase in volume flow rate. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.)

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Figure 22-10 Correlation of simultaneous Doppler echocardiography and ascending aortic transit time-stroke volume (SV) and cardiac output (CO) during 75 separate interventions. (From Burwash IG, Forbes AD, Sadahiro M, et al: Am J Physiol 1993;265:H1734–1743.)

transesophageal imaging. In addition, significant calcification of the valve can limit accurate delineation of the aortic valve orifice.[62] Some investigators have reported favorable correlations between planimetered stenotic orifice areas obtained on multiplane transesophageal echocardiography and continuity equation valve areas and/or Gorlin valve areas, but this approach is likely to be needed Figure 22-11 Anatomic specimen showing calcific aortic stenosis with nodular deposits of calcium within the aortic cusps and no commissural fusion.

in only a small subset of patients.[52] [53] [63] [64] Other investigators have found planimetry of the aortic orifice to be difficult and less accurate than continuity equation valve areas obtained from transthoracic imaging. [65] Multiplane transesophageal echocardiography does appear to provide more accurate determination of aortic valve morphology (bicuspid versus tricuspid valve) than biplane imaging.[66] More recently, Doppler transesophageal echocardiography has been applied using both biplane and

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multiplane imaging from the transgastric view.[67] [68] Aortic valve area as derived from Doppler transesophageal echocardiography was similar to that measured by planimetry but could not be obtained in approximately 70% of patients because of failure to align the Doppler beam adequately.[67] The amount of work expended by the left ventricle in keeping the aortic valve open in systole compared with the amount of work resulting in effective forward blood flow has appeal as a potential measure of stenosis severity. This measure may reflect the intrinsic stiffness of the valve leaflets, and thus be less dependent on volume flow rate.[48] [54] [69] With a normal aortic valve, work calculated from left ventricular or aortic pressure tracings will be nearly identical. However, when aortic stenosis is present, the difference between work calculated from left ventricular pressures versus aortic pressures should be related to the amount of work "lost" in opening the stiff leaflets. To calculate work, a power curve is generated by multiplying instantaneous flow times pressure, with total potential stroke work calculated by integrating power over the systolic ejection period[69] using either left ventricular (for total work) or aortic (for effective work) pressures. The steady component of work is defined as mean systolic pressure times stroke volume; pulsatile work is defined as total minus steady work. Stroke work loss then represents the difference between left ventricular and effective work and can be calculated for total, steady, and pulsatile components[48] as follows:

LV stroke work loss = LV work − effective work Since potential work obviously will increase with increases in flow rate, the potential work loss across the stenotic valve is indexed for volume flow rate and expressed as the percentage of left ventricular stroke work loss: Given that stroke work is calculated as the instantaneous product of pressure and flow, and stroke work loss is simply the ratio of left ventricular to aortic work, this proposed index of stenosis severity also is likely to vary with volume flow rate if the actual degree of valve opening varies. Note that when the ratio of left ventricular to aortic work is calculated, the terms for transaortic volume flow rate cancel each other, so that stroke work loss can be determined from Doppler pressure calculations alone.

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A new index of energy loss that takes body surface area into account and can be calculated from Doppler-derived data was recently evaluated in an experimental model.[70] The model used fixed stenoses and bioprosthetic valves 479

of two sizes that were evaluated at different flow rates. With use of this model, the effective orifice area was compared to the energy loss index. In a retrospective analysis of 138 patients with moderate or severe aortic stenosis, the index and valve area were compared in predicting clinical outcome, defined as death or need for valve replacement. This energy loss index was the better predictor of clinical outcome, with a positive predictive value of 67%. Valve resistance is calculated from invasive or Doppler data as follows[56] [57]

Resistance = (∆Pmean \ Qmean ) × 1333 where ∆Pmean is mean transaortic pressure gradient in mm Hg, Qmean is

mean volume flow rate in milliliters per second, 1333 is a conversion factor, and resistance is in units of dynes per second per cm-5 . Several investigators have observed a curvilinear relationship between valve resistance and valve area (with both invasive and Doppler data[56] [57] ) (Fig. 22-12) . This observation is not surprising given the mathematical derivation of the valve area and resistance concepts. In fact, the concepts of valve area and valve resistance are to some extent mutually exclusive. Valve area calculations with the Gorlin formula assume a quadratic relationship between pressure gradient and flow rate. Conversely, the valve resistance concept assumes a linear relationship between these two variables. Most clinical and experimental data support the concept of a quadratic, rather than linear, relationship between pressure gradient and flow rate across a stenotic valve[71] (Fig. 22-13) (Figure Not Available) . More complete modeling of the interaction between the left ventricle, valve, and peripheral vasculature may enhance our understanding of the hemodynamics of valvular aortic stenosis.[72] Aortic valve resistance has largely been used as a research tool and has not gained widespread acceptance into clinical practice. The reasons for

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Figure 22-12 Relationship between aortic valve resistance and aortic valve area for patients with severe aortic stenosis confirmed at surgery (group I; circles) and the 95% confidence limits of this relation (dashed curves). Values for patients with milder, noncritical stenosis (group II triangles) were plotted against this relation; in seven of eight group II patients, values were outside the confidence limits. (From Cannon JDJ, Zile MR, Crawford FAJ, Carabello BA: J Am Coll Cardiol 1992; 20:1517–1523.) Figure 22-13 (Figure Not Available) Plot of square-law dependence of pressure gradient on flow demonstrated for circular stenoses with orifices from 0.5 to 2.0 cm2 . (From Voelker W, Reul H, Heinhaus G, et al: Circulation 1995;91:1196–1204.)

this are multifactorial and include familiarity of most cardiologists with gradients and valve areas and a lack of consensus among studies in terms of the added information valve resistance provides above more traditional measures of stenosis severity.[56] [73] [74] Aortic valve area changes during the cardiac cycle, and the valve has been shown to open and close more slowly in patients with aortic stenosis than in those with normal valves.[75] The rate of change in the aortic valve area during the cardiac cycle has therefore been proposed as an additional measure of aortic stenosis severity and in predicting disease progression. [58] When the rate of change in the aortic valve area throughout the ejection phase of the cardiac cycle was expressed as a ratio (AVA ratio), patients with a large AVA ratio were found have more rapid disease progression than those with a lower AVA ratio. This new measure may prove useful in patients with valve areas of borderline significance (i.e., 1.0 cm2 ) by identifying patients with a higher probability for rapid disease progression (Fig. 22-14) (Figure Not Available) . Three-dimensional echocardiography has largely been used as a research tool to evaluate left and right ventricular chamber size and structural dimensions of the mitral valve. However, this imaging modality was used to planimeter the inner surface of the aortic valve leaflets in 23 patients undergoing aortic valve replacement.[76] Measurements were feasible in all but one patient, and valve area was comparable to that derived by the Gorlin formula. Progressive calcification of the aortic valve occurs with all causes of aortic stenosis and eventually leads to impaired leaflet mobility and valve obstruction. The degree of aortic valve calcification can be evaluated on the short-axis view with transthoracic echocardiographic imaging. In a recent

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study of 126 asymptomatic patients with severe aortic stenosis (aortic jet velocity of at least 4 m per second), the extent of aortic valve calcification was the only independent predictor of clinical outcome, defined as death or need for valve replacement (Fig. 22-15) .[61] In addition, the combination of severe valve calcification and a rapid increase in aortic jet velocity (at least 0.3 m per second per year) predicted an extremely poor prognosis with 79% of patients undergoing surgery or dying within 2 years. In this study, calcification was graded on a scale of 1 (no calcification) to 4 (extensive thickening and 480

Figure 22-14 (Figure Not Available) Relationship of the change in valve area during the systolic ejection to the rate of progression of aortic stenosis. The aortic valve area ratio (AVA ratio) was calculated as the aortic valve area during the midpoint of deceleration divided by the valve area during the mid-point of acceleration. A larger AVA ratio indicates stiffer aortic valve leaflets. Rapid progression was defined as a decrease in valve area of 0.20 cm2 per year or more. In patients with a baseline AVA of 1.2 cm2 or greater, the number of rapid and slow progressors for a ratio less than 1.25 and 1.25 or greater is shown (A). In patients with a baseline AVA of 1.2 cm2 or greater, the receiver operating curve for AVA ratio (B) indicates the sensitivity and specificity of various AVA ratios for predicting rapid progression of disease. AUC, area under the curve. (From Lester SJ, McElhinney DB, Miller JP, et al: Circulation 2000;101:1947–1952.)

calcification of all cusps). Other studies have also found aortic valve calcification to predict more rapid disease progression.[60]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Physiologic Variability in Measures of Stenosis Severity Exercise Hemodynamics in Valvular Aortic Stenosis Although exercise testing should be performed with caution, if at all, in symptomatic patients with valvular aortic stenosis because of the high risk of complications,[55] studies in asymptomatic patients have provided insight into the relationship between hemodynamic severity and clinical symptoms (Table 22-2) . [46] [47] [48] [49] [51] , [77] [78] [79] [80] In patients with asymptomatic aortic stenosis, exercise is associated with an appropriate rise in heart rate and cardiac output. The increase in cardiac output with upright exercise is mediated almost entirely by heart rate, with little change in stroke volume. However, even though stroke volume does not change, mean and maximum transaortic volume flow rates are increased because of concurrent shortening of the systolic ejection period. Thus, exercise results in an increase in maximum aortic jet velocity, with a corresponding increase in the mean transaortic gradient as predicted by the Bernoulli equation. The continuity equation predicts a linear relationship between maximum volume flow rate (Qmax ) and maximum jet velocity (Vmax ) for any given valve area.[78] This linear relationship has been verified using both invasive and noninvasive data in an animal model of valvular aortic 481

Figure 22-15 Kaplan-Meier analysis of event-free survival among 25 patients with no or mild aortic valve calcification, as compared with 101 patients with moderate or severe calcification. The vertical bars indicate standard errors. All the subjects in this study had an initial aortic jet velocity of at least 4.0 m per second (mean 5.0 ± 0.6 m per second). (From Rosenhek R, Binder T, Porenta G, et al: N Engl J Med, 2000;343:611–617.)

stenosis.[81] In clinical studies, only two data points typically can be

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acquired, but the slope of the change in Vmax relative to Qmax in patients with no change in valve area with exercise parallels the slope predicted by this relationship. In patients with an increase in valve area with exercise, the observed slope is greater than predicted for a fixed valve area. Changes in Aortic Valve Area with Changes in Volume Flow Rate The effect of changes in volume flow rate on Gorlin and continuity equation valve areas also has been examined in in vitro models, in animal models, [82] and in patients with valvular aortic stenosis (Fig. 22-16) . These studies consistently show an increase in valve area with an increase in transaortic volume flow rate for most stenotic aortic valves.[46] [47] [48] [49] [50] [51] [83] [84] [85] Although these apparent increases, to some extent, could be due to errors in the valve area formulas, both in vitro pulsatile flow model data [71] and video imaging of flow-dependent changes in valve opening support the concept that valve area itself, both anatomic and physiologic, varies with transaortic volume flow rate.[86] This conclusion is not all that surprising given the well-known observation that even normal aortic valve leaflets open less when volume flow rate is decreased, for example, in patients with a dilated cardiomyopathy. Change in Other Measures of Stenosis Severity with Change in Volume Flow Rate Although some investigators have suggested that valve resistance is independent of flow rate,[50] [87] other investigators have shown changes in valve resistance with changes in volume flow rate in in vitro models,[71] in animal models, and in patients with asymptomatic aortic stenosis.[15] [83] In part, the relative stability of valve resistance with changes in flow rate observed in some studies[56] [57] may relate to the range of stenosis severity evaluated (see Fig. 22-12) . Because of the curvilinear relationship between resistance and valve area, with "larger" valve areas (right side of 482

TABLE 22-2 -- Physiologic Changes with Exercise in Adults with Valvular Aortic Stenosis Bache et al[47]

Ettinger et al[79]

Otto et al[78]

Martin Burwash et al[49] et al[51]

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Patients, N Measurements

20 10 Invasive Invasive

Type of Exercise

Supine bicycle

Heart Rate, bpm Rest Exercise Systolic Blood Pressure, mm Hg Rest Exercise Stroke Volume, mL Rest Exercise Qmean , mL/sec Rest Exercise

Supine bicycle

28 85 110 Doppler Invasive Doppler echo echo Treadmill Supine Treadmill bicycle

79 ± 3 87 ± 5 112 ± 5 109 ± 5

71 ± 17 71 ± 2 147 ± 28 98 ± 2

63 ± 14 104 ± 23

120 ± 3 118 ± 8 136 ± 3 133 ± 8

139 ± 15 — 155 ± 24 —

143 ± 22 163 ± 29

— —

— —

98 ± 29 89 ± 32

245 ± 14 318 ± 21

— —

300 ± 85 275 ± 8 319 ± 80 366 ± 325 ± 10 400 ± 140 159

Cardiac Output, L/min Rest Exercise

5.4 ± 0.3 8.6 ± 1.1 8.5 ± 0.6 9.2 ± 0.9

Mean Pressure Gradient, mm Hg Rest Exercise

59 ± 4 74 ± 5

37 ± 9 38 ± 11

— —

103 ± 30 96 ± 30

6.5 ± 1.7 6.0 ± 0.2 6.3 ± 1.7 10.7 ± 9.3 ± 0.2 9.9 ± 3.8 4.4

39 ± 20 52 ± 26

37 ± 2 41 ± 2

30 ± 14 41 ± 18

Vmax (m/sec) Rest Exercise

— —

— —

4.0 ± 0.9 4.6 ± 1.1

—

3.6 ± 0.8

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— Aortic Valve Area, cm2 Rest 0.8 ± 0.1 1.8 ± 0.3 Exercise 0.9 ± 0.1 1.9 ± 0.3 Valve Resistance, dyne/sec/cm-5 Rest — — Exercise — — Stroke Work Loss, % Rest — — Exercise — — Left Ventricular EndDiastolic Pressure; mm Hg Rest 12 ± 6 15 ± 3 Exercise 20 ± 2 15 ± 4 Vmax , maximum aortic jet velocity.

4.3 ± 0.8

1.2 ± 0.5 1.1 ± 0.1 1.4 ± 0.5 1.3 ± 0.7 1.3 ± 0.1 1.6 ± 0.7

— —

191 ± 12 137 ± 81 182 ± 12 155 ± 97

— —

26 ± 1 25 ± 1

17 ± 7 20 ± 9

— —

— —

— —

curve) resistance changes very little even with substantial changes in valve area, whereas with smaller valve areas (left side of curve), large changes in resistance are expected with only small changes in valve area. Similarly, left ventricular stroke work loss has been found to vary with changes in volume flow rate.[51] [71] [88] Overall, both total and steady left ventricular stroke work losses correlate inversely with valve area. However, for a specific valve anatomy, work loss increases with an increase in stroke volume despite a concurrent increase in valve area. This suggests that for a given degree of leaflet stiffness, greater opening of the valve is achieved at the expense of greater work loss. Alternatively, since work includes both potential and kinetic energy, a decrease in the percentage of potential work converted to kinetic work would lead to this observation. In studies to date, only potential work has been measured because of the conceptual and technical difficulties in measurement of kinetic work. Changes in the effective frictional loss component with changes in volume flow rate also

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may affect calculated measures of stenosis severity. Which Measure of Stenosis Severity Is Best? The anatomy of degenerative valvular aortic stenosis is characterized by thickened and stiff leaflets without commissural fusion (see Fig. 22-11) . Given this anatomic substrate, it is not surprising that the degree of valve opening varies with the amount of "force" applied to the valve, whether this force is represented by the surgeon's finger, a balloon valvuloplasty catheter, or the rate and volume of blood ejected by the left ventricle. Most investigators to date have found that each proposed measure of stenosis severity, when examined in detail, varies with changes in volume flow rate. These measures include peak left ventricular to aortic pressure gradient, mean transaortic pressure gradient, maximum Doppler aortic jet velocity, Gorlin valve area, continuity equation valve area, left ventricular stroke work loss, and valve resistance. Of note, despite this potential limitation, most clinical decisions can be made with a high degree of reliability using these, albeit imperfect, indices of disease severity. To 483

Figure 22-16 Relationship of rest and continuity equation aortic valve area (A), aortic valve resistance (B), and percentage of left ventricular stroke work loss (C) in 110 exercise studies. The slopes of the regression lines (solid line) are greater than the line of identity (dashed line), demonstrating an increase in all three indexes with exercise. AVA, aortic valve area; LVSW, left ventricular stroke work. (From Burwash IG, Pearlman AS, Kraft CD, et al: J Am Coll Cardiol 1994;24:1342–1350.)

define the "best" measure of stenosis severity, the specific goals in quantitating the degree of stenosis must be clarified. These goals fall into two distinct categories: clinical patient management and research applications. In terms of clinical decision making, the ideal measure of stenosis severity should reflect disease severity and should have an acceptable intraobserver and interobserver reproducibility. In addition, it should be easily applicable, noninvasive, and inexpensive. Most importantly, it should be predictive of clinical outcome. Clearly, Doppler echocardiographic measures of jet velocity and valve area meet these criteria, as discussed subsequently. In the clinical setting, the impetus to derive a flow-independent measure of stenosis severity arises from the relatively unusual clinical situation in

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which there is coexisting left ventricular systolic dysfunction and an anatomically abnormal aortic valve. Potential approaches to this clinical dilemma are discussed in the following sections. For specific research applications, the "best" measure of stenosis severity must possess additional characteristics. One research goal is to explain the paradox of the marked overlap in hemodynamic severity between symptomatic and asymptomatic patients with aortic stenosis. Some patients with hemodynamically severe disease remain asymptomatic, whereas other patients with only moderate valve obstruction develop definite symptoms. [89] [90] [91] Whether these apparent discrepancies between hemodynamic severity and clinical manifestations of disease are related to other factors (such as ventricular diastolic function[92] ) or whether they reflect the inadequacy of available measures of stenosis severity remains unclear. A second and more important research goal is to follow disease severity over time to define the natural history of this disease and to identify factors that predict progression in individual patients. This goal requires measures of stenosis severity that have a high degree of reproducibility over time and among institutions. This application will allow use of Doppler echocardiographic measures of aortic stenosis severity as end points in intervention trials to prevent or slow disease progression.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Left Ventricular Response to Valvular Aortic Stenosis Diastolic Function The initial physiologic response to chronic pressure overload of the left ventricle is impaired early diastolic relaxation as manifested by a prolonged time constant of relaxation (tau), a lengthened isovolumic relaxation time (IVRT), and a reduced early diastolic filling velocity, similar to the changes seen in patients with systemic hypertension ( see Chapter 6 and Chapter 32 ). [93] [94] [95] [96] [97] Changes in diastolic function typically precede evidence of systolic dysfunction and thus may be present early in the disease course. Although some investigators suggest that Doppler measures of early and late diastolic filling velocities (or rates) may not be sensitive for detection of early diastolic dysfunction,[94] others propose that diastolic parameters can distinguish symptomatic from asymptomatic patients.[92] Later in the disease course, decreased diastolic compliance plus a rightward shift on the passive diastolic pressure-volume relationship may result in a filling pattern characterized by a shortened IVRT, increased early diastolic filling velocity, rapid early deceleration slope, and reduced atrial contribution to diastolic filling, a pattern often referred to as pseudonormalization. [96] Wall Stress and Concentric Hypertrophy

484

As the severity of stenosis increases, concentric left ventricular hypertrophy develops in response to the chronic elevation in left ventricular systolic pressure. This increase in myocardial wall thickness allows maintenance of normal wall stress given that wall stress is directly related to chamber pressure and dimension, but inversely related to wall thickness. Left ventricular hypertrophy is assessed most reliably by calculation of left

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ventricular mass from two-dimensional images, although simple chamber dimensions and diastolic wall thickness may be adequate for clinical evaluation in many patients. Meridional and circumferential wall stress can be calculated from two-dimensional echocardiographic data in conjunction with Doppler evaluation of the aortic valve gradient and a cuff blood pressure measurement, as described in Chapter 4 . In general, the time course for development of left ventricular hypertrophy parallels the course of stenosis severity in most patients. In some individuals, the degree of hypertrophy appears out of proportion to the severity of aortic stenosis. In these cases, other causes for hypertrophy, such as hypertension, coexisting hypertrophic cardiomyopathy, or an infiltrative myocardial process should be considered. It is particularly important to evaluate these possibilities carefully on two-dimensional imaging because the clinical presentation of hypertrophic cardiomyopathy may be similar to that of valvular aortic stenosis. Genetic factors also play a role in the degree of left ventricular hypertrophy. For example, a recent study found that certain polymorphisms of the angiotensin-converting enzyme gene were associated with increased left ventricular hypertrophy.[98] Gender Differences in the Left Ventricular Response to Aortic Stenosis Several investigators have found significant gender differences in the left ventricular response to the chronic pressure overload of aortic stenosis. [99] In symptomatic patients referred for aortic valvuloplasty, although women and men had similar valve areas, women had higher transaortic gradients, higher relative wall thicknesses, and a higher prevalence of left ventricular hypertrophy using gender-specific hypertrophy criteria. In addition, women had a lower functional status score for the same degree of aortic valve obstruction.[100] Another study observed higher peak left ventricular pressures, higher ejection fractions, smaller left ventricular end-diastolic dimensions, and a higher relative wall thickness in women, as compared with men, with aortic stenosis.[101] Although left ventricular mass did not differ in women versus men, left ventricular geometry differed as reflected in a lower circumferential wall stress for a given degree of hypertrophy. Similar findings were observed in a consecutive series of asymptomatic aortic stenosis patients.[102] Even though there were no gender differences in aortic stenosis severity, women reported more functional limitation and had smaller left ventricular end-diastolic and end-systolic volumes and mass index, but had a higher relative wall thickness and fractional shortening as compared with men. In addition, women had a shorter treadmill exercise

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duration and a smaller increase in cardiac output with exercise, even though heart rate and blood pressure responses were similar in men and women.[102] The importance of gender differences in the left ventricular response to chronic pressure overload are illustrated by the observation that after aortic valve replacement in patients with depressed left ventricular systolic function (ejection fraction < 45%), women had a greater improvement in ejection fraction at a mean of 1.4 years after valve replacement, although survival was similar between men and women. The ejection fraction increased from 33% ± 8% to 48% ± 15% in women, compared with an increase from 32% ± 9% to 42% ± 15% in men (P < .02).[103] In summary, the degree of increase in left ventricular mass is variable, in both men and women. However, women tend to have small ventricles with thick walls, low wall stress, and normal or hyperdynamic systolic function (Fig. 22-17) . In contrast, men tend to have left ventricular dilation with normal wall thickness, increased wall stress, and depressed systolic function. Systolic Dysfunction Left ventricular systolic dysfunction due to valvular aortic stenosis usually occurs late in the disease course. Given the high ventricular afterload caused by the stenotic valve, left ventricular contractility typically remains normal, despite a low ejection fraction. Relief of the high afterload with valve replacement often leads to rapid normalization of systolic function. In adult patients, however, left ventricular systolic dysfunction may be due to causes other than aortic stenosis, such as coronary artery or myocardial disease. Patients with these conditions often fail to improve with valve replacement. In the patient with a moderate aortic valve gradient, distinguishing poor left ventricular systolic function caused by severe aortic stenosis from that caused by concurrent ischemic or myocardial disease with only moderate aortic valve disease remains a difficult dilemma. One approach to this problem is to use a flow-independent measure of stenosis severity or to look at the change in stenosis severity with a change in volume flow rate; an alternate approach is to utilize a load-independent measure of left ventricular contractility to evaluate myocardial function. Unfortunately, a load-independent measure of contractility has proven as elusive as a flow-independent measure of stenosis severity.[94] [101]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Coexisting Coronary Artery Disease In the patient undergoing valve replacement for symptomatic aortic stenosis, most cardiac surgeons recommend concurrent coronary artery bypass grafting if significant coronary artery disease is present. Although the need for coronary bypass grafting in the aortic stenosis patient remains somewhat controversial, reported operative mortality 485

Figure 22-17 In this elderly woman with calcific aortic stenosis and mitral annular calcification, severe concentric hypertrophy is present as shown in an end-diastolic image in an apical four-chamber view (A). Aortic jet velocity is 5.1 m per second corresponding to a maximum gradient of 104 and a mean gradient of 62 mm Hg (B). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

in patients with both aortic stenosis and coronary artery disease is only 1.1% to 4.8% when valve replacement plus coronary bypass grafting is performed, versus 4.0% to 13.2% when valve replacement alone is performed.[104] [105] In aortic stenosis patients with angina, the prevalence of significant coronary artery disease ranges from 40% to 80%, so that coronary angiography is needed for planning the operative procedure. Aortic stenosis patients without symptoms of angina also have a prevalence of significant coronary artery disease between 0% and 54% (average 16%). The appropriate diagnostic approach to these patients is less clear. Exercise treadmill testing in aortic stenosis patients is often nondiagnostic for the presence of coronary artery disease because most of these patients (even when asymptomatic) have significant ST segment depression with exercise, possibly related to left ventricular hypertrophy. [78] [106] In addition, it is important to recognize the potential risk of exercise testing in symptomatic aortic stenosis patients.

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The utility of echocardiographic stress imaging for the diagnosis of coronary artery disease in aortic stenosis patients has not been extensively evaluated. Studies on the exercise physiology of aortic stenosis or on the response to inotropic stimulation with dobutamine have focused on Doppler evaluation of aortic stenosis severity and cardiac output rather than on segmental wall motion abnormalities of the left ventricle.[87] A recent study of 50 patients with severe aortic stenosis evaluated the use of adenosine stress echocardiography for the detection of coronary artery disease.[107] The sensitivity and specificity of stress echocardiography were 85% and 97%, respectively. In addition, no major complications occurred during the procedure. Clearly, these observations need confirmation in other studies. In our experience, definite exercise-induced reversible segmental wall motion abnormalities have been seen in a few patients with aortic stenosis in whom subsequent coronary angiography confirmed significant coronary artery disease. More often, however, no definite wall motion abnormalities are seen, even though subsequent catheterization does show greater than 50% narrowing in the coronary arteries. Whether this lack of sensitivity relates to exercise limitation by aortic stenosis itself (the ischemic threshold is not reached), to diffuse subendothelial ischemia obscuring segmental abnormalities, or whether the degree of stenosis being treated with bypass grafting is insufficient to cause ischemia remains unclear. Further studies of stress echocardiography in aortic stenosis patients may clarify this issue. Exercise tomographic thallium imaging in aortic stenosis patients has a sensitivity of 90% and a specificity of 70% for the presence of significant (greater than 50% luminal diameter narrowing) coronary artery disease.[108] Similarly, adenosine thallium stress testing in aortic stenosis patients has a sensitivity of 92% and a specificity of only 71%.[109] When combined with a pretest likelihood of disease (based on gender, age, and cardiac risk factors), the post-test likelihood of coronary artery disease can be helpful in deciding whether coronary angiography is necessary and may result in a reduction in overall costs of patient evaluation.[110] However, many clinicians choose to perform coronary angiography because of the low risk associated with this procedure and the potential impact of the diagnosis on the operative procedure and survival in a specific individual.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Disease Progression Natural History of Aortic Valve Stenosis The natural history of valvular aortic stenosis is characterized by a long time period during which the patient is asymptomatic but there is gradually increasing obstruction 486

to left ventricular outflow (Table 22-3) .[111] [112] The duration of this asymptomatic period is variable. With a congenital unicuspid valve, symptoms typically are recognized in childhood or adolescence. Occasionally, however, young adults may present with symptomatic congenital aortic stenosis, either due to restenosis after a surgical valvotomy as a child or in the absence of previous surgical procedures. In patients with a congenital bicuspid aortic valve, the onset of symptoms typically is at 50 to 60 years of age.[113] [114] In the elderly patient with degenerative valve disease, symptom onset typically is at 70 to 80 years of age, but the interval between observing aortic valve "sclerosis" by echocardiography and clinical evidence of severe stenosis may be only 5 to 10 years. Rheumatic valvular aortic stenosis has a variable course with significant aortic valve obstruction (in conjunction with mitral valve involvement) occurring over a wide age range. Because disease progression results in reduced leaflet opening, the antegrade velocity across the valve increases in direct relation to the degree of valve obstruction. Transaortic pressure gradients increase as predicted by the Bernoulli equation; although it is noteworthy that little increase in the pressure gradient is seen until the valve area is reduced to one half the normal area, whereas an increase in velocity will be noted with only minimal TABLE 22-3 -- Natural History of Valvular Aortic Stenosis

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Study Frank et al[111]

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Entry Criteria ∆Ppeak ≥ 50 mm Hg or AVI < 0.7 cm2 /m2

Chizner et Cardiac cath, al[133] no AVR

O'Keefe et al[134]

Symptom Status 80% symptomatic

Patients, Age, N yrs 15 32– 59

Aortic Mea Stenosis Follo up Severity AVI 0.4 > 2 y ± 0.1 cm2 /m2

76% symptomatic

42 22– AVA 0.7 5.4 y 77 ± 0.3 (0.2–1.1) cm2

Severe aortic Symptomatic stenosis, no AVR, age ≥ 60

50 77 Vmax 4.5 1.7 y

Turina et Cardiac cath, al[91] no AVR

Symptomatic

Asymptomatic

m/sec, AVA 0.6 (0.3–8) cm2

(60– 89) 125 43 Mean ∆P 6.6 y 69 mm Hg AVA 0.56 cm2 (16– 73) 65 Mean ∆P 57 mm Hg AVA 0.76 cm2

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Horstkotte Catheterization Asymptomatic et al[89] for other reasons Catheterization Asymptomatic for other reasons

Refused surgery

Kelly et al Vmax ≥ 3.6 [131]

Symptomatic

Asymptomatic

m/sec

Symptomatic Pellikka et al[132]

Doppler Vmax Asymptomatic ≥ 4 m/sec

142

Mild AS (AVA > 1.5 cm2 ) 236 Moderate AS (AVA 0.8–1.5 cm2 ) 35 Severe AS (AVA < 0.8 cm2 ) 51 63 ± ∆P 68 ± 15 ± 19 19 mos 39 72 ± ∆P 68 ± 11 19 143 72 Vmax 4.4 20 m (4–6.4) m/sec

(40– 94)

18% Kennedy Moderate [135] aortic stenosis asymptomatic et al at cath, no AVR Otto et al Abnormal Asymptomatic [128] valve with Vmax > 2.6

66 67 ± AVA 35 m 10 0.92 ± 0.13 (0.7–1.2) 2.5 y 123 63 ± Vmax < 16 3.0 m/sec

m/sec

Vmax 3–4

m/sec Vmax >

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Rosenhek Abnormal et al[61] valve with Vmax > 4.0

Asymptomatic

4.0 m/sec 128 60 ± Vmax 5.0 27 ± mos 18 ± 0.6 m/sec

m/sec

AS, aortic stenosis; AVA, aortic valve area; AVI, aortic valve index, AVR valve replacement; cath, catheterization; ∆P, pressure gradient; Vmax , maxim jet velocity.

* Event-free survival.

obstruction. Continuity equation valve areas will reflect accurately the degree of impairment of valve opening. In the past, "severe" or "critical" aortic stenosis has been defined in terms of a specific valve area or valve area index. More recent studies[89] [91] [115] have shown marked overlap in hemodynamic severity between symptomatic and asymptomatic patients, indicating that the "critical" degree of valve narrowing varies from patient to patient (Fig. 22-18) . This observation has been confirmed in prospective studies showing that symptom onset occurs with a jet velocity as low as 3.0 m per second or may be delayed until the jet velocity is over 5.0 m second. Similarly, some patients remain asymptomatic with a valve area less than 0.7 cm2 , whereas others have definite symptoms with a valve area greater than 1.0 cm2 . Hemodynamic Progression Until recently, data on the hemodynamic progression of valvular aortic stenosis was limited to studies of patients in whom two cardiac catheterizations had been performed (Table 22-4) . [116] [117] [118] [119] [120] [121] The impact of selection bias on these data is difficult to assess, since only patients who did not die or undergo valve replacement after the first catheterization,

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487

Figure 22-18 Hemodynamically severe aortic stenosis: mean aortic pressure gradient, valve orifice area, cardiac index, and left ventricular end-diastolic pressure in severely symptomatic (open circles) and asymptomatic or mildly symptomatic (closed circles) patients. Mean value (horizontal line) and statistical difference between both groups are indicated. NS, not significant. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–473.)

yet required a second catheterization for clinical indications, are included in these series. In general, these studies showed an average rate of increase in mean pressure gradient between 0 and 12 mm Hg per year and a decrease in valve area between 0.02 and 0.3 cm2 per year. Marked individual variability in the rate of progression was noted, however, and no clear factors were identified that predicted the rate of progression. The availability of an accurate, noninvasive method to evaluate hemodynamic severity has allowed larger and more detailed studies on the rate of hemodynamic progression.[58] [60] , [61] [90] , [115] [122] [123] [124] [125] [126] [127] In these studies, the average rate of increase in aortic jet maximum velocity ranges from 0.2 to 0.4 m per second per year, with an increase in mean gradient of 6 to 7 mm Hg per year and a decrease in valve area of 0 to 0.3 cm2 per year. Again, marked individual variability in the rate of hemodynamic progression Figure 22-19 Change in maximal aortic jet velocity (Vmax ) and pressure gradient during follow-up in 45 patients. (From Faggiano P, Ghizzoni G, Sorgato A, et al: Am J Cardiol 1992;70:229–233.)

was observed ( Fig. 22-19 and Fig. 22-20 ). Although Dopplerechocardiographic studies have the advantage of larger patient numbers and potentially less selection bias (a repeat echocardiographic study is likely to be requested more often than a repeat cardiac catheterization), many of these studies are retrospective, with the data extracted from ongoing clinical databases. Thus, patients with rapid progression, those developing symptoms, or those requiring surgical intervention may be overrepresented. Conversely, repeat studies may not have been performed in clinically stable patients. The results of more recent prospective studies may avoid some of these biases.[61] [128]

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It is important to remember that as the disease progresses, increasing obstruction to left ventricular outflow most often is reflected by both a decrease in valve area and an increase in jet velocity and pressure gradient. However, if there is a concurrent decrease in transaortic 488

TABLE 22-4 -- Hemodynamic Progression of Valvular A

Study Bogart et al[116]

Clinical Status at Entry 2 cardiac caths

Cheitlin et al[117] Wagner and Selzer

2 cardiac caths 2 cardiac caths

Mean Follow up Type of Measurement Patients, Interva Study Method N yr Retrospective Invasive 11 4.9

Retrospective Invasive

29 4

Retrospective Invasive

50 3.5

Retrospective Invasive

26 9

[120]

Jonasson et al[118] Nestico et al[119] Davies et al[121] Otto et al

Calcific AS

2 cardiac Retrospective Invasive caths 2 cardiac Retrospective Invasive caths Asymptomatic Prospective Doppler

29 5.9 47 42 1.7

[90]

Roger et al AS on echo

Retro cohort Doppler

112 2.1

Retrospective Doppler

25 4.8

[123]

Thoreau et AS on echo al[122]

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AS on echo

Peter et al AS on echo

Prospective

Doppler

45 1.5

Retrospective Doppler

49 2.7

Retrospective Doppler

394 6.3

[126]

Brener et al[125] Otto et al

AS on echo

Asymptomatic Prospective

Doppler

123 2.5

Retrospective Doppler

91 1.8

Retrospective Doppler

170 1.9

Prospective

128 1.8

[128]

Bahler et AS on echo al[60] Palta et al AS on echo [127]

Roshenhek AS on echo et al[61] with Vmax

Doppler

>4.0 m/sec

AS, aortic stenosis; AVA, aortic valve area; ∆P, pressure gradient; Vmax , volume flow rate, a decrease in valve area alone may be seen with no change in jet velocity or transaortic gradient. A decrease in transaortic volume flow rate may occur secondary to comorbid disease, such as increasing mitral regurgitation or myocardial infarction, but also may occur late in the disease course of isolated aortic stenosis as left ventricular stoke volume decreases because of the onset of subtle systolic dysfunction (Fig. 22-21) . Conversely, some patients may have an interval increase in jet velocity and pressure gradient with no change in valve area if transaortic stroke volume is increased because of systemic factors (e.g., anemia, fever, pregnancy) or increasing aortic regurgitation. At this point, it is not clear whether the rate of hemodynamic progression in an individual patient is either predictable or "steady." In fact, it is most likely that the rate of progression is nonlinear; that is, a fairly slow rate of Figure 22-20 Maximal aortic jet velocity (Vmax ) is plotted for the initial

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and final Doppler echocardiographic studies in 42 asymptomatic patients. Group means are indicated by the symbol . (From Otto CM, Pearlman AS, Gardner CL: J Am Coll Cardiol 1989; 13:545–550.)

progression may change to a rapid increase in severity when the opposing forces of left ventricular ejection and leaflet stiffness can no longer be balanced. Predictors of Hemodynamic Progression Factors that predict the rate of hemodynamic progression in an individual patient have not been well defined. Clearly, valve anatomy is an important factor in disease progressive, since most patients with a bicuspid stenotic valve require surgical intervention at a younger age than patients with degenerative aortic stenosis.[114] Gender also is important, since the ratio of men to women with aortic stenosis is approximately 2:1. Other factors associated with the rate of disease progression are the severity of aortic stenosis when initially seen (more severe disease 489

Figure 22-21 A 32-year-old man had asymptomatic valvular aortic stenosis with a jet velocity of 5.0 m per second and a continuity equation valve area of 1.2 cm2 (A and B). Over the next year, he developed the onset of exercise intolerance and early symptoms of aortic stenosis. Repeat examination showed a decrease in aortic jet velocity to 4.5 m per second (C) in association with a decreased transaortic volume flow rate (D). Aortic valve area had decreased to 1.0 cm2 . Two-dimensional echocardiography showed normal left ventricular systolic function, but ejection fraction had decreased from 72% to 60%.

leads to symptoms more rapidly than milder disease) and age (older patients have more rapid disease progression than younger patients). Clinical factors such as elevated serum lipid levels, hypertension, smoking, and diabetes have been found to be associated with aortic stenosis.[129] In addition, a recent study found that smoking, hypercholesterolemia, and elevated creatinine and calcium levels were associated with more rapid disease progression.[127] However, further studies are needed to confirm these results. Two recent studies suggested that the amount of aortic valve calcium is an important determinant of disease progression.[60] [61] Despite using different grading scales to evaluate valve calcium, both of these studies found that the rate of disease progression was more rapid when

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more valve calcium was present. These studies also confirmed previous observations that the rate of disease progression is highly variable for individual patients. Given the continued uncertainty regarding which factors predict progression in an individual patient, it is prudent to follow patients with aortic valve thickening closely, monitoring for early symptoms of valve obstruction. Periodic echocardiographic examinations also are warranted, particularly for any change in symptoms or functional status. Uncertainty as to the rate of hemodynamic progression in an individual patient complicates the decision as to whether concurrent aortic valve replacement should be performed in patients with only moderate aortic stenosis who are undergoing coronary artery bypass surgery. Some surgeons recommend "prophylactic" valve replacement, since otherwise reoperation may be needed in less than 5 years.[130] Symptomatic versus Asymptomatic Aortic Stenosis The clinical course of the patient with aortic stenosis changes dramatically once symptoms supervene. The 490

Figure 22-22 (Figure Not Available) A, Event-free survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circle) in severely symptomatic (solid lines and solid symbols) and asymptomatic or mildly symptomatic (dashed lines and open symbols) patients. B, Effective survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circles) in severely symptomatic (solid lines) and asymptomatic or mildly symptomatic (dashed line) patients. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–483.)

asymptomatic patient (regardless of hemodynamic severity) has a low risk of sudden death with an actuarial survival rate no different from that of agematched normal subjects[89] [91] [131] [132] (Fig. 22-22 (Figure Not Available) and Fig. 22-23 ). In contrast, the symptomatic patient has a grim prognosis, with a 5-year actuarial survival rate of only 12% to 50% without surgical intervention. These data were derived from studies of patients who refused surgical intervention.[89] [91] , [111] , [131] [133] [134] [135] In patients with severe, symptomatic aortic stenosis, predictors of survival include the transaortic gradient or velocity, left ventricular systolic function as assessed qualitatively on echocardiography, age, and gender.[136] Of note, patients with a higher transaortic gradient have a better prognosis, most likely

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because when severe stenosis is present, a low gradient indicates a low transaortic stoke volume. In any case, valve surgery for relief of stenosis remains the appropriate treatment for symptomatic patients, even the elderly.[137] [138] Only rarely does severe comorbid disease result in an unacceptably high operative morbidity and mortality.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Role of Echocardiography in Clinical Decision Making Timing of Intervention in the Symptomatic Patient Calcific aortic valve disease is prevalent in the elderly.[139] [140] Most of these patients have a systolic murmur on auscultation, but not all are symptomatic. The first step in the clinical decision making process for the timing of intervention in a patient with valvular aortic stenosis is a careful history as to whether symptoms (angina, exertional dizziness, exercise intolerance, or heart failure) are present or absent ( Table 22-5 ; ; Fig. 2224 ). Most clinicians defer intervention until definite symptoms are present, since the risk of sudden death is very low in the asymptomatic patient.[89] [91] [131] [132] , The presence of moderate or severe valve calcification in combination with a rapid increase in jet velocity over time (i.e., rapid progressors) identifies a subgroup of asymptomatic patients with a very poor short-term prognosis who are likely to develop symptoms soon.[61] If the patient has symptoms that may be due to aortic stenosis, the next step is to confirm the anatomic diagnosis and quantitate the degree of valve obstruction by Doppler echocardiography. The most appropriate standard of reference for the diagnostic utility of echocardiography in the management of symptomatic aortic stenosis patients is survival and functional status (not catheterization results), as our goal is to predict clinical outcome correctly.[16] Based on this reference standard, aortic jet velocity alone is a simple and useful initial diagnostic test. When jet velocity is very high (>4.0 or 4.5 m per second), severe stenosis is confirmed.[140] [141] [142] Some patients with mixed moderate aortic stenosis and aortic regurgitation will have a jet velocity over 4 or 4.5 m per second even though valve area is in the range of 1.0 to 1.5 cm2 . Comparing Doppler data with subsequent clinical outcome suggests that these patients benefit from valve replacement if symptoms of valve disease are present.[40] Decision making in patients with mixed aortic stenosis and aortic regurgitation is confounded by the need to take the degree of left

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ventricular dilation and systolic dysfunction into account as well as the severity of valve obstruction (see Chapter 4) . When jet velocity is very low (<3.0 m per second), severe stenosis is unlikely and valve replacement is not needed.[140] [142] Of course, exceptions do occur in clinical practice and an occasional patient may be seen with a jet velocity less than 3.0 m per second and a valve area less than 1.0 cm2 in association with severely reduced left ventricular systolic function. Similarly, this numerical approach applies only to the symptomatic patient in whom valve replacement is being considered. A high jet velocity in an asymptomatic patient certainly does not mandate surgical intervention. The use of two break points (upper and lower) allows both severity and specificity to be maximized but leaves an intermediate group in whom further evaluation is needed. When the jet velocity is 3 to 4 m per second, calculation of valve area and assessment of the degree of coexisting aortic regurgitation are helpful in clinical decision making. If the valve area is 1.0 cm2 or less and the patient has symptoms of aortic stenosis, valve replacement is indicated. If the valve area is greater than 1.5 cm2 , valve 491

Figure 22-23 Cumulative life table incidence of death in aortic stenosis patients. Asymptomatic persons (closed circles) had a significantly better survival with respect to all-cause mortality, cardiac death, and sudden death than symptomatic patients (open circles). (From Kelly TA, Rothbart RM, Cooper CM, et al: Am J Cardiol 1988;61:123–130.)

TABLE 22-5 -- Clinical Decision Making in Adults with Symptomatic Ao Stenosis Lower V max

Patients, Study N Method Otto 104 Split sample 1988 [40]

Upper V max

Break Break Diag End Point, Point, Accu Point % m/sec Midrange m/sec 9 Surgical <3.0 AVA, AR >4.0 findings plus 1 yr

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mortality Oh 100 Comparison Aortic Single AVA >4.5 1988 with cath data stenosis value [141] severity at cath Galan 510 Observational, Actual <3.0 AVA >4.5 1991 retrospective outcome [3] (AVR) Shah 93 Blinded Actual <3.0 AVA >4.0 1991 decision re: outcome [142] AVR (AVR) AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; Vmax , maximum aortic jet velocity.

6

9

9

replacement is unlikely to be helpful. When the valve area is between 1.0 and 1.5 cm2 , valve replacement may be indicated if there is at least moderate coexisting aortic regurgitation. Again, clinical decision making is problematic in this patient group. One prudent approach in the mildly symptomatic patient is to repeat the Doppler echocardiographic study after a reasonably short time interval (3–12 months). Evidence of disease progression will tip the balance toward intervention, whereas a stable examination and the absence of worsening symptoms argues for further waiting with close clinical follow-up. In clinical practice, the basic echocardiographic examination of a patient with valvular aortic stenosis includes measurement of maximum aortic jet velocity (with optional gradient calculations); continuity equation valve area; assessment of the degree of coexisting aortic regurgitation; evaluation of left ventricular size, hypertrophy, and systolic function; evaluation of the degree of mitral regurgitation; and estimation of pulmonary artery pressures. All of these parameters are included in the clinical decisionmaking process, along with any other specific measurements needed in an individual patient. Aortic Stenosis with Decreased Left Ventricular Function In some patients it is unclear whether valve opening is restricted due to excessive leaflet stiffness or whether there is only mild leaflet sclerosis with limited motion due to low transaortic stroke volume (Fig. 22-25) .

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There have been two basic research approaches to resolving the problem of distinguishing severe aortic stenosis with consequent depressed left ventricular systolic function from only mild to moderate stenosis with reduced leaflet motion due to intrinsic left ventricular dysfunction: (1) a flow-independent measure of stenosis severity or (2) a load-independent measure of left ventricular systolic function. Although significant progress has been made with both of these approaches, as discussed earlier, neither approach has provided a clear answer. A pragmatic clinical approach to this patient group is to (1) look at the valve, (2) look at the patient, (3) look at the options, and (4) consider further diagnostic evaluation (Table 22-6) . Direct assessment of the degree of leaflet thickening and calcification by fluoroscopy, transthoracic or transesophageal echocardiography, or, if 492

Figure 22-24 Flow chart for clinical decision making in aortic stenosis. AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; F/U, follow-up; Vmax , maximum velocity of aortic jet.

Figure 22-25 A 61-year-old man presented with heart failure symptoms. Echocardiographic examination showed a moderately calcified valve with reduced leaflet opening (A) and reduced systolic function (ejection fraction, 20%) in association with marked left ventricular dilation as seen in the apical four-chamber view (B). Transaortic stroke volume was reduced as shown by pulsed Doppler echocardiographic examination of left ventricular outflow velocity in an anteriorly angulated four-chamber view (C). The aortic jet velocity (D) was 3.0 m per second corresponding to a maximum gradient of 36 mm Hg and a mean of gradient of 22 mm Hg. Continuity equation valve area was 0.9 cm2 . After multiple readmissions for heart failure on medical therapy, the patient underwent aortic valve replacement. Postoperatively, there has been no change in left ventricular function and persistent symptoms of heart failure are present. Ao, aorta; AS-jet, aortic stenosis jet; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium; RV, right ventricle.

493

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TABLE 22-6 -- Clinical Decision Making: Aortic Stenosis with Decreased Left Ventricular Function 1. Look at the valve Severely calcified versus Flexible leaflets 2. Look at the patient LV dysfunction due to end-stage ischemic disease or cardiomyopathy versus LV dysfunction due to aortic stenosis 3. Look at the options Risk of surgery Comorbid disease Outcome without surgery 4. Evaluate stenosis severity at two different flow rates (dobutamine or exercise): Increased transaortic flow rate Increased AVA suggests flexible valve leaflets No change in AVA suggests stiff, rigid valve leaflets No change in transaortic volume flow rate Severe AS versus unresponsive myocardium? AS, aortic stenosis; AVA, aortic valve area; LV, left ventricular. necessary, direct inspection at the time of surgery often is very helpful. A heavily calcified valve suggests that valve replacement will be beneficial, whereas thin, flexible leaflets argue against valve surgery. Additional clinical information about the patient may clarify the problem. If left ventricular systolic dysfunction is due to aortic stenosis, improvement is expected after valve replacement. However, if left ventricular dysfunction is due to end-stage ischemic disease or a primary cardiomyopathy, little improvement is expected after aortic valve surgery. Next, the therapeutic options and expected outcomes can be estimated for the individual patient. If the risk of surgery is acceptable or if the patient is having surgery for coexisting coronary artery disease, the threshold for valve replacement is reasonably low. If the risk of valve replacement is excessively high because of comorbid disease, medical therapy may be

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appropriate. If the patient has failed aggressive medical therapy, surgical intervention may be indicated, even if the risk is high. If the clinical decision still remains unclear, evaluation of stenosis severity at two different flow rates may be helpful. With mild to moderate aortic stenosis, augmentation of transaortic volume flow rate with exercise or a positive inotropic agent (e.g., dobutamine) will result in a significant increase (>0.2 cm2 ) in valve area as the flexible leaflets open to a greater extent. Conversely, with critical aortic stenosis, valve area will change little despite increased transaortic volume flow due to stiff, rigid valve leaflets. However, an increase in aortic valve area can be seen in some patients with surgically confirmed severe aortic stenosis, which therefore does not exclude fixed valve disease.[143] If the ventricle fails to respond to inotropic stimulation (i.e., no increase in cardiac output), interpretation is more difficult.[50] [144] [145] The failure of volume flow rate to increase may be due to limitation of flow by a severely stenotic valve or may be due to an unresponsive myocardium. In some patients, it may be preferable to evaluate stenosis severity at baseline and after several weeks of therapy to optimize preload and afterload, rather than using maneuvers to acutely increase volume flow rate. Instead of assessing changes in valve area, another approach is to calculate the end-systolic wall stress to fractional shortening relationship and compare the patient's data with those of published series[101] to assess whether improvement after valve replacement is likely. Unfortunately, despite meticulous diagnostic evaluation, outcome is likely to be poor in patients with aortic stenosis and low output, regardless of the therapy chosen.[146] [147] [148] [149] [150] Patients with reduced systolic function and a history of a prior myocardial infarction experience a particularly poor outcome following valve replacement.[151] A recent study that included patients with a low transvalvular gradient in addition to impaired systolic function found that the ejection fraction improved in the majority of patients following surgery, but that the 30-day mortality rate was 21%.[152] Evaluation of the Asymptomatic Patient Undergoing Noncardiac Surgery In the asymptomatic patient with valvular aortic stenosis undergoing noncardiac surgery, echocardiography allows (1) assessment of disease severity, (2) monitoring of left ventricular function before, during, and after the procedure, and (3) alerting the clinician to the need for invasive

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hemodynamic monitoring. Many of these patients, even with severe obstruction, can be managed without valve replacement if loading conditions are optimized preoperatively and careful invasive monitoring is continued in the postoperative period.[153] [154] Common postoperative complications include pulmonary edema or congestive heart failure associated with tachycardia that usually resolves quickly with rate control and diuresis. Similar considerations apply to the management of the pregnant patient with aortic valve disease (see Chapter 31) . Optimizing the Surgical Approach Once the decision has been made to proceed with relief of stenosis, the echocardiographic examination plays a key role in choosing the optimal surgical approach. Valve replacement remains the standard therapy for relief of valvular aortic stenosis. The optimal valve size and type typically are selected in the operating room based on direct measurement of the annulus by the surgeon. Echocardiographic prediction of prosthetic valve size has been only fair because of the limited number of valve sizes and the goal of implanting a larger valve when possible to improve hemodynamics. [155] For homograft valve replacements, an estimate of the optimal size is more important than for mechanical valves, so that the correct size will be available at the time of surgery.[156] For homograft aortic valves, diastolic left ventricular outflow tract diameter correlates best with implanted valve size. Note that the diastolic outflow tract diameter measurement averages 2 mm smaller than the systolic measurement (which is used in valve area calculations). A dilated aortic root commonly is seen as a result of poststenotic dilation and, in some cases, may be large enough to merit root replacement. In patients with a 494

small aortic annulus, an enlarging procedure may be considered or a specific valve chosen to avoid suboptimal hemodynamics postoperatively. Recognition of a subvalvular membrane, which can be mistaken for valvular stenosis on echocardiography, will alter the surgical approach and may allow resection of the membrane without valve replacement. Coexisting hypertrophic cardiomyopathy, although rare, is important to recognize to avoid postoperative dynamic subaortic obstruction.

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Echocardiographic Evaluation after Valve Replacement for Aortic Stenosis Evaluation of the Valve Replacement Surgical procedures that preserve the native aortic valve have not yet been successful for treatment of valvular aortic stenosis,[157] nor has percutaneous balloon valvuloplasty shown long-term benefit in adult patients. [136] A mechanical or stented tissue prosthetic valve is most often implanted after removal of the stenotic valve leaflets. The fluid dynamics of prosthetic valves, evaluation of valve function, and other postoperative complications are discussed at length in Chapter 23 , Chapter 24 , and Chapter 25 . Newer surgical approaches to treatment of valvular aortic stenosis include the development of stentless tissue valves[158] [159] [160] [161] [162] [163] and the use of aortic valve homografts.[157] [164] [165] Both these valves types offer the advantages of improved hemodynamics compared with conventional valves, the absence of the need for chronic anticoagulation, and the hope of increased durability. Some centers also have reported success with the pulmonic valve autograft procedure in young adults, as well as adolescent patients.[166] [167] [168] In this procedure, the patient's stenotic aortic valve is replaced with his or her own native pulmonic valve. A homograft then is used in the pulmonic position. Potential advantages of this procedure include optimal hemodynamics and low thrombogenicity. In addition, tissue viability of the pulmonic autograft provides the possibility of tissue growth and repair, which are particularly important features in adolescent patients. In one series including patients up to age 35 years, event-free survival rate after the pulmonic autograft procedure was 90% at 7 years.[166] Events included reoperation for either aortic or pulmonic valve dysfunction, significant aortic regurgitation, and death. More recently, echocardiographic follow-up of 100 patients undergoing the pulmonic valve autograft procedure was reported.[169] The reintervention rate was 2% at a mean follow-up period of 33 months, with a range of 6 months to 7

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years. A unique complication of the pulmonic autograft procedure is the development of homograft failure, either from stenosis or regurgitation. With homograft stenosis, patients typically develop progressive dyspnea approximately 3 to 6 months following surgery, at a time when continued physical recovery from the surgical procedure would be expected. Tissue from these failed explanted homografts show a prominent inflammatory cell infiltrate and therapy has thus focused on suppressing the heightened immune response with oral steroids. When a course of oral steroids fails to control the disease process, reoperation may be required. Since stentless tissue valve, homografts, and pulmonic autografts appear similar to a native aortic valve on echocardiographic examination,[160] [165] it is important that details about the surgical procedure be available at the time of the echocardiographic examination. Doppler findings for these valves also are similar to findings in native valves except that antegrade velocities may be slightly higher. Pulmonic autografts tend to have some degree of regurgitation early postoperatively, which typically decreases over the next several months, presumably due to collagen synthesis and increased structural stability of the valve in response to the increased mechanical stress on the valve leaflets. Other Hemodynamic Changes Postoperatively If left ventricular end-diastolic pressure has been chronically elevated preoperatively, as the ventricle remodels and filling pressures normalize, there may be a corresponding decrease in pulmonary artery pressures. If pulmonary pressures are elevated because of coexisting lung disease, little change is expected postoperatively. Moderate pulmonary hypertension (pulmonary artery pressures of 31 to 50 mm Hg) occurs in approximatly 50% of patients evaluated preoperatively with right heart catheterization.[170] However, the presence and magnitude of pulmonary hypertension do not appear to be related to the severity of aortic stenosis. It remains unclear whether preoperative pulmonary hypertension is related to postoperative survival, because studies have yielded conflicting results. [171] The effect of aortic valve replacement on coexisting mitral regurgitation remains controversial. In theory, mitral regurgitant severity should decrease given the "afterload reducing effect" of aortic valve replacement.[172] However, the magnitude of this effect may be small, particularly if there is anatomic abnormality of the mitral valve apparatus.[173] When significant mitral regurgitation accompanies severe aortic stenosis, it is prudent to consider a surgical intervention to reducing mitral regurgitant severity at

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the time of aortic valve replacement. Intracavity gradients due to dynamic obstruction at the midventricular level are seen in one quarter to one half of aortic stenosis patients in the early postoperative period.[174] [175] The severity of obstruction varies from trivial to severe, and clinical evidence of hemodynamic compromise may be seen in some patients. Patients with small hypertrophied and hyperdynamic ventricles at baseline are more likely to have obstruction postoperatively. [176] Typically, obstruction is manifested as a late-peaking systolic velocity curve, which is similar to the pattern seen in hypertrophic obstructive cardiomyopathy. However, the level of obstruction is at the midventricular or papillary muscle level, rather than subaortic, and systolic anterior motion of the mitral valve is not seen. Obstruction is dynamic in that the presence and severity of obstruction varies from day to day (peaking at the third postoperative day) and in that obstruction can be provoked or increased 495

by maneuvers that decrease left ventricular preload or increase contractility. Echocardiographic recognition of midcavity ventricular obstruction in the postoperative period affects clinical management, since intravascular volume loading and avoidance of agents that increase contractility or reduce afterload can result in significant clinical improvement. The echocardiographic finding of dynamic obstruction after aortic valve replacement also has significant prognostic implications. Patients with obstruction have more frequent postoperative complications (hypotension, arrhythmias), a longer hospital stay, and a higher mortality rate than those without obstruction.[175] [176] [177] The Effect of Valve Replacement on the Left Ventricle When left ventricular systolic function is depressed because of valvular aortic stenosis, improvement is seen early in the postoperative period. Predictors of improvement in the ejection fraction include female gender and less severe coexisting coronary artery disease.[103] When measured by quantitative angiography, left ventricular mass and wall thickness decrease substantially in the postoperative period. By 10 months postoperatively, left ventricular mass has decreased by about 30% as compared with the preoperative left ventricular mass, with a further decrease in left ventricular mass observed at studies performed 8 years

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postoperatively. Left ventricular mass may remain elevated in some patients, particularly if the prosthetic valve has suboptimal hemodynamics. Despite the apparent improvement in left ventricular geometry and systolic function seen in most patients, irreversible (or only very slowly reversible) changes in myocardial structure persist late postoperatively, with a relative increase in myocardial interstitial fibrosis as compared with normal and persistent diastolic dysfunction.[178] These myocardial changes, in combination with the mild pressure overload of the prosthetic valve, can result in persistent systolic overload at the myofibrillar level.[93]

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Future Directions Echocardiographic evaluation of aortic stenosis is an established and effective clinical tool. However, to explain the relationship between hemodynamic severity and symptom onset, a flow-independent measure of stenosis severity still is needed. At this point, the most promising research approach to a flow-independent measure of stenosis severity is to determine the change in the degree of valve narrowing measured at two different volume flow rates rather than utilizing data obtained only at rest. Continuity equation valve area and the slope of the maximum velocity/maximum volume flow rate relationship both are potentially useful approaches to this problem. A plausible hypothesis is that early in the disease course of "degenerative" aortic stenosis, increases in volume flowrate result in increased opening of the valve leaflets. As leaflet stiffness increases, this increase in leaflet motion diminishes until, eventually, increases in left ventricular ejection force no longer result in increased leaflet motion. We propose that symptom onset correlates with a stiff and rigid valve that limits the patient's ability to increase cardiac output with exercise. Other investigators have proposed a similar approach measuring stenosis severity at different flow-rates using exercise or dobutamine.[50] [78] [87] Further studies are needed to assess the potential prognostic value of this approach. As studies using Doppler approaches provide additional insight into the natural history of this disease, these data will allow prediction of disease progression in individual patients. In addition, these data will allow sample size calculation and appropriate risk stratification for interventional trials. In the future, these techniques will be used as end points in clinical trials of interventions to prevent or delay progression of "degenerative" valvular aortic stenosis.

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501

Chapter 23 - Fluid Dynamics of Prosthetic Valves Ajit P. Yoganathan PhD Brandon R. Travis PhD

Doppler echocardiography has made noninvasive examination of prosthetic heart valve function a clinical reality. Unfortunately, there are still many imperfections in echocardiographic examinations, including acoustic shadowing, reflections caused by implanted valves, and limitations in ultrasound technology. Despite these limitations, a number of important parameters can be calculated or estimated to aid in the assessment of prosthetic heart valve function and performance. Once a valve has been implanted, its function is governed primarily by its hemodynamic characteristics. In order to understand the hemodynamic performance of prosthetic heart valves, it is necessary to have a solid background in the physical laws that govern their function; therefore, the purpose of this chapter is to introduce cardiologists to the governing principles of fluid dynamics, relevant formulations used in prosthetic valve assessment, and fluid mechanical characteristics of specific prosthetic heart valves.

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Fluid Dynamics With few exceptions, a material can be characterized as a fluid if it deforms continuously under the action of shear stress.[1] Shear stress is defined as a force per unit area applied tangentially to a surface. Viscosity is related to the amount of deformation that a fluid experiences when a shear stress is imposed on it. A constant viscosity fluid, called a Newtonian fluid, is one in which the relationship between viscous shear stress and strain rate is linear, as shown in Equation 1: where µ is the viscosity, usually defined in centipoise (grams/cm·s). The coefficient in this linear relationship is the dynamic viscosity. Equation 1 states the relationship between viscous shear stress (τ), viscosity (µ), and strain rate for flow in the x-direction with the derivative taken in the ydirection, perpendicular to the direction of flow. Blood behaves as a Newtonian fluid in regions of high strain rate. For flow in large arteries, 3.5 cp is often used as a viscosity estimate for blood.[2] Conservation of Mass Conservation of mass governs all materials, and it is the logical starting point for an introduction to fluid motion. Consider an imaginary volume, a control volume, enclosed by a surface through which fluid can flow, as shown in Figure 23-1 . It is not necessary for this control volume to coincide with any physical boundaries; it is purely a tool for the analysis of physical systems. Conservation of mass, or continuity, states that the change in mass within this control volume is equal to the mass of fluid that enters the volume, minus the mass that exits. [3] A very good assumption for cardiovascular applications is that 502

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Figure 23-1 Control volume for the conservation of mass. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 . ρ, fluid density.

blood is incompressible, meaning its density does not vary. Assuming that there are only two surfaces across which fluid flows, surfaces 1 and 2, the velocities (v) and areas (A) can be related by conservation of mass, as shown in Equation 2.

pρv1 (t)A1 = ρv2 (t)A2 (2) Conservation of Momentum The principle of conservation of momentum was initially formulated as Newton's second law of motion—mass times the acceleration of an object is equal to the sum of the forces acting on that object. For application to fluid mechanics, it is more convenient to define this in terms of the fluid momentum. The momentum of a fluid is a measure of the mechanical force it is able to transfer and is equal to the product of fluid mass and fluid velocity. A change in momentum of a fluid can only be accomplished by the application of a force. The general form of the principle of conservation of momentum for an incompressible Newtonian fluid is called the NavierStokes equations.[3] The forces that merit consideration within the cardiovascular system are pressure, gravity, viscous shear stresses, and turbulent stresses. Conservation of Energy Consider the conservation of energy statement, again using the control volume approach. The change in energy within a control volume is equal to the net rate of energy crossing the surface of the control volume plus the net rate of energy generated within the control volume. Energy loss occurs when the net rate of energy generated within the control volume is negative. In cardiovascular applications, energy loss usually occurs because the viscosity of the fluid converts its kinetic energy to heat. The general equation for energy conservation is difficult to apply to cardiac blood flow; however, with a number of simplifying assumptions a useful relation can be obtained. The Bernoulli equation,[4] as shown in Equation 3, is used

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extensively in noninvasive cardiology:

where p is the static pressure and v is the velocity, along the streamline, h is the vertical distance above some reference point, and s is the distance between points one and two along the streamline. This equation can be derived from either the conservation of energy or the conservation of momentum. Each term in Equation 3 has a physical definition that aids in comprehension and application of the Bernoulli equation. The left side of the equation represents the difference in pressure acting on the fluid between the positions one and two. The first term on the right side is called the inertial term and represents the change in fluid acceleration owing to temporal changes in the applied force. The second term on the right side is the kinetic energy associated with the fluid at each location. This term can also be considered the convective acceleration term, which is associated with a change in the velocity of a fluid as it travels from one location to another. The classic example of convective acceleration is the steady flow of fluid through a converging nozzle, such as a funnel. Because of continuity, the velocity is higher at the exit of the funnel than at the entrance, and acceleration occurs even though the flow is steady. The third term on the right side of the equation is the hydrostatic pressure difference, owing to the difference in elevation between the two points. The final term on the right side of the equation is the irreversible loss of mechanical energy or momentum owing to viscous effects. The limitations that arise when using Equation 3 are important to understand. Initially, Bernoulli's equation was derived for inviscid flow, in which there are no viscous effects. Because it is not physically possible to obtain such a flow, the term on the far right was added to account for losses caused by viscous effects. Equation 3 must also be applied between two points that lie along a streamline within a flow field. Streamlines are imaginary lines in a flow field to which the velocity vector is always parallel. In steady flow situations, streamlines can be traced by placing a particle or dye into the fluid and following their motion throughout the flow field. If the flow is unsteady, however, streamlines change from one time to another, and the particle paths no longer coincide with streamlines. Because of the difficulty in defining streamlines, rigorous application of Equation 3 is not possible in cardiovascular flows.

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Dimensionless Quantities The structures of cardiovascular flows are governed by chamber geometry and two dimensionless quantities. The first of these quantities, the Reynolds number, is defined as follows: where v is the velocity, µ is the viscosity, ρ is the fluid density, and d is a length representative of the flow regime 503

in question. For flow in a pipe, d is the pipe diameter, whereas for jet flows, it is the diameter of the orifice through which the jet exits. Physically, the Reynolds number represents the ratio of the fluid inertia to the viscous forces acting on a fluid. The other important dimensionless quantity in cardiovascular flows, the Womersley number (α), represents the ratio of the local acceleration a fluid experiences to the viscous forces acting on it. The Womersley number is defined as follows:

where ω is the frequency (heart rate) and all other variables are the same for those used in the definition of the Reynolds number. These dimensionless numbers can be used to define a transition regime to turbulence common to all cardiovascular flows occurring in a similar geometry. Turbulence Consider a car traversing a winding road. As long as the car stays below a certain speed, the frictional force between its tires and the road enable the car to follow the path in which its front wheels are aligned. When the car surpasses a certain speed and passes around a large curve, however, the inertia of the car overcomes the frictional force holding the tires to the road. Similarly, flows with large inertia relative to the frictional, or viscous, forces acting on them become turbulent. Under these conditions, a small instability in the flow field (e.g., surface roughness within a pipe) can initiate fluctuations in fluid motion. When these fluctuations propagate to the point where fluid motion can only be described as random fluctuations about a mean velocity, the flow is said to be turbulent.

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In steady flows, the tendency of a flow to be turbulent is governed only by the Reynolds number and the chamber geometry. Two geometries that have been studied extensively and have direct applications to cardiovascular fluid mechanics are flow through a straight pipe and flow through a small, circular orifice. Flow through a straight pipe transitions to turbulence at Reynolds numbers of approximately 2000.[5] Flow through small, circular orifices create a phenomenon known as a free jet. For steady free jet flows, which are inherently more unstable than pipe flows, the critical Reynolds number is approximately 1000, with fully turbulent flow occurring at Reynolds numbers greater than 3000.[6] [7] In pulsatile flow, the transition to turbulence depends on the Womersley number and the shape of the flow waveform as well as the Reynolds number and chamber geometry.[8] [9] The critical Reynolds numbers for the transition to turbulence in pulsatile flow is much higher than the corresponding numbers in steady flow. Estimates of transition to turbulence in the ascending aorta by Yoganathan et al[4] (based on work by Nerem and Seed[10] ) indicated that the critical Reynolds number for transition is approximately 8000. It is also important to note that in pulsatile flow, turbulence may not be present during the entire cycle. Because flow acceleration is inherently more stable than flow deceleration, turbulence is more often observed during the deceleration phase of pulsatile flow. [9] Shear Stress Both viscous and turbulent shear stresses, if large enough, can potentially lyse or activate cells of the blood[11] [12] [13] [14] however, the origin, and consequently the scale, of viscous and turbulent shear stresses is different. Viscous shear stresses act on a molecular scale; they arise from the tendency of one molecule to remain near its neighbors. This tendency is quantified in fluids by their viscosity. Because viscous stresses act on a scale much smaller than the diameter of a blood cell, blood cells always experience a viscous shear stress if such a stress is present. In contrast, turbulent shear stresses arise from the inertia contained within the fluctuations of turbulent flow. Turbulent shear stresses act on a scale comparable to the length of the smallest turbulent fluctuations, often much larger than the diameter of a blood cell. Even if a turbulent shear stress is present, a blood cell may not experience this stress if the cell diameter is much smaller than the length scale of the smallest turbulent fluctuations. Boundary Layer Separation

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Due to viscosity, when a flowing fluid contacts a solid body, because of viscosity, the fluid that is immediately adjacent to the body must be the same velocity as the body. For this reason, a boundary layer is formed. The boundary layer is a region in which the velocity changes from zero at the wall to that of the free stream value. Boundary layers are extremely thin but very important, for it is only in this region of the flow that viscous effects are significant. As a fluid moves downstream, viscous diffusion occurs and the viscous effects are felt farther from the wall, and the boundary layer grows. When a fluid flows over a solid body, it must change direction to pass around the body. A pressure gradient is required for this to occur. When an adverse pressure gradient (i.e., a pressure gradient against the flow direction, tending to decrease fluid velocity) is applied, if the magnitude of the pressure gradient is large enough, the fluid within the boundary layer reverses and boundary layer separation occurs. Downstream of the separation point, a region exists in which there may be reversed, turbulent, or disturbed flow. Recirculating or vortical flows are characteristic of this region; they can lead to high particle residence times and oscillatory shear stresses, both of which can have a wide variety of clinical implications, including atherosclerosis.[15] [16] In pulsatile flows, separation can be generated by a geometric adverse pressure gradient or by temporal changes in the driving pressure. Geometric adverse pressure gradients are present behind all prosthetic heart valves because of the small orifice area. As the area increases downstream of a prosthetic heart valve, the velocity decreases, in accordance with the continuity equation. The decrease in velocity is caused by an adverse pressure gradient. Because of the contractile nature of the heart, 504

the blood that flows through it also experiences both acceleration and deceleration during a cardiac cycle. It is during the deceleration phase of a particular flow, when an adverse pressure gradient is present, that boundary layer separation is most likely to occur. Thus, in regions in which there are both geometric and temporal adverse pressure gradients, separation is even more likely. Cavitation Cavitation is the formation of vaporous bubbles resulting from a sudden

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drop in local pressure below the vapor pressure of the fluid. The abrupt closure of a mechanical prosthesis has been shown to induce cavitation in in vitro flow circuits,[17] [18] [19] and a few works have linked cavitation with mechanical valve closure in vivo as well.[20] , [21] The formation and subsequent collapse of cavitation bubbles releases a tremendous amount of energy within a very localized area; cavitation has been known to crack steel turbomachinery. Cavitation during the mechanical valve closure event is thought by some to be responsible for pitting on mechanical prosthesis surfaces[22] and the blood damage induced by mechanical prostheses.[18] The sharp drops in local pressure created by mechanical prosthesis closure lasts less than 2 ms,[18] [19] [20] [21] so the resulting cavitation bubbles collapse soon after they are created. Vaporous cavitation bubbles could act as nucleation sites, however, drawing in blood gasses such as nitrogen and carbon dioxide. The resulting gaseous emboli could last much longer than the cavitation event. Indeed, gaseous emboli have been detected in the circulation of patients with mechanical prostheses by transcranial Doppler. [23] Such emboli have been dubbed with the acronym HITS (high intensity transient signals). Pressure Recovery Consider steady flow of fluid through a pipe with a restrictive orifice placed downstream of the pipe entrance. Because of continuity, as the fluid enters the restriction, it accelerates. Assuming that the flow is streamlined when the particle enters the restriction, the velocity increases and the static pressure decreases, according to the Bernoulli equation. Once it exits the restriction and the cross-sectional area increases, the particle's velocity decreases and the pressure increases. The increase in pressure distal to a restrictive orifice is called pressure recovery. If there are no viscous energy losses, the pressure recovers to the value it had at the entrance to the restriction; however, viscous losses always occur, pressure does not recover completely, and irreversible mechanical energy losses occur.[3] Consider two similar steady flow situations. The first geometry is that of a Venturi flow meter, as shown in Figure 23-2 . The second case involves flow through an orifice meter, in which a restrictive orifice is placed in the center of a straight pipe (see Fig. 23-2A) . In the first case, because of the smooth contraction before the Venturi throat and the gradual area expansion downstream, there is no separation and very little energy loss. Most of

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Figure 23-2 A, Orifice meter with pressure drop. B, Venturi meter with pressure drop.

the velocity at the Venturi throat is converted back to pressure. For the same flow through the orifice meter, the velocity at the orifice would be approximately the same as the velocity at the Venturi throat. Because of the very rapid area contraction and expansion surrounding the orifice, however, a large separation region forms downstream and energy is lost. Pressure measurements at the location of the greatest contraction within each model would yield approximately the same value, which could lead one to believe that the energy losses in both models are identical. If the pressure is measured further downstream, however, it is evident that the Venturi meter has a much smaller energy consumption than the orifice meter, owing to downstream recovery of pressure. The same concepts may hold true for stenoses within the cardiovascular system. In the Venturi model, the peak velocity and the smallest pressure occur at or very near to the throat of the model, whereas in the orifice meter, because fluids cannot turn sharp corners, the peak velocity occurs slightly downstream of the orifice. The location at which this occurs is called the vena contracta because the area that the fluid passes through is less than the orifice area. Therefore, according to the Bernoulli and continuity equations, the maximum pressure drop across a prosthetic valve occurs at the location of the vena contracta and not at the valve orifice.

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Application of Fluid Mechanics to Prosthetic Heart Valves Pressure Drop The pressure drop (∆P) across a prosthetic valve is related to the energy losses caused by its presence. Pressure 505

drops across natural valves can be measured with invasive catheter techniques; however, it is both difficult and dangerous to pass a catheter through a prosthetic valve. Fortunately, the Bernoulli equation can provide a noninvasive estimate of the pressure drop across prosthetic or natural valves. Neglecting the viscous effects and applying Equation 3 at mean conditions, so that the integral term vanishes, yields Equation 4: Point 1 is proximal to the valve and point 2 is at the orifice. If the velocity upstream of the valve is much smaller than at the valve, v1 can be neglected and Equation 5 is obtained:

If the velocity is measured with continuous wave Doppler ultrasound (in meters per second), the pressure drop can be obtained from this equation in millimeters of mercury. When measuring pressure distal to prosthetic valves, it is important to note whether or not the recovered pressure is measured. It is especially important when using continuous wave Doppler ultrasound to evaluate prosthetic heart valves. Continuous wave Doppler ultrasound measures the highest velocity, which occurs at the vena contracta. Consequently, the Doppler-derived pressure drops are always based on the pressure at the vena contracta, before pressure recovery occurs. Thus, one is likely to

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overestimate the transvalvular pressure drop because pressure recovery is not considered. Although Doppler ultrasound may overestimate transvalvular pressure drops, however, they are extremely useful in patient diagnosis. A study by Marcus et al[24] has shown that Doppler-derived pressure drops measured across small-diameter prosthetic mechanical valves (Medtronic-Hall and St. Jude) correlate just as strongly with fluid mechanical energy losses as the recovered pressure drops measured by catheterization. Pressure drop and recovery through prosthetic valves can be significant factors affecting the pressure within the left ventricle. A larger pressure drop across a prosthetic valve requires a larger systolic pressure in the left ventricle to drive flow through the circulation. Because it has been shown that left ventricular pressure is the primary determinant of myocardial oxygen consumption,[25] it is imperative that the pressure in the left ventricle is minimized when dealing with prosthetic valves. Numerous studies detailing the effects of recovery on pressure drop measurements for both natural and prosthetic heart valves have been published, and this topic continues to be an area of active research.[26] [27] [28] [29] [30] [31] [32] [33] [34] [35] Valve Area Cardiologists have used a variety of methods to determine the forward flow area of a valve. Because of acoustic anomalies caused by prosthetic valves and the limited spatial resolution of echocardiography, it is often impossible Figure 23-3 Control volume in the left ventricle for determining aortic valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 .

to measure the valve area directly. Applying a control volume analysis to a prosthetic valve in the aortic position (Fig. 23-3) and rewriting Equation 1, however, allows for estimation of the mean area over which fluid flows, as shown in Equation 6: The integral is taken with respect to time over the systolic flow period, v1 is

the velocity upstream of the aortic valve, and v2 is the velocity at the vena

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contracta. A2 is the area of the vena contracta or the effective valve area and A1 is the area at the upstream face of the control volume, measured by

echocardiography. Inherent to Equation 6 is the assumption that the spatial velocity profile is uniform over the entire orifice area; however, because the velocity profile is nonuniform in mechanical prostheses, it is difficult to apply Equation 6 accurately. By extending the control volume from the left ventricular outflow tract to encompass the entire left ventricle (Fig. 23-4) , it is possible to use this technique to determine the mean mitral valve area. The time-velocity integral of both the mitral and the left ventricular outflow tract positions must be calculated over the entire cardiac cycle. It is only necessary to integrate the velocity at the mitral valve during diastole and that of the aortic valve during systole, because these are the only times in which there is flow through the valves. If regurgitation is not present in either valve, Equation 6 can be applied and the effective area of the mitral valve can be obtained. When aortic regurgitation is present, the velocity and area at the light ventricular outflow tract can be used instead for calculation of effective mitral orifice area. Another method for determining valve area can be 506

Figure 23-4 Control volume in the left ventricle for determining mitral valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2

derived using the Bernoulli equation and conservation of mass. A contraction coefficient (Cd ) can be defined as the area of the vena contracta

divided by the area of the valve orifice (Ao ).[3] The continuity equation for flow through an orifice, including the contraction coefficient, appears in Equation 7, where Q is the flow rate and v is the velocity at the vena contracta: Q = Ao vCd (7) Substituting Equation 5 into Equation 7 and solving for velocity yields an

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equation that can be used to determine the effective orifice area of a cardiac valve:

The constant was determined by using the density of blood (ρ = 1050 kg/m3 ) and converting the units to those convenient for biomedical use.

The effective area will be square centimeters, if the root mean square systolic or diastolic flow rate (Qrms ) is in cubic centimeters and the mean systolic or diastolic pressure drop (∆P) is measured in millimeters of mercury.

Another method that has been developed involves measuring the pressure half-time of an orifice to estimate the orifice area. The pressure half-time (Pt/2 ) is the time required for left ventricular pressure to decrease to half of its peak value. An empiric relation between the pressure half-time and the area of the mitral valve (Amv ) has also been established. It was based on observations that changes in the mitral pressure drop with time were constant for a particular orifice area[36] [37]

The constant 220 was empirically determined,[38] but this equation has been shown to be dependent on a number of factors other than the valve area, including the severity of aortic regurgitation and ventricular wall properties. This equation is ineffective for prosthetic heart valves, limiting its application.[39] [40] Regurgitant Flow Rate Because mechanical prosthetic valves are fairly rigid, they are unable to form tight seals when closed. Consequently, regurgitant jets are present in prosthetic valves under normal conditions, although the amount of regurgitation is usually small. Normal regurgitant flow is characterized by a closing volume during valve closure and leakage after closure (see Figure 23-11) . Regurgitant flow is often characterized by the regurgitant volume. The regurgitant volume is the total volume of fluid through the valve per beat owing to the retrograde flow. It is equal to the sum of the closing volume and the leakage volume. The closing volume is the volume of fluid flowing retrograde through the valve during valve closure. Any fluid volume accumulation after valve closure is caused by leakage and is

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referred to as the leakage volume. These quantities are dependent on valve size, increasing with increasing valve diameter. Typically, the regurgitant volume is higher for mechanical valves than for bioprosthetic valves; however, prosthetic valves can exhibit substantial regurgitation when they malfunction. To distinguish normal from abnormal valve function, it is important to differentiate between normal regurgitant volume and additional regurgitation owing to disease. Fluid mechanical analysis of this problem has provided two different techniques that at least partially fulfill this requirement. Turbulent Jet Theory

Using free turbulent jet theory, Cape et al[41] [42] [43] (and later Sugawara et al [44] ) were able to derive relations for the regurgitant flow rate based solely on Doppler ultrasound measurements. Turbulent jets have a number of unique characteristics. Upon entering a chamber they spread radially, pulling or entraining stationary fluid with them. Initially, though, the jet has a core of fluid that is not affected by the stationary fluid. This potential core has the same velocity as the jet at the orifice and persists for a few orifice diameters downstream, as shown in Figure 23-5 . Once the core vanishes, the jet reaches a state that is amenable to theoretical analysis. It is important to recognize, however, the assumptions inherent in this theoretical analysis. Unsteady flow effects are neglected, and the analysis assumes that the jet enters a stationary fluid and does not impinge on solid boundaries. In the heart, regurgitant jets are unsteady, often impinge on the walls of the heart, and always encounter incoming forward flow. Additional work has been performed that treats jets in confined and impinging geometries; these geometries more closely resemble the chambers of the left heart. Burleson et al [45] [46] constructed a dimensional analysis model of valvular regurgitation based on the center line velocity decay of the jet and the width and length of the receiving chamber. Their equation has been shown to 507

Figure 23-5 Free jet center line velocity decay showing jet velocity (v) plotted versus distance (x).

be accurate for a number of in vitro geometries and conditions.[45] [47]

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Proximal Flow Convergence

The principle of conservation of mass was also applied in the region proximal to the valvular orifice to measure regurgitant volume.[48] [49] [50] [51] When fluid enters a regurgitant orifice it must accelerate to reach a peak velocity at the throat of the orifice. If the orifice is circular, this acceleration region should be axisymmetric about the center of the orifice. Thus, upstream of the regurgitant orifice, a series of concentric isovelocity contours hemispherical in shape can be defined within the flow field. This physical argument is the basis for the proximal flow convergence method of quantifying regurgitant flow rate. If a control volume is constructed to coincide with a hemispherical contour and the regurgitant orifice, as shown in Figure 23-6 , the same amount of fluid that enters the volume from an isovelocity contour exits the control volume through the regurgitant orifice. The control volume statement is represented mathematically in Equation 9. Qo = (2πr2 )Vr (9) The term within parentheses is the surface area of the hemispherical control surface. Vr is the velocity measured with color Doppler echocardiography

and r is the distance at which the velocity is measured. Qo is the flow rate at the regurgitant orifice.

Because of its simplicity and ease of application, this technique has received a great deal of attention, especially for mitral regurgitation. The effects of regurgitant orifice motion,[52] orifice geometry variation,[53] [54] [55] [56] and ultrasound machine settings[53] have all been addressed with both in vitro and in vivo investigations. In addition, its application to prosthetic valve regurgitation has also been considered.[57] Studies in our laboratory have found that isovelocity contours from regurgitant orifices can be described better by a hemielliptical shape than by a hemispherical shape, yielding more accurate estimations of regurgitant flow rate in vitro.[58] [59] Unfortunately, rigorous in vivo validation of the proximal flow convergence technique is difficult.

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Hemodynamic Characteristics of Native Valves In order to effectively analyze flow through prosthetic heart valves in the mitral or aortic positions, it is important to understand the conditions under which natural valves function. Figure 23-7 illustrates typical pressure and flow waveforms for healthy individuals at both the aortic and the mitral valves. During systole, the pressure difference required to drive the blood through the aortic valve is on the order of a few millimeters of mercury. Diastolic pressure differences across the aortic valve are much larger than systolic, the pressure usually being about 80 mm Hg. The valve closes near the end of the deceleration phase of systole with very little reverse flow. The blood flow through the mitral valve is biphasic during diastole, as shown in Figure 23-4 . The first peak, the E wave, is due to ventricular relaxation, whereas the second peak, the A wave, is caused by contraction of the left atrium; therefore, all valves in the mitral position open and close twice during each cardiac cycle. It is also evident that all cardiac valves are closed during both isovolumic contraction and isovolumic relaxation. Measurements of the velocity profile just distal to the aortic valve have been performed with Doppler echocardiography in normal subjects.[60] The peak systolic velocity is Qo = (2πr2 )Vr . (12) Figure 23-6 Proximal isovelocity surface area schematic. Vr is the velocity on a hemispheric shell defined by the radius (r) with surface area A1 . A2 is the regurgitant orifice area and Vo is the peak regurgitant jet velocity.

508

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Figure 23-7 Pressure and flow waveforms for the left heart.

1.35 ± 0.35 m per second and the velocity profile at the level of the aortic valve annulus is relatively flat; however, there is usually a slight skew toward the septal wall (<10% of the center line velocity) caused by the orientation of the aortic valve relative to the long axis of the left ventricle. This skew in the velocity profile has been shown by many experimental techniques, including hot film anemometry,[61] [62] Doppler ultrasound,[60] and magnetic resonance imaging.[63] The flow patterns distal to the aortic valve also play an important role in proper valve function. During systole, vortices form behind each leaflet in the sinus region. In vitro studies have attempted to relate these vortices to effective valve closure.[64] [65] It has been shown that the ventricular vortices are unnecessary for valve closure; however, they do ensure that the valve closes quickly, reducing leakage.[66] The velocity profile at the mitral valve has been determined in detail in pigs and should be comparable to the velocity profile in humans because of the similarity in cardiac anatomy.[67] Again there is a slight skew to the profile, but there does not seem to be a preferred orientation. It is dependent on the particular geometry of the mitral valve, the diastolic flow patterns within the left ventricle and the location at which the pulsed Doppler sample volume is placed.[67] When the sample volume was placed at the mitral annulus, the peak early diastolic velocity was 63.6 ± 16.1 cm per second, whereas the late diastolic peak velocity was 53.7 ± 10.8 cm per second.[67] When the sample volume was at the tip of the mitral valve leaflets, the peak early diastolic velocity was 82.9 ± 30.8 cm per second and the peak late diastolic velocity was 39.6 ± 14.2 cm per second. Vortices develop in the left ventricle during diastole as blood enters through the mitral valve. Bellhouse[68] proposed that the vortices helped to close the mitral valve at the end of diastole. Later work has shown that the vortices play a role in early closing of the mitral valve, but late closure is dominated by left ventricular pressure.[69] Because of the restrictive area of prosthetic valves, the peak velocities are usually higher, and the spatial velocity profiles are dramatically different from those in natural valves. The shear stresses in prosthetic valves also are

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much larger because of the higher velocities and turbulence. The magnitude of the shear stress varies greatly depending on the type of prosthetic valves. It is important to note the differences and similarities between valve types in terms of shear stress magnitudes, peak velocities, and flow patterns so that an effective assessment of prosthetic valve function can be performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Fluid Mechanics of Specific Prosthetic Valve Designs Prosthetic heart valves have been successfully used in heart valve replacement over the past 40 years. Currently, heart valve prostheses can be classified into two primary categories, mechanical and biologic. Mechanical valves in current clinical use are composed of three basic designs or classifications: ball-and-cage, tilting disc, and bileaflet. The biologic valves can be further classified into three categories: stented, unstented, and homograft valves. Although significant progress has been made in the development of better prostheses through new materials and more physiologic valve designs, several problems associated with prosthetic valves have not been eliminated. Existing problems that can be related to the valve hemodynamics or local fluid mechanics are (1) thrombosis and thromboembolism, (2) hemolysis, (3) tissue overgrowth, (4) damage to endothelial lining, and (5) regurgitation. The presence of high shear stresses can lead to damage of formed blood elements, platelet activation, and initiation of biochemical processes affecting coagulation. Lethal damage to red cells can occur with fluid shear stresses as low as 1500 dyn/cm2 .[11] These levels can be significantly lower (10 to 100 dyn/cm2 ) in the presence of foreign surfaces, such as those presented by a valve prosthesis.[12] [13] Sublethal damage can occur in stress fields as low as 500 dyn/cm2 .[14] In addition, platelet activation and damage have been shown to occur in shear stresses ranging from 100 to 500 dyn/cm2 .[70] The residence time of the cell in the damaging fluid environment is a significant factor in determining lethal stress levels that further complicates the mechanism for damage. Additionally, regions of flow separation and stagnation form local environments suitable for accumulation and growth of thrombi and fibrous or pannus tissue.[71] The fluid mechanic performance of prosthetic heart valves is often assessed

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through in vitro testing to determine transvalvular pressure drops, regurgitant volumes (closure and leakage), distal and proximal velocity fields, 509

and the locations and levels of turbulent stresses. The relationship between valve fluid mechanics and the development of problematic function have been studied by numerous investigators over the past two decades. In vitro studies have concentrated on quantifying local fluid stress levels through state-of-the-art flow measurement techniques such as laser Doppler anemometry,[72] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [91] hot film anemometry,[92] [93] [94] and ultrasound velocimetry.[95] The fluid mechanics of the various prosthetic valve designs are discussed in this section. Comparisons between the many valve designs within each classification of prostheses are left to the many references dealing with the assessment of individual valves. Antegrade and retrograde flow fields are described, including turbulence levels, regurgitation, and pressure drop characteristics for the different valve designs. All flow characteristics are referenced from in vitro experiments conducted in our laboratory unless otherwise specified. In most citations, the data are representative of 25- or 27-mm aortic prostheses tested under physiologic pulsatile flow conditions providing a cardiac output (CO) of 5.0 to 6.0 L per minute and a heart rate (HR) of 70 bpm. Exact test conditions (valve size, CO, HR, pressures) are noted for each citation. The measurement of pressure drop is intrinsically related to the distal flow fields of valves. The effect of pressure recovery depends strongly on flow structure and the vessel geometry in which the flow is entering. Stewart et al[29] have assessed the differences in determining transvalvular pressure drops across aortic valves owing to pressure recovery effects, when using standard in vivo techniques such as Doppler ultrasound or cardiac catheterization. Doppler-measured pressure drops are not equal to cathetermeasured drops, unless the catheter is placed at the same location where the peak velocity is measured by Doppler, typically the vena contracta of the jet. Pressure recovery is very dependent on valve type, size, orientation, and position (i.e., aortic or mitral), and it is particularly likely with mechanical valves, which exhibit complex jet flow patterns with more than one jet, and in smaller aortic valves at higher flow rates. In general, the Doppler technique measured higher pressure drops in mechanical aortic valves,

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especially in the larger sizes, than did the catheterization technique. In addition, some valve designs such as the Medtronic Freestyle unstented bioprosthesis and larger size bileaflet and tilting disc mechanical valves require that the upstream approach velocity (i.e., the term v1 in Equation 4) be measured and used in the modified Bernoulli equation, owing to small pressure drops. When pressure drops are expected to be small, neglecting the approach velocity in the calculations can lead to significant overestimation in the pressure drop. Clinicians should be aware of these effects when interpreting pressure drop data in diagnostic exams. Mechanical Valves The three major mechanical valve designs or classes are the tilting disc, bileaflet, and ball-and-cage. These valves differ primarily in the type and function of the occluder. Although these different designs influence the valvular Figure 23-8 Schematic showing the geometry of commonly used mechanical valve prostheses.

fluid mechanics, all three share common flow structures such as welldefined jet flows, wakes with some degree of flow reversal, and turbulent shear layers. The antegrade flow, regurgitant flow, and pressure drop characteristics for each valve design are discussed separately in the following sections. Because the design of a valve can strongly influence the local fluid dynamics, a brief discussion of the pertinent design features of each class of valve is provided. Figure 23-8 illustrates the design features of the three classes of mechanical valve prostheses. Tilting Disc Valves

The tilting disc valve has one occluder (disc) generally of a circular cross section. The disc is often mounted such that it is free to rotate about a pivot axis, typically displaced from the disc diameter. Metal struts are used to secure the disc within the valve housing and control its range of motion. Numerous design variations on the tilting disc valve exist. These different designs vary in the pivot mechanism or strut design, the range of disc motion allowed, or in the geometry of the disc, which can range from flat to curved. Typically, the occluder opens to angles between 60 and 80 degrees with respect to the valve annulus.

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The tilting disc valve is characterized by two orifices separated by the occluder. The major orifice is the larger open area formed between the disc pivot axis and the housing, as the disc swings distally to the open position. This orifice is free of blockage owing to mounting struts and causes little resistance to transvalvular flow. As the disc opens, the remaining part of the disc, on the other side of the pivot axis, swings in the proximal direction to form the minor orifice. Mounting struts, which can vary from one to two depending on valve design, typically span the minor orifice. Because of the upstream protrusion of the disc into the minor orifice tract and the presence of the mounting struts, a slight obstruction of flow is encountered. Antegrade Flow.

Figure 23-9 and Figure 23-10 illustrate the antegrade flow patterns of the Björk-Shiley monostrut and Medtronic-Hall tilting disc valves. The antegrade flow is characterized by a major orifice jet and a minor orifice jet. The major orifice jet is spatially larger than the minor orifice jet. It is semicircular in cross section with 510

Figure 23-9 Velocity and turbulent shear stress profiles downstream of a 27-mm Björk-Shiley monostrut tilting disc valve at peak systole. A and C, Profile through the major and minor orifices at 11 mm downstream. B and D, Center line profile 17 mm downstream across the major and minor orifices (major orifice to the right).

peak systolic velocities of approximately 2 m per second in the aortic position. Under comparable flow conditions, most tilting disc valves exhibit similar major orifice jet structures and peak velocity magnitudes. The spatial structure of the minor jet varies depending on the number of struts used to secure the disc. In single-strut designs such as the BjörkShiley monostrut and the Medtronic-Hall tilting disc, the minor orifice jet appears as two jets separated by a well-defined wake behind the strut. The flow on each side of the strut is nearly symmetric with similar spatial structure and velocity magnitude. Valves with two struts display a minor orifice jet structure consisting of a strong central jet bounded by two weaker jets. The adjacent weaker jets are separated from the central jets by the wakes of the struts. Their velocity magnitude is roughly 30% to 40% of the velocity magnitude of the central jet. The peak velocities of the minor orifice jet are typically of the same magnitude or slightly less than the peak

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velocity in the major orifice jet in nearly all tilting disc designs. Wake regions are observed behind the valve struts and disc. These wake regions are areas of flow separation with significant velocity defect and nearly stagnant flow. Wake regions persist for 10 to 20 mm downstream of the valve annulus. Owing to the opening angle of the disc, the major and minor orifice jets are directed toward the wall on the major orifice side of the valve, following the occluder. In the aortic position, this results in a region of separated flow in the sinuses located below or near the minor jet at peak systole. Because of the strong major orifice jet and the orientation of the disc with respect to the flow, strong secondary flow structures are encountered downstream of the valve. These secondary flows form a pair of counter-rotating vortices or helical motions. The vortices are generated by the high-momentum fluid in the major jet wrapping around the sides of the disc and flowing into the low-momentum, separated flow regions immediately behind the disc. Flow over the disc generates vortex shedding similar to that observed with flow over a delta wing airfoil. Turbulent stresses associated with the titling disc design are located in the jet shear layers and in the wakes of the discs and struts. The turbulent shear stress profiles for the monostrut and Medtronic-Hall valves are shown in Figure 23-9 511

Figure 23-10 Velocity and turbulent shear stress profiles downstream of a 27-mm Medtronic-Hall tilting disc valve at peak systole. A and C, Center line profile 15 mm downstream across the major and minor orifices (major orifice to the right). B and D, Profile through the major and minor orifices at 13 mm downstream.

and Figure 23-10 . Peak turbulent shear stresses, in the aortic position, can range from 1500 to 3500 dyn/cm2 depending on the particular tilting disc design. These stress levels were measured 10 to 15 mm downstream of the valve housing and may be even higher closer to the valve. Large stresses persist almost into the aorta, indicating that a significant volume of the fluid is occupied by the turbulent shear layers, which may be relevant in that sufficiently long residence times may exist for formed blood elements exposed to turbulent stresses. Table 23-1 summarizes the peak velocity and turbulent shear stress levels for many of the 27-mm aortic valves in clinical use.

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Normal Regurgitant Flow.

The tilting disc design shows slightly lower regurgitant volumes than the bileaflet design, owing to reduced closing and leakage volumes (Fig. 2311) . Ranges for the regurgitant volume of the tilting disc valve vary from approximately 5.5 mL per beat for 19- and 20-mm valves to 9 mL per beat for 29-mm valves. Table 23-2 and Table 23-3 list the regurgitant volumes for several prosthetic valve designs. The leakage flow in mechanical valves is often in the form of small-scale regurgitant jets. In the tilting disc design these jets emanate from small gaps around the perimeter of the valve between the disc and the valve housing. [76] [96] [97] , Baldwin et al[96] measured the gap width of a Björk-Shiley monostrut valve with Delrin rings and obtained widths of approximately 75 µm, which varied nonuniformly around the valve perimeter. These leakage jets were believed to be advantageous because of the potential for washing of the perimeter of the valve housing 512

TABLE 23-1 -- Peak Systolic Velocity and Turbulent Shear Stress Levels for Common 27-mm Aortic Valve Prostheses †

Valve Type Valve Ball-and-cage Starr-Edwards 1260 Tilting disc

Björk-Shiley convexo-concave

Björk-Shiley Monostrut

Medtronic-Hall

Peak Turbulent Shear Peak Measurement Velocity Stress Location (cm/s) (dyn/cm2 ) 12 mm 220 1850 downstream 7 mm 200 3400 downstream 11 mm 200 1800 downstream 8 mm 200 1250 downstream 11 mm 200 800 downstream 13 mm 200 1500

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downstream Omnicarbon 14 mm downstream Bileaflet St. Jude Medical 13 mm Standard downstream Duramedics 13 mm downstream Carbomedics 12 mm downstream Stented Carpentier-Edwards 15 mm bioprostheses Porcine 2625 downstream Carpentier-Edwards 15 mm Porcine 2650 downstream Carpentier-Edwards 17 mm Pericardial 2900 downstream Hancock MO Porcine 10 mm 250 downstream Hancock II Porcine 18 mm 410 downstream Ionescu-Shiley 27 mm Standard Pericardial downstream Hancock Pericardial 18 mm downstream Nonstented Medtronic Freestyle * Leaflet tips bioprostheses 10 mm from tips St. Jude Medical Leaflet tips * TSPV 10 mm from tips

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225

2000

210

1500

210

2300

228

1520

370

4500

200

2000

180

1000

330

2900

260

2500

230

2500

170

2100

125 100 150 125

†Data obtained at 5 L/min CO, 70 bpm HR, and 120/80 mm Hg aortic pressure. *Data obtained from in vitro Doppler ultrasound measurements.

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during closure. Other studies have shown that the regurgitant jets are of a significant velocity magnitude, ranging from 2 to 5 m per second, and turbulent stresses are several times greater than in the antegrade flow field. Measurements in the regurgitant jets of the Björk-Shiley valve indicate that peak turbulent shear stresses are as high as 10,000 dyn/cm2 .[96] Turbulent scales in these jets are estimated to be of the same order of magnitude as the size of red cells and may result in higher rates of hemolysis than in the antegrade turbulent fields. Pressure Drop Characteristics.

To minimize the workload on the heart, a prosthetic valve should not impose resistance to forward flow. In general, prosthetic Figure 23-11 Regurgitant, closing, and leakage volumes of a valve in the aortic position.

valves impose more forward flow resistance than do natural valves. Prosthetic valves are often characterized by their pressure drop or through their effective orifice areas (Equation 8), which can be used to estimate the resistance a valve imposes on forward flow across it. The effective orifice area (Aeff ) is an index of how well a valve design uses its primary or internal orifice area. Another measure of a valve's resistance to forward flow is the performance index (PI), the ratio of Aeff to the valve sewing ring area. The PI provides a measure of how well a valve design uses its total mounting area, the area the flow would see without the valve. Although the Aeff is a function of the valve size, the PI attempts to normalize for valve size, providing a more uniform measure of a valve's resistance characteristics independent of the size and nearly independent of the flow rate. The tilting disc design presents a relatively streamlined configuration to the flow and thus shows relatively low gradients. Tilting disc valves typically show a PI ranging from 0.4 to 0.65. Aeff and PI for several prosthetic valve designs in clinical use today are provided in Table 23-2 and Table 23-3 . Orientation.

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The orientation of the tilting disc valve in the mitral position has been studied in vivo by Jones et al.[98] These authors made comparisons of the orientations of the major orifice jet of tilting disc valves with respect to the left ventricular geometry. The studies indicated that the preferred orientation for tilting disc valves in the mitral position is with the major orifice oriented toward the left ventricular free wall, as opposed to the septum. Greater intraventricular turbulence was observed with a septal orientation of the major orifice than with a free wall orientation. Orientation of the major orifice toward the septal wall produced large areas of velocity reversal, directed against the minor orifice. In contrast, 513

TABLE 23-2 -- In Vitro Hemodynamic Data for Common Aortic Valve Prostheses *

Valve Type Ball-and-cage

Tilting disc

Regurgitant Size Volume Valve (mm) (mL/beat) Starr-Edwards 1260 27 5.5 25 4.3 21 2.5 Björk-Shiley convexo27 8.5 concave 25 7.3 21 5.5 Björk-Shiley Monostrut 27 9.2 25 7.6 23 6.9 21 5.9 19 5.5 Medtronic-Hall 27 9.6 25 8.4 23 7.3 20 6.2

EOA †

(cm2 ) 1.75 1.62 1.23 2.59

PI 0.30 0.33 0.36 0.45

2.37 1.54 3.34 2.62 2.00 1.45 1.07 3.64 3.07 2.26 1.74

0.48 0.45 0.58 0.53 0.48 0.42 0.38 0.64 0.62 0.54 0.51

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Bileaflet

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St. Jude Medical Standard

St. Jude Medical Regent

Carbomedics

Sorin Bicarbon ‡

Stented bioprostheses

Carpentier-Edwards Porcine 2625

Carpentier-Edwards Porcine 2650

27

10.8 4.09 0.71

25 23 21 19 29

9.9 8.3 6.8 6.8 13.5

27 25 23 21 19 17 27 25 23 21 19 27 25 23 21 19 27

12.3 11.2 10.3 9.0 7.6 6.3 7.5 6.1 6.5 3.4 3.0

3.23 2.24 1.81 1.21 4.98

0.66 0.54 0.52 0.43 0.75

4.40 3.97 3.47 2.81 2.06 1.56 3.75 3.14 2.28 1.66 1.12 3.06 2.39 2.07 1.54 0.97 <3 1.95

0.77 0.81 0.83 0.81 0.73 0.69 0.65 0.64 0.55 0.48 0.40 0.71 0.69 0.73 0.67 0.55 0.34

25 21 27

<2 1.52 0.31 <2 1.28 0.37 <2 2.74 0.48

25

<2 2.36 0.48

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Carpentier-Edwards Pericardial 2900

Hancock Porcine 242

Hancock MO Porcine 250

Hancock II Porcine 410

Ionescu-Shiley Standard Pericardial Mosaic Porcine

Mitroflow Pericardial

21 19 27

<2 1.38 0.40 <2 1.17 0.41 <3 3.70 0.64

25 21 19 27 25 23 21 19 25

<2 <2 <2 <3 <2 <2 <2 <2 <2

3.25 1.88 1.56 2.14 1.93 1.73 1.31 1.15 2.16

0.66 0.54 0.55 0.37 0.39 0.42 0.38 0.41 0.44

23 21 19 27 25 23 21 27

<2 <2 <2 <2 <2 <2 <2 <3

1.94 1.43 1.22 2.36 2.10 1.81 1.48 2.35

0.47 0.41 0.43 0.41 0.43 0.44 0.43 0.41

29 27 25 23 21 29 23 19

<3 <2 <2 <2 <1 <4 <3 <2

3.15 2.81 2.11 1.74 1.54 3.71 2.12 1.34

0.48 0.49 0.43 0.42 0.44 0.56 0.51 0.47

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Nonstented bioprostheses

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Medtronic Freestyle Porcine

27

25 23 21 19 EOA, effective orifice area; PI, performance index.

<4 3.75 0.65 <4 <3 <2 <2

3.41 2.69 2.17 1.84

0.69 0.65 0.63 0.65

*5 L/min CO typical, 70 bmp HR, 120/80 mm Hg aortic pressure. †EOA Computed from Equation 8. ‡Values from Badano L, Mocchegiani R, Bertoli G, et al: J Am Soc Echocardiogr 1997; 10:632–643.

514

TABLE 23-3 -- In Vitro Hemodynamic Data for Common Mitral Valve Prostheses *

Valve Type Ball-and-cage

Valve Starr-Edwards 1260

Tilting disc

Björk-Shiley Standard

Björk-Shiley convexoconcave

Medtronic-Hall

Regurgitant EOA † Size Volume (mm) (mL/beat) (cm2 ) PI 30 1.99 0.28 28 1.66 0.27 26 1.56 0.29 31 3.40 0.45 29 6.7 2.79 0.42 25 2.15 0.44 29 10.1 2.96 0.45 27 25 31

8.3 2.28 0.40 2.03 0.41 10.0 3.53 0.47

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Bileaflet

Stented bioprostheses

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St. Jude Medical Standard

Hancock Porcine 342

Hancock II Porcine

Carpentier-Edwards Porcine 6650 Carpentier-Edwards Porcine 6900 Carpentier-Edwards Porcine 6625 Ionescu-Shiley Standard Pericardial

Mosaic Porcine

29 27 25 31

10.0 8.9 7.2 13.1

3.53 2.73 2.23 3.67

0.53 0.47 0.45 0.48

29 27 35

10.9 3.40 0.51 9.7 2.81 0.49 <4 2.72 0.28

33 31 29 27 25 33 31 29 27 25 27

<4 <4 <4 <2 <2 <4 <3 <3 <2 <2 <2

2.54 2.36 2.11 1.77 1.63 2.66 2.29 2.05 1.78 1.59 2.03

27

<2

2.68 0.47

31

<4

2.58 0.39

31

<5

3.00 0.40

27 25 33 31 29

<2 <2 <4 <3 <3

1.77 1.61 2.38 2.26 2.02

0.30 0.31 0.32 0.31 0.33 0.31 0.30 0.31 0.31 0.32 0.35

0.31 0.33 0.28 0.30 0.31

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Nonstented bioprostheses

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Mitral Valve Allograft ‡

27 25 25

23 EOA, effective orifice area; PI, performance index.

<2 <2

1.71 0.30 1.55 0.32 3.38 0.69 1.80 0.43

*5 L/min CO typical, 70 bpm HR. †EOA computed from Equation 8. ‡In vitro measurements at 5 L/min CO.

free wall orientation of the major orifice produced more physiologic left ventricular flow patterns. These results have been corroborated in in vitro flow visualization studies conducted in our laboratory, under physiologic flow conditions in an anatomically correct left ventricular model.[99] Studies by Travis et al[100] and Kleine et al[101] have examined the effects of valve orientation on forward flow hemodynamics through mechanical prostheses in the aortic position. Travis et al studied the effects of valve orientation on fluid mechanical energy loss and transvalvular pressure drop in angled in vitro models of the aortic inflow tract. Their study showed that orientation of the disc so that it is parallel to the proximal flow direction when the valve is in the open position minimizes energy loss and pressure drop for the tilting disc valve. Kleine et al used an in vivo pig model to examine the effects of prosthesis orientation on turbulent stresses. These researchers found a minimum in turbulent stress magnitude with orientation of the major orifice to the right posterior aortic wall, which is the area of highest velocities during ejection. Bileaflet Valves

The bileaflet design is characterized by two semicircular leaflets typically made of pyrolytic carbon that are hinged to the valve housing. The leaflets divide the flow into three regions, two lateral orifices and a central orifice. The primary differences between the many bileaflet valves are in the hinge design, the leaflet opening angle, and curvature of the leaflets. Hinge design variations are employed to control opening angle and influence the local fluid mechanics, washout, and flow patterns generated in the hinge, which may affect leaflet function and pressure

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515

drop. Leaflet opening angles vary from 75 to 90 degrees in the bileaflet designs in current clinical use. The bileaflet valves tend to show better bulk flow hemodynamics than the tilting disc or ball-and-cage designs. The characteristic geometry of the bileaflet design is illustrated in Figure 23-8 . Antegrade Flow.

The antegrade flow fields of bileaflet designs are characterized by three jets. Two jets emanate from the lateral orifices and one from the central orifice, as illustrated in Figure 23-12 . All three jets tend to show similar peak velocity magnitudes, independent of valve design. Greater forward flow emerges from the lateral orifices, however, than from the central orifice. The cross section of the lateral jets tends to be of a crescent shape, whereas the central jet is nearly planar in cross section. Wakes generated from the leaflets separate the three jets and persist for several centimeters downstream. The triple jet pattern is also discernible in two-dimensional color flow maps, using color Doppler ultrasound techniques as Figure 23-12 Velocity and turbulent shear stress profiles 13 mm downstream of a 27-mm St. Jude Medical bileaflet valve at peak systole. A and C, Center line profile through lateral and central orifices. B and D, Profile through the central orifice only.

illustrated in Figure 23-13 . This color Doppler flow map was obtained in pulsatile flow in vitro studies of a 31-mm St. Jude Medical bileaflet valve in the mitral position. The central jet loses its coherence after 2 or 3 cm as the lateral jets grow and merge into the central flow region. The lateral jets do maintain their coherence and relatively high velocity magnitude over a greater distance. The flow is initially well ordered during the early acceleration phase and becomes turbulent before peak systole. Separated regions with flow reversal are generally observed around the perimeter of the housing. The separated regions tend to be asymmetric around the valve with larger spatial dimensions near the hinges than adjacent to the lateral jets. This asymmetric behavior may be related to the increased thrombogenecity of the bileaflet design that occurs in the hinge regions.

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Turbulent stresses are concentrated in the leaflet wakes and in the shear layers alongside the three jets. The bileaflet design exhibits lower turbulent stresses than the 516

Figure 23-13 (color plate.) Two-dimensional color Doppler flow mapping of the downstream triple jet flow fields of a bileaflet valve design under physiologic pulsatile flow conditions.

tilting disc and ball-and-cage designs, with peak aortic values ranging from 1000 to 1500 dyn/cm.2 Peak stresses in the mitral position are less because of the lower peak diastolic transvalvular velocities. Three-component turbulent stress measurements have shown that the turbulent stress distribution is similar to that of local two-dimensional jets and wakes.[102] The onset of turbulence can be related to a Reynolds number based on the local flow properties of the jets and wakes and not on a Reynolds number based on global geometry, such as the size of the annulus or the diameter of the aorta. Understanding this turbulence structure may also provide potential leaflet design changes to minimize stress levels. As a result of this similarity with jet and wake structures, computational techniques may be able to use low Reynolds number turbulence models developed for jet and wakes. Peak aortic velocity and turbulent stress levels for clinically used 27-mm bileaflet valves are provided in Table 23-1 . Normal Regurgitant Flow.

Retrograde flow characteristics for the bileaflet design are similar to those for the tilting disc valve. Regurgitant volume characteristics are summarized in Table 23-2 and Table 23-3 . The bileaflet design shows slightly larger regurgitant volumes than the tilting disc valve. Leakage flow through the bileaflet valve design occurs primarily through the pivots. In addition, leakage is also observed around the periphery and from the gap between the two leaflets. Figure 23-14 illustrates typical two-dimensional color Doppler flow mapping images of these regurgitant jets. Velocity and turbulence measurements, obtained both within the pivots and 1 mm upstream of the valve housing in the aortic position, indicate that the major jets persist through nearly all of diastole. The mean velocity magnitudes in the jets are on the order of 2 or 3 m per second with turbulent shear stress

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levels exceeding 3000 dyn/cm.2 These high turbulent stresses, when coupled with a relatively stagnant adjacent flow regime, could lead to thrombus formation. Such a region of stagnation was noted in the pivots of the Medtronic Parallel valve. This design was voluntarily withdrawn from the market after a high incidence of thrombosis was noted in clinical trials. Explant data revealed that this thrombus was located preferentially within the inflow region of the valve pivots. Ellis et al,[103] Gross et al,[104] and Healy et al[105] subsequently performed extensive laser Doppler velocimetry measurements, computational simulations, and flow visualization studies that linked the thrombus formation within the Medtronic Parallel pivot to a persistent stagnation region at the same location. In contrast, in studies of bileaflet prostheses that have clinically acceptable rates of thrombosis, such as the St. Jude Medical Standard and Regent valve designs, no persistent regions of stagnation were found within the pivots.[106] [107] Pressure Drop Characteristics.

The bileaflet design in general has lower pressure drops than do any of the three mechanical valve designs, although the pressure drop of the Medtronic-Hall tilting disc valve is comparable to that of the St. Jude Medical Standard valve. [82] Recent bileaflet prosthesis designs, such as the St. Jude Medical Regent valve, have incorporated narrower sewing cuffs and a thinner, reinforced valve orifice to increase the Aeff and PI for a given valve size. These values as well as data from other bileaflet valve designs are tabulated in Table 23-2 and Table 23-3 . Orientation.

The bileaflet valve is mounted in one of two orientations in the mitral position. The first position is the anatomic position, with the leaflet hinge plane of the valve oriented in a direction perpendicular to the plane of the aortic outflow and mitral inflow tracts. The leaflets pivot in a similar plane as that of the native mitral valve leaflets. The second position is the antianatomic position, with the valve mounted such that the leaflet hinge plane is rotated 90 degrees from the anatomic position. The orientation of the St. Jude Medical bileaflet valve in the mitral position has been studied in in vitro flow visualization experiments conducted in our laboratory. The results of these studies indicate that the antianatomic Figure 23-14 (color plate.) Two-dimensional color Doppler flow mapping of the regurgitant jet flow field of a bileaflet valve design

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under physiologic pulsatile flow conditions.

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position provides better flow patterns along the posterior wall of the ventricle. Potentially better lateral flow expansion in the plane perpendicular to the plane of the aortic outflow and mitral inflow tracts is also observed. The anatomic position, however, provides adequate flow patterns within the left ventricle with slightly narrower lateral expansion of the inflow jets. Van Rijk-Zwikker et al[108] investigated the effects of orientation of the Carbomedics bileaflet valve in in vivo pig studies. Two-dimensional echocardiographic and color Doppler measurements were analyzed to determine the influence of valve orientation on valve function and the transvalvular flow patterns within the left ventricle. The 90-degree, antianatomic orientation was found to be superior to the anatomic orientation of the valve. The anatomic orientation resulted in diastolic backflow directed toward the valve, which may lead to asymmetric motion of the valve leaflets. The antianatomic position produced diastolic backflow patterns that enter the left ventricular outflow tract. Minimal interference with the function of the leaflets is expected from these flow patterns. The studies of Travis et al[100] and Kleine et al[101] examined the effects of aortic bileaflet valve orientation as well as tilting disc valve orientation on forward flow hemodynamics. Travis et al found that orienting the leaflets of the open valve parallel to the proximal flow direction resulted in decreases in energy losses and pressure drops in vitro. Kleine et al found that turbulence created by bileaflet valves was minimal when one of the lateral orifices faces the right posterior wall of the aorta. Ball-and-Cage Valve The ball-and-cage valve is characterized by a silicone ball mounted into a wire cage, as illustrated in Figure 23-8 . The Figure 23-15 Center line velocity and turbulent shear stress profiles 30 mm downstream of a 27-mm Starr-Edwards ball-and-cage valve at peak systole.

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only ball-and-cage valve in use today is the Starr-Edwards 1260. The cage is constructed from three wire struts separated by 120 degrees. The struts emanate from the valve housing and converge at the distal end of the valve, the apex of the cage. The ball is free to travel along the cage, typically over a 1- to 2-cm distance. Antegrade Flow.

The flow fields of these valves consist of annular jets that emerge from around the occluder or poppet. In the aortic position, the jets are initially directed toward the wall of the aorta where they impact and then follow the contour of the aortic wall. Peak systolic velocities in the aorta are comparable to those encountered in the other valve designs, approximately 2 m per second at peak systole. The annular jets show rapid development early in systole during the acceleration phase of flow. A gradual divergence and growth of the jet is observed with increasing displacement downstream, where the jet maintains its structure over a considerable axial distance. Velocity profiles at peak systole are shown in Figure 23-15 , 30 mm downstream of the valve. Large mean velocity gradients are observed alongside the annular jet, with values exceeding 1500 L per second. The flow field in the mitral position is similar to the jet structure in the aortic position; however, the jet peak velocities are lower, the jet decays more rapidly, and greater lateral expansion of the jet occurs in the ventricle. The ball generates a large wake in the central part of the flow field that starts in early systole and grows into a region of reverse flow lasting from peak to end-systole. The lateral extent of this region of reverse flow is on the order of 8 to 10 mm distal to the apex of the cage. Peak reverse velocities can be as high as 20 to 25 cm per second. These regions of large separation are responsible for the thrombogenecity of these valves.[109] The ball in these types of valves is often observed to fluctuate at the apex, which is most likely caused by flow instabilities within the wake or vortex shedding from the ball. This 518

phenomenon increases the lateral extent of the wake and produces an increase in the relative velocity between the ball and the model wall and an increase in pressure drop across the prosthesis. The turbulent stresses are concentrated in the large velocity gradients associated with the annular jets of these valves. Turbulent shear stresses as

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high as 1900 dyn/cm2 have been measured downstream of these valves in the aortic position. High turbulent stresses are observed through most of systole over a significant length downstream of the valve. The rapid turbulent stress generation indicates a quick temporal development of the jet and prolonged perseverance of the jet structure. Immediately adjacent to the ball, peak turbulent shear stresses are estimated to be as high as 3500 dyn/cm2 . The large wall shear stresses associated with the ball valve could cause damage to the endothelial lining of the aorta. The turbulent stresses measured in the annular jets are more than sufficient to cause lethal damage to red blood cells, as well as platelet damage and activation. Coupled with the large separated region behind the ball, thrombus formation on the apex of the cage is likely and has been documented in the medical literature. Normal Regurgitant Flow.

The normal regurgitant flow of the ball-and-cage design is composed mainly of the closing volume flow. The seating of the ball valve is generally very good with little or no leakage flow. Typical values of the regurgitant volume are roughly 5 mL per beat for the 25- and 27-mm valve sizes. These values are also provided in Table 23-2 and Table 23-3 . Pressure Drop Characteristics.

These valves typically show larger pressure drops than do the tilting disc and bileaflet designs. The PI and Aeff of the Starr-Edwards valve range from 0.36 and 1.62 cm2 for 25-mm size valves to 0.3 and 1.71 cm2 for the 27-mm valve. Typical values of the Aeff and PI are tabulated in Table 23-2 and Table 23-3 . The large wake region is principally responsible for the large pressure drop across the valve. Figure 23-16 Center line velocity and turbulent shear stress profiles 17 mm downstream of a 27-mm Carpentier-Edwards pericardial valve at peak systole.

Bioprostheses The most common bioprosthetic valves are composed of three biologic leaflets made from the porcine aortic valve or bovine pericardium. They are

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constructed similarly to the natural aortic valve. The annular ring is cloth covered and molded to function similarly to the aortic annulus. Metal or polymeric stents provide support to the leaflets at their commissures in the stented design, whereas the leaflet commissures in nonstented aortic valves must be attached to the native aorta for support. The clinically available designs vary mainly in the support structure and in the leaflet material and construction. All trileaflet bioprostheses, however, open to a centrally located orifice with respect to the valve annulus and mimic the open geometry of the normal aortic valve but with a smaller orifice area. Tissue valves are less thrombogenic than mechanical valves and thus do not require anticoagulant treatment; however, tissue valves exhibit higher pressure gradients than do most commonly used mechanical valves, particularly in the small sizes that exhibit stenotic characteristics. These valves also suffer from calcification of the leaflets, material fatigue leading to valve failure because of leaflet rupture or tearing, or both. Calcification of the tissue is often a precursor to leaflet rupture and tearing, as these are often observed adjacent to calcified lesions. Stented Valves Antegrade Flow.

All stented bioprosthetic valves have central jet type flow fields as illustrated in Figure 23-16 and Figure 23-17 . The newer generation porcine valves and most pericardial valves create flatter velocity profiles than do the earlier porcine valve designs. Flatter velocity profiles 519

Figure 23-17 Center line velocity and turbulent shear stress profiles 15 mm downstream of a 27-mm Carpentier-Edwards 2625 porcine valve at peak systole.

result in more evenly distributed downstream flow fields and lower turbulent shear stress levels. Early designs, such as the Carpentier-Edwards porcine model 2625 and the Hancock I porcine valves, generated asymmetric jet profiles. The jets were directed slightly away from the stent in a plane that bisected one leaflet and the stent opposite that leaflet, as illustrated in Figure 23-17 . Peak aortic velocities exceed 3 m per second at peak systole for normal flow conditions.

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The newer porcine designs, such as the Carpentier-Edwards porcine 2650, and the pericardial valves produce jets that are wider and have more blunted profiles. These jets exhibit a more axisymmetric velocity profile with large mean velocity gradients (viscous stresses) alongside the jets. Peak velocities range from 2 to 3 m per second under normal flow conditions in the aortic position. These jets still show a slight laterally directed motion similar to the older porcine valve designs, but it is not as pronounced. In in vitro experiments, stagnant flow can be observed throughout systole between the outflow surfaces of the valve leaflets and the flow model wall. In earlier valve designs, these stagnation regions were larger and exhibited regions of flow reversal. Stented bioprosthesis stagnant regions can be amplified in conditions of low cardiac output, in which one of the three leaflets may fail to open fully. Flow stasis can lead to deposition of thrombogenic elements on the outflow surfaces of the leaflets. In all stented valve designs, the turbulent shear stresses are confined to narrow regions in the shear layers of the central jets. Peak turbulent shear stresses in the aorta ranged from greater than 2000 dyn/cm2 to greater than 4500 dyn/cm2 in the early valve designs. The pericardial and newer porcine aortic valve designs exhibit lower stress levels, in the range of 1000 to 2500 dyn/cm.2 Additionally, turbulent shear stresses show a more confined spatial structure along the jet shear layers in the newer valve designs, as shown in Figure 23-15 . Turbulent shear stress levels are high enough to cause hemolysis and platelet activation. Considering the location of peak stresses adjacent to the regions of reverse flow, it may be speculated that the tissue valve would also be prone to thrombogenic events or tissue overgrowth of the sewing ring. Normal Regurgitant Flow.

All tissue valves exhibit some degree of regurgitant flow in the closing volume. Leakage volume is essentially zero in properly functioning valves. The closing volumes, however, are generally lower in bioprostheses than in the mechanical prostheses. The lower closing volumes are caused by more rapid closure of the valve leaflets for tissue valves compared with the occluders of the mechanical valve designs. Regurgitant volumes are on the order of 1 mL per beat for most tissue valves. The Ionescu-Shiley pericardial valve, however, has closing volumes ranging from 2.5 to 6.5 mL per beat, depending on valve size and position (aortic or mitral). Typical values of the regurgitant volumes for several bioprosthetic valves are given in Table 23-2 and Table 23-3 . Regurgitant jets are normally nonexistent

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and the presence of such a jet indicates valve incompetence. Pressure Drop Characteristics.

All stented porcine tissue valves are mildly stenotic compared with the natural valve in large sizes, and they are moderately to severely stenotic in the small sizes. Porcine valves in small sizes exhibit a higher degree of stenosis than do comparably sized mechanical valves. As a result, the PI of common stented porcine tissue valves ranges from 0.3 to 0.4, compared with values around 0.6 to 0.7 for similarly sized mechanical valves. This stenotic behavior is due in part to the construction of the leaflets, the stiffness of the fixed tissue, and the man-made commissures. The stents also act to restrict the motion of the leaflets somewhat during opening. Typical Aeff ranges from 1.3 to 2.5 cm2 for 21- to 27-mm porcine aortic valves, respectively.[110] The new generation of stented pericardial valves (e.g., Carpentier-Edwards, MitroFlow), however, have pressure drop characteristics comparable to the St. Jude Medical Standard and MedtronicHall mechanical valve designs in all sizes. For example, the CarpentierEdwards aortic pericardial valves (sizes 27 to 19 mm) have Aeff values ranging from 3.7 to 1.56 cm2 . The Aeff and PI values for several tissue 520

valves, both porcine and pericardial, are listed in Table 23-2 and Table 233. Nonstented Valves

Nonstented aortic valve prostheses are composed of a natural porcine valve and usually some length of the intact aorta. The original right and left coronary arteries are also ligated with short remnants to aid in reimplantation of the patient's coronaries. In vitro testing of nonstented aortic bioprostheses requires a compliant test chamber capable of simulating the human aortic root. Hemodynamic data show that aortic nonstented valves have pressure drops comparable to mechanical prostheses. [111] [112] [113] During the past few years, several investigators have begun testing and using mitral valve heterografts.[114] These mitral heterografts typically use fixed valves with or without intact papillary muscles. These new mitral replacements can be considered to be nonstented bioprostheses. Currently,

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quantitative in vitro testing of the flow fields of these valve designs is limited; however, our laboratory has begun assessing the hemodynamic characteristics of these mitral replacements. A study by Jensen et al[115] has shown that the fixation of porcine mitral heterografts in glutaraldehyde reduces orifice area and increases total regurgitation in these valves. Although no mitral valve replacements are currently approved in the United States, one design is in clinical trials in Europe. This valve, the St. Jude Medical Quattro valve, is fashioned from pericardium and offers reasonable hemodynamics. Mitral heterografts have the potential for better hemodynamic performance, reduced thrombogenesis, and improved left ventricular function. Antegrade Flow.

Currently, quantitative data on the antegrade flow fields for both aortic and mitral nonstented tissue valves are under study. Ultrasound Doppler results for a 27-mm Medtronic Freestyle valve[111] indicate that the flow accelerates uniformly through the valve with an apparent uniform and flat profile downstream of the valve. Doppler-measured peak velocities at the leaflet tips ranged from 75 to 125 cm per second at cardiac outputs from 3.0 to 5.0 L per minute. The peak velocities decreased to a range of 60 to 100 cm per second at 5 to 10 mm from the leaflet tips over the same range of cardiac outputs. There is no appearance of a jet with steep velocity gradients, as is observed in stented bioprostheses. Similar results were obtained from ultrasound Doppler measurements conducted with a 29-mm St. Jude Medical TSPV valve design. Normal Regurgitant Flow.

The nonstented aortic valves exhibit regurgitant volumes that are comparable to closing volumes of valves exhibiting similar Aeff . Good coaptation is observed with little or no leakage. Nonstented mitral valve heterografts tested in our laboratory exhibited comparable closing volumes to unfixed natural valves tested in the same flow loop. Good coaptation was observed with no leakage. The function of mitral heterografts is strongly dependent on the implantation technique, which is expected when considering the complicated function of the mitral complex compared with the aortic valve. Pressure Drop Characteristics.

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The unstented Medtronic Freestyle valve has a lower pulsatile pressure drop than comparably sized stented valves. In the 25 and 27 mm size Freestyle valves, Aeff was comparable to the St. Jude Medical Standard bileaflet valve, whereas in smaller sizes it was comparable to the St. Jude Medical Regent valve. The Medtronic Freestyle and Mosaic porcine valves use the exact same tissue, treated with the same processes. The Aeff of a 23mm Medtronic Freestyle stentless valves, however, was found to be similar to that of a 27-mm stented Mosaic valve. Thus, removal of bioprosthetic valve stents definitely creates less forward flow obstruction and significantly improves overall hemodynamic performance. The Aeff for several sizes of the Medtronic Freestyle porcine valve are listed in Table 23-2 and Table 23-3 . Because of the added complexity of the unstented design and the increased factors governing selection and style, optimal flow performance of these valves both in vitro and in vivo depends on the type of valve configuration used for a particular patient geometry and on the proper sizing of the valve. Improper selection of style and size can compromise hemodynamic performance of the valve. In vitro tests of the Medtronic Freestyle valve indicate that the Aeff can be optimized by using a valve one size larger than the size of the simulated aorta. Thus, a 23-mm valve should be used in a 21-mm aorta. Total root or an inclusion cylinder valve geometry technique showed better Aeff results than partially or fully scalloped valve configurations. Pressure drops for mitral valve heterografts are generally higher than normal mitral valves, owing to stiffening of the valve tissue resulting from fixation. Homograft Valves

Homograft valves are cryopreserved human valves, and they have been used for more than two decades in the aortic position. With the advent of improvements in surgical techniques and viable mitral heterografts, a mitral homograft is also a possibility. Aortic homografts are typically implanted as a complete valve, annulus, and aortic section. As a result, the effective annulus area is reduced from the original aortic valve annulus before replacement. Mitral homografts consist of intact mitral valves with annulus, papillary muscles, and chordae tendineae. Antegrade Flow.

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The flow field characteristics of the homograft aortic valves are similar to those of the natural valve, although peak velocities are slightly higher because of a reduced Aeff resulting from the smaller area of the outflow tract. Peak velocities, however, are smaller in homograft valves than those observed in other prosthetic designs for comparably sized valves. The aortic homograft shows excellent hemodynamics over the entire size range in contrast to the stented bioprostheses, which show increased stenosis in the smaller valve sizes. Studies conducted in our lab indicate that sheep allograft mitral valves and untreated normal mitral valves have excellent hemodynamics compared with that of stented valves.[115] The unfixed mitral valves exhibit both qualitatively and quantitatively similar forward flow characteristics to those observed clinically for normal human mitral 521

Figure 23-18 Planar two-dimensional transmitral flow patterns in the left ventricle during diastole. Images were obtained from in vitro planar flow visualization experiments of natural, untreated mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.)

valves. The qualitative left ventricular flow fields during diastole are illustrated in Figure 23-18 . This figure shows the in vitro flow patterns for the natural mitral valve using a two-dimensional planar flow visualization technique outlined in Lefebvre.[99] These experiments were conducted in an anatomically correct left ventricular model constructed of polished transparent acrylic. The models were manufactured so that the native mitral valve complex, including papillary muscles and chordae tendineae, could be implanted and tested under normal physiologic conditions. Figure 23-19 illustrates the model and relationship of a native valve mounted in the model. Normal Regurgitant Flow.

As with other bioprosthetic valves, the homograft valves exhibit small closing volumes. Properly functioning homograft valves should exhibit little or no regurgitation caused by leakage. The mitral homografts show the same dependency of implantation technique on overall hemodynamics. Proper implantation of the valve complex including proper alignment of the

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papillary muscles with the valve annulus results in superior function with no regurgitation other than normal closing volume. Pressure Drop Characteristics.

The homograft valves show low pressure drops with large Aeff compared with mechanical and stented valves. Vetter et al[116] conducted in vitro tests of 23- and 25-mm mitral homograft valves at physiologic conditions of 5 L per minute CO and 70 bpm HR to measure the pressure drop and Aeff characteristics of these valves. Measured pressure drops ranged from 10.4 to 3.4 mm Hg for the 23- and 25-mm valves, respectively. The corresponding Aeff ranged from 1.8 to 3.4 cm2 . These values are comparable to 25- and 27-mm Hancock 342 and Hancock II bioprostheses, indicating a significant improvement in hemodynamics for similar valve size. Typical values for the Aeff and PI of homograft valves are listed in Table 23-2 and Table 23-3 .

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions We foresee that the future direction of prosthetic valve research will follow several courses: tissue-engineered bioprosthetic valves; invention of novel tissue fixation techniques; improved mechanical valve design; improved in vitro, computational, and animal testing protocols; and development of noninvasive diagnostic capabilities. Conceptually, tissue-engineered valves would hold the most promise for a near-perfect valve replacement. The goal of this research is to grow living human aortic valves in the laboratory, preferably using the patient's own tissue. Potential advantages involve total acceptance of the living tissue, with hemodynamic and cellular function similar to the normal human aortic valve, resulting in a lifetime equal to that of native valves. Tissue xenografts are currently fixed in glutaraldehyde, which stiffens the compliance of the valve material and hinders hemodynamic performance. [115] Other fixative techniques may improve hemodynamic performance or increase the functional lifetime of xenografts. For mechanical valves, the focus will be on reducing their thrombogenic properties. This goal could possibly be achieved by development of biocompatible surface coatings and materials, or by changing valve geometry to improve closure and leakage flow through these valves. [117] A first step in this research should be to improve understanding of blood element damage, thromboembolic events, and thrombus formation. As we enrich our understanding of these topics, in vitro evaluation techniques and in vivo diagnostic capabilities should also improve.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Acknowledgments The work reported from our laboratory has been supported by grants from the Food and Drug Administration, Figure 23-19 The anatomically correct left ventricular in vitro model used in the testing of nonstented and homograft mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.)

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the American Heart Association, the heart valve industry, and generous gifts from Tom and Shirley Gurley and the Lilla Boz Foundation.

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525

Chapter 24 - Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction Miguel Zabalgoitia MD

After more than 3 decades of clinical experience, the search for the "ideal" artificial heart valve continues with increasing interest. Thirty years ago, prosthetic valves were limited to the ball-and-cage mechanism; since then, single and double tilting discs and several stented and nonstented biologic devices have been introduced. Each of these valves is accompanied by individual ultrasonic and hemodynamic characteristics (see Chapter 23) , making the roles of the echocardiographer and sonographer understandably more complex. The optimal management of patients with prosthetic valves requires serial assessment of valve function and left ventricular performance. Symptoms of fatigue, dyspnea, and exercise intolerance may be caused by valve dysfunction or a variety of comorbid conditions. Doppler echocardiography is the imaging modality of choice in evaluating patients with known or suspected prosthetic valve dysfunction because it provides information regarding valve structure, hemodynamics, native valve status, and left ventricular function.[1] [2] [3] Since its clinical introduction more than a decade ago, transesophageal echocardiography (TEE) has been widely

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accepted as a tool that allows superior anatomic and functional assessment of native and prosthetic valves.[4] [5] [6] TEE now is a routine diagnostic procedure in assessing prosthetic heart valves. Three-dimensional (3D) echocardiography is an evolving new technology with a wide range of potential clinical applications, and evaluation of prosthetic heart valves, particularly tissue valves, may be one of them. Other available methods for assessing prosthetic valves include cardiac catheterization with angiography for both hemodynamic and structural information. Cardiac catheterization also provides the opportunity to perform fluoroscopy in the case of metallic valves. The potential use of magnetic resonance imaging in assessing prosthetic valve function has been suggested by a comparative study detecting pathologic prosthetic regurgitation.[7] Further studies are needed to determine the most appropriate clinical setting for this imaging modality. Nowadays, it is impossible to ignore the impact that economics has on our daily practice. Evaluation of cost and effectiveness of diagnostic testing is complex; it involves the test itself and the treatment strategies that follow. [8] In this regard, one must answer the following questions: Do the test results affect the decision-making process?; Do the test results lead to the treatment of choice?; What is accuracy of the testing?; What is the cost?; and What is the morbidity due to the test? Although a detailed ultrasound cost analysis of prosthetic heart valves is lacking, the subject offers a useful frame of thought, and the answer to each of the above-mentioned questions is clearly favorable. In fact, the perception of most clinicians is that Doppler echocardiography in patients with prosthetic heart valves is a highly cost-effective tool.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prosthetic Heart Valve Classification Several types of prosthetic heart valves, divided into mechanical and biologic categories based on their primary 526

TABLE 24-1 -- Classification of Prosthetic Heart Valves Mechanical Ball-and-cage (Starr-Edwards) Single tilting disc (Medtronic-Hall, OmniScience) Double tilting disc (St. Jude Medical, Carbomedics) Biologic Heterograft stented (Hancock, Carpentier-Edwards) Heterograft nonstented for aortic valve (Toronto SPV, Medtronic Freestyle, and CryoLife-O'Brien) Heterograft nonstented for pulmonic valve (CryoLife-Ross) Homografts (aortic, pulmonic, and mitral) manufacturing material, are available for implantation. Table 24-1 lists the most common prosthetic heart valves currently used in clinical practice. Mechanical Valves Ball-and-Cage.

The first successful valve replacement used a ball-and-cage design, [9] [10] and after several modifications, only the Starr-Edwards valve has endured with an estimated usage of more than 200,000. It consists of a Silastic ball

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with a circular sewing ring and a cage formed by metal arches located around the sewing ring (Fig. 24-1) . The silicone rubber ball retracts toward the apex of the cage as antegrade blood flows through the valve orifice and between the ball and the stents. [11] Single Tilting Disc.

A single disc tilting valve consists of a circular sewing ring with a circular disc eccentrically attached by lateral or central metal struts. MedtronicHall, Figure 24-1 Mechanical heart valves. Starr-Edwards (S-E), MedtronicHall (M-H), OmniScienct (Omni), and St. Jude Medical (SJM).

Björk-Shiley, and OmniScience are representatives of this group. The first successful low-profile design was the Björk-Shiley, introduced in 1969,[12] with an estimated usage of 360,000. The Björk-Shiley valve has been discontinued from the United States market. When the pyrolytic carbon disc opens, blood flows through two unequal (major and minor) orifices and the disc opens with an angle ranging from 60 to 80 degrees, which favors closure by a backflow mechanism (see Fig. 24-1) . This angle results in resistance to flow around the disc and stagnated flow behind the disc, a site of potential thrombus formation. Double Tilting Disc.

Bileaflet valves have two semicircular pyrolytic carbon discs attached to the valve ring by two small midline hinges. St. Jude Medical and Carbomedics are the prototypes of this group (see Fig. 24-1) . The bileaflet design was introduced by St. Jude Medical in 1977 and has been used over 600,000 times. Mechanical valves are extremely durable with overall actuarial survival rates ranging from 94% ± 2% at 10 years for the St. Jude Mechanical valve to between 60% and 70% at 10 years for the Starr-Edwards valve.[13] [14] [15] Primary structural abnormalities are very rare,[16] [17] [18] and most valve malfunctions are caused by perivalvular leak, endocarditis, and thrombosis. Chronic anticoagulation is required in all patients with mechanical valves to prevent valve thrombosis and embolic events. With adequate

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anticoagulation, the rate of thrombosis is 0.6% to 1.8% per patient-year for bileaflet valves.[13] [19] [20] Biologic (Tissue) Valves Stented Bioprostheses.

Porcine valves currently in use are the Hancock and Carpentier-Edwards. The leaflets are treated with glutaraldehyde to reduce antigenicity, but they are less pliable than normal human valves.[21] The Carpentier-Edwards porcine valve has a stent made from a single piece of wire and the three leaflets are mounted above the sewing ring, allowing a larger orifice area and a better hemodynamic profile. Both porcine bioprostheses have a similar macroscopic appearance, but they are easily distinguishable by their radiographic appearance; Hancock appears as a circular ring whereas Carpentier-Edwards appears as a crown. The Ionescu-Shiley bioprosthesis from bovine pericardial tissue was discontinued after 10 years of use because of dehiscence.[22] The Carpentier-Edwards pericardial (Perimount) valve is currently available, but unlike the Ionescu-Shiley, which used retention sutures to attach the leaflets, the Perimount valve is mounted within the stent to maximize cusp opening and to reduce abrasion between tissue and stent. The long-term results with this valve are very encouraging. A major advantage of bioprosthetic valves is the low rate of thromboembolism (1.6% per patient-year) in the absence of chronic anticoagulation[23] however, stented heterograft valves are subject to progressive calcific degeneration and failure typically after 6 to 8 years of implantation.[24] [25] [26] [27] [28] [29] Calcific degeneration is faster in children, young adults, and patients with abnormal calcium metabolism.[30] [31] In several large series, the rate of degeneration for porcine valves was 3.3% per patient-year and a freedom 527

from valve failure rate for aortic valves was 78% ± 2% and for mitral valves was 69% ± 2%.[23] [32] [33] After 10 years, the rate of deterioration accelerates abruptly with freedom from valve failure rates of 49% ± 4% for aortic and 32% ± 4% for mitral prostheses.[32] Using the porcine bioprosthesis in patients over 70 years of age, a 90% freedom from valve replacement at 12 to 15 years has been reported.[33] [34] This finding may be related to a decreased rate of degeneration in elderly patients or an increased rate of death from other than valve-related causes in the group of

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patients who did not outlive their prostheses. Nonstented Bioprostheses.

Nonstented heterografts are expected to improve hemodynamics and longterm durability while retaining the fundamental advantages of tissue valves. The goals are to return the patients to their own baseline conditions as is feasible, prolong survival, and improve quality of life. The absence of the stent and sewing cuff make it possible to implant a larger valve for a given annular size, resulting in a greater effective orifice area. A nonstented bioprosthesis uses the patient's aortic root as the valve stent, absorbing the motion stress induced during the cardiac cycle and leading to better hemodynamic performance. Nonstented bioprostheses include the Toronto SPV,[35] [36] Medtronic Freestyle,[37] [38] [39] [40] and CryoLife-O'Brien.[41] [42] [43] There are several variations within the same valve, depending on the patient's needs and the surgeon's preference. These variations include the full root technique with reimplantation of the coronary arteries, the root inclusion technique with preservation of the native coronary arteries, or the subcoronary technique. Figure 24-2 depicts a subcoronary implantation. Removal of the stent appears to eliminate much of the stress that promotes calcification and valve deterioration. Nonstented bioprostheses typically are manufactured from intact porcine aortic valves processed at very low fixation pressures. Moreover, some valves (i.e., Medtronic Freestyle) are treated with the anticalcificant amino-oleic acid, which may further decrease calcific deposits. The addition of a layer of polyester fabric around the graft adds support and aids implantation.[44] [45] Nonstented valves have been used primarily in the aortic position in men older than 60 years of age. The reported operative mortality rate for patients with nonstented valves is 3% to 6%,[46] [47] but these figures are probably affected by patient selection. Postoperative complications at 12 months appear to be low, with endocarditis reported at 1% to 2%, thromboembolism at 2% to 3%, and hemorrhage at 1.5%.[44] [46] [47] There have been no reports of primary structural failure, and the reported survival rates have been as high as 91% ± 4% at 6 years.[44] [47] [48] The CryoLife-Ross valve is a pulmonary nonstented bioprosthesis made of three noncoronary porcine cusps used to correct congenital defects involving the pulmonic valve, and they can also be used during the Ross procedure as described later.

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Homografts.

Homografts are antibiotic-sterilized, cryogenically-preserved valves harvested from cadaveric human hearts.[49] Their major advantages are relative resistance to infection, lack of need for chronic anticoagulation, and excellent hemodynamic profile, most notably in Figure 24-2 Drawing of a nonstented aortic valve (Toronto SPV) at the subcoronary position. (Courtesy of St. Jude Medical, Inc., St. Paul, Minn. All rights reserved. Copyright © 2001 St. Jude Medical, Inc. Toronto SPV is a registered trademark of St. Jude Medical, Inc.)

smaller aortic root sizes.[50] [51] As illustrated in Figure 24-3 (Figure Not Available) , homografts have been developed for the aortic, pulmonic, and even for mitral valves. The technical aspects of homograft preparation and the meticulous and highly skilled freehand surgical technique required for implantation in some cases have limited their use on a routine basis. Typically, homografts are inserted without a stent, using the patient's natural fibrous annular tissue for support. Ross Procedure.

The pulmonic autograft (or Ross procedure), first described in 1967,[52] consists of replacing the abnormal aortic valve with the native pulmonic valve of the same patient, then placing a nonstented homograft or porcine bioprosthesis in the pulmonic position. The operation is technically demanding; the pulmonic valve is removed with healthy tissue above and below the valve insertion. This procedure requires some reconstruction of the right ventricular outflow tract. In addition, the coronary arteries are reimplanted into the pulmonary artery trunk that serves as the new aortic root. Although the Ross procedure involves two valve operations (aortic valve autograft and pulmonic valve nonstented allograft) to correct one diseased valve, it provides optimal hemodynamics and echocardiographic performance and low valve-related complication rates.[53] The main longterm problem with this operation has been degeneration and failure of the right-sided valve caused by obstruction in the distal segment of the homograft conduit.[54] [55] Early 528

Figure 24-3 (Figure Not Available) Drawing of cardiac anatomy depicting the

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availability of homografts for the pulmonary, aortic, and mitral valves. (Courtesy of CryoLife, Kennesaw, Ga.)

autograft failure (<6 months) most often is due to technical errors or persistent endocarditis, and late failures generally are due to aortic annulus dilation, endocarditis, or valve degeneration.[56] [57]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Fundamental Principles Pertaining to Prostheses Modified Bernoulli Equation Blood flow velocity through a narrow orifice is related to the pressure difference between two chambers as described by the Bernoulli principle used to convert flow velocity (m/sec) to pressure gradient (mm Hg). The modified Bernoulli equation used in prosthetic valves is the same as that used in native valves: Pressure gradient = 4(VMAX )2 where VMAX is the maximal (peak) velocity across the valve orifice. It is

important to recognize that the modified Bernoulli equation neglects the effects of acceleration and viscous losses, and yet it has proved to be remarkably accurate when compared with catheter-derived pressure gradients when both are obtained simultaneously.[58] [59] [60] [61] [62] [63] When the left ventricular outflow tract velocity (V1 ) is greater than 1 m per

second, such as in patients with concomitant aortic regurgitation, V1 should

be subtracted from VMAX . Maximal instantaneous and mean gradients

should be calculated for aortic valves, and mean gradient should be calculated for mitral valves. A high gradient in the setting of anemia, tachycardia, or sepsis does not necessarily indicate stenosis; conversely, an upper normal limits gradient in the setting of severe left ventricular dysfunction may indicate significant stenosis. Pressure Recovery Recording valve gradients that appear to be an "overestimation" when compared with those at catheterization may result from distal pressure recovery, which refers to the conversion of kinetic energy present at the

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valve level to pressure energy distal to the valve.[64] [65] When flow passes through the prosthesis, components of velocity and momentum are directed centrally, causing the flow stream to contract distally for a short distance. This point of maximal constriction is called vena contracta and occurs downstream distally from the anatomic location of the prosthesis. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure or pressure recovery. Under these circumstances, when the aortic pressure is measured in the upper ascending aorta (distal to the vena contracta), the pressure difference between the left ventricle and the aorta is less than the aortic pressure measured at the vena contracta. The degree of pressure recovery may be as high as a mean of 10 mm Hg in small St. Jude Medical valves challenged under physiologic flow rates. The magnitude of pressure recovery is greater with larger valve areas and with smaller aortic roots; therefore, patients with severe prosthetic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and normal aortic root diameter. Pressure recovery and vena contracta are important concepts to keep in mind when Doppler- and catheter-derived pressure gradients are being compared. Because continuous wave Doppler measures velocity at the level of the vena contracta (physiologic variable) and catheterization measures the difference between left ventricle and the fully recovered static pressure in the aorta, catheter-derived data must be interpreted with caution. Failure of the invasive technique to record the gradient at the vena contracta level may explain some of the reported discrepancies.[66] Continuity Equation An important limitation of Doppler velocities (and pressure gradients derived thereof) is that they are flow volume rate dependent. When transvalvular flow is decreased, such as in patients with significant left ventricular systolic dysfunction, Doppler velocities may only be moderately elevated despite severe obstruction. Thus, comparisons may be confounded by interval changes in flow volume rate. For these reasons, estimation of valve areas, in addition to mean pressure gradients, should be routinely calculated. The equation of continuity can be used to estimate aortic and mitral valve areas. Figure 24-4 illustrates how to apply the continuity equation in aortic prostheses:

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AVA = (ALVOT × VTILVOT )/VTITRANSPROSTHESIS

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Figure 24-4 Effective orifice area (EOA) calculation for an aortic valve prosthesis. The left panel corresponds to the outflow tract (subvalvular) velocity, also known as V1 . The middle panel corresponds to the prosthesis velocity, also known as V2 . The right panel corresponds to the parasternal long-axis view, showing the outflow tract diameter (arrows). Ac, aortic closure; AO, aorta; Ao, aortic opening; LA, left atrium; LV, left ventricle; RV, right ventricle; subvalve, subvalvular; vel. int., velocity integral.

where ALVOT is the cross-sectional area of the outflow tract at end-systole measured just underneath the prosthesis from the parasternal long-axis view. VTILVOT is the velocity time integral proximal to the valve as seen

from an apical view using pulsed wave Doppler. One must be careful placing the sample volume immediately adjacent to the aortic prosthesis from the apical five-chamber view while avoiding the region of subvalvular acceleration. The Doppler wave form should be smooth with minimal spectral broadening and a well-defined peak. VTITRANSPROSTHESIS is the

velocity time integral across the prosthesis using continuous wave Doppler. Because the direction of the jet may be eccentric, all acoustic aortic windows (apical, suprasternal, and right parasternal) should be carefully examined to detect the highest velocity signal. Continuity equation valve areas have been compared with invasively obtained data for bioprosthetic[67] [68] [69] and mechanical valves.[70] [71] The largest source of variability is the accurate and reliable measurement of the left ventricular outflow tract. When this diameter is difficult to obtain from the precordial window, TEE offers an excellent alternative for calculation of aortic valve area.[72] For mitral valve area (MVA), the continuity equation is as follows: MVA = (AVA × VTIAORTIC )/VTITRANSPROSTHESIS where AVA is the cross-sectional aortic valve area as measured from the

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parasternal long-axis view, VTIAORTIC is the velocity time integral across the native aortic valve, and VTITRANSPROSTHESIS is the velocity time

integral across the mitral prosthesis.[73] Because the continuity equation is based on the principle of conservation of mass, it assumes that flow across the mitral prosthesis and that across the second valve are equal. Thus, in patients with greater than mild mitral regurgitation, the preferred method to estimate valve area is the pressure half-time. In the presence of aortic regurgitation, the pulmonic valve area and flow can be used in lieu of the aortic valve. The limiting step in using the pulmonic valve is the accurate and reproducible measurement of the right ventricular outflow tract diameter from the precordial approach. An important advantage of the continuity equation is its relative independence from valvular gradient and chamber compliance.[74] Data acquisition for the continuity equation, however, is more cumbersome than the pressure half-time. Doppler Velocity Index The Doppler velocity index (DVI) is a dimensionless ratio of the left ventricular outflow tract to prosthesis velocities: DVI = VLVOT /VTRANSPROSTHESIS Because it is independent of valve size, this index can be particularly helpful when the cross-sectional area of the outflow tract cannot be obtained. Because the velocity proximal to the valve is subtracted from that across the prosthesis, the patient serves as his or her own control, 530

with flow being the main dependent factor. The higher the index, the larger the area; the lower the index, the smaller the area. Index values calculated from 25 patients with normally functioning St. Jude Medical aortic valves were 0.39 ± 0.07, range 0.28 to 0.55. In a small group of patients with severe stenosis of St. Jude Medical aortic valves requiring reoperation, the DVI was 0.19 ± 0.05, range 0.12 to 0.27, which was significantly different from normal values at the 0.05 level.[75] Valve Resistance Resistance is the quotient of gradient and flow (R = ∆P/Q). This

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hemodynamic parameter suggested by Ford et al[76] is an alternative to the Gorlin formula in assessing severity of native aortic stenosis. It can be calculated from echo-Doppler data as follows: Resistance = 1.33 ∆P (ET/SV) where ∆P is the mean pressure gradient in mm Hg, ET is the ejection time in seconds, and SV is the stroke volume in mL per minute. The ratio of mm Hg to mL per minute is converted to dyne-sec-cm5 when multiplied by 1.33. In conditions characterized by variation of flow, valve resistance remained more constant than the Gorlin estimated area. In considering valve resistance, however, one must recognize that most data have been derived from native valve stenosis, not from prostheses; no information is available during changing flow conditions, such as exercise; and there is virtually no clinical data in prosthetic mitral valves. Saad et al[75] studied two groups of patients with prosthetic aortic malfunction (predominant stenosis versus predominant regurgitation) and compared them with a control group. Effective orifice area (continuity equation), Doppler velocity index, and valve resistance were all very helpful in separating the groups. It is unclear, however, whether valve resistance per se added clinically significant information beyond that derived by valve area and Doppler velocity index. An important role of valve resistance in artificial valves may be in patients with small aortic valve areas, relatively low flow velocities, and severe left ventricular systolic dysfunction, to differentiate severe prosthetic valve stenosis from a low cardiac output state, which has been shown to be useful in patients with native aortic stenosis.[77] Pressure Half-Time The pressure half-time is the time required for the peak velocity to decline by a factor of 1 divided by the square root of 2, and it can be helpful in separating normal from obstructed prostheses. The pressure half-time is dependent on several factors, including atrial and ventricular compliance, ventricular stiffness, and, of course, the actual effective orifice area (EOA). Pressure half-time is used to calculate the EOA of mitral and tricuspid valve prostheses based on the inverse relationship between pressure halftime and valve area[78] EOA (cm2 ) = 220 / pressure half-time (msec)

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Validation of this method with invasive data has showed good correlation. Kapur et al[79] compared mitral valve areas derived by pressure half-time with those derived by the Gorlin formula in 32 patients with mitral valve prosthesis and found correlations of 0.94 and 0.79 for bioprosthetic and mechanical valves, respectively. In contrast, Wilkins et al,[59] using simultaneous catheterization and Doppler techniques in 11 patients with mitral prosthesis, found poor correlation. This method relies on the constant, 220, which was originally derived for native rheumatic mitral stenosis. Application of this constant to the wide variety of valve types and sizes cannot be expected to yield predictable results.[3] The continuity equation is an excellent alternative to the pressure half-time to calculate mitral valve area. [80] Leakage Backflow Prosthetic mechanical valves have a normal regurgitant volume known as leakage backflow that occurs when the valve occluder has already been seated and blood leaks into the proximal chamber between and around the occluder assembly. In theory, this "built-in" regurgitation prevents stasis and thrombus formation by a "washing" mechanism. The jets of leakage backflow are characterized by being short in duration, narrow, symmetrical (bileaflet valves), and having low velocities (nonaliasing) encoded in a homogeneous color—red or blue, depending on the transducer location (assuming Nyquist limit >0.53 m/sec). [81] [82] The normal regurgitant jets in the Carbomedics valve are larger than those of the St. Jude Medical. Abnormal jets, on the other hand, are longer in duration, wider, larger, asymmetrical across the valve midline, frequently eccentric ("hugging the wall"), extending far into the receiving chamber, and display a mosaic pattern reflecting high-velocity, turbulent flow. A jet with an unusual angle (i.e., one anteriorly directed toward the atrial appendage) is also typical of a paravalvular leak. Figure 24-5 depicts the typical appearance of a normal backflow in a bileaflet mitral valve (see Fig. 24-5A) . In contrast, a larger, wider, eccentric jet "hugging" the left atrial lateral wall characteristic of severe perivalvular regurgitation is seen (see Fig. 25-5B) . Table 24-2 highlights the differences between physiologic leakage backflow and pathologic regurgitant jets. TABLE 24-2 -- Physiologic Leakage versus Pathologic Regurgitation of

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Mechanical Prosthesis Jet Feature Size Symmetry Aliasing Eccentric

Physiologic Leakage Short and narrow Symmetrical (bileaflet valves) No (low velocity) No

Pathologic Regurgitation Large and wide Asymmetrical Yes (high velocity) Yes

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Figure 24-5 (color plate.) TEE longitudinal views of a normal CarboMedics valve in the mitral position (A). Two symmetrical regurgitant backflow jets are seen within the left atrium (LA). These jets are low velocity, nonaliased, and encoded in red. In contrast, a pathologic periprosthetic leak is seen in an abnormal valve (B). The jet is high velocity, mosaic in color, and eccentric, and it encircles the left atrial wall (open arrow). The normal regurgitant backflow jets (solid arrows) are also seen. See Table 24-2 for differentiation of physiologic versus pathologic jets.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography of Normal Prosthetic Valve Function In general, the same principles used in native valves are applicable to artificial valves. Echocardiography has some limitations related to reverberations and shadowing from the interface between ultrasound and the foreign material composing the valve.[83] Intense reverberations projected behind the prosthesis can mask normal structures or instead create artifacts, leading to a misdiagnosis. Table 24-3 describes common limitations and technical errors or "pitfalls" as well as suggestions on how to overcome or minimize their impact. A complete examination should include estimation of pressure gradients and valve area, degree of normal or TABLE 24-3 -- Echocardiography of Prosthetic Valves: Pitfalls Technical Limitations or Pitfalls Suggestions Acoustic shadowing Use window in which ROI is not obscured by the valve's artifact. Consider TEE. Failure to detect peak Image from multiple windows. velocity Under- or Include proximal velocity in continuity equation if overestimation of it is >1 m/sec. valve gradient or effective orifice area Consider pressure recovery. Use mean valve gradient, not "peak-to-peak" or maximal instantaneous gradient. Unexpectedly high Consider high cardiac output setting, i.e., valve gradient or small tachycardia, anemia, sepsis.

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effective orifice area Calculate DVI and valve resistance. Compare to previous echo study. Consider prosthesis-patient mismatch. Consider valve thrombosis (TEE?). Consider pannus formation (TEE?). DVI, Doppler velocity index; ROI, region of interest; TEE, transesophageal echo. abnormal regurgitation, left ventricular size and function, native valve structure and function, and calculation of the pulmonary artery systolic pressure. M-mode recording may assist in evaluating disc or leaflet excursion, whereas color M-mode recording may assist in timing regurgitant jets. Two-dimensional (2D) imaging should begin by identifying the sewing ring, the occluder mechanism, and the surrounding area. The ball or disc is often indistinctly imaged because of echo reverberations. The leaflets of normal tissue valves should be thin with an unrestricted motion. A very helpful and frequently overlooked parameter for evaluation of prosthetic valves is comparison with prior studies. The importance of a timely baseline postoperative study cannot be overemphasized. In our institution we routinely perform an ultrasound examination prior to hospital discharge, or in the patient's first clinic visit. This initial study establishes the baseline gradients and area, the postoperative ventricular systolic function, and the systolic pulmonary artery pressure for that particular patient, at that particular time. This anatomic and hemodynamic profile is subsequently used whenever prosthetic dysfunction becomes a concern. How often "routine" echocardiographic follow-up studies should be performed is a controversial topic. Table 24-4 lists the recommended schedule for early and long-term follow-up of prosthetic heart valve evaluation. Follow-up for nonstented bioprostheses and homografts clearly should be different from stented bioprostheses, because nonstented bioprothesis deterioration rates are lower. The effective orifice area is not the sewing ring orifice; it is the remaining area not occupied by the valve occluder assembly. Normally functioning mechanical and stented bioprostheses, therefore, have higher velocities than native valves. The smaller the size of the bioprosthesis, the smaller the

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effective orifice area, and the higher the flow velocities. For homografts and the newest nonstented bioprostheses, the hemodynamic profile is near normal. Table 24-5 and Table 24-6 provide the normal range of in vivo velocities for mechanical and bioprosthetic valves in the aortic and mitral positions, respectively.

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TABLE 24-4 -- Recommended Doppler Echocardiography Follow-up in Patients with Prosthetic Heart Valves Patient Category EARLY POSTOPERATIVE Any type of valve LONG-TERM FOLLOW-UP Stented Bioprosthesis Clinically normal

Recommendation Baseline study in all patients

Every 2 years for the first 6 years, then every year for 4 years, then every 6 months Patient-prosthesis mismatch Once a year Chronic renal failure Once a year Nonstented Bioprosthesis and Homografts Clinically normal Every 2 or 3 years Mechanical Valves Clinically normal Every 2 or 3 years Patient-prosthesis mismatch Once a year

Echocardiographic Features by Valve Type Ball-and-Cage.

The Silastic ball produces multiple echoes from its leading edge, obscuring other aspects of its structure. Flow through a normally functioning ball-andcage valve is characterized by turbulence created by the high-profile ball in the center of the blood stream and by the eddies created as flow circulates retrogradely (Fig. 24-6) . Consequently, when compared with single and

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double tilting disc valves, the hemodynamic performance of the ball-andcage valve is less, with higher pressure gradients. This hemodynamic profile increases its intrinsic thrombogenicity because of blood cell damage.[15] Color flow in a normal ball-and-cage valve includes lowvelocity closure backflow (2 to 5 mL per beat).[11] [84] Single Tilting Disc.

Figure 24-7 illustrates a single tilting disc valve in the mitral position. The left panel illustrates the typical antegrade flow through the major and minor orifices in the correct orientation (major orifice toward the lateral aspect, away from the outflow tract) as opposed to the incorrect orientation seen on the right panel. Typical flow velocity of a single tilting disc valve is TABLE 24-5 -- Normal Doppler Values for Aortic Prostheses ‡

Type Starr-Edwards Björk-Shiley St. Jude Medical Medtronic-Hall OmniScience Hancock CarpentierEdwards Aortic Homograft Toronto SPV † Freestyle † O'Brien †

Peak Velocity (m/sec) 3.1 ± 0.5 2.5 ± 0.6 3.0 ± 0.8 2.6 ± 0.3 2.8 ± 0.4 2.4 ± 0.4 2.4 ± 0.5

Mean Area Mean Gradient (mm Hg) (cm2 ) * 24 ± 4 * 14 ± 5 * 11 ± 6 * 12 ± 3 * 14 ± 3 11 ± 2 1.8 14 ± 6 1.8

Area Range (cm2 ) * * * * *

1.4–2.3 1.2–3.1

1.8 ± 0.4

7±3

2.2

1.7–3.1

2.2 ± 0.4 2.2 ± 0.4 2.2 ± 0.4

3±4 3±4 3±4

2.2 2.2 2.2

2.0–2.8 2.0–2.8 2.0–2.8

‡Data from references [5] [11] [14] [18] [19] [23] [38] [40] [41] [46] [51] [58] [67] [68] [69] [75] [88] [90] [95] and [103] . *Insufficient data available. †Nonstented bioprostheses.

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Figure 24-6 A, Normal diastolic intracavitary flow pattern. B, Disturbed antegrade flow across a ball-and-cage valve. Note the high-profile ball located in the center of the blood stream, creating turbulence and eddying as flow changes direction.

around 2 m per second. Flow through the minor orifice consists of two jets separated by a well-defined wake behind the tilting disc but with a velocity similar to the major orifice. The appearance of the disc is characterized by echoes produced by its motion. Color flow in these valves includes a small amount of normal backflow (5 to 9 mL per beat), originated from small gaps around the perimeter of the valve. [85] [86] Hixson et al[81] have reported that the Medtronic-Hall valve has a large central regurgitant backflow that can extend back into the left atrium with aliasing, whereas the peripheral jets are nonaliasing, low-velocity flow. Double Tilting Disc.

Figure 24-8 illustrates the anatomic orientation of a bileaflet valve in the mitral position during diastole and normal mitral inflow. The blood flow is near-laminar with a path similar to the laminar flow of the native valve. In the opening position, the hemidiscs appear as parallel lines with a short angle between them. Imaging of the normal valve includes the sewing ring and two distinct echoes in the opening position and a wide obtuse angle in the closing position. Identification of the two hemidiscs may be problematic with the standard approach of transthoracic echocardiography (TTE), particularly in the aortic position. However, multiplane TEE at the upper and midesophageal level can better visualize the hemidiscs for aortic and mitral positions.

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TABLE 24-6 -- Normal Doppler Values for Mitral Prostheses *

Type Starr-Edwards Björk-Shiley

Peak Velocity (m/sec) 1.8 ± 0.4 1.6 ± 0.3

Mean Gradient (mm Hg) 4.6 ± 2.4 5.0 ± 2.0

Area Mean (cm2 ) 2.1 2.4

Area Range (cm2 ) 1.2–2.5 1.6–3.7

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1.6 ± 0.3 1.7 ± 0.3 1.8 ± 0.3 1.5 ± 0.3 1.8 ± 0.2

5.0 ± 2.0 3.1 ± 0.9 3.3 ± 0.9 4.3 ± 2.1 6.5 ± 2.1

2.9 2.4 1.9 1.7 2.5

1.8–4.4 1.5–3.9 1.6–3.1 1.3–2.7 1.6–3.5

1.8 ± 0.4

6.4 + 3.0

2.2

1.9–2.9

*Data from references [5] [14] [58] [59] [69] [73] [80] [88] and [103] .

In normally functioning bileaflet valves, color demonstrates a small amount of normal backflow (5 to 10 mL per beat) designed to decrease the risk of thrombosis by a "wash out" mechanism. TEE visualization of the bileaflet valve depends on the image orientation in the parallel or perpendicular position of the discs in relation to the sound beam. In the parallel position, the discs appear in profile as two lines. Color may reveal up to three distinct jets: two at the edges of the valve directed upward and outward; one centrally located and directed straight up. In the perpendicular position, the leaflets reflect dense reverberations into the ventricular cavity and color reveals a semicircular flare on the atrial aspect. As the probe is pulled or advanced, the central flare becomes narrower. [81] [82] The Carbomedics is a newer version of bileaflet mechanism with recessed pivots that may result in larger regurgitant jets.[87] Stented Bioprostheses.

The cross-sectional appearance of porcine valves is that of three cusps and three struts with an echogenic sewing ring. Normal flow pattern is a bellshaped central flow with a relatively flat velocity profile. Peak flow velocities commonly found in the aortic position are around 2.5 m per second, and in the mitral position are around 1.7 m per second. Mild backflow in normally functioning bioprostheses is less common than in mechanical valves, and it has been reported in up to 10% of the cases.[88] Nonstented Bioprostheses.

Careful measurement of the patient's outflow tract or the sinotubular junction is

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Figure 24-7 Single tilting disc mitral prosthesis. A, Correct anatomic disc orientation, allowing the major orifice flow to be directed away from the left ventricular (LV) outflow tract. B, Incorrect anatomic disc orientation, in which the major orifice flow is directed toward the LV outflow tract, creating turbulence.

an important contribution of ultrasound in determining nonstented valve size.[89] After implantation, the appearance is of a normal trileaflet valve, with increased echogenicity in the annular region from the layer of fabric supporting the graft. [90] Reported hemodynamics are very encouraging with nearly-natural transvalvular gradients resulting in significant reduction in afterload and wall stress.[46] [47] [48] Ventricular remodeling through regression of cardiac hypertrophy may be an important predictor of survival after valve replacement, and hypertrophy regression as early as 6 months after valve replacement has been reported with nonstented valves.[91] Homografts.

Preoperative or intraoperative TEE measurement of the aortic annulus has been used to select the correct homograft size.[51] The 2D imaging of the nonstented homograft is similar to the native aortic valve, with increased echoes at the level of the annulus resulting from the retaining sutures as the only hint that a new valve has replaced the native valve. Homograft failure commonly results from progressive aortic insufficiency; valve stenosis is rare.[92] [93] Long-term outcome with homograft valves is complicated by differences in harvesting, sterilization, and preservation, as well as differences in the surgical techniques applied. In the Ross procedure, TEE plays an important role in providing accurate measurement of the right ventricular outflow tract for choosing the homograft size. In addition, color flow Doppler within the left and right ventricular outflow tracts provides essential information regarding aortic and pulmonic regurgitation, respectively. For Figure 24-8 Double tilting disc mitral valve. A, Normal mitral inflow. B, Mitral inflow across a double tilting disc valve, with flow passing through three separate orifices, creating a near-normal flow pattern.

534

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these reasons, in our institution intraoperative TEE is routinely performed during the Ross procedure. Valved Conduits and Composite Grafts.

Valved conduits have been used most often in the repair of congenital heart disease. Reestablishing flow from the right heart to the pulmonary artery is often performed with a bioprosthesis. The echocardiographic evaluation should include definition of the anatomic relation of the valve conduit to the heart and the flow velocity through the proximal and distal aspects of the conduit. Careful Doppler evaluation of the entire conduit is necessary because stenosis can occur at either end or anywhere along the conduit. The extracardiac course of the conduit can result in variable angles and directions of flow; therefore, color Doppler may be helpful in defining the location of high-velocity flow. Additional windows from the subcostal, subclavian, and right parasternal windows may be necessary to align the Doppler beam. Composite grafts for left-sided valves are most commonly seen in patients with aortic valve and aortic root diseases such as connective tissue disorders (e.g., Marfan's syndrome), leading to aortic aneurysm or dissection. Complications include pseudoaneurysm of the ascending aorta caused by dehiscence, which can occur at the annulus, at the distal anastomosis with the native aorta, or at the coronary artery reimplantation site.[94] TTE is essential for serial follow-up. TEE can provide additional views of the aortic valve and ascending aorta and should be considered in the evaluation of symptomatic patients or in those in whom the precordial imaging suggests an aneurysm or pseudoaneurysm formation. Echocardiographic Features by Valve Position Aortic.

Gradients and areas should be measured and averaged from at least three (sinus rhythm) to five (atrial fibrillation) beats. A clear understanding of the differences among peak gradient, maximal instantaneous gradient, peak-topeak gradient, and mean gradient is essential to avoid confusion when they are compared to those derived by catheterization. The peak gradient obtained by Doppler closely correlates with the maximal instantaneous gradient derived by catheterization. The mean gradient obtained with either technique correlates very closely with each other. When Doppler and fluidfilled pressure gradients are recorded at the same time in the catheterization

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suite, the degree of concordance is superb.[58] [59] [79] For example, Burstow et al[58] found excellent correlation for the mean gradient (tissue valves, r = 0.93; mechanical valves, r = 0.96) when data were recorded simultaneously; however, when they were not simultaneous, the correlations fell slightly (tissue valves, r = 0.85; mechanical valves, r = 0.87). Values derived with the continuity equation have correlated well with prosthesis size.[95] [96] Peak velocities as high as 3.5 to 4.0 m per second have been recorded in normally functioning prosthetic mechanical aortic valves. These high-flow velocities exist briefly at valve opening; however, the mean gradient usually falls within the normal range. The mean pressure gradient, therefore, and not the peak pressure gradient, Figure 24-9 (Figure Not Available) Simultaneous catheterization and Doppler recordings in a Starr-Edwards prosthesis (A) and a Braunwald-Cutter prosthesis (B) in the mitral position. Note the excellent pressure gradient correlations. (From Burstow DJ, Nishimura RA, Bailey KR, et al: Circulation 1989;80:504–514.)

should be used in making clinical decisions, and it is the one to be reported for subsequent comparative studies on the same patient. If the mean pressure gradient is abnormally elevated, prosthetic valve stenosis should be suspected and TEE (or fluoroscopy) should be considered. Mitral.

Echocardiographic assessment of mitral prostheses includes calculation of the mean pressure gradient and the effective orifice area. Similar to aortic prostheses, the mitral mean pressure gradient correlates very well with the mean gradient derived at the time of catheterization when both data are recorded simultaneously. As illustrated in Figure 24-9 (Figure Not Available) , the mean pressure gradient is the average of multiple gradient calculations across the Doppler spectral envelope. Assessment of mitral regurgitation is often difficult because reverberations shadow the left atrium. The parasternal long-axis view may be helpful in eccentric jets; however, for accurate determination of mitral regurgitation, multiplanar TEE is the method of choice. This approach is ideally suited for assessing the mitral valve because of its close proximity to the left atrium and the use of high-frequency transducers. The exact appearance of the mitral

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535

valve depends on the valve's orientation and the degree of left atrial enlargement. During the examination, the valve sewing ring should be carefully searched at the midesophageal and transgastric levels. The left atrium and its appendage should be searched for spontaneous echo contrast and thrombus because they may be present in patients with prosthetic mitral valves even if they are in sinus rhythm and have normal left ventricular function.[97] Evaluation of pulmonary venous flow may be important in assessing severity of regurgitation. Tricuspid.

Data with tricuspid valve prostheses are far more limited than data with left-sided valves. In many respects Doppler evaluation is similar to mitral prostheses. The prosthesis should be imaged from all available views (parasternal short-axis, parasternal right ventricular inflow, apical fourchamber, and subcostal views). Bioprostheses are preferred over mechanical valves because of their high thrombogenic potential in this position. Because flow across the right-sided chambers increases with inspiration, one should expect mild variations in the peak E wave velocity; therefore, three (sinus rhythm) to five (atrial fibrillation) beats should be taken for an average. Severe tricuspid regurgitation is frequently caused by dilation of the native annulus; therefore, annular rings are nowadays preferred over prosthetic valves to correct hemodynamically significant tricuspid regurgitation. TEE plays an important role in these cases by confirming annular dilation as the origin of the regurgitation and not an intrinsic leaflet abnormality. Pulmonic.

Prostheses in this position are relatively uncommon in part because percutaneous balloon valvuloplasty Figure 24-10 Step-by-step recommended approach for evaluating a patient with suspected prosthetic valve dysfunction. Note that auscultation and TTE examination are the initial steps. TEE and cinefluoroscopy are intermediate steps; cardiac catheterization is the last.

is an effective tool in hemodynamically significant stenosis.[98] When a surgical intervention is needed, valvotomy is frequently used to palliate the

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valve, and later in life a bioprosthesis can be used. As with the native pulmonic valve, the bioprosthesis is best seen from the parasternal shortaxis and subcostal views. The more commonly used TEE views include the basal short-axis and the longitudinal views, which may be helpful in choosing the appropriate homograft size. Color flow Doppler examination within the right ventricular outflow tract is essential to document any residual regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography of Prosthetic Valve Dysfunction Figure 24-10 illustrates the recommended step-by-step approach in patients with suspected prosthetic valve dysfunction. A careful clinical examination has no substitute. TTE should always be included in the initial assessment. If a high gradient is detected, additional tests may be needed, including TEE and cinefluoroscopy. Cardiac catheterization and angiography provides important hemodynamic and pathologic confirmation in many cases; however, its use should be restricted to patients in whom TEE and cinefluoroscopy have not provided a definitive diagnosis.[5] For mechanical valves, cinefluoroscopy renders a better means to evaluate the actual valve opening and closing motion. It is clearly indicated whenever valve thrombosis is suspected. One needs to determine the valve's rotational 536

Figure 24-11 Radiographic side view of a bileaflet valve. In the opening position (A), the two discs form a 10-degree angle, whereas in the closing position (B), they form a 120-degree (<25 mm) or 130-degree (>27 mm) angle, depending on valve size. C, Photograph of a bileaflet mechanical valve in the opening position.

orientation by positioning the imaging intensifier in a view perpendicular to the valve plane. The right anterior oblique cranial view is frequently used for this purpose, although occasionally a left anterior oblique caudal view may be needed. Depending on the valve type and radiographic characteristics (i.e., radiolucency, radiopacity), the discs appear as dense lines inside the circle formed by the valve housing mechanism. The fluoroscopic side view renders important information in determining the closing angle degree. To achieve the side view, the image intensifier

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should be moved longitudinally 90 degrees and rotated transversely to a position in line with the valve leaflets. For the St. Jude Medical valve, the opening angle between the two parallel lines should be 10 degrees (Fig. 2411A) . In the closing position, the two lines form a wide obtuse angle in the form of a "V" (see Fig. 24-11B) ; for valves less than 25 mm the angle should be 120 degrees, and for valves greater than 27 mm it should be 130 degrees. A complete cinefluoroscopic examination can be performed in 15 minutes or less. Figure 24-12 Radiographic representation of a bileaflet valve in the opening position. A, A "frozen" leaflet. By cinefluoroscopy, only one leaflet moves during the cardiac cycle. B, Normal appearance as rotated 90 degrees.

In the typical case of thrombosis of a double tilting disc prosthesis, only one leaflet may be moving, indicating leaflet entrapment. Figure 24-12 shows still frames recorded during cinefluoroscopy in a patient with valve thrombosis and entrapment. The opening (A) and closing (B) positions of a St. Jude Medical valve clearly indicate that the right-sided leaflet (near the patient's spine) remains "frozen" during the entire cardiac cycle, indicative of leaflet entrapment by the thrombus. Primary Mechanical Failure Dysfunction from an intrinsic valve problem is known as primary mechanical failure. This complication is rare in the use of current mechanical valves. The Starr-Edwards valve had a rare intrinsic problem called ball variance, in which changes of the ball resulted in emboli either from ball material or thrombi formed on the irregular or cracked ball.[99] [100] Figure 24-13 illustrates a classic example of ball variance with a crack seen across the 537

Figure 24-13 Pathologic specimen showing ball variance in a StarrEdwards valve. Notice the crack seen across the midportion of the ball and a large thrombus entrapped between the ball and the cage.

midportion of the ball and a large thrombus trapped between the ball and

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the cage. Disc embolization from single or double tilting disc valves is rare. The older version of the Björk-Shiley valve had several reported cases of fractured struts resulting in disc embolization. The Björk-Shiley valve is no longer available in the United States, but this valve was implanted in thousands of patients who continue to require follow-up. Monostrut (available in Europe), a new Björk-Shiley valve, is designed so the inflow and outflow struts are machined from a single piece of alloy.[18] Disc fracture has been reported in 3 Medtronic-Hall and in 10 St. Jude valves.[18] Stented bioprostheses on the other hand, may undergo primary failure called calcific degeneration. This type of valve failure is characterized by restricted cusp motion leading to stenosis or cusp tears, which then leads to regurgitation and different degrees of mixed lesions.[101] [102] Flail cusp owing to leaflet tears is associated with severe regurgitation; therefore, the echocardiographic detection of a flail cusp has important therapeutic implications. Figure 24-14A illustrates the TEE image at the midesophageal level of a patient with a flail cusp in a stented bioprosthesis. Figure 24-14B shows the explanted bioprosthesis depicting the flailed cusp. A musical or "cooing" sound has been reported with pulsed Doppler in patients with perforated or torn leaflets, which result in a striated, "shuddering" appearance to the signal, referred to as harmonics. [103] [104] [105] Leaflet thickening in the absence of endocarditis most likely represents milder degrees of calcific degeneration; however, a thickened and often irregular appearance can also be seen in endocarditis. In patients with "fibrocalcific" changes on their cusps, the differentiation between calcific degeneration and endocarditis should be based on the clinical context.[103] [106]

Thrombosis Thrombosis occurs almost exclusively in mechanical valves, leading to predominant stenosis with or without some regurgitation. Figure 24-15 illustrates a thrombosed Beall valve (disc-in-cage) in the mitral position in a patient presenting in pulmonary edema; in addition, a large left atrial thrombus is sitting in the posterior aspect of the left atrium. The onset of symptoms may be gradual or sudden, and its incidence does not vary significantly Figure 24-14 TEE, horizontal four-chamber view, demonstrating a flail cusp (FC) in a mitral stented bioprosthesis (A). The patient presented to the

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hospital with progressive dyspnea on exertion, orthopnea, and fatigue. Ten years earlier, his mitral valve was replaced with a Hancock bioprosthesis. B, The excised valve with one of the cusps flailed and the other two with signs of degeneration. LA, left atrium; LV, left ventricle; RA, right atrium.

538

Figure 24-15 Prosthetic valve thrombosis in a Beall valve. A, Parasternal long-axis view from a patient with a disc-in-cage prosthesis (c) in the mitral position. A large thrombus (th) is noted in the posterior left atrial (LA) wall. B, The excised valve with a large thrombus obstructing the disc motion. AO, aorta; RV, right ventricle.

among different mechanical valves, except when the valve is in the tricuspid position. The low flow rate through the right-sided chambers is the most likely predisposing factor for the thrombosis rate as high as 20%, [107] limiting the use of mechanical valves in this position. Echocardiography should focus on determining the range of occluder motion. Several views should be used to determine the plane of maximal excursion. Bileaflet valves present a unique problem because thrombosis can affect only one hemidisc (see Fig. 24-12) . TEE is a sensitive and accurate tool for diagnosing prosthetic valve thrombosis and for evaluating the efficacy of thrombolytic therapy in the emergency room.[107] [108] [109] [110] Although reoperation is frequently recommended in these patients, thrombolysis has been used many times in critically ill patients who are not otherwise candidates for reoperation. Emergent surgery for acute valve thrombosis has a perioperative mortality of 30% to 40%, with the risk linked to the preoperative New York functional class, status of the left ventricular systolic function by echocardiography, urgency of operation, and concomitant coronary artery disease.[111] [112] [113] Thrombolytic therapy is a logical alternative to surgery in these high-risk patients. Numerous reports of the use of thrombolytics in acutely thrombosed mechanical valves have been published mostly in the form of case reports. [107] [109] [110] Table 24-7 includes the four largest series, representing nearly 90% of the total patients so far reported.[114] [115] [116] [117] As can be appreciated, the success rate is 81%; however, there are unavoidable complications including systemic emboli in 18% and an overall mortality rate of about 15%. In clinically stable patients with stuck leaflets and no

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high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence.[117] The best thrombolytic regimen is yet to be established, but streptokinase has been the most commonly used. For patients with high-risk (i.e., large) thrombus, valve replacement is clearly indicated unless the surgical risk is prohibitive. Thromboembolism Despite the routine use of anticoagulants in patients with mechanical valves, thromboembolism remains a major cause of morbidity and mortality. The incidence of thromboembolic episodes, however, has been significantly reduced with anticoagulation to between 1% and 4% per patient per year, and the risk of serious bleeding on anticoagulation is between 1% and 5% per patient per year.[118] [119] [120] According to the two largest trials, there is no difference in embolization with stented bioprosthetic versus adequately anticoagulated mechanical valves.[118] [120] In the decision of valve replacement, one must consider underlying risk factors such as prior thromboembolism, atrial fibrillation, significant left ventricular dysfunction, left atrial enlargement, left atrial appendage thrombus, and hypertension. The single most attractive advantage of bioprostheses is that in most cases anticoagulation is not needed. The increased risk of reoperation noted with stented bioprostheses, however, is a high price to pay for the reduced risk of bleeding through avoiding anticoagulation. Newer tissue valves such as nonstented bioprostheses and homografts may prove to be durable and yet enjoy the benefit of avoiding anticoagulation. An interesting observation described with TEE is fibrin strands. [121] Fibrin strands are commonly located on the atrial aspect of mitral prostheses or on the ventricular aspect of aortic prostheses. As illustrated in Figure 24-16 , their appearance is that of thin structures a few millimeters in length moving independently from the leaflets. Fibrin strands should be distinguished from vegetations or thrombi by their chaotic movement in and out of the imaging plane. They are more commonly seen on mechanical valves, but they also have been reported on tissue valves, and they have been associated with a higher incidence of embolic events.[122] [123] In a study by Isada et al,[122] 539

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TABLE 24-7 -- Combined Data for Patients with Left-Sided Prosthetic V Thrombosis Undergoing Thrombolytic Therapy Complications

Deaths

No. of Valve Clinical Reference Patients Location Success EMB HEM SURG TOTAL SURG TH Witchitz 12 8M/4A 69% 0 2 5 3 2 [114] et al Lorient 26 15M/11A 89% 5 0 4 4 2 Roudaut et al[115] 12 12M 83% 4 3 2 0 1 Shapira et [116] al Özkan et 89% 1 3 0 1 0 36 * 28M/8A [117] al Total 86 63M/23A 82% 10 8 11 8 5 A, aortic; Emb, embolic; Hem, hemorrhagic; M, mitral; Surg, surgical; th thombotic or thromboembolic. *36 episodes in 32 patients.

fibrin strands were found in 15 (18%) of 83 prosthetic mitral valve patients, and of those 15 patients, 8 (53%) had embolic events compared with 12 (18%) of 68 patients without strands. In contrast, fibrin strands have also Figure 24-16 (color plate.) TEE, horizontal four-chamber view, demonstrating fibrin strands (arrows) on the atrial side of a St. Jude Medical prosthesis (A). Chaotic movement of these structures in and out of the imaging plane characterizes real-time imaging. LA, left atrium; RA, right atrium; RV, right ventricle. Mild mitral regurgitation is noted in the medial aspect of the prosthesis.

been detected in otherwise normal prosthetic valves.[121] Further studies are needed to determine the clinical significance of fibrin strands before clinical decisions are made based solely on their presence. Endocarditis

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Prosthetic valves are at a high risk for endocarditis because of their foreign material and abnormal flows. Prosthetic valve endocarditis carries a significant morbidity and mortality. Older series reported a mortality rate as high as 75% with early endocarditis (<60 days) and 45% with late endocarditis (>60 days). In a more recent study evaluating echocardiographic findings and their relation to morbidity and mortality,[124] the presence of an infected prosthetic valve was a major risk factor for death. Five of 11 deaths related to endocarditis occurred in patients with prosthetic valves. The annual rate for late prosthetic endocarditis is estimated at 0.5% per year. [13] [19] , [118] , [120] According to the Veterans Cooperative[118] and the Edinburgh study,[120] there is no significant difference of endocarditis between mechanical and stented bioprosthetic valves; however, when compared with native valves, prosthetic valve endocarditis is more likely to be associated with ring abscess, conduction abnormalities, and a more grave prognosis. [125] Vegetations typically appear as irregular masses of echoes attached to the valve components commonly moving with the blood path. On tissue valves vegetations usually result in leaflet destruction, whereas on mechanical valves they may interfere with the occluder mechanism, resulting in stenosis, regurgitation, or both. Large vegetations (>10 mm) are associated with increased embolic complications.[126] , [127] Figure 24-17 shows a TEE at the midesophageal level in a septic patient with a stented bioprosthesis in the aortic position. The large echodense mass seen within the left ventricular outflow tract is consistent with a vegetation. Differentiation of vegetation from thrombus may be difficult and often impossible. An important hint is that endocarditis more commonly is associated with regurgitant lesions, whereas thrombosis more commonly is associated with stenotic lesions. Either condition, however, can be seen as mobile echodense masses. Thus, such separation primarily should be based on the clinical presentation and bacteriologic results. Rarely, both complications 540

Figure 24-17 TEE at the midesophageal level from the transverse (T) and longitudinal (L) views in a septic patient with a stented bioprosthesis in the aortic position. A large echodense mass in the left ventricular outflow tract is clearly seen (arrows). LA, left atrium; LV, left ventricle; RA, right atrium, RVOT, right ventricular outflow tract.

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may be present in the same valve. Figure 24-18 corresponds to a midesophageal view in a septic patient with a St. Jude Medical valve in the mitral position and a bioprosthesis in the tricuspid position. A large vegetation and a thrombus can be seen on the atrial aspect of the mitral valve. Early and accurate identification of septic complications TABLE 24-8 -- Sensitivity (Sens) and Specificity (Spec) of TTE versus TEE for the Diagnosis of Vegetations and Associated Abscesses in Patients with Endocarditis TTE

Reference Mugge et al (1989)[127] * Taams et al (1990)

No. of Patients Studied 105

No. of Patients with PVE 25

SENS (%) 58

33

12

36

118

34

28

TEE

SPEC SENS SPEC (%) (%) (%) ‡ 90 ‡ 100 100 100

[128] *

Daniel et al (1991)

99

87

95

[129] †

PVE, prosthetic valve endocarditis; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *Identification of vegetations. ‡Insufficient data available, but smaller studies have reported specificity of TEE at 100%. †Identification of abscesses.

Figure 24-18 TEE at the midesophageal level from the transverse view in a septic patient with a St. Jude Medical valve in the mitral position and a stented bioprosthesis in the tricuspid position. A large vegetation (veg) and a thrombus (th) are clearly identified within the left atrium. LV, left ventricle; RA, right atrium; RV, right ventricle.

in patients with prosthetic valves have a significant impact on the decisionmaking process. TEE has dramatically improved the diagnostic accuracy in detecting vegetations, abscesses, and other complications associated with

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prosthetic valve endocarditis. [127] [128] [129] [130] Studies comparing TTE and TEE have included both native and prosthetic valves in their analysis. Table 24-8 lists studies comparing the two modalities in which patients with prosthetic valves were included. Although prosthetic valves are not analyzed separately, the data clearly favors TEE as a superior imaging modality; therefore, TEE should be performed routinely in patients with suspected prosthetic valve endocarditis, most notably in patients who fail to improve on therapy. Development of a perivalvular abscess is associated with a grave prognosis and indicates the need for aggressive medical and surgical therapies.[131] [132] Clinical findings suggestive of an abscess include persistent sepsis despite appropriate antibiotics, new or worsening heart failure symptoms, and development of first-degree atrioventricular block or incomplete right bundle branch block. Figure 24-19 illustrates a range of possible outcomes of a prosthetic valve abscess. Rupture may occur into adjacent structures, including the pericardial sac creating cardiac 541

Figure 24-19 A to D, Clinical, electrocardiographic, and echocardiographic characteristics in septic complications of mechanical valves. AV, atrioventricular; CHF, congestive heart failure; RBBB, right bundle branch block.

tamponade; however, a rather common outcome is the development of perivalvular dehiscence with a tunnel communicating the aorta with the left ventricular outflow tract and consequently severe perivalvular regurgitation. Emergent surgical treatment may be a lifesaving procedure in these acutely ill patients. Echocardiographic findings of perivalvular abscess include valve rocking, periaortic root thickening, or perivalvular echolucency.[133] As noted in Table 24-8 , identification of an abscess is very difficult from TTE; therefore, TEE is mandatory when this complication is clinically suspected. In addition, fistulous tracts connecting the perivalvular space with adjacent structures can be imaged and tracked down with color flow. Figure 24-20 represents the mid- and upper esophageal images in a septic, critically ill patient with a St. Jude Medical aortic prosthesis who presented to the emergency room with acute aortic insufficiency and pulmonary edema; a large perivalvular abscess is clearly noted.

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Patient-Prosthesis Mismatch The term patient-prosthesis mismatch refers to the clinical setting in which the prosthesis is structurally normal but the hemodynamic data are consistent with a greater stenosis than expected for the valve type and size. [134] [135] The mismatch occurs because the valve area is relatively insufficient to fit the patient's body surface area. A given valve area perfectly acceptable for a small relatively inactive subject may be inadequate for a larger physically active individual. This problem is usually seen in patients with small aortic annulus sizes and in whom the valve replacement was performed because of native valve stenosis rather than regurgitation.[134] From the clinical point of view, the patient fails to improve or may even be symptomatically worse. The long-term implications of this condition are not known. After successful aortic valve replacement, regression of cardiac hypertrophy is commonly detected. Failure to regress 6 months after surgery may be a subtle indication that residual aortic stenosis is present and that the hemodynamic burden persists.[136] [137] In some patients inadequate hemodynamics may be apparent only at higher cardiac output stages (i.e., during exercise). For patients with exertional symptoms suggesting high valve resistances without evidence of a primary valve dysfunction, stress echocardiography (see later) should be considered. The diagnosis of patient-prosthesis mismatch requires exclusion of an intrinsic valve dysfunction, which further emphasizes the need for a baseline postoperative study. Prosthetic Aortic Stenosis The initial suspicion of prosthetic valve stenosis may be the incidental finding of abnormally high flow velocities detected during a routine examination. This finding should prompt careful inspection from the parasternal long- and short-axis views to determine possible causes. In addition to thrombus formation, obstruction also can occur from gradual ingrowth of fibrous tissue called pannus formation. An encapsulated perivalvular abscess may reduce the outflow tract area leading to stenosis. Figure 24-21 shows images from a patient with a homograft and a sterile perivalvular cavity reducing the effective orifice area. In the absence of symptoms and if there is normal valve motion otherwise, close follow-up is probably appropriate. Alternatively, stress echocardiography may be necessary to unmask a truly symptomatic stenosis or to address the patient's or referral physician's concerns. If the valve area calculated from TTE data

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is markedly reduced, 542

Figure 24-20 TEE in a septic patient with a St. Jude Medical aortic valve. A, Partial dehiscence and a large abscess cavity (arrow). B, Cross-sectional view of the same pathology. The abscess cavity is composed of echodense and echolucent material (arrow). AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium.

we commonly reassess the aortic valve area (continuity equation) by combining the diameter of the left ventricular outflow tract accurately determined by TEE at the upper-midesophageal level with the transthoracic velocity time integrals obtained during the same setting. Prosthetic Mitral Stenosis Valve area should be routinely calculated from the pressure half-time or the continuity equation (or both) in patients with suspected prosthetic mitral stenosis. Although an E wave velocity greater than 2 m per second may be indicative of prosthesis stenosis, increased velocities in the absence of a prolonged pressure half-time may be a result of prosthetic regurgitation.[2] Color flow can aid in aligning the Doppler beam parallel to the mitral inflow in obtaining the most representative Doppler signal. Mean valve gradient should be combined with pressure half-time or flow volume determination to differentiate prosthesis stenosis from increased transvalvular volume. As noted earlier, TEE is a very useful tool for detecting thrombosed mitral prosthesis and guiding thrombolytic therapy; thus, TEE should always be performed in patients in whom stenosis is suspected. Prosthetic Aortic Regurgitation The approach to grading prosthetic regurgitation is similar to that of native valves and involves evaluation of several echo-Doppler indices. As with native valve regurgitation, ventricular size and function are important clues to the severity of regurgitation. Normal left ventricular internal dimensions is incompatible with severe chronic Figure 24-21 TTE of a patient with stenosis of an aortic homograft. A, Parasternal long-axis view showing an encapsulated antibiotic-sterilized

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cavity (C), which reduces the outflow tract diameter (LVOT) in half (arrows). B, Continuous wave Doppler from the five-chamber view in the same patient with elevated velocities up to 4.0 m/sec, maximal gradient of 64 mm Hg, and a mean gradient of 34 mm Hg. The continuity equation valve area was estimated at 0.7 cm2 . LA, left atrium.

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aortic regurgitation. Jet height and area from the short-axis view have been compared with angiographic grading in native valve regurgitation with excellent correlations of 0.93 and 0.91, respectively.[138] [139] In our laboratory we have found the parasternal long-axis view a more useful view to assess the jet area in relation to the left ventricular outflow tract area. Eccentric valvular or perivalvular jets may overestimate the severity of prosthetic regurgitation because they may be directed perpendicular to the outflow tract, occupying a larger portion of the ventricular outflow tract area. The apical five-chamber view should also be used to determine jet characteristics. The pressure-half time can be helpful in differentiating chronic from acute regurgitation. In general, acute (commonly severe) aortic regurgitation has a rapid slope decay indicative of acute elevation of left ventricular pressures at end-diastole. Although highly specific, this finding is poorly sensitive because the decay slope may be altered by changes in diastolic function, particularly ventricular compliance, heart rate, and rhythm. Thus, patients with severe chronic aortic regurgitation and a compliant left ventricle may have an aortic-ventricular diastolic pressure slope similar to patients with milder degrees of aortic regurgitation. Consequently, in many patients the Doppler diastolic slope decay helps in differentiating acute from chronic regurgitation, but not severe from moderate regurgitation. The intensity of the continuous wave Doppler signal may help in assessing severity of regurgitation. In patients with severe regurgitation, the signal intensity of the forward and regurgitant flows are similar. Unfortunately, such estimation is subject to wide interobserver variations. In addition, signal intensity depends highly on the specific gain settings on different ultrasound systems and even in the same machine. Thus, in our laboratory an intense Doppler signal of aortic insufficiency is a hint that the severity of regurgitation is more than mild. The amount of flow reversal in the descending thoracic aorta also has been correlated with severity. Normal flow reversal in the ascending aorta is confined to the early part of diastole,

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whereas flow reversal that persists throughout diastole is seen in patients with severe regurgitation.[3] [81] TEE may provide important etiologic information such as primary mechanical failure (i.e., flail cusp), ring dehiscence, vegetations, or abscess formation with a paravalvular fistula (see Fig. 24-19D) . Additionally, TEE offers an excellent visualization of the ventricular outflow tract area for severity assessment based on the relation of jet area and ventricular outflow tract area. Finally, evaluation of the ascending aorta for aneurysmal dilation or dissection should be part of the TEE examination in these patients. Prosthetic Mitral Regurgitation Assessment of mitral regurgitation by TTE is problematic because reverberations from the metallic material of the prosthesis commonly obscure the left atrium. This problem is less noticeable with bioprostheses. Nevertheless, the common practice in our laboratory is to turn to TEE every time there is clinical or TTE suspicion of pathologic mitral regurgitation, regardless of the type of prosthesis. Color Doppler demonstrating flow convergence or a clearly visible proximal isovelocity surface area on the ventricular aspect of the valve is suggestive of severe regurgitation. The maximal area of the acceleration signal has been used to assess severity of mitral regurgitation.[140] Similar to aortic insufficiency, the intensity of the continuous wave Doppler signal is related to severity; the more intense the signal, the more severe the regurgitation.[71] Significant regurgitation has a density similar to the antegrade flow signal.[141] A recent evaluation of TTE for evaluating prosthetic mitral regurgitation compared proximal isovelocity surface area, intensity of the Doppler signal, and color Doppler jet within the left atrium.[142] Flow convergence was more sensitive but less specific for predicting significant prosthetic mitral regurgitation. Doppler indices used for severe native valve regurgitation also may be helpful in prosthesis regurgitation, such as increased E wave velocity (>2 m/sec), increased mean gradient (>5 to 7 mm Hg), short pressure half-time (<100 m/sec), and increased time velocity integral (>40 cm).[6] [142] [143] Unexplained, worsening, or new pulmonary hypertension may be indicative of significant regurgitation. TEE has substantially improved the diagnostic accuracy of the jet characteristics for determining severity and etiology of prosthetic regurgitation. [4] [144] Remember that color Doppler is a measure of velocity and not of volume, and although the jet area may be relatively small,

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eccentric jets may result from severe regurgitation, particularly when they wrap around ("hug") the left atrial wall (Fig. 24-22) . An eccentric jet of severe mitral regurgitation loses momentum and velocity as it contacts the atrial wall despite a large volume, a phenomenon known as the Coanda effect.[145] In our laboratory, we use an eccentric jet as an evidence of severity. In fact, most cases of eccentric regurgitation hugging the lateral wall of the left atrium Figure 24-22 (color plate.) TEE from the transverse plane (0 degrees) illustrating a large, eccentric jet of severe mitral regurgitation.

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enter into one of the pulmonary veins or into the left atrial appendage, confirming severe mitral regurgitation. Prosthetic valve dehiscence, that is, a separation of the prosthetic sewing ring from the native fibrous ring, is caused by detachment of the retaining sutures. Careful TEE evaluation of the annulus at the midesophageal and transgastric levels can reveal a dropout of echoes; when color Doppler is applied, an eccentric jet may become obvious. Detection of valve dehiscence is important because it usually means severe regurgitation requiring surgical repair or replacement. Figure 24-23 is a set of TEE images illustrating a patient with a Hancock bioprosthesis in the mitral position with dehiscence and severe eccentric regurgitation. The morphology of the pulmonary vein Doppler waveform is dependent on both volume of regurgitation and left atrial properties. Pulmonary vein flow characteristics have been useful in assessing severity of native mitral valve regurgitation. Typically, there is loss of the systolic wave amplitude and eventually reversal of systolic flow as the Figure 24-23 (color plate.) TEE showing dehiscence in a stented mitral bioprosthesis with perivalvular regurgitation. A and C, The dehiscent site (arrows) is seen as a dropout of echoes at the annular attachment. B and D, Eccentric severe paravalvular regurgitation is seen through the dehiscence. LA, left atrium; LAA, left atrial appendage; LV, left ventricle; RA, right atrium; RV, right ventricle.

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severity of regurgitation increases from moderate to severe. These changes should not be interpreted as an absolute measure of regurgitant severity, however. In vivo models suggest that pulmonary venous flow reversal is more likely in acute versus chronic mitral regurgitation because the atrium is less compliant and has a smaller initial volume.[146] In addition, characterization of the pulmonary vein flow in prosthetic mitral regurgitation is lacking, and extrapolation of the data from native to prosthetic valves has not been documented.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Stress Echocardiography in Assessing Prosthetic Valve Function In patients with suspected prosthetic valve dysfunction, one may encounter symptomatic patients in whom the 2D and Doppler imaging indicates normal valve function at rest. Under these circumstances, exercise echocardiography may elicit abnormal hemodynamics indicating valve 545

TABLE 24-9 -- Prosthetic Valve Exercise Doppler Hemodynamics No. of Patients Aortic Position CarpentierEdwards MedtronicHall MedtronicHall St. Jude Medical Mitral Position Björk-Shiley

Valve Sizes (mm)

Mean Gradient (mm Hg) * EXERCISE INCREASE † REST (%)

4 21

15 ± 3

21 ± 3

70

14 21

15 ± 4

24 ± 6

80

14 21–27

9±4

15 ± 6

83

17 21–27

11 ± 4

18 ± 7

81

11 25–31

4.9 ± 1.8

10.3 ± 2.9

100

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6 28–32

4.6 ± 12.6 ± 130 1.2 4.1 St. Jude 17 26–32 2.5 ± 5.1 ± 3.5 102 Medical 1.4 Medtronic15 26–32 3.0 ± 7.0 ± 2.9 116 Hall 1.1 Data from Tatineni et al,[147] Wiseth et al,[148] and Halbe et al.[150]

*Mean ± SD. †Exercise protocols used were symptom-limited treadmill and upright or supine bicycle.

dysfunction or patient-prosthesis mismatch. In our laboratory, we prefer supine bicycle ergometry over treadmill because serial hemodynamic data can be obtained at different exercise stages. Normal hemodynamics with stress in these patients excludes valve dysfunction as the cause of the patient's symptoms. Valve gradient, valve area, degree of regurgitation, and systolic pulmonary artery pressure can all be calculated at rest and at peak stress (or immediately afterward). Despite its clinical potential, relatively few stress echocardiographic studies in patients with suspected prosthetic valve dysfunction have been published.[61] [147] [148] [149] [150] Table 24-9 summarizes data available regarding valve gradients at rest and with exercise. Dobutamine provides an excellent alternative for evaluating valve hemodynamics when the patient is unable or unwilling to undergo treadmill exercise or bicycle ergometry.[151] In our laboratory we use a protocol similar to that for ischemic heart disease; that is, we attempt to reach at least 85%, or ideally 90%, of the maximal predicted heart rate according to the patients' age and gender. We start with IV administration of dobutamine at 10 µg/kg per minute and increase sequentially every 3 minutes to 20, 30, and 40 µg/kg per minute. If the Doppler signal intensity of tricuspid regurgitation is weak because of trivial or mild regurgitation, we routinely add a small amount of diluted Optison to enhance signal intensity, allowing calculation of systolic pulmonary artery pressure. In patients with single tilting disc prostheses in the aortic position, peak and mean gradients are higher with the dobutamine stress echocardiography compared with symptom-limited treadmill exercise.[152]

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Evaluation of the patient with decreased left ventricular systolic function and possible prosthetic aortic stenosis is problematic. In 24 adults with native aortic valve stenosis (area ≤ 0.5 cm2 /m2 ), mean gradient less than 30 mm Hg, and ventricular dysfunction (ejection fraction ≤ 0.45), deFilippi et al[153] performed echocardiography at baseline and at peak dobutamine stress to distinguish severe fixed aortic stenosis from flow-dependent (relative) aortic stenosis. Three hemodynamic subsets were identified: (1) fixed aortic stenosis with increased cardiac output and transvalvular gradient and no change in valve area; (2) relative aortic stenosis with increased valve area but no change in gradient; and (3) lack of contractile reserve with indeterminate stenosis because of inability to increase cardiac output.[153] Theoretically, a similar study may be applicable, although not yet proved, in patients with severe ventricular dysfunction and prosthetic stenosis of undetermined severity.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Three-Dimensional Echocardiography in Assessing Prosthetic Valve Function Current echocardiographic approaches to determination of effective orifice area are based on flow characteristics. Flow characteristics, however, also depend on several factors in addition to the actual orifice area, including ventricular compliance, systolic function, and loading conditions. A classic dilemma is the patient with a mechanical aortic valve with high flow velocities detected in a routine Doppler examination. Is this a normal finding? Is it consistent with pannus formation and therefore with some stenosis? Is this a patient-prosthesis mismatch? An echocardiographic technique that actually allows us to visualize the orifice size would likely improve our diagnostic abilities. Three-dimensional echocardiography involves the acquisition and display of cardiac structures in three spatial dimensions allowing their visualization and analysis as they move in time and space. Figure 24-24 illustrates a commonly used rotational scanning mechanism in which the transducer is rotated at 3-degree increments up to 180 degrees. Dynamic 3D imaging may provide a more realistic representation of prosthetic morphology than 2D images. Recent advances in ultrasound equipment, digital storage, and display techniques have made 3D clinically feasible; however, the clinical potential of 3D imaging has just begun to be recognized, and there are no published data on the use of 3D technology in assessing prosthetic valve function. Figure 24-25 depicts a 3D reconstruction of a St. Jude Medical valve performed in our laboratory. The two hemicircular lateral orifices and the central rectangular orifice are clearly indicated. Mitral annular rings have been reconstructed with 3D 546

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Figure 24-24 Left, The rotational mechanism for acquisition of two-dimensional images at 3-degree intervals from 0 to 180 degrees. Right, The twodimensional images are piled up one after another, gated by the electrocardiogram. Figure 24-25 Three-dimensional reconstruction of a St. Judge Medical valve in the mitral position as seen from the left atrium or "surgeon's view." The semicircular orifices (curved arrows) and the rectangular orifice (straight arrow) are seen.

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technology.[153] Dall'Agata et al[154] used TEE to analyze mitral valve rings in 19 consecutive patients who underwent annuloplasty because of severe regurgitation. Fifteen patients received a Cosgrove-Edwards (flexible) ring and four received a Carpentier (rigid) ring. Imaging acquisition used the rotational technique immediately after the operation and was considered to be adequate in 17 of 19 patients. The authors were able to differentiate values from end-systolic to end-diastolic orifice areas (4.2 ± 1.5 cm2 versus 4.8 ± 1.5 cm2 ; P < .0001) in the Cosgrove-Edwards ring, and no significant change in the Carpentier ring.[154]

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551

Chapter 25 - Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves William A. Zoghbi MD

The surgical approach to treating diseases of the aorta and cardiac valves has evolved dramatically over the past two decades. Concurrent with these developments, echocardiography and particularly Doppler techniques have been refined, allowing a better definition of cardiac structures and flow dynamics. Furthermore, transesophageal echocardiography (TEE) has improved the diagnostic capabilities of sonographic techniques by providing superior imaging of the aorta and cardiac structures, thus increasing the diagnostic impact of echocardiography in patients with diseases of the aorta and cardiac valves. A variety of complications, however, may occur in patients undergoing surgery on the great vessels and cardiac valves. These complications may occur early or late in the postoperative period and include infection, thrombosis, obstruction or dehiscence of prosthetic material, and progression of the underlying disease disorder, particularly in diseases of the aorta. Recognition of diseases of the aorta and of the infectious complications and dysfunction of prosthetic valves has been addressed elsewhere in detail ( see Chapter 23 and Chapter 24 ). This chapter focuses

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on unusual complications following surgery on the aorta and cardiac valves and the role of echocardiographic techniques in assessing these complications.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Unusual Complications Following Surgery on the Aorta Pseudoaneurysms of Composite Aortic Grafts Clinical Setting

In patients with aortic aneurysm or those with dissection of the aortic root involving the aortic sinuses and aortic valve, which are not amenable to repair, replacement of the aortic root with a composite graft is now widely accepted. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] First reported, in 1968, by Bentall and De Bono,[1] and more recently modified since then, [5] , [6] [10] [11] [12] [13] this surgical procedure has significantly prolonged the life expectancy of patients affected with annuloaortic ectasia.[5] [9] [14] Knowledge of this procedure, its variations, and complications is crucial for the echocardiographer, particularly because echocardiography with Doppler has emerged as a powerful diagnostic modality in assessing the function and complications of composite aortic grafts. The original Bentall procedure consists of replacing the aortic root and valve with a composite aortic graft 552

(ascending aortic graft and prosthetic aortic valve). The coronary arteries are reimplanted onto the graft, and the aorta is wrapped around the graft to improve hemostasis.[1] [2] [3] [4] [15] Among the complications of composite aortic grafts is the development of a pseudoaneurysm of the ascending aorta. This pseudoaneurysm occurs secondarily to dehiscence of the suture line at the aortic annulus, the coronary ostia, or the distal graft anastomosis. In patients with composite grafts who underwent the original Bentall procedure, this potentially lethal complication was reported to occur at a rate of 7% to 25%. [3] [16] [17] [18] [19] Modifications of the original method have since been proposed to decrease the incidence of pseudoaneurysm

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formation.[2] [5] [6] [11] [12] [13] In 1981, Cabrol et al[2] modified the operation by introducing a second tube graft connecting the coronary ostia and the main ascending aortic graft (Fig. 25-1) . In 1991, Kouchoukos and co-workers[5] showed that the "open," or "button," technique for reimplantation of the coronary arteries led to a lower incidence of pseudoaneurysms. With the present modifications, the incidence of pseudoaneurysm formation has decreased to less than 6%.[5] [7] [8] [9] [12] [19] [20] [21] [22] The clinical symptoms associated with pseudoaneurysm formation vary. Whereas some patients have nonspecific symptoms or may be completely asymptomatic, other patients may be severely limited by dyspnea and fatigue. Given the possibility of aortic rupture, early diagnosis of aortic pseudoaneurysm is therefore essential. Echocardiography with Doppler and, more recently, TEE have had a significant impact on the detection of pseudoaneurysms and the evaluation of patients with composite grafts.[18] [23] [24] [25] [26] [27] [28] [29] [30]

Figure 25-1 (color plate.) Diagram of the surgical reconstruction of the aortic root in a patient with ruptured aortic dissection, using a composite aortic graft (modified Cabrol technique). The native aortic root is excised and replaced with a composite graft. A tube graft connects the aortic graft to the left main coronary artery. A vein graft (dark blue) was used in this case to bypass a stenosed right coronary artery. (Courtesy of Dr. Hazim J. Safi.) Echocardiographic and Doppler Findings

A normal composite aortic graft is visualized with echocardiography as an echo-dense ascending aortic root, with a prosthetic valve in the aortic position. The maximal diameter of the composite graft depends on the size of the graft. In 27 patients with normal composite grafts evaluated in the author's institution, the diameter of the ascending aorta ranged from 3.2 to 5 cm (mean of 4.2 cm).[18] In patients whose native aorta wrapped the graft, a small echo-free space between the graft and the wall of the aorta was seen in most patients (80%) and usually was small, ranging from 0 to 1.4 cm (mean 0.6 cm).[18] In all cases of normal composite graft, Doppler examination showed no evidence of flow in this small echo-free space and the presence of only trivial aortic insufficiency. Echocardiography can provide important diagnostic information about the presence of the pseudoaneurysm and the site of dehiscence of the surgical anastomosis.[18] [31] [32] [33] The identification of an enlarged ascending aorta with an echo-free space around the aortic graft should prompt investigation

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for the presence of a pseudoaneurysm. Other considerations include a hematoma without pseudoaneurysm or, depending on the clinical setting, the presence of graft infection with abscess formation. The space around the graft may contain varying amounts of echo-dense debris or thrombus. A pseudoaneurysm is diagnosed as an enlarged ascending aorta with an echofree space between the aortic graft and the wall of the aorta, along with the demonstration of flow into the echo-free space (Fig. 25-2) .[18] [31] [32] In a series of patients with pseudoaneurysms diagnosed in the author's institution, [18] 553

Figure 25-2 (color plate.) Echocardiographic and Doppler findings using transthoracic echocardiography in a patient with a large pseudoaneurysm of the ascending aorta complicating a composite graft. The dehiscence was at the aortic annulus anastomosis. A and C show the extent of the pseudoaneurysm as delineated by the arrows in short-axis (A) and long-axis (C) views. The origin and extent of the systolic jet into the pseudoaneurysm are shown in B and D in the same image planes as in A and C. During diastole (E), blood converges from the pseudoaneurysm toward the aortic annulus and enters the left ventricle (arrow) through the dehiscence, mimicking aortic insufficiency. The corresponding angiographic findings are shown in Figure 25-9 . GR, aortic graft; LA, left atrium; LV, left ventricle; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

the maximal diameter of the ascending aorta ranged from 6 to 14 cm. The maximal echo-free space between the aortic graft and the wall of the ascending aorta ranged from 2 to 7 cm. This space may be eccentric or concentric around the graft. Although most cases of pseudoaneurysms report more than 2 cm of echo-free space surrounding the graft, the demonstration of flow into the space outside the graft is essential for the diagnosis, irrespective of the size of the echo-free space. Once a pseudoaneurysm is suspected, special attention is directed to imaging the ascending aorta, aortic root, the plane of the prosthetic valve, and the coronary ostia from the left and right parasternal and suprasternal windows. In cases of pseudoaneurysms, color-flow Doppler imaging frequently demonstrates evidence of a pulsatile flow jet into the echo-free space between the graft and the wall of the ascending aorta (see Fig. 2) . This finding confirms the entity of pseudoaneurysm, as opposed to the mere presence of blood or fluid collected around the graft (Fig. 25-3) . In

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the author's experience, however, transthoracic color-flow examination may not identify flow in the echo-free space in some patients. In these cases, transesophageal examination clearly demonstrates flow into the pseudoaneurysm (Fig. 25-4) . This limitation is the result of the lower resolution and sensitivity of surface echocardiography combined with posterior shadowing from the graft and aortic prosthesis. Transthoracic and transesophageal echocardiography do provide complementary information regarding the status of a composite aortic graft. If any suspicion arises about the presence of a pseudoaneurysm, a TEE is clearly indicated for further evaluation of the abnormality. Following is a description of Doppler echocardiographic findings observed with composite graft pseudoaneurysms.

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Figure 25-3 Transesophageal horizontal plane demonstrating a large hematoma (arrows) surrounding a composite aortic graft (G) in a patient early after operation. There was no flow detected around the graft by Doppler echocardiography at any level. Th, Thrombus. The hematoma was secondary to postoperative bleeding complications. Aortic Annulus Dehiscence

In cases of dehiscence at the aortic annulus anastomosis, with ensuing communication between the left ventricle and the pseudoaneurysm, colorflow Doppler identifies a systolic jet arising from the paraprosthetic valve area, directed cranially into the pseudoaneurysm ( see Fig. 25-2 and Fig. 25-4 ). Because the jet frequently is eccentric, the imaging plane showing the flow jet in the long axis of the aortic root usually is lateral or medial to the plane showing the aortic graft. Thus, the flow jet and aortic graft may not be seen in the same longitudinal plane (see Fig. 25-2) . The short-axis view at the level of the prosthetic aortic valve demonstrates the jet arising in the Figure 25-4 (color plate.) Transesophageal echocardiographic frames and corresponding color Doppler systolic frames in a patient with composite graft pseudoaneurysm. The transthoracic examination in this patient did not demonstrate flow in the pseudoaneurysm. The upper panels are at the level of the ascending aorta; the lower panels are at the prosthetic aortic valve level. The dehiscence at the aortic annulus is depicted by a

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straight arrow. Color flow Doppler demonstrates flow into the pseudoaneurysm. GR, aortic graft; LA, left atrium; LV, left ventricle; PrV, prosthetic valve; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

paravalvular area and oriented into the pseudoaneurysm. Short-axis views from a more cranial angle demonstrate the orientation of the jet in the pseudoaneurysm in relation to the aortic graft. These considerations apply for both transthoracic and TEE imaging ( see Fig. 25-2 and Fig. 25-4 ). Generally, detection of the dehiscence and flow into the pseudoaneurysm is much easier with TEE than with the transthoracic approach. In most cases of dehiscence at the aortic annulus, continuous-wave Doppler views from the apical window demonstrate two distinct systolic jets: one coursing through the prosthetic valve and another coursing through the left ventricular-pseudoaneurysm communication (Fig. 25-5) . In the author's experience, the maximal velocity and derived pressure gradient through the communication have been higher than those through the prosthesis.[18] The systolic jet through the dehiscence frequently starts before the opening click of the prosthetic valve, and its duration is usually longer than the ejection time through the valve (see Fig. 25-5) . In all cases of dehiscence of the aortic annulus, a diastolic jet is seen in the left ventricular outflow, simulating valvular aortic insufficiency. In these cases, concomitant aortic insufficiency arising from within the valve usually cannot be excluded with confidence; however, with TEE, the mechanism of regurgitation can be much better defined. Continuous-wave Doppler recording of these diastolic jets also shows a short pressure half-time, mimicking severe aortic insufficiency. In some cases, an abrupt termination of diastolic flow before the prosthetic aortic-valve click at the onset of early systolic flow through the communication supports the conclusion that this regurgitation is not occurring through the aortic valve (see Fig. 25-5) . Coronary Artery Dehiscence

Coronary artery dehiscence is diagnosed by color-flow Doppler as a jet arising from the level of the coronary ostia or coronary anastomosis and directed into the pseudoaneurysm. Dehiscence 555

Figure 25-5 Continuous wave Doppler from the apical window of the

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patient with aortic annulus dehiscence shown in Figure 25-2 . Recordings are obtained from the same position on the chest wall, with minor change in angulation. Compared with the systolic jet velocity through the prosthetic aortic valve, the systolic jet through the ventricular-pseudoaneurysm communication has a higher maximal velocity (Vmax), is of longer duration, and starts (oblique arrow) before the first click of the prosthetic valve (horizontal arrow). The diastolic regurgitant jet into the left ventricle has a steep deceleration slope and ends before the first systolic aortic valve click (upper panel, straight arrow) at the time of onset of systolic flow into the pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

usually is easier to define in patients in whom the pseudoaneurysm is large because of the more defined spatial distribution of the jet. Various flow patterns may be recorded, as shown in Figure 25-6 . Whether the flow is predominantly systolic into the pseudoaneurysm or systolic and diastolic depends on factors such as the compliance of the pseudoaneurysm and whether a communication exists between the pseudoaneurysm and the left ventricle. Compression of the Composite Graft or Adjacent Structures

Compression of the graft may result from hematoma or pseudoaneurysm formation[27] and is most commonly observed with aortic annulus dehiscence. With two-dimensional echocardiography, pulsatile compression of the graft can be seen during systole (Fig. 25-7) , most likely because of the high pressure surrounding the graft and possibly a Venturi phenomenon occurring within the graft. Using continuous-wave Doppler, a high-velocity systolic jet can be recorded, a finding similar to that seen in an obstructed prosthetic aortic valve. Differentiation of the two entities may be difficult; however, visualization of the pulsatile compression of the graft provides a good assessment of the underlying condition. If the pseudoaneurysm is extensive, it may compress adjacent structures. Compression of the pulmonary artery with resultant pulmonary arterial stenosis was recently reported as a complication of a large pseudoaneurysm.[33] Role of Transesophageal Echocardiography

The use of TEE clearly is advantageous in the overall definition of complications of composite aortic grafts.[18] , [27] [30] [31] [32] [33] [34] For delineation of pseudoaneurysms, the aortic suture ring is clearly visualized with TEE, thereby enhancing the evaluation of dehiscence at this level with both echocardiography and Doppler techniques. Furthermore, the

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anastomosis of the coronary arteries to the aortic graft is better assessed. Evaluation of flow in the potential space between the graft and native wrapped aorta or fibrous tissue (in the case of excision of the native aorta) is improved. Dehiscence at the distal anastomosis of the aortic graft to the aortic arch remains difficult to assess because of limitations of imaging in this area; however, this type of dehiscence is the least frequent and rarely occurs alone. In cases of pseudoaneurysm formation secondary to endocarditis, TEE may detect vegetations that can further substantiate the diagnosis (Fig. 25-8) . In the absence of such a finding, however, exclusion of an infected graft based on echocardiographic examination, or based on any structural imaging alone, is difficult. Because of anterior 556

Figure 25-6 (color plate.) Examples of different velocity patterns observed by continuous wave Doppler in two patients with coronary artery dehiscence. In A, the color jet arising from the left main dehiscence is depicted in the parasternal long- (A1 ) and short- (A2 ) axes by a large arrow. In this patient with concomitant aortic annulus dehiscence, continuous wave Doppler (A3 ) shows increased systolic and diastolic velocities directed from the graft into the pseudoaneurysm. The patient in B has a sole dehiscence at the right coronary anastomosis depicted in short axis (B1 and B2 ). Continuous wave Doppler recording (B3 ) shows flow directed from the graft into the pseudoaneurysm in systole and flow reversal from the pseudoaneurysm into the graft in diastole (small arrows). GR, graft; LV, left ventricle; PA, pulmonary artery; PSA, pseudoaneurysm; RV, right ventricle. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

shadowing produced from the prosthetic valve and graft, an optimum assessment of the aortic root in composite grafts involves combined transthoracic and transesophageal studies. In cases of suspected pseudoaneurysm formation in which a collection of blood and thrombus is seen around the graft, and without demonstration of flow by transthoracic echocardiography or other imaging modalities, a transesophageal study is crucial in providing the diagnosis.[18] Other Imaging Modalities

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Several modalities have been suggested as diagnostic screens for the development of pseudoaneurysm after Figure 25-7 Right parasternal transthoracic echocardiographic images of composite graft pseudoaneurysm demonstrating systolic compression of the graft by the pseudoaneurysm. Gr, graft; PSA, pseudoaneurysm.

composite graft surgery, including chest radiography, computed tomography (CT), digital subtraction angiography, and more recently, magnetic resonance imaging (MRI).[3] [17] [35] , [36] Although chest radiography may warn of the possibility, its sensitivity and specificity for the diagnosis of pseudoaneurysm are poor. Computed tomography and MRI are currently recommended as diagnostic imaging modalities for the serial evaluation of composite grafts and progression of the underlying disease to other segments of the aorta. [10] As for diagnosing pseudoaneurysm, although CT scanning or MRI can provide the diagnosis of blood or fluid collection around the graft, whether this finding represents a mere collection of fluid around the graft or is the result of communication with the ventricle, coronary arteries, or aorta may not be adequately differentiated. Until recently, aortography was the most widely used method for diagnosis of pseudoaneurysms and was the primary diagnostic modality for further evaluation of fluid collection around the composite graft.[36] Aortography still is an excellent modality for diagnosing dehiscence of the composite graft at the coronary artery anastomosis and distal graft (Fig. 25-9) ; however, in cases of isolated dehiscence of the graft at the aortic annulus anastomosis, aortography has been found to completely miss the diagnosis of pseudoaneurysm.[18] [27] This is explained by the fact that in these cases, the pseudoaneurysm communicates only with the left ventricle; a contrast injection in the aortic root would therefore not opacify the left ventricle or the pseudoaneurysm. An example of such a case is 557

Figure 25-8 (color plate.) Transesophageal echocardiographic frames (left) and corresponding color Doppler systolic frames (right) in a patient with endocarditis and composite graft pseudoaneurysm secondary to aortic annulus dehiscence. The upper panels are at the level of the prosthetic valve; the lower panels are at the level of the left main coronary artery. Two large vegetations are depicted (top, arrows) near the site of dehiscence.

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Systolic flow into the pseudoaneurysm is shown, and the limits of the pseudoaneurysm are indicated (bottom, arrows). Gr, graft; LA, left atrium; LVO, left ventricular outflow; P, pseudoaneurysm; RV, right ventricle; Veg, vegetations. Figure 25-9 Aortograms of the thoracic aorta in two patients with pseudoaneurysm complicating composite aortic graft. A, The pseudoaneurysm around the ascending graft is opacified (arrows). B, Aortogram of the patient whose echocardiographic images are in Figure 252 . In this case with single aortic annulus dehiscence, the large pseudoaneurysm is not opacified. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

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presented in Figure 25-2 and Figure 25-9 . Echocardiography in these cases is superior to aortography in the detection of pseudoaneurysms. Because in most of these cases the prosthetic aortic valve is not crossed at catheterization, opacification of the pseudoaneurysm necessitates a left ventriculogram using the transseptal technique or the levo phase of a pulmonary angiogram. In cases with concomitant dehiscence at the coronary or distal graft anastomoses, or in those with coexisting aortic insufficiency, the pseudoaneurysm may be opacified with aortography. [18] Complications of Aortic Allografts for Replacement of the Aortic Valve and Aortic Root Clinical Setting

Allograft or homograft replacement of the aortic root also has provided an effective therapy for diseases of the aortic root and the aortic valve. [37] [38] [39] [40] Three general techniques for insertion have been used: subcoronary valve implantation, a mini- or inclusion-root implantation, and an aorticroot replacement. Compared with composite graft replacement of the aortic root, the use of an allograft is particularly helpful in recurrent complications of the aortic root, especially in the presence of infection. Aortic allografts, therefore, have been performed predominantly in patients with destruction of the aortic root resulting from endocarditis, in patients with congenitally narrowed or hypoplastic aortic roots, in patients with complications involving previous root replacement such as heavy calcifications, and in those for whom anticoagulation is contraindicated.

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Among the most commonly reported complications of aortic allografts are calcifications of the root, aortic regurgitation, and infectious complications occurring primarily in patients whose underlying indication for aortic root replacement was endocarditis. Similar to composite aortic grafts, reports of unusual complications include problems with anastomotic sites (dehiscence with pseudoaneurysm formation), problems with coronary artery anastomosis, and possible compression of the graft. [38] [40] [41] [42] Figure 25-10 (color plate.) Transesophageal echocardiographic findings in a patient with systolic compression of aortic homograft secondary to dehiscence at the aortic annulus anastomosis. The upper panels display the dynamic compression of the homograft in short axis. Color M-mode echocardiography at the same level shows the systolic compression of the graft (white arrows) and systolic flow in both the pseudoaneurysm (above the arrows) and the homograft. Continuous wave Doppler recording from the transgastric view depicts the high gradient through the obstruction. The aortic valve was normal. Gr, gradient; H, aortic homograft; LA, left atrium; RV, right ventricle. (From Nagueh SF, Bozkurt B, Li GA, et al: Am Heart J 1996;132(5):1070–1073, with permission.) Echocardiographic and Doppler Findings

Data are scarce on the echocardiographic findings in aortic root allografts. [42] [43] A normal aortic root allograft, especially early after surgery, may be difficult to differentiate from a native aortic root. Late after surgery, however, calcifications of the homograft are common and are detected by echocardiography as increased echogenicity in the aortic root. If leaflet degeneration occurs, varying degrees of aortic insufficiency, with or without aortic stenosis, may be present. In a recent study, paravalvular aortic insufficiency and eccentric jets were more common in patients with subcoronary aortic allograft implantation (41%) than in those with root replacement (11%).[43] Some unusual complications may affect the allograft, but these complications have occurred early in the postoperative period and can be detected with intraoperative TEE. Recently, cases have been reported with complications related to anastomosis of the coronary arteries with the allograft.[41] Aliasing by color flow was detected along with ischemia in the distribution of the involved anastomosis (left main or right coronary artery). Other reported complications included dehiscence of the homograft with resultant pseudoaneurysm formation. Compression of the graft by the pseudoaneurysm may occur, simulating valve stenosis (Fig. 2510) .[42] With more extensive experience in cardiac imaging of these patients, the spectrum of complications and the role of echocardiography and other imaging modalities in patients undergoing aortic allograft surgery

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will be better defined. Replacement of the Aorta with an "Elephant-Trunk" Procedure In patients with extensive aortic aneurysmal disease or in dissection involving the ascending aorta, arch, and descending aorta, replacement of the aortic arch and varied lengths of the aorta can be a major undertaking. In 1983, Borst et al[44] described a dual-stage technique whereby the ascending aorta and arch are replaced first, leaving a segment of the distal tubular graft in the descending 559

Figure 25-11 (color plate.) Transesophageal imaging of the descending aorta (Desc Ao) (longitudinal plane) in a patient with aortic aneurysm involving the arch and descending aorta following a successful first stage of an "elephant trunk" procedure. The free distal end of the tubular graft is seen in the descending thoracic aneurysm. Color flow Doppler shows flow into the descending aorta arising from the distal end of the graft (Gr).

thoracic aorta. Borst coined the name "elephant-trunk" technique for this procedure. [44] At a second stage, the distal aorta is repaired beyond the subclavian artery. Since its original description, few modifications have been applied to the technique.[6] [45] [46] After the first stage of the operation, TEE imaging of the descending aorta shows the free position of the distal tubular graft in the descending aneurysm, with blood flow detected in the graft emptying into the aneurysm (Fig. 25-11) . This finding at this stage is normal and should not be mistaken for dehiscence of the graft. Following a successful first stage of the procedure, the most serious and usually fatal complication is rupture of the remaining descending thoracic aneurysm while awaiting the second stage of the surgery. The author has observed an unusual interim complication of severe hemolytic anemia following the first stage, which resolved after the second stage of the repair. The intravascular hemolysis was caused by insertion of the distal graft into the false lumen during the first operation. Because insertion of the graft into the descending aorta during the first stage is performed blind, some surgeons in the author's institution currently use intraoperative TEE to assess the position of the inserted graft in the descending aorta. Other Complications Progression of aortic disease with further aneurysm formation or dissection

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in additional segments of the aorta is the most common cause for reoperating on patients with diseases of the aorta.[19] [47] [48] [49] Monitoring the progression of aortic disease after the initial surgery affects prognosis and is crucial in the overall management of these patients. In addition to the complications mentioned earlier, rupture of the great vessels with fistula formation, although infrequent, can occur as a complication of aortic dissection or aneurysm. Communication between the aorta and pulmonary artery is clinically suspected by the findings of a continuous murmur, similar to patent ductus arteriosus or the presence of heart failure. Echocardiographic findings depend on the size of the shunt and may include volume overload of the left ventricle and elevated pulmonary pressures. Doppler echocardiographic findings are those of continuous flow into the pulmonary artery from the aorta.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Unusual Complications Following Valve Surgery Left Ventricular Pseudoaneurysm After Mitral Valve Replacement Clinical Setting

Rupture of the left ventricle with pseudoaneurysm formation is a rare but serious complication following mitral valve replacement. Overall, the incidence appears to range from 0.5% to 2% in isolated or combined mitral valve procedures. [50] [51] [52] [53] [54] Rupture of the left ventricle may occur immediately after surgery, presenting with hemodynamic collapse, or may present in the delayed postoperative period as a false aneurysm of the left ventricle. Anatomic characteristics and other factors have been described as predisposing to rupture of the ventricle such as heavy mitral or annular calcifications, the operative procedure itself, the number of surgical procedures previously undergone, or other hemodynamic considerations; however, often no clear cause for the pseudoaneurysm formation can be found.[55] The clinical presentation of pseudoaneurysm formation is variable. In the early postoperative period, it can present as poor postoperative progress, chest pain, heart failure, or as the development of a new murmur.[51] [52] [56] Late postoperative presentation may be similar or may be totally asymptomatic. In unusual cases, the pseudoaneurysm can compress the coronary arteries, leading to ischemia or myocardial hibernation.[57] Echocardiographic and Doppler Findings

Echocardiographic techniques play a significant role in the diagnosis of left ventricular pseudoaneurysm.[58] [59] A pseudoaneurysm, in contrast to a true aneurysm, is visualized as a saccular or globular chamber communicating with the left ventricle through a narrow and abrupt discontinuity in the ventricular myocardium. Over the past few years, the important role of Doppler echocardiography in the diagnosis of pseudoaneurysms has been increasingly appreciated. The demonstration of flow into the

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pseudoaneurysm by pulsed- and color-flow Doppler substantiates the diagnosis and may at times be the only clue for its presence in cases where the origin of the pseudoaneurysm cannot be visualized.[60] [61] [62] Doppler echocardiography is crucial in differentiating a pseudoaneurysm from other entities such as pericardial cysts, loculated pericardial effusion, or hematoma, especially in cases in which communication of the cavity with the left ventricle is not seen. As with true left ventricular aneurysm, a pseudoaneurysm demonstrates akinesis or dyskinesis during ventricular systole. Characteristic Doppler patterns can be seen with systolic filling and diastolic emptying of the pseudoaneurysm.[63] In patients with sinus rhythm, filling of the pseudoaneurysm during atrial contraction 560

can also be seen. With the availability of intravenous contrast echo agents that can cross the pulmonary circulation,[64] the administration of contrast can be of important diagnostic value in these situations by identifying whether such a communication exists with the left ventricle and by localizing its site. The use of contrast is particularly helpful when the communication with the ventricle is rather large and blood velocity in the cavity is too low to be clearly detected with Doppler. The location of the pseudoaneurysm can vary in relation to the prosthetic valve. Transthoracic echocardiography can demonstrate its presence and characteristic features; however, because of technical difficulties and imaging in the far field, the pseudoaneurysm may be frequently missed with the transthoracic approach. TEE is currently the echocardiographic method of choice in evaluating patients with suspected left ventricular pseudoaneurysm complicating mitral valve replacement.[63] [65] [66] [67] An example of a pseudoaneurysm complicating mitral valve replacement demonstrated by TEE and missed by transthoracic imaging is shown in Figure 25-12 . Other Imaging Modalities

Nonsurgical detection of pseudoaneurysm previously has depended on left ventriculography. Angiography is still important in the diagnosis of pseudoaneurysms in patients in whom the transthoracic examination may be difficult and also provides a spatial distribution of the Figure 25-12 (color plate.) Transverse transesophageal

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echocardiography planes at four levels (A to D) are shown along with contrast left ventriculography in the right oblique view, demonstrating opacification of a left ventricular pseudoaneurysm complicating mitral valve replacement. The approximate locations of the transverse echo planes are schematically shown on the angiogram. A1 and A2 show the maximal extent of the pseudoaneurysm and respective color flow demonstrating flow in the cavity. B and C show the neck of the pseudoaneurysm by color Doppler and its proximity and impingement on the proximal circumflex artery (C, arrows). The most caudal plane (D) is at the level of the prosthetic valve (PrV), which is normal. Ao, aorta; LA, left atrium; LV, left ventricle; PsAN, pseudoaneurysm; RV, right ventricle. (From Baker WB, Klein MS, Zoghbi WA: J Am Soc Echocardiogr 1993;6:548–552.)

pseudoaneurysm (see Fig. 25-12) ; however, because of its tomographic nature, TEE can further add to left ventricular angiography in pinpointing the site of origin of the pseudoaneurysm and its relation to adjacent structures for later surgical correction. The intraoperative use of TEE in surgical repair of these lesions can also be crucial when the repair involves areas close to the coronaries, in the assessment of ventricular function immediately postoperatively, and to indirectly detect whether injury occurred in the area of the coronary vessels with the evaluation of regional myocardial function.[63] It is generally agreed that management of patients with pseudoaneurysm formation of the left ventricle necessitates surgical intervention because of the risk of rupture and potential sudden death. Although surgical correction has been carried out almost uniformly in highrisk patients, some authors have advocated continued TEE follow-up in asymptomatic patients.[67] Left Atrial Dissection after Mitral Valve Replacement Clinical Setting

Dissection of the left atrium with resultant pseudoaneurysm formation is a rare complication of mitral valve replacement.[68] [69] [70] [71] [72] Predisposing factors for this unusual complication are similar to those for left ventricular pseudoaneurysms and include mitral annulus calcifications, 561

Figure 25-13 Dissection of the left atrium demonstrated with intraoperative transesophageal echocardiography after mitral valve surgery. A, horizontal view; B, 73-degree view. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (From Genoni M, Jenni R, Schmid ER, et al: Ann Thorac Surg 1999;68:1394–1396.)

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external cardiac massage, friable atrial wall tissue, preexisting pericardial adhesions, and technical considerations during surgery. Clinical presentation varies from detection in the operating room with TEE, to the presence of a systolic murmur of mitral regurgitation, heart failure, or an asymptomatic state. Surgical correction is recommended for symptomatic cases or those with severe left atrial compression. Spontaneous healing has been reported in only one case.[70] Internal drainage of the false lumen into the right atrium has been recently proposed in cases where the dehiscence at the mitral annulus is small.[71] Echocardiographic and Doppler Findings

On echocardiography, a cavity formation is seen within the left atrium, with a linear echo density consisting of the dissection of the atrial wall. This is best delineated with TEE (Fig. 25-13) .[71] [72] Paraprosthetic valve regurgitation is usually seen, with flow by Doppler entering into the false lumen through the communication.[72] Recording of the jet with continuouswave Doppler provides various degrees of velocity and duration of flow, depending on the size of the communication, and compliance of the false lumen. Pseudoaneurysm of the Ascending Aorta After Aortic Valve Replacement Clinical Setting

False aneurysm of the ascending aorta is a rare but serious complication of aortic valve replacement. Potential factors contributing to this complication include leaking aortotomy suture lines, needle punctures for air-evacuation procedures after surgery, postoperative endocarditis, or friability of the aortic wall.[73] [74] [75] [76] Clinical presentation is variable, including an asymptomatic, incidental finding on chest radiography or echocardiography, symptoms of atypical chest discomfort or dyspnea, and the finding of a continuous murmur because of fistula formation with adjacent cardiac chambers.[73] [74] [75] [76] Surgical repair generally is recommended because these pseudoaneurysms have a high propensity for rupture. Echocardiographic and Doppler Findings

Echocardiography shows a typical pseudoaneurysmal cavity arising from the ascending aorta in the vicinity of the prosthetic aortic valve. Usually the aorta is of normal size, and the neck of the pseudoaneurysm is small and

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may be difficult to appreciate on transthoracic echocardiography. TEE enhances imaging and definition of the pseudoaneurysm, which could be lined with thrombus. Color Doppler identifies flow into the cavity in systole, emptying in diastole (Fig. 25-14) . In a typical aortic pseudoaneurysm, there is no associated aortic insufficiency or flow in the cavity. In case of further complications of the pseudoaneurysm, however, continuous flow can be detected at the site of rupture into the right atrium or right ventricle.[75] [76] Similar to other pseudoaneurysms of the aorta, aortography, CT, or MRI also can delineate the pseudoaneurysm 562

Figure 25-14 (color plate.) Echocardiographic and Doppler images of an aortic pseudoaneurysm obtained with transesophageal echocardiography in the 30-degree and 90-degree planes. Flow is seen entering the pseudoaneurysm in systole and emptying in diastole. The corresponding aortogram delineates the extent of the pseudoaneurysm. Ao, aorta; An, pseudoaneurysm; LA, left atrium.

(see Fig. 25-14) . In these cases, Doppler echocardiography and aortography can aid surgical correction by more accurately pinpointing the site of rupture and flow into the pseudoaneurysm. Pseudoaneurysm of the Mitral-Aortic Intervalvular Fibrosa Clinical Setting

The region of the mitral-aortic continuity or mitral-aortic intervalvular fibrosa (MAIVF) contains mostly fibrous, relatively avascular tissue. Because of its composition, the MAIVF is the weakest segment of the aortic ring,[77] is prone to infection, and is more sensitive to trauma. The roof of the MAIVF is formed of pericardium, and its ventricular side is the posterior portion of the left ventricular outflow tract. Dehiscence in the MAIVF region, secondary to infection, trauma, or even surgical manipulation may result in the formation of an abscess or a pouch between the medial wall of the left atrium and the aorta. An intervalvular pseudoaneurysm ensues when the abscess or pouch communicates with the left ventricular outflow tract.[78] [79] [80] [81] An example of an MAIVF pseudoaneurysm is shown in Figure 25-15 . Most pseudoaneurysms in the MAIVF region occur secondarily to infection and are more common in

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patients with prosthetic valves.[82] Other causes include trauma, surgical trauma, and congenital pseudoaneurysms.[82] [83] [84] Detecting these pseudoaneurysms is important because of their potential complications, which may include rupture into the left atrium or aorta, resulting in mitral or aortic regurgitation, respectively, or even rupture into the pericardial space, with ensuing cardiac tamponade and death.[78] [81] [83] Determining the incidence of MAIVF pseudoaneurysms is difficult. Prior to the use of TEE, the few reports available surfaced at pathology or during angiography. With the advent of TEE, the most sensitive technique for evaluating these lesions, MAIVF pseudoaneurysms were detected in 9% of patients undergoing TEE for suspected aortic valve or ring disease.[82] The clinical presentation varies but is most commonly that of endocarditis, congestive heart failure, valvular regurgitation, or it may be asymptomatic, without a history of endocarditis. Because the pseudoaneurysm is located between the left atrium and aorta, and its origin is in the left ventricular outflow, it is not readily identified at surgery and may be missed. Thus, accurate detection, delineation, and differentiation of MAIVF pseudoaneurysms from ring abscesses is important in overall patient management and in the guidance of surgical correction. Echocardiographic and Doppler Findings

Transthoracic echocardiography has been used for the diagnosis of aortic root complications.[85] [86] Its sensitivity, however, recently has been shown to be limited in the evaluation of posterior lesions, particularly in the presence of prosthetic aortic valves; by contrast TEE substantially improves the diagnosis of such lesions.[87] [88] In a series from the author's institution, transthoracic echocardiography detected 43% of a total of 23 lesions affecting the aortic root, whereas TEE identified 90% of the lesions.[82] The importance of the transthoracic approach in detecting anterior ring abscesses cannot be ignored, however, particularly in the presence of prosthetic aortic valves, where TEE may have significant limitations because of shadowing of the prosthesis in the region of the anterior aortic ring. Combining transthoracic and transesophageal imaging, therefore, would allow a comprehensive evaluation of the aortic root and is strongly recommended. In contrast to aortic ring abscesses, intervalvular pseudoaneurysms exhibit a characteristic dynamic feature during the cardiac cycle. Marked pulsatility is observed in most MAIVF pseudoaneurysms, with expansion during early systole and collapse in diastole (see Fig. 25-15) . [82] This

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feature is explained by the fact that the pressure in the pseudoaneurysm reflects left ventricular pressure and 563

that a large portion of the pseudoaneurysm is surrounded by the left atrium. Thus, when left atrial pressure exceeds left ventricular pressure in diastole, the pseudoaneurysm collapses, whereas it expands in systole. This dynamic behavior during the echocardiographic examination is indeed the first clue to the presence of an MAIVF pseudoaneurysm. In contrast, aortic ring abscesses located anteriorly or posteriorly in the aortic root do not exhibit this marked pulsatility, which may be explained by several factors. In walled-off abscesses without detectable flow, pulsatility is not expected. In ring abscesses with systolic and diastolic flow owing to paraprosthetic aortic regurgitation, the pressure remains high throughout the cardiac cycle in these cavities compared with adjacent chambers so that pulsatility is not seen. Although collapsibility provides indirect evidence for the presence of an MAIVF pseudoaneurysm, confirmation of this diagnosis requires visualization of the neck of the pseudoaneurysm in the left ventricular outflow. This communication rarely can be seen by transthoracic echocardiography[82] however, it is usually well visualized with the transesophageal approach. In the author's experience, the size of the neck has ranged from 0.5 to 2.1 cm in diameter. In cases where there is still doubt about whether the cavity communicates with the aorta or left ventricle, the administration Figure 25-15 (See also color plate.) Echocardiographic and color Doppler frames from the transverse plane during transesophageal echocardiography showing a typical simple mitral-aortic intervalvular fibrosa pseudoaneurysm with its location, pulsatility, and flow patterns during the cardiac cycle. Top, Pseudoaneurysm (straight arrow) and communication with the left ventricular outflow (curved arrow) are shown. The pseudoaneurysm begins to expand during early systole, remains distended in late systole, and collapses during diastole. Bottom, Magnified color Doppler views of the area within the box seen in the top middle panel. During early systole, the pseudoaneurysm fills, showing high, aliased velocities. Low, nonaliased velocities are seen during the remainder of systole while the pseudoaneurysm remains expanded (middle). During diastole, the pseudoaneurysm empties and collapses. LA, left atrium; LV, left ventricle.

of intravenous contrast agents that cross the pulmonary circulation can help resolve this issue.

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Color Doppler imaging is crucial in the evaluation of MAIVF pseudoaneurysms. Its application helps to assess whether rupture of this cavity into adjacent chambers has occurred and define its communication. The following are characteristic Doppler features in unruptured and ruptured MAIVF pseudoaneurysms. In the case of unruptured pseudoaneurysms, Doppler evaluation usually is less impressive. Only a brief duration of flow into the pseudoaneurysm occurs during early systole (20–60 msec), at which time pressure between the pseudoaneurysm and left ventricle is equalized, and no further flow is detected by Doppler (see Fig. 25-15) .[82] During diastole, a brief period of flow exiting from the pseudoaneurysm may be seen but frequently can be missed because of its low velocity. In contrast, in pseudoaneurysms that have ruptured, into either the left atrium or aorta, an intense color-flow signal can be seen during the cardiac cycle. In cases of rupture into the left atrium, color Doppler shows holosystolic, intense flow signal in the pseudoaneurysm and eccentric "mitral" regurgitation through the perforation of the pseudoaneurysm, the latter acting as a conduit for blood flow from the left ventricle to the left atrium (Fig. 25-16) . The use of color Doppler actually facilitates 564

Figure 25-16 (See also color plate.) Two-dimensional and color flow transesophageal echocardiography images of a complicated mitralaortic intervalvular fibrosa pseudoaneurysm with rupture into the left atrium in the setting of endocarditis after mitral valve annuloplasty and aortic valve replacement. The pseudoaneurysm (slender arrow) and its neck (large arrow) are shown. The pseudoaneurysm is septate, has mobile vegetations, and expands significantly in systole. An intense color flow jet in systole is seen through the pseudoaneurysm with subsequent, eccentric regurgitation into the left atrium. Ao, aorta; LA, left atrium; LV, left ventricle.

the identification of the rupture site of the pseudoaneurysm by tracking the origin of the regurgitant jet. The ruptured site is rarely seen by transthoracic echocardiography but can be suspected by the presence of eccentric mitral regurgitation arising close to the aortic root. Similar to unruptured pseudoaneurysms, those pseudoaneurysms communicating with the left atrium show systolic expansion and diastolic collapse (see Fig. 25-16) . In cases where rupture of the pseudoaneurysm occurs into the aorta, with or without concomitant dehiscence of the prosthetic aortic valve, aortic insufficiency is detected (Fig. 25-17) . In systole, color Doppler shows

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antegrade flow from the ventricle through both the pseudoaneurysm and the prosthetic aortic valve. In diastole, retrograde flow of "aortic" insufficiency is seen, directed from the aortic root into the pseudoaneurysm and into the ventricle. Other Imaging Modalities

Until recently, cineangiography has been the standard for diagnosing aortic root lesions.[89] With the advent of echocardiography with Doppler, and more recently TEE, however, these techniques have rivaled the invasive diagnostic modality. Few cases of MAIVF pseudoaneurysms have been described with angiography.[80] [90] [91] The pulsatility described earlier is also seen on angiography (Fig. 25-18) . In a case series in which patients underwent both diagnostic modalities, MAIVF pseudoaneurysms were more frequently detected by TEE than by aortography.[82] Only 2 of 9 pseudoaneurysms were identified by aortography, both of which had associated aortic insufficiency (Fig. 25-19) . The direct communication between the left ventricular outflow tract and pseudoaneurysm explains the need for a ventricular injection of dye to detect this abnormality. This finding is similar to that described earlier for pseudoaneurysms of composite aortic grafts with a single dehiscence at the aortic annulus anastomosis. Thus, in patients without aortic insufficiency, demonstration of the pseudoaneurysm with angiography requires left ventriculography. Compared with angiography, TEE more clearly delineates the origin of the intervalvular pseudoaneurysms and their communication elucidating 565

Figure 25-17 (See also color plate.) Two-dimensional and color Doppler frames during omniplane transesophageal examination at an angulation of 120 degrees, showing a ruptured mitral-aortic intervalvular fibrosa pseudoaneurysm into the aorta. During systole, blood flows into the pseudoaneurysm and from the pseudoaneurysm into the aorta through small fenestrations (white arrow). Normal flow direction through the prosthesis (black arrow) is also shown. During diastole, blood regurgitates into the left ventricle through the pseudoaneurysm (black arrows). An, pseudoaneurysm; Ao, aorta; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

the origin of concomitant mitral regurgitation or aortic insufficiency and, therefore, assisting in planning surgical repair.[82]

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Patients with cavitary lesions complicating aortic valve disease, particularly prosthetic valves, require extensive surgical intervention, including in some cases aortic root replacement. Because of the risk of rupture into the pericardium, surgical correction of MAIVF pseudoaneurysm is warranted in most cases. Although the natural history of uncomplicated pseudoaneurysm is unclear, surgical repair was performed in the majority of cases reported. In patients who do not undergo an immediate operation, TEE may be useful in identifying serial changes in the pseudoaneurysm or the development of a rupture into adjacent chambers, which can help plan appropriate therapy. Intracardiac Fistula following Valve Replacement Clinical Setting

Intracardiac fistula formation is an uncommon complication following valve replacement surgery. Several types of fistulae may occur following mitral valve replacement, Figure 25-18 Left anterior oblique view during aortography in a patient with mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm and aortic insufficiency. The MAIVF pseudoaneurysm (arrows) shows pulsatility during the cardiac cycle. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

including left ventricular–to–right atrial communications and left ventricular–to–coronary sinus fistulae.[92] [93] [94] [95] These complications are attributed mainly to excessive débridement and injury to the mitral annulus during surgery. Concomitant endocarditis, however, may be an underlying mechanism in late postoperative cases. In the early postoperative period, the clinical presentation may include a new systolic murmur, findings of high cardiac output, or a high oxygen saturation in the pulmonary artery; however, this condition may be often misdiagnosed as remnant tricuspid regurgitation or periprosthetic valve regurgitation. Conversely, fistula formation following aortic valve replacement, between the aorta and cardiac chambers, such as left or right atrium or right ventricle, is usually secondary to infectious causes but could also occur in the setting of a ruptured pseudoaneurysm.[75] [76] Findings in these conditions are similar to those of rupture of sinus of Valsalva, including a continuous murmur. Echocardiographic and Doppler Findings

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A left ventricular-to-right atrial fistula mimics tricuspid insufficiency, and differentiating it from the latter may be difficult. A few direct and indirect clues may raise suspicion for this diagnosis. In contrast to most tricuspid insufficiency 566

Figure 25-19 Example of a patient with an unruptured mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm diagnosed with transesophageal echocardiography (TEE), missed at aortography. Top, TEE transverse planes show the MAIVF pseudoaneurysm expanding during systole (left) and collapsing during diastole (right). Communication between the pseudoaneurysm and left ventricular outflow region (arrow) is seen. Bottom, Aortogram during systole and diastole in the same patient appears normal. An, MAIVF pseudoaneurysm; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

jets, which are directed towards the interatrial septum, the jet from the fistula seen by color Doppler arises near the crux of the heart and is usually directed centrally or toward the free wall of the right atrium. Unconventional imaging planes used to assess the origin of the jet may provide visualization of proximal velocity acceleration on the left ventricular side, raising suspicion for the diagnosis. Recording of jet velocity by continuous-wave Doppler will invariably lead to registering a high-velocity jet, similar to mitral regurgitation. If there is concomitant mitral regurgitation, the jet velocities will be almost equal—this will lead to an overestimation of pulmonary artery pressure when using the modified Bernoulli equation. A close examination of right ventricular function, septal motion, pulmonary flow velocity contour, and pulmonary insufficiency jet, if available, may reveal a discordance between findings of normal pressure by these indices and that derived from the "tricuspid insufficiency" jet, raising suspicion for the diagnosis. Further confirmation may be carried out with TEE aiming at better definition of the origin of the jet. In the case of left ventricular–to–coronary sinus fistula, a high-velocity intense color jet is seen in the coronary sinus, which in these cases is usually dilated. The differential diagnosis includes a coronary artery–to– coronary sinus fistula, where, in contrast, a continuous flow occurs.[96] On the other hand, fistula formation between the aorta and cardiac chambers through a periprosthetic aortic valve abscess rupture is diagnosed as a

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continuous systolic and diastolic jet into the respective chamber, with a continuous and intense recording by continuous-wave Doppler of high velocity reflecting the high-pressure difference between aorta and the communicating chamber. In the above conditions, the most often used alternative diagnostic modality is contrast cineangiography for demonstrating the communications. Pulmonary Valve Autotransplantation: The Ross Operation In 1967, Ross described the use of an autologous pulmonary valve to replace the diseased aortic valve. The procedure, presently known as the Ross operation, consists of implanting the patient's own pulmonary valve within the aortic root and replacing the pulmonary valve with either an aortic or pulmonary allograft. This procedure is performed predominantly in young adult patients and children with aortic valve disease and offers the advantages of valve viability and potential for growth in young patients, and the elimination of the need for long-term anticoagulation, in addition to increased durability compared with aortic allografts and bioprosthetic valves in this age group.[97] [98] Complications of the Ross operation include the potential for aortic insufficiency because of malalignment of the pulmonic valve in the aortic position, and valve degeneration occurring late after surgery. More recently, replacement of the aortic root with a pulmonary root autograft has been proposed.[99] [100] [101] The potential advantage of this procedure, compared with simple pulmonary valve autograft, is the more optimal alignment and function of the valve leaflets, because the sinuses of Valsalva also are transplanted. Short-term follow-up data from these patients have not revealed significant dilatation of the wall of the pulmonary artery in the aortic position. Over the past few years, more experience with the procedure has been acquired.[40] [102] [103] [104] [105] [106] The incidence of progressive aortic insufficiency has been low and has improved with the root-replacement technique.[40] [107] Annular dilatation of the pulmonary autograft occurs after implantation in the aortic position (20% increase on average).[107] [108] Infrequently, however, aneurysmal or pseudoaneurysmal formation may develop at this site, complicating pulmonary autograft surgery and necessitating reoperation.[109] [110] Progressive stenosis of the allograft in the pulmonary position has been infrequently reported, usually at the distal anastomosis in the pulmonary artery[101] [111] however, reoperating on the pulmonary allograft may be necessary in up to 20% of patients, at 20 years.[40] Echocardiographic techniques are ideally suited for the follow-up and

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detection of complications in patients with pulmonary valve or pulmonary root autografts.[101] [107] [108] [109] [110] [111] [112] [113] In most cases, transthoracic echocardiography with Doppler is sufficient to evaluate the aortic root and the presence and severity of aortic insufficiency. In suspected complications, TEE improves the definition of aortic root pathology.[109] Similarly, echocardiography can provide serial assessment of allograft function in the pulmonary position. Stenosis at the distal anastomosis has been recently reported with Doppler echocardiography, requiring reoperation in few patients.[101] [111] The transesophageal approach may be needed to evaluate complex lesions or the mechanism of postoperative complications.

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Section 5 - Cardiomyopathies and Pericardial Disease

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Chapter 26 - Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient Jannet F. Lewis MD

Background It is estimated that there are 2 million individuals in the United States with a diagnosis of congestive heart failure, and nearly 400,000 new patients are diagnosed each year. Among 652 members of the Framingham Heart Study who developed congestive heart failure between 1948 and 1988, median survival after onset of heart failure was 1.7 years in men and 3.2 years in women.[1] One-year and 5-year survival rates were 57% and 25% in men and 64% and 38% in women, respectively. No significant change in the prognosis of congestive heart failure was identified during the 40 years of observation. However, the course of the disease is not uniformly poor, and considerable variability exists among individual patients. [2] [3] [4] [5] [6] [7] [8] [9]

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Moreover, newer therapeutic interventions, both pharmacologic treatment [10] [11] [12] [13] and cardiac transplantation,[14] [15] [16] promise improved survival in patients with congestive heart failure. Improvement in survival depends in part on the ability to correctly characterize the disease and stratify patients with regard to prognosis to make the most appropriate therapeutic plan. Two-dimensional and Doppler echocardiography have markedly improved our understanding of the pathophysiology of congestive heart failure and have also provided noninvasive techniques for accurate diagnosis of underlying causes, hemodynamic evaluation at baseline and during medical intervention, and important prognostic information to guide further management. This chapter is devoted primarily to the use of twodimensional and Doppler echocardiography in the evaluation and management of congestive heart failure due to dilated cardiomyopathy. Other diseases associated with heart failure (coronary artery disease, valvular heart disease, other cardiomyopathies) are the subjects of separate chapters.

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Echocardiography in the Diagnosis of Cardiomyopathy 572

The widespread use of echocardiography in the management of patients with suspected or known cardiac disease has facilitated our appreciation of the spectrum of diseases that present with the constellation of signs and symptoms of congestive heart failure. Thus, while many patients with manifestations of decompensated congestive heart failure have reduced left ventricular ejection fraction, congestive symptoms and signs may be present in other conditions.[17] [18] Previous observations in patients undergoing noninvasive assessment of systolic function have shown that as many as 50% of patients with clinically diagnosed congestive heart failure have a normal left ventricular ejection fraction. Most of these patients have systemic hypertension alone or in combination with ischemic heart disease. A substantial minority have nondilated cardiomyopathies, such as hypertrophic or restrictive cardiomyopathy, with heart failure occurring primarily as a consequence of diastolic dysfunction. Echocardiography provides excellent visualization of the left ventricle in most patients and readily distinguishes the three major forms of cardiomyopathy. Dilated cardiomyopathy is characterized by dilated cardiac chambers, most prominently the left ventricle, and reduced ejection fraction[3] [8] [19] , [20] (Fig. 26-1) . Echocardiographic diagnosis of hypertrophic cardiomyopathy is based on identification of severe asymmetric hypertrophy of the left ventricle, usually most marked in the ventricular septum with sparing of the posterior wall, and normal or increased ejection fraction[21] [22] [23] [24] [25] (see Chapter 27) . The disease shows considerable morphologic diversity, however, and recognition of this diversity is essential for diagnosis. Thus, while septal hypertrophy is the most prominent and best-recognized feature of the

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disease, hypertrophy may be confined to the apical segments of the left ventricle[26] [27] or most marked in the posterior free wall.[28] Also, there appear to be definite age-related morphologic differences among patients with hypertrophic cardiomyopathy[29] [30] [31] (Fig. 26-2) . Elderly patients with this disease, compared with younger patients, generally show less severe hypertrophy that is more often localized to the ventricular septum. Restrictive cardiomyopathy, most commonly due to cardiac amyloidosis, may also present with signs and symptoms of congestive heart failure (see Chapter 28) . The disease is characterized by a symmetrically thickened left ventricular wall with a "ground-glass" appearance of the myocardium, and normal left ventricular chamber size and systolic function until the very advanced stages of the disease (Fig. 26-3) . Doppler echocardiographic studies in patients with amyloid heart disease have identified a spectrum of transmitral filling patterns that correlate with the severity of disease and prognosis.[32] [33] Echocardiographic diagnosis of ischemic heart disease is based on identification of segmental wall motion abnormalities ( see Chapter 11 Chapter 12 Chapter 13 Chapter 14 ). In most patients, the distinction between ischemic heart disease and dilated cardiomyopathy is readily apparent. However, in some Figure 26-1 Diastolic (A) and systolic (B) frames in an apical four-chamber echocardiographic view from a 23-year-old man with dilated cardiomyopathy. The left ventricle is dilated and the ejection fraction is markedly depressed. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

patients with severe ischemic heart disease, there may be substantial left ventricular dilation and global systolic dysfunction.[34] Alternatively, patients with nonischemic dilated cardiomyopathy may demonstrate segmental areas of akinesis as well as regions with apparently preserved contractility, usually the basal segments of the inferior and posterior walls. [35] Consequently, in patients with severely depressed left ventricular systolic function, the distinction between nonischemic and ischemic disease may present an important diagnostic problem. Although coronary arteriography provides definitive diagnosis in such cases, other noninvasive modalities such as dobutamine stress echocardiography also give important diagnostic and therapeutic information.

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Figure 26-2 Echocardiographic images in a parasternal long-axis view from a 23-year-old woman (A) and a 66-year-old woman (B) with hypertrophic cardiomyopathy. In the younger patient, the ventricular septum (VS) is markedly and diffusely thickened and bulges into the left ventricular chamber. In the older patient, the septum is more modestly thickened (arrowheads), and the ventricular chamber shape appears normal. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

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Assessment of Dilated Cardiomyopathy by Echocardiography Morphologic Description Cardiac enlargement is a central feature in dilated cardiomyopathy. [3] [19] , [36] However, echocardiographic assessment has demonstrated a spectrum of findings with regard to the degree of chamber enlargement, magnitude of left ventricular dysfunction, myocardial thickness, and size and systolic function of the right ventricle.[8] [20] [37] , [38] For example, although most patients show a marked increase in the size of the left ventricular chamber, Keren et al[38] described a group of patients with "minimally dilated cardiopathy." The cause of lack of dilation is not entirely clear, but pathologic examination shows less myofibrillar loss in these subjects than in patients with more dilation. The prognosis for these patients appears to be similar to the prognosis for those with the more classic form of the disease. The morphologic variability in dilated cardiomyopathy has also been demonstrated at postmortem examination. Benjamin et al[39] found variability in the degree of left ventricular wall thickness and relation of wall thickness to chamber size. A review of clinical records revealed greater wall thickness in long-term survivors than in short-term Figure 26-3 Echocardiographic images from a 62-year-old man with cardiac amyloidosis. The ventricular wall thickness is markedly increased, and the ventricular septum has a typical "ground-glass" appearance. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 26-4 Two-dimensional echocardiographic images in an apical four-chamber view from two patients with dilated cardiomyopathy. A, Predominant and disproportionate dilation of the left ventricular chamber can be seen. The right ventricle in this patient appears relatively small. B, More pronounced right ventricular chamber dilation can be seen. Right ventricular systolic function is also depressed in this patient. Pacemaker leads (arrowheads) are present in the right cardiac chambers. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

survivors, and a smaller radius-to-thickness ratio appeared to confer a somewhat protective effect. Similarly, Gaasch and Zile[40] found wall stress to be an important predictor of outcome in patients with dilated cardiomyopathy. Investigations of patients with dilated cardiomyopathy have focused largely on description of the left ventricle. However, right ventricular size and systolic function also vary among patients with dilated cardiomyopathy and have important implications for prognosis and treatment.[9] [41] In a clinical and echocardiographic study of patients with dilated cardiomyopathy, two morphologic subsets were identified: patients with relatively equal degrees of ventricular enlargement, and patients with predominant and disproportionate dilation of the left ventricle but relative sparing of the right [9] (Fig. 26-4) . Severe mitral and tricuspid regurgitation were more common among patients with pronounced right ventricular enlargement. Survival over a mean follow-up period of 28 months was better among patients with primarily left ventricular dilation. Pinamonti et al [42] subsequently reported right ventricular systolic function as a strong predictor of death or cardiac transplantation in 79 consecutive patients with dilated cardiomyopathy followed for a mean of 22 months. Noninvasive Hemodynamic Assessment The hemodynamic parameters assessable by two-dimensional and Doppler echocardiography are listed in Table 26-1 . Assessment of Left Ventricular Systolic Function

Left ventricular systolic function in the setting of congestive heart failure has important diagnostic and prognostic implications. In addition, parameters of systolic function may be useful in evaluating the response to therapeutic intervention. The most widely used clinical index of systolic function is ejection fraction (calculated as [end-diastolic volume − end-

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systolic volume]/end-diastolic volume). Left ventricular volume has been assessed by echocardiography on the basis of a number of geometric assumptions (see Chapter 4) . Because the left ventricle commonly loses its normal elliptical geometry in TABLE 26-1 -- Noninvasive Hemodynamic Data Obtainable by TwoDimensional (2D) and Doppler Echocardiography 2D Alone X X X

Hemodynamic Parameter LV diastolic volume LV stroke volume/cardiac output LV ejection fraction LA/LV diastolic pressure Pulmonary artery pressure RA pressure X Valvular regurgitation severity X LA, left atrial; LV, left ventricular; RA, right atrial.

Doppler Alone

Both

X

X

X X X X

X

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TABLE 26-2 -- Measurement of Stroke Volume/Cardiac Output by Doppler Echocardiography Study Fisher et al[46] † Dubin et al[49] Lewis et al[47]

Subjects, n 15 18 39

Huntsman et al

45

r Value * (SEE) Variability, % 0.97 (0.23 L/m) 0.87 (11 mL) 0.91 (0.63 L/m) inter: 6.8 ± 1.5 0.87 (0.59 L/m) inter: 16.4 ± 13.8 0.94 (0.58 L/m)

Method Mitral LV outflow Mitral inflow Aorta

[45]

Nicolosi et al[48] ‡

30

—

inter: 6.8

Six methods

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intra: 5.9 methods 16.0 Inter, interobserver variability; intra, intraobserver variability; method, variability of the method; LV, left ventricular; SEE, standard error of estimate. * Correlation with stroke volume/cardiac output measured by roller pump and thermodilution cardiac output. † Canine studies. ‡ Healthy volunteers without thermodilution measurements.

the setting of heart failure, however, the biplane "method of discs" is less dependent on geometric assumptions and provides a more accurate determination of ventricular volume.[43] The major limitation to this method is the requirement for apical four- and two-chamber views with endocardial definition of sufficient technical quality to permit manual tracing during freeze-frame analysis. Developments in automated border detection may resolve this problem (see Chapter 7) . Aside from these technical considerations, ejection fraction is largely dependent on the loading conditions of the left ventricle, and therefore may not serve as an accurate surrogate of myocardial contractility. For example, in the setting of mitral regurgitation, ejection fraction poorly reflects myocardial contractility. Determination of stroke volume and cardiac output provides more accurate assessment of ventricular performance. Stroke volume can be calculated from diastolic and systolic left ventricular volumes by echocardiography.[43] [44] However, as with calculation of ejection fraction, significant error may occur because of suboptimal visualization of endocardial borders during freeze-frame analysis. Studies by several investigators in different laboratories have demonstrated excellent correlation between cardiac outputs obtained by Doppler echocardiography and flow measured by invasive techniques[45] [46] [47] [48] [49] (Table 26-2) . Doppler echocardiographic assessment of stroke volume is based on the principle that flow (Q) across an orifice can be calculated as the product of the cross-sectional area of the orifice (CSA) and the time velocity integral (TVI) across the orifice: Q = CSA × TVI

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Stroke volume = CSA × TVI Cardiac output = stroke volume × heart rate Theoretically, flow can be assessed across any vessel or cardiac valve. Thus, stroke volume has been calculated using Doppler sampling of left ventricular outflow, ascending aorta, and mitral, tricuspid, and pulmonic valves.[45] [46] [47] [48] [49] [50] Each method is limited by the ability to measure orifice size accurately. Calculation of stroke volume and cardiac output from the flow velocity in the left ventricular outflow tract (Fig. 26-5) utilizes cross-sectional area calculated from diameter measurement of the left ventricular outflow tract, assuming a circular geometry: Area = π(diameter / 2)2 As is apparent, small differences in diameter measurement result in relatively larger differences in calculation of cross-sectional area and stroke volume. Nonetheless, the overall correlation of cardiac output determined from the left ventricular outflow Doppler method and output measured by thermodilution is excellent, and reproducibility of this method is approximately 16%.[47] Use of ascending aortic flow velocity for calculation of stroke volume is technically more difficult and has been less commonly applied.[48] [49] Several approaches have been assessed for measurement of stroke volume from the mitral inflow velocity waveform.[46] [47] [48] [49] The simplest method employs Doppler sampling in the center of the mitral annulus and measurement of the mitral annulus, assuming a circular geometry for calculation of cross-sectional area (Fig. 26-6) . The mitral annular method for calculation of stroke volume and cardiac output also shows close correlation with thermodilution measurement but with larger interobserver variability than with the outflow method. Because of the noncircular geometry of the mitral annulus, alternative approaches to the calculation of mean mitral valve area during diastole utilize M-mode correction of twodimensional measurements as well as biplane measurement of mitral annulus diameter, assuming an elliptical geometry. These approaches have also shown good correlation with thermodilution cardiac output but are more tedious and do not appear to offer significant advantage. Pulmonary artery flow calculation of stroke volume has been less widely used in adult patients because of limited visualization of the pulmonary

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artery boundaries but has been extensively applied in pediatric patients.[50] The pulmonary artery dilation often observed in patients with dilated cardiomyopathy may improve visualization of the pulmonary boundaries and thus facilitate the use of this method in adults. Because of the difficulties encountered with calculation of cross-sectional area, use of the flow velocity integral alone to obtain a stroke distance has been proposed as a correlate of stroke volume.[51] Measurement of stroke distance 576

Figure 26-5 Calculation of cardiac output using the left ventricular outflow method. The diameter of the left ventricular outflow immediately proximal to the aortic cusp is measured from the parasternal long-axis view (A, upper and lower). Pulsed Doppler sample volume is placed proximal to the aortic valve in the apical view (B, upper) to obtain the left ventricular outflow flow velocity waveform (B, lower). LA, left atrium; LV, left ventricle.

for serial evaluation of patients undergoing therapeutic intervention appears to be a reasonably accurate alternative to stroke volume measurement. Ejection phase indices derived from M-mode and Doppler echocardiographic measurements have also been used to assess left ventricular systolic function. These indices are significantly influenced by loading conditions of the ventricle. On the other hand, indices related to isovolumic contraction, such as the rate of pressure rise Figure 26-6 Calculation of cardiac output using the mitral inflow method. A, Diameter of the mitral annulus is measured from the apical four-chamber view during maximal excursion of the mitral valve. B, Doppler sample volume is placed in the center of the mitral annulus to obtain the mitral flow velocity waveform (lower). LA, left atrium; LV, left ventricle.

during this period (dP/dt), appear to be less influenced by load and are especially useful for evaluating directional changes of myocardial contractility. The mitral regurgitant jet velocity is largely a consequence of temporal changes in the relationship between left ventricular and left atrial pressures. During isovolumic contraction, left atrial pressure does not change appreciably in patients with chronic mitral regurgitation and a

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compliant left atrium. Thus, the rate of change in velocities (and derived pressures) in 577

Figure 26-7 (Figure Not Available) Drawing of a mitral regurgitant flow velocity jet illustrating the basis for determining rate of pressure rise (RPR) in the left ventricle. Two points are selected along the velocity curve (A, 1 m/sec = 4 mm Hg; B, 3 m/sec = 36 mm Hg), and the time interval (t) between them is measured. ECG, electrocardiogram. (From Bargiggia GS, Bertucci C, Recusani F, et al: Circulation 1989; 80:1287–1292, with permission.)

this pre-ejection phase provides information about ventricular systolic performance. [52] [53] [54] [55] Bargiggia et al[52] used Doppler echocardiography to obtain dP/dt from mitral regurgitant jet velocities and found good correlation with peak dP/dt measured at cardiac catheterization (Fig. 26-7) (Figure Not Available) . Doppler-derived dP/dt is obtained by digitization of mitral regurgitant jet velocities at 1 msec intervals to obtain the rate of increase in velocity. This rate of velocity change is converted to rate of pressure increase using the modified Bernoulli equation (pressure gradient = 4[velocity]2 ). In the normal heart, the rate of pressure rise exceeds 1200 mm Hg per second. A pressure rise of less than 400 mm Hg per second is consistent with severe systolic dysfunction.[54] Assessment of Left Ventricular Diastolic Function and Estimation of Left Ventricular Filling Pressure

Left ventricular diastolic function plays an important role in the pathophysiology of a variety of diseases.[17] [18] , [56] [57] [58] [59] In patients with systolic dysfunction, abnormalities of diastolic function may importantly contribute to clinical manifestations of disease. Indeed, diastolic function appears to be significantly related to the severity of cardiac symptoms and prognosis in patients with heart failure.[41] [42] [60] [61] [62] [63] [64] [65] [66] [67] Transmitral flow velocity obtained by pulsed Doppler echocardiography has been extensively used to assess left ventricular diastolic function[68] [69] [70] [71] [72] [73] [74] [75] (see Chapter 6) . The normal mitral waveform is characterized by an early peak flow velocity and a second, late peak with atrial systole (Fig. 26-8) . A number of diastolic indices have been used to assess left ventricular diastolic function, including peak velocity during early filling (E), peak velocity following atrial contraction (A), the time integrals of early and late filling velocities, the ratio of early and late peak

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velocities (E/A), and deceleration time (measured as the time from peak early filling to descent of filling to the baseline). Mitral inflow waveform patterns have been correlated with hemodynamic findings and therefore provide important noninvasive hemodynamic information.[66] [67] [70] A pattern of impaired relaxation is characterized by reduced early peak flow velocity, prolonged deceleration time, and augmented late flow velocity [70] (see Fig. 26-8) . This pattern has been observed in a variety of conditions (e.g., systemic hypertension, coronary artery disease, and early amyloidosis) and is associated with abnormal left ventricular relaxation with relatively normal left ventricular diastolic pressure. In comparison, a "restrictive" pattern of filling has been observed with marked elevation of left atrial and left ventricular diastolic pressure and is most commonly observed in advanced congestive heart failure[41] [42] [66] , [67] [70] [76] (see Fig. 26-8) . Although the transmitral flow velocity waveform provides important information regarding left ventricular diastolic function, the appearance of the transmitral waveform is also influenced by a number of variables, including age, heart rate, and left atrial/left ventricular crossover pressure at the time Figure 26-8 Spectrum of mitral inflow patterns. A, Normal mitral velocity flow pattern. B, Pattern of impaired relaxation with decreased peak early velocity (E) and increased peak late velocity (A). C, Restrictive filling pattern showing increased E velocity, short deceleration time, and reduced A velocity.

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Figure 26-9 Illustration of left ventricular and left atrial pressures with simultaneous mitral flow velocity waveforms in a normal ventricle, a ventricle with impaired relaxation, and a ventricle with increased preload. Note the relation of the atrioventricular gradient on the appearance of the mitral waveform. Hatched areas represent the atrial filling fraction; large arrows denote isovolumic relaxation time; small arrows indicate deceleration time (Dec Time). A, peak late velocity; E, peak early velocity; LA, left atrium; LV, left ventricle. (From Mulvagh S, Quinones MA, Kleiman NS, et al: J Am Coll Cardiol 1992;20:112– 119, with permission from the American College of Cardiology.)

of mitral opening[70] [72] [77] [78] [79] (Fig. 26-9) . The latter accounts for the "pseudonormal" pattern observed in patients with impaired relaxation and

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elevated left atrial pressure. The dependence of transmitral filling on factors other than left ventricular diastolic dysfunction presents an important consideration for the use of mitral indices of left ventricular filling for assessment of diastolic function. Assessment of pulmonary vein flow velocity waveforms provides information complementary to that obtained from the transmitral flow patterns.[80] [81] [82] [83] Pulmonary venous sampling is most readily obtained from a transesophageal study but with practice can be obtained with the transthoracic approach in most patients. The normal pulmonary vein flow pattern is characterized by antegrade systolic and diastolic waves and a retrograde diastolic wave following atrial systole (Fig. 26-10) . During forward systolic pulmonary vein flow, the left atrium functions as a reservoir. Systolic flow from the pulmonary vein into the left atrium is influenced by contractility of the left ventricle and descent of the mitral annulus, as well as left atrial pressure. Thus, impaired left ventricular systolic function and elevated left atrial (or pulmonary capillary wedge) pressure are associated with decreased systolic antegrade flow in the pulmonary veins[81] [83] (Fig. 26-11) (Figure Not Available) . A ratio of pulmonary vein systolic to diastolic velocity integrals of less than 0.40 correlates with left atrial pressures of greater than 15 mm Hg. During forward diastolic flow of the pulmonary vein, the left atrium functions as a conduit. Pulmonary venous diastolic flow is therefore largely influenced by left ventricular diastolic pressure, as well as factors that affect early transmitral filling: age, heart rate, and differences in left atrial/left ventricular crossover pressure at the time of mitral opening. Retrograde diastolic flow (atrial reversal) depends on the integrity of atrial systole and left atrial pressure. Elevated left atrial pressure is usually associated with a pulmonary vein retrograde diastolic flow velocity of greater than 40 cm per second.[81] An integrated approach to assessment of left ventricular diastolic function utilizes both transmitral and pulmonary venous flow velocities. In the presence of impaired relaxation with relatively normal left ventricular diastolic pressure, transmitral filling shows the classic pattern of E to A reversal (E/A ratio <1.0) and prolonged deceleration time (>150 msec). The pulmonary venous waveform shows a ratio of forward systolic to diastolic flow of 1.0 or greater and a retrograde diastolic flow velocity of less than 40 cm per second. In the presence of elevated left Figure 26-10 Pulmonary vein flow velocity waveforms obtained by

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transesophageal study in a patient with normal flow pattern (A) and a patient with severe mitral regurgitation (B). There is marked systolic flow reversal in the presence of severe mitral regurgitation.

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Figure 26-11 (Figure Not Available) Scatterplot of correlation of systolic fraction (pulmonary venous velocity time integral as fraction of the sum of systolic and early diastolic velocity time integral) with pulmonary capillary wedge pressure (PCWP). SEE, standard error of estimate. (From Kuecherer HF, Muhiudeen IA, Kusumoto FM, et al: Circulation 1990;82:1127–1139, with permission.)

atrial pressure, early peak mitral flow velocity is increased, followed by shortened deceleration and reduced late peak velocity. Pulmonary venous flow in this situation shows reduced forward systolic flow, a systolic to diastolic ratio of less than 0.4, and increased retrograde diastolic (atrial systolic) flow velocity. The duration of transmitral late flow velocity (A) relative to the duration of pulmonary vein retrograde diastolic flow (Ar) is a useful indicator of left ventricular end-diastolic pressure. In a study by Rossvoll and Hatle, a duration of the pulmonary venous Ar wave exceeding the transmitral A wave duration predicted an end-diastolic pressure of greater than 15 mm Hg, with a sensitivity of 85% and specificity of 79%[84] (Fig. 26-12) . A number of formulas have been derived for estimation of pulmonary capillary wedge and left ventricular end-diastolic pressures (Table 26-3) .[84] [85] [86] [87] [88] [89] [90] The formulas vary considerably in complexity but provide reasonable assessment TABLE 26-3 -- Calculation of Left Ventricular Diastolic Pressure by Echocardiography Study Pozzoli et al[50] Giannuzzi et al[87] Nagueh et al[89] Nagueh et al[84] Garcia et al[86] Mulvagh et al[85]

Equation PCWP = 1.85 × DR - 0.10 × SF + 10.9 PCWP = 32.16 - 0.104E + 0.1345A - 0.17DT + 4.95E/A PCWP = 45 - 0.16DT PCWP = 1.24 (E/Ea) + 1.9 PCWP = 5.27 (E/Vp) + 4.66 PWCP = 46 - 0.22IVRT - 0.10AFF - 0.03DT - 2E/A + 0.05MAR

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Mulvagh et al[85] LVEDP = 46 - 0.22IVRT - 0.03DT - 0.01AFF - (2/E/A) + 0.05MAR Nagueh et al[88] mean PCWP = 17 + 5.3E/A - 0.11IVRT Pozzoli et al[90] PCWP = 0.93DR - 0.155F + 0.03 (dZ - dA) + 0.87E/A + 16.2 A, mitral inflow peak late diastolic velocity; AFF, mitral atrial filling fraction; DT, early mitral velocity deceleration time; DR, early mitral inflow velocity deceleration rate; dZ - dA, difference in duration of reverse pulmonary venous and mitral velocity at atrial contraction; E, mitral inflow peak early velocity; Ea, peak early velocity measured by tissue Doppler at mitral annulus; IVRT, isovolumic relaxation time; MAR, time from mitral closure by Doppler to R wave on ECG; PCWP, pulmonary capillary wedge pressure; SF, peak pulmonary venous flow velocity systolic fraction; Vp, early diastolic color flow propagation velocity. of pressures in patients with reduced left ventricular systolic function. Assessment of Pulmonary Artery Systolic Pressure

Pulmonary artery pressure measured invasively has been commonly employed to assess left ventricular diastolic function. The relation of tricuspid regurgitant jet velocity to right ventricular pressure (and pulmonary artery pressure) as estimated by the modified Bernoulli equation (pressure gradient = 4[velocity]2 ), combined with the frequent finding of Doppler-detected tricuspid regurgitation, even in the absence of structural cardiac disease, affords the opportunity to noninvasively estimate pulmonary artery systolic pressure.[91] Thus, PASP = 4V2 + RAP where PASP is pulmonary artery systolic pressure, V is peak velocity of the tricuspid regurgitant jet, and RAP is estimated right atrial pressure. Figure 26-12 Bar charts showing the effect of different left ventricular (LV) pressures before atrial contraction (pre-a) (A) and of LV pressure (awave) increases at atrial systole (B) on the mean duration of pulmonary venous retrograde velocity (PV-a) and mitral A wave, and the difference in flow duration. The duration of flow on the vertical axis is in milliseconds. + P <.05 versus normal pressure. + + P < .01 versus mildly increased pressure. + P < .05 versus normal pressure. + + P < .05 versus mildly increased pressure. (From

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Rossvoll O, Hatle LK: J Am Coll Cardiol 1993; 21:1687–1696, with permission from the American College of Cardiology.)

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Several approaches have been taken to the estimation of right atrial pressure.[91] [92] [93] Clinical measurement of jugular venous pressure shows significant error. Assumption of a right atrial pressure of 10 mm Hg has been used but has obvious limitations. Right atrial pressure can be more accurately estimated on the basis of the size and respiratory changes of the inferior vena cava. The normal vena cava measures less than 20 mm and shows a 50% reduction in size with inspiration. As right atrial pressure rises, vena caval size increases and the inspiratory decrease in size is blunted, ultimately disappearing when right atrial pressure exceeds 20 mm Hg.[92] Assessment of hepatic vein flow also affords more quantitative determination of right atrial pressure.[93] Pulmonary artery end-diastolic pressure can be estimated from the pulmonary regurgitant jet velocity using the modified Bernoulli equation. This assessment appears to be less reproducible and is less commonly employed in clinical practice. Secondary Valvular Regurgitation

Mitral and tricuspid regurgitation are commonly present in congestive heart failure, particularly in heart failure occurring as a consequence of dilated cardiomyopathy.[3] [9] [20] Mitral competence depends on the integrity of all the components of the mitral valve apparatus (including the mitral annulus, leaflets, chordae tendineae, and papillary muscles) as well as the function of the underlying left ventricular myocardium.[94] [95] Several mechanisms have been proposed for mitral regurgitation occurring in the presence of dilated cardiomyopathy. Mitral annular dilation occurring as a consequence of left ventricular dilation has been implicated as an important cause of mitral regurgitation,[96] whereas other reports have disputed the role of annular dilation as a significant factor in functional regurgitation. [97] Papillary muscle dysfunction is a well-accepted cause of mitral regurgitation in ischemic heart disease and is believed to contribute to the development of regurgitation in dilated cardiomyopathy. In support of this view, recent investigations suggest that mitral regurgitation in the presence of dilated cardiomyopathy is related largely to the abnormal shape of the left ventricle. In the presence of heart failure, the left ventricle not only dilates but also loses its normal elliptical shape and becomes more spherical. The presence and severity of mitral regurgitation have been

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shown to be related to the sphericity of the left ventricular chamber during diastole and systole.[97] The mechanism by which this alteration in chamber shape causes mitral regurgitation may be explained by abnormal papillary muscle alignment and abnormal leaflet apposition during systole. Although the degree of regurgitation is usually mild to moderate in severity, severe regurgitation may be present and may contribute significantly to symptoms as well as prognosis. The importance of mitral regurgitation in dilated cardiomyopathy is underscored by reports demonstrating worse symptomatic status, poorer response to therapy, and reduced survival in patients with severe mitral regurgitation. [98] [99] [100] Doppler echocardiography is exquisitely sensitive for detection of atrioventricular valve regurgitation. However, quantitation of regurgitation is among the more difficult challenges in echocardiography. Experience with Doppler color flow imaging to quantitate the severity of mitral regurgitation has shown reasonable correlation between regurgitant jet size and angiographic grade of mitral regurgitation,[101] [102] but the significant overlap among patients with mild, moderate, or severe regurgitation limits the use of jet size alone for quantitation. Size of the color regurgitant jet is influenced by a number of factors other than regurgitant flow, including pressure difference between left ventricle and left atrium, left ventricular systolic function, size and compliance of the left atrium, entrainment of blood in the atrium, and direction of the jet (central versus eccentric jet)[103] [104] [105] [106] [107] (see Chapter 17) . Doppler echocardiographic quantitation of regurgitant stroke volume and regurgitant fraction has also been used to assess the severity of mitral regurgitation. [108] [109] Thus, the difference between stroke volume through the mitral annulus and stroke volume through the left ventricular outflow represents the regurgitant stroke volume (RSV). This method shows good correlation with angiographic grade of mitral regurgitation, but has shown a tendency toward overestimation of regurgitant stroke volume. This tendency appears to be overcome with experience.[109] Calculation of valve orifice size has conventionally been used to evaluate valvular stenosis but can also be applied to regurgitant lesions to obtain an effective regurgitant orifice area (ERO)[110] (see Chapter 17) : ERO = RSV/TVI where TVI is the time velocity integral of the mitral regurgitant jet recorded

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with continuous wave Doppler ultrasonography. In the presence of severe mitral regurgitation, regurgitant orifice area generally exceeds 35 to 40 mm2 . Examination of the pulmonary veins is useful for evaluation of the severity of mitral regurgitation. Normal pulmonary vein flow demonstrates phasic forward systolic and diastolic flow and retrograde diastolic flow with atrial contraction. In the presence of mitral regurgitation, forward systolic flow shows an inverse relation to the severity of mitral regurgitation and flow reversal with severe disease [111] (see Fig. 26-10) . Importantly, discordance in pulmonary vein flow velocity may occur in up to 25% of patients with mitral regurgitation and in nearly 40% with severe regurgitation. This discordance occurs most commonly with eccentric regurgitant jets and less commonly with central jets typical of dilated cardiomyopathy. Observations of flow through a restricted orifice (such as that occurring in mitral regurgitation) show that flow converges toward the orifice in a series of proximal isovelocity hemispheric surfaces.[112] This flow convergence region can be demonstrated by Doppler echocardiography as a color mosaic on the ventricular side of the valve (Fig. 26-13) . The continuity principle dictates that regurgitant flow rate (Q) can be calculated as the product of the hemispheric surface area of the flow convergence region and the velocity at that hemispheric surface Q = 2πr2 Vn

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Figure 26-13 (See also color plate.) Apical four-chamber views from a patient with dilated cardiomyopathy and mitral regurgitation. Color flow imaging shows a region of flow convergence on the ventricular side of the mitral valve. LV, left ventricle; RA, right atrium; RV, right ventricle.

where r is the radial distance between the color reversal at the first aliasing and the regurgitant orifice and Vn is the Nyquist velocity. Calculation of

regurgitant flow and regurgitant orifice size by the flow convergence method has shown excellent correlation with angiographic assessment.[112] , [113] Moreover, reduction in mitral regurgitant orifice size appears to be an

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Serial Two-Dimensional and Doppler Echocardiography in Guiding Treatment and Assessing Prognosis Several pharmacologic and nonpharmacologic treatments are available for treatment of congestive heart failure, including digoxin, diuretics, vasodilators, angiotensin converting enzyme inhibitors, beta-adrenergic blocking agents, and cardiac transplantation.[10] [11] [12] [13] [15] [16] , [115] Therapy can be tailored to the individual patient with the use of noninvasive hemodynamic information obtained by two-dimensional and Doppler echocardiography. For example, although most patients with heart failure and left ventricular systolic dysfunction benefit from positive inotropic agents, either oral digoxin administration or parenteral drugs such as dobutamine, appropriate additional therapy should be geared toward the hemodynamics of the individual patient. Thus, patients with elevated left ventricular filling pressure generally receive significant symptomatic benefit from diuretics and venodilators such as nitroglycerin. On the other hand, patients with normal or only mildly elevated filling may have further deterioration of cardiac output with the use of diuretics and preload reduction. In such patients, management should be directed at optimizing cardiac output with afterload reduction using angiotensin converting enzyme inhibitors or other vasodilators or both. Cardiac transplantation is generally reserved for severely symptomatic patients who do not respond to pharmacologic intervention.[14] [116] At present, the 5-year survival rate after transplantation is approximately 75%. Because of the limited resources and significant cost, however, this intervention is available to only a small minority of patients with heart failure. Thus, assessment of the prognosis, and therefore the urgency of transplantation, is of major importance. Doppler Echocardiography in Intensive Care Unit Monitoring Invasive cardiac monitoring in intensive care units allows objective and

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serial hemodynamic assessment of critically ill patients. This information is often vital to the selection of an optimal therapeutic regimen as well as to determining the efficacy of treatment. However, invasive cardiac monitoring is not without considerable costs and finite risks attributable to complications from placement of intravenous or intra-arterial catheters, including pneumothorax, infection, and blood loss. In contrast, noninvasive hemodynamic assessment obtained by two-dimensional and Doppler echocardiography is not associated with these adverse events and presents an important alternative to invasive monitoring. However, effective use of these noninvasive techniques depends largely on the reliability and reproducibility as compared with invasive measurements. Table 26-2 summarizes the accuracy and reproducibility of these noninvasive measures in several major studies. The author's experience with two-dimensional and Doppler echocardiography suggests that there are few situations in which a careful noninvasive hemodynamic assessment yields clinically important differences from similar information obtained invasively. Thus, in most patients, determination of left ventricular volume, ejection fraction and cardiac output, pulmonary artery systolic pressure, and diastolic filling indices provides adequate data for assessment of overall hemodynamic status.

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TABLE 26-4 -- Echocardiographic Parameters Correlated with Clinical Outcome in Dilated Cardiomyopathy Parameter References [42] [67] [119] LV size [42] LA size [8] [12] [64] [119] [126] LV ejection fraction [117] PA pressure [9] [42] RV size/function [41] [42] [66] [68] [126] [127] Mitral inflow pattern [98] [99] Mitral regurgitation LA, left atrial; LV, left ventricular; PA, pulmonary artery; RV, right ventricular.

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Prognostic Value of Echocardiography Determination of prognosis in patients with dilated cardiomyopathy (Table 26-4) remains a challenging clinical problem. A variety of clinical symptoms and signs and invasive hemodynamic and echocardiographic factors have been reported to be predictive of prognosis in patients with dilated cardiomyopathy and may be helpful in guiding therapy[4] [8] [14] , [35] [41] [42] [65] [66] [86] [117] [118] [119] [120] [121] [122] [123] [124] [125] [126] [127] [128] [129] [130] , , (Fig. 26-14 and Table 26-5) . Among the echocardiographic parameters, left ventricular ejection fraction, chamber size and shape, and wall thickness are strong independent predictors of prognosis. Marked reduction of ejection fraction, progressive left ventricular dilation, and increased sphericity of the left ventricle are associated with poor survival in patients with dilated cardiomyopathy. In populations with uniformly markedly depressed ejection fraction (<25%), there is weaker correlation with survival. Increased right TABLE 26-5 -- Univariate Analysis of Clinical, Doppler Echocardiographic, and Hemodynamic Variables Predicting Death or Transplantation in Dilated Cardiomyopathy Parameter EDT Age mAoP LVEDVI RVFSA NYHA LVESVI LAAI E/A ratio E mPAP LADI CTR B point

Cut-off Points <115 msec <26 yr <71 mm Hg >179 mL/m2 36% III + IV >150 mL/m2 >18 cm2 /m2 >1.9 >0.6 m/sec >29 mm Hg >23 mm/m2 >57% Present

P value <.0001 <.0001 <.0001 <.0001 <.0001 .0001 .0001 .0001 .0003 .0005 .0007 .0008 .0018 .0041

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A S3

<0.4 m/sec Present

.0051 .006

LVESDI

>37 mm/m2 >17 mm Hg

.01

mPAWP A, peak velocity of A wave; CTR, cardiothoracic ratio; E, peak velocity of E wave; EDT, E deceleration time; LAAI, left atrial area index; LADI, left atrial diameter index; LVESDI, left ventricular endsystolic diameter index; LVEDVI, left ventricular enddiastolic volume index; LVESVI, left ventricular endsystolic volume index; mAoP, mean aortic pressure; mPAP, mean pulmonary artery pressure; mPAWP, mean pulmonary artery wedge pressure; NYHA, New York Heart Association functional class; S3 ,

.02

third heart sound; RVFSA, right ventricular fractional shortening area. From Pinamonti B, DiLenarda A, Sinagra G, Camerii F: J Am

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Coll Cardiol 1993;22:808–815. ventricular size and poor systolic function are also associated with poorer prognosis [9] [42] (Fig. 26-15) . A spectrum of transmitral flow velocity patterns have been observed in heart failure that reflect the hemodynamic milieu and severity of disease, as discussed previously.[41] [42] [66] [67] [68] [69] Transmitral filling in patients with dilated cardiomyopathy shows a strong correlation with functional status and survival.[41] [42] [66] , [68] A "restrictive" pattern of filling characterized by increased early transmitral flow velocity, shortened deceleration time, and reduced late velocity is more commonly observed in patients with severe cardiac symptoms and markedly depressed systolic function of the right and left ventricles[42] , [68] (see Fig. 26-8) . This pattern correlates with elevated left ventricular Figure 26-14 Survival curves in patients with congestive heart failure demonstrating the effect of New York Heart Association (NYHA) functional class (A) and gender (B) on cumulative cardiac mortality. (From Xie G-Y, Martin RB, Smith MD, et al: J Am Coll Cardiol 1994;24:132–139, with permission from the American College of Cardiology.)

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Figure 26-15 Kaplan-Meier survival curves in two morphologic subsets of patients with dilated cardiomyopathy. The top curve (closed circles) depicts survival in patients with predominant and disproportionate dilation of the left ventricular chamber. The bottom curve (triangles) depicts survival in patients with a relatively equal degree of left and right ventricular chamber enlargement. (From Lewis JF, Webber JD, Sutton LL, et al: J Am Coll Cardiol 1993; 21:649–654, with permission from the American College of Cardiology.)

diastolic and pulmonary capillary wedge pressure and more severe mitral regurgitation. As much as a 10-fold difference in the 1-year mortality rate has been identified in patients with dilated cardiomyopathy and a restrictive transmitral filling pattern compared with a nonrestrictive pattern[41] (Fig. 2616) . Pulmonary artery pressure assessed by Doppler echocardiography is also an

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important predictor of survival in patients with congestive heart failure. In a series of 108 patients with both ischemic and nonischemic disease, tricuspid regurgitant jet velocity exceeding 2.5 m per second was associated with more frequent hospitalization and increased mortality due to heart failure over a follow-up period of 28 months.[117] Aside from these specific echocardiographic measurements, a recent report suggests that the use of echocardiography, in general, is associated with better outcome in patients with congestive heart failure. Patients with heart Figure 26-16 Survival curve in patients with congestive heart failure demonstrating the effect of transmitral flow velocity patterns on cumulative cardiac mortality. (From Xie G-Y, Martin RB, Smith MD, et al: J Am Coll Cardiol 1994;24:132–139, with permission from the American College of Cardiology.)

failure who did not undergo echocardiography were less often treated with angiotensin converting enzyme inhibitors and experienced poorer overall survival.[131] Limitations of Echocardiography in Assessment of Heart Failure A significant limitation of echocardiography in the evaluation of congestive heart failure relates to the variability in echocardiographic measurements. This variability is a consequence of both technical factors and intraobserver and interobserver interpretation variability of the serial studies. These factors can be minimized by close adherence to standardized protocols in both performance and interpretation of studies. Despite the previously discussed inherent limitations, ejection fraction remains the most commonly used measure of left ventricular systolic function, with clinically acceptable variability. Ejection fraction can also be accurately obtained by radionuclide angiography, albeit with a small but finite radiation exposure. However, radionuclide angiography does not provide the information about chamber sizes, wall thickness, and valvular function afforded by echocardiography. Ejection fraction obtained by contrast ventriculography has several important limitations, including the use of geometric assumptions that may be less applicable in dilated cardiomyopathy, inherent risk of cardiac catheterization, and impracticality and costs of serial evaluations. Cardiac output measured by Doppler echocardiography also has important limitations for use in evaluation and serial follow-up of patients with heart

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failure. Observer variability for this technique is substantial, ranging from about 6% to 16%. This variability is largely attributable to discrepancies in measurement of orifice cross-sectional area and is more marked in measurement of transmitral stroke volume. Some investigators have proposed the use of stroke distance to avoid the inherent error incurred by calculating stroke volume and cardiac output.[51] Stroke distance appears to be particularly applicable to serial evaluation after therapeutic intervention. [132] Several circumstances preclude the use of Doppler echocardiography for assessment of cardiac output. These include poor acoustic windows, suboptimal image quality, and valvular regurgitation or stenosis. Despite these limitations, noninvasive estimation of stroke volume and cardiac output is an important adjunct in the evaluation of patients with heart failure.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications Research applications of echocardiography in patients with dilated cardiomyopathy can be divided into two major categories: use of existing techniques to evaluate the effects of novel therapeutic interventions and application of newer echocardiographic techniques for improved diagnostic and prognostic information. The former use was discussed in the preceding sections. Several new and innovative echocardiographic developments have potential application to the diagnosis and management of congestive heart failure. The development of newer contrast agents allows better endocardial definition and may be 584

useful for quantitation of ventricular volume and ejection fraction in patients with technically suboptimal study results.[133] [134] In addition, the ability to more reproducibly assess ventricular volume and ejection fraction in general has important implications for assessment of pharmacologic management and therapeutic interventions. The use of contrast agents for measurement of regional coronary perfusion offers potential for noninvasive distinction between ischemic and nonischemic disease (see Chapter 8) .[135] [136] [137] [138] Myocardial characterization using ultrasonic backscatter has been used to distinguish normal from abnormal myocardial tissue[139] [140] [141] [142] (see Chapter 9) . This technique has been most widely applied in the evaluation of ischemic heart disease, but recent investigations have demonstrated distinctive ultrasonic tissue characterization in dilated cardiomyopathy, which may be useful for diagnosis, assessment of disease progression, and evaluation of response to therapy. [141] Three-dimensional echocardiography offers promise of more accurate assessment of ventricular volume and mass[143] [144] [145] (see Chapter 10) . Further developments of these techniques are expected to refine the echocardiographic assessment of individuals with dilated cardiomyopathy and provide important noninvasive data for diagnosis and management.

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588

Chapter 27 - Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Anna Woo MD E. Douglas Wigle MD Harry Rakowski MD

Hypertrophic cardiomyopathy is a cardiac disorder characterized by a wide spectrum of clinical, echocardiographic, and hemodynamic findings.[1] [2] This condition is defined as unexplained ventricular hypertrophy that predominantly affects the left ventricle and is usually asymmetric (Fig. 271) .[3] The histopathologic features of hypertrophic cardiomyopathy include myocyte hypertrophy, myocardial fiber disarray, and interstitial fibrosis. Since its modern description more than four decades ago,[4] [5] there have been significant advances in the diagnosis of hypertrophic cardiomyopathy, the understanding of its complex pathophysiology, and the evolution of its management. Echocardiography has played a crucial role in defining hypertrophic cardiomyopathy, determining its pathophysiology, quantitating its morphologic and hemodynamic severity, and assessing the acute and chronic responses to various therapies. [6] Echocardiographic studies have provided invaluable insight into the epidemiology,[7] inheritance,[8] and

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prognosis[9] of this condition. The ability to perform serial safe, noninvasive, real-time studies makes echocardiography the diagnostic modality of choice in the screening,[10] [11] diagnosis,[12] and serial monitoring of patients with hypertrophic cardiomyopathy. In recent years, the role of echocardiography in this condition has extended to intraprocedural decision making, with the use of intraoperative transesophageal echocardiography during surgical myectomy[13] and the application of myocardial 589

Figure 27-1 Hypertrophic cardiomyopathy. Gross pathologic specimen of the heart from a patient with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction who died suddenly. Note the asymmetric hypertrophy with a markedly thickened interventricular septum and the narrow outflow tract between the basal septum and anterior mitral leaflet, which is thickened and fibrosed from repeated mitral leafletseptal contact (arrow).

contrast echocardiography to the guidance of septal ethanol ablation.[14]

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Epidemiology Hypertrophic cardiomyopathy was initially believed to be a rare disorder affecting young adults.[5] This concept was reinforced by studies that focused on highly selected patients with the obstructive form of hypertrophic cardiomyopathy.[15] However, modern studies using echocardiography in the evaluation of subjects suggest a much higher prevalence of this condition than previously anticipated. The Coronary Artery Risk Development in Adults (CARDIA) study, a prospective study of 4111 apparently healthy adults younger than 40 years of age from a general population, detected hypertrophic cardiomyopathy by echocardiographic examination in 0.17% of subjects.[7] There was a similar prevalence of hypertrophic cardiomyopathy in a large study of 33,735 young athletes undergoing preparticipation medical screening in Italy, with a total of 22 cases (0.07%) identified from this cohort.[16] Studies of more selected subjects have reported the prevalence of hypertrophic cardiomyopathy as 0.17% in a study of Japanese workers who underwent electrocardiographic screening and targeted echocardiography,[17] and as 0.5% in a study of 714 consecutive patients referred to an echocardiography laboratory.[18] The reported incidence of hypertrophic cardiomyopathy has ranged from an incidence rate of 0.4 per 100,000 person-years from 1980 to 1981 in Western Denmark[19] to a rate of 2.5 per 100,000 person-years between the years 1975 and 1984 in Olmsted County, Minnesota.[20]

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Molecular Genetics Hypertrophic cardiomyopathy is a genetic disorder with an autosomal dominant pattern of inheritance. This condition is believed to arise from a genetic defect involving one of the proteins of the cardiac myofibrillar apparatus (Fig. 27-2) (Figure Not Available) [21] (1) β-myosin heavy chain (β-MHC), (2) myosin binding protein C, (3) troponin T, (4) α-tropomyosin, (5) troponin I, (6) ventricular myosin essential light chain, (7) ventricular myosin regulatory light chain, (8) α-cardiac actin, or (9) titin. The initial genetic defect was described more than a decade ago.[22] Since then, more than 100 different mutations have been associated with this condition. Various molecular diagnostic techniques have been used to detect these mutations. An abnormal genotype cannot be identified in approximately one third of patients with a definite family history of hypertrophic cardiomyopathy.[2] It remains controversial whether the underlying genotype contributes to the overall phenotypic expression of hypertrophic cardiomyopathy and whether it should be considered in the risk stratification and management of patients.[2] Previous studies have suggested that certain genetic defects, such as missense mutations of the β-MHC gene resulting in an amino acid charge change[23] or cardiac troponin T mutations, [24] are associated with a poor prognosis. A study of six different missense mutations of the β-MHC gene showed no significant relationship between the genetic defect and the degree or morphologic pattern of hypertrophy.[25] Other studies, however, have suggested that patients with troponin T[24] or cardiac myosin binding protein C defects[26] may have a milder degree of hypertrophy compared with patients with β-MHC mutations.

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Diagnosis The diagnosis of hypertrophic cardiomyopathy is based on the demonstration of left ventricular hypertrophy in the absence of other causes, such as systemic hypertension or aortic stenosis.[3] M-mode echocardiography assumed an early role in the diagnosis of hypertrophic cardiomyopathy.[27] The echocardiographic finding of a septal-to-posterior Figure 27-2 (Figure Not Available) (See also color plate.) Schematic diagram of the cardiac myofibrillar apparatus. Hypertrophic cardiomyopathy is a genetic disorder involving one of the nine cardiac sarcomeric proteins. The percentages (in parentheses) represent the relative frequency of the mutations of the individual sarcomeric proteins reported from various studies. (From Spirito P, Seidman CE, McKenna WJ, Maron BJ: N Engl J Med 1997;336:775–785. Copyright © 1997 Massachusetts Medical Society.)

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Figure 27-3 Cross-sectional, two-dimensional echocardiographic views obtained at the midpapillary level from a normal heart (A) and from two cases of hypertrophic cardiomyopathy (B and C). In B and C, there is an asymmetric increase in septal wall thickness without involvement of the posterior free wall. Hypertrophy is limited to the septum (arrows) in B, whereas there is anterolateral extension of the hypertrophy (arrows) in C. (From Wigle ED, Sasson Z, Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83.)

wall thickness ratio of greater than 1.3 is strongly associated with hypertrophic cardiomyopathy (Fig. 27-3) . [28] The use of a septal-toposterior wall thickness ratio of 1.5:1 increases the specificity of asymmetric septal hypertrophy for this condition.[6] Other M-mode findings associated with obstructive hypertrophic cardiomyopathy, such as systolic anterior motion and mid-systolic notching of the aortic valve, have been detected in other conditions and are no longer considered pathognomonic

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for this condition. Family Screening The first-degree relatives of patients with hypertrophic cardiomyopathy should be screened for this condition.[29] Possible screening methods for family members include molecular genetic analysis,[12] [21] 12-lead electrocardiogram,[30] and echocardiography. M-mode and two-dimensional echocardiography have been used as investigational tools in the family screening of this condition for the past three decades,[8] and echocardiography is the most widely accepted diagnostic screening test for hypertrophic cardiomyopathy.[29] The diagnosis of this condition is made in children when left ventricular wall measurements are more than two standard deviations above the mean for weight and age.[31] New criteria for the diagnosis of hypertrophic cardiomyopathy in first-degree adult relatives of patients with hypertrophic cardiomyopathy have been proposed (Table 27-1) .[10] The diagnosis in first-degree relatives would be made in the presence of (1) one major echocardiographic or electrocardiographic criterion, (2) two minor echocardiographic criteria, or (3) one minor echocardiographic and two minor electrocardiographic criteria. These criteria were formulated on the premise that mild echocardiographic or electrocardiographic abnormalities will have a high probability of being the phenotypic expression of a genotypic abnormality in first-degree relatives. Screening throughout adulthood, usually at 5-year intervals, is currently recommended because hypertrophic cardiomyopathy may have delayed penetrance, particularly in those patients with underlying cardiac myosin binding protein C defects. [26] Preparticipation Screening in Athletes The screening of young athletes prior to involvement in competitive sports remains a contentious issue.[32] Previous studies of medical screening (a combination of history, physical examination, and 12-lead electrocardiogram or echocardiography alone) of a total of 766 American college athletes found no cases of hypertrophic cardiomyopathy.[33] [34] The investigators concluded that systematic medical screening was not beneficial, especially since there was confusion between possible physiologic versus pathologic ventricular hypertrophy (see "Differential Diagnosis"). However, a large Italian study of 33,735 young athletes undergoing preparticipation medical screening detected 22 individuals with hypertrophic cardiomyopathy. [16] All of these subjects were barred from competitive athletic activities and none of these subjects died during a

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mean TABLE 27-1 -- Proposed Diagnostic Criteria for Hypertrophic Cardiomyopathy in Adult First-Degree Relatives Major Criteria Echocardiographic Criteria Left ventricular wall thickness: • ≥13 mm in anterior septum or posterior wall • ≥15 mm the posterior septum or free wall Severe SAM (septal-leaflet contact) Electrocardiographic Criteria Left ventricular hypertrophy and repolarization changes (Romhilt & Estes criteria) T wave inversion in one of the following sets of leads: • ≥3 mm in leads I and a VL (with QRS-T wave axis difference ≥30 degrees) • ≥3 mm in leads V3–V6 • ≥5 mm in leads II, III, aVF Abnormal Q (>40 msec or >25% R wave) in at least two leads from following sets of leads: • Leads II, III, aVF (in absence of left anterior hemiblock) • Leads V1–V4 • Leads I, aVL, V5–V6

Minor Criteria Left ventricular wall thickness: • 12 mm in anterior septum or posterior wall • 14 mm in posterior septum or free wall Moderate SAM (no leaflet-septal contact) Redundant mitral valve leaflets Complete BBB or (minor) interventricular conduction defect (in left ventricular leads) Minor repolarization changes in left ventricular leads

Deep S wave in lead V2 (>25 mm)

Unexplained chest pain, dyspnea or syncope SAM, systolic anterior motion.

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Modified from McKenna WJ, Spirito P, Desnos M, et al: Heart 1997;77:130–132.

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follow-up of 8 years. There was one case of sudden death due to hypertrophic cardiomyopathy in an athlete in whom the condition was not detected during life. The results of this study suggest that preparticipation screening may prevent sudden death in hypertrophic cardiomyopathy.

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Differential Diagnosis The differential diagnosis of asymmetric or disproportionate septal hypertrophy includes such lesions as right ventricular hypertension secondary to valvular pulmonary stenosis, pulmonary hypertension, and dtransposition of the great arteries. Increased septal wall thickness has been described in such various conditions as amyloidosis,[35] septal sarcomas, glycogen and mucopolysaccharide storage diseases, Friedreich's ataxia, and myxedema (Fig. 27-4) .[36] Hypertrophy secondary to such known conditions as systemic hypertension or valvular aortic stenosis may commonly have a prominent degree of focal septal hypertrophy. Other Causes of Left Ventricular Hypertrophy: Common Clinical Dilemmas Athlete's Heart

The clinical and echocardiographic differentiation between hypertrophic cardiomyopathy and athlete's heart may be difficult.[37] [38] [39] The left ventricular wall thickness may be 13 to 16 mm in 2% of elite athletes, raising the possibility of underlying hypertrophic cardiomyopathy.[37] Multivariate analyses have shown that the major determinants of cardiac morphologic adaptations to training include body size (body surface area or height) and participation in certain endurance sports. Therefore, alterations in left ventricular wall thickness may be more striking in athletes engaging in rowing or canoeing, cycling, and cross-country skiing.[38] The distinction between athlete's heart and pathologic hypertrophy may be less of an issue Figure 27-4 (See also color plate.) Two-dimensional echocardiographic parasternal long-axis (A) and short-axis (B) views from a 45-year-old woman with heart failure referred for evaluation of hypertrophic cardiomyopathy. Echocardiographic evaluation revealed asymmetric increased wall thickness of the septum, no systolic anterior motion, thickened mitral

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and aortic valve leaflets, central mitral regurgitation, and moderate aortic regurgitation. Subsequent investigations revealed underlying systemic amyloidosis.

in women, since the left ventricular wall thickness of elite female athletes is in the range of 6 to 12 mm, which does not exceed normal age-adjusted limits for wall thickness. This suggests that athletic training may not be a stimulus for significant hypertrophy in females.[40] Septal Hypertrophy in the Elderly

It may be difficult to distinguish between elderly patients with hypertrophic cardiomyopathy and those with hypertensive heart disease.[41] Elderly subjects may develop a sigmoid-shaped septum as an age-related phenomenon. [42] Terms that have been used to describe this finding are sigmoid septum, septal bulge,[43] or discrete upper septal hypertrophy. It is controversial whether this finding should be considered a subtype of hypertrophic cardiomyopathy or whether it represents a benign anatomic variant.[44] [45] Other findings on echocardiographic examination that are more compatible with a septal bulge rather than hypertrophic cardiomyopathy of the elderly include focal hypertrophy limited to less than 3 cm length of the basal anterior septum, protrusion of the focal hypertrophy into the left ventricular outflow tract, a normal left ventricular end-diastolic diameter, and the absence of other characteristic echocardiographic findings of hypertrophic cardiomyopathy.[44] Echocardiographic and clinical features of hypertrophic cardiomyopathy in the elderly are discussed later (see "Hypertrophic Cardiomyopathy of the Elderly").

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Evaluation by Echocardiography Left Ventricular Hypertrophy: Severity, Distribution, and Patterns of Hypertrophy The advent of two-dimensional echocardiography greatly increased the ability to detect the full extent, distribution, and severity of myocardial hypertrophy. [46] [47] [48] Comprehensive echocardiographic assessment requires imaging of the left ventricle from several transthoracic 592

Figure 27-5 Optimal echocardiographic evaluation of the degree, extent, and distribution of hypertrophy in hypertrophic cardiomyopathy requires imaging from multiple transthoracic windows. Parasternal long-axis (A),, parasternal short-axis at the basal level (B), apical longaxis (C), and apical four-chamber (D) views in a 22-year-old woman with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction. Massive hypertrophy was detected with a maximal septal thickness of 34 mm, anterolateral wall involvement, and extension of hypertrophy to the apical level. The patient had New York Heart Association class III symptoms, severe systolic anterior motion, and a resting outflow tract gradient of 70 mm Hg and was referred for surgical myectomy.

windows, including the parasternal long-axis view, serial parasternal shortaxis views, and the apical windows (Fig. 27-5) . Measurements of the anterior septum, posterior septum, posterior wall, and anterolateral wall obtained from cross-sectional parasternal short-axis views are made at three levels: basal (at the level of the mitral valve), midventricular (at the level of the papillary muscles), and apical.[6] A 10-point scoring system to quantify the extent of left ventricular hypertrophy in hypertrophic cardiomyopathy has been developed by Rakowski and Wigle (Table 27-2) .[47] [49] This score incorporates the degree of septal hypertrophy at the basal level, the length

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of septal hypertrophy, and the extension of hypertrophy to the anterolateral free wall. The parasternal short-axis view of the left ventricle at the level of the mitral leaflet tips can be used to define anterolateral wall involvement. The apical four-chamber TABLE 27-2 -- Extent of Hypertrophy According to Echocardiographic Point Score Extent of Hypertrophy Septal thickness, mm (basal third of septum) 15–19 20–24 25–29 >30 Extension to papillary muscles (basal two thirds of septum) Extension to apex (total septal involvement) Anterolateral wall extension Maximum total From Wigle ED, Sasson Z, Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83.

Points 1 2 3 4 2 2 2 10

and long-axis views can determine the length of septal involvement. In a study of 100 consecutive patients with hypertrophic cardiomyopathy presenting to our echocardiography laboratory, 25% of cases had localized subaortic hypertrophy, 27% had septal hypertrophy extending to the midpapillary level, and 48% had hypertrophy extending to the apex. There was a significant relationship between the hemodynamic subtype of hypertrophic cardiomyopathy (resting left ventricular outflow tract obstruction, latent or provocable outflow tract obstruction, or the nonobstructive form) and the extent of hypertrophy (Table 27-3) .[47] [49] Maron et al[48] classified asymmetric septal hypertrophy into four types (Table 27-4) . A minority of patients had involvement of the anterior septum alone (type I). Panseptal hypertrophy, with involvement of both the anterior and posterior septum, was detected in 20% of patients (type II). More than half of the patients with hypertrophic cardiomyopathy had extension of hypertrophy to the anterolateral wall (type III). All other patterns of hypertrophy (type IV), such as isolated posteroseptal, apical septal, or lone anterolateral wall involvement (Fig. 27-6) , constituted 18%

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of the study cohort. Technical Factors and Echocardiographic Pitfalls Echocardiographic studies have demonstrated changes in the acoustic texture of the myocardium in patients with hypertrophic cardiomyopathy.[46] [50] There may be increased ultrasonic reflectivity of the left ventricular walls, especially the interventricular septum. Diffuse bright echoes 593

TABLE 27-3 -- Extent of Hypertrophy Related to Hemodynamic Subg Hypertrophic Cardiomyopathy Basal Basal No. One Two Whole Hemodynamic of Interventricular Third, Third, Septum, Anterola Subgroup Cases Septum (mm) % % % Extensio Resting 39 2.45 ± 0.55 8% 20% 72% 83% obstruction Latent 34 1.89 ± 0.35 53% * 35% 12% * 13% obstruction 63% † No obstruction 27 2.09 ± 0.57 14% † 26% 59% † From Rakowski H, Fulop J, Wigle ED: Postgrad Med J 1986;62:557–561 *P < 0.001 latent vs both resting and no obstruction †P < 0.05 no obstruction vs resting obstruction

may be seen throughout the myocardium and may give a ground-glass appearance. One study demonstrated significantly greater reflectivity of the septal and posterior walls in patients with hypertrophic cardiomyopathy compared with age-matched control subjects. There are important technical considerations in the echocardiographic assessment of hypertrophic cardiomyopathy. Oblique cuts of the left ventricle can spuriously produce the appearance of asymmetric septal hypertrophy and overestimate wall thickness.[36] [51] Two-dimensional echocardiographic studies have demonstrated that hypertrophy can be quite

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localized or eccentric in distribution.[6] [52] More atypical forms of hypertrophic cardiomyopathy, such as isolated lateral wall hypertrophy or asymmetric apical hypertrophy, may be missed from standard parasternal long-axis views, since the septum and anterior wall appear normal in thickness and there is no systolic anterior motion of the mitral valve. The diagnosis of apical hypertrophy by echocardiography may be missed in patients with difficult or suboptimal apical windows or if the apical segments are foreshortened.

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Left Ventricular Outflow Tract Obstruction Pathophysiology M-mode echocardiographic studies demonstrated narrowing of the left ventricular outflow tract,[53] systolic anterior motion of the mitral valve,[54] and mid-systolic notching of the aortic valve,[55] and established the important role of echocardiography in the assessment of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy.[56] Advances in two-dimensional echocardiography and Doppler techniques would provide additional insights into the mechanisms responsible TABLE 27-4 -- Morphologic Classification of Hypertrophic Cardiomyopathy Percentage of Cases 10 20

Maron Type Distribution of Hypertrophy I Isolated anterior septum II Panseptal (anterior and posterior septum) without free wall involvement III Septum and anterolateral free wall IV Regions other than basal anterior septum From Maron BJ, Gottdiener JS, Epstein SE: Am J Cardiol 1981;48:418–428, with permission from Excerpta Medica Inc.

52 18

for dynamic outflow tract obstruction,[6] summarized in Table 27-5 . Morphologic features of hypertrophic cardiomyopathy that contribute to left ventricular outflow tract obstruction include narrowing of the outflow tract by ventricular septal hypertrophy, [57] intrinsic abnormalities of the mitral leaflets, [58] [59] [60] anterior displacement of the mitral apparatus,[46] [56] [58] and anterior malposition of the papillary muscles.[61] There is a close relationship between the extent of left ventricular

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hypertrophy and the presence of left ventricular outflow tract obstruction. The presence of resting left ventricular outflow tract obstruction is associated with a higher hypertrophy point score (see Table 27-3) .[49] The mitral leaflets in hypertrophic cardiomyopathy are typically elongated.[59] These mitral leaflets coapt abnormally in the body of the leaflets, rather than at the tip.[58] [59] The degree of anterior displacement of the mitral apparatus has been related to the degree of obstruction.[46] [56] [58] Furthermore, in hypertrophic cardiomyopathy, the papillary muscle tips are displaced anteriorly and toward one another. This results in a decrease in the relative tension on the chordae tendineae to the body of the anterior mitral leaflet, producing relative chordal slack in the central and anterior leaflet portions.[59] [62] Reduced chordal tension is more likely when the distance from the papillary muscle tips to the mitral leaflets is decreased by a combination of hypertrophy at the base of the papillary muscles and increased leaflet length. Mitral Leaflet Systolic Anterior Motion Although the nature of the hydrodynamic forces on the anterior mitral leaflet remains controversial, it is believed that the anterior leaflet distal to the site of coaptation is subjected to Venturi[1] or drag forces, or both.[62] [63] Therefore, systolic anterior motion occurs, and the tip of the anterior mitral valve leaflet typically develops a sharp TABLE 27-5 -- Factors Contributing to Dynamic Left Ventricular Outflow Tract Obstruction Narrowing of left ventricular outflow tract Septal hypertrophy Anterior displacement of mitral apparatus Anterior displacement of papillary muscles Hydrodynamic forces (Venturi and drag forces) causing systolic anterior motion Rapid early left ventricular ejection Elongated mitral leaflets

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Figure 27-6 Atypical pattern of hypertrophy with predominant

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anterolateral wall hypertrophy in a 36-year-old woman with a strong family history of hypertrophic cardiomyopathy. Two-dimensional end-diastolic frames from parasternal long-axis (A) and short-axis (B) views show an anterior septal thickness of 13 mm and maximal hypertrophy involving the basal anterolateral wall, with a wall thickness of 19 mm.

anterior and superior angulation, leading to mitral leaflet-septal contact in early to mid-systole (Fig. 27-7) . There is a significant relationship between systolic anterior motion (SAM) and the onset of the obstructive pressure gradient, which was demonstrated in patients undergoing simultaneous cardiac catheterization and M-mode echocardiographic studies (Fig. 27-8) . [64] The presence of mitral leaflet–septal contact occurs almost simultaneously with the onset of the pressure gradient. M-mode, two-dimensional, and Doppler echocardiography are established noninvasive techniques in the assessment of the degree of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. An M-mode echocardiographic study classified the degree Figure 27-7 (See also color plate.) Schematic diagram of a transesophageal echocardiogram (frontal long-axis plane) demonstrating the anterior and basal motion of the anterior mitral leaflet leading to leaflet-septal contact and failure of leaflet coaptation in midsystole. At the onset of systole (A), the coaptation point (thick arrow) is in the body of the mitral leaflets. During early systole (B) and mid-systole (C), there is anterior and basal movement of the residual length of the anterior mitral leaflet (thick arrow) with septal contact and failure of leaflet coaptation (thin arrow). The interleaflet gap (arrow) results in a posteriorly directed jet of mitral regurgitation into the left atrial cavity (stippled area). Corresponding two-dimensional transesophageal views (D and E) with color flow imaging in a patient with obstructive hypertrophic cardiomyopathy show septal hypertrophy, anterior motion of the anterior mitral leaflet, and color turbulence in the outflow tract with the posteriorly directed mitral regurgitation. (A to C, From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.)

of SAM into three categories: (1) mild (SAM-septal distance > 10 mm) (2) moderate (SAM-septal distance ≤10 mm or brief mitral leaflet–septal contact), and (3) severe (prolonged SAM-septal contact, lasting at least 30% of echocardiographic systole).[54] A subsequent study documented severe SAM in all patients with resting obstruction. There was a linear relationship between the time of onset of SAM and the severity of left ventricular outflow tract obstruction (Fig. 27-9) (Figure Not Available) .[65]

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Color M-mode echocardiography is a valuable technique for demonstrating SAM-septal contact as the site of left ventricular outflow tract obstruction. [6] Blood flow toward the site of mitral leaflet-septal contact is seen as a blue jet while the signal aliases to red as flow velocity 595

Figure 27-8 Simultaneous hemodynamic and M-mode echocardiographic recordings in a patient with obstructive hypertrophic cardiomyopathy and a gradient of 86 mm Hg. Arrow indicates simultaneous onset of systolic anterior motion-septal contact and onset of pressure gradient (defined as peak of aortic percussion wave). AO, central aortic pressure; ECG, echocardiogram; IVS, interventricular septum; LV, left ventricular pressure; MV, mitral valve; PW, posterior wall. (From Pollick C, Morgan CD, Gilbert BW, et al: Circulation 1982;66:1087–1094.)

increases during rapid early ejection into the aorta. At the site of mitral leaflet-septal contact, the site of left ventricular outflow tract obstruction, two turbulent mosaic jets develop: one is directed into the posterior portion of the Figure 27-9 (Figure Not Available) Method of quantitating pressure gradient (PG) from degree of systolic anterior motion (SAM)-septal contact is shown in M-mode echocardiogram (ECG). The two time periods used to calculate PG are as follows: X = duration of SAM-septal contact and Y = period from onset of SAM to onset of SAMseptal contact. IVS, interventricular septum; MV, mitral valve; PW, posterior wall. (From Pollick C, Rakowski H, Wigle ED: Circulation 1984;69:47.)

obstructed left ventricular outflow tract and the second is an eccentric, posteriorly directed jet of mitral regurgitation into the left atrium. Two-dimensional echocardiography further defines the structures involved in causing systolic anterior motion. The distal anterior mitral leaflet and chordae tendineae move anteriorly to contact the septum in the presence of severe systolic anterior motion. The parasternal short-axis views demonstrate that mitral leaflet-septal contact may be extensive, involving much of the circumference of the anterior leaflet, which leads to significant narrowing of the left ventricular outflow tract.[46] [49] Finally, left ventricular outflow tract obstruction may develop secondary to posterior leaflet SAM and posterior leaflet-septal contact (Fig. 27-10) .[66] [67] Doppler Assessment

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Pulsed wave and continuous wave Doppler have been used to determine the pressure gradient across the left ventricular outflow tract in patients with hypertrophic cardiomyopathy. Pulsed wave Doppler signals can be recorded sequentially from the left ventricular apex to the outflow tract. The peak velocity increases as the sample volume approaches the site of mitral leaflet-septal contact.[6] Continuous wave Doppler assessment from an apical approach with the beam directed across the left ventricular outflow tract can be used to determine the peak velocity (V) at the site of obstruction. Patients with outflow tract obstruction have a characteristic spectral profile with an asymmetric leftward concave shape (Fig. 27-11) .[68] This results from a relatively rapid initial rise in velocity followed by a more gradual increase in the outflow tract velocity to cause a peak in late systole, resulting in a dagger-shaped configuration. [69] There may be some variability in the waveform contour, and some spectral profiles will demonstrate lesser degrees of asymmetry with the outflow tract jet peaking earlier in systole. The peak gradient (∆P) can be estimated using the modified Bernoulli equation2 : ∆P = 4V2 There is an excellent correlation between the pressure gradient determined by continuous wave Doppler measurements and that determined by highfidelity micromanometer recordings during cardiac catheterization.[68] [70] Color flow mapping has been used to characterize the level of obstruction, either in the left ventricular outflow tract or in the midventricle.[71] Serial Doppler studies have shown that there is significant spontaneous variability in the left ventricular outflow tract gradient in hypertrophic cardiomyopathy.[72] Technical Aspects of Doppler Evaluation There are important technical considerations in the performance and interpretation of Doppler studies in patients with hypertrophic cardiomyopathy. It was not possible 596

Figure 27-10 (color plate.) Two-dimensional frames from a transesophageal echocardiogram illustrating posterior leaflet-septal contact. A, During diastole, the mitral leaflets open. Note the unusually

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elongated posterior leaflet. The mitral annulus is tilted so that the posterior leaflet extends into the left ventricular cavity farther than normal. B, In early systole, the anterior leaflet coapts behind the posterior leaflet. C through E, In mid- to late systole, anterior motion of the posterior leaflet occurs (C), and posterior leafletseptal contact develops (D), resulting in left ventricular outflow tract obstruction (E). F, Color flow imaging demonstrates the development of a turbulent mosaic jet in the left ventricular outflow tract and a jet of mitral regurgitation.

to obtain a discernible signal from the left ventricular outflow tract in 16% of patients in one study comparing continuous wave Doppler echocardiography to cardiac catheterization.[68] This inability to acquire a clear spectral display from the outflow tract may be secondary to inadequate transthoracic windows or distortion of left ventricular geometry. In addition, it is imperative to distinguish the high-velocity systolic signal coming from the outflow Figure 27-11 Continuous wave Doppler recordings of the left ventricular outflow tract in a young patient with hypertrophic cardiomyopathy and severe systolic anterior motion and severe mitral regurgitation. The spectral profile has a characteristic dagger-shaped configuration. The peak velocity in the outflow tract is 4.4 m per second, which corresponds to a peak outflow tract gradient of 77 mm Hg, based on the modified Bernoulli equation.

tract from the signal of mitral regurgitation. The spectral profile of mitral regurgitation is characterized by an earlier onset, a more abrupt initial increase in velocity, and a higher peak velocity than that of an outflow tract signal. Systolic jets with a peak velocity of greater than 5.5 m per second (gradient >120 mm Hg) are most likely secondary to mitral regurgitation rather than left ventricular outflow tract obstruction.[68] Further differentiation of these two jets can be accomplished by orienting the transducer more medially and anteriorly and away from the mitral regurgitant jet. Nevertheless, there may still be contamination of the highvelocity signal of outflow tract obstruction from the jet of mitral regurgitation (Fig. 27-12) . This pitfall is particularly more common in patients with concomitant intrinsic mitral valve disease and a more centrally directed jet of mitral regurgitation. Despite optimal imaging, adjustments in instrument settings, and consideration of the differences in the timing and contour of these systolic jets, the distinction between these different Doppler signals may occasionally still be difficult.[73]

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Mitral Regurgitation in Hypertrophic Cardiomyopathy Anterior mitral leaflet-septal contact results in failure of coaptation with the posterior mitral leaflet, creating a funnel-shaped gap through which mitral regurgitation can develop, predominantly in mid-systole to late systole.[13] Studies of patients undergoing myectomy for obstructive 597

Figure 27-12 In a patient with obstructive hypertrophic cardiomyopathy, continuous wave Doppler signals from the left ventricular outflow tract at the site of obstruction (A), from the intermediate position (B), and at the site of mitral regurgitation in posterior left atrium (C). Obstructive outflow tract jet starts after the QRS wave, is preceded by low velocity presystolic flow, and has characteristic change in acceleration velocity (arrow, A). Mitral regurgitation is typically of higher velocity and starts earlier in systole. Care must be taken to avoid contamination of left ventricular outflow tract jet with mitral regurgitation. (From Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47.)

hypertrophic cardiomyopathy have demonstrated a predominant posteriorly directed jet in the majority of patients without independent mitral valve disease (Fig. 27-13) .[13] , [74] Mitral valve leaflet size contributes to the development of systolic anterior motion. A study combining echocardiographic features and pathologic findings in hypertrophic cardiomyopathy detected enlarged mitral valves in 44% of patients.[60] Patients with enlarged mitral valves had echocardiographic evidence for "typical" systolic anterior motion, characterized by the presence of a sharp, right-angled bend of the distal half of the anterior mitral valve leaflet and contact of the distal and central portions of the anterior mitral leaflet with the ventricular septum. In contrast, in patients with normal-sized mitral valves, systolic anterior motion was "atypical," involving greater portions of the body of the anterior mitral leaflet body and related chordae

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tendineae, and with little bending of the anterior mitral valve leaflet. Mitral regurgitation associated with obstructive hypertrophic Figure 27-13 (color plate.) Patient with severe obstructive hypertrophic cardiomyopathy and severe mitral regurgitation. A, Parasternal longaxis view showing turbulent left ventricular outflow tract and severe mitral regurgitation directed toward the posterior left atrial (LA) wall. B, Color Mmode study from the apical four-chamber view. C, Color M-mode line highlighted by arrow. Systolic flow at the midventricular level is homogeneously blue and then laminar. As the flow approaches the area of obstruction at the site of anterior leaflet septal contact, aliasing to red occurs over a depth of about 1 cm. The obstructed area of the outflow tract then has a mosaic pattern indicative of turbulent flow. In early systole, there is a narrow band of blue flow with brief duration of aliasing to red, followed by turbulent flow, indicating early development of turbulent flow and of outflow tract obstruction, which was timed with the onset of systolic anterior motion. LV, left ventricle; AO, aortic root. (From Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47.)

cardiomyopathy has been shown to be related to the degree of anterior leaflet systolic anterior motion and to the length and mobility of the posterior leaflet, which determine the size of the interleaflet gap and the degree of mid-systolic coaptation of the mitral leaflets.[75] These findings were corroborated by an intraoperative transesophageal echocardiographic study of 104 patients that demonstrated a significant correlation between the degree of mitral regurgitation, as assessed by color jet area and pulmonary venous flow pattern, and the degree of left ventricular outflow tract obstruction.[74] The presence of a nonposterior jet of mitral regurgitation suggests intrinsic mitral valve leaflet disease independent of SAM. Independent mitral valve lesions can be identified by echocardiography and are usually related to mitral valve prolapse, [76] ruptured chordae,[77] mitral annular calcification,[78] anomalous insertion of a papillary muscle into the anterior mitral leaflet,[79] or leaflet trauma (Fig. 27-14) . Repeated mitral leaflet-septal contact is associated with fibrosis and thickening 598

Figure 27-14 (color plate.) Transesophageal echocardiographic images from the long-axis view in three patients with obstructive hypertrophic cardiomyopathy. A, Posteriorly directed jet of mitral regurgitation (arrow) in a patient without independent mitral valve disease. B, Anteriorly directed mitral regurgitant jet

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(arrow) in a patient with posterior mitral valve leaflet prolapse. C, Centrally directed jet of mitral regurgitation (arrow) in a patient with rheumatic mitral stenosis. Ao, aorta; LV, left ventricle; MR, mitral regurgitation. (From Yu E, Omran AS, Wigle ED, et al: J Am Coll Cardiol 2000;36:2219–2225.)

of the anterior mitral leaflet and with subaortic septal endocardial fibrosis and thickening, previously described as a septal "callus."[46] Myectomy alone is generally successful in relieving mitral regurgitation, without the requirement for associated mitral valve replacement.[74]

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Atypical Forms of Hypertrophic Cardiomyopathy Asymmetric Apical Hypertrophy Asymmetric apical hypertrophic cardiomyopathy was initially reported by Japanese investigators in the 1970s.[80] [81] This unusual variant of hypertrophic cardiomyopathy has Figure 27-15 Two-dimensional echocardiographic and pulsed-wave Doppler recordings in a patient with asymmetric apical hypertrophic cardiomyopathy. A and B, Parasternal long-axis and short-axis views demonstrating normal septal wall thickness and no systolic anterior motion. C, Apical four-chamber view shows increased thickness of the apicolateral wall and spade-shaped configuration of the left ventricle at end-diastole. D, Pulmonary venous inflow pattern with sampling of right upper pulmonary vein demonstrates increased velocity of PV(a) (arrow), reflecting increased left ventricular end-diastolic pressure.

subsequently been described in non-Asian populations.[82] The striking features of patients with apical hypertrophy include the presence of giant negative T waves (≥10 mm) in the precordial electrocardiographic leads and an "ace of spades" configuration to the left ventricle (Fig. 27-15) . The diagnosis may be missed if acoustic windows are suboptimal and endocardial definition is poor. Contrast echocardiography may be useful in enhancing endocardial definition for identification of apical hypertrophy.[83] Echocardiography plays an important role in the assessment of the degree of hypertrophy at the apex, the extent of hypertrophy, and the development of such complications as impaired diastolic filling, apical aneurysm formation, apical infarction and subsequent midventricular obstruction, 599

and left atrial enlargement. Magnetic resonance imaging studies have

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identified a non-spade-shaped type of apical hypertrophy.[84] Serial magnetic resonance imaging of patients with this condition has suggested that apical hypertrophy can begin with the involvement of a single apical segment, which may produce a non-spade-shaped configuration. Circumferential hypertrophy of all four apical segments may subsequently develop and lead to the classic spade-shaped configuration.[85] Midventricular Obstruction The midventricular form of obstructive hypertrophic cardiomyopathy, initially described in 1976,[86] is an uncommon variant of this condition. Invasive angiographic and hemodynamic features of this condition include an hourglass-shaped left ventricular cavity, systolic midcavity obliteration, a distinct apical chamber, and a systolic pressure gradient at the midventricular level. Echocardiographic and Doppler findings include septal hypertrophy with hypertrophy extending to the midpapillary level, midcavity obliteration in systole, a persistent residual apical cavity in systole, and color turbulence at the midventricular level (Fig. 27-16) .[47] [71] [87] Subtypes of midventricular obstruction include lone midcavity obstruction, combined left ventricular outflow tract and midventricular obstruction, or midventricular obstruction associated with apical infarction or apical aneurysm formation. The combination of color flow mapping, pulsed wave, and continuous wave Doppler techniques is useful in localizing the site or sites and severity of obstruction.[71] Figure 27-16 (color plate.) A, Diastolic two-dimensional echocardiographic apical long-axis view of a patient with midventricular obstruction, apical infarction, and apical aneurysm formation. B, Note the poorly contractile and partially dyskinetic apical chamber in early systole. Flow away from the transducer is depicted in blue. C, Continuous wave Doppler recording through the area of midventricular obstruction shows a peak gradient of approximately 60 mm Hg. D, Midventricular obstruction develops in mid-systole and a mosaic color jet is seen at the level of the obstruction.

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Hypertrophic Cardiomyopathy of the Elderly Hypertrophic cardiomyopathy of the elderly is a subset of this condition with some distinguishing clinical and echocardiographic features (Fig. 2717) .[88] [89] [90] Hypertrophic cardiomyopathy of the elderly is more commonly identified in women. The pattern of hypertrophy tends to be focal and localized to the anterior or posterior interventricular septum.[91] Elderly patients with hypertrophic cardiomyopathy tend to have a milder degree of hypertrophy. The shape of the left ventricular cavity in elderly patients is typically ovoid with normal septal curvature. In contrast, younger patients tend to have a crescent-shaped left ventricular cavity and an abnormal convexity to the septum, characterized as a reversal of septal curvature.[43] Concomitant mitral annular calcification was detected in 30% of patients older than 40 years with hypertrophic cardiomyopathy in one autopsy series.[92] The mechanisms leading to left ventricular outflow tract obstruction in hypertrophic cardiomyopathy of the elderly are different from those seen in younger patients. Elderly patients have a relatively small heart and distorted geometry of the left ventricular outflow tract.[78] Mitral annular calcification results in anterior displacement of the mitral apparatus, narrowing of the outflow tract, and less angulation of the mitral leaflets. In contrast to younger patients, there is restricted systolic anterior motion of the anterior leaflet, with leaflet-septal contact occurring in the body of the leaflet rather than at the tip. Outflow tract obstruction, either at rest or with provocation, is associated with the majority of patients with hypertrophic cardiomyopathy of the elderly.[93] Furthermore, 600

Figure 27-17 (color plate.) Transesophageal echocardiographic images in the long-axis view obtained from a patient with hypertrophic

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cardiomyopathy of the elderly. A, There is narrowing of the left ventricular outflow tract secondary to septal hypertrophy and anterior displacement of the mitral apparatus from mitral annular calcification. Outflow tract obstruction results from systolic anterior motion and anterior leaflet septal contact. B, Color flow imaging demonstrates a mosaic jet of color turbulence in the outflow tract and a large jet of mitral regurgitation, which is more central in origin, unlike in younger patients who have a predominant eccentric posterior mitral regurgitant jet. Ao, aorta; IVS, interventricular septum; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; SAM, systolic anterior motion. (From Rakowski H, Freedman D, Wigle ED: Cardiol Elderly 1995;3:415–422.)

the presence of mitral annular calcification distorts the mitral annulus and may lead to an independent jet of mitral regurgitation, which is often centrally directed and distinct from the posteriorly directed mitral regurgitant jet caused by systolic anterior motion. In one study of patients with hypertrophic cardiomyopathy of the elderly, the significant risk factors associated with an adverse prognosis were class III dyspnea and left atrial size.[94]

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Stress Echocardiography in Hypertrophic Cardiomyopathy The application of stress echocardiography is important in the management of patients with hypertrophic cardiomyopathy, since the outflow tract gradients obtained after exercise may be very different from those measured after amyl nitrite inhalation and more accurately reflect patients' symptoms.[95] There may be a 50% increase in the left ventricular outflow tract gradient during supine exercise.[96] The magnitude of the pressure gradient has been shown to increase almost twofold with upright bicycle exercise. [97] Exercise echocardiography is beneficial in assessing the results of such interventions as septal ethanol ablation or surgical myectomy.[98] In addition, exercise testing has important prognostic implications.[99] [100] Exercise-induced hypotension may occur in one third of patients with hypertrophic cardiomyopathy and has been associated with a family history of hypertrophic cardiomyopathy or sudden death and with a smaller left ventricular cavity size.[99]

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Evaluation of Diastolic Function Factors Contributing to Impaired Diastolic Function In the past two decades, the application of Doppler techniques has been extremely beneficial in the evaluation of diastolic function in hypertrophic cardiomyopathy (Fig. 27-18) . [101] Diastolic filling of the left ventricle is impaired in hypertrophic cardiomyopathy and may result in dyspnea on exertion, elevated filling pressures, and progressive left atrial enlargement. Table 27-6 outlines the factors that contribute to diastolic filling in hypertrophic cardiomyopathy.[6] , [47] [102] Impaired relaxation of the left ventricle is secondary to increased contraction load, decreased relaxation loads, decreased inactivation, and increased nonuniformity. The early contraction load of outflow tract obstruction impairs and delays the onset of relaxation. The major relaxation loads, coronary and ventricular filling, are decreased. Calcium overload secondary to hypertrophy or ischemia leads to myofibril inactivation of actinmyosin cross-bridges. Relaxation is further impaired by the nonuniformity of load and inactivation in different segments of the left ventricle. Chamber stiffness is directly proportional to the myocardial mass and the degree of TABLE 27-6 -- Factors Affecting Diastolic Function in Hypertrophic Cardiomyopathy Relaxation Loads Contraction load Subaortic stenosis Relaxation loads Late systolic loading End-systolic deformation (restoring forces) Coronary filling

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Ventricular filling Inactivation Myocardial calcium overload Nonuniformity of load and inactivation (nonuniformity of contraction and relaxation) Chamber Stiffness Myocardial mass Left ventricular volume Myocardial stiffness (fibrosis) Adapted from Wigle ED, Sasson Z. Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83; and Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47.

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Figure 27-18 (color plate.) Patient with hypertrophic cardiomyopathy and midventricular obstruction. Diastolic function is evaluated by pulsed-wave Doppler recording from the right upper pulmonary vein (A), tissue Doppler imaging of the mitral annulus (B), and pulsed-wave Doppler recording of the mitral leaflet tip (C). The mitral inflow velocities appear normal. The pulmonary venous inflow pattern shows blunting of the systolic wave and an increased PV(a) velocity, compatible with increased left ventricular filling pressures, suggesting pseudonormalization of the diastolic mitral inflow pattern.

myocardial fibrosis and is inversely proportional to the left ventricular chamber volume. Pulsed Wave Doppler Assessment Pulsed wave Doppler assessment of mitral inflow velocities at the level of the mitral leaflet tips is the most commonly used method to assess diastolic left ventricular filling. Impaired relaxation is the predominant diastolic abnormality identified in patients with hypertrophic cardiomyopathy.[103] The mitral inflow pattern typically demonstrates a prolonged isovolumic relaxation time (IVRT), reduced early rapid filling (E), a prolonged deceleration time (DT), and increased atrial filling (A). The early diastolic velocity gradually increases and the deceleration time decreases with

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worsened left ventricular compliance and increased left atrial pressure. However, unlike in patients with ischemic or dilated cardiomyopathy, a study of simultaneous Doppler and invasive hemodynamic assessments showed that there was no significant correlation between the mean left atrial pressure and the deceleration time in patients with hypertrophic cardiomyopathy.[104] These findings are supported by other Doppler studies that showed no significant relationship between diastolic filling abnormalities and exercise capacity[105] or the magnitude of left ventricular hypertrophy.[106] Asynchronous Relaxation The inhomogeneity of relaxation seen in patients with hypertrophic cardiomyopathy may result in left ventricular intracavitary flow during isovolumic relaxation. Asynchronous relaxation in patients with asymmetric septal hypertrophy leads to earlier relaxation of the apex. Blood flow from the left ventricular base to apex is detected during isovolumic relaxation and has been termed intracavitary IVRT flow.[107] In contrast, patients with asymmetric apical hypertrophic cardiomyopathy may have intracavitary apex-to-base flow, previously described as a paradoxic jet flow, with earlier relaxation of proximal left ventricular segments.[108] Tissue Doppler Imaging Tissue Doppler imaging is an emerging modality for the evaluation of diastolic function in patients with hypertrophic cardiomyopathy.[109] A study of simultaneous cardiac catheterization, Doppler echocardiography, and tissue Doppler imaging showed that the ratio of E velocity to flow propagation velocity and the ratio of E velocity to early diastolic annular velocity (Ea) correlated reasonably well with left ventricular filling pressures. Left atrial pressure (LAP) is determined by the following equation[110] LAP = E/Ea × 1.25 + 1.9 Improvements in left ventricular relaxation and compliance, left atrial size reduction, and decreased symptoms were demonstrated following the relief of left ventricular outflow tract obstruction by septal ethanol ablation (see "Septal Ablation").[111] [112] In addition, tissue Doppler imaging has identified left ventricular regional relaxation

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602

abnormalities and asynchrony in patients with hypertrophic cardiomyopathy.[113]

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Prognostication by Echocardiography Multiple risk factors for sudden cardiac death have been associated with hypertrophic cardiomyopathy.[2] Clinical risk factors that have been implicated as risk factors include younger age of presentation, a malignant family history of hypertrophic cardiomyopathy, a history of syncope, and a history of ventricular tachycardia. The overall extent of left ventricular hypertrophy, as determined by a left ventricular wall thickness index, was significantly greater in one study of patients with sudden death.[114] Patients with marked and diffuse hypertrophy, defined as a maximal wall thickness of 30 mm or greater or a wall thickness of 25 mm or greater in two or more segments, had an eightfold increase in sudden death compared with control patients, who had lesser degrees of hypertrophy. One recent study stratified patients according to five subgroups of maximal left ventricular wall thickness (≤15 mm, 16 to 19 mm, 20 to 24 mm, 25 to 29 mm, and ≥30 mm) and demonstrated a significant increasing risk for sudden death based on maximal wall thickness.[9] The cumulative 20-year risk of sudden death for patients with a maximal wall thickness of 15 mm or less was minimal, whereas the risk was nearly 40% for patients with a maximal wall thickness of 30 mm or greater at initial presentation. Atrial fibrillation is a significant complication of hypertrophic cardiomyopathy. Left atrial enlargement is a common finding in this condition, secondary to the presence of mitral regurgitation, left ventricular outflow tract obstruction, impaired diastolic function, and elevation of left ventricular end-diastolic pressure. Early studies have correlated the development of atrial fibrillation with the severity of left atrial enlargement. [115] [116] The onset of atrial fibrillation is frequently associated with rapid clinical deterioration. The incidence of systemic embolism and stroke increases significantly with left atrial enlargement and atrial fibrillation.[117]

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Medical Therapy Medical management in hypertrophic cardiomyopathy is optimized by monitoring the response to therapy with serial echocardiographic and Doppler studies (Table 27-7) .[6] The three different classes of pharmacologic agents used for the treatment of obstructive hypertrophic cardiomyopathy are beta blockers, disopyramide, and calcium channel blockers. The mechanism of benefit of these agents is felt to be a decrease in myocardial contractility, which results in decreased left ventricular ejection velocity, the delayed onset of mitral leaflet systolic anterior motion and, consequently, decreased outflow tract obstruction and mitral regurgitation. Beta-adrenergic blocking agents are beneficial in the management of symptomatic obstruction, particularly in patients with latent or provocable outflow tract obstruction.[1] They may indirectly improve left ventricular diastolic filling by reducing the heart rate and increasing passive ventricular filling.[118] Disopyramide TABLE 27-7 -- Echocardiographic and Doppler Assessment of Effects of Therapy Decreased/Abolished Obstruction • Decrease in or abolition of SAM • Decreased LVOT velocity • Disappearance of systolic aortic valve narrowing • Decrease in or abolition of mitral regurgitation Improved Diastolic Function • More rapid time to peak filling • Longer diastasis • Increased LV filling during early diastole • Lower atrial LV filling velocity LV, left ventricular; LVOT, left ventricular outflow tract; SAM, systolic

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anterior motion. Adapted from Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47. is a type Ia antiarrhythmic agent with significant negative inotropic properties. [119] Cardiac symptoms and exercise capacity are generally improved in patients with obstructive hypertrophic cardiomyopathy following the institution of disopyramide. Calcium channel blockers may enhance ventricular filling and decrease myocardial ischemia in patients with hypertrophic cardiomyopathy. Multiple studies have demonstrated improvement in diastolic filling parameters with such calcium channel blockers as verapamil,[120] [121] nifedipine,[122] and diltiazem.[123] However, verapamil should be used with caution in patients with hypertrophic cardiomyopathy because it can lead to vasodilation and worsening outflow tract obstruction.[124]

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Dual-Chamber Pacing Dual-chamber (DDD) atrioventricular pacing reduces left ventricular outflow tract obstruction by inducing both acute and chronic changes.[125] [126] Pacing from the right ventricular apex may cause paradoxic or diminished inward movement of the ventricular septum and asynchronous and late activation at the base of the septum, which may contribute to widening of the left ventricular outflow tract during systole, and decreased myocardial contractility. The atrioventricular delay must be optimized to achieve complete ventricular capture. Initial studies had suggested significant symptomatic improvement and left ventricular mass regression with DDD pacing.[127] However, the results of multiple subsequent studies have been less encouraging. DDD pacing may result in impairment of both systolic and diastolic function, possibly related to asynchronous contraction and relaxation.[128] Randomized crossover studies of DDD pacing (treatment arm) versus AAI pacing (control arm) have been completed by Nishimura et al,[129] the PIC study investigators,[130] and the MPATHY study investigators.[131] These studies have shown an incomplete reduction in the left ventricular outflow tract gradient, no significant decrease in left ventricular wall thickness, and no significant increase in peak myocardial oxygen consumption (VO2 ) during follow-up.[132] The perceived decline in symptoms following pacemaker implantation may be due to a placebo effect.[129] [132] These findings were corroborated by a nonrandomized study comparing DDD pacing and septal myectomy, which showed a significantly greater improvement in the functional 603

class, peak VO2 , and left ventricular outflow tract gradient in the patients who underwent surgery.[133] The patients who seem to benefit from DDD pacing are the subset of older patients with lower baseline peak VO2 levels. [130] [131]

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Septal Ablation Septal ethanol ablation is an innovative interventional technique that consists of the selective injection of ethanol into the septal perforator branch of the left anterior descending artery. This leads to occlusion of the septal branch and localized infarction of the hypertrophied interventricular septum. Synonymous terms for this technique include nonsurgical septal reduction therapy, percutaneous transluminal septal myocardial ablation, and transmyocardial ablation of septal hypertrophy. The targeted infarction results in acute myocardial stunning, decreased SAM, and relief of the left ventricular outflow tract obstruction.[134] [135] The initial clinical experience with septal ethanol ablation was reported in 1995.[136] The selection of the appropriate septal branch to be injected was determined by the reduction in the left ventricular outflow tract gradient following transient occlusion of the targeted vessel by a balloon catheter. However, a key development in this technique was the use of intraprocedural echocardiography. Transesophageal echocardiography is infrequently required.[134] [137] Myocardial contrast echocardiography with transthoracic imaging[138] [139] has become essential for the guidance and monitoring of septal ethanol ablation. Myocardial Contrast Echocardiography During Septal Ethanol Ablation The intra-arterial injection of an echo-enhancing agent allows for the specific localization of the vascular beds perfused by individual septal perforator branches of the left anterior descending artery. Contrast agents that have Figure 27-19 (color plate.) Intraprocedural myocardial contrast echocardiography during septal ethanol ablation. A, Following injection of Levovist into the first septal perforator of the left anterior descending artery, a contrast depot is identified in the region of the basal septum by transthoracic two-

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dimensional apical imaging. This opacified area overlies the region of anterior mitral leaflet–septal contact, is adjacent to the site of left ventricular outflow tract turbulence, and is the targeted region of interest. B, Following alcohol injection into the first septal branch, an alcohol depot is identified in the same region as the area of contrast depot. Alcohol injection results in further increased echogenicity of the basal septum. C, Repeat transthoracic apical view with color flow imaging in a patient 3 months following septal ethanol ablation. There is now laminar flow in the left ventricular outflow tract. D, Continuous wave Doppler recording showing a nonsignificant resting gradient of 6 mm Hg across the left ventricular outflow tract. (From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079.)

been used during septal ethanol ablation are sonicated human albumin (Albunex, Mallinckrodt Inc, St. Louis, Mo[138] ) Optison (Mallinckrodt Inc), and Levovist (Schering AG, Berlin, Germany[139] ). Sonicated albumin is administered as a bolus injection of 1.0 to 1.5 mL of sonicated albumin diluted with normal saline (range of dilution 1:3 to 1:1). Levovist is a galactose-based agent, and 1 to 2 mL in a concentration of 350 ng/mL is injected through the inflated intra-arterial balloon catheter. High gain settings are required to visualize rapidly the effects of Levovist injection. [140] Following the injection of the contrast agent, the segments of the interventricular septum supplied by the septal branch become opacified. The spatial extent of myocardial opacification can be determined from multiple transthoracic windows. The vascular territory targeted by contrast echocardiography is the region of anterior mitral leaflet–septal contact, adjacent to the zone of flow acceleration and color turbulence in the left ventricular outflow tract (Fig. 27-19) .[139] In addition, contrast echocardiography is invaluable in detecting contrast opacification in regions remote from the site of mitral leaflet–septal contact.[14] [140] The demonstration of contrast enhancement in nonseptal sites necessitates the selection of another vessel to be targeted. The opacifying effects of intraarterial Levovist usually disappear within 10 minutes, thus allowing for reinjection of this contrast agent into subsequent vessels. The contrast effect of ethanol has the same distribution as that of the contrast agent, and intra-arterial ethanol injection frequently results in increased echogenicity and reflectivity. The area of contrast enhancement with human sonicated albumin has been correlated with infarct size, as determined by the peak creatine kinase level and by the size of the perfusion defect on singlephoton emission computed tomography thallium imaging (Table 27-8) .[138] Improved Outcomes with Contrast Echocardiography Two groups with extensive experience with intraprocedural contrast echocardiography during septal ethanol

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604

TABLE 27-8 -- Myocardial Contrast Echocardiography During Septal Ethanol Ablation With MCE (n = No MCE (n = 131/132) 28/30) P Value 65 (32) 96 (62) <0.001

Variable Maximum creatine kinase-MB rise (U/L) DDD-Pacemaker 5 17 0.05 implantation rate, % Follow-up success rate 94 64% <0.001 (LVOT gradient reduction >50%) LVOT gradient (rest) at 3 9 (17) 27 (34) <0.01 months (mm Hg) LVOT, left ventricular outflow tract; MCE, intraprocedural myocardial contrast echocardiography. From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079.

ablation have demonstrated that this echocardiographic approach results in improved outcomes.[14] [139] [141] The use of intra-arterial sonicated albumin limited the number of vessels injected and the volume of ethanol used and resulted in fewer cases of atrioventricular block requiring permanent pacemaker implantation, one of the significant complications associated with septal ethanol ablation.[141] Faber et al[14] have reported on the largest experience with intraprocedural myocardial contrast echocardiography during septal ethanol ablation. They showed improved outcomes with contrast echocardiography using Levovist as compared with the strategy of target vessel selection by probatory balloon occlusion (see Table 27-8) . Contrast-guided septal ethanol ablation resulted in smaller infarcts, a 5% versus 17% pacemaker implantation Figure 27-20 A to H, Two-dimensional transthoracic echocardiographic still frames obtained during septal ethanol ablation in various patients. The opacification of such left ventricular regions as the posteromedial

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papillary muscle (A, arrow), basal lateral wall (B, arrow), posterolateral wall (C and G, arrows), inferior wall (F, arrows) have been reported. Opacification of such rightsided structures as the right ventricular papillary muscles may also occur, in association with small (E) and large (D and H) contrast depots seen in the septum. LA, left atrium; RA, right atrium; RV, right ventricle. (From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079.)

rate, and greater reductions in the left ventricular outflow tract gradient. The opacification of myocardial segments distal to the target region of mitral leaflet–septal contact resulted in a change in the target vessel in 7% of cases (Fig. 27-20) . Therefore, myocardial contrast echocardiography optimizes septal ethanol ablation by permitting the targeted delivery of ethanol, limiting the induced infarction to the culprit region of mitral leaflet–septal contact, and by minimizing procedural complications. Clinical Results Following Septal Ethanol Ablation The major early outcomes of septal ethanol ablation from three recognized international centers are summarized in Table 27-9 (Table Not Available) . [137] [141] [142] [143] Subsequent studies beyond 1 year following this procedure have shown ongoing symptomatic improvement. [144] [145] The immediate relief in left ventricular outflow tract obstruction seen following ethanol injection is secondary to acute myocardial stunning following the controlled infarction. [135] There is a gradual and continued decrease in the degree of left ventricular outflow tract obstruction with healing and replacement fibrosis[137] and thinning of the infarcted septal segment and enlargement of the outflow tract.[146] The long-term risk of late ventricular arrhythmias following induced infarction in patients with hypertrophic cardiomyopathy remains unclear, although early studies have not demonstrated an increased risk.[137] Echocardiographic and Doppler studies are beneficial in the serial noninvasive follow-up of patients following septal ethanol ablation. Multiple studies have documented 605

TABLE 27-9 -- Summary of Results of Septal Ethanol Ablation (Not Available) LVOTG, left ventricular outflow tract gradient; PPM, Permanent

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Pacemaker. significant progressive reductions in basal septal thickness and in the resting and provocable left ventricular outflow tract gradients over the first 2 years of follow-up (Fig. 27-21) .[147] These developments have been associated with favorable changes in the geometry of the left ventricular outflow tract[135] and with improvements in left ventricular diastolic function.[111] [112]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Surgical Myectomy Ventricular myotomy or myectomy has been performed for the past four decades for the management of severe obstructive hypertrophic cardiomyopathy refractory to maximally tolerated medical therapy. Septal myectomy relieves outflow tract obstruction by widening of the left ventricular outflow tract, which leads to decreased systolic anterior motion of the mitral valve and decreased dynamic outflow tract obstruction. Echocardiography is useful in the identification of patients suitable for surgical myectomy. The preoperative echocardiographic characteristics predictive of symptomatic benefit from surgical myectomy include asymmetric hypertrophy, severe SAM of the mitral leaflets, and a prolonged isovolumic relaxation time.[148] In addition, echocardiography plays an important role in Figure 27-21 Serial transthoracic echocardiograms in a 25-year-old patient prior to and 2 years following septal ethanol ablation for drugrefractory symptomatic obstructive hypertrophic cardiomyopathy. A, Parasternal long-axis view obtained prior to the procedure demonstrates prominent septal hypertrophy (arrow) and resting systolic anterior motion. B, During follow-up 2 years after septal ethanol ablation, there is striking localized thinning of the anterior septum (arrow), resolution of systolic anterior motion, and a resting outflow tract gradient of 6 mm Hg.

detecting additional lesions requiring surgical management. Comprehensive preoperative echocardiographic imaging in patients referred for surgical myectomy includes the evaluation of independent mitral valve disease, concomitant aortic valve disease, and the assessment of additional levels of obstruction (midventricular or right ventricular outflow tract).[13] Intraoperative Echocardiography Surgical myectomy is performed from the transaortic approach and is technically challenging given the limited exposure and visualization of the

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hypertrophied septum. Prior to the introduction of intraoperative echocardiography, the extent and degree of septal hypertrophy was estimated by surgical palpation[149] and by preoperative transthoracic echocardiographic studies. A key development in the surgical management of obstructive hypertrophic cardiomyopathy has been the use of intraoperative echocardiography with epicardial or transesophageal imaging (Fig. 27-22) . Intraoperative echocardiography guides the surgical interventions, assesses immediate results, and excludes important complications.[13] [150] Intraoperative transesophageal echocardiography allows for detailed 606

Figure 27-22 (color plate.) Intraoperative echocardiography in a patient with obstructive hypertrophic cardiomyopathy. A to D, Transesophageal study. A, Two-dimensional systolic frame obtained prior to myectomy, demonstrating marked anterior and basal motion of the anterior mitral leaflet with leaflet-septal contact (arrow). B, Same frame with Doppler color flow imaging demonstrating turbulence in the left ventricular outflow tract (arrowheads) arising at the site of leaflet-septal contact and a jet of posteriorly directed mitral regurgitation (arrow). C, Two-dimensional frame obtained after myectomy. Note the widened left ventricular outflow tract and absence of systolic anterior motion despite persistence of abnormal coaptation point (arrow). D, Same frame with Doppler color flow imaging demonstrating lack of turbulence in the outflow tract (arrowheads) and only a small centrally directed jet of mitral regurgitation (arrow). E and F, Intraoperative epicardial study of the same patient after myectomy. E, Parasternal long-axis frame demonstrating the absence of systolic anterior motion despite persistence of an abnormal coaptation point between the mitral leaflets. F, Parasternal short-axis frame demonstrating the site of myectomy (arrow). (From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52.)

delineation of the depth, width, and length of the required myectomy, the degree of systolic anterior motion and left ventricular outflow tract obstruction, and the quantitation and mechanisms of mitral regurgitation.[13] [74] Imaging from multiple transesophageal and transgastric views using a multiplane transducer allows for the careful Figure 27-23 A, Intraoperative transesophageal echocardiogram in the long-axis plane in a patient referred for myectomy. The depth, width, and length of the hypertrophied septum (measured from the base of the right coronary cusp of the aortic valve) and the point of anterior leaflet-septal contact are obtained to guide the resection. B, Transgastric views of the mitral valve and left

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ventricular outflow tract permit detailed examination of the morphology of the mitral leaflets, the point of leaflet-septal contact (arrow) and the assessment of systolic anterior motion. LA, left atrium; Ao, aorta.

assessment of the thickness of the anterior and posterior portions of the interventricular septum. The length of septal hypertrophy is measured from the base of the right coronary cusp of the aortic valve (Fig. 27-23) . The targeted length of resection is 1 cm below the point of anterior mitral leaflet–septal contact. The left ventricular 607

Figure 27-24 (color plate.) Intraoperative transesophageal echocardiogram (frontal long-axis plane) before (upper panels) and after (lower panels) myectomy in a patient with no independent mitral valve disease (A) and in a patient with thickened mitral leaflets (B). A, Upper left panel, Two-dimensional systolic frame demonstrating anterior leaflet-septal contact with failure of mitral leaflet coaptation. Upper right panel, Same frame with Doppler color flow imaging demonstrating turbulent left ventricular outflow and a large jet of posteriorly directed mitral regurgitation arising from the gap between the two mitral leaflets. Lower left panel, Two-dimensional systolic frame now showing a widened left ventricular outflow tract and abolition of systolic anterior motion. Lower right panel, Same frame with Doppler color flow imaging demonstrating nonturbulent left ventricular outflow with a marked reduction in the severity of mitral regurgitation and the presence of only a small residual central jet. B, Upper left panel, Two-dimensional systolic frame demonstrating thickened mitral leaflets and septal hypertrophy. Upper right panel, Same frame with color flow imaging demonstrating a posteriorly directed jet of mitral regurgitation. Lower panels, Following myectomy, two-dimensional and Doppler color flow imaging now show widening of the outflow tract, no significant turbulence in the outflow tract and the resolution of mitral regurgitation. (A, from Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.)

outflow tract gradient can be measured by transgastric imaging in the longaxis view with the continuous wave Doppler beam aligned parallel to the left ventricular outflow tract. Following surgical excision of the basal septum, repeat echocardiographic imaging permits the instantaneous evaluation of the adequacy of the myectomy (Fig. 27-24) .[13] [150] Intraoperative echocardiography can determine whether there is significant residual outflow tract obstruction or hemodynamically important residual mitral regurgitation (Fig. 27-25) . In addition, intraoperative echocardiography allows for the immediate

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detection of such operative complications as a ventricular septal defect[151] Figure 27-25 (color plate.) Transesophageal echocardiogram demonstrating an unsatisfactory result after myectomy. A, Before myectomy. Turbulence is shown in the left ventricular outflow tract and a jet of mitral regurgitation is seen in the left atrium (arrow). B through D, After myectomy. B, Two-dimensional frame in the frontal long-axis plane demonstrating the persistence of systolic anterior motion. C, Doppler color flow imaging shows persistence of turbulence in the outflow tract and severe mitral regurgitation (arrow). D, Two-dimensional frame demonstrating a very small myectomy site (arrowheads). (From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.)

and left ventricular dysfunction.[13] Three-dimensional transesophageal echocardiographic imaging with three-dimensional reconstruction has been used to assess the geometry of the hypertrophied septum and the crosssectional area of the left ventricular outflow tract prior to and following extended myectomy. [152] Outcomes Following Myectomy Studies of the results of surgical myectomy from experienced tertiary referral centers have shown excellent early and long-term postoperative outcomes. [153] [154] [155] Potential 608

Figure 27-26 (color plate.) Echocardiographic imaging obtained following surgical myectomy. A and B, Two-dimensional and color flow imaging in the parasternal long-axis view (A) and short-axis view (B) demonstrate a widened outflow tract, a small jet of aortic regurgitation, and a separate jet of color flow turbulence secondary to septal perforator flow. Aortic regurgitation following myectomy is most commonly due to the postoperative loss of aortic annular support. C, Continuous wave Doppler imaging across the outflow tract confirms the presence of mild aortic regurgitation. D, Gross pathologic specimen of excised basal septum in a patient who underwent myectomy. Note the lumen of the septal perforator vessel within the excised septum (arrow).

complications following myectomy include heart block, ventricular septal defect, aortic regurgitation, and arrhythmias. Aortic regurgitation is felt to be secondary to trauma of the aortic valve or secondary to the loss of aortic

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annular support following myectomy (Fig. 27-26) . [156] Echocardiographic studies performed at rest and with provocative maneuvers are important in the serial monitoring of patients following myectomy.[98] Many studies have documented a significant reduction or abolition of the resting outflow tract gradient in the majority of patients following myectomy, resulting in substantial and lasting symptomatic improvement.[153] [154] [155] [157] , [158] Nonrandomized studies of medical therapy versus myectomy[159] and pacing versus myectomy[133] have suggested more favorable overall outcomes with myectomy.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary of Treatment Strategies Many therapeutic options are currently available in the management of symptoms attributable to outflow tract obstruction in hypertrophic cardiomyopathy. Pharmacologic agents such as beta blockers, disopyramide, and calcium channel blockers have variable effects in reducing the outflow tract gradient and in improving diastolic function. Patients with drug-refractory symptoms are candidates for DDD pacing, septal ethanol ablation, or surgical myectomy. There is a lesser magnitude of gradient reduction with pacing and septal ethanol ablation. Many studies from experienced centers suggest that the resting outflow tract gradient declines approximately 50% with pacing and more than 70% following septal ethanol ablation.[132] The subgroup of older, severely limited patients who are not candidates for surgical myectomy may benefit most from dual chamber pacing. The decreased outflow tract obstruction following septal ethanol ablation has been accompanied by significant improvements in symptomatic status, exercise tolerance, and left ventricular mass. The left ventricular outflow tract gradient may be completely abolished with surgical myectomy, which results in long-term symptomatic benefit. Trials are currently ongoing that compare the relative merits and outcomes of these different treatment modalities. [143]

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References 1. Wigle ED, Rakowski H, Kimball BP, Williams WG: Hypertrophic cardiomyopathy:

Clinical spectrum and treatment. Circulation 1995;92:1680–1692. 2. Spirito P, Seidman CE, McKenna WJ, Maron BJ: The management of hypertrophic

cardiomyopathy. N Engl J Med 1997;336:775–785. 3. Richardson P, McKenna W, Bristow M, et al: Report of the 1995 World Health

Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841–842. 4. Brock RC: Functional obstruction of the left ventricle. Guys Hosp Rep

1957;106:221–238. 5. Teare RD: Asymmetrical hypertrophy of the heart in young adults. Br Heart J

1958;20:1–8. 6. Rakowski H, Sasson Z, Wigle ED: Echocardiographic and Doppler assessment of

hypertrophic cardiomyopathy. J Am Soc Echocardiogr 1988;1:31–47. 7. Maron BJ, Gardin JM, Flack JM, et al: Prevalence of hypertrophic cardiomyopathy

in a general population of young adults: Echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation 1995;92:785–789. 609

8. Clark CE, Henry WL, Epstein SE: Familial prevalence and genetic transmission of

idiopathic hypertrophic subaortic stenosis. N Engl J Med 1973;289:709–714.

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9. Spirito P, Belone P, Harris KM, et al: Magnitude of left ventricular hypertrophy and

risk of sudden death in hypertrophic cardiomyopathy. N Engl J Med 2000;324:1778– 1785. 10. McKenna WJ, Spirito P, Desnos M, et al: Experience from clinical genetics in

hypertrophic cardiomyopathy: Proposal for new diagnostic criteria in adult members of affected families. Heart 1997;77:130–132. 11. Corrado D, Basso C, Schiavon M, Thiene G: Screening for hypertrophic

cardiomyopathy in young athletes. N Engl J Med 1998;339:364–369. 12. Maron BJ, Moller JH, Seidman CE, et al: Impact of laboratory molecular diagnosis

on contemporary diagnostic criteria for genetically transmitted cardiovascular diseases: Hypertrophic cardiomyopathy, long-QT syndrome, and Marfan syndrome. A statement for healthcare professionals from the Councils on Clinical Cardiology, Cardiovascular Disease in the Young, and Basic Science, American Heart Association. Circulation 1998;98:1460–1471. 13. Grigg LE, Wigle ED, Williams WG, et al: Transesophageal Doppler

echocardiography in obstructive hypertrophic cardiomyopathy: Clarification of pathophysiology and importance in intraoperative decision making. J Am Coll Cardiol 1992;20:42–52. 14. Faber L, Ziemssen P, Seggewiss H: Targeting percutaneous transluminal septal

ablation for hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. J Am Soc Echocardiogr 2000;13:1074–1079. 15. Frank S, Braunwald E: Idiopathic hypertrophic subaortic stenosis: Clinical analysis

of 126 patients with emphasis on the natural history. Circulation 1968;37:759–788. 16. Corrado D, Basso C, Schiavon M, Thiene G: Screening for hypertrophic

cardiomyopathy in young athletes. N Engl J Med 1998;339:364–369. 17. Hada Y, Sakamoato T, Amano K, et al: Prevalence of hypertrophic

cardiomyopathy in a population of adult Japanese workers as detected by echocardiographic screening. Am J Cardiol 1987;59:183–184. 18. Maron BJ, Peterson EE, Maron MS, et al: Prevalence of hypertrophic cardiomyopathy in an outpatient population referred for echocardiographic study. Am J Cardiol 1994;73:577–580. 19. Bagger JP, Baandrup U, Rasmussen K, et al: Cardiomyopathy in Western

Denmark. Br Heart J 1984;52:327–331.

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20. Codd MB, Sugure DD, Gersh BJ, Melton LJ III: Epidemiology of idiopathic

dilated and hypertrophic cardiomyopathy: A population-based study in Olmsted County, Minnesota, 1975–1984. Circulation 1989;80:564–572. 21. Seidman C: Hypertrophic cardiomyopathy: From man to mouse. J Clin Invest

2000;106:S9–S13. 22. Jarcho JA, McKenna W, Pare JAP, et al: Mapping a gene for familial hypertrophic

cardiomyopathy to chromosome 14q1. N Engl J Med 1989;321:1372–1378. 23. Watkins H, Rosenzweig A, Hwang DS, et al: Characteristics and prognostic

implications of myosin missense mutations in familial hypertrophic cardiomyopathy. N Engl J Med 1992;326:1108–1114. 24. Watkins H, McKenna WJ, Thierfelder L, et al: Mutations in the genes for cardiac

troponin T and α-tropomyosin in hypertrophic cardiomyopathy. N Engl J Med 1995;332:1058–1064. 25. Solomon SD, Wolff S, Watkins H, et al: Left ventricular hypertrophy and

morphology in familial hypertrophic cardiomyopathy associated with mutations of the beta-myosin heavy chain gene. J Am Coll Cardiol 1993;22:498–505. 26. Niimura H, Bachinski LL, Sangwatanaroj S, et al: Mutations in the gene for

cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy. N Engl J Med 1998;338:1248–1257. 27. Shah PM, Gramiak R, Kramer DH: Ultrasound location of left ventricular outflow

obstruction in hypertrophic obstructive cardiomyopathy. Circulation 1969;40:905. 28. Henry WL, Clark CE, Epstein SE: Asymmetric septal hypertrophy:

Echocardiographic identification of the pathognomonic anatomic abnormality of IHSS. Circulation 1973;47:225–233. 29. Wald D: Screening for hypertrophic cardiomyopathy. J Med Screen 1999;6:159–

162. 30. Ryan MP, Cleland JGF, French JA, et al: The standard electrocardiogram as a

screening test for hypertrophic cardiomyopathy. Am J Cardiol 1995;76:689–694. 31. Humez FU, Houston AB, Watson J, et al: Age and body surface area related

normal upper and lower limits of M mode echocardiographic measurements and left ventricular volume and mass from infancy to early adulthood. Br Heart J 1994;7:276– 280.

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32. Epstein SE, Maron BJ: Sudden death and the competitive athlete: Perspectives on

preparticipation screening studies. J Am Coll Cardiol 1986;4:220–230. 33. Maron BJ, Bodison SA, Wesley YE, et al: Results of screening a large group of

intercollegiate competitive athletes for cardiovascular disease. J Am Coll Cardiol 1987;10:1214–1221. 34. Lewis JF, Maron BJ, Diggs JA, et al: Preparticipation echocardiographic screening

for cardiovascular disease in a large, predominantly black population of collegiate athletes. Am J Cardiol 1989;64:1029–1033. 35. Klein AL, Oh JK, Miller FA, et al: Two-dimensional and Doppler echocardiographic assessment of infiltrative cardiomyopathy. J Am Soc Echocardiogr 1988;1:48–59. 36. Prasad K, Atherton J, Smith GC, et al: Echocardiographic pitfalls in the diagnosis

of hypertrophic cardiomyopathy. Heart 1999;82(Suppl III):III8–III15. 37. Pellicia A, Maron BJ, Spataro A, et al: The upper limit of physiological cardiac

hypertrophy in highly trained elite athletes. N Engl J Med 1991;324:295–301. 38. Spirito A, Pellicia A, Proschan MA, et al: Morphology of "athlete's heart" assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol 1994;74:802–806. 39. Maron BJ, Pellicia A, Spirito P: Cardiac disease in young trained athletes: Insights

into the methods for distinguishing athlete's heart from structural heart disease, with particular emphasis on hypertrophic cardiomyopathy. Circulation 1995;91:1596–1601.

40. Pellicia A, Maron BJ, Culasso F, et al: Athlete's heart in women. JAMA

1996;276:211–215. 41. Karam R, Lever HM, Healy BP: Hypertensive hypertrophic cardiomyopathy or

hypertrophic cardiomyopathy with hypertension? A study of 78 patients. J Am Coll Cardiol 1989;13:580–584. 42. Dalldorf FG, Willis PW IV: Angled aorta ("sigmoid septum") as a cause of

hypertrophic stenosis. Hum Pathol 1985;16:457–462. 43. Lever HM, Karam RF, Currie PJ, Healy B: Hypertrophic cardiomyopathy in the

elderly: Distinction from the young based on cardiac shape. Circulation 1989;79:580–

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589. 44. Krasnow N: Subaortic septal bulge simulates hypertrophic cardiomyopathy by

angulation of the septum with age, independent of focal hypertrophy: An echocardiographic study. J Am Soc Echocardiogr 1997;10:545–555. 45. Belenkie I, MacDonald RPR, Smith ER: Localized septal hypertrophy: Part of the spectrum of hypertrophic cardiomyopathy or an incidental echocardiographic finding? Am Heart J 1988;115:385–390. 46. Martin RP, Rakowski H, French J, Popp RL: Idiopathic hypertrophic subaortic

stenosis viewed by wide-angle, phased-array echocardiography. Circulation 1979;59:1206–1217. 47. Wigle ED, Sasson Z, Henderson M, et al: Hypertrophic cardiomyopathy: The

importance of the site and extent of hypertrophy. A review. Prog Cardiovasc Dis 1985;28:1–83. 48. Maron BJ, Gottdiener JS, Epstein SE: Patterns and significance of distribution of

left ventricular hypertrophy in hypertrophic cardiomyopathy. Am J Cardiol 1981;48:418–428. 49. Rakowski H, Fulop J, Wigle ED: The role of echocardiography in the assessment

of hypertrophic cardiomyopathy. Postgrad Med J 1986;62:557–561. 50. Lattanzi F, Spirito P, Picano E, et al: Quantitative assessment of ultrasonic

myocardial reflectivity in hypertrophic cardiomyopathy. J Am Coll Cardiol 1991;17:1085–1090. 51. Fowles RE, Martin RP, Popp RL: Apparent asymmetric septal hypertrophy due to

angled interventricular septum. Am J Cardiol 1980;46:386–392. 52. Klues HG, Schiffers A, Maron BJ: Phenotypic spectrum and patterns of left

ventricular hypertrophy in hypertrophic cardiomyopathy: Morphologic observations and significance as assessed by two dimensional echocardiography in 600 patients. J Am Coll Cardiol 1995;26:1699–1708. 610

53. Henry WL, Clark CE, Glancy DL, Epstein SE: Echocardiographic measurement of the left ventricular outflow gradient in idiopathic hypertrophic subaortic stenosis. N

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Engl J Med 1973;288:898. 54. Gilbert BW, Pollick C, Adelman AG, Wigle ED: Hypertrophic cardiomyopathy:

Subclassification by M-mode echocardiography. Am J Cardiol 1980;45:861–872. 55. Krajcer Z, Orzan F, Pechacek LW, et al: Early systolic closure of the aortic valve

in patients with hypertrophic subaortic stenosis and discrete subaortic stenosis. Am J Cardiol 1978;41:823–829. 56. Henry WL, Clark CE, Griffith JM, Epstein SE: Mechanism of left ventricular

outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic subaortic stenosis). Am J Cardiol 1975;35:337–345. 57. Spirito P, Maron BJ: Significance of left ventricular outflow tract cross-sectional

area in hypertrophic cardiomyopathy: A two-dimensional echocardiographic assessment. Circulation 1983;67:1100–1108. 58. Shah PM, Taylor RD, Wong M: Abnormal mitral valve coaptation in hypertrophic obstructive cardiomyopathy: Proposed role in systolic anterior motion of mitral valve. Am J Cardiol 1981;48:258–262. 59. Jiang L, Levine RA, King ME, Weyman AE: An integrated mechanism for systolic

anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J 1987;113:663–644. 60. Klues HG, Roberts WC, Maron BJ: Morphologic determinants of

echocardiographic patterns of mitral valve systolic anterior motion in obstructive hypertrophic cardiomyopathy. Circulation 1993;87:1570–1579. 61. Reis R, Bolton MR, King JF, et al: Anterior-superior displacement of papillary

muscles producing obstruction and mitral regurgitation in idiopathic hypertrophic subaortic stenosis. Circulation 1974;49–50(Suppl):181–188. 62. Sherrid MV, Chu CK, Delia E, et al: An echocardiographic study of the fluid

mechanics of obstruction in hypertrophic cardiomyopathy. J Am Coll Cardiol 1993;22:816–825. 63. Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G: Systolic anterior motion

begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2000;36:1344–1354. 64. Pollick C, Morgan CD, Gilbert BW, et al: Muscular subaortic stenosis: The

temporal relationship between systolic anterior motion of the anterior mitral leaflet and the pressure gradient. Circulation 1982;66:1087–1094.

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65. Pollick C, Rakowski H, Wigle ED: Muscular subaortic stenosis: The quantitative relationship between systolic anterior motion and the pressure gradient. Circulation 1984;69:43–49. 66. Maron BJ, Harding AM, Spirito P, et al: Systolic anterior motion of the posterior

mitral leaflet: A previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation 1983;68:282–293. 67. Spirito P, Maron BJ: Patterns of systolic anterior motion of the mitral valve in

hypertrophic cardiomyopathy: Assessment by two-dimensional echocardiography. Am J Cardiol 1984;54:1039–1046. 68. Panza JA, Petrone RK, Fananapazir L, Maron BJ: Utility of continuous wave

Doppler echocardiography in the noninvasive assessment of left ventricular outflow tract pressure gradient in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1992;19:91–99. 69. Bryg RJ, Pearson AC, Williams GA, Labovitz AJ: Left ventricular systolic and

diastolic flow abnormalities determined by Doppler echocardiography in obstructive cardiomyopathy. Am J Cardiol 1987;59:925–931. 70. Sasson Z, Yock PG, Hatle LK, et al: Doppler echocardiographic determination of

the pressure gradient in hypertrophic cardiomyopathy. J Am Coll Cardiol 1988;11:752–756. 71. Schwammenthal E, Block M, Schwartzkopff B, et al: Prediction of the site and

severity of obstruction in hypertrophic cardiomyopathy by color flow mapping and continuous wave Doppler echocardiography. J Am Coll Cardiol 1992;20:964–972. 72. Kizilbash AM, Heinle SK, Grayburn PA: Spontaneous variability of left

ventricular outflow tract gradient in hypertrophic obstructive cardiomyopathy. Circulation 1998;97:461–466. 73. Yock PG, Hatle L, Popp RL: Patterns and timing of Doppler-detected intracavitary

and aortic flow in hypertrophic cardiomyopathy. J Am Coll Cardiol 1986;8:1047– 1058. 74. Yu E, Omran AS, Wigle ED, et al: Mitral regurgitation in hypertrophic obstructive

cardiomyopathy: Relationship to obstruction and relief with myectomy. J Am Coll Cardiol 2000;36:2219–2225. 75. Schwammenthal E, Nakatani S, He S, et al: Mechanism of mitral regurgitation in

hypertrophic cardiomyopathy. Circulation 1998;98:856–865.

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76. Petrone RK, Klues HG, Panza JA, et al: Coexistence of mitral valve prolapse in a consecutive group of 528 patients with hypertrophic cardiomyopathy assessed with echocardiography. J Am Coll Cardiol 1992;20:55–61. 77. Zhu WX, Oh JK, Kopecky SL, et al: Mitral regurgitation due to ruptured chordae

tendineae in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1992;20:242–247. 78. Rakowski H, Freedman D, Wigle ED: Echocardiographic evaluation of

hypertrophic cardiomyopathy in the elderly. Cardiol Elderly 1995;3:415–422. 79. Klues HG, Roberts WC, Maron BJ: Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy: Significance in producing left ventricular outflow obstruction. Circulation 1991;84:1188–1197. 80. Sakamoto T, Tei C, Muramaya M, et al: Giant negative T wave inversion as a

manifestation of asymmetric apical hypertrophy (AAH) of the left ventricle: Echocardiographic and ultrasonocardiotomographic study. Jpn Heart J 1976;17:611. 81. Yamaguchi H, Ishimura T, Nishiyama S, et al: Hypertrophic non-obstructive

cardiomyopathy with giant negative T-waves (apical hypertrophy): Ventriculographic and echocardiographic features in 30 patients. Am J Cardiol 1979;44:401. 82. Webb JG, Sasson Z, Rakowski H, et al: Apical hypertrophic cardiomyopathy:

Clinical follow-up and diagnostic correlates. J Am Coll Cardiol 1990;15:83–90. 83. Thanigaraj S, Perez JE: Apical hypertrophic cardiomyopathy: Echocardiographic

diagnosis with the use of intravenous contrast image enhancement. J Am Soc Echocardiogr 2000;13:146–149. 84. Suzuki J, Watanabe F, Takenaka K, et al: New subtype of apical hypertrophic

cardiomyopathy identified with nuclear magnetic resonance imaging as an underlying cause of markedly inverted T waves. J Am Coll Cardiol 1993;22:1175–1181. 85. Suzuki J, Shiamamoto R, Nishikawa J, et al: Morphological onset and early

diagnosis in apical hypertrophic cardiomyopathy: A long term analysis with nuclear magnetic resonance imaging. J Am Coll Cardiol 1999;33:146–151. 86. Falicov RE, Resnekov L, Bharati S, Lev M: Midventricular obstruction: A variant

of obstructive cardiomyopathy. Am J Cardiol 1976;37:432–437. 87. Kuhn H, Mercier J, Köhler E, et al: Differential diagnosis of hypertrophic

cardiomyopathies: Typical (subaortic) hypertrophic cardiomyopathy, atypical (mid-

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ventricular) hypertrophic cobstructive cardiomyopathy and hypertrophic nonobstructive cardiomyopathy. Eur Heart J 1983;4(Suppl F):93–104. 88. Whiting RB, Powell JW, Dinsmore RE, Sanders C: Idiopathic hypertrophic

subaortic stenosis in the elderly. N Engl J Med 1971;285:196–200. 89. Krasnow N, Stein RA: Hypertrophic cardiomyopathy in the aged. Am Heart J

1978;96:326–336. 90. Lewis JF, Maron BJ: Clinical and morphologic expression hypertrophic

cardiomyopathy in patients (65 years of age). Am J Cardiol 1994;73:1105–1111. 91. Chikamori T, Doi Y, Yonazawa Y, et al: Comparison of clinical features of

patients >60 years of age to those <40 years of age with hypertrophic cardiomyopathy. Am J Cardiol 1990;66:875–877. 92. Mohamed HE, Roberts WC: Frequency and significance of mitral annular calcium

in hypertrophic cardiomyopathy: Analysis of 200 necropsy patients. Am J Cardiol 1987;60:877–884. 93. Lever HM, Karam RF, Currie PJ, Healy BP: Hypertrophic cardiomyopathy in the

elderly. Circulation 1989;79:580–589. 94. Fay WP, Taliercio C, Histrup DM, et al: Natural history of hypertrophic

cardiomyopathy in the elderly. J Am Coll Cardiol 1990;18:821–826. 95. Marwick TH, Nakatani S, Haluska B, et al: Provocation of latent left ventricular

outflow tract gradients with amyl nitrite and exercise in hypertrophic cardiomyopathy. Am J Cardiol 1995;75:805–809. 611

96. Decoulx E, Goullard L, Millaire A, et al: Left intraventricular gradients measured

by Doppler echocardiography at rest, during exercise and during isoproterenol test in hypertrophic cardiomyopathy. Arch Mal Coeur Vaiss 1992;85:839–845. 97. Schwammenthal E, Schwartzkopff B, Block M, et al: Doppler echocardiographic

assessment of the pressure gradient during bicycle ergometry in hypertrophic cardiomyopathy. Am J Cardiol 1992;69:1623–1628. 98. Göl MK, Emir M, Keles T, et al: Septal myectomy in hypertrophic obstructive

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cardiomyopathy: Late results with stress echocardiography. Ann Thorac Surg 1997;64:739–745. 99. Frenneaux MP, Counihan PJ, Caforio ALP, et al: Abnormal blood pressure

response during exercise in hypertrophic cardiomyopathy. Circulation 1990;82:1995– 2002. 100. Sadoul N, Prasad K, Elliott PM, et al: Prospective prognostic assessment of blood

pressure response during exercise in patients with hypertrophic cardiomyopathy. Circulation 1997;96:2987–2991. 101. Spirito P, Maron BJ, Bonow RO: Noninvasive assessment of left ventricular

diastolic function: Comparative analysis of Doppler echocardiographic and radionuclide angiographic techniques. J Am Coll Cardiol 1986;7:518–526. 102. Louie E, Edwards L: Hypertrophic cardiomyopathy. Prog Cardiovasc Dis

1994;34:275–308. 103. Maron BJ, Spirito P, Green KJ, et al: Noninvasive assessment of left ventricular

diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1987;10:733–742. 104. Nishimura RA, Appleton CP, Redfield MM, et al: Noninvasive Doppler

echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: A simultaneous Doppler echocardiographic and cardiac catheterization study. J Am Coll Cardiol 1996;28:1226–1233. 105. Nihoyannopoulos P, Karatasakis G, Frenneaux M, et al: Diastolic function in hypertrophic cardiomyopathy: Relation to exercise capacity. J Am Coll Cardiol 1992;19:536–540. 106. Spirito P, Maron BJ: Relation between extent of left ventricular hypertrophy and

diastolic filling abnormalities in hypertrophic cardiomyopathy. J Am Coll Cardiol 1990;15:808–813. 107. Sasson Z, Hatle L, Appleton CP, et al: Intraventricular flow during isovolumic

relaxation: Description and characterization by Doppler echocardiography. J Am Coll Cardiol 1987;10:539–546. 108. Nakamura T, Matsubara K, Jurukawa K, et al: Diastolic paradoxic jet flow in

patients with hypertrophic cardiomyopathy: Evidence of concealed apical asynergy with cavity obliteration. J Am Coll Cardiol 1992;19:516–524. 109. Nagueh SF, Lakkis NM, Middleton KJ, et al: Doppler estimation of left

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ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation 1999;99:254–261. 110. Nagueh SF, Middleton KJ, Kopelen HA, et al: Doppler tissue imaging: A

noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527–1533. 111. Nagueh SF, Lakkis NM, Middleton KJ, et al: Changes in left ventricular diastolic

function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation 1999;99:344–347. 112. Nagueh SF, Lakkis NM, Middleton KJ, et al: Changes in left ventricular filling

and left atrial function six months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1999;34:1123–1128. 113. Oki T, Mishiro Y, Yamada H, et al: Detection of left ventricular regional

relaxation abnormalities and asynchrony in patients with hypertrophic cardiomyopathy with the use of tissue Doppler imaging. Am Heart J 2000;139:497–502. 114. Spirito P, Maron BJ: Relation between extent of left ventricular hypertrophy and

occurrence of sudden cardiac death in hypertrophic cardiomyopathy. J Am Coll Cardiol 1990;15:1521–1526. 115. Henry WL, Morganroth J, Pearlman AS, et al: Relation between

echocardiographically determined left atrial size and atrial fibrillation. Circulation 1975;53:273–279. 116. Glancy DL, O'Brien KP, Gold HK, Epstein E: Atrial fibrillation in patients with

idiopathic hypertrophic subaortic stenosis. Br Heart J 1970;32:652–659. 117. Robinson K, Frenneaux MP, Stockins B, et al: Atrial fibrillation in hypertrophic

cardiomyopathy: A longitudinal study. J Am Coll Cardiol 1990;15:1279–1285. 118. Thompson DS, Naqvi N, Juul SM, et al: Effects of propranolol on myocardial

oxygen consumption, substrate extraction, and haemodynamics in hypertrophic obstructive cardiomyopathy. Br Heart J 1980;44:488–498. 119. Pollick C: Muscular subaortic stenosis: Hemodynamic and clinical improvement

after disopyramide. N Engl J Med 1982;307:997–999. 120. Rosing DR, Kent KM, Maron BJ, Epstein SE: Verapamil therapy: A new

approach to the pharmacologic treatment of hypertrophic cardiomyopathy. II. Effects on exercise capacity and symptomatic status. Circulation 1979;60:1208–1213.

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121. Bonow RO, Rosing DR, Bacharach SL, et al: Effects of verapamil on left ventricular systolic function and diastolic filling in patients with hypertrophic cardiomyopathy. Circulation 1981;64:787–796. 122. Lorell BH, Paulus WJ, Grossman W, et al: Modification of abnormal left

ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy. Circulation 1982;64:499–507. 123. Iwase M, Sotobata I, Takagi S, et al: Effects of diltiazem on left ventricular

diastolic behavior in patients with hypertrophic cardiomyopathy: Evaluation with exercise pulsed Doppler echocardiography. J Am Coll Cardiol 1987;9:1099–1105. 124. Epstein SE, Rosing DR: Verapamil: Its potential for causing serious

complications in patients with hypertrophic cardiomyopathy. Circulation 1981;64:437–441. 125. Fananapazir L, Cannon RO, Tripodi D, Panza JA: Impact of dual-chamber

permanent pacing in patients with obstructive hypertrophic cardiomyopathy with symptoms refractory to verapamil and β-adrenergic blocker therapy. Circulation 1992;85:2149–2161. 126. Slade AKB, Sadoul N, Shapiro L, et al: DDD Pacing in hypertrophic

cardiomyopathy: A multicentre clinical experience. Heart 1996;75:44–49. 127. Fananapazir L, Epstein ND, Curiel RV, et al: Long-term results of dual-chamber

(DDD) pacing in obstructive hypertrophic cardiomyopathy: Evidence for progressive symptomatic and hemodynamic improvement and reduction of left ventricular hypertrophy. Circulation 1994;90:2731–2742. 128. Nishimura RA, Hayes DL, Ilstrup DM, et al: Effect of dual-chamber pacing on

systolic and diastolic function in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1996;27:421–430. 129. Nishimura RA, Trusty JM, Hayes DL, et al: Dual-chamber pacing for patients

with hypertrophic obstructive cardiomyopathy: A prospective randomized, doubleblind cross-over study. J Am Coll Cardiol 1997;29:435–441. 130. Kappenberger L, Linde C, Daubert C, et al: Pacing in hypertrophic obstructive

cardiomyopathy. A randomized crossover study. Eur Heart J 1997;18:1249–1256. 131. Maron BJ, Nishimura RA, McKenna WJ, et al: Assessment of permanent dual-

chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy: A randomized, double-blind, cross-over

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study (M-PATHY). Circulation 1999;99:2927–2933. 132. Sorajja P, Elliott PM, McKenna WJ: Pacing in hypertrophic cardiomyopathy.

Cardiol Clin 2000;18:67–79. 133. Ommen SR, Nishimura RA, Squires RW, et al: Comparison of dual-chamber

pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1999;34:191–196. 134. Kuhn H, Gietzen F, Schäfers M, et al: Changes of left ventricular outflow tract

after transcoronary ablation of septum hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transesophageal echocardiography and measuring of myocardial glucose utilization and perfusion. Eur Heart J 1999;20:1808– 1817. 135. Flores-Ramirez R, Lakkis NM, Middleton KJ, et al: Echocardiographic insights

into the mechanisms of relief of left ventricular outflow tract obstruction after nonsurgical septal reduction therapy in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;37:208–214. 136. Sigwart U: Non-surgical myocardial reduction for hypertrophic obstructive

cardiomyopathy. Lancet 1995;346:211–214. 612

137. Gietzen FH, Leuner CJ, Raute-Kreinsen U, et al: Acute and long-term results after

transcoronary ablation of septal hypertrophy (TASH): Catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 1999;20:1342– 1354. 138. Nagueh SF, Lakkis NM, He ZH, et al: Role of myocardial contrast

echocardiography during septal reduction therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1998;32:225–229. 139. Faber L, Seggewiss H, Gleichmann U: Percutaneous transluminal septal

myocardial ablation in hypertrophic obstructive cardiomyopathy: Results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998;98:2415– 2421. 140. Faber L, Seggewiss H, Ziemssen P, Gleichmann U: Intraprocedural myocardial

contrast echocardiography as a routine procedure in percutaneous transluminal septal myocardial ablation: Detection of threatening myocardial necrosis distant from the

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septal target area. Cathet Cardiovasc Intervent 1999;47:462–466. 141. Lakkis NM, Nagueh SF, Kleiman NS, et al: Echocardiography-guided ethanol

septal reduction for hypertrophic obstructive cardiomyopathy. Circulation 1998;98:1750–1755. 142. Seggewiss H, Faber L, Gleichmann U: Percutaneous transluminal septal ablation

in hypertrophic obstructive cardiomyopathy. Thorac Cardiovasc Surg 1999;47:94– 100. 143. Kuhn H, Gietzen FH, Leuner C, et al: Transcoronary ablation of septal

hypertrophy (TASH): A new treatment option for hypertrophic obstructive cardiomyopathy. Z Kardiol 2000;89(Suppl 4):IV-41–IV-54. 144. Faber L, Meissner A, Ziemssen P, Seggewiss H: Percutaneous transluminal septal

myocardial ablation for hypertrophic obstructive cardiomyopathy: Long term follow up of the first series of 25 patients. Heart 2000;83:326–331. 145. Lakkis NM, Nagueh SF, Dunn K, et al: Nonsurgical septal reduction therapy for

hypertrophic obstructive cardiomyopathy: One-year follow-up. J Am Coll Cardiol 2000;36:852–855. 146. Schulz-Menger J, Strohm O, Waigand J, et al: The value of magnetic resonance

imaging of the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy after septal artery embolization. Circulation 2000;101:1764–1766. 147. Mazur W, Nagueh SF, Lakkis NM, et al: Regression of left ventricular

hypertrophy after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation 2001;103:1492–1496. 148. McCully RB, Nishimura RA, Bailey KR, et al: Hypertrophic obstructive

cardiomyopathy: Preoperative echocardiographic predictors of outcome after septal myectomy. J Am Coll Cardiol 1996;27:1491–1496. 149. Morrow AG: Hypertrophic subaortic stenosis: Operative methods utilized to

relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg 1978;76:423– 430. 150. Marwick TH, Stewart WJ, Lever HM, et al: Benefits of intraoperative

echocardiography in the surgical management of hypertrophic cardiomyopathy. J Am Coll Cardiol 1992;20:1066–1072. 151. Siegman IL, Maron BJ, Permut LC, et al: Operative treatment in hypertrophic

subaortic stenosis: Techniques, and the results of pre and postoperative assessments in

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83 patients. Circulation 1975;52:88–102. 152. Franke A, Schöndube FA, Kühl HP, et al: Quantitative assessment of the

operative results after extended myectomy and surgical reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy using dynamic three-dimensional transesophageal echocardiography. J Am Coll Cardiol 1998;31:1641–1649. 153. Williams WG, Wigle ED, Rakowski H, et al: Results of surgery for hypertrophic

obstructive cardiomyopathy. Circulation 1987;76(Suppl V):V-104–V-108. 154. Robbins RC, Stinson EB: Long-term results of left ventricular myotomy and

myectomy for obstructive hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg 1996;11:586–594. 155. McCully RB, Nishimura RA, Tajik AJ, et al: Extent of clinical improvement after

surgical treatment of hypertrophic cardiomyopathy. Circulation 1996;94:467–471. 156. Sasson Z, Prieur T, Skrobik Y, et al: Aortic regurgitation: A common

complication after surgery for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1989;13:63–67. 157. Maron BJ, Merrill WH, Freier PA, et al: Long-term clinical course and

symptomatic status of patients after operation for hypertrophic subaortic stenosis. Circulation 1978;57:1205–1213. 158. Spirito P, Maron BJ: Perspectives on the role of new treatment strategies in

hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 1999;33:1071–1075. 159. Seiler C, Hess OM, Schoenbeck M, et al: Long-term follow-up of medical versus

surgical therapy for hypertrophic cardiomyopathy: A retrospective study. J Am Coll Cardiol 1991;17:634–642.

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613

Chapter 28 - Restrictive Cardiomyopathy Diagnosis and Prognostic Implications Maran Thamilarasan MD Allan L. Klein MD

General Principles Classification Cardiomyopathies are disorders of the myocardium characterized by systolic or diastolic dysfunction. They are further broadly categorized into restrictive, dilated, hypertrophic, and arrhythmogenic right ventricular cardiomyopathy. [1] [2] [3] [4] Restrictive cardiomyopathy includes the entities of idiopathic restrictive cardiomyopathy, endomyocardial fibrosis, and Loeffler's cardiomyopathy.[4] Other disease entities include noncompaction of the left ventricle.[4] [5] The term has also come to encompass myocardial infiltrative processes that occur in the context of systemic diseases. These secondary forms of restrictive cardiomyopathies are probably more common than the primary form.[6] The classic example is primary amyloidosis. Other interstitial or storage diseases that can lead to restrictive hemodynamics include sarcoidosis, hemochromatosis, Fabry's disease, glycogen storage disease, and radiation heart disease. Figure 28-1 lists the classification of cardiomyopathies as defined by the World Health Organization. [4] We further suggest the working

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classification of restrictive cardiomyopathy shown in Figure 28-2 . It should be emphasized that the presence of restrictive physiology is by no means diagnostic of restrictive cardiomyopathy, which may be diagnosed in the absence of demonstrable restrictive physiology. Pathophysiology and Hemodynamics Restrictive cardiomyopathy is characterized by impaired ventricular filling, as a result of increased myocardial and/or endocardial stiffness, resulting in abnormally high filling pressures (left atrial pressure typically greater than 12 mm Hg). The increased stiffness arises from an abnormality both of ventricular compliance and, to a lesser extent, of ventricular relaxation.[7] Systolic function is typically normal until advanced stages of the disease. Elevation in left-sided pressures can lead to passive elevation of right-sided pressures, but often there is also concomitant diastolic dysfunction of the right ventricle as well. Elevated atrial pressures lead to pulmonary congestion, distention of central veins, hepatic distention, and peripheral edema. This 614

Figure 28-1 Classification of cardiomyopathies.

gives rise to the typical clinical features of effort intolerance in early cases, and rest dyspnea and symptoms of low cardiac output in more advanced cases. Atrial fibrillation is not uncommon, secondary to the atrial enlargement (which arises as a compensatory mechanism to the elevated pressures). Ventricular arrhythmias or advanced heart block may be present in advanced cases and are often the cause of death in these patients. Symptoms of the underlying systemic disease, if present, will also be evident. In cases of restrictive cardiomyopathy, there is rapid ventricular filling in early diastole, with sudden cessation of further filling in late diastole as a result of the constraint by the stiff ventricles. This gives rise to the characteristic dip and plateau ("square root" sign) in the ventricular diastolic pressure waveform. Corresponding to the rapid early ventricular filling, a prominent y descent is often seen in the jugular venous pulse. Left and right ventricular end-diastolic pressures are elevated, with the left

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ventricular Figure 28-2 Working classification of restrictive cardiomyopathy.

diastolic pressure often being 5 mm Hg higher than the right. Pulmonary hypertension is usually present in advanced cases. In early-stage disease or with marked diuresis, these characteristic changes may be brought on only by intravenous fluid challenge. However, these hemodynamic patterns are by no means diagnostic of restrictive cardiomyopathy, and other diseases may produce similar abnormalities. Echocardiographic Approach to Restrictive Cardiomyopathy Echocardiography plays an important role in the initial diagnosis, and subsequent follow-up, of patients with restrictive cardiomyopathy.[8] [9] A comprehensive echocardiographic evaluation of restrictive cardiomyopathy includes M-mode and two-dimensional imaging as well as Doppler examination of mitral and tricuspid inflow, pulmonary 615

venous flow, and hepatic venous flow. Color M-mode and tissue Doppler imaging are also important newer adjuncts. Transesophageal echocardiography plays a complementary role, especially in cases of suboptimal transthoracic echocardiographic images and in examination of the pulmonary veins.[10] As is discussed later, phasic respiratory changes in Doppler patterns are important to look for when trying to differentiate constrictive pericarditis from restrictive cardiomyopathy. A nasal thermistor is used for this purpose: the change in temperature with inspiration, expiration, and apnea is assessed and displayed together with the continuous and pulsed wave Doppler spectral display. Two-Dimensional Echocardiography Findings on two-dimensional echocardiography reflect the underlying pathophysiology. Typically ventricular wall thickness is increased, with normal cavity size (except in the case of idiopathic restrictive cardiomyopathy, in which ventricular wall thickness is typically normal).[4] Thrombi may be present, both in the ventricles and atria. Biatrial enlargement is present, reflective of the chronic elevation in filling

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pressures. Other manifestations of increased filling pressures include dilation of the hepatic veins, superior and inferior venae cavae, and pulmonary veins. The normal inspiratory collapse of the inferior vena cava may be diminished. Varying degrees of mitral and tricuspid regurgitation are usually present. The cause of the regurgitation is multifactorial. In endomyocardial fibrosis, there is direct involvement of the mitral or tricuspid valve leaflets, or both, by the disease process. Pulmonary hypertension can lead to secondary tricuspid regurgitation. Diastolic mitral or, less commonly, tricuspid regurgitation may be present as a result of elevation of ventricular end-diastolic pressures. Doppler Echocardiographic Assessment of Diastolic Properties Table 28-1 summarizes the useful Doppler echocardiographic measurements in assessing left ventricular diastolic function that are further elucidated in the following discussion. Pulsed Wave Doppler

Pulsed wave Doppler evaluation of mitral and tricuspid inflow is useful in interpreting the degree of diastolic dysfunction present in restrictive cardiomyopathy.[11] [12] However, interpretations must be made cautiously, as the pattern of filling is affected by numerous other factors, including age, loading conditions, and the presence of other diseases. The left and right ventricular filling patterns can be obtained by pulsed Doppler interrogation of the mitral and tricuspid inflow, with the sample volume placed at the tips of the mitral and tricuspid leaflets, respectively. The TABLE 28-1 -- Useful Doppler Echocardiographic Parameters of Left and Right Ventricular Diastolic Function Left Ventricular Filling Right Ventricular Filling Left ventricular inflow Right ventricular inflow E wave velocity (cm/sec) E wave velocity (cm/sec) A wave velocity (cm/sec) A wave velocity (cm/sec) E/A ratio E/A ratio Deceleration time (msec) Deceleration time (msec) Isovolumic relaxation time (msec) Pulmonary vein flow Superior vena cava and hepatic vein

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Forward flow Forward flow S wave velocity (cm/sec) S wave velocity (cm/sec) D wave velocity (cm/sec) D wave velocity (cm/sec) Reverse flow Reverse flow Atrial reversal wave velocity V wave reversal (cm/sec) (cm/sec) Atrial reversal wave duration Atrial reversal wave velocity (msec) (cm/sec) Tissue Doppler echocardiography of Tissue Doppler echocardiography of mitral annulus tricuspid annulus Color M-mode flow propagation velocity of mitral inflow Adapted from Klein AL, Cohen GI: Cleve Clin J Med 1992;59:278–290. ventricular Doppler filling pattern (Fig. 28-3) , in normal sinus rhythm, consists of a filling wave during early diastole (E wave) and a filling wave associated with atrial contraction (A wave). The E wave deceleration time is measured by extrapolating the deceleration slope of the outer edge of the E wave tracing from the peak velocity to the baseline.[11] [12] By placing the cursor between the aortic and mitral valve, the examiner can measure isovolumic relaxation time as the time interval between the closing click of the aortic valve and the onset of mitral inflow. Left ventricular chamber stiffness has been shown to be inversely related to the square of the deceleration time.[13] Pulmonary Vein Flow

Pulsed wave Doppler examination of the pulmonary veins is valuable in assessing left ventricular diastolic function.[14] This examination can be performed in the apical four- or two-chamber view from the transthoracic approach, where the right upper pulmonary vein can be examined. It is important that the sample volume be placed at least 1 cm into the pulmonary vein, to optimize the signal and avoid artifact from atrial blood flow. It is often helpful to use color Doppler echocardiography (with lower Nyquist limits) to aid in localizing the pulmonary vein. Recently it has been shown that the use of contrast agents may help to enhance visualization of pulmonary venous flow.[15] Transesophageal echocardiography is better suited to assess pulmonary vein flow patterns because of the proximity of

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the transducer to the pulmonary veins. The left and right upper and lower pulmonary veins can usually be examined from the transesophageal approach. The normal pulmonary venous flow consists of two systolic forward flows (S waves), a slightly smaller 616

Figure 28-3 A, Pulmonary vein Doppler flow pattern in relation to left ventricular filling pattern. Pulmonary venous flow consists of two systolic (S) and one diastolic (D) forward flow. The early systolic forward flow is secondary to atrial relaxation. In normal sinus rhythm, there is a small flow reversal with atrial contraction (AR). B, The left ventricular inflow velocity is composed of an early diastolic E wave and a late diastolic A wave. AVC, aortic valve closure; DT, deceleration time; IVRT, isovolumic relaxation time; MVC, mitral valve closure; MVO, mitral valve opening. (From Klein AL, Tajik AJ: J Am Soc Echocardiogr 1991;4:379–392.)

diastolic forward flow (D wave), and a smaller flow reversal coinciding with atrial contraction (AR wave) (see Fig. 28-3) . Often, the sample volume position that optimizes the AR wave may not be the same one that results in the best analysis of the S and D waves. The atrial reversal is usually absent in atrial fibrillation, with no effective atrial contraction. The systolic forward flow can be seen to consist of two components: an early and a late systolic flow. The early flow occurs during atrial relaxation, and the late flow occurs during ventricular contraction, with movement of the mitral annulus toward the apex. This biphasic systolic flow was observed in 37% of cases with a transthoracic approach[16] and in up to 100% of cases with a transesophageal approach.[17] Right ventricular stroke volume, pulmonary vascular compliance, and phasic changes in left atrial pressure, left ventricular compliance, and atrial contractility all affect pulmonary venous flow.[14] As left atrial pressure increases, there is a gradual decrease in systolic flow and an increase in diastolic flow, with an increase in the atrial reversal wave. In advanced cases, the systolic forward flow may be greatly diminished or may cease altogether. Sensitive indices of increased left ventricular filling pressure include the ratio of the systolic forward flow to the total forward flow, as well as the duration and peak velocity of the atrial reversal wave.[18] [19] Rossvoll and Hatle[18] demonstrated that if the duration of the atrial reversal wave exceeded that of the mitral inflow A wave, then left ventricular diastolic pressure was typically elevated to greater than 15 mm Hg (Fig. 28-

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4) . Klein et al[19] showed that this difference between the duration of the mitral A wave and the pulmonary venous atrial reversal wave is relatively age independent and therefore of value even in elderly patients as an indicator of left ventricular filling pressure. This increase in the duration and peak velocity of the atrial reversal wave with left atrial hypertension and elevation of left ventricular diastolic pressure occurs as a result of increased resistance to atrial emptying into the left ventricle. Mitral regurgitation, if present, also contributes to the blunting of the systolic forward flow, and with significant mitral regurgitation, frank flow reversal is often observed in the pulmonary veins in systole. [20] [21] [22] Hepatic Vein and Superior Vena Cava Flow

Central venous flow patterns are analogous to flow patterns in the pulmonary veins. There is a systolic forward flow (corresponding to the x descent on examination of the venous pulsations) and a smaller diastolic forward flow (y descent). There are also small flow reversals with ventricular (VR wave) and atrial (AR wave) contraction (Fig. 28-5) . With restrictive cardiomyopathy, there is a predominant diastolic forward flow (corresponding to the rapid y descent in the central venous pulses), while the systolic flow is reduced (diminished x descent).[23] The predominant diastolic compared with systolic forward flow occurs during all phases of respiration. The diminished systolic forward flow in restrictive cardiomyopathy occurs as a result of several factors, including increased right atrial pressure, right ventricular stiffness, and tricuspid regurgitation. Flow reversals (VR and AR waves) are increased during inspiration compared with expiration and apnea. With significant tricuspid regurgitation, systolic flow reversal may also be observed in the hepatic veins.

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Figure 28-4 Diagram demonstrating how to compare width of pulmonary venous atrial reversal and width of mitral A wave. A pulmonary venous duration that is 20 msec or greater than the mitral A wave duration suggests elevated left ventricular end-diastolic pressure. (From Abdalla IA, et al: J Am Soc Echocardiogr 1998;11:1125–1133.)

Color M-mode Echocardiography Color M-mode echocardiography is a pulsed Doppler technique that can

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display a spatiotemporal map of blood flow velocities across a vertical scan line. Whereas pulsed Doppler gives information on flow velocity at a fixed spatial point, color M-mode echocardiography allows acquisition of information on flow velocities at different points from the mitral orifice to the left ventricular apex over time (Fig. 28-6) . This can be done with a temporal resolution of 5 msec, a spatial resolution of less than Figure 28-5 Diagram demonstrating normal tricuspid and hepatic venous (or superior vena caval) velocity profiles. There is biphasic forward flow, with a greater systolic (S) than diastolic (D) flow. Small flow reversals are noted during late ventricular systole (VR) and with atrial contraction (AR). TVC, tricuspid valve closure, TVO, tricuspid valve opening. (From Klein AL et al: J Am Coll Cardiol 1990;15:99–108.)

1 mm, and a velocity measurement with an error of about 5%.[24] Color M-mode analysis is performed from the apical four-chamber view. Color Doppler is turned on and the imaging plane is adjusted so that the direction of blood flow will be parallel to the M-mode cursor, which is placed through the center of the inflow. It is important that the entire depth from the mitral annulus to the apex Figure 28-6 Diagram representing the relationship between pulsed Doppler echocardiography of mitral inflow and color M-mode flow propagation velocity (Vp). TD, time delay of the peak E velocity from the mitral tips to the apex. (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875, with permission from the American College of Cardiology.)

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Figure 28-7 (color plate.) Example of a color M-mode recording, demonstrating the E and A waves and the measurement of the flow propagation velocity (Vp). (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875, with permission from the American College of Cardiology.)

of the ventricle be displayed. The slope measured is that of the first aliasing velocity of the early filling wave, measured from the mitral tips to a position 4 cm distally into the left ventricle (Fig. 28-7) .[24] This differs from

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the original description, which measured the slope of the transition from color to no color.[25] Clinical studies utilizing this flow propagation velocity have found it to be a sensitive index of left ventricular relaxation.[25] [26] A normal flow propagation velocity (Vp) in an adult is greater than 45 cm per second.[24] Brun et al[25] showed that the velocity of flow propagation was significantly decreased in diseases associated with impaired left ventricular relaxation, and this decrease was independent of ventricular dilation. They demonstrated an inverse relationship between Vp and the time constant of relaxation. Stugaard et al[26] found a similar decrease in velocity propagation in the setting of acute ischemia in an animal model. An advantage of color M-mode is that it appears to be less preload dependent than the traditional Doppler parameters. Takatsuji et al[27] demonstrated that Vp was free of pseudonormalization and correlated well with invasively derived measures of LV relaxation. Garcia et al[28] likewise demonstrated minimal effects of varying preload on Vp, both in animal models using inferior vena cava occlusion and in patients undergoing cardiac surgery before and during partial cardiopulmonary bypass. Using an in vitro model, Pai et al[29] demonstrated that the rate of propagation of the E wave was only weakly related to mean left atrial pressure and strongly related to left ventricular diastolic stiffness. There is some suggestion, however, that Vp may be more load dependent in patients with congestive heart failure and may be influenced by LV cavity geometry.[30] Tissue Doppler Echocardiography Tissue Doppler echocardiography allows for the analysis of myocardial wall motion velocities.[24] [31] [32] [33] Unlike blood flow velocity, which is of low amplitude and high velocity, myocardial velocities are of high amplitude and low velocity. Traditional Doppler systems use a high-pass filter to eliminate these low-velocity signals, such that only blood flow velocity is displayed. By bypassing this filter and using lower gain amplification, the lower velocity tissue signals can be displayed. This can be done either in a color or in a pulsed display.[32] [33] For diastolic function assessment, pulsed tissue Doppler echocardiographic analysis of the mitral annulus has been used. Similar information was used in the past with digitized M-mode echocardiography, but this technique was time intensive and required off-line measurements. Isaaz et al[31] were the first to apply this new technique to measure the motion of the cardiac base in normal subjects. Because primary myocardial disease affects the rate of left

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ventricular relaxation, direct determination of myocardial wall expansion velocities has been shown to be useful in assessing diastolic function. Tissue Doppler echocardiographic measurements are made from the apical four- or two-chamber view by placing the sample volume at the desired aspect of the mitral annulus (anterior, inferior, lateral or septal). The lateral and medial aspects are commonly used; however, it may be better to obtain an average of these measurements, especially if segmental wall motion abnormalities are present. A pulsed sample is then obtained. The sample is ideally obtained during apnea, to minimize translational movement. Three major signals will be apparent (Fig. 28-8) . The first is a systolic one (above the baseline), representing the descent of the annulus toward the apex with systole (S wave). The second major signal is a below the baseline deflection, reflecting elastic recoil of the left ventricle during early diastole (Em ). It is this measure that is used in diastolic function assessment. In normal adults, Em is greater than 10 cm per second.[24] The third major

signal is another below the baseline deflection, reflecting atrial contraction (Am ). In addition to these three signals, other smaller isovolumic signals

may also be apparent.

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Figure 28-8 Example of a pulsed tissue Doppler echocardiographic velocity profile as obtained from the lateral mitral annulus in the apical four-chamber view. Am , annular velocity with atrial contraction; Em , annular velocity during early diastole. (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875, with permission from the American College of Cardiology.)

Em appears to be a sensitive marker of impaired left ventricular relaxation.

There are data to suggest that this marker is also less preload sensitive than traditional Doppler parameters. Oki et al[34] found a good correlation between tau and Em , regardless of left ventricular filling pressures. Sohn et al[35] demonstrated that administration of nitroglycerin did not significantly alter Em in patients with documented diastolic dysfunction. In an animal

model, Firstenberg et al[36] demonstrated that Em was less preload dependent

as tau increased.

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These variables are not completely independent of loading and filling conditions, however. The Valsalva maneuver has been shown to reduce early and late annular TABLE 28-2 -- The Stages of Diastolic Dysfunction Normal Stage 1 Stage 3/4 (Delayed Stage 2 (Restrictive YOUNG ADULT Relaxation) (Pseudonormal) Filling) >1 >1 <1 1–2 >2 <220 <220 >220 150–200 <150

Parameter E/A ratio Deceleration time, msec Isovolumic <100 <100 >100 60–100 <60 relaxation time, msec Pulmonary <1 ≥1 ≥1 0.5–≤1 <0.5 veins (S/D ratio) Pulmonary <35 <35 <35 ≥35 (if in sinus ≥35 (unless rhythm) atrial vein atrial systolic reversal, cm/sec failure) Color M>55 >45 <45 <45 <45 mode (flow propagation velocity, cm/sec) Tissue >10 >8 <8 <8 <8 Doppler (early myocardial velocity, cm/sec) Adapted from Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875. velocities in a proportional fashion in normal subjects.[37] In a series of 15 patients on chronic hemodialysis, fluid removal was associated with a reduction in septal annular velocities.[38] Heart rate has also been shown to

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have an impact on tissue Doppler velocities. In an animal model, Greenberg et al[39] found that increasing heart rate negatively influenced Em , independent of changes in contractility and relaxation. Hatle and Sutherland[40] have shown that the presence of severe mitral regurgitation can result in a significant increase in wall motion velocities, effectively masking the presence of diastolic dysfunction.

Combining tissue Doppler and pulsed Doppler may also provide useful information in assessing left ventricular diastolic parameters. The ratio of the transmitral E wave to the early diastolic annular velocity (E/Em ) has

been used as an index of left ventricular filling pressures. In a recent study from the Mayo clinic,[41] an E/Em ratio of less than 8 predicted normal mean left ventricular diastolic pressure, whereas a ratio of greater than 15 identified elevated diastolic pressure. A wide range of filling pressures was seen in patients with ratios between 8 and 15. In these patients, integration of other Doppler indices was helpful in predicting elevated diastolic pressure.

Newer applications include using color tissue Doppler echocardiography to calculate regional myocardial strain rates, which have been used to assess regional systolic and diastolic motion.[40] The myocardial velocity gradient between the epicardium and endocardium is another promising approach to evaluation of restrictive cardiomyopathy.[41] Diastolic Filling Patterns Utilizing traditional Doppler indices of mitral and tricuspid inflow, pulmonary venous flow, as well as color M-mode and Doppler tissue imaging, four stages of diastolic function can be recognized ( Table 28-2 and Fig. 28-9 ). [24] Patients with restrictive cardiomyopathy will typically progress through the various stages of diastolic dysfunction as disease severity increases.[24] [42] Normal Filling Pattern.

As a result of the rapid ventricular relaxation in early diastole, the E wave velocity is characteristically higher than the A wave velocity, so that the E/A ratio is greater than 1. The E wave deceleration is usually between 150 and 220 msec. The isovolumic 620

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Figure 28-9 Schematic of the phases of diastolic function, as characterized by mitral inflow, pulmonary venous (PV) flow, tissue Doppler echocardiography (TDE), and color M-mode (CMM) flow propagation velocity (Vp). (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865– 875, with permission from the American College of Cardiology.)

relaxation time is less than 100 msec (usually between 60 and 100 msec). In very young adults, the pulmonary vein S/D ratio will be less than 1, while it is typically greater than 1 in the general adult population. The atrial reversal is not prominent, less than 35 cm per second in velocity. Color Mmode flow propagation velocity is fast, greater than 55 cm per second in the younger adults and 45 cm per second in older adults. Em is typically greater than 10 cm per second. Delayed Relaxation Pattern.

The early stages of the disease may be characterized primarily by impaired ventricular relaxation, rather than by elevations in atrial pressure and restricted filling. The E wave velocity is therefore typically diminished as a result of the slower ventricular relaxation, and there is a compensatory increase in A wave velocity. The isovolumic relaxation time is usually prolonged (>100 msec). The deceleration time is usually normal or prolonged (>220 msec). The E/A ratio is typically less than 1. Pulmonary vein S/D ratio remains greater than 1, and the atrial reversal is not especially prominent. The abnormal relaxation is reflected in a slow color M-mode flow propagation velocity (Vp <45 cm/sec) and lower mitral annular Doppler tissue imaging velocity (Em <8 cm per second).[24] Pseudonormal Pattern.

As the disease progresses and ventricular compliance decreases, atrial pressures rise. Thus, there is a gradual increase in E wave velocity and a decrease in A wave velocity. The deceleration time also becomes progressively shortened. Therefore, at some stage of disease progression, the delayed relaxation pattern associated with early disease evolves into a pseudonormal pattern in which the E/A ratio is greater than 1, often indistinguishable from the normal pattern seen in young healthy individuals. Examination of the pulmonary venous flow pattern is helpful in differentiating the pseudonormal pattern of mitral inflow from the true normal pattern. The pseudonormal pattern is typically associated with an increased atrial reversal wave of the pulmonary venous flow (>35 cm per

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second).[18] [43] [44] The pulmonary vein systolic flow may be normal but may also demonstrate blunting. In contrast, the true normal pattern of mitral inflow will be associated with a normal pulmonary venous flow pattern; that is, a systolic forward flow, a smaller diastolic forward flow, and a small atrial reversal. Typically the atria will be dilated in these patients with a pseudonormal filling pattern. Color M-mode and Doppler tissue imaging are also very useful in this differentiation. Vp and Em (Fig. 28-10) will typically remain low.[24]

Restrictive Filling Pattern.

In a typical case of advanced restrictive cardiomyopathy, the E wave velocity is usually elevated, with a shortened isovolumic relaxation time (<60 msec) as a result of increased atrial pressure. Because of the elevated ventricular end-diastolic pressure, there is rapid equalization of pressures across the atrioventricular valves in diastole, resulting in a shortened deceleration time (<150 msec). In diastasis and with atrial contraction, little or no further flow is seen, and therefore the A wave velocity is greatly diminished. This distinct morphologic pattern is analogous to the dip and plateau pattern in the ventricular diastolic pressure waveform. Therefore, the E/A ratio is significantly increased. There will be significant blunting of the systolic component of pulmonary venous flow. Atrial reversal may be prominent; however, if atrial mechanical failure is present, it will be decreased. Vp (Fig. 28-11) and Em remain low.[24] The restrictive pattern is

further divided into a reversible (stage 3) and irreversible (stage 4) phase. This distinction is made by assessing response to maneuvers that decrease preload (i.e., sitting the patient up, administration of nitrates). Stage 4 is characterized by lack of change in these diastolic parameters with reduction in preload. Progression of Disease.

With disease progression, the ventricular filling pattern will gradually change from an impaired relaxation pattern through a pseudonormal pattern with gradual increase in E wave velocity and decrease in A wave velocity to a typical restrictive pattern.[11] [42] In contrast, a restrictive pattern has not been seen to evolve into a delayed relaxation pattern with disease progression.[42] This gradual change is thought to be mediated by a progressive increase in atrial and ventricular filling pressures that occurs with progressively stiffer ventricles.

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Figure 28-10 Figure demonstrating the utility of tissue Doppler echocardiography (TDE) in differentiating a pseudonormal filling pattern from a normal pattern. Standard pulsed Doppler evaluation is displayed in the upper panels. E/A ratio is greater than 1 in both panels. The lower panels demonstrate pulsed TDE findings, which show a reduction in early annular velocity (Em ). (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875, with permission from the American College of Cardiology.)

Limitations of Echocardiographic Assessment of Diastolic Function Although pulsed Doppler flow evaluation of left and right ventricular filling and of pulmonary and central venous flow have added significantly to the assessment of diastolic function, they must be interpreted with caution, Figure 28-11 (color plate.) Pulsed Doppler (upper panels) and color Mmode (lower panels) findings with normal diastolic function, delayed relaxation pattern, and restrictive pattern. Flow propagation velocity remains delayed in both delayed relaxation and restrictive patterns. (From Garcia MJ, et al: J Am Coll Cardiol 1998;32:865–875, with permission from the American College of Cardiology.)

as they can be affected by a multitude of physiologic and technical factors. The same applies to the newer modalities of color M-mode and Doppler tissue imaging. Technical Factors

A comprehensive Doppler echocardiographic examination for diastolic dysfunction requires meticulous care and 622

Figure 28-12 Changes with age in left ventricular inflow early wave (A), late wave (B), E/A ratio (C), deceleration time (D), and isovolumic relaxation time (E) in male and female subjects. Bold lines, mean; lightface lines, 95% confidence interval. (From Klein AL, et al: Mayo Clin Proc 1994;69:212–224.)

attention to detail. The location of the sample volume, and proper

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instrument settings such as the filter level, are important for optimal pulsed Doppler recordings. Optimal sweep speed is 50 or 100 cm per second (especially for measuring the deceleration time). In obtaining the inflow patterns, the sample volume should be placed at the tips of the mitral and tricuspid leaflets, respectively, where the highest velocities are recorded. Placing the sample volume into the atrium may make the A wave appear relatively larger. The mitral E wave deceleration time should be measured with the sample volume at the midposition of the leaflet tips. More medial placement of the sample volume (adjacent to the left ventricular outflow tract) may give an apparent shortened deceleration time.[45] With tachycardia, there will be fusion of the E and A waves. In this circumstance, an accurate deceleration time cannot be obtained. In addition, the mitral A wave velocity increases relative to the E wave velocity, and the isovolumic relaxation time decreases as heart rate increases. Proper positioning of the sample volume in the pulmonary veins is also very important in obtaining an accurate 623

flow profile. The forward flow velocity, especially the S wave, may decrease as the sample volume is moved from the orifice of the pulmonary veins into the left atrium.[45] Sinus tachycardia may cause the pulmonary S and D waves to merge. Tachycardia can likewise result in fusion of the early and late filling waves by color M-mode, making it difficult to get an accurate assessment of Vp. If the M-mode cursor is not parallel to the inflow, then assessment will be inaccurate. Attention must be paid to ensure that intracavitary flow occurring prior to the onset of mitral inflow is not mistaken for mitral inflow.[24] The geometry of the ventricle may likewise have an impact on propagation. The aliasing velocity must be adjusted (to approximately two thirds of the pulsed Doppler E wave) to allow for a complete envelope, and the sample sector must include the entire left ventricle. For curvilinear slopes, it is important that the slope only be measured from the annulus to a point 4 cm into the ventricle. The sample volume must be accurately placed at the annulus for Doppler tissue imaging measurements. In the setting of regional wall motion abnormalities, analysis and averaging of all four annular positions may be

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prudent to obtain a global assessment of left ventricular relaxation, although the impact of regional dysfunction on annulus Figure 28-13 Changes with age in pulmonary venous systolic forward flow velocity (A) and diastolic forward flow velocity (B), systolic to diastolic velocity ratio (C), and atrial reversal velocity (D) in male and female subjects. Bold lines, mean; lightface lines, 95% confidence interval. (From Klein AL, et al: Mayo Clin Proc 1994;69:212–224.)

motion is not yet completely understood. The effects of rotational movement and translation of the myocardium are minimized by use of an apical window but are not completely eliminated. Effects of Age and Gender

The normal aging process affects ventricular diastolic function, and hence has an impact on the ventricular filling and pulmonary venous flow patterns ( Fig. 28-12 and Fig. 28-13 ). In children and young adults, left ventricular relaxation is rapid, allowing a significant percentage of left ventricular filling (90% ± 5%) to occur in early diastole. Therefore, the E/A ratio is usually greater than 1.5, with a short isovolumic relaxation time (20 to 60 msec) and deceleration time (120 to 160 msec).[37] Likewise, Vp is fast (typically >55 msec) and Em is elevated (>10 cm per second).[24] In a study of 117 normal persons, Klein et al[46] reported that the mitral peak E wave velocity and E/A ratio were significantly higher in patients younger than 50 years of age than in those aged 50 years and older. The peak A wave velocity was significantly lower and the deceleration time and isovolumic relaxation time were shorter in patients younger than 50 years. In general, female subjects 624

tend to have higher velocities and a more prolonged deceleration time than male subjects. [46] With increasing age and a progressive slowing of left ventricular relaxation,[46] [47] there is a gradual decrease in E wave velocity, a compensatory increase in A wave velocity, and prolongation of isovolumic relaxation time and deceleration time. By the seventh decade, the E/A ratio is roughly 1:1, isovolumic relaxation time has lengthened to between 80 and 100 msec, and mitral deceleration time has increased to between 200 and 220 msec.[43] Color M-mode flow propagation velocity likewise appears

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to vary with age. Mego et al[48] demonstrated a 44% reduction in Vp between the youngest and the oldest volunteers in their study group, which consisted of individuals without any clinically evident cardiovascular disease. Sohn et al[35] likewise demonstrated age dependence of Doppler tissue velocities. In a study of 59 normal volunteers, they found that Em

decreased while Am increased with age, leading to lower E/A ratios with age.

In normal individuals, the peak velocity and velocity integral of the pulmonary S wave and the atrial reversal wave gradually increase, while the peak velocity and velocity integral of the pulmonary D wave gradually decrease from the third decade of life onward. The relatively higher D wave velocity in young subjects most likely reflects the rapid ventricular relaxation, creating a ventricular "suction" and decreased left atrial pressure during this phase of the cardiac cycle. As left ventricular relaxation gets progressively slower with age, the peak E wave velocity of the mitral inflow, and hence the D wave velocity of the pulmonary vein flow, decrease. Both the velocity and the duration of the atrial reversal wave increase with age for similar reasons. Klein et al[19] showed that the increase in duration of the atrial reversal wave with age parallels the increase in duration of the mitral A wave. Therefore, the difference in duration between the pulmonary vein atrial reversal wave and the mitral A wave is relatively age independent. Effects of Loading Conditions

Loading conditions significantly affect Doppler-derived indices of left ventricular diastolic function.[45] [49] [50] [51] [52] With a reduction in preload, mitral E wave velocity decreases and deceleration time increases. The A wave velocity remains relatively unchanged, and therefore the E/A ratio is significantly decreased. The isovolumic relaxation time increases and the atrial reversal wave of the pulmonary venous flow decreases. These changes in the Doppler indices mimic those changes associated with aging and impaired left ventricular relaxation. Thus, the presence of marked diuresis or dehydration may mask the true diastolic filling pattern. Increases in preload result in opposite changes that mimic those associated with typical restrictive cardiomyopathy. Thomas and Weyman[53] in a computer simulation model, showed that increasing atrial pressure leads to a shortening of isovolumic relaxation time, an increased acceleration rate, and significantly increased peak velocity and time velocity integrals.

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Color M-mode and Doppler tissue imaging appear less preload sensitive, but they are not completely unaffected by loading conditions, as has been alluded to in the earlier discussion. Coexisting Diseases

The presence of atrial fibrillation, with the absence of an A wave and varying RR intervals, reduces the utility of transmitral flow velocity measurements. Although the atrial reversal wave in the pulmonary flow may disappear with atrial fibrillation, the S/D ratio may still give an indication of left atrial pressure, although some degree of systolic blunting is expected. Atrial fibrillation itself will shorten deceleration time. Phasic respiratory changes can still be present in the setting of atrial fibrillation and can be useful in the diagnosis of constrictive pericarditis, as will be discussed later. Atrial flutter also interferes with assessment of diastolic function, as the fluttering of the atria alters the normal biphasic transmitral flow. Severe left ventricular systolic dysfunction may be associated with a restrictive pattern of transmitral flow.[43] [54] [55] E wave velocity is increased and isovolumic relaxation time decreased as a result of high left atrial pressure. The high left ventricular end-diastolic pressure leads to a rapid equalization of pressures across the mitral valve, and therefore the deceleration time is shortened. Such a pattern of transmitral flow appears to be associated with a poor prognosis.[55] The presence of valvular heart disease can make assessment of diastolic function quite difficult. Significant mitral regurgitation will result in an increase in the E wave. Systolic blunting and even systolic flow reversal can be seen in the pulmonary veins. Mitral stenosis results in mechanical impedance to inflow, rendering deceleration time and isovolumic relaxation time inaccurate in the assessment of ventricular diastolic function. Nevertheless, valvular heart disease can lead to both systolic and diastolic dysfunction.[56] Possible mechanisms for diastolic abnormalities include increased wall stress, altered myocardial structure, subendocardial hypoperfusion, diastolic calcium overload, and interstitial fibrosis. Alternative Diagnostic Approaches Other diagnostic investigations may be employed in addition to Doppler echocardiography in suspected cases of restrictive cardiomyopathy. These may include cardiac catheterization with measurement of intracardiac

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pressures, although Doppler echocardiography has made such invasive measurement unnecessary in many cases. Endo-myocardial biopsy may be required in some cases to give a histologic diagnosis, but patchy infiltration of the myocardium may give rise to false-negative results. For differentiating restrictive cardiomyopathy from constrictive pericarditis, additional imaging modalities, such as magnetic resonance imaging or computed tomographic scanning of the chest to demonstrate pericardial thickening, may be used.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Cardiac Amyloidosis 625

Cardiac amyloidosis is the best studied and most classic example of restrictive cardiomyopathy. Amyloidosis is a multisystem disease of unknown cause in which there are extracellular deposits of amyloid protein fibrils in various organs of the body, resulting in tissue damage and organ malfunction. Primary amyloidosis is the most common form; in this form, the fibrils that are deposited are immunoglobulin light chains, often associated with multiple myeloma. Secondary amyloidosis occurs less often and involves a nonimmunoglobulin protein. Most cases of cardiac involvement occur with primary amyloidosis.[57] [58] Cardiac involvement is often the main determinant of prognosis in patients with this disorder. The typical clinical features are those of a male patient aged 40 years or older presenting with progressive biventricular failure, refractory supraventricular and ventricular arrhythmias, or conduction defects. The cardiac silhouette on chest radiography is usually mildly to moderately enlarged. Pulmonary congestion is evident in later stages of the disease. The electrocardiogram typically is of low voltage. Echocardiography is the procedure of choice in the noninvasive diagnosis and serial follow-up of patients with cardiac amyloidosis. Echocardiographic Findings Cardiac amyloidosis usually gives a distinctive appearance on twodimensional echocardiography (Fig. 28-14) . Left ventricular cavity size is usually normal or small with markedly thickened myocardium, which typically displays a highly abnormal texture, often described as "granular and sparkling"[59] or like ground glass in appearance. The

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Figure 28-14 Apical four-chamber view from a patient with amyloidosis. Note the increased wall thickness, thickened atrioventricular valves, biatrial enlargement, and a small pericardial effusion.

granular appearance is thought to be due to the acoustic mismatch between the highly reflectile amyloid deposits and the normal myocardial tissue.[60] These abnormal echoes appear to have an anatomic basis, as autopsy studies have demonstrated the presence of amyloid fibrils at the site of these granular sparkling echoes.[61] Global left ventricular systolic function is usually preserved until advanced stages of the disease, at which point systolic dysfunction ensues. The interatrial septum and valve leaflets are also thickened. Both atria are enlarged, and small to moderate pericardial effusions are usually present.[59] [62] A variety of two-dimensional and Doppler-derived indices have been shown to be useful prognostic markers in this disease. Among these is the mean left ventricular wall thickness.[59] In a series of more than 100 patients with biopsy-proven amyloidosis, median survival was only 0.4 years in those with a mean wall thickness of greater than 15 mm, compared with 2.4 years for those with a mean wall thickness of less than 12 mm. Right ventricular wall thickness greater than 7 mm has also been suggested to be a marker of more advanced disease. The ratio of electrocardiographic voltage to echocardiographic cross-sectional muscle area is thought to be specific to cardiac amyloidosis and is suggested to be predictive of clinical symptoms and prognosis.[63] A ratio of greater than 1.5 was 82% sensitive and 83% specific for cardiac amyloidosis in a more recent study.[64] However, the usefulness of this ratio is limited by the presence of other coexisting disease such as hypertension or pericardial effusion. Although amyloidosis has traditionally been associated with a restrictive filling pattern, a spectrum of left ventricular filling abnormalities are observed in patients with this disease.[23] [42] [65] In one series, patients with a mean left ventricular wall thickness between 12 and 15 mm demonstrated a Doppler pattern consistent with impaired relaxation.[42] The transmitral E/A ratio was less than 1, with an increased S/D ratio in the pulmonary veins (Fig. 28-15) . The isovolumic relaxation time (>86 msec) and deceleration time (>240 msec) were also prolonged.[42] In patients with advanced disease (in those patients with a mean left

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ventricular wall thickness of greater than 15 mm), a restrictive pattern of left ventricular filling was observed.[42] Deceleration time and isovolumic relaxation time were shortened, with marked systolic blunting of pulmonary venous flow and an increase in diastolic forward flow velocity (Fig. 28-16) . Moreover, serial echocardiographic studies in these patients [42] showed that the impaired relaxation pattern gradually evolved into a restrictive pattern through a pseudonormal phase as the disease progressed (Fig. 28-17) . Symptom progression was associated with an increase in the E/A ratio and shortening of the deceleration time. In contrast, patients with the restrictive pattern on the baseline study showed no significant changes on follow-up. It is thought that as the disease evolves, there is progressive deposition of amyloid fibril in the myocardium leading to subsequent loss of myocardial cells from pressure necrosis, thereby leading to a gradual decrease in left ventricular compliance.[66] As compliance decreases, left ventricular end-diastolic and left atrial pressure increase. This is reflected in the serial change in the left ventricular filling pattern.[66] [67] Klein et al[65] have also shown that in patients with advanced 626

Figure 28-15 Early case of amyloidosis associated with impaired relaxation pattern of mitral inflow (A) with a decreased E/A ratio, prolonged deceleration time (DT) of 300 msec, and a relatively normal pulmonary venous Doppler flow pattern (B) with a small atrial reversal wave (AR). Exp, expiration; Insp, inspiration. (From Klein AL, et al: J Am Coll Cardiol 1989;13:1017–1026, with permission from the American College of Cardiology.)

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Figure 28-16 A, Advanced case of amyloidosis associated with a restrictive pattern of mitral inflow with an increased E/A ratio and a shortened deceleration time (DT) of 120 msec. B, Another example of an advanced case of amyloidosis with a normal E/A ratio but a shortened deceleration time. C and D, Note the shortened isovolumic relaxation time (C) and blunted pulmonary systolic forward flow (S) and increased atrial reversal wave (AR) (D). (From Klein AL, et al: J Am Coll Cardiol 1989;13:1017–1026, with permission from the American College of Cardiology.)

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Figure 28-17 Serial pulsed Doppler evaluation in a patient with cardiac amyloidosis, demonstrating progression of diastolic dysfunction from an abnormal relaxation pattern to a pseudonormal pattern. (From Klein AL, et al: J Am Coll Cardiol 1990;16:1135–1141, with permission from the American College of Cardiology.)

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Figure 28-18 A, Pulsed wave Doppler echocardiographic patterns of right ventricular filling and systemic venous flow patterns in an early case of amyloidosis showing a delayed relaxation pattern of right ventricular filling. B, Pulsed wave Doppler echocardiographic patterns of right ventricular filling and systemic venous flow patterns in an advanced case of amyloidosis with a restrictive pattern of right ventricular filling. (From Klein AL, et al: J Am Coll Cardiol 1990;15:99–108, with permission from the American College of Cardiology.)

disease, the difference in the duration of the pulmonary venous atrial reversal wave and the mitral inflow A wave is significantly higher compared with normal subjects and patients with early disease. The right ventricular filling pattern has been shown to be similar to that of the left ventricle.[68] In early cases, as in patients with a right ventricular free wall thickness of less than 7 mm, the tricuspid A wave velocity was increased, with a decreased E/A ratio and prolonged deceleration time suggesting abnormal relaxation (Fig. 28-18A) . In advanced cases (right ventricular wall thickness greater than 7 mm), the tricuspid E/A ratio was increased and the deceleration time markedly shortened, characteristic of restriction (see Fig. 28-18B) . Central venous flow patterns were consistent with this pattern, with diminished systolic forward flow and augmented diastolic flow in the superior vena cava and hepatic veins. Flow reversals Figure 28-19 Survival in 63 patients with cardiac amyloidosis (patients subdivided according to the deceleration time [DT] of 150 msec). Patients with a shortened deceleration time of 150 msec or less (dashed line) had a significantly reduced survival compared with those with DT greater than 150 msec (solid line). (From Klein AL, et al: Circulation 1991;83: 808– 816.)

were increased compared with normal values and showed further increase with inspiration.

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Prognostic Stratification Doppler echocardiography has proved useful for prognostic stratification of patients with cardiac amyloidosis. In a series of 63 consecutive patients with biopsy-proven cardiac amyloidosis that were followed for a mean of 18 ± 12 months, a shortened mitral E wave deceleration time at the baseline study was a powerful predictor of mortality. Patients with a deceleration time of less than 150 msec had significantly reduced survival compared with those whose deceleration time was greater than 150 msec (1-year probability of survival 49% vs. 92%, P < .001)[69] (Fig. 28-19) . Bivariate analysis showed that 629

the combination of shortened deceleration time of 150 msec or less and increased mitral E/A ratio was a stronger predictor of cardiac death than two-dimensional variables of mean left ventricular wall thickness and fractional shortening. Its association with elevated left atrial and left ventricular diastolic pressures, which occur with advanced disease, can most likely explain the prognostic value of a shortened deceleration time.[70] Thus, it is not unexpected that such patients generally have a poorer prognosis. Right ventricular dilation has also been reported to be associated with a poorer prognosis in patients with cardiac amyloidosis.[71] A Doppler-derived index, which combines indices of systolic and myocardial performance (isovolumic contraction time + isovolumic relaxation time/ejection time), has also been shown to predict clinical outcome in these patients.[72] Differentiation from Hypertrophic Cardiomyopathy Left ventricular hypertrophy and hypertrophic cardiomyopathy are also associated with increased myocardial wall thickness. Differentiation is important because the treatment and prognosis of these conditions are very different. Cardiac amyloidosis can sometimes give rise to asymmetric septal hypertrophy.[65] Low voltage on the electrocardiogram favors a diagnosis of amyloidosis rather than hypertrophic cardiomyopathy. Although the constellation of markedly dilated atria, small-sized but thickwalled ventricles, thickened valves, and pericardial effusion are suggestive of cardiac amyloidosis, endomyocardial biopsy may be necessary in some cases to give a definitive diagnosis, especially with a history of hypertension, because of the prognostic implications of a diagnosis of

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cardiac amyloidosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Other Examples of Restrictive Cardiomyopathy Idiopathic Restrictive Cardiomyopathy Idiopathic restrictive cardiomyopathy is usually a sporadic disease characterized by diastolic dysfunction in the setting of a nonhypertrophied, nondilated ventricle with initially preserved systolic function. Endomyocardial biopsy in these cases is nonspecific. Echocardiographic findings include the presence of large atria and abnormal diastolic filling. This disease primarily affects the elderly, but a childhood variant has been described. In a recent Mayo Clinic review of 94 patients with this disease, a left atrial dimension of greater than 60 mm was associated with increased risk of death.[73] Clinical parameters that were predictive included male gender and higher New York Heart Association functional class. Endomyocardial Disease The hypereosinophilic syndromes include endomyocardial fibrosis and Loeffler's endocarditis. These diseases are characterized by direct myocardial damage as a result of cytotoxic eosinophils. Loeffler's endocarditis is part of the idiopathic hypereosinophilic syndrome. Endomyocardial fibrosis is endemic in parts of Africa, India, and South America[74] and has been associated with a number of parasitic infections.[75] [76] It is usually the result of the presence within the myocardium of parasites that die, leading to inflammatory reaction and fibrosis. Occasionally, drug reactions and allergic granulomatosis and vasculitis (Churg-Strauss syndrome) may produce eosinophilic myocarditis. Pathologically, these diseases are marked by intense endocardial fibrosis, initially affecting the apical regions of one or both ventricles (with obliteration of the apex) and extending to the subvalvular apparatus of both atrioventricular valves. Significant atrioventricular valvular regurgitation may result from the fibrotic involvement of the valve leaflets and mural thrombi in one or both ventricles may also be found.

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Pinar Sopena et al[77] compared echocardiographic findings in 10 patients with idiopathic hypereosinophilic syndrome with 10 patients with secondary hypereosinophilia. In the idiopathic group, echocardiographic abnormalities were detected in six patients with more than one abnormality in most (four had apical obliteration of the right ventricle, three had left ventricular apical obliteration, six had endocardial thickening of the left ventricle, three had subvalvular mitral thickening, three had subvalvular tricuspid thickening, and two had a pericardial effusion). Two patients had hemodynamic patterns consistent with restriction. In secondary eosinophilia, only one patient had right ventricular obliteration and tricuspid subvalvular thickening. In a more recent review of endomyocardial fibrosis, Berensztein et al[78] found biventricular involvement in 8 of 10 patients. Pericardial effusions of varying sizes were noted in all 10 of their patients. Nine of the 10 had involvement of the atrioventricular valves. Figure 28-20 is an example of the echocardiographic findings that can be seen in endomyocardial disease. The hemodynamic consequences of endomyocardial fibrosis are those of restrictive cardiomyopathy. There is increased stiffness of the ventricles to filling and a gradual reduction in ventricular cavity size as a result of fibrotic obliteration. The presence of ventricular thrombus further decreases ventricular cavity size. Systolic function is usually preserved. Noncompaction Although not classified as a restrictive cardiomyopathy, ventricular noncompaction is worth describing because it is an entity that has received increasing attention in the literature. It is caused by intrauterine arrest of the normal compaction of the loose meshwork and myocardial fibers, producing a thin epicardial layer and a thickened endocardial layer with prominent trabeculations and deep recesses.[5] Figure 28-21 is an example of the classic echocardiographic findings found in this disease. Diastolic function is typically abnormal in these patients, ranging from a delayed relaxation pattern to a restrictive pattern. This 630

Figure 28-20 Apical four-chamber (A) and apical long-axis (B) views from a patient with endomyocardial fibrosis. Note the apical obliteration noted in both the left and right ventricles.

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Figure 28-21 A and B, Two-dimensional echocardiographic findings in a patient with noncompaction of the left ventricle. Note the prominent recesses and trabeculations, which are enhanced by the use of contrast (B) for endocardial delineation. C, This patient demonstrates a delayed relaxation pattern of diastolic function on pulsed Doppler recording of left ventricular inflow.

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disease is associated with significant cardiovascular morbidity and mortality. Hemochromatosis Primary hemochromatosis is an iron storage disease with multiorgan involvement, including the heart, pancreas, liver, and skin. Echocardiography is useful in assessing cardiac involvement in primary hemochromatosis. A variety of structural and functional abnormalities have been described. Olson et al[79] studied 19 patients with idiopathic hemochromatosis without other known heart disease. Seven patients (37%) had chamber dilation and systolic dysfunction attributable to the hemochromatosis, whereas 12 did not. In another series from the same authors, [80] five of six patients (83%) with biopsy-proven cardiac hemochromatosis had left ventricular enlargement and marked global dysfunction. Increased ventricular wall thickness and mass may also be observed, although Olson et al[80] suggested that this is not a typical feature of cardiac hemochromatosis. Patterns consistent with dilated or restrictive cardiomyopathy have also been described in patients with primary hemochromatosis. Ventricular dysfunction and increased ventricular mass may normalize after successful venesection.[81] The presence of systolic dysfunction usually signifies a poor prognosis.[79] Cecchetti et al[82] have suggested a progression of cardiac involvement in this disease, with reversible increase in wall thickness being the initial manifestation. With further increase in iron deposition, chamber dilation and left ventricular dysfunction ensue. Secondary hemochromatosis may develop in patients who are transfusion dependent, as in those with congenital anemia. Henry et al[83] performed echocardiography in 54 patients with congenital anemia and compared the results with normal subjects. Left ventricular wall thickness, transverse

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dimension and mass, and left atrial transverse dimension were increased in most patients despite the fact that only 32% showed chest radiographic evidence of cardiac enlargement and 16% showed electrocardiographic abnormalities. Only four patients had decreased systolic function, and all of these died within 6 months. Cardiac Sarcoidosis Sarcoidosis is a multisystem, noncaseating granulomatous disorder that may involve the heart. Sarcoid granulomas are found in the myocardium at autopsy in up to 25% of patients with sarcoidosis.[84] Characteristically, granulomas are found in the superior interventricular septum, although other areas such as the papillary muscles and ventricular free walls can also be affected. Although the presence of granulomas is not uncommon, clinically evident heart disease is not commonly seen in patients with sarcoidosis.[85] In those patients who do manifest cardiac symptoms, conduction abnormalities, ventricular arrhythmias, progressive heart failure, and even sudden death can be seen. Angomachalelis et al[86] performed Doppler echocardiography in 10 patients with sarcoidosis and 10 normal control subjects. They found evidence of left ventricular diastolic dysfunction in 50% of patients at a stage when no systolic dysfunction was evident. Compared with control subjects, patients had a lower mitral A wave velocity and lower E/A ratio. Fahy et al[87] examined 50 patients with pulmonary sarcoidosis without suspected cardiac involvement and found evidence for diastolic dysfunction in 7 of them (14%). They concluded that these patients might have had a subclinical sarcoid cardiomyopathy. Burstow et al[88] reviewed echocardiograms in 88 patients with systemic sarcoidosis and found evidence for left ventricular systolic function attributable to cardiac sarcoidosis in 12 of them (14%). Eight of these patients had segmental wall motion abnormalities, and the remaining four had global impairment of left ventricular function. Twodimensional echocardiographic criteria,[89] such as mitral valve prolapse, pericardial effusion,[90] increased right ventricular anterior wall thickness, and asymmetric septal hypertrophy, are seldom of much clinical use in assessing for cardiac involvement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Differentiation from Constrictive Pericarditis Eliciting the cause of diastolic dysfunction can often be difficult, particularly in the differentiation between constrictive pericarditis and restrictive cardiomyopathy,[91] because the presenting symptoms and clinical features of the these conditions are very similar. It is vitally important to make this distinction, as the management and prognostic implications of these conditions are very different (see Chapter 29) . Constrictive pericarditis can be effectively treated with surgical stripping of the pericardium. Invasive hemodynamic studies showed some initial promise in differentiating the two conditions. Elevation and equalization of right and left ventricular end-diastolic pressures (difference <5 mm Hg) was suggested to favor constriction.[92] The "dip and plateau" pattern or the "square root sign" on the left ventricular hemodynamic tracings were also said to be suggestive of constriction.[93] Constriction was believed to be associated with a right ventricular end-diastolic pressure exceeding one third of right ventricular systolic pressure. In contrast, elevation of pulmonary systolic pressure to greater than 50 mm Hg was said to be suggestive of restriction. However, restrictive cardiomyopathy has been known to produce hemodynamic pictures that are otherwise suggestive of constriction.[93] Indeed, there can be considerable overlap in the hemodynamic profile of these conditions. It was also thought that exercise might be useful in making this differentiation. It was thought that exercise in constriction would result in elevation of right and left ventricular end-diastolic pressure to an equal degree, whereas in restriction there would be a greater degree of elevation in left-sided pressures. However, the available data would suggest that this is not the case.[94] [95] Doppler Echocardiographic Assessment of Ventricular Filling

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The imprecision of hemodynamic criteria in differentiating constriction from restriction has stimulated considerable 632

interest in the use of echocardiographic techniques. Initial studies focused mainly on early diastolic left ventricular filling parameters. The rationale was that in constrictive pericarditis, early left ventricular relaxation is usually "supernormal" and very rapid. However, this rapid early filling is followed shortly by a complete halt to left ventricular filling as a result of external constraint by the rigid pericardium, which limits further ventricular expansion and filling. In contrast, in restrictive cardiomyopathy, left ventricular relaxation is slow as a result of primary myocardial disease, and therefore left ventricular filling is impaired throughout diastole. Tyberg et al[96] demonstrated that patients with constriction completed 85 ± 4% of left ventricular filling in the first half of diastole, compared with only 45 ± 4% in patients with restriction. However, these findings are most consistent with early stages of restrictive cardiomyopathy that are associated with an impaired relaxation pattern of ventricular filling. With disease progression, elevations in atrial pressure result in a similar rapid early emptying phase (i.e., a pseudonormal or restrictive filling pattern). Radionuclide ventriculography has also been used to examine the time-volume curve of the left ventricle,[97] [98] with similar findings. More recently, Doppler echocardiography with respirometry has been shown to be useful in the differentiation of constriction from restriction. Hatle et al[99] compared 12 patients with restriction with 7 with constriction. Baseline hemodynamics in the two groups were very similar. Compared with control subjects, patients with constriction showed marked changes in left ventricular isovolumic relaxation time and in early mitral and tricuspid inflow velocities at the onset of inspiration and expiration. Moreover, Figure 28-22 A, Typical transesophageal pulsed wave Doppler echocardiographic recordings of mitral inflow (bottom) and pulmonary vein flow (top) in a normal control subject. B, In a patient with constrictive pericarditis showing changes with respiration, with inspiration (uparrows), there are significant decreases in the pulmonary systolic (S) and diastolic (D) forward flow and mitral inflow E wave. C, In a patient with restrictive cardiomyopathy, there are no significant changes in the pulmonary S and D waves and the mitral E-wave velocities with respiration. (From Klein AL, et al: J Am Coll Cardiol 1993;22:1935–1943, with permission from the American College of

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Cardiology.)

these changes resolved after successful surgical pericardiectomy. In contrast, these changes were not observed in control subjects, nor in patients with restriction. Diastolic mitral and tricuspid regurgitation were more common in patients with restriction. Mancuso et al[100] studied seven patients with constriction and six with restriction. In patients with constriction, the mitral peak E wave velocity increased significantly at the onset of expiration and decreased at the onset of inspiration, whereas reciprocal changes were observed in tricuspid peak E wave velocities. Figure 28-22 and Figure 28-23 (Figure Not Available) show the patterns of left ventricular inflow velocities during different phases of respiration in normal subjects, in patients with constrictive pericarditis, and in patients with restrictive cardiomyopathy.[23] In normal subjects, there is little change in mitral E and A wave velocity, deceleration time, and isovolumic relaxation time during inspiration, apnea, and expiration. In classic restriction, mitral E wave velocity and E/A ratio is increased with markedly shortened deceleration and isovolumic relaxation times. However, there is little variation in these parameters (<5%) during the various phases of respiration. In constriction, there is a significant decrease in mitral E wave velocity and prolongation of isovolumic relaxation time with inspiration, and an increase in E wave velocity and shortening of isovolumic relaxation time with expiration (see Fig. 28-22) . Reciprocal changes are observed in the right ventricular inflow pattern (see Fig. 28-23) (Figure Not Available) . Klodas et al[101] used tricuspid regurgitation velocity curves to help differentiate patients with constriction from those with other causes of heart failure. They found that in patients with constriction, there were significant elevations 633

Figure 28-23 (Figure Not Available) Respiratory variation of mitral (A) and tricuspid (B) inflow and hepatic (C) and pulmonary (D) vein pulsed wave Doppler echocardiographic flow patterns in normal subjects, those with constrictive pericarditis, and those with restrictive myocardial disease. (From Klein AL, Cohen GI: Cleve Clin J Med 1992;59:278–290.)

in the peak tricuspid regurgitant velocity, the time velocity integral, and the duration of the tricuspid regurgitant jet with inspiration.[101] In patients with other causes for heart failure, no significant inspiratory increases were

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noted. In the study by Hatle et al,[99] the greatest decrease in mitral E wave velocity and the longest increase in isovolumic relaxation time were observed on the first beat after inspiration; the opposite changes were observed on the first beat after expiration. Thus, it is important to use a respirometer to document the onset of inspiration and expiration. Similar changes were seen in the aortic and pulmonary flow velocities, but the magnitude of these changes was less and they occurred later in the respiratory cycle. These marked respiratory variations in left and right ventricular inflow patterns occur as a result of effective isolation of the cardiac chambers by the thickened pericardium from the normal respiratory changes in intrathoracic pressure. In normal individuals and in patients with restriction, intrathoracic and intracardiac pressures decrease slightly but equally with inspiration; therefore, the same forward flow from the pulmonary veins into the left atrium is maintained throughout different phases of respiration. In constriction, however, there are no significant respiratory changes in intracardiac pressure, whereas intrathoracic pressure (including pressure in the pulmonary veins) decreases with inspiration. As a result, the flow from the pulmonary veins into the left atrium, and hence into the left ventricle, is decreased in inspiration (less driving pressure), leading to a decrease in mitral E wave velocity and lengthening of isovolumic relaxation time. The enhanced interventricular dependence in constriction also adds to these respiratory variations in the ventricular filling pattern. In a typical case of pericardial constriction, from expiration to inspiration, isovolumic relaxation time increases more than 50%, mitral E wave decreases more than 33%, and tricuspid E wave increases more than 44%. Pulmonary Vein Flow Pulsed Doppler examination of the pulmonary veins by transesophageal echocardiography also aids in differentiating constrictive pericarditis and restrictive cardiomyopathy. In a series by Klein et al,[102] patients with constriction had a higher pulmonary venous peak systolic flow (S wave) and lower peak diastolic flow (D wave) both during inspiration and during expiration when compared with patients with restriction. Patients with constriction, compared with those with restriction, had a moderate decrease in pulmonary venous S wave velocity with inspiration (19% vs. 10%, P = .09). However, there was a greater decrease in D wave velocity with the onset of inspiration

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(29% for constriction vs. 16% with restriction, P = .008). The pulmonary venous peak atrial reversal flow velocity and integral also tended to be smaller in constriction than in restriction in expiration (P = .02 and P = .05, respectively). A combination of a pulmonary venous S/D ratio of 0.65 or greater in inspiration and a 40% or greater change of the pulmonary vein D wave from expiration to inspiration had a sensitivity of 86% and specificity of 94% in differentiating constrictive pericarditis from restrictive cardiomyopathy.[102] Figure 28-23 (Figure Not Available) summarizes the changes in pulmonary venous flow velocities in the different phases of respiration. In normal subjects, there is very little respiratory change in pulmonary venous flow, with a greater systolic to diastolic flow velocity and a small atrial reversal wave. In restriction, there is marked blunting of the systolic forward flow and a markedly increased atrial reversal, with little change with respiration. In constriction, there is systolic blunting throughout the different phases of respiration with a marked decrease in diastolic forward flow with inspiration. Figure 28-22 shows the typical respiratory variation in mitral inflow and pulmonary vein flow in a patient with constrictive pericarditis. Hepatic Vein Flow Figure 28-23 (Figure Not Available) summarizes the Doppler hepatic venous flow patterns in normal subjects, in patients with restrictive cardiomyopathy, and patients with constrictive pericarditis. In normal subjects, there is a greater peak systolic to diastolic flow velocity, with small flow reversals associated with ventricular contraction and atrial contraction. These reversals are usually more prominent in expiration than in inspiration and apnea. In restriction, there is blunting of systolic forward flow and prominent flow reversals. In constriction, there is significant decrease in both systolic and diastolic forward flow with expiration associated with markedly increased flow reversals. Pitfalls and Limitations Pulsed Doppler examination of ventricular filling and venous flow patterns has proved a reliable tool that may help to differentiate restriction from constriction.[23] [99] [102] However, it is important to realize that significant respiratory variation in flow velocities does not occur exclusively in constrictive pericarditis. Severe chronic obstructive pulmonary disease, asthma, or severe right ventricular dysfunction can also lead to these

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respiratory changes and may lead to diagnostic confusion. Assessment of superior vena caval flow may be helpful in differentiating chronic obstructive pulmonary disease from constrictive pericarditis in patients who have respiratory variation in mitral inflow. Boonyaratavej et al[103] demonstrated that patients with chronic obstructive pulmonary disease had marked increases in inspiratory superior vena caval systolic forward flow, a finding that was lacking in patients with constriction. Meticulous attention must be paid during sampling, because changes in sample volume position during deep inspiration and expiration can artifactually affect changes in Doppler parameters. Atrial fibrillation is not uncommon in both restrictive cardiomyopathy and constrictive pericarditis and can make interpretation of flow velocities difficult. Nevertheless, Tabata et al[104] recently demonstrated that significant respiratory changes in mitral and pulmonary venous flow are present in patients with constrictive pericarditis in atrial fibrillation. Again, the use of respirometry is very important in these patients to demonstrate that the changes are not due solely to varying RR intervals. Moreover, as mentioned earlier, loading conditions affect flow velocities profoundly, and fluid challenge may sometimes be necessary to bring out the typical respiratory changes of constriction. Bush et al[105] and other investigators[106] used volume infusion in patients with occult constriction. When the hemodynamic profile is not consistent with constriction in the presence of other suggestive features, a fluid challenge of 500 to 1000 mL of normal saline infusion over 5 to 10 minutes may result in hemodynamics more typical of constriction. Klein et al[107] showed that volume loading with rapid infusion of 0.5 to 1 L of fluid during transesophageal echocardiography is safe. The respiratory variation in the velocity of the pulmonary venous D wave was accentuated with volume loading in patients with constrictive pericarditis, as compared with no significant change in respiratory variation in patients with restrictive cardiomyopathy. On the other hand, patients with constrictive pericarditis may be so overloaded with fluid that the typical respiratory variations in ventricular filling and pulmonary venous flow pattern may be masked. Sometimes, it may be necessary to place patients in an upright sitting position (and hence reduce preload) to bring out the characteristic Doppler flow patterns.[108] Two-Dimensional Echocardiographic Features M-mode and two-dimensional echocardiography are also useful in the

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diagnosis of constrictive pericarditis.[109] [110] [111] The presence of pericardial thickening or calcified pericardium suggests constrictive pericarditis. Tethering of the atrium and ventricle are also suggestive of constriction. A jerky motion of the interventricular septum in diastole (septal bounce) and inferior vena cava plethora also suggest constriction. Pericardial thickening may be demonstrable on two-dimensional echocardiography, but often transesophageal echocardiography is needed. Transesophageal echocardiography allows visualization of pericardial thickening around the right-side chambers and at the ventricular apex but is relatively limited in visualizing thickening adjacent to the lateral left ventricular wall.[112] Digitized M-mode Echocardiography Janos et al[113] used digitized M-mode echocardiography in four patients with constrictive disease and three with restrictive disease and compared the results with those obtained in normal subjects. Patients with constrictive pericarditis had a significantly higher maximal rate of 635

left ventricular posterior wall thinning than patients with restriction. Morgan et al[114] used digitized M-mode echocardiography to differentiate between constrictive pericarditis and restrictive cardiomyopathy. Fifteen patients with restrictive cardiomyopathy, 10 patients with constrictive pericarditis, and 20 age- and sex-matched control subjects were studied. Compared with patients with constrictive pericarditis, those with restrictive cardiomyopathy had significantly decreased peak left ventricular posterior wall thickening and thinning rates. Digitization of M-mode echocardiograms, with particular attention to posterior wall function, may be a useful adjunct in distinguishing restrictive cardiomyopathy from constrictive pericarditis. Color M-mode and Doppler Tissue Imaging The newer echocardiographic tools of color M-mode and Doppler tissue imaging are also useful in helping to make the differentiation between constrictive pericarditis and restrictive cardiomyopathy. In pure constrictive pericarditis, there is no inherent abnormality in ventricular relaxation. The impairment in ventricular filling occurs as a result of external pericardial constraint, which abruptly limits ventricular filling. As a result, Vp will not be slow in these patients (as compared to those with restriction, who by

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definition have impairment in ventricular relaxation), and in fact may be faster than in normal subjects.[24] A similar finding is seen with Doppler tissue imaging. Em will be normal or even above normal in pure constriction, whereas it is low in restriction. Garcia et al[115] have demonstrated that a cut-off value of 8 cm per second is useful in differentiating these two entities. Measurement of Em may be especially helpful in difficult cases of constrictive pericarditis in which respiratory variation of Doppler flows may be absent or illuminated.[115] Other Imaging Modalities In constrictive pericarditis, chest radiography may reveal pericardial calcification. Computed tomography or magnetic resonance imaging of the chest can also be used to visualize the thickened pericardium. Mixed Constriction/Restriction Constrictive disease can occur in conjunction with primary myocardial disease. A classic example of this is radiation-induced heart disease, with concomitant myocarditis and pericarditis. Features of both diseases will be present and it is often difficult to sort out which disease is predominant. Pericarditis can also develop in patients with other disorders of diastolic dysfunction. In these cases, pericardial thickening will be apparent (either by magnetic resonance imaging or by transesophageal echocardiography); however, the classic respiratory changes in Doppler inflows will not be present. Advanced stages of diastolic dysfunction are present. These patients are particularly challenging to manage, as the degree of benefit to be obtained from pericardial stripping can be difficult to gauge. In general, prognosis appears poor in these patients.[116]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Exercise Echocardiography in Diastolic Dysfunction Dyspnea on exertion is often the only symptom in patients with early restrictive cardiomyopathy. Therefore, evidence of diastolic dysfunction may be revealed only by exercise. The mechanism of these exertional symptoms has been studied in animal models.[117] [118] [119] The normal hemodynamic response to exercise is an increase in ejection fraction and cardiac output with a decrease in the duration of diastole. A fall in left ventricular pressure in early diastole is thought to be responsible for the increased diastolic filling without a concomitant increase in left atrial pressure. However, in the presence of diastolic dysfunction, failure of left ventricular pressure to fall results in an abnormal rise in left atrial pressure to maintain the transmitral gradient and left ventricular filling. Kitzman et al [120] performed exercise testing with invasive hemodynamic monitoring in seven patients with suspected diastolic dysfunction and in 10 matched control subjects. Compared with control subjects, patients had a significantly lower stroke volume index and end-diastolic volume index, but the end-systolic volume index was not different. Patients, but not control subjects, had a markedly increased pulmonary capillary wedge pressure with peak exercise. Exercise echocardiography enables the examination of patterns of ventricular filling during or immediately after exercise and may prove a useful tool in detecting latent ventricular dysfunction that may not be evident at rest. It has also been shown recently that regional assessment of diastolic function during stress testing may be useful in the identification of ischemia.[121]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Restrictive cardiomyopathies encompass a group of disease states characterized by primary diastolic dysfunction. Evolution in the noninvasive assessment of diastolic function, especially by echocardiography, has contributed greatly to our understanding of these diseases. Developments in Doppler echocardiography, color M-mode, and Doppler tissue imaging have paralleled our enhanced understanding of the physical, physiologic, and pathophysiologic factors that affect ventricular filling. These modalities not only have contributed to the diagnosis of these conditions but also allow for prognostic stratification and differentiation from other disease states such as constrictive pericarditis. These applications of echocardiography to the assessment of diastolic function are exciting, but it is important to bear in mind their limitations. With these recent advances, echocardiography may contribute to better patient management, which may in turn result in an improved clinical outcome.

636

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Goodwin JF: Cardiomyopathies and specific heart muscle diseases: Definitions,

terminology, classifications and new and old approaches. Postgrad Med J 1992;68 (suppl 1):S3–S6. 2. Goodwin JF: Overview and classification of the cardiomyopathies. Cardiovasc Clin

1988;19:3–7. 3. Goodwin JF: The frontiers of cardiomyopathy. Br Heart J 1982;48:1–18. 4. World Health Organization/International Society and Federation of Cardiology:

Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation 1996;93:841–842. 5. Oechslin EN, Attenhofer Jost CH, Rojas JR, et al: Long-term follow-up of 34 adults

with isolated left ventricular noncompaction: A distinct cardimyopathy with poor prognosis. J Am Coll Cardiol 2000;36:493–500. 6. Click RL, Olson LJ, Edwards WD, et al: Echocardiography and systemic diseases

[review]. J Am Soc Echocardiogr 1994;7:201–216. 7. Wilmshurst PT, Katritsis D: Restrictive cardiomyopathy. Br Heart J 1990;63:323–

324. 8. Thomas JD: Doppler echocardiography and left ventricular diastolic function. In

Gaasch WH, LeWinter MM (eds): Left Ventricular Diastolic Dysfunction and Heart Failure. Malvern, PA, Lea & Febiger, 1994, pp 192–218. 9. Hatle L: Diastolic dysfunction in restrictive and constrictive heart disease. In

Gaasch WH, LeWinter MM (eds): Left ventricular diastolic dysfunction and heart

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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Pagina 2 di 12

failure. Malvern, PA, Lea & Febiger, 1994, pp 390–407. 10. Klein AL, Cohen GI, Pietrolungo JF, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943. 11. Appleton CP, Hatle LK, Popp RL: Relation of transmitral flow velocity patterns to

left ventricular diastolic function: New insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12:426–440. 12. Appleton CP, Hatle LK, Popp RL: Demonstration of restrictive ventricular

physiology by Doppler echocardiography. J Am Coll Cardiol 1988;11:757–768. 13. Little WC, Ohno M, Kitzman DW, et al: Determination of left ventricular chamber

stiffness from the time for deceleration of early left ventricular filling. Circulation 1995;92:1933–1939. 14. Klein AL, Tajik AJ: Doppler assessment of pulmonary venous flow in healthy

subjects and in patients with heart disease. J Am Soc Echocardiogr 1991;4:379–392. 15. Ellaham S, Haunerova E, Gottdiener J: Intravenous Optison (FS069) enhances

pulmonary vein flow velocity signals. Clin Cardiol 2000;23:91–95. 16. Smallhorn JF, Freedom RM, Olley PM: Pulsed Doppler echocardiographic

assessment of extraparenchymal pulmonary vein flow. J Am Coll Cardiol 1987;9:573– 579. 17. Bartzokis T, Lee R, Yeoh TK, Schnittger I: Transesophageal echo-Doppler echocardiographic assessment of pulmonary venous flow patterns. J Am Soc Echocardiogr 1991;4:457–464. 18. Rossvoll O, Hatle LK: Pulmonary venous flow velocities recorded by transthoracic

Doppler ultrasound: Relation to left ventricular diastolic pressures. J Am Coll Cardiol 1993;21:1687–1696. 19. Klein AL, Abdalla I, Murray RD, et al: Age independence of the difference in

duration of pulmonary venous atrial reversal flow and transmitral A-wave flow in normal subjects. J Am Soc Echocardiogr 1998;11:458–465. 20. Klein AL, Stewart WJ, Bartlett J, et al: Effects of mitral regurgitation on

pulmonary venous flow and left atrial pressure: An intraoperative transesophageal echocardiographic study. J Am Coll Cardiol 1992;20:1345–1352.

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21. Klein AL, Obarski TP, Stewart WJ, et al: Transesophageal Doppler echocardiography of pulmonary venous flow: A new marker of mitral regurgitation severity. J Am Coll Cardiol 1991;18:518–526. 22. Klein AL, Bailey AS, Cohen GI, et al: Importance of sampling both pulmonary

veins in grading mitral regurgitation by transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:115–123. 23. Klein AL, Cohen GI: Doppler echocardiographic assessment of constrictive

pericarditis, cardiac amyloidosis, and cardiac tamponade [review]. Cleve Clin J Med 1992;59:278–290. 24. Garcia MJ, Thomas JD, Klein AL: New Doppler echocardiographic applications

for the study of diastolic function. J Am Coll Cardiol 1998;32:865–875. 25. Brun P, Tribouilloy C, Duval AM, et al: Left ventricular flow propagation during

early filling is related to wall relaxation: A color M-mode Doppler analysis. J Am Coll Cardiol 1992;20:420–432. 26. Stugaard M, Smiseth OA, Risoe C, et al: Intraventricular early diastolic filling

during acute myocardial ischemia, assessment by multigated color M-mode Doppler echocardiography. Circulation 1993;88:2705–2713. 27. Takatsuji H, Mikami T, Urasawa K, et al: A new approach for evaluation of left

ventricular diastolic function: Spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography. J Am Coll Cardiol 1996;27:365–371. 28. Garcia MJ, Smedira NG, Greenberg NL, et al: Color M-mode Doppler flow

propagation velocity is a preload insensitive index of left ventricular relaxation: Animal and human validation. J Am Coll Cardiol 2000;35:201–208. 29. Pai RG, Yoganathan AP, Toomes C, et al: Mitral E wave propagation as an index

of left ventricular diastolic function. I. Its hydrodynamic basis. J Heart Valve Dis 1998;7:438–444. 30. Van Dantzig JM, Dassen WR, Lucas CMHB, et al: Propagation velocity of mitral

inflow by color-M mode is load-dependent in congestive heart failure [abstract]. Circulation 1999;100:I295–296. 31. Isaaz K, Munoz del Romeral L, Lee E, et al: Quantitation of the motion of the

cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr 1993;6:166–176.

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Pagina 4 di 12

32. Garcia MJ, Rodriguez L, Ares MA, et al: Myocardial wall velocity assessment by

pulsed Doppler tissue imaging: Characteristic findings in normal subjects. Am Heart J 1996;132:648–656. 33. Miyatake K, Yamagishi M, Tanaka N, et al: New method for evaluating left

ventricular wall motion by color-coded tissue Doppler imaging: In vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 34. Oki T, Tabata T, Yamada H, et al: Clinical application of pulsed Doppler tissue

imaging for assessing abnormal left ventricular relaxation. Am J Cardiol 1997;79:921–928. 35. Sohn DW, Chai IH, Lee DJ, et al: Assessment of mitral annulus velocity by

Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474–480. 36. Firstenberg MS, Greenberg NL, Main ML, et al: Determinants of diastolic

myocardial tissue Doppler velocities: Influences of relaxation and preload. J Appl Physiol 2001;90:299–307 37. Pai PY, Oh JK, Ommen SR, et al: Acute preload alteration affects mitral annulus

velocities measured by tissue Doppler [abstract]. Circulation 1999;1000:I–777. 38. Pizigo E, Extramiana F, Larrazet F, et al: Load-dependence assessment of Doppler-

tissue velocity in the posterior wall and mitral annulus in patients undergoing hemodialysis [abstract]. Circulation 1999;1000:I–777. 39. Greenberg NL, Firstenberg MS, Castro P, et al: Doppler tissue early diastolic

myocardial velocities are independently influenced by heart rate [abstract]. J Am Soc Echocardiogr 2000;13:433. 40. Hatle L, Sutherland GR: Regional myocardial function: A new approach. Eur Heart

J 2000;21:1337–1357. 41. Ommen SR, Nishimura RA, Appleton CP, et al: Clinical utility of Doppler

echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler-catheterization study. J Am Coll Cardiol 2000;102:1788–1794. 41A. Palka P, Lange A, Donnelly JE, et al: Differentiation between restrictive

cardiomyopathy and constrictive pericarditis by early diastolic Doppler myocardial velocity gradient at the posterior wall. Circulation 2000;102:655–662.

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Pagina 5 di 12

42. Klein AL, Hatle LK, Taliercio CP, et al: Serial Doppler echocardiographic follow-

up of left ventricular diastolic function in cardiac amyloidosis. J Am Coll Cardiol 1990;16:1135–1141. 637

43. Appleton CP, Hatle LK: The natural history of left ventricular filling

abnormalities: Assessment by two-dimensional and Doppler echocardiography. Echocardiography 1992;9:437–457. 44. Appleton CP, Galloway JM, Gonzalez MS, et al: Estimation of left ventricular

filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease: Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coll Cardiol 1993;22:1972–1982. 45. Grodecki PV, Klein AL: Pitfalls in the echo-Doppler assessment of diastolic

dysfunction. Echocardiography 1993;10:213–234. 46. Klein AL, Burstow DJ, Tajik AJ, et al: Effects of age on left ventricular

dimensions and filling dynamics in 117 normal persons. Mayo Clin Proc 1994;69:212–224. 47. Hirota Y: A clinical study of left ventricular relaxation. Circulation 1980;62:756–

763. 48. Mego DM, DeGeare VS, Nottestad SY, et al: Variation of flow propagation

velocity with age. J Am Soc Echocardiogr 1998;11:20–25. 49. Nishimura RA, Housmans PR, Hatle LK, et al: Assessment of diastolic function of

the heart: Background and current applications of Doppler echocardiography. Part I. Physiologic and pathophysiologic features [review]. Mayo Clin Proc 1989;64:71–81. 50. Nishimura RA, Abel MD, Hatle LK, et al: Relation of pulmonary vein to mitral

flow velocities by transesophageal Doppler echocardiography: Effect of different loading conditions. Circulation 1990;81:1488–1497. 51. Choong CY, Abascal VM, Thomas JD, et al: Combined influence of ventricular

loading and relaxation on the transmitral flow velocity profile in dogs measured by Doppler echocardiography. Circulation 1988;78:672–683.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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Pagina 6 di 12

52. Choong CY, Herrmann HC, Weyman AE, et al: Preload dependence of Doppler-

derived indexes of left ventricular diastolic function in humans. J Am Coll Cardiol 1987;10:800–808. 53. Thomas JD, Weyman AE: Echocardiographic Doppler evaluation of left

ventricular diastolic function. Physics and physiology [review]. Circulation 1991;84:977–990. 54. Giannuzzi P, Imparato A, Temporelli PL, et al: Doppler-derived mitral deceleration

time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction. J Am Coll Cardiol 1994;23:1630–1637. 55. Xie GY, Berk MR, Smith MD, et al: Prognostic value of Doppler transmitral flow

patterns in patients with congestive heart failure. J Am Coll Cardiol 1994;24:132–139.

56. Hess OM, Felder L, Krayenbuehl HP: Diastolic function in valvular heart disease

[review]. Herz 1991;16:124–129. 57. Kyle RA, Greipp PR: Amyloidosis (AL): Clinical and laboratory features in 229

cases [review]. Mayo Clin Proc 1983;58:665–683. 58. Smith TJ, Kyle RA, Lie JT: Clinical significance of histopathologic patterns of

cardiac amyloidosis. Mayo Clin Proc 1984;59:547–555. 59. Cueto-Garcia L, Reeder GS, Kyle RA, et al: Echocardiographic findings in

systemic amyloidosis: Spectrum of cardiac involvement and relation to survival. J Am Coll Cardiol 1985;6:737–743. 60. Chiaramida SA, Goldman MA, Zema MJ, et al: Real-time cross-sectional

echocardiographic diagnosis of infiltrative cardiomyopathy due to amyloid. J Clin Ultrasound 1980;8:58–62. 61. Nicolosi GL, Pavan D, Lestuzzi C, et al: Prospective identification of patients with

amyloid heart disease by two-dimensional echocardiography. Circulation 1984;70:432–437. 62. Siqueira-Filho AG, Cunha CL, Tajik AJ, et al: M-mode and two-dimensional

echocardiographic features in cardiac amyloidosis. Circulation 1981;63:188–196. 63. Cueto-Garcia L, Tajik AJ, Kyle RA, et al: Serial echocardiographic observations in

patients with primary systemic amyloidosis: An introduction to the concept of early

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Pagina 7 di 12

(asymptomatic) amyloid infiltration of the heart. Mayo Clin Proc 1984;59:589–597. 64. Falk RH, Plehn JF, Deering T, et al: Sensitivity and specificity of the

echocardiographic features of cardiac amyloidosis. Am J Cardiol 1987;59:418–422. 65. Klein AL, Oh JK, Miller FA, et al: Two-dimensional and Doppler

echocardiographic assessment of infiltrative cardiomyopathy [review]. J Am Soc Echocardiogr 1988;1:48–59. 66. St. John Sutton MG, Reichek N, Kastor JA, et al: Computerized M-mode

echocardiographic analysis of left ventricular dysfunction in cardiac amyloid. Circulation 1982;66:790–799. 67. Abdalla I, Murray RD, Lee JC, et al: Duration of pulmonary venous atrial reversal

flow velocity and mitral inflow A wave: A new measure of severity of cardiac amyloidosis. J Am Soc Echocardiogr 1998;11:1125–1133. 68. Klein AL, Hatle LK, Burstow DJ, et al: Comprehensive Doppler assessment of right ventricular diastolic function in cardiac amyloidosis. J Am Coll Cardiol 1990;15:99–108. 69. Klein AL, Hatle LK, Taliercio CP, et al: Prognostic significance of Doppler

measures of diastolic function in cardiac amyloidosis: A Doppler echocardiography study. Circulation 1991;83:808–816. 70. Klein AL, Hatle LK, Burstow DJ, et al: Doppler characterization of left ventricular

diastolic function in cardiac amyloidosis. J Am Coll Cardiol 1989;13:1017–1026. 71. Patel AR, Dubrey SW, Mendes LA, et al: Right ventricular dilatation in primary

amyloidosis: An independent predictor of survival. Am J of Cardiol 1997;80:486–492.

72. Tei C, Dujardin KS, Hodge DO, et al: Doppler index combining systolic and

diastolic myocardial performance: Clinical value in cardiac amyloidosis. J Am Coll Cardiol 1996;28:658–664. 73. Ammash NM, Seward JB, Bailey KR, et al: Clinical profile and outcome of

idiopathic restrictive cardiomyopathy. Circulation 2000;101:2490–2496. 74. Hutt MS: Epidemiology aspects of endomyocardial fibrosis. Postgrad Med J

1983;59:142–146. 75. Patel AK, D'arbela PG, Somers K: Endomyocardial fibrosis and eosinophilia. Br

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

Book Text

Pagina 8 di 12

Heart J 1977;39:238–241. 76. Spry CJ, Take M, Tai PC: Eosinophilic disorders affecting the myocardium and

endocardium: A review. Heart Vessels 1985 (suppl);1:240–242. 77. Pinar Sopena J, Candell Riera J, San Jose Laporte A, et al: Echocardiographic

manifestations in patients with hypereosinophilia (in Spanish). Rev Esp Cardiol 1990;43:450–456. 78. Berensztein CS, Pineiro D, Marcotegui M, et al: Usefulness of echocardiography

and Doppler echocardiography in endomyocardial fibrosis. J Am Soc Echocardiogr 2000;13:385–392. 79. Olson LJ, Baldus WP, Tajik AJ: Echocardiographic features of idiopathic

hemochromatosis. Am J Cardiol 1987;60:885–889. 80. Olson LJ, Edwards WD, Holmes DR Jr, et al: Endomyocardial biopsy in

hemochromatosis: Clinicopathologic correlates in six cases. J Am Coll Cardiol 1989;13:116–120. 81. Dabestani A, Child JS, Henze E, et al: Primary hemochromatosis: Anatomic and

physiologic characteristics of the cardiac ventricles and their response to phlebotomy. Am J Cardiol 1984;54:153–159. 82. Cecchetti G, Binda A, Piperno A, et al: Cardiac alterations in 36 consecutive

patients with idiopathic hemochromatosis: Polygraphic and echocardiographic evaluation. Eur Heart J 1991;12:224–230. 83. Henry WL, Nienhuis AW, Wiener M, et al: Echocardiographic abnormalities in

patients with transfusion-dependent anemia and secondary myocardial iron deposition. Am J Med 1978;64:547–555. 84. Silverman KJ, Hutchins GM, Bulkley BH: Cardiac sarcoid: A clinicopathologic

study of 84 unselected patients with systemic sarcoidosis. Circulation 1978;58:1204– 1211. 85. Lewin RF, Mor R, Spitzer S, et al: Echocardiographic evaluation of patients with

systemic sarcoidosis. Am Heart J 1985;110:116–122. 86. Angomachalelis N, Hourzamanis A, Vamvalis C, et al: Doppler echocardiographic

evaluation of left ventricular diastolic function in patients with systemic sarcoidosis. Postgrad Med J 1992;68(suppl 1):S52–56.

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Book Text

Pagina 9 di 12

87. Fahy GJ, Marwick T, McCreery CJ, et al: Doppler echocardiographic detection of

left ventricular diastolic dysfunction in patients with pulmonary sarcoidosis. Chest 1996;109:62–66. 88. Burstow DJ, Tajik AJ, Bailey KR, et al: Two-dimensional echocardiographic

findings in systemic sarcoidosis. Am J Cardiol 1989;63:478–482. 89. Gregor P, Widimsky P, Sladkova T, et al: Echocardiography in sarcoidosis. Jpn

Heart J 1984;25:499–508. 90. Angomachalelis N, Hourzamanis A, Salem N, et al: Pericardial effusion

concomitant with specific heart muscle disease in systemic sarcoidosis. Postgrad Med J 1994;70(suppl 1):S8–12. 638

91. Vaitkus PT, Kussmaul WG: Constrictive pericarditis versus restrictive

cardiomyopathy: A reappraisal and update of diagnostic criteria [review]. Am Heart J 1991;122:1431–1441. 92. Meaney E, Shabetai R, Bhargava V, et al: Cardiac amyloidosis, constrictive

pericarditis and restrictive cardiomyopathy. Am J Cardiol 1976;38:547–556. 93. Benotti JR, Grossman W, Cohn PF: Clinical profile of restrictive cardiomyopathy.

Circulation 1980;61:1206–1212. 94. Fowler NO: Constrictive pericarditis: New aspects. Am J Cardiol 1982;50:1014–

1017. 95. Vogel JH, Horgan JA, Strahl CL: Left ventricular dysfunction in chronic

constrictive pericarditis. Chest 1971;59:484–492. 96. Tyberg TI, Goodyer AV, Hurst VW, et al: Left ventricular filling in differentiating

restrictive amyloid cardiomyopathy and constrictive pericarditis. Am J Cardiol 1981;47:791–796. 97. Aroney CN, Ruddy TD, Dighero H, et al: Differentiation of restrictive

cardiomyopathy from pericardial constriction: Assessment of diastolic function by radionuclide angiography. J Am Coll Cardiol 1989;13:1007–1014. 98. Gerson MC, Colthar MS, Fowler NO: Differentiation of constrictive pericarditis

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and restrictive cardiomyopathy by radionuclide ventriculography. Am Heart J 1989;118:114–120. 99. Hatle LK, Appleton CP, Popp RL: Differentiation of constrictive pericarditis and

restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357– 370. 100. Mancuso L, D'Agostino A, Pitrolo F, et al: Constrictive pericarditis versus

restrictive cardiomyopathy: The role of Doppler echocardiography in differential diagnosis. Int J Cardiol 1991;31:319–327. 101. Klodas E, Nishimura RA, Appleton CP, et al: Doppler evaluation of patients with

constrictive pericarditis: Use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction. J Am Coll Cardiol 1996;28:652–657. 102. Klein AL, Cohen GI, Pietrolungo JF, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943. 103. Boonyaratavej S, Oh JK, Tajik AJ, et al: Comparison of mitral inflow and

superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol 1998;32:2043–2048. 104. Tabata T, Kabbani SS, Murray RD, et al: Difference in the respiratory variation

between pulmonary venous and mitral inflow Doppler velocities in patients with constrictive pericarditis, with and without atrial fibrillation. J Am Coll Cardiol 2001;37:1936–1942. 105. Bush CA, Stang JM, Wooley CF, et al: Occult constrictive pericardial disease:

Diagnosis by rapid volume expansion and correction by pericardiectomy. Circulation 1977;56:924–930. 106. Schiavone WA, Rice TW: Pericardial disease: Current diagnosis and management

methods. Cleve Clin J Med 1989;56:639–645. 107. Klein AL, Al-Assaad N, Pietrolungo JF, et al: Does rapid volume loading during

transesophageal echocardiography differentiate constrictive pericarditis from restrictive cardiomyopathy? [abstract]. J Am Soc Echocardiogr 1994;7:S38. 108. Oh JK, Tajik AJ, Appleton CP, et al: Preload reduction to unmask the

characteristic Doppler features of constrictive pericarditis: A new observation. Circulation 1997;18:796–799.

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109. King SW, Pandian NG, Gardin JM: Doppler echocardiographic findings in

pericardial tamponade and constriction. Echocardiography 1988;5:361–372. 110. Lewis BS: Real time two dimensional echocardiography in constrictive

pericarditis. Am J Cardiol 1982;49:1789–1793. 111. Voelkel AG, Pietro DA, Folland ED, et al: Echocardiographic features of

constrictive pericarditis. Circulation 1978;58:871–875. 112. Thamilarasan M, Schvartzman P, White RD, et al: The accuracy of

transesophageal echocardiography in the assessment of pericardial thickness in patients with constrictive pericarditis: A comparison with magnetic resonance imaging [abstract]. Circulation 1999;100:I–294. 113. Janos GG, Arjunan K, Meyer RA, et al: Differentiation of constrictive pericarditis

and restrictive cardiomyopathy using digitized echocardiography. J Am Coll Cardiol 1983;1:541–549. 114. Morgan JM, Raposo L, Clague JC, et al: Restrictive cardiomyopathy and

constrictive pericarditis: Non-invasive distinction by digitized M mode echocardiography. Br Heart J 1989;61:29–37. 115. Garcia MJ, Ares MA, Rodriguez L, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler tissue imaging: Measurement of mitral annular velocity. J Am Coll Cardiol 1996;27:108–114. 115A. Rajagopalon N, Garcia MJ, Rodriguez L, et al: Comparison of new Doppler

echocardiographic methods to differentiate constrictive pericardial disease and restrictive cardiomyopathy. Am J Cardiol 2001;87:86–94. 116. Zelin S, Skiles JA, Klein AL: Echocardiographic and clinical features of mixed

constriction/restriction [abstract]. J Am Coll Cardiol 2000;35(suppl 2):434A–435A. 117. Cheng CP, Igarashi Y, Little WC: Mechanism of augmented rate of left

ventricular filling during exercise. Circ Res 1992;70:9–19. 118. Cheng CP, Noda T, Nozawa T, et al: Effect of heart failure on the mechanism of

exercise-induced augmentation of mitral valve flow. Circ Res 1993;72:795–806. 119. Ohno M, Cheng CP, Little WC: Mechanism of altered patterns of left ventricular

filling during the development of congestive heart failure. Circulation 1994;89:2241– 2250.

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120. Kitzman DW, Higginbotham MB, Cobb FR, et al: Exercise intolerance in patients

with heart failure and preserved left ventricular systolic function: Failure of the FrankStarling mechanism. J Am Coll Cardiol 1991;17:1065–1072. 121. Von Bibra H, Tuchnitz A, Klein AL, et al: Regional diastolic function by pulsed

Doppler myocardial mapping for the detection of left ventricular ischemia during pharmacologic stress testing: A comparison with stress echocardiography and perfusion scintigraphy. J Am Coll Cardiol 2000;36:444–452.

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639

Chapter 29 - Pericardial Disease Bradley I. Munt MD Tim Kinnaird MB Christopher R. Thompson MD, CM

Basic Principles Anatomy of the Pericardium The pericardium consists of two layers that surround the heart and proximal segments of the aorta, pulmonary artery, pulmonary veins, and venae cavae. The outermost layer is a thick fibrous structure, which blends with the adventitia of the aorta and pulmonary arteries to provide firm support for the heart. This layer also has supporting ligamentous attachments to the diaphragm, sternum, and vertebrae.[1] [2] The inner layer is a serous membrane consisting of a single layer of mesothelial cells, which directly overlies the epicardial fat to form the visceral pericardium. This membrane reflects back on itself to line the inside of the fibrous layer and forms the parietal pericardium. The pericardial space is enclosed between the two layers of serous pericardium. This space is limited superiorly by the attachments of the fibrous pericardium to the great arteries. It is limited posteriorly by reflections of the pericardium as the pulmonary veins and venae cavae enter the atria. These reflections result in the formation of two blind-ending tunnels or sinuses. The oblique sinus lies behind the left atrium and is limited superiorly by the pericardial reflection to the upper pulmonary veins, laterally by the reflections of the pericardium around the

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left pulmonary veins, and medially by the reflections of the pericardium around the right pulmonary veins and venae cavae. The transverse sinus lies above the pulmonary vein reflection and is bound anteriorly by the great arteries and posteriorly by the left atrial roof (Fig. 29-1) (Figure Not Available) . Pericardial Fluid The pericardial space normally contains 10 to 50 mL of fluid that lubricates the contact between the two serosal layers of the pericardium.[3] This fluid is an ultrafiltrate of plasma and contains proteins, electrolytes, and phospholipids. The pericardial fluid is believed to be formed in the visceral pericardium. The pericardial space drains via the thoracic and right lymphatic ducts. Any condition obstructing lymphatic flow or raising central venous pressure leads to accumulation of pericardial fluid. Fluid also accumulates in conditions that increase the normal pericardial permeability. Functions of the Pericardium The pericardium reduces friction between the heart and the surrounding mediastinal structures and provides a barrier against the local spread of infection or malignancy to the heart.[2] However, because the pericardium is a semi-rigid layer that completely encloses the heart, it also serves to modulate the pressure within the pericardial 640

Figure 29-1 (Figure Not Available) Pericardial anatomy showing attachments of the pericardium to the great vessels and junction of the pulmonary veins and atria after removal of the heart. (From Edmunds HL: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1304. Reproduced with permission of The McGraw-Hill Companies.)

space and the cardiac structures enclosed within the pericardium. In addition, the pericardium mediates ventricular coupling or interaction.[4] Understanding the role of the pericardium in pressure modulation and ventricular interaction is important in order to appreciate the echocardiographic characteristics of pericardial pathology and other cardiac diseases. Pericardial Pressure

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More than a century ago, Bernard concluded that the pericardium significantly constrained cardiac filling.[5] The concept of transmural pressure, the intracavity end-diastolic pressure minus the pericardial pressure, subsequently evolved to take into account this pericardial restraint. This concept is extremely important because transmural pressure is likely to be a closer representation of preload than the intracavity enddiastolic pressure. Controversy exists, however, regarding the magnitude of this constraint because of difficulties in accurate determination of pericardial pressure. Fluid-filled catheters probably underestimate pericardial pressure and suggest higher transmural pressures. Pericardial balloons, however, suggest that pericardial pressure is very close to right atrial and right ventricular end-diastolic pressures and that right ventricular transmural pressure, therefore, is close to zero.[6] Slinker et al[7] have further modified these concepts, suggesting that pericardial balloons overestimate pericardial pressure and therefore underestimate true transmural pressure. Nevertheless, it is important to consider pericardial restraint and pericardial pressure when assessing ventricular filling and function. The pericardium is a relatively stiff structure, so intrapericardial pressure rises rapidly as intrapericardial volume increases acutely[8] (Fig. 29-2) (Figure Not Available) . Shirato et al[9] studied dogs following acute volume loading, showing that the left ventricular pressure-volume relationship shifts upward and leftward (i.e., at any given intracavity pressure, the chamber volume was lower). The explanation for this finding is that an increase in intrapericardial volume (caused by an increase in right-sided chamber volumes) increases intrapericardial pressure, restraining left ventricular filling. The opposite effects were seen with reductions in cardiac volume using nitroprusside. These authors also demonstrated that after removal of the pericardium, changes in pressure-volume relationships took place along a single curve. Belenkie et al[10] eliminated the influence of pericardial pressure by plotting transmural pressure rather than intracavity pressure against volume and found also that changes occurred along a single curve (Fig. 29-3) . These Figure 29-2 (Figure Not Available) Pericardial pressure-volume relationships in a patient with normal pericardial anatomy (solid line) and a patient who has gradually developed a pericardial effusion (dashed line). (From Edmunds HL: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1305. Reproduced with permission of The McGraw-Hill Companies.)

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Figure 29-3 The effect of acute right ventricular pressure loading (experimental pulmonary embolism) on diastolic compliance (left) and ventricular function (right). The conventional approach (top) defines compliance and function in terms of left ventricular end diastolic pressure (LVEDP). Transmural (chamber-pericardial) left ventricular end diastolic pressure (LVEDPTM ) is also shown (bottom). The transmural plots demonstrate that there is no change in diastolic compliance or contractility. The decrease in left ventricular performance is explained by left ventricular hypovolemia caused by increased external constraint resulting in a left and upward shift in the diastolic compliance curve and a right and downward shift in the ventricular function curve. LVEDV, left ventricular end diastolic volume; LVSW, left ventricular stroke work. (Redrawn from Tyberg JV, Belenkie I, Manyari DE, Smith ER: Can J Cardiol 1996;12:1058–1064, with permission.)

results indicate that the hemodynamic effects of acute volume loading are significantly influenced by pericardial restraint and that intrinsic myocardial compliance is not altered. Although similar effects have been seen in human studies,[11] it is interesting to speculate that because the human pericardium is much thicker than the canine pericardium, pericardial influence may be even more pronounced in humans. The restraining effects of the pericardium are much less apparent in the chronic volume overloaded state because pericardial compliance and surface area are able to increase under chronic strain conditions[8] (see Fig. 29-2) (Figure Not Available) . Ventricular Coupling (Interaction)

An increase in pericardial pressure resulting from pericardial fluid accumulation also reduces transmural pressure and shifts ventricular pressure-volume relationships (see later). The left and right ventricle interact to influence each other's diastolic behavior. The interaction can be either series interaction (i.e., the output of the right ventricle influencing venous return and, consequently, filling of the left ventricle), or direct interaction (i.e., ventricular filling characteristics changed by the side-byside nature of the ventricles within the relatively stiff pericardium). An increase in the volume of one ventricle increases pericardial pressure, thus moving the pressure-volume relationship of the other ventricle upward and leftward. Direct ventricular interaction can occur even in the absence of a pericardium because of septal bulging,[12] but interaction is much more marked when the pericardium is intact.[13] Studies in dogs with absent pericardia have shown that large increases in right ventricular volume and

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pressure are required before left ventricular pressures increase. [14] Conversely, left ventricular pressure increases in parallel with that of the right ventricle in the presence of an intact pericardium. In constrictive pericarditis, this interaction is markedly accentuated. Several groups have studied the clinical relevance of ventricular interaction. Belenkie et al[15] showed that in the dogs with experimental pulmonary emboli (and consequent right ventricular pressure and volume overload), left ventricular filling was markedly impaired with a leftward shift of left ventricular intracavity pressure-volume relationship. When transmural left ventricular pressure was plotted against volume, however, all values lay on a single curve. This finding illustrates that a pericardial pressure increase, as a result of right heart dilation, significantly influences left ventricular filling (i.e., it reduces left ventricular operating chamber compliance without altering intrinsic myocardial compliance). The effects of ventricular interaction also have been studied in heart failure. Atherton et al[16] showed that the paradoxical increase in cardiac output with lower body suction seen in some patients was a consequence of a reduction in right heart size, resulting in improved left ventricular filling (as demonstrated by radionuclide ventriculography). It is clear, therefore, that the pericardium plays a major role in limiting cardiac distention, modulating intracavity pressure and ventricular filling characteristics, and mediating direct ventricular interaction. Echocardiographic Examination of the Pericardium The pericardium covers the entire external surface of the heart and therefore is visualized from all standard echocardiographic acoustic windows. Echocardiographically, the pericardium appears as a thin, usually single echogenic structure that is more obvious posteriorly than anteriorly (Fig. 29-4) . Most pericardial processes are evident in the parasternal longaxis view because these processes generally result in diffuse pericardial involvement and pericardial fluid tends to accumulate in the oblique sinus initially.[17] [18] As well, complete or partial absence of the pericardium results in marked cardiac displacement or left atrial appendage herniation or enlargement,[19] and pericardial cysts are usually located at the left or right costophrenic angle.[20] All of these areas are well visualized from the parasternal long-axis view, especially if leftward and rightward angulation of the transducer is performed. An important exception is postsurgical pericardial effusions. In the nonsurgical patient, when the clinical suspicion of a primary pericardial disease is low, a normal parasternal long-axis view

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is believed to be adequate to rule out pericardial pathology. Unfortunately, in a series 642

Figure 29-4 Parasternal long-axis view of the normal pericardium. In this patient, the visceral pericardium (VP) and parietal pericardium (PP) are appreciated anteriorly, whereas the pericardium (P) appears as a single, bright echogenic structure posteriorly. AO, descending thoracic aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

of patients who underwent pericardiocentesis for tamponade,[21] the diagnosis of pericardial effusion was not considered in 44% of patients before echocardiography, and an alternative working diagnosis was thought to be more likely in a further 36%. Twenty-four percent of the patients were not postoperative. The authors concluded that "the proper diagnosis does not appear to be initially considered in up to 80% of patients who present with cardiac tamponade." Therefore, we advocate that the pericardial space be studied in all standard echocardiographic acoustic windows as part of the standard echocardiographic examination, with special attention in all postoperative patients. There is a relatively poor correlation between measurements of pericardial thickness by transthoracic echocardiography and pathological examination. [22] Although a good correlation has been suggested between pericardial thickness derived by transesophageal echocardiography and computed tomography,[23] we still prefer computed tomography or magnetic resonance imaging to evaluate the pericardium because a more thorough examination can be performed. Visualization of the right ventricular and right atrial free walls, often with high frame rate M-mode or two-dimensional recordings of motion, is required to determine the hemodynamic significance of pericardial effusions. As well, pulsed wave Doppler recordings of right ventricular filling, often with respiratory tracking, are needed as a minimum. We strongly advocate that all patients with pericardial effusions undergo an initial full, detailed echocardiographic examination to rule out conditions that may affect echocardiographic indicators of hemodynamically significant pericardial fluid (e.g., atrial septal defects, right ventricular hypertrophy), and detect coexisting cardiac conditions. Follow-up

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examinations may be of a more directed, limited nature.

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Constrictive Pericarditis Several types of disorders can cause pericardial inflammation and subsequent thickening, fibrosis, and calcification (Table 29-1) . Pericardial thickening results in impaired cardiac filling and characteristic echocardiographic signs. Pathophysiology The thickened, fibrotic pericardium constricts the heart and reduces operative chamber compliance. Consequently, diastolic filling is impeded and the end-diastolic cardiac volume is determined by the pericardial volume. The thickening usually involves the whole pericardial surface and leads to elevation and equalization of diastolic pressures in all four cardiac chambers. In early diastole, ventricular filling occurs at a more rapid rate than normal because of elevated atrial pressures and a cardiac volume that is less than the limiting volume of the pericardium. Once the pericardial volume is reached, however, filling halts abruptly and total chamber volume increases only slightly. This limitation to filling in mid and late diastole leads to M-mode, two-dimensional, and Doppler abnormalities (discussed later) and the typical "square root sign" seen with invasive hemodynamic measurement.[24] The thickened pericardium isolates the heart from the normal respiratory swings in intrathoracic pressure; however, respiratory fluctuations in pulmonary venous pressure still occur, and a decrease in pulmonary venous pressure with inspiration leads to a decrease in the driving TABLE 29-1 -- Causes of Constrictive Pericarditis Idiopathic origin Infectious diseases Tuberculous Bacterial

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Fungal Viral Parasitic Trauma Blunt or penetrating trauma Cardiac surgery Connective tissue disorders Rheumatoid arthritis Systemic lupus erythematosus Neoplasia Primary benign or malignant pericardial tumors Secondary local or metastatic spread Miscellaneous Chronic renal failure Mediastinal irradiation Pulmonary asbestosis

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pressure across the mitral valve. This decrease prolongs the isovolumetric relaxation time, reduces early diastolic transmitral flow velocity, and prolongs the decleration time.[25] These changes are not seen in normal patients or in patients with restrictive cardiomyopathy. The pericardial limitation to filling also serves to exaggerate normal ventricular coupling. A reduction in left ventricular filling with inspiration allows a compensatory increase in right heart filling. These respiratory fluctuations in left and right heart filling cause characteristic changes in mitral and tricuspid Doppler inflow patterns, ventricular dimensions, and aortic and pulmonary peak velocities (discussed later). Echocardiographic Diagnosis M-mode and Two-Dimensional Abnormalities

The abrupt cessation of flow in mid-diastole results in flattening of the

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motion of the posterior left ventricular wall in mid and late diastole. This result follows relatively normal motion in early diastole associated with rapid ventricular filling and is the M-mode equivalent of the square root sign. This sign is relatively sensitive, being reported in 85% of patients with constriction; however, it is also seen in 20% of normal subjects.[26] Abnormalities of interventricular septal motion are common in constriction. Septal position is influenced by pressure gradients between the left and right ventricle, and changes in septal position with respiration are exacerbated by the constricting effect of the rigid pericardium. Both Mmode and two-dimensional echocardiography can demonstrate marked movement of the septum posteriorly with inspiration and anteriorly with expiration and consequent respiratory changes in left and right ventricular volumes.[27] A further M-mode sign seen with constriction is a "double component" of septal motion. The normal anterior movement of the septum after atrial systole is preceded by brief posterior displacement, which is caused by a transient increase in the right ventricular pressure above that of the left ventricle with the onset of atrial systole. A second posterior septal movement occurs in early diastole because left ventricular pressure decays more quickly than right ventricular pressure. This second posterior septal movement is an exaggeration of the normal diastolic posterior septal movement that occurs at this time in the cardiac cycle. Premature pulmonary valve opening also occurs and can be appreciated using M-mode echocardiography. The abnormally elevated filling pressure associated with constriction leads to right ventricular diastolic pressure exceeding pulmonary artery diastolic pressure in mid-diastole and consequent premature pulmonary valve opening. Pericardial thickening and calcification can be appreciated using M-mode and two-dimensional modalities although the sensitivity and specificity have been questioned. Early reports of M-mode sensitivity of almost 100% in diagnosing pericardial thickening[28] or diagnosing constrictive pericarditis from other findings[29] have not been confirmed in later studies. [26] [30] [31] [32] A systematic over-estimation of true thickness using transthoracic echocardiography was found in dogs with experimental constrictive pericarditis.[22] These difficulties have been related to technical difficulties such as gain settings and resolution, and to fibrosis obscuring cardiac boundaries. Patchy pericardial thickening also may cause diagnostic difficulties. A more recent study found that transesophageal echocardiography was more accurate, with a sensitivity of 95% and specificity of 86% in the detection of thickened pericardium.[23]

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The inferior vena cava is also typically dilated with blunting of the normal respiratory variation in its diameter.[33] This sign, however, is nonspecific and frequently seen in other conditions with elevated right atrial pressures. Despite all of these signs, no single M-mode or two-dimensional echocardiographic feature is diagnostic of constrictive pericarditis. Doppler Abnormalities

In keeping with rapid early diastolic flow, the left ventricular (mitral) inflow pattern typically shows a high E wave velocity, short deceleration time, and a low A wave velocity. This pattern, however, reflects impaired diastolic function and therefore is not specific to pericardial constriction. Of much more use is the change in left and right (tricuspid) ventricular inflow patterns seen with respiration, because these signs appear to be much more reliable in diagnosing constriction. Several studies[25] [34] have reported that patients with pericardial constriction have (1) a prolongation of the isovolumetric relaxation time with inspiration greater than 25% in all patients with constriction compared with less than 5% in normal patients; (2) greater than 25% reduced peak early left ventricular flow velocity with inspiration in all patients compared with less than 5% in normal patients; (3) larger expiratory decreases in right ventricular inflow velocity than in normal patients; (4) a 14% reduction in aortic velocity with inspiration compared with 4% reduction in normal patients; (5) a 16% increase in pulmonary artery velocity with inspiration compared with 5% in normal patients; (6) changes in all parameters being greatest in the first beat following inspiration compared with changes two or three beats later in those patients with pulmonary disease; and (7) an absence of these significant respiratory fluctuations after pericardectomy. Respiratory fluctuations in mitral inflow velocity are not always present. One study suggests normal respiratory fluctuations in 12% of patients with proved constriction.[34] The authors speculated that the mechanism was a markedly elevated left atrial pressure forcing mitral valve opening to occur on a steeper part of the left ventricular curve, thus masking inspiratory changes in inflow velocity and isovolumic relaxation time.[34] This finding was supported in a subsequent study that showed that in patients with constriction, but with blunted respiratory changes, preload reduction unmasked the characteristic respiratory variation.[35] The increased flow through the right heart with inspiration in patients with constriction alters tricuspid regurgitation jet parameters. Increased right

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ventricular preload 644

increases the cavity pressure, increasing the regurgitation velocity and velocity time integral. Klodas et al[36] reported a 13% increase in tricuspid regurgitation velocity with inspiration in patients with constrictive pericarditis, compared with an 8% decrease in jet velocity in normal patients. Abnormalities of pulmonary and hepatic vein flow also have been described in association with constrictive pericarditis. The predominant forward hepatic vein flow in constriction occurs typically during early diastole because of an elevated right atrial pressure inhibiting inflow during systole and driving flow across a high early diastolic transtricuspid gradient.[34] This pattern, however, is not uniform, and systolic forward flow also can predominate. Augmentation of right heart filling during inspiration increases hepatic forward flow, and expiration causes a marked increase in flow reversal with atrial systole and a decrease or paradoxical reversal of flow in early diastole. In a series of patients with surgically proved constrictive pericarditis, echocardiographic criteria based on respiratory variations in mitral and hepatic vein flow correctly diagnosed constriction in 22 of 25 patients.[34] This result leads us to use Doppler flow abnormalities, especially fluctuations with respiration, as our primary echocardiographic criteria in the evaluation of patients for whom constrictive pericarditis is in the differential diagnosis. Pulmonary vein flow abnormalities described in association with constrictive pericarditis include a reduction in systolic wave and diastolic wave velocities and a reduction in the systolic-to-diastolic ratio.[34] As with mitral inflow, these patterns are a reflection of diastolic dysfunction and elevated filling pressures and are not specific to constriction. Respiratory fluctuations in pulmonary venous flow, however, also have been reported in constriction and are used to differentiate patients with constriction from those with restriction and from normal subjects.[37] In patients with constriction, both diastolic and systolic flow velocities increase during expiration, but the degree of increase is greater for diastolic flow velocity. [34]

Doppler Tissue Imaging Abnormalities

It has been shown that in patients with pericardial constriction, the velocity

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of early diastolic posterior left ventricular wall motion is increased (consistent with rapid early filling) and the time from aortic valve closure to peak left ventricular wall velocity appears to be shortened.[38] Abnormalities of septal motion were also demonstrated by Doppler tissue imaging consistent with the M-mode abnormalities described earlier. Recent work suggests that Doppler tissue imaging may be very useful in differentiating pericardial constriction from restriction, with myocardial relaxation velocities (reflecting intrinsic myocardial disease) being significantly lower in restriction than in constriction.[39]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Pericardial Effusion A wide variety of conditions, broadly divided into inflammatory, neoplastic, endocrine, and traumatic, can lead to an increase in pericardial fluid. An increase results in separation of the parietal pericardium from the visceral pericardium and fluid accumulation in this physiological potential space. Clinically, the consequences of this pericardial effusion are alterations in the physiology of cardiac function as the normally negative intrapericardial pressure becomes less negative and is then transformed into a positive pressure, which reduces intracardiac filling pressures. Because right-sided pressures tend to be lower than left-sided pressures, direct effects of the pericardial fluid are usually first seen in right-sided chambers. [40]

M-mode and Two-Dimensional Echocardiography Echocardiographic Appearance of Pericardial Fluid and Other Common Disorders Simulating Pericardial Effusion

The hallmark of a pericardial effusion is visualization of echolucent material with properties consistent with fluid in the pericardial space. If pericardial anatomy is relatively normal before fluid accumulation, fluid first accumulates in the oblique sinus posterior to the left ventricle[17] (see Fig. 29-1) (Figure Not Available) , and it is best viewed in the parasternal long-axis view. Once approximately 100 mL of fluid has accumulated in the pericardium, the fluid tends to become circumferential, filling the entire pericardial space. It is important to differentiate normal anatomic variants and nonpericardial processes from pericardial fluid. Left-sided pleural effusions can appear posterior to the heart. The echocardiographic hallmark separating pericardial from pleural effusions is that pericardial fluid tracks anteriorly to the proximal descending thoracic aorta, whereas pleural effusions do not ( Fig. 29-5 and Fig. 29-6 ). As well, large amounts of pericardial fluid tend

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to be located circumferentially around the heart, whereas large left pleural effusions remain predominantly posterior. Visualization of partially atelectatic lung in the fluid cavity also can aid in the diagnosis of a pleural effusion (Fig. 29-7) . Epicardial fat also leads to an echolucent space in the area of the pericardium (Fig. 29-8) . Epicardial fat, however, tends to occur anteriorly; using standard imaging settings, epicardial fat has echogenicity between that of the blood pool and myocardium,[41] [42] whereas pericardial effusion has echogenicity closer to the blood pool (see later for exceptions). Epicardial fat is more common in older individuals (prevalence <1% in subjects 20 to 30 years old to >15% for those older than 80 years) and in subjects who are female, obese, hypertensive, and who have elevated glucose and low-density lipoprotein levels.[43] Factors Affecting the Appearance of Pericardial Effusions

The echogenicity of the pericardial fluid can be influenced by features intrinsic to the fluid (e.g., fluid composition including protein content, hemorrhage, chyle, cholesterol, or bacteria) or related to the same process that 645

Figure 29-5 Parasternal long-axis view of a large, circumferential pericardial effusion. The pericardial fluid is seen tracking between the left atrium and aorta (imaged obliquely). There is right ventricular diastolic collapse. AO, descending thoracic aorta; PE, pericardial effusion; RV, right ventricle.

leads to the fluid (e.g., tumor infiltration of the pericardium). In general, as the protein or cellular content of the fluid increases, the echogenicity of the fluid increases. Characterization of the exact fluid composition is not possible, however, from echocardiography.[44] Clinical Considerations A common clinical scenario is a request for determination of the presence or absence of pericardial effusion, and if present, a determination of the effusion size and hemodynamic effect. It must be remembered that an incompletely understood complex interaction of factors leads to the ultimate physiologic consequences of pericardial effusion and influences

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the hemodynamic effects in a given patient. These factors include the pericardial pressure-volume relationship, the rapidity of fluid accumulation, underlying cardiac pathology (particularly hypertrophy and shunts), and systemic volume status.[45] Clinical experience and animal experimentation have determined that small acute pericardial effusions (occurring most commonly post intervention or traumatically) can lead to dramatic physiologic effects, whereas moderate or even large pericardial effusions that accumulate slowly can be hemodynamically well tolerated.[8] Localized cardiac compression may lead to dramatic hemodynamic consequences without producing classic echocardiographic indications of tamponade.[46] [47] [48]

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Pericardial Tamponade Two-Dimensional Echocardiographic Findings Right Ventricular Compression, Inversion, or Collapse

Perhaps the most useful echocardiographic indicator of a hemodynamically significant pericardial effusion is right ventricular diastolic collapse. Right ventricular diastolic collapse is seen on M-mode or two-dimensional echocardiography Figure 29-6 Subcostal view of a large, predominantly anterior pericardial effusion. In early ventricular systole (A), right atrial and ventricular size and contour appear relatively normal. In early ventricular diastole (B), marked right atrial and ventricular collapse are seen. PE, pericardial effusion; RA, right atrium; RV, right ventricle.

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recordings as a persistent inward motion of the right ventricular free wall during diastole ( see Fig. 29-5 and Fig. 29-6 ). By the time it is noted in experimental preparations, a significant reduction (approximately 20%) in forward cardiac output and elevation in heart rate without a change in mean arterial pressure have already occurred.[49] There is no precise relationship between the duration or degree of right ventricular diastolic collapse and the degree of elevation of intrapericardial pressure or the severity of the hemodynamic effect of the pericardial fluid.[50] Clinically, one can appreciate all degrees of this phenomenon, from a barely perceptible dip, only appreciated with high frame rate recordings, to complete collapse and obliteration of the right ventricle throughout diastole ( see Fig. 29-5 and Fig. 29-6 ).

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Increases in right ventricular intracavitary volume,[51] [52] right ventricular pressure,[53] and increased chamber stiffness all reduce the amount of right ventricular diastolic collapse for any given increase in intrapericardial pressure. Clinically, these increases may be seen in patients with pulmonary hypertension, left-to-right shunts (especially atrial septal defects), or right ventricular ischemia not manifesting right ventricular diastolic collapse despite significant elevations of pericardial pressure.[51] [52] [53]

Because the sensitivity and specificity and therefore the negative and positive predictive values of right ventricular diastolic collapse depend on the definition of tamponade (Table 29-2) , we use a clinical approach to this finding. In a patient with clinical findings of tamponade, we interpret right ventricular diastolic collapse to indicate a significant hemodynamic contribution of the effusion to the patient's clinical state, and are an indication for immediate therapy to remove pericardial fluid. In a patient without clinical tamponade, we interpret right ventricular diastolic collapse to indicate intrapericardial pressure at or above right ventricular diastolic pressure and the potential for Figure 29-7 View of the right pleural cavity with a wedge-shaped slice of atelectatic lung. LI, liver; LL, lung; PLE, pleural effusion.

Figure 29-8 Parasternal long-axis view of a small, circumferential pericardial effusion (PE) with epicardial fat (EF). The pericardial fluid is seen anteriorly and posteriorly between the parietal pericardium (PP) and visceral pericardium (VP). The epicardial fat is seen lying between the right ventricular wall and visceral pericardium. LV, left ventricle; RV, right ventricle.

relatively acute hemodynamic deterioration. Although this is not an indication for immediate pericardial fluid removal, urgent action is indicated to reverse any factors worsening the hemodynamic effect of the effusion. Large pleural effusions can cause right ventricular diastolic collapse.[54] In our experience, this fact has not lead to confusion regarding diagnosis. If we encounter a patient with tamponade physiology and a large pleural

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effusion who also has a pericardial effusion, we drain the pleural effusion first and then clinically and echocardiographically reassess the patient for hemodynamic status. Right Atrial Compression, Inversion, or Collapse

Right atrial pressures are lower than right ventricular pressures throughout the cardiac cycle. Because intrapericardial pressure is evenly distributed over the heart, one can surmise that right atrial compression occurs before right ventricular compression as pericardial pressure is raised. This assumption is borne out in imaging studies in which the right atrium and ventricle are continuously imaged during pericardiocentesis.[40] Subsequently, right atrial inversion, which tends to begin in late ventricular diastole (just before or at the P wave if sinus rhythm is present) but persists into early ventricular systole, is an extremely sensitive sign of cardiac tamponade[55] ( Fig. 29-9 ; see also Fig. 29-6 ). Right atrial inversion, however, is less specific than right ventricular diastolic collapse (see Table 29-2) . The 647

TABLE 29-2 -- Echocardiographic Features of Pericardia No. of Patients Echocardiographic with Definition of Se Study Sign Evaluated Tamponade Tamponade 17 of 86 Presence of a Armstrong (1982) Right ventricular [117] moderate to large diastolic collapse; et al pericardial M-mode (posterior effusion with at movement of the least two of the right ventricular following: (1) free wall in early elevated venous and mid-diastole as pressure, (2) timed from the systemic echocardiogram) hypotension, (3) pulsus paradoxus and resolution of signs after

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Armstrong (1982) Right ventricular diastolic collapse; et al[117] 2D (any indentation of the right ventricular free wall during diastole) Engel et al (1982) Right ventricular [118] diastolic collapse; M-mode, (persistent posterior motion of the right ventricular free wall greater than 50 msec after mitral valve opening) Gillam et (1983) Right atrial collapse al[56] (inversion of the right atrial free wall at any point of the cardiac cycle)

Gillam et (1983) Right atrial diastolic al[56] collapse (right atrial inversion time index > 0.34 [number of video frames demonstrating right atrial inversion ÷ total number of frames per cardiac cycle])

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10 of 41

pericardiocentesis (as above)

21 of 37

Pulsus paradoxus >10 mm Hg, elevated systemic venous pressure, and resolution of signs with pericardiocentesis

19 of 123

Two or more of the following: (1) elevated jugular venous pressure, (2) relative hypotension, (3) pulsus paradoxus greater than 10 mm Hg and resolution of the symptoms with pericardiocentesis (as above)

18 of 36

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Kronzon et al[55]

(1983) Right atrial collapse; 2D (any reduction in right atrial size during diastole) Kronzon (1983) Left atrial collapse; et al[55] 2D (posterior left atrial wall motion of at least 10 min in diastole) Singh et al (1984) Right ventricular [40] diastolic collapse; 2D (persistent inward motion of the right ventricular endocardial surface after opening of the mitral valve)

Singh et al (1984) Right atrial collapse; 2D (right atrial free wall appears to be inverted at any point during the cardiac cycle) Singh et al (1984) Right ventricular [40] diastolic collapse; 2D (persistent inward motion of the right ventricular endocardial surface after mitral valve opening)

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9 of 29

Clinical with relief after pericardiocentesis

9 of 29

(as above)

12 of 16

Equalization of right atrial, pulmonary capillary wedge and intrapericardial pressures and elevation of these pressures to >10 mm Hg (as above)

8 of 12

[40]

Himelman (1988) Inferior vena cava et al[33] plethora; 2D (a decrease in

16 of 21

33 of 115

Equalization of the intrapericardial, right atrial, and pulmonary wedge pressures with elevations of these pressures to > 10 mm Hg Either of the following: (1) elevation [mean

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proximal vena caval diameter by <50% after a deep inspiration)

> 12 mm Hg] and equalization [≤ 5 mm Hg] of diastolic filling pressures or (2) systolic blood pressure < 100 mm Hg that increased by > 20 mm Hg after pericardiocentesis (as above)

Himelman (1988) Right atrial 33 of 115 [33] et al collapse: 2D (dynamic inversion of the right atrial wall occurring in late diastole or early systole) 33 of 115 (as above) Himelman (1988) Right ventricular [33] et al diastolic collapse: 2D (early diastolic inversion of the right ventricular free wall that varied with respiration) NPV, negative predictive value (true negatives/true negatives + false nega value (true positive/true positives + false positives). *Some of the values differ from those reported in the original studies; data from patients with "equivocal" tamponade have not been used. †True positives/true positives + false negatives. ‡ True negatives/true negatives + false positives.

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Figure 29-9 A, Off-axis apical view of a moderate pericardial effusion (PE), pleural effusion (PLE), and a metastatic tumor (TU) deposit in a patient with

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known small cell lung cancer. There is right atrial diastolic collapse. B, A subcostal view of the same patient showing tumor deposit on the right atrium (RA), as well as the moderate pericardial effusion. LA, left atrium; LV, left ventricle; RV, right ventricle.

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degree of right atrial collapse bears an imprecise relationship to the intrapericardial pressure or hemodynamic effect of the fluid.[46] [56] Conversely, the right atrial inversion time index (total number of frames showing inversion divided by the total number of frames in the cycle), has been reported to have a high sensitivity and specificity for the presence of clinical cardiac tamponade[56] (see Table 29-2) . It should be noted that respiration and the same factors that interfere with right ventricular diastolic collapse, although less well studied, may diminish right atrial collapse. Ventricular pacing also has been reported to affect the accuracy of this sign.[56] Left Atrial Compression, Inversion, or Collapse

Normally, left atrial pressure is higher than right atrial pressure throughout the cardiac cycle; therefore, one can speculate that left atrial compression, inversion, or collapse is less sensitive but more specific than right atrial findings for tamponade. This assumption also has been borne out in studies. [55] Left atrial collapse may be useful in settings of abnormally high rightsided pressures (e.g., pulmonary embolism) and may be the only sign of tamponade in the postoperative patient.[48] Phasic Respiratory Changes and Plethora of the Inferior Vena Cava

Decreased phasic respiratory changes and plethora of the inferior vena cava have been reported in tamponade.[33] It is well recognized that multiple other conditions can lead to this finding, and it therefore has a high sensitivity but low specificity for tamponade[33] (see Table 29-2) . Other M-mode and Two-Dimensional Features of Altered Pericardial Pressure

Other features suggested in the echocardiographic literature to indicate the presence of a hemodynamic effect of tamponade are predominantly related to the increases in right-sided flow and the ventricular interaction that occurs with raises in intrapericardial pressures. These features include decreased mitral valve opening with inspiration (with a decrease in the

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excursion of the anterior leaflet and diminished EF slope),[57] [58] and increases in right and decreases in left heart sizes with inspiration.[59] In general, we feel these physiologic phenomena are better assessed in the modern era with Doppler flow recordings than with M-mode or twodimensional recordings. Determination of Pericardial Fluid Volume Although two-dimensional (using a prolate ellipse model[60] ) and especially three-dimensional echocardiography[61] have the ability to determine the volume of a pericardial effusion, we find our referring physicians prefer characterization of the effusion as minimal, small, moderate, or large in size. For circumferential pericardial effusions, we characterize any pericardial effusion with less than 5 mm of pericardial separation (corresponding to a fluid volume of 50 to 100 mL) as minimal, 5 to 10 mm of separation as small (corresponding to a fluid volume of 100 to 250 mL), 10 to 20 mm of separation as moderate (corresponding to a fluid volume of 250 to 500 mL), and greater than 20 mm of separation as large (corresponding to a fluid volume of > 500 mL). We also routinely report (for any moderate or large effusion, or any effusion with a hemodynamic effect) the location of the fluid, loculations, the presence of an appropriate approach for percutaneous drainage, and our estimation of the risk of complications from percutaneous intervention. Localized and Loculated Pericardial Fluid Collections In some cases, loculation or combinations of localized with more generalized cardiac compression can occur, making both the diagnosis and potential contribution of the pericardial process to cardiac pathology difficult. In our experience and that of others,[46] [47] [48] this situation is especially problematic following cardiac surgery. In these instances, it is not possible to rely on the absence of traditional echocardiographic markers of hemodynamic effect of the fluid to rule out a contribution of the pericardial fluid. A careful search for localized chamber compression, echogenic structures suggesting collections of blood inside or adjacent to the pericardial space, and nontraditional markers of hemodynamic perturbations, such as left ventricular or left atrial diastolic collapse,[62] must be performed. Transesophageal echocardiography often adds incremental information. [63] [64] [65] If doubt remains as to the presence or hemodynamic effect of a collection, alternative imaging techniques, catheter-based hemodynamic monitoring with volume manipulation, or even surgical exploration may be required for both diagnostic and therapeutic purposes.

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Often the most important role of the echocardiogram is to rule out other cardiac causes of the patient's clinical state.

[48]

Doppler Echocardiography The determination of variations in intracardiac flows with respiration, specifically using pulsed wave Doppler, has proved to aid clinical decision making in the treatment of patients with pericardial effusions. During inspiration, intrathoracic, intrapericardial, and intracardiac pressures normally decrease in unison and to a similar extent. There is normally a small augmentation of right-sided transvalvular flows and a decrease in left-sided transvalvular flows accompanying inspiration[66] because of a combination of increased venous return secondary to decreased intrathoracic pressure and a decrease in pulmonary vascular impedance and ventricular interaction. With accumulation of pericardial fluid there is a blunting of transmission of pressure changes from the intrathoracic compartment to 650

the intrapericardial compartment and subsequently to the intracardiac structures that are surrounded by the pericardium.[66] Continued transmission of intrathoracic pressure to cardiac structures located outside the pericardium occurs. Because of the presence of lower right-sided pressures, larger changes in transvalvular flows on the right than on the left occur as fluid accumulates. [67] A summary of the magnitude and direction of flow disturbance in intracardiac flows are presented in Table 29-3 . The magnitude of this flow disturbance is greater, and statistical separation of values from normal occurs earlier, with right-sided flows than with leftsided flows. Because of ventricular interaction, however, aortic and mitral decreases in flow velocity do occur with inspiration (part of the mechanism of pulsus paradoxus). Although most of the literature has concentrated on changes in transvalvular flow velocities, a decrease in left ventricular ejection time and left ventricular inflow duration also occur.[67] The combination of a decrease in both of these quantities results in an increase in left ventricular isovolumetric relaxation time as measured by echocardiography with inspiration.[67] The vena cava and pulmonary veins are less enclosed and therefore less influenced by pericardial forces. More subtle flow disturbances are seen in these structures.[68]

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Clinically, we depend primarily on left ventricular and right ventricular inflow variations with respiration. We find they are the most easily obtainable in dyspneic patients, who, because of orthopnea, are reluctant to lay flat. The Role of Echocardiography in Patient Management It is important to recognize that significant decreases in cardiac output and increases in filling pressures occur before the appearance of clinical tamponade (which we define as a fall in mean arterial pressure and a pulsus paradoxus > 10 mm Hg caused by raised pericardial pressure).[49] As well, the clinical transformation from stable to unstable can occur abruptly with small changes in any of the factors that influence the hemodynamic effect of a given pericardial effusion. Therefore, echocardiography plays a pivotal role in the management of patients with pericardial effusion, because some echocardiographic findings occur when intrapericardial pressure is elevated, but before clinical compromise. It must be appreciated that the physiologic effects of an increasing pericardial effusion lie on a continuum, and therefore any separation into distinct stages is arbitrary. We find it useful clinically, however, to divide patients with pericardial effusions echocardiographically into three hemodynamic categories. First, we describe those without echocardiographic evidence of hemodynamic compromise (no right ventricular collapse, no right or left atrial collapse, physiologic changes in intracardiac flows with inspiration) as "no evidence of hemodynamic effect" on the echocardiographic report. Second, we describe those with any degree of right ventricular diastolic collapse, prolonged (>35% of the cardiac cycle) right atrial collapse, or marked respiratory flow variation (>25% left ventricular or >80% right ventricular early filling [E] velocity changes with inspiration) as showing echocardiographic indications of "tamponade." Tamponade is in quotation marks to acknowledge our understanding that tamponade is a clinical syndrome. Thirdly, we report patients that fit into neither of the abovementioned categories as having echocardiographic indicators of elevated pericardial pressure without echocardiographic features of tamponade. These rules are applicable to patients with relatively normal pericardial and cardiac physiology; however, it cannot be overemphasized that with localized cardiac compression, or abnormal physiological states, hemodynamic compromise may be present owing to elevated pericardial pressure without any classic M-mode, two-dimensional or Doppler echocardiographic indicators of raised intrapericardial pressure.[46] [47] [48]

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Echocardiographically Guided Pericardiocentesis Before two-dimensional echocardiography, percutaneous pericardiocentesis was viewed with trepidation by even the most experienced clinicians. In cardiac catheterization laboratories, with the procedure performed under continuous fluoroscopic, electrocardiographic, and hemodynamic monitoring, experienced clinicians in large volume centers achieved success rates of only 86% in obtaining fluid, with death rates of 4%, and a further 4% risk of other major complications.[69] In contrast, echocardiographically guided series have indicated success rates of greater than 99%, with no deaths and total complication rates of 3% to 5% (pneumothorax, hemothorax, subsequent purulent pericarditis, transient ventricular tachycardia). [70] [71] [72] Multiple techniques exist for echocardiographically guided pericardiocentesis, [72] [73] [74] and the best technique in an individual case depends on the amount and location of the pericardial fluid, the clinical status of the patient, and the operator's experience. In all but emergency situations, we prefer to perform the procedure in our coronary care unit, under continuous echocardiographic, electrocardiographic, noninvasive or invasive blood pressure, and oximetry monitoring. The steps we employ for nonemergency echocardiographically guided pericardiocentesis are as follows: 1. The patient's echocardiogram is reviewed to determine the amount and location of pericardial fluid, the presence of loculations, the possible percutaneous approaches, and any underlying cardiac pathology. 2. As a minimum the patient's chart is reviewed; if needed a history is taken and a directed physical examination is performed. We determine the clinical effects of the pericardial effusion, the presence of any bleeding diathesis, and underlying general medical or specific cardiac issues that could modify our approach (e.g., avoidance of areas documented to have adhesions, allergies). 3. Laboratory tests are ordered or reviewed. As a minimum we suggest a hemoglobin, platelet count, electrolytes, creatinine, INR, * and APTT. † Any coagulopathy or * INR, international normalized ratio. † APTT, activated partial thromboplastin time. 651

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652

electrolyte disturbance (especially hypokalemia) should be corrected. If the patient is significantly anemic, a cross-match or blood type and antibody screen should be performed. In the presence of severe renal failure, we may choose to administer desmopressin (DDAVP) to improve platelet function. 4. Informed consent is obtained, a large bore peripheral IV is placed, a noninvasive blood pressure cuff (if an arterial line is not present) is applied and readings taken every 2 minutes. Oxygen (O2 ) saturation monitoring is performed and O2 by nasal prongs is provided.

5. If an echocardiographer is performing the study, we prefer to image the patient ourselves to obtain a "feel" for the correct approach. We choose the approach that provides the most direct route to the largest collection of fluid, as far removed from vital structures as possible. Special attention should be made to avoid the internal thoracic arteries (located 0.5 to 2 cm lateral to the sternum). We then mark a proposed entry point (with a permanent marker or indentation of the skin with the top of a syringe cap), and then re-image from this location to determine the depth to the fluid, the depth to the nearest cardiac structure, and the correct angle. We then determine if an acoustic window is available, remote to the proposed puncture site (that will not interfere with the sterility of the procedure), to directly visualize the procedure. If so, we have our sonographers image from this window while the procedure is performed. If not, we cover the imaging probe with a sterile cover and have it available for the physician performing the procedure to use if needed. 6. We then prepare and drape the patient and open a commercial pericardiocentesis kit. If the effusion is at a depth greater than 5 cm from the surface, or if there is less than 2 cm of fluid between the pericardium and any cardiac structure at the proposed puncture site, we prepare a three-way stop-cock device for injection of echo contrast. This is performed by connecting two 10-mL Luer lock syringes, one syringe filled with 5 mL of sterile saline agitated with 0.25 to 0.5 mL of air (similar to the set up used for a peripheral venous contrast study). We perform the procedure while wearing sterile gown and gloves. 7. The skin (including an area for an eventual suture) and subcutaneous tissue along the proposed approach are then thoroughly anesthetized

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with 1% or 2% lidocaine using a small (19- to 25-gauge) needle. We use a needle, if possible, that is long enough to reach the pericardial fluid, but not any cardiac structures. Adequate local anesthetic is a must. The needle is advanced along the previously determined pathway until the pericardial fluid is reached, or the predetermined appropriate length of the needle is inserted. 8. We then attach a needle (that we have confirmed will accommodate the guidewire) to a 10-mL Luer lock syringe with 5 mL of 1% lidocaine. Under direct imaging if possible, the needle is advanced until pericardial fluid is obtained, or a depth of needle is inserted that could contact a cardiac structure (i.e., if the pericardial fluid is 4 cm from the skin surface at the entry point and there is 2 cm of fluid in this area, we limit our insertion to <6 cm). Constant aspiration during the advancement of the needle followed by a slight pause for injection should be performed to ensure that a plug of tissue or clot is not occluding the needle tip. A small amount of additional lidocaine may need to be injected during the needle advancement. There is a characteristic "feel" to the needle's contact with pericardium and its puncture. Because of the tomographic nature of two-dimensional imaging and the high reflectivity of the pericardial puncture needle, care must be taken to avoid misinterpretation of the image during the procedure. Direct visualization does not substitute for clinical judgment or allow one to continue insertion of the needle to depths where cardiac puncture can occur. 9. Once the pericardium is entered (Fig. 29-10) , there should be free flow of fluid into the syringe. If there is any doubt as to the structure punctured, and in all cases of small effusions, we confirm the position of the needle with the injection of 0.5 to 1.0 mL of agitated saline through the needles (using the three-way stop-cock configuration described earlier). Visualization of the contrast only in the pericardial space confirms the needle position (see Fig. 29-10) . A J-shaped guidewire is introduced, once again under direct vision, into the pericardial space. The needle is withdrawn, a small "nick" is placed in the skin at the wire's entry point, and dilators are employed. A pigtail catheter is placed over the wire into the pericardial space, the guidewire is removed, and a 50-mL Luer lock syringe is attached to withdraw fluid for analysis. Once 50 to 500 mL of fluid has been withdrawn, we attach a suction drainage device to the pigtail and suture the pigtail in place. If it is clear we are in the pericardial space after the initial puncture, we often omit the stage of contrast injection into the pericardium. In these

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cases, we advance the needle an additional 1 to 2 mm after the initial pericardial puncture, remove the 10-mL syringe, and attach a 50-mL Luer lock syringe to withdraw fluid for analysis. The needle in the pericardial space must not be allowed to advance to depths where a cardiac structure could be punctured. The 50-mL Luer lock syringe is removed and the guidewire is advanced. Care should be taken to keep the proximal 5 to 10 cm of the external pigtail sterile in case repositioning is required. We routinely send pericardial fluid for a gram and acid fast bacillus stain, culture, cell count, and cytology. Other more specialized tests may be ordered depending on the clinical scenario. The yield of routine tests appears to be low.[75] One report suggests that determination of adenosine deaminase and carcinoembryonic antigen may be useful in separating neoplastic, tuberculous, and viral pericardial effusions.[76] Animal work indicates a possible future role for the determination of pericardial fluid pH.[77] 10. The puncture site is treated with an iodine-based antibacterial and the site is covered with an occlusive dressing. Once drainage from the catheter ceases we reimage the patient and remove the catheter once only a minimal amount of fluid remains. Analgesia is given as required to eliminate the discomfort, usually mild, from the indwelling catheter. TABLE 29-3 -- Respiratory Variation in Intraca

Study Pandian et al (1985)

Normal Tampo Subjects INSPIRATION EXPIRATION INSPIRATION E

[119]

Mitral mean flow velocity

Tricuspid mean flow velocity

9 dogs (at baseline, effusion without tamponade, and with tamponade) ↓ 10 ± 2% 3 patients (all with tamponade) ↑ 17 ± 2%

↓ 42 ± 3% ↑ 117 ± 19%

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Leeman et al (1987) 19 (11 [120] tamponade) Mitral ↓ 8% ↓ 35% TVI Tricuspid ↑ 9% ↑ 80% TVI Aortic ↓ 3% ↓ 33% TVI Pulmonary TVI ↑ 9% ↑ 86% Appleton et (1988) 27 (7 al[67] tamponade) Mitral E wave velocity (cm/s) 82 ± 17 85 ± 18 39 ± 12 6 Tricuspid E wave velocity (cm/s) 64 ± 10 56 ± 9 60 ± 6 3 Aortic flow velocity (cm/s) 109 ± 9 113 ± 9 80 ± 22 IVRT 72 ± 14 6 (msec) 74 ± 15 117 ± 39 E, early diastolic filling wave of the left (mitral) or right (tricuspid) ventri time; TVI, time velocity integral. To remove the catheter, we give the patient a small IV dose of sedative and analgesia if possible, disconnect the pigtail from the drainage device, and remove the dressing. We 653

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Figure 29-10 Off-axis, short-axis subcostal view of a large pericardial effusion (PE) during pericardiocentesis. A, The needle (NE) has been advanced into the pericardial space under direct visualization. B, Marked echogenicity of the pericardial space after 1 mL of saline agitated with 0.05 mL of air is injected, confirming that the needle is in the pericardial space. LV, left ventricle.

then cut the suture, attach a 10- to 50-mL Luer lock syringe (depending on the amount of residual effusion) to the pigtail, and withdraw at a rate of 2 to 5 cm per second while applying gentle suction on the system with the syringe. To reposition the catheter, we give the patient a small IV dose of sedative and analgesia if possible, and with sterile technique, disconnect the pigtail from the drainage device, remove the dressing, cut the suture, attach a 10-mL Luer lock syringe to the pigtail, and advance or withdraw the catheter up to 5 cm per second while applying gentle suction on the system with the syringe. In an emergency situation, the physicians at our institution still prefer to have echocardiographic confirmation of an effusion, if at all possible. When effusions are found, they use the information obtained to guide the percutaneous approach. Most often, this occurs during percutaneous interventions. This so-called "rescue pericardiocentesis" is successful in relieving tamponade in 99% of cases, and it may be the only and definitive therapy in 82% of cases.[71] Often the patient is prepared and draped by the time the equipment and echocardiographer arrive at the catheterization laboratory. Usually, the interventional cardiologist performs the pericardiocentesis, with the echocardiographer performing the imaging and guiding. Outpatient echocardiographically guided pericardiocentesis,[78] percutaneous pericardial biopsy,[79] as well as the creation of pericardial windows with balloon techniques[80] [81] [82] and sclerotherapy[83] have been described. Imaging probes that allow needle insertion in the center of the imaging plane are available. [84]

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Acute Pericarditis The clinical syndrome of acute pericarditis frequently includes chest pain, fever, malaise, and less often myalgia, cough, dysphagia, and hiccup. [2] On physical examination, the hallmark of acute pericarditis is the pericardial friction rub. The sound is usually scratchy, superficial ("walking on dry snow") and may be monophasic, biphasic, or triphasic. The electrocardiographic features, predominantly those of widespread elevation of ST segments (with upward concavity) and PR depression, with a characteristic evolution, are well described. [2] [85] The spectrum of the disease is vast, however, from virtually asymptomatic patients with minor electrocardiogram changes to a fulminant illness with extension of the inflammation to the myocardium (myopericarditis) and life-threatening hemodynamic compromise. [86] An echocardiogram is often ordered in patients in whom acute pericarditis is suspected. No echocardiographic feature is pathognomonic of the disease. Patients with uncomplicated viral pericarditis have a normal echocardiogram. The value of echocardiography in acute pericarditis lies in its unique ability to detect complications, at times aid in the diagnosis of the underlying etiology, or detect other cardiac processes that may account for the patient's clinical presentation. Complications include pericardial effusion, and in myopericarditis, ventricular systolic or diastolic dysfunction. The echocardiogram may reveal tumor (see Fig. 29-9) or a regional wall motion abnormality, suggesting previous myocardial infarction as an underlying etiology. A myriad of other cardiac diagnoses can mimic acute pericarditis, and the echocardiogram may be useful in this regard (e.g., detecting a vegetation and mitral regurgitation in a patient with fever and a systolic auscultatory event).

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We occasionally find echocardiography to be useful in patients presenting with chest pain (especially of <12-hours duration in which thrombolysis may be indicated) and electrocardiogram changes in which the differential diagnosis includes an acute coronary syndrome and pericarditis. The finding of a regional wall motion abnormality in an anatomic distribution without pericardial effusion suggests therapy toward an acute coronary syndrome is warranted. The finding of a pericardial effusion without a regional wall motion abnormality suggests pericarditis is more likely. Unfortunately, not even these findings are absolute, and thrombolytic therapy has been administered to patients in whom, in retrospect, the real diagnosis was pericarditis.[87] [88] In a substantial number of cases the echocardiogram is normal or shows pathology consistent with either diagnosis. In this case, we often proceed to immediate coronary angiography.

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Congenital Disorders of the Pericardium Congenital Absence of the Pericardium Congenital absence of the pericardium is a rare clinical entity. Most reported cases involve complete absence of the pericardium. Partial absence of the pericardium, either left or right, has also been reported. Reported symptoms in the literature include paroxysmal stabbing chest pain (largely nonexertional), heart murmur, an abnormal chest x-ray study, and rarely incarceration of the left atrium or ventricle.[19] The echocardiographic features of congenital absence of the pericardium include unusual echocardiographic windows, cardiac hypermotility, abnormal ventricular septal motion, and abnormal swinging motion of the heart.[89] At least one, and usually two of these findings, are reported in all patients with complete absence of the pericardium.[89] In patients with partial absence, displacement and enlargement of a pericardial structure as it herniates through the pericardium may be noted. This finding has significant importance as case reports exist of coronary artery obstruction,[90] [91] [92] [93] left atrial strangulation,[94] [95] herniation of the left atrium causing syncope, [96] or herniation of the left or right ventricle causing mitral or tricuspid regurgitation. [97] [98] Although a diagnosis of complete absence of the pericardium may be established with a combination of clinical presentation, chest radiography and echocardiography, partial absence of the pericardium often requires ancillary imaging techniques to fully delineate the nature and extent of the defect. In this regard, magnetic resonance imaging has proved to be especially useful.[19] [99] [100] Reports of combined congenital pericardial and diaphragmatic defects also exist.[98] Pericardial Cysts Pericardial cysts are congenital, benign intrathoracic lesions thought to be remnants of a defect in embryologic development of the pericardium. Prenatal diagnosis has been reported.[101] They usually involve the left or

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right costophrenic angle, although they may be found adjacent to any cardiac structure.[20] [102] [103] Rarely, hydatid pericardial cysts[104] or a cardiac hemangioma[105] may have echocardiographic features mimicking pericardial cysts. Reported complications of pericardial cysts include cardiac tamponade,[106] [107] hemorrhage,[108] or erosion of cardiac structures. [102] [103] [109] , The echocardiographic hallmark of a pericardial cyst is a round or oval echo-free structure, related to one of the cardiac chambers, from which it is separated by a definite wall of echoes.[110] [111] The presence of internal echoes or a more solid structure should alert the clinician to the possibility of a less benign process. A report exists of a pericardial cyst that was not diagnosed on transthoracic echocardiography being apparent on a transesophageal study.[112] Differentiation of benign pericardial cysts from other cardiac pathology appears important, as numerous therapeutic, relatively noninvasive treatments exist for benign pericardial cysts. Treatments include videoscopic resection,[113] ethanol sclerosis,[114] or needle aspiration and drainage.[115] [116]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Acknowledgments The authors would like to thank our cardiac sonographers, Rosalind Gilles, Kitty Perry, Vickie Echelli, Julie Hall, and Patricia Walley, for providing the images and advice on the chapter, and Leanne Williams for help in preparation.

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References 1. Holt J: The normal pericardium. Am J Cardiol 1970;26:455–465. 2. Hoit B: Pericardial heart disease. Curr Probl Cardiol 1997;22:353–400. 3. Spodick D: The normal and diseased pericardium: Current concepts of pericardial

physiology, diagnosis and treatment. J Am Coll Cardiol 1983;1:240–251. 4. Baker A, Dani R, Smith E, et al: Quantitative assessment of independent

contributions of pericardium and septum to direct ventricular interaction. Am J Physiol 1998;275:H476–483. 5. Bernard H: The functions of the pericardium. J Physiol 1898;22:43. 6. Smiseth O, Refsum H, Tyberg J: Pericardial pressure assessed by right atrial

pressure: A basis for calculation of left ventricular transmural pressure. Am Heart J 1984;108:603–605. 7. Slinker BK, Ditchey RV, Bell SP, Le Winter MM: Right heart pressure does not

equal pericardial pressure in the potassium chloride–arrested canine heart in situ. Circulation 1987;76:357–362. 8. Freeman G, Le WM: Pericardial adaptations during chronic cardiac dilation in dogs.

Circ Res 1984;54:294–300. 9. Shirato K, Shabetai R, Bhargava V, Franklin D, Ross JJ: Alteration of the left

ventricular diastolic pressure–segment length relation produced by the pericardium. Effects of cardiac distension and afterload reduction in conscious dogs. Circulation 1978;57:1191–1198. 10. Belenkie I, Dani R, Smith E, Tyberg J: The importance of pericardial constraint in

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experimental pulmonary embolism and volume loading. Am Heart J 1992;123:733– 742. 11. Atherton J, Moore T, Lele S, et al: Diastolic ventricular interaction in chronic heart

failure [see comments]. Lancet 1997;349:1720–1724. 12. Brinker J, Weiss J, Lappe D, et al: Leftward septal displacement during right

ventricular loading in man. Circulation 1980;61:626–633. 13. Hoit B, Dalton N, Bhargava V, Shabetai R: Pericardial influences on right and left

ventricular filling dynamics. Circ Res 1991;68:197–208. 655

14. Lorell B, Palacios I, Daggett W, et al: Right ventricular distension and left

ventricular compliance. Am J Physiol 1981;240:H87–98. 15. Belenkie I, Dani R, Smith E, Tyberg J: Ventricular interaction during experimental

acute pulmonary embolism. Circulation 1988;78:761–768. 16. Atherton J, Moore T, Thomson H, Frenneaux M: Restrictive left ventricular filling

patterns are predictive of diastolic ventricular interaction in chronic heart failure [published erratum appears on p 744]. J Am Coll Cardiol 1998;31:413–418. 17. Martin R, Rakowski H, French J, Popp R: Localization of pericardial effusion with

wide angle phased array echocardiography. Am J Cardiol 1978;42:904–912. 18. Martin R, Bowden R, Filly K, Popp R: Intrapericardial abnormalities in patients

with pericardial effusion. Findings by two-dimensional echocardiography. Circulation 1980;61:568–572. 19. Gatzoulis M, Munk M, Merchant N, et al: Isolated congenital absence of the

pericardium: Clinical presentation, diagnosis, and management. Ann Thorac Surg 2000;69:1209–1215. 20. Salyer D, Salyer W, Eggleston J: Benign developmental cysts of the mediastinum.

Arch Pathol Lab Med 1977;101:136–139. 21. Larose E, Ducharme A, Mercier L, et al: Prolonged distress and clinical

deterioration before pericardial drainage in patients with cardiac tamponade. Can J Cardiol 2000;16:331–336.

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22. Pandian N, Skorton D, Kieso R, Kerber R: Diagnosis of constrictive pericarditis by two-dimensional echocardiography: Studies in a new experimental model and in patients. J Am Coll Cardiol 1984;4:1164–1173. 23. Ling L, Oh J, Tei C, et al: Pericardial thickness measured with transesophageal

echocardiography: Feasibility and potential clinical usefulness. J Am Coll Cardiol 1997;29:1317–1323. 24. Kern M, Aguirre F: Interpretation of cardiac pathophysiology from pressure

waveform analysis: Pericardial compressive hemodynamics, Part III. Cathet Cardiovasc Diagn 1992;26:152–158. 25. Hatle L, Appleton C, Popp R: Differentiation of constrictive pericarditis and

restrictive cardiomyopathy by Doppler echocardiography [see comments]. Circulation 1989;79:357–370. 26. Voelkel A, Pietro D, Folland E, et al: Echocardiographic features of constrictive

pericarditis. Circulation 1978;58:871–875. 27. Gibson T, Grossman W, McLaurin L, et al: An echocardiographic study of the

interventricular septum in constrictive pericarditis. Br Heart J 1976;38:738–743. 28. Chandraratna P, Aronow W, Imaizumi T: Role of echocardiography in detecting

the anatomic and physiologic abnormalities of constrictive pericarditis. Am J Med Sci 1982;283:141–146. 29. Janos G, Arjunan K, Meyer R, et al: Differentiation of constrictive pericarditis and

restrictive cardiomyopathy using digitized echocardiography. J Am Coll Cardiol 1983;1:541–549. 30. Hinds S, Reisner S, Amico A, Meltzer R: Diagnosis of pericardial abnormalities by

2D-echo: A pathology-echocardiography correlation in 85 patients. Am Heart J 1992;123:143–150. 31. Morgan J, Raposo L, Clague J, et al: Restrictive cardiomyopathy and constrictive

pericarditis: Non-invasive distinction by digitised M mode echocardiography. Br Heart J 1989;61:29–37. 32. Engel P, Fowler N, Tei C, et al: M-mode echocardiography in constrictive

pericarditis. J Am Coll Cardiol 1985;6:471–474. 33. Himelman RB, Kircher B, Rockey DC, Schiller NB: Inferior vena cava plethora

with blunted respiratory response: A sensitive echocardiographic sign of cardiac

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tamponade. J Am Coll Cardiol 1988;12:1470–1477. 34. Oh J, Hatle L, Seward J, et al: Diagnostic role of Doppler echocardiography in

constrictive pericarditis [see comments]. J Am Coll Cardiol 1994;23:154–162. 35. Oh J, Tajik A, Appleton C, et al: Preload reduction to unmask the characteristic

Doppler features of constrictive pericarditis. A new observation [see comments]. Circulation 1997;95:796–799. 36. Klodas E, Nishimura R, Appleton C, et al: Doppler evaluation of patients with

constrictive pericarditis: Use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction [see comments]. J Am Coll Cardiol 1996;28:652– 657. 37. Klein A, Cohen G, Pietrolungo J, et al: Differentiation of constrictive pericarditis

from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943. 38. Oki T, Tabata T, Yamada H, et al: Right and left ventricular wall motion velocities

as diagnostic indicators of constrictive pericarditis. Am J Cardiol 1998;81:465–470. 39. Garcia MJ, Rodriguez L, Ares M, et al: Differentiation of constrictive pericarditis

from restrictive cardiomyopathy: Assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108–114. 40. Singh S, Wann LS, Schuchard GH, et al: Right ventricular and right atrial collapse

in patients with cardiac tamponade—a combined echocardiographic and hemodynamic study. Circulation 1984;70:966–971. 41. Rifkin R, Isner J, Carter B, Bankoff M: Combined posteroanterior subepicardial fat

simulating the echocardiographic diagnosis of pericardial effusion. J Am Coll Cardiol 1984;3:1333–1339. 42. Wada T, Honda M, Matsuyama S: Extra echo spaces: Ultrasonography and

computerised tomography correlations. Br Heart J 1982;47:430–438. 43. Savage D, Garrison R, Brand F, et al: Prevalence and correlates of posterior extra

echocardiographic spaces in a free-living population based sample (the Framingham study). Am J Cardiol 1983;51:1207–1212. 44. Lopez-Sendon J, Garcia-Fernandez M, Coma-Canella I, et al: Identification of

blood in the pericardial cavity in dogs by two-dimensional echocardiography. Am J Cardiol 1984;53:1194–1197.

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45. Reddy P, Curtiss E, O'Toole J, Shaver J: Cardiac tamponade: Hemodynamic

observations in man. Circulation 1978;58:265–272. 46. Kronzon I, Cohen ML, Winer HE: Cardiac tamponade by loculated pericardial

hematoma: Limitations of M-mode echocardiography. J Am Coll Cardiol 1983;1:913– 915. 47. Duvernoy O, Larsson S, Persson K, et al: Pericardial effusion and pericardial

compartments after open heart surgery. An analysis by computed tomography and echocardiography. Acta Radiol 1990;31:41–46. 48. Chuttani K, Tischler M, Pandian N, et al: Diagnosis of cardiac tamponade after cardiac surgery: Relative value of clinical, echocardiographic, and hemodynamic signs. Am Heart J 1994;127:913–918. 49. Leimgruber PP, Klopfenstein HS, Wann LS, Brooks HL: The hemodynamic

derangement associated with right ventricular diastolic collapse in cardiac tamponade: An experimental echocardiographic study. Circulation 1983;68:612–620. 50. Gaffney F, Keller A, Peshock R, et al: Pathophysiologic mechanisms of cardiac

tamponade and pulsus alternans shown by echocardiography. Am J Cardiol 1984;53:1662–1666. 51. Cogswell TL, Bernath GA, Wann LS, et al: Effects of intravascular volume state

on the value of pulsus paradoxus and right ventricular diastolic collapse in predicting cardiac tamponade. Circulation 1985;72:1076–1080. 52. Klopfenstein HS, Cogswell TL, Bernath GA, et al: Alterations in intravascular

volume affect the relation between right ventricular diastolic collapse and the hemodynamic severity of cardiac tamponade. J Am Coll Cardiol 1985;6:1057–1063. 53. Cogswell TL, Bernath GA, Keelan MH Jr, et al: The shift in the relationship

between intrapericardial fluid pressure and volume induced by acute left ventricular pressure overload during cardiac tamponade. Circulation 1986;74:173–180. 54. Kaplan L, Epstein S, Schwartz S, et al: Clinical, echocardiographic, and

hemodynamic evidence of cardiac tamponade caused by large pleural effusions. Am J Respir Crit Care Med 1995;151:904–908. 55. Kronzon I, Cohen ML, Winer HE: Diastolic atrial compression: A sensitive

echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 1983;2:770–775. 56. Gillam L, Guyer D, Gibson T, et al: Hydrodynamic compression of the right

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atrium: A new echocardiographic sign of cardiac tamponade. Circulation 1983;68:294–301. 57. D'Cruz I, Cohen H, Prabhu R, Glick G: Diagnosis of cardiac tamponade by

echocardiography: Changes in mitral valve motion and ventricular dimensions, with special reference to paradoxical pulse. Circulation 1975;52:460–465. 58. Vignola P, Pohost G, Curfman G, Myers G: Correlation of echocardiographic and

clinical findings in patients with pericardial effusion. Am J Cardiol 1976;37:701–707. 656

59. Settle H, Adolph R, Fowler N, et al: Echocardiographic study of cardiac

tamponade. Circulation 1977;56:951–959. 60. D'Cruz I, Hoffman P: A new cross sectional echocardiographic method for

estimating the volume of large pericardial effusions. Br Heart J 1991;66:448–451. 61. Vazquez de Prada JA, Jiang L, Handschumacher M, et al: Quantification of

pericardial effusions by three-dimensional echocardiography. J Am Coll Cardiol 1994;24:254–259. 62. Chuttani K, Pandian N, Mohanty P, et al: Left ventricular diastolic collapse. An

echocardiographic sign of regional cardiac tamponade. Circulation 1991;83:1999– 2006. 63. Kochar G, Jacobs L, Kotler M: Right atrial compression in postoperative cardiac

patients: Detection by transesophageal echocardiography. J Am Coll Cardiol 1990;16:511–516. 64. Jadhav P, Asirvatham S, Craven P, et al: Unusual presentation of late regional

cardiac tamponade after aortic surgery. Am J Card Imaging 1996;10:204–206. 65. Brooker R, Farah M: Postoperative left atrial compression diagnosed by

transesophageal echocardiography. J Cardiothorac Vasc Anesth 1995;9:304–307. 66. Sharp J, Bunnell I, Holland J, et al: Hemodynamics during induced cardiac

tamponade in man. Am J Med 1960;29:640–646. 67. Appleton C, Hatle L, Popp R: Cardiac tamponade and pericardial effusion:

Respiratory variation in transvalvular flow velocities studied by Doppler

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echocardiography. J Am Coll Cardiol 1988;11:1020–1030. 68. Nishimura R, Housmans P, Hatle L, Tajik A: Assessment of diastolic function of

the heart: Background and current applications of Doppler echocardiography. Part I. Physiologic and pathophysiologic features. Mayo Clin Proc 1989;64:71–81. 69. Krikorian J, Hancock E: Pericardiocentesis. Am J Med 1978;65:808–814. 70. Callahan J, Seward J, Nishimura R, et al: Two-dimensional echocardiographically

guided pericardiocentesis: Experience in 117 consecutive patients. Am J Cardiol 1985;55:476–479. 71. Tsang T, Freeman W, Barnes M, et al: Rescue echocardiographically guided

pericardiocentesis for cardiac perforation complicating catheter-based procedures. The Mayo Clinic experience. J Am Coll Cardiol 1998;32:1345–1350. 72. Salem K, Mulji A, Lonn E: Echocardiographically guided pericardiocentesis—the

gold standard for the management of pericardial effusion and cardiac tamponade. Can J Cardiol 1999;15:1251–1255. 73. Pandian N, Brockway B, Simonetti J, et al: Pericardiocentesis under two-

dimensional echocardiographic guidance in loculated pericardial effusion. Ann Thorac Surg 1988;45:99–100. 74. Tsang T, Freeman W, Sinak L, Seward J: Echocardiographically guided

pericardiocentesis: Evolution and state-of-the-art technique. Mayo Clin Proc 1998;73:647–652. 75. Mueller X, Tevaearai H, Hurni M, et al: Etiologic diagnosis of pericardial disease:

The value of routine tests during surgical procedures. J Am Coll Surg 1997;184:645– 649. 76. Koh K, In H, Lee K, et al: New scoring system using tumor markers in diagnosing

patients with moderate pericardial effusions. Int J Cardiol 1997;61:5–13. 77. Edwards N: The diagnostic value of pericardial fluid pH determination. J Am

Anim Hosp Assoc 1996;32:63–67. 78. Ziskind A, Rodriguez S, Lemmon C, Burstein S: Percutaneous pericardial biopsy

as an adjunctive technique for the diagnosis of pericardial disease. Am J Cardiol 1994;74:288–291. 79. Uthaman B, Endrys J, Abushaban L, et al: Percutaneous pericardial biopsy:

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Technique, efficacy, safety, and value in the management of pericardial effusion in children and adolescents. Pediatr Cardiol 1997;18:414–418. 80. Kouvaras G, Polydorou A, Hatziantoniou G: Percutaneous balloon pericardiotomy

for management of cardiac tamponade in a patient with lung cancer and large pericardial effusion. Acta Cardiol 1994;49:549–553. 81. Iaffaldano RA, Jones P, Lewis BE, et al: Percutaneous balloon pericardiotomy: A

double-balloon technique. Cathet Cardiovasc Diagn 1995;36:79–81. 82. Law DA, Haque R, Jain A: Percutaneous balloon pericardiotomy: Non-surgical

treatment for patients with cardiac tamponade. W V Med J 1997;93:310–312. 83. Girardi L, Ginsberg R, Burt M: Pericardiocentesis and intrapericardial sclerosis:

effective therapy for malignant pericardial effusions. Ann Thorac Surg 1997;64:1422– 1428. 84. Hanaki Y, Kamiya H, Todoroki H, et al: New two-dimensional, echocardiographically directed pericardiocentesis in cardiac tamponade. Crit Care Med 1990;18:750–753. 85. Ginzton L, Laks M: The differential diagnosis of acute pericarditis from the normal

variant: New electrocardiographic criteria. Circulation 1982;65:1004–1009. 86. Remes J, Helin M, Vaino P, Rautio P: Clinical outcome and left ventricular

function 23 years after acute coxsackie virus myopericarditis. Eur Heart J 1990;11:182–188. 87. Millaire A, de Groote P, Decoulx E, et al: Outcome after thrombolytic therapy of nine cases of myopericarditis misdiagnosed as myocardial infarction. Eur Heart J 1995;16:333–338. 88. Ferguson D, Dewey R, Plante D: Clinical pitfalls in the noninvasive thrombolytic

approach to presumed acute myocardial infarction. Can J Cardiol 1986;2:146–151. 89. Connolly H, Click R, Schattenberg T, et al: Congenital absence of the pericardium:

Echocardiography as a diagnostic tool. J Am Soc Echocardiogr 1995;8:87–92. 90. Amiri A, Weber C, Schlosser V, Meinertz T: Coronary artery disease in a patient

with a congenital pericardial defect. Thorac Cardiovasc Surg 1989;37:379–381. 91. Rees A, Risher W, McFadden P, et al: Partial congenital defect of the left

pericardium: Angiographic diagnosis and treatment by thoracoscopic pericardiectomy:

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Case report. Cathet Cardiovasc Diagn 1993;28:231–234. 92. Larsen R, Behar V, Brazer S, et al: Chest pain presenting as ischemic heart disease.

Congenital absence of the pericardium. N C Med J 1994;55:306–308. 93. Saito R, Hotta F: Congenital pericardial defect associated with cardiac

incarceration: Case report. Am Heart J 1980;100:866–870. 94. Vanderheyden M, De SJ, Nellens P, et al: Herniation of the left atrial appendage

due to partial congenital absence of the left pericardium. Acta Clin Belg 1996;51:91– 93. 95. Finet G, Bozio A, Frieh J, et al: Herniation of the left atrial appendage through a

congenital partial pericardial defect. Eur Heart J 1991;12:1148–1149. 96. Hoorntje J, Mooyaart E, Meuzelaar K: Left atrial herniation through a partial

pericardial defect: A rare cause of syncope. Pacing Clin Electrophysiol 1989;12:1841– 1845. 97. Reginao E, Speroni F, Riccardi M, et al: Post-traumatic mitral regurgitation and

ventricular septal defect in absence of left pericardium. Thorac Cardiovasc Surg 1980;28:213–217. 98. Tosson R, Korbmacher B, Schulte H: Combined congenital pericardial and

diaphragmatic defects: A case report. Cardiovasc Surg 1996;4:57–59. 99. Croisille P, Revel D: Magnetic resonance imaging of cardiac and pericardial

disease. J Belge Radiol 1997;80:133–136. 100. Gassner I, Judmaier W, Fink C, et al: Diagnosis of congenital pericardial defects,

including a pathognomic sign for dangerous apical ventricular herniation, on magnetic resonance imaging. Br Heart J 1995;74:60–66. 101. Lewis K, Sherer D, Goncalves L, et al: Mid-trimester prenatal sonographic

diagnosis of a pericardial cyst. Prenat Diagn 1996;16:549–553. 102. Chopra P, Duke D, Pellett J, Rahko P: Pericardial cyst with partial erosion of the

right ventricular wall. Ann Thorac Surg 1991;51:840–841. 103. Williamson B, Spotnitz W, Gay S, Parekh S: Pericardial cyst. A rare mass

abutting the aorta. J Comput Tomogr 1988;12:264–266. 104. Gurlek A, Dagalp Z, Ozyurda U: A case of multiple pericardial hydatid cysts. Int

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J Cardiol 1992;36:366–368. 105. Landolphi D, Belkin R, Hjemdahl-Monsen C, LaFaro R: Cardiac cavernous

hemangioma mimicking pericardial cyst: Atypical echocardiographic appearance of a rare cardiac tumor. J Am Soc Echocardiogr 1997;10:579–581. 106. Bandeira F, de Sa V, Moriguti J, et al: Cardiac tamponade: An unusual

complication of pericardial cyst. J Am Soc Echocardiogr 1996;9:108–112. 107. Bava G, Magliani L, Bertoli D, et al: Complicated pericardial cyst: Atypical

anatomy and clinical course. Clin Cardiol 1998;21:862–864. 657

108. Borges A, Gellert K, Dietel M, et al: Acute right-sided heart failure due to

hemorrhage into a pericardial cyst [see comments]. Ann Thorac Surg 1997;63:845– 847. 109. Mastroroberto P, Chello M, Bevacqua E, Marchese A: Pericardial cyst with partial

erosion of the superior vena cava. An unusual case. J Cardiovasc Surg (Torino) 1996;37:323–324. 110. Pezzano A, Belloni A, Faletra F, et al: Value of two-dimensional

echocardiography in the diagnosis of pericardial cysts. Eur Heart J 1983;4:238–246. 111. Bini R, Nath P, Ceballos R, et al: Pericardial cyst diagnosed by two-dimensional

echocardiography and computed tomography in a newborn. Pediatr Cardiol 1987;8:47–50. 112. Padder F, Conrad A, Manzar K, et al: Echocardiographic diagnosis of pericardial

cyst. Am J Med Sci 1997;313:191–192. 113. Ferguson M: Thoracoscopic management of pericardial disease. Semin Thorac

Cardiovasc Surg 1993;5:310–315. 114. Kinoshita Y, Shimada T, Murakami Y, et al: Ethanol sclerosis can be a safe and

useful treatment for pericardial cyst. Clin Cardiol 1996;19:833–835. 115. Rice T: Benign neoplasms and cysts of the mediastinum. Semin Thorac

Cardiovasc Surg 1992;4:25–33.

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116. Volpino P, De Cesare A, Bononi M, et al: Pericardial cysts. Report on 9 treated

cases. G Chir 1997;18:811–814. 117. Armstrong WF, Schilt BF, Helper DJ, et al: Diastolic collapse of the right

ventricle with cardiac tamponade: An echocardiographic study. Circulation 1982;65:1491–1496. 118. Engel PJ, Hon H, Fowler NO, Plummer S: Echocardiographic study of right

ventricular wall motion in cardiac tamponade. Am J Cardiol 1982;50:1018–1021. 119. Pandian N, Wang S, Mclnerney K, et al: Doppler echocardiography in cardiac

tamponade: Abnormalities in tricuspid and mitral inflow responce to respiration in experimental and clinical tamponade. J Am Coll Cardiol 1985;5:485. 120. Leeman D, Riley M, Carl L, Come P: Doppler echocardiography in cardiac

tamponade: Exaggerated respiratory variation in transvalvular blood flow velocity integrals. J Am Coll Cardiol 1987;9:17A.

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658

Chapter 30 - The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Hannah A. Valantine MD Ingela Schnittger MD

Heart transplantation offers improved survival and an improved quality of life to patients with end-stage heart failure.[1] [2] Despite anticipated 1- and 5-year survival rates of 85% and 70%, respectively, however, acute and chronic rejection of the allograft are major factors that negatively affect patient outcome.[1] [3] Whereas survival during the initial year after transplantation is limited primarily by acute rejection and the complications associated with therapy, the most important factor affecting long-term survival is transplant coronary artery disease, which is probably a manifestation of chronic rejection. [4] The application of echocardiography to facilitate earlier diagnoses of acute rejection and allograft vascular disease has been a major challenge in heart transplantation. In clinical practice, surveillance for acute rejection, particularly during the initial year after transplantation, is based on routine endomyocardial biopsies performed at predefined intervals. This strategy, which involves at least 10 right-ventricular biopsies during the first year, has the potential for sampling error and is associated with complications inherent in such an

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invasive procedure, including damage to the tricuspid valve[5] furthermore, the biopsy procedures are expensive, time-consuming, and inconvenient for patients. Likewise, surveillance for allograft vascular disease by annual coronary angiography presents problems such as delayed diagnosis, underestimation of disease severity, [6] [7] and expense. These limitations have fueled the continuing challenge to develop noninvasive methods to detect acute rejection and to monitor response to therapy. The first two sections of this chapter review the echocardiographic methods that have been applied to acute rejection surveillance, with reference to normal cardiac allograft structure and function, and the pathophysiologic basis for the changes observed during acute rejection. Also discussed are the factors that limit established echocardiographic parameters that are used as primary end points for monitoring acute rejection. The third section of this chapter reviews the applications of stress echocardiography and intravascular ultrasonography for the diagnosis, 659

prognostic stratification, and applications to recent clinical trials of transplant coronary artery disease.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Normal Structural and Functional Characteristics of the Transplanted Heart M-mode Echocardiographic Characteristics of the Nonrejecting Heart The most striking abnormality recognizable from the M-mode recording is the abnormal septal motion with a net decrease in posterior motion of the left-sided septal endocardium, or frankly paradoxical septal motion (Fig. 30-1) , as observed after most cardiac operations. In heart transplant patients there is diminished septal thickening compared with that of normal subjects (38% vs. 57%).[8] This contrasts with normal or exaggerated systolic posterior-wall thickening, which results in normal left ventricular cavity dimensions and the percentage fractional shortening. Left ventricular posterior wall thickness and mass are increased however, compared with those of normal controls, [8] even when indexed for body surface area. Among the multiple factors examined, only systolic blood pressure was found to be an independent correlate of left Figure 30-1 M-mode recording of the left ventricle, parasternal long-axis view. Paradoxical septal motion (arrow) is noted with normal to slightly exaggerated posterior wall (PW) excursion. ECG, electrocardiogram; S, septum.

Figure 30-2 Influence of recipient atrial contraction on mitral leaflet motion. Top, Simultaneous phonocardiogram and M-mode mitral valve echocardiogram showing the influence of recipient atrial contraction (long arrows labeled P) on mitral valve motion. Recipient atrial contraction in late systole (beat 2) is associated with a steeper E-F slope than what is seen when atrial contraction occurs in early systole (beat 1) or diastole (beat 3). Recipient atrial contraction in early diastole results in a decrease in amplitude of the a-wave (beat 3). Bottom, Simultaneous contractions of donor (short arrows) and recipient atria result in increased amplitude of the a-wave in beat 3 compared with the

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preceding beat 2 of the bottom panel and with beat 3 of the top panel.

ventricular mass in the nonrejecting heart.[8] Digitized M-mode echocardiographic data indicate abnormal rates of posterior-wall motion during diastole, consistent with impaired relaxation even in the absence of acute rejection. M-mode echocardiographic examination reveals the donor left atrial dimension to be enlarged compared with normal. Dissociated recipient and donor atrial contraction also affects the M-mode echocardiographic appearance of mitral valve and posterior wall movement.[9] Typically, beatto-beat variation is seen in mitral valve motion that is dependent on the timing of recipient atrial contraction relative to the donor atrial cardiac cycle (Fig. 30-2) . Pericardial effusion is a common initial finding after heart transplantation, at a point when it is usually small and unassociated with any clinical sequelae, except for a pericardial friction rub. These small pericardial effusions rapidly become organized and evolve into a pattern of pericardial thickening that is often seen posteriorly when the left ventricular cavity is recorded (Fig. 30-3) . Two-Dimensional Echocardiographic Characteristics of the Nonrejecting Heart Transthoracic echocardiography offers a more detailed assessment of the structure and function of the orthotopically 660

Figure 30-3 M-mode recording of the left ventricle, parasternal longaxis view. A, Moderate pericardial effusion (solid arrow), with echogenicity suggesting formation of fibrinous strands, with the parietal pericardium moving forward in systole (open arrow). B, Similar view from the same patient with consolidation of effusion and only a pattern of pericardial thickening remaining (solid arrow). ECG, electrocardiogram; PW, posterior wall; S, septum.

transplanted cardiac allograft. The most characteristic anatomic finding relates to the surgical procedure of orthotopic heart transplantation, namely the biatrial anastomoses that are apparent as suture lines of enhanced

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Figure 30-4 Two-dimensional echocardiogram, apical four-chamber view, demonstrating enlarged atria with very prominent suture lines (arrows), characteristic for the transplanted patient. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

echogenicity (Fig. 30-4) . This abnormality is best viewed in the apical four-chamber view. Aside from providing a nidus for thrombus formation, the anastomosis of recipient atrial remnants with donor atria results in biatrial 661

enlargement. Although the recipient atrial remnant retains electrical and mechanical function, its electrical activity is dissociated from that of the donor atrium, resulting in abnormal overall atrial function.[10] Recently, there has been a shift from using the Stanford procedure of biatrial anastomosis to a bicaval approach, resulting in a nearly normal overall size of the left atrium and normal integrity of the right atrium. The two-dimensional echocardiographic images of the left ventricle reveal normal cavity dimensions, with considerable variability in contractility. Generally, left ventricular contractility appears at the upper limit of normal, [11] a finding that may relate to denervation with increased circulating catecholamines. Left ventricular hypertrophy also is a frequent finding; however, some studies have reported normal left ventricular mass in stable heart transplant patients beyond 1 year after transplantation.[12] Early after transplantation, right ventricular dimensions usually are within normal limits, except in patients who have had significant pulmonary hypertension during the preoperative or perioperative period. Under these conditions, right ventricular dilation is a frequent finding. Detailed descriptions of right ventricular echocardiographic characteristics in patients beyond 1 year after transplantation reported by Gorcsan et al[8] indicate that right ventricular wall thickness and cavity size are significantly increased compared with those of normal subjects. End-systolic and end-diastolic maximal right ventricular short-axis dimensions and areas are increased compared with those of normal control subjects; however, the right ventricular fractionalarea change is not significantly different from the normal value (35 ± 9.0% vs. 32 ± 13%). The prevalence of left ventricular segmental wall motion abnormalities in

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the cardiac allograft is poorly defined. One study reported that segmental wall motion abnormalities were never found in a cohort of heart transplant patients studied beyond 1 year after heart transplantation.[12] This differs from our experience at Stanford in which segmental wall motion abnormalities have been observed in both early and long-term patients. In patients studied during the first and second years after heart transplantation, wall motion abnormalities are usually unassociated with angiographically apparent epicardial coronary artery stenosis. Resting segmental wall motion abnormalities seen in the initial postoperative period likely reflect preexisting donor microvascular coronary artery disease that is not apparent by angiography, in contrast to the abnormalities seen in long-term patients. During the early postoperative period, a small pericardial effusion is frequently found. This effusion is usually located posteriorly and laterally, is rarely associated with signs of hemodynamic compromise, and becomes organized, with echocardiographic signs of pericardial thickening, in the absence of any clinical sequelae. These "normal variants" in pericardial appearances of the transplanted heart contrast with the occasional finding of increasing pericardial effusion[13] or signs of pericardial constriction.[14] The significance of increasing pericardial effusion with respect to acute rejection is discussed below. Transesophageal echocardiography has been used more recently in examination of the cardiac transplant patient and provides special diagnostic value in several situations. The close proximity of the esophagus to the left and right atria, atrial appendices, interatrial septum, and pulmonary veins clearly is an advantage of this technique, providing improved visualization of these structures. Derumeaux et al[15] prospectively performed transesophageal recordings in 64 transplanted patients and found a high incidence of spontaneous echocardiographic contrast (55% [35/64 pts]) and left atrial thrombus (28% [18/64 pts]) in patients who had undergone orthotopic heart transplantation, were treated with aspirin, dipyridamole, or both, and were in sinus rhythm. Other investigators have reported similar findings.[16] [17] Several case studies[18] [19] have reported on the occasional finding of sutureline obstruction of the left atrium. Canivet et al[18] described a patient with a mean gradient of 13 mm Hg across a prominent left atrial suture line, causing profound hemodynamic embarrassment. Doppler Echocardiographic Characteristics of the Nonrejecting Heart

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To develop noninvasive parameters for monitoring cardiac allograft function, Doppler echocardiography has been used to measure isovolumic relaxation time and the patterns of blood flow across atrioventricular valves and within the pulmonary and hepatic veins. A number of characteristic findings that relate to acute rejection have been described, including the left ventricular isovolumic relaxation time, peak early mitral flow velocity (E wave), and mitral valve pressure half-time (Fig. 30-5) . Typically, the left ventricular isovolumic relaxation time and pressure half-time are shortened immediately after heart transplantation but increase during the initial weeks, reaching a plateau after 6 weeks.[20] These increases likely reflect improvement in diastolic function as the allograft recovers from early ischemia. In the stable, nonrejecting allograft, the left ventricular isovolumic relaxation time and pressure half-time are prolonged compared with normal, suggesting a persistent relaxation abnormality in the presence of normal filling pressures.[21] This occult diastolic dysfunction may be unmasked by volume loading, as has been described from hemodynamic studies. Generally, the mitral flow velocity at atrial contraction is diminished compared with that of normal subjects or recipients of heartlung transplants.[22] Doppler-echocardiographic assessment of venous return to the heart provides indirect information regarding diastolic function of the heart. Blood flow in the hepatic veins and superior vena cava reflects right ventricular diastolic function, whereas patterns of blood flow in the pulmonary veins are indicators of left ventricular diastolic function. Venous flow typically is biphasic, and in the native heart in middle-aged adults, the systolic time-velocity integral is greater than the diastolic time-velocity integral. This contrasts with the pattern seen in the nonrejecting cardiac allograft, in which diastolic venous flow exceeds systolic venous flow. Further loss of systolic filling may represent an early manifestation of diastolic allograft dysfunction, which at its extreme is manifested by prominent 662

Figure 30-5 Methods for obtaining the diastolic indices. A, Apical fourchamber view and positioning of the pulsed Doppler sample volume (circle) at the tip of the mitral leaflet to obtain optimal perpendicular orientation with respect to mitral valve flow for recording of maximum velocities across the mitral valve. Sample volume is also positioned to obtain the signal of aortic valve closure. LA, left atrium; LV, left ventricle; RA, right atrium;

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RV, right ventricle. B, Analysis of pulsed Doppler mitral flow velocity curve. The upper panel shows simultaneous recording of the electrocardiogram (ECG), phonocardiogram (PHONO), and mitral flow velocity curve. The arrows indicate aortic valve closure, which is confirmed by the first high-intensity signal on the phonocardiogram (arrow). Calibration marks at the top of the panel are at 200-msec intervals. Velocity calibration marks are at 0.2 m/s intervals. The lower panel is a schematic representation of the mitral flow velocity curve to indicate the method of measurement of diastolic indices. Isovolumic relaxation time (A) is measured from aortic valve closure to the onset of mitral flow. Mitral valve pressure half-time is calculated from the base time (B), which is measured as the distance between the perpendicular line from the peak mitral flow velocity extended to the baseline, and the line of the deceleration slope also extended to the baseline. To obtain the pressure half-time, the base time is multiplied by a constant 0.29. Peak early mitral flow velocity (C) is measured from the baseline to the peak velocity recorded.

systolic flow reversal and diastolic flow reversal at donor atrial contraction. [23]

Clinically insignificant valvular regurgitation in the transplanted heart is well documented.[10] Overall frequencies of valvular regurgitation parallel reports for the native heart, but an association of mitral regurgitation with acute rejection also has been suggested. In contrast, tricuspid regurgitation in the allograft is a more frequent finding compared with the native heart and most likely occurs as a consequence of biopsy-related trauma. Frankly flail tricuspid leaflets requiring valve replacement have been described. [24]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Changes in Cardiac Allograft Morphology and Function Related to Acute Rejection Echocardiographic Changes Morphologic changes have been most frequently described in association with acute rejection (Table 30-1) . Changes in Left Ventricular Mass

An increase in left ventricular mass observed by M-mode and twodimensional echocardiography has been associated with acute rejection in adult[25] and pediatric[26] heart transplantation. Sagar et al[27] used the Troy formula to evaluate changes in left ventricular mass observed by M-mode echocardiography. During 19 consecutive episodes of acute rejection, an increase in left ventricular mass exceeding 100% was reported in all patients. Using two-dimensional echocardiography, Dubroff et al[28] showed that an increase in left ventricular mass was associated with allograft rejection, although the changes were TABLE 30-1 -- Echocardiographic Changes in Acute Rejection Increase in left ventricular mass Decrease in left ventricular systolic function Increase in myocardial texture New or increased pericardial effusion

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less dramatic than those observed by M-mode echocardiography. On subsequent evaluation of seven patients, the same investigations concluded that the inherent variation in left ventricular mass determined by echocardiography was substantial and, thus, represented a significant

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limitation for the diagnosis of acute rejection by two-dimensional echocardiography alone. Hence, although changes in left ventricular mass do occur with rejection, the magnitude of these changes is variable and often falls within the variability of the measurement. These limitations have prevented the use of left ventricular mass as a single parameter for routine rejection surveillance. To improve the utility of echocardiography for rejection surveillance, algorithms that combine multiple measured parameters have been applied, as discussed below. In a recent trial comparing two formulations of cyclosporine, echocardiography was used to monitor and compare graft function in the two treatment arms. Patients receiving the preparation known to have a superior pharmacokinetic profile (i.e., Neoral) demonstrated less increase in left ventricular (LV) mass during the initial 12 months after transplantation, compared with those receiving an older formulation of cyclosporine (i.e., Sandimmune). These differences in LV mass were also paralleled by differences in parameters of relaxation. This observation is consistent with an effect of the drug (Neoral) in inhibiting myocyte responses to rejection and ischemia that lead to LV hypertrophy after transplantation. Importantly, this trial confirmed the feasibility of echocardiography for monitoring heart transplant patients in multicenter clinical trials.[29] Changes in Left Ventricular Systolic and Diastolic Function

Before the use of cyclosporine as the primary maintenance immunosuppressive drug, acute rejection was monitored by clinical parameters of allograft function. Specifically, auscultation for the development of an S3 gallop and a decrease in electrocardiographic (ECG)

voltages formed the basis of clinical monitoring. The use of cyclosporine altered the pattern of acute rejection such that these clinical signs were not reliable for the detection of histologically proven rejection. In adult patients whose maintenance immunosuppression includes cyclosporine, left ventricular systolic function deteriorates late during acute cellular rejection. This contrasts with the situation in pediatric transplantation, in which a decline in the percentage fractional shortening is highly predictive of acute rejection.[26] The reason for the differences in systolic dysfunction between adult and pediatric heart transplant patients who experience rejection is unclear. Differences may be explained in part by the histologic diagnosis of acute rejection, particularly with reference to the diagnosis of humoral rejection.

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Indeed, recent studies indicate that in adult patients the decline in the percentage fractional shortening is a sensitive predictor of humoral rejection, particularly when accompanied by increased left ventricular mass.[30] Furthermore, patients who show a decline in systolic function with hemodynamic compromise have a poor long-term outcome.[31] Thus, in patients who are in the initial year of heart transplantation, a decline in systolic function should raise the possibility of acute rejection and warrants prompt endomyocardial biopsy. If the biopsy fails to show at least moderate rejection, the possibility of acute vascular rejection should be entertained and appropriate investigation instituted. In the absence of facilities for histologic confirmation of vascular rejection, empirical treatment is instituted, and a response to therapy is determined by echocardiographic monitoring of left ventricular function. In a patient who presents beyond 1 year after transplantation with a decline in systolic function on echocardiography and a biopsy that fails to demonstrate rejection, the possibility of transplant coronary artery disease should be considered and investigated. Preliminary reports suggest that the presence of intimal thickening by intracoronary ultrasound imaging is of prospective significance in this setting. M-mode echocardiographic assessment of ventricular relaxation has been validated by comparison with hemodynamic and radionuclide studies. Using standard digitizing methods, reproducible measurements of left ventricular filling and emptying rates, as well as rates of myocardial thinning and thickening, can be obtained. Parameters of left ventricular systolic and diastolic function of the transplanted heart were initially investigated by Paulsen et al.[32] Acute rejection was associated with decreased left ventricular lengthening rate and posterior wall thinning, consistent with diastolic dysfunction. Similar observations were reported by Dodd et al[33] who reported on multiple parameters obtained from the digitized M-mode echocardiographic recordings obtained during the initial 3 months after transplantation. The parameters found to be significantly different between patients with biopsies showing rejection versus those showing no rejection were left ventricular end-diastolic volume (LVEDV), left ventricular filling velocity, maximal left ventricle posterior wall velocity (normalized for chamber size at the time of maximal velocity), and velocity of left ventricular posterior wall thinning. No single parameter, however, was sufficiently sensitive to be useful clinically because of considerable overlap between nonrejecting and rejecting hearts. Sensitivities and specificities were much improved by using a multipleparameter algorithm.

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More recently, Moidl et al[34] have used acoustic quantification for online measurement of cardiac volumes and their changes from two-dimensional echocardiographic recordings, to facilitates quantitative assessment of systolic and diastolic function in heart transplant patients. During rejection, there was a significant decrease in left ventricular peak filling rate (PFR) compared to measurements made in the absence of rejection, consistent with diastolic dysfunction induced by acute rejection. A PFR value of greater than 4 predicted the absence of rejection in 100% of cases, and a decrease of more than 18% from previous non-rejection values successfully predicted acute rejection. Pericardial Effusion as a Marker of Acute Rejection

Although a small pericardial effusion is frequent early after heart transplantation, a sudden increase in the size 664

Figure 30-6 Two-dimensional echocardiogram, apical four-chamber view, demonstrating a large pericardial effusion in a patient with acute rejection. LV, left ventricle; PE, pericardial effusion.

or the appearance of a new effusion (Fig. 30-6) is often an indicator of acute rejection.[13] Observational studies indicate that frequently the concurrent endomyocardial biopsy is negative, but the subsequent biopsy is usually positive for rejection and requires a more protracted course of antirejection therapy to achieve complete resolution. These observations suggest that the immune response may be directed at the epicardial surface of the heart, a concept that is supported by the finding of a marked epicardial lymphocytic infiltrate at autopsy examination.[13] Recent studies in large cohorts of patients confirm that pericardial effusion in transplant recipients is associated with a higher incidence and more severe histologic grading of acute rejection.[35] Thus, an unexplained increase in pericardial effusion is an indication for enhanced rejection surveillance. Ultrasound Tissue Characterization

Alterations in echogenicity (myocardial texture) of the myocardium in various pathologic states have been reported.[36] Prominent myocardial texture (Fig. 30-7) can sometimes be observed on two-dimensional

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echocardiography in the setting of acute rejection, but qualitative assessment of this feature alone is too unreliable for the diagnosis of acute rejection. Several investigators have studied the potential use of ultrasound tissue characterization for the detection of acute transplant rejection. Different approaches to measuring changes in echogenicity have been sought, with the hypothesis in all approaches that acute rejection results in measurable alterations in acoustic properties. The changes in echogenicity that occur during acute rejection are subtle, and it is not entirely clear what accounts for the changes seen in ultrasound tissue characterization. Investigators have postulated that changes in local elasticity and density, as well as changes in fiber architecture, geometry, orientation, and contractile performance[37] are sufficient to affect myocardial texture, altering the acoustic properties of tissue. The techniques used in the assessment of acute cardiac rejection include analysis of the video-processed signal[38] and measurements of integrated backscatter, using either cyclic variation[39] or time-averaged, integrated backscatter.[40] Dawkins et al[41] studied the intensity of the echocardiography myocardial ultrasound signal, expressed as median pixel intensity, during acute unmodified rejection in the canine model. They found that a progressive increase in the pixel intensity correlated well with the histologic severity of rejection. Masuyama et al[39] used the cyclic variation of integrated ultrasonic backscatter to study the changes in signal strength expressed in decibels (dB) that occur in transplant patients during rejection. In 12 patients, the magnitude of the cyclic variation of integrated ultrasonic backscatter for the septum and posterior wall decreased, with moderate to severe rejection, from 4.2 (± 2.1) to 2.9 (± 1.8) dB and from 6.7 (± 1.2) to 5.1 (± 1.4) dB, respectively. A sensitivity of 86%, a specificity of 85%, and an accuracy of 85% for detection of rejection were achieved. There was no significant difference in integrated ultrasonic backscatter between normal subjects and nonrejecting transplant patients without myocardial hypertrophy; however, in a group of eight heart transplant Figure 30-7 Two-dimensional echocardiogram, apical four-chamber view, demonstrating prominent texture of the myocardium (arrows), increased wall thickness of the ventricles, and a significant pericardial effusion (pe) recorded in a patient with acute severe rejection. The ventricles also were poorly contractile (not shown). la, left atrium; lv, left ventricle.

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patients with significant cardiac hypertrophy, there was a lower integrated ultrasonic backscatter of the septum at baseline compared with those without hypertrophy. Thus, caution must be exercised when measuring integrated backscatter from the septum in patients with myocardial hypertrophy. In a study by Stempfle et al,[38] 12 dogs underwent heterotopic cervical heart transplantation, with serial measurements taken of myocardial echo amplitudes analyzed by gray-level histogram statistics. Regions of interest were studied to show that acute cardiac rejection was associated with a progressive increase in the mean gray level. It was also noted, however, that an increase in mean gray-level values after resolution of rejection may not indicate persistent rejection but rather permanent structural abnormalities. Although several reports cumulatively suggest that there are statistically significant alterations in acoustic properties during acute rejection, sufficient individual variation exists to indicate that a single measurement in a patient cannot be taken as a definite criterion for rejection. This fact underscores the importance of serial measurements in which each individual serves as his or her own control. Indeed, Angermann et al[42] suggested that serial end-diastolic integrated backscatter measurements of the posterior wall and septum permit reliable identification of not only moderate to severe acute rejection but also of mild acute rejection. Other limitations still exist in using ultrasound tissue characterization as a tool for the assessment of cardiac rejection. One important factor is the variability in the normalization of acoustic properties after a rejection episode. Further refinement of this tool is needed to allow its routine use in the detection of acute rejection. Currently, however, these techniques may serve as an adjunctive screening test, provided careful serial measurements are obtained in individual patients. Doppler Echocardiographic Assessment of Diastolic Function for Monitoring Acute Rejection Changes in the mitral inflow velocity signal correlate well with hemodynamic parameters of left ventricular function, thus providing noninvasive markers of left ventricular diastolic function for serial monitoring of patients (Table 30-2) .[43] [44] [45] Among the parameters most

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frequently studied are the left ventricular isovolumic relaxation time, mitral valve pressure half-time, and peak mitral valve early-flow velocity (E wave). The left ventricular isovolumic relaxation time was initially measured by M-mode echocardiography TABLE 30-2 -- Doppler Changes in Acute Rejection Impairment of diastolic function Decrease in pressure half-time Decrease in isovolumic relaxation time Increase in early diastolic filling velocity New onset of mitral regurgitation and phonocardiography and shown to correlate with acute rejection.[46] Doppler Echocardiographic Examination

All studies are performed with the patient in the left lateral decubitus position after 15 minutes of recumbency to achieve a basal heart rate and blood pressure. Doppler echocardiographic recordings are obtained with a combined imaging and Doppler transducer. Blood-flow velocity and valve movements at the mitral orifice are recorded using pulsed-wave Doppler ultrasound with the transducer positioned at the cardiac apex. From a standard four-chamber view, mitral flow velocities are recorded with the sample volume placed within the valve orifice near the leaflet tips to obtain maximal velocity of forward flow (Fig. 30-8A) . The discrete signal of aortic valve closure, seen as a high-intensity signal, is recorded simultaneously by orienting the transducer to encounter both mitral and aortic flow velocities. In each patient, all subsequent Doppler recordings of mitral flow velocity and mitral and aortic valve movements are performed with the sample volume at the same position. Simultaneous recordings of electrocardiogram and Doppler ultrasound are obtained at 100 mm/sec and analyzed without prior knowledge of the right ventricular endomyocardial biopsy findings. Analysis of Doppler Recordings

The parameters of left ventricular diastolic function that are assessed are isovolumic relaxation time, measured from aortic valve closure (confirmed by phonocardiogram) to the onset of transmitral flow; peak E-wave velocity; and mitral valve pressure half-time (see Fig. 30-8B) . Doppler values are calculated from an average of 10 consecutive beats after the

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exclusion of cycles in which recipient atrial contraction occurred between late systole and mitral valve opening. The decision to omit such beats is based on previous observations[9] showing that recipient atrial contraction occurring in late systole significantly shortens the measurement of left ventricular isovolumic relaxation time and pressure half-time, and increases E-wave velocity, most likely caused by an increase in left atrial pressure. All measurements are obtained with an automated software program, and the mean value for each diastolic index is computed. The group mean and standard deviation of all variables are calculated. Reproducibility of Doppler measurements is determined from calculating the mean square difference between paired measurements. Intra- and interobserver correlation coefficients have previously been defined as 0.85 and 0.95, respectively, for measurements of left ventricular isovolumic relaxation time and pressure half-time.[47] Diagnosis of Left Ventricular Diastolic Dysfunction Caused by Acute Rejection

Average values for the diastolic indices are computed as described above. From detailed reproducibility studies, 666

Figure 30-8 Changes in the diastolic indices during acute rejection measured from the pulsed Doppler mitral flow velocity curve. A, Recordings were obtained from a patient when right ventricular endomyocardial biopsy showed no evidence of rejection. The upper image is a four-chamber view indicating positioning of the pulsed Doppler sample volume. The lower image is the simultaneous recording of the electrocardiogram (ECG), phonocardiogram (PHONO), and mitral flow velocity curve. Aortic valve closure (arrows), which can be seen in the pulsed Doppler recording and confirmed as aortic valve closure by the first high-intensity signal on the phonocardiogram, is shown. The calibration marks at the top are at 200-msec intervals. Velocity calibration is at 0.2m/sec intervals. Isovolumic relaxation time (IVRT) = 101 msec, pressure half-time = 36 msec, and peak early mitral flow velocity = 0.6 m/sec. B, Recording from the same patient when endomyocardial biopsy showed acute rejection. The upper panel shows positioning of the pulsed Doppler sample volume at the tip of the mitral leaflets; the lower panel shows simultaneous recording of electrocardiogram (ECG), phonocardiogram (PHONO), and mitral flow velocity curve. In comparison with A, IVRT and pressure half-time have shortened, and peak early mitral flow velocity has increased. IVRT = 60 msec, pressure half-time = 24 msec, peak early mitral flow velocity = 1.1 m/sec.

a wide intersubject variability in diastolic indices was described previously.

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Thus, each patient must serve as his or her own control; changes from baseline measurements in a given patient provide the index for Doppler diagnosis of left ventricular diastolic dysfunction. Stable baseline values are defined as "two consecutive measurements which do not change beyond the threshold of spontaneous variations of the method," as previously reported.[47] Prior studies have defined the threshold for statistically significant changes in left ventricular isovolumic relaxation time and pressure half-time to be 15% or greater, and for mitral E-wave velocity to be 20% or greater. Thus, the severity of diastolic dysfunction can be graded as mild, moderate, or severe, according to the decrease in either left ventricular isovolumic relaxation time or pressure half-time (mild if the decrease was 15% to 19%, moderate if 20% to 39%, and severe if ≥40%) compared with stable baseline data of the patient. An increase in mitral Ewave velocity in the presence of stable isovolumic relaxation time and pressure half-time measurements is not regarded as indicative of diastolic dysfunction, owing to the propensity for this parameter to be influenced by heart rate. In the rare event that the left ventricular isovolumic relaxation time and pressure half-time change in opposite directions, an increase of greater than 20% in mitral E-wave velocity is used as an indicator of left ventricular diastolic [43]

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dysfunction. Such an observation occurs if aortic valve closure is early because of diminished stroke volume, causing prolongation of isovolumic relaxation time, where as pressure half-time shortens because of restrictive left ventricular physiology. In the future we need to examine the application of other Doppler parameters for the evaluation of diastolic functions that are not currently used in the assessment of acute rejection. Such parameters include, for example, venous inflow. In nontransplanted hearts, Doppler assessment of pulmonary venous flow serves as an important adjunct in the evaluation of left ventricular diastolic dysfunction. Limited reports from studies of superior vena cava flows during acute rejection suggest that inflow to the right side of the heart does change with acute rejection. [23] Other modalities to assess diastolic function, such as acoustic quantification or automated border detection, with analysis of diastolic filling patterns, may prove to be valuable. Limitations of Doppler Indices for Rejection Surveillance

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The application of Doppler indices of diastolic function to monitor rejection in heart transplant recipients (Table 30-3) makes several assumptions. The first assumption is that the acute development of a pattern characteristic of restrictive left ventricular physiology is caused primarily by the effects of acute rejection and not to changes in heart rate and loading conditions. The development of restrictive physiology as a direct consequence of acute rejection is plausible because there seems to be little correlation between the Doppler indices and evidence for fluid retention or heart rate increase when patients are serially studied[21] however, attention to possible confounding factors in the interpretation of results is crucial. Two further limitations unique to the transplanted heart could affect left ventricular physiology. The first is the unique physiology imposed by the anatomy of the orthotopically transplanted heart, in which variable proportions of recipient atria are anastomosed to donor atria. These atrial remnants retain both electrical and mechanical function and have been shown to contribute significantly to parameters of systolic and diastolic function, whether determined by hemodynamic or echocardiographic criteria. In early Doppler echocardiographic studies in heart transplant patients, it was demonstrated that TABLE 30-3 -- Limitations of Doppler Indices to Monitor Acute Rejection Alterations in heart rate and loading conditions Variable timing of recipient and donor atrial contraction Intersubject variation Interstudy variation Restrictive physiology early after transplantation Persisting occult restrictive physiology Acute rejection superimposed on chronic diastolic dysfunction Measurement of respiratory variation in mitral and tricuspid valve flow velocities limited by dissociated donor and recipient atrial contraction the timing of recipient atrial contraction could significantly affect Doppler indices of diastolic function, emphasizing the importance of selecting appropriate cardiac cycles for serial monitoring in patients.[9] As might be anticipated, recipient atrial contraction occurring in late systole increases atrial pressure, causing earlier mitral valve opening and shortening of the isovolumic relaxation time. Earlier mitral valve opening at a steeper point

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in the ventricular pressure decline results in a greater instantaneous left atrial to left ventricular pressure gradient on mitral valve opening, which might explain the higher peak early mitral flow velocity. Likewise, a higher mitral valve opening pressure caused by recipient atrial contraction could account for rapid deceleration of antegrade transmitral flow velocity and, thus, a shortened pressure half-time. Thus, if similar cycles are not used for measurements in serial studies, there is potential for measurement of some beats that are affected by late systolic recipient atrial contraction, and others in which recipient atrial contraction occurred in early systole or diastole, giving rise to averaged values that do not differ from study to study. These results would confound correlation with biopsy changes that could affect left ventricular relaxation properties. In studies in which attention has not been paid to standardized selection of cycles for measurement, it has been difficult to demonstrate the association of diastolic dysfunction with acute rejection.[48] Without the application of specific methods to exclude beats in which recipient atrial contraction occurred in late systole, one must guard against any interpretation of the presence or absence of differences between serial measurements, particularly with respect to rejection. The intersubject and interstudy variation seen in the mitral flow velocity curve is another potential limitation. Frequently, only one component of the mitral flow velocity curve can be seen in diastole, corresponding to early diastolic filling, with the absence of an atrial component. Occasionally, the early diastolic velocity signal is lost and only the velocity at atrial contraction is apparent. Therefore, it is crucial to distinguish between the signal of early diastolic flow and that of atrial contraction for any interpretation of changes between studies and between patients. Furthermore, serial measurements of diastolic function in heart transplant patients may be quite abnormal as a consequence of factors other than those attributable to immunologic injury during the initial few weeks after transplantation. The mitral flow velocity pattern typically seen in the initial postoperative period is characterized by a shortened isovolumic relaxation time and pressure half-time and a high mitral E-wave velocity. During the ensuing 6 weeks there is a gradual increase in pressure half-time and isovolumic relaxation time, and a decrease in Evelocity consistent with a decrease in left ventricular diastolic pressure and improved diastolic function.[20] Clearly, making a diagnosis of diastolic dysfunction due to acute rejection poses a major challenge in this setting, in which there is a propensity for improving cardiac function both as the allograft recovers

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from ischemia and as catecholamine levels decrease. This gives rise to the potential for considerable variation in individual values. It is, thus, essential that each patient serve as his or her own control 668

for the determination of the significance of observed changes between serial studies. When results are reported, it is helpful to clearly define the duration posttransplantation, because time posttransplantion is one of the factors influencing the changes in diastolic indices. Thus, a failure in recovery of diastolic function during the initial weeks after transplantation, even in the absence of further shortening of left ventricular isovolumic relaxation time or pressure half-time, may reflect diastolic dysfunction caused by rejection. The intersubject variation in diastolic indices may relate to variable recovery of left ventricular function after mechanical, pharmacologic, or ischemic injury during the transplantion procedure. Alternatively, persistent diastolic dysfunction can occur as a consequence of incomplete resolution of the immunologic events that affect cardiac function. Furthermore, chronic mild rejection, which is not treated in most transplant centers, may occur concurrently with significant impairment in cardiac function, as reported by Yeoh et al.[49] Thus, in the presence of chronically impaired diastolic function, irrespective of its cause, relatively small changes in diastolic indices may go unrecognized as significant indicators of immunologic injury. Measurement of blood flow during the isovolumic relaxation phase has been applied to the detection of diastolic dysfunction as a marker of acute rejection. This measurement is seen as a positive signal directed toward the apex, detected by continuous-mode Doppler in the apical position, arising along the interventricular septum in the mid part of the left ventricle, or from the basal region of the septum and lasting throughout the phase of isovolumic relaxation. The ability to detect an isovolumic relaxation flow signal is decreased in cardiac rejection, with no significant changes in the other Doppler-echocardiographic parameters, except for a significant decrease in the ejection fraction in the group with severe rejection. The absence of an isovolumic relaxation blood-flow signal in a cardiac transplant patient was associated with a specificity of 94% and a sensitivity of 86% for severe rejection, 58% for moderate rejection, and 44% for mild rejection.[50]

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Tissue Doppler Imaging Tissue Doppler imaging (TDI) has recently been introduced as a tool to assess changes in left ventricular systolic and diastolic function. Using TDI, one can measure the contraction and relaxation velocities of the myocardium. Solid tissue moves at slow velocities of 0.1 m/sec or less, as compared to red blood cells, which may reach velocities of 1.0 m/sec or more. The low-velocity, high-amplitude signals from myocardium are detected selectively, allowing quantification of tissue velocities. TDI can be displayed as a color two-dimensional scan, color M-mode, or in pulsedwave Doppler mode (see Chapter 6) . Several recent reports[51] , [52] have suggested using TDI in assessing systolic and diastolic dysfunction in heart transplant recipients. Puleo et al[51] studied the pulsed-wave tissue Doppler signals from the inferior LV wall in 121 transplant recipients. The peak relaxation velocity in nonrejecting allograft recipients was 0.21 m/sec. During moderate allograft rejection, peak relaxation velocities decreased to 0.14 m/sec and subsequently increased to 0.23 m/sec after successful treatment. With a cutoff value of 0.16 m/sec, the sensitivity of peak myocardial relaxation velocities for detecting rejection was 76%. The specificity and negative predictive values were 88% and 92%, respectively. These investigators did not find any significant change in peak systolic velocities during rejection. Mankad et al [52] measured the peak systolic and peak diastolic velocity gradients in 78 heart transplant patients, obtaining the myocardial velocity gradient from color M-mode tissue Doppler imaging. Previous studies[53] have shown that there is a difference in velocities in the endocardial myocardial layer as compared to the epicardial layer. The velocity gradient is then defined as the difference in myocardial velocity between the endocardium and epicardium, divided by the myocardial wall thickness. Mankad et al[52] found that there was a significant reduction in the peak systolic and peak diastolic velocity gradients in the posterior wall during rejection. Furthermore, they noted that a tissue Doppler peak-to-peak mitral annular velocity gradient of 135 mm/sec had a 93% sensitivity, a 71% specificity, and a 98% negative predictive value for detecting rejection. TDI could not discriminate between rejection and other causes of low velocities, such as ischemia, but high values were supportive for excluding the diagnosis. Despite these encouraging results, further investigations are needed to fully determine if any of the TDI measurements are accurate enough for routine use in the diagnosis of acute rejection. Fabregas et al,[54] in a brief report of

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7 patients studied serially after transplantation with TDI, did not find a consistent correlation between rejection and the contraction and relaxation velocities of the mitral and tricuspid annuli. Although TDI measurements of diastolic relaxation velocities may be independent of preload,[55] other limitations to the technique still exist such as discrimination between acute rejection and other causes of myocardial fibrosis seen in chronic rejection, or with ischemia-infarction secondary to transplant coronary artery disease. Another limitation is the impact that the Doppler angle of incidence and poor image quality have on TDI measurements. Combined Echocardiographic Parameters for Monitoring Acute Rejection Although echocardiography can identify several morphologic and functional changes that relate to acute rejection, sensitivity that falls short of the ideal 100% has prevented its use as the primary method of rejection surveillance. Clustering of multiple echocardiographic parameters has been suggested as an approach to enhancing the sensitivity of echocardiography without sacrificing specificity. [33] Dodd et al[33] have developed a computerized algorithm that incorporates changes in left ventricular mass, volume, and function to detect rejection. In this study, quantitative analyses of two-dimensionally guided M-mode echocardiograms of the left ventricle were performed using a digitized measurement format. The left ventricular end-diastolic (LVED) minor axis dimension, 669

interventricular septum thickness (IVS), and posterior wall thickness (PWT) were measured. The left ventricular end-diastolic volume (LVEDV) was calculated from the left ventricular minor axis dimension according to the relationship LVEDV = (LVED/10)3 and expressed as the percentage of normal predicted for body surface area. Left ventricular mass (LVM) was estimated according to the following relationship: LVM = 1.04 ([(LVED + LVPW + IVS)/10]3 − [LVED/10]3 ) Systolic function was estimated from the left ventricular shortening fraction, interventricular septum thickening, and left ventricular posterior wall thickening. Left ventricular diastolic function was obtained from the following indices: the filling velocity of the ventricular cavity; the maximal velocity of posterior wall thinning, normalized for the chamber size at the

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time of maximal velocity; and the average velocity of left ventricular posterior wall thinning. When these echocardiographic measurements were compared between patients whose concurrent biopsy showed no rejection or mild rejection versus those patients showing moderate or severe rejection, significant differences were observed for left ventricular enddiastolic volume, filling velocity, maximal velocity of the left ventricular posterior wall, and velocity of left ventricular posterior wall thinning. No single measurement, however, was adequately sensitive to be useful clinically because of considerable patient overlap between the none-to-mild and moderate-to-severe groups. To determine whether multiple M-mode parameters would be more sensitive in discriminating moderate to severe rejection, parameters that were significantly different between these grades of rejection were assigned a score of 1 or 2, depending on the level of significance of the difference and on the scatter of data. Indices of systolic function and mass were also given a score, and a scoring algorithm was developed. The resulting score in patients with normal to mild rejection on biopsy was 2.95 (± 1.98) versus 6.15 (± 1.45) (P < 0.001) in patients with moderate to mild rejection. A threshold score of 4 or greater was associated with a sensitivity of 100% and a positive predictive value of 77% for the detection of moderate to severe rejection. The negative predictive value of a score of 4 or less was 100% and specificity was 84%. These investigators further refined the algorithm and documented a sensitivity of 100% in a prospective analysis. Similar results have been observed in pediatric patients.[26] More recently, Ciliberto et al[56] investigated an extensive combination of echocardiographic criteria for the detection of rejection. In 130 patients, 1400 serial echocardiograms recorded within 24 hours of endomyocardial biopsy were analyzed for previously reported markers of acute rejection including (1) increasing wall thickness greater than 4 mm (interventricular septum plus left ventricular posterior wall); (2) increased myocardial echogenicity; (3) the appearance of or increase in pericardial effusion; (4) a greater than 20% decrease in pressure half-time; (5) a greater than 20% decrease in left ventricular isovolumic relaxation time; and (6) a greater than 10% decrease in left ventricular ejection fraction. The number and distribution of echocardiographic criteria were significantly related to the biopsy grade, the presence of two or more echocardiographic criteria being highly specific (96% to 100%) for rejection of all grades. Of the echocardiographic false-positives, 40% occurred as a consequence of viral myocarditis or pericarditis or in patients with accelerated coronary artery disease.

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In contrast, the sensitivity for the detection of moderate rejection was only 80%, and for mild rejection, 60%. All the false-negatives, however, were coincident with biopsies showing only one focus of myocyte necrosis, that is, moderate focal rejection. When the cases of mild rejection were analyzed for outcome related to the evolution of rejection, it was apparent that poor sensitivity was mainly the result of low sensitivity in patients whose biopsy grade did not warrant antirejection treatment (untreated patients). Thus, the sensitivity of two or more echocardiographic criteria for diagnosis of mild rejection requiring treatment (diffuse multifocal lymphocyte infiltrate or clinically significant rejection) was 70%. Analysis of the evolution of rejection in 46 patients with mild untreated rejection revealed that patients with two or more echocardiographic criteria at the onset had a less benign course and were more likely to require subsequent treatment for rejection. After antirejection therapy, changes in echocardiographic criteria paralleled the evolution of the rejection grade, suggesting that the echocardiographic response during the initial 2 weeks of therapy was predictive of outcome. Thus, patients with a benign course showed an improved echocardiographic picture as early as the first week after treatment, with further improvement during the second week. In contrast, those with an unfavorable course had a further worsening in echocardiographic criteria during the initial week and only a slight improvement after 2 weeks. The investigators concluded that poor sensitivity of echocardiography for the detection of mild rejection precludes its replacement of endomyocardial biopsy for rejection surveillance. It is now recognized by most transplant centers, however, that mild rejection, that is, a lymphocytic infiltrate in the absence of myocyte necrosis, does not require antirejection treatment because at least 50% of such cases resolve spontaneously.[57] Thus, the application of combined echocardiographic criteria for detecting rejection that requires treatment is a method that could considerably reduce the number of endomyocardial biopsies required for surveillance. Furthermore, by diagnosing and treating acute rejection in a more timely fashion, echocardiographic surveillance has the potential to significantly affect transplant coronary artery disease and the long-term outcome in heart transplant patients. At our institution, the timetable for performing echocardiography and other surveillance tests is outlined in Figure 30-9 . Future developments in this area will be facilitated by advances in ultrasound technology that allow more accurate measurements of each of the individual echocardiographic parameters that have been associated with

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rejection. Paralleling these technologic advancements will be the need for the prospective collection of data to create sufficiently large databases for computer modeling, using multiple parameters to determine which combinations 670

Figure 30-9 Simplified flow chart of the timing of diagnostic studies after cardiac transplantation in a patient with no complications and no evidence of rejection. When these study results are abnormal, further evaluation may be needed, but a simple algorithm is problematic because of the need to consider both allograft function and biopsy findings, the possibility of humoral as well as cellular rejection, and variations in the criteria used for grading and treating rejection. Angio, coronary angiography; Bx, biopsy; Echo, echocardiography; IVUS, intravascular ultrasound.

adequately predict acute rejection. Of crucial importance for the advancement of noninvasive diagnosis of acute rejection is improvement in the current histologic diagnosis of rejection that focuses on only one part of the alloimmune response. An improved understanding of the role of cytokines and microvascular injury as the mediators of allograft dysfunction could significantly affect the clinical application of markers of allograft function for rejection surveillance. Indeed, recent observations indicate a significant association of diastolic dysfunction with acute microvascular injury and upregulation of a spectrum of cytokines that also might play an important role in transplant coronary artery disease.[58] Strategies based on the early detection and treatment of allograft dysfunction could significantly affect the long-term outcome of heart transplant recipients. Echocardiographic Guidance of Right Ventricular Biopsies With escalating healthcare costs, there is an ongoing effort to reduce expenses while avoiding a decrease in the quality of healthcare. Several reports on the feasibility and safety of performing right ventricular biopsies with the aid of echocardiographic guidance have been published.[59] [60] This technique potentially reduces cost if the procedure is performed in a regular examination room or ward bed instead of in a fully equipped catheterization laboratory. We currently perform right ventricular biopsies during the immediate posttransplantion period, using echocardiographic guidance, in the intensive care unit. Preliminary reports suggest this technique is safe

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and provides adequate or even better biopsy samples than fluoroscopically guided biopsies. It is important that there be excellent communication and trust between the sonographer and the invasive operator. Endomyocardial biopsy under transesophageal echocardiographic guidance may be a viable option in certain situations, such as in critically ill patients[61] or in the pediatric population.[62]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transplant Coronary Artery Disease Accelerated coronary artery disease is the most important limitation to long-term survival after heart transplantation.[1] , [63] Clinical and pathologic studies have shown the prevalence of occlusive coronary artery disease of the cardiac allograft (transplant coronary artery disease) to be 10% to 15% at 1 year and 40% to 50% at 5 years after transplantation. Transplant coronary artery disease frequently presents with sudden death, myocardial infarction, and a decline in cardiac function, and is the leading cause of death in patients who survive beyond the first year after heart transplantation. [64] Although the pathophysiology underlying this process is poorly understood, an immune hypothesis has been postulated, based on its localization to the transplanted heart while native vessels are spared; the accelerated course and diffuse involvement of conduit vessels in conjunction with changes in the microvasculature; and some correlation with the incidence for acute rejection. Supporting the immune hypothesis is the relatively weak correlation of transplant coronary artery disease diagnosed angiographically, with risk factors conventionally implicated in nontransplant coronary artery disease. Irrespective of the mechanisms leading to this complication, there are a number of clinical features of transplant coronary disease, distinct from native coronary disease, that result in its delayed diagnosis and, thus, may contribute significantly to the high mortality rates. Perhaps the most important of these is the absence of angina because 671

of afferent denervation, which has led to the strategy of routine annual screening angiography as the method of choice for the detection of transplant coronary artery disease. Clinicopathologic studies and recent intracoronary ultrasound experience, however, have challenged the role of coronary arteriography as the "gold standard" for the diagnosis of transplant

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coronary artery disease. Several lines of evidence indicate that angiography underestimates transplant coronary artery disease because of the diffuse involvement of vessels. Furthermore, angiography cannot detect those early stages of the disease that are characterized by intimal thickening without luminal narrowing, nor can it detect microvascular disease. These limitations have fueled the search for methods to detect the functional consequences of transplant coronary artery disease that might arise from myocardial ischemia, whether related to disease in the conduit vessels or disease in the microvasculature. Several noninvasive techniques, including exercise testing, thallium scintigraphy, and stress echocardiography, have been evaluated as methods for establishing the diagnosis of transplant coronary artery disease, using coronary angiography as the gold standard. Exercise testing alone often is of limited value because of the suboptimal peak heart rates achieved, and which is further compounded by physical limitations related to deconditioning, orthopedic, or pulmonary factors. Dipyridamole (Persantine) thallium scintigraphy[65] has also been reported to have low sensitivity and specificity for the diagnosis of transplant coronary artery disease. One clear challenge is the fact that even mild transplant coronary artery disease (e.g., a 30% narrowing of the lumen) represents a significant process that accelerates faster and is associated with more ischemic events and sudden death than in the nontransplant population. Thus, a 2-year mortality rate exceeding 50% was reported to be associated with stenosis of 40% or greater once diagnosed angiographically.[63] Stress Echocardiography for Detection of Transplant Coronary Artery Disease Stress echocardiography has been investigated for the diagnosis of transplant coronary artery disease. We reported our findings in 51 patients undergoing exercise echocardiography testing before their routine annual coronary arteriogram. [66] Fourteen patients (27%) had transplant coronary artery disease according to angiographic criteria; six had mild, six had moderate, and two had severe stenosis. One patient with mild and two patients with severe transplant coronary artery disease had abnormal exercise echocardiograms; however, none of the six patients with moderate coronary artery disease had an abnormal exercise echocardiogram (i.e., false-negative results). Of the 43 patients with mild or no stenosis, 19 had moderate to severe intimal proliferation, as seen with intracoronary ultrasonography. Of eight patients with moderate or severe stenosis, four

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were tested with intracoronary ultrasonography, and all had moderate to severe intimal proliferation. Six patients had a false-positive exercise echocardiogram when compared with angiography, but of four who were tested with intracoronary ultrasonography, two had mild and two had moderate to severe intimal thickening (Fig. 30-10) . Thus, exercise echocardiography was correctly associated with a high falsenegative rate for the detection of moderate coronary artery stenosis. Conversely, a false-positive exercise echocardiogram was associated with intimal proliferation by intracoronary ultrasonography in several patients, suggesting that coronary angiography may underestimate significant coronary artery disease. Subsequent reports suggest that dobutamine-stress echocardiography may be the preferable noninvasive technique for the detection of ischemia in this patient population. Since chronotropic incompetence sometimes is the limiting factor for optimal stress testing, dobutamine (or other pharmacologic) stress testing may have an advantage over exercise stress testing. Also, transplant patients frequently have decreased exercise tolerance because of orthopedic or pulmonary problems and are unable to reach 85% of their predicted maximal peak heart rate. With dobutamine, patients have a greater chance to overcome these problems. Further studies are needed to confirm the sensitivity, specificity, and accuracy of pharmacologic stress echocardiography in the transplanted heart. Akosah et al[67] studied the hemodynamic response to beta-adrenergic stimulation by dobutamine in heart transplant patients. They found that an augmented chronotropic response did occur but the expected decline in diastolic blood pressure in response to dobutamine in heart transplant patients was similar to that in nontransplanted patients. The increase in myocardial oxygen demand and decrease in coronary perfusion may be an important mechanism in the development of ischemic abnormalities in the transplant population. Akosah et al[68] also found a high sensitivity (95%) and negative predictive accuracy (92%) for dobutamine stress echocardiography but a specificity of only 55% and a positive predictive value of only 69%, suggesting this test is most useful in excluding transplant coronary disease. Dobutamine stress echocardiography also appears to have prognostic value. Spes et al[69] examined the value of serial dobutamine stress echocardiographic studies in 109 transplant patients and compared the

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results with coronary angiography and intravascular ultrasound. Worsening of serial dobutamine stress tests indicated an increased risk of events compared with no deterioration (relative risk 7.26) A normal dobutamine stress test, on the other hand, predicted an uneventful course. Furthermore, the prognostic value of the test was comparable to that of intravascular ultrasound and angiography. Similar results have been reported by others. [70]

It is important to recognize that patients with significant transplant coronary artery disease often have resting wall-motion echocardiographic abnormalities, especially if triple-vessel disease is present. In patients studied beyond 1 year after heart transplantation, a resting segmental wallmotion abnormality is virtually diagnostic of transplant coronary artery disease. Detecting transplant coronary artery disease by noninvasive methods continues to be a challenge for the clinician. In heart transplant patients, anatomic narrowing of epicardial coronary arteries may be present in the absence of demonstrable ischemia. Conversely, patients may demonstrate 672

Figure 30-10 Distal anteroseptal wall motion abnormality induced during treadmill exercise testing in a patient 5 years after heart transplantation. A, Left ventricle, apical four-chamber view at rest. B, Left ventricle at peak exercise. Bulging and lack of thickening of the distal anteroseptal segment are noted (arrowheads). C, Coronary arteriogram (right anterior oblique projection) in the same patient showing a patent left anterior descending (LAD) coronary artery (arrow) without discernible disease. D, Intracoronary ultrasonography in this patient at the level of the proximal LAD coronary artery. Eccentric intimal thickening is noted with the luminal area (A) and the total vessel area (B) outlined to highlight the extent of thickening.

ischemia related to small-vessel disease, despite the absence of angiographically significant disease. Our current recommendation is to combine dobutamine stress echocardiography, for the detection of myocardial ischemia, with annual coronary angiography and intracoronary ultrasonography, and to have a low threshold for repeat coronary arteriography if there is unexplained allograft failure. Intravascular Ultrasonography for Detection of Transplant Coronary Artery Disease

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General Principles and Methods for Image Acquisition

Detailed descriptions of the ultrasound technology involved in intravascular ultrasound imaging systems are supplied in Chapter 15 . The system most frequently used in studying heart transplant patients uses a 30-MHz ultrasound transducer enclosed within an acoustic housing on the tip of a 5F, flexible rapid-exchange catheter. The ultrasound beam is reflected against an angulated mirror rotating at 1800 rpm, creating a 360-degree cross-sectional image perpendicular to the catheter. The procedure for intravascular ultrasound image acquisition and analysis has been described in detail.[71] Up to four distinct locations, separated by at least 1 cm, are selected for ultrasound measurements. These sites are selected where the lumen is circular, and vessel bifurcations and side branches are avoided. Recent morphometric analysis suggests that this method can be optimized by obtaining a pull-back recording and making measurements at 10 randomly selected sites along the vessel.[72] The studies are recorded on 0.5inch (1.29 cm) S-VHS videotape for subsequent offline analysis. The typical image recorded is composed 673

Figure 30-11 Intravascular ultrasound image obtained from a heart transplant patient. A, Typical image shows the catheter artifact at the center, the lumen, the intima, and the hypoechoic media. Vertical and horizontal calibration marks (white dots) are at 0.5-mm intervals. B, Methods of quantitation of intimal layer (color plate). The luminal area (LA) is obtained by planimetering the intima-lumen interface denoted by the yellow (inner) circle. The total area (TA) is obtained by planimetering the intima-media interface denoted by the red (outer) circle. The intimal area is calculated as follows: Intimal area = TA − LA. Intimal index = (TA − LA)/TA. Vertical and horizontal calibration marks are at 0.5-mm intervals.

of the catheter artifact in the center, the lumen, the intima, the media, and the adventitial surfaces (Fig. 30-11A) . The largest vessel lumen at enddiastole is used for quantitative analysis. The typical image obtained is composed of the catheter artifact, the lumen, and the three-layered appearance of the vessel wall if intimal thickening is present (see Fig. 3011A) . The lumen–vessel interface and, in the presence of intimal thickening, the external border of the intimal layer (intima–media interface) are traced by planimetry. This allows the calculation of mean intimal thickness, obtained from multiple intimal area measurements, and calculation of the intimal index, defined as the ratio of the intimal area to

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the sum of the intimal and luminal areas (Fig. 30-11B) . Measurements from all sites are averaged for each study. In addition to the measurements of mean intimal thickness and intimal index, a classification system that takes into consideration the degree of circumferential involvement of the artery is used (Table 30-4) . A spectrum of different images may be recorded from heart transplant patients surviving beyond 1 year after transplant (Fig. 30-12) . Intimal thickening may be minimal, as shown in Fig. 30-12A , or TABLE 30-4 -- Ultrasound Classification of Coronary Artery Disease in Cardiac Transplant Recipients Class I Severity Minimal Intimal thickness <0.3 mm Circumferential involvement

<180°

II Mild <0.3 mm >180°

III Moderate 0.3–0.5 mm or >0.5 mm <180°

IV Severe >1.0 mm or >0.5 mm >180°

severe, as shown in Fig. 30-12B , irrespective of the duration after transplantation. Validation with Coronary Angiography and Histologic Examination

Early studies compared measurements of the coronary artery lumen derived from intracoronary ultrasound with measurements determined by angiography. [71] In 20 cardiac transplant patients with no angiographic coronary artery disease, measurements from multiple sites in the left anterior descending artery were performed using both methods. Luminal dimensions using the two imaging systems correlated closely, with a correlation coefficient of 0.86. Of note was that the more the imaging catheter deviated from the long axis of the vessel, the greater was the discrepancy between ultrasound and angiographic measurements. Validation of the three-layered appearance of the coronary artery was obtained from histologic studies that included transplanted hearts imaged in vivo early after transplantation and again at autopsy.[73] In this important study, 16 hearts from patients aged 16 to 55 years with no history of coronary artery disease were examined. By comparing 72 cross sections with corresponding histologic sections, the authors concluded that the intracoronary ultrasound image appearance of young, morphologically

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normal coronary artery walls is homogeneous, with no layering. A threelayered appearance suggests the presence of at least 0.2 mm of intimal thickening. Taken together with further autopsy studies that indicate an intimal thickness of greater than 0.3 mm to be pathologic,[74] [75] these data have allowed the application of intravascular ultrasonography to prospectively evaluate the 674

Figure 30-12 Spectrum of images recorded from heart transplant recipients. A, Images recorded from a patient 8 years after cardiac transplantation showing minimal intimal thickening (arrow). B, Images from a patient with severe intimal thickening (arrow) 4 years after transplantation. Horizontal and vertical calibration marks are at 0.5-mm intervals.

prognostic significance of intimal thickening in heart transplant patients. Safety in Heart Transplant Patients

After the initial introduction of intravascular ultrasonography to assess coronary artery morphology in heart transplant patients, concerns were raised regarding the risks for endothelial damage leading to accelerated atherosclerosis. To address this question, coronary artery lumen dimensions of 38 heart transplant patients were measured by quantitative angiography in matched angiograms, at an interval of 1 year after the initial intravascular ultrasound examination.[76] The angiographic measurements in the vessel that had previously held the intravascular ultrasound catheter were compared with vessels that had not been catheterized. There were no differences in the absolute and percentage change in the angiographically measured mean-vessel diameters in intravascular ultrasound-imaged and nonimaged vessels. Acute coronary spasm, however, occurred in 8% of the patients undergoing intravascular ultrasound imaging but resolved promptly in response to nitroglycerin in all cases. Intravascular ultrasonography was not associated with any clinical morbidity. Clinical Application

Intravascular ultrasonography (IVUS) has been used to characterize the in vivo morphologic characteristics of transplant coronary artery disease in terms of incidence and severity, and to define the relationship of intimal thickening to angiographic evidence of coronary artery disease. The relationship of stress-test results to intimal thickening, as detected by

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IVUS, has been evaluated with the hypothesis that coronary angiography may not provide a sufficiently sensitive gold standard against which to test the reliability of stress-induced myocardial ischemia as a marker of transplant coronary artery disease. The technique has also been applied to the evaluation of risk factors that predispose to intimal thickening distinct from coronary artery stenosis and to define the prognostic significance of intimal thickening for predicting mortality and angiographic disease. Focusing on the pathophysiologic basis of transplant coronary artery disease, recent studies have applied IVUS to examine the relationship of intimal thickening with microvascular endothelial cell surface markers and cytokine expression in endomyocardial biopsy. Finally, IVUS is emerging as the gold standard with which to evaluate the efficacy of new therapies in clinical trials for prevention of transplant coronary artery disease. Incidence and Severity of Transplant Coronary Artery Disease.

The severity, distribution, and characteristics of transplant coronary artery disease, as defined by IVUS were reported from 304 intravascular ultrasound studies performed in 174 heart transplant patients.[77] Images were obtained during the initial 2 months following transplantation and up to 15 years after heart transplantation. This study provides a reference point for IVUS measurements of mean intimal thickness, index, and classification, and for morphologic characteristics, including calcification. Compared with studies obtained during the initial months after heart transplantation, patients studied at year 1 had greater intimal thickness, a greater intimal index, and a high intimal class. Thereafter, all three parameters increased over time, reaching peak values between 5 and 15 years. Calcification was detected in 12% of patients at years 0 to 5 but increased to detection in 24% of patients 5 to 15 years after transplantation. This study demonstrated that the greatest rate of progression of transplant coronary artery disease occurred during the initial 2 years after transplantation. This information is crucial because it suggests that measurements obtained from IVUS can provide end points for testing the effect 675

of therapeutic strategies targeted at the prevention of transplant coronary artery disease. Relationship of Coronary Artery Intimal Thickening to Angiographic Findings.

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Several studies have now reported underestimation of transplant coronary artery disease by coronary angiography, confirming earlier pathologic observations. In the initial 80 heart transplant patients undergoing IVUS examination,[78] 60 patients studied at 1 year or greater had some intimal thickening, which was graded as minimal or mild in 35%, moderate in 28%, and severe in 35%. Despite normal angiographic findings in 42 of the 60 patients, however, 50% of the patients had moderate or severe intimal thickening. This observation led to the concept of "angiographically silent" intimal thickening and to the possibility that patients with moderate or severe intimal thickening may be at risk for the subsequent development of angiographically significant disease or for cardiac events. Of 20 patients studied within 1 month of transplantation, an intimal layer was visualized in 13, all of whom had normal coronary angiographic findings. This observation has led to the question of whether disease that is present in the donor heart before transplantation accounts for intimal thickening seen within 3 months after transplantation. It has been suggested that the presence of eccentric lesions, particularly in older donor hearts, probably reflects pre-existing disease. [79] Because most of the baseline studies were not performed until 6 weeks after transplantation, the possibility that intimal thickening occurs as a consequence of the acute alloimmune response requires further evaluation. Prognosis Stratification and Risk-Factor Assessment.

The initial experience with IVUS indicated that 50% of heart transplant patients with moderate or severe intimal thickening had normal coronary angiographic findings, thus confirming that coronary angiography underestimated the severity of the disease. A 3-year follow-up of 120 patients confirmed the prognostic importance of intimal thickening, as detected by IVUS examination.[80] Intimal thickness in excess of 0.3 mm predicted the development of angiographic disease, overall survival, and graft loss resulting from transplant coronary artery disease. Our results on the reproducibility, safety, and prognostic significance of IVUS measures of intimal thickness paved the way for the application of this technology for the quantitative assessment of the early phase of transplant coronary artery disease. To examine the pathophysiology of transplant coronary artery disease, several groups, including our own, have defined the immunologic, metabolic, infectious, donor, and recipient risk factors for intimal thickening.[80] [81] By univariate analysis of metabolic versus immunologic risk for transplant coronary artery disease, 14 of 37 factors were

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significantly associated with intimal thickening. Factors that positively correlated with mean intimal thickness included the pretransplant lowdensity lipoprotein cholesterol level, the duration after transplantation, the average posttransplantation body weight, the number of moderate rejection episodes, the total number of rejection episodes, and the average plasma glucose and insulin levels 2 hours after an oral glucose load. Factors that inversely correlated with intimal thickening included the posttransplant average high-density lipoprotein cholesterol level, the average daily weight-adjusted dose of cyclosporine, and diltiazem treatment. By multivariate regression analysis with the presence of disease shown by IVUS as the dependent variable, average triglyceride levels and the mean post-transplantation body weight remained the only independent predictors for intimal thickening (R = 0.55, P < .0001). Likewise, angiographic evidence of transplant coronary artery disease was significantly correlated with average triglyceride levels and weakly with donor age. In a subgroup analysis of 39 patients studied 1 year after transplantation, a higher average triglyceride level (R = 0.55, P < .003) was the only factor associated with intimal thickening by intravascular ultrasonography. The results of these statistical analyses, as in prior studies, do not indicate acute cellular rejection as an independent predictor of transplant coronary artery disease but rather implicate an important role for lipoprotein abnormalities in the development of both early and late disease. Furthermore, prevention of transplant coronary artery disease by lipid-lowering agents[82] and calcium antagonists[83] suggests that factors other than acute cellular rejection are involved in the pathophysiology of transplant coronary artery disease. Thus, the results of clinicopathologic studies using IVUS to detect early and late disease provide a number of insights into potential pathophysiologic mechanisms of transplant atherosclerosis. Further investigation is needed about the role of vascular injury and the ensuing injury-response model, as postulated for nontransplant atherosclerosis. Relationship of Intimal Thickening to Microvascular Cell Surface Markers and Inflammatory Cell Phenotypes on Endomyocardial Biopsy.

Our group has performed studies aimed at defining the cellular and molecular mechanisms in transplant coronary artery disease. We examined the hypothesis that alterations of microvascular cell surface markers occur in parallel in the microvasculature and epicardial vessels, and that these changes may be important in the pathophysiology of intimal proliferation. [84] Forty-three heart transplant patients beyond 1 year posttransplantation were examined by IVUS, with concurrent analysis of right ventricular endomyocardial biopsies obtained at the time of IVUS. An inverse

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relationship between intimal thickening and microvascular cell surface markers was noticed. The rejection incidence was higher, and the duration after transplantation longer, in intimal classes II, III, and IV, compared with class I. These results are consistent with alterations of microvascular endothelial cell surface markers occurring in association with intimal thickening in epicardial coronary vessels. The changes in the expression of surface antigens by vascular cells could provide the substrate for coronary artery intimal proliferation and narrowing. Relationship of Intimal Thickening to Stress Test Results.

Dobutamine stress results indicate that positive tests coincident with normal angiographic findings are frequently associated with coronary artery intimal thickening, suggesting that ischemia may be occurring as a consequence of intimal hyperplasia in the microvasculature.[85] Similarly, intimal thickening was a frequent finding in exercise echocardiographic false-positive tests. Intravascular ultrasonography provides information regarding 676

early stages of transplant coronary artery disease in patients in vivo, before the development of obstructive lesions. It can be performed safely and is unassociated with a risk of an increasing rate of disease progression or of acute complications. It is superior to coronary angiography because it provides prognostically important information before the development of severe obstructive disease. Thus, it can be used in parallel with molecular analysis methods to characterize the pathophysiologic mechanisms that lead to rapid intimal proliferation in heart transplantation. Finally, because the most rapid phase of intimal proliferation occurs during the initial 2 years after heart transplantation, IVUS provides an invaluable method for monitoring the response to pharmacologic strategies for prevention of transplant coronary artery disease. Application of Intravascular Ultrasound in Clinical Trials.

The studies cited previously set the stage for the use of intravascular coronary artery ultrasound in clinical trials. Kobashigawa et al[82] demonstrated that patients randomized to pravastatin had significantly less intimal thickening 1 year after transplant compared with controls. A similar observation was reported by Wenke et al,[86] who used IVUS and coronary

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angiography to evaluate the effect of another HMG-CoA reductase inhibitor, simvastatin. In a randomized trial of mycophenolate mofetil (MMF) versus azathioprine, patients treated with MMF demonstrated less intimal area compared with controls. This was the first evidence in humans to suggest that the drug inhibits the disease process.[87] Given the limitations of coronary angiography to detect transplant coronary artery disease, as discussed earlier, it is anticipated that in the future clinical trials will use IVUS as the primary end point with which to test efficacy.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Section 6 - Echocardiography in the Pregnant Patient

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Chapter 31 - The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Catherine M. Otto MD Thomas R. Easterling MD Thomas J. Benedetti MD

Echocardiography is often requested in pregnant women either to evaluate known pre-existing heart disease or to check the possibility of heart disease in women with cardiac symptoms or abnormal findings on physical examination. Evaluation of heart disease in pregnancy is complicated by the fact that many healthy women experience symptoms of fatigue, decreased exercise tolerance, or dyspnea during pregnancy. Clinical examination alone may be nondiagnostic, prompting a request for echocardiographic evaluation. Similarly, although a "flow murmur" is present in most pregnant women, this normal finding cannot always be distinguished from a pathologic murmur on physical examination. With

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diagnostic testing, it is important to differentiate the normal alterations in cardiovascular 680

physiology and anatomy due to pregnancy from pathologic findings. In pregnant patients with known cardiac disease, expected findings (and appropriate normal reference values) may be different from those in nonpregnant patients. In some cases, echocardiography may be used to monitor cardiovascular function during pregnancy and in the peripartum period. In pregnant patients with concurrent systemic disease or with preeclampsia, echocardiography can provide important insights into the effect of the disease process on cardiovascular physiology and can assist in the management of individual patients. In this chapter, the normal hemodynamic and echocardiographic changes of pregnancy are reviewed and the role of echocardiography in the management of pregnant women with known or suspected cardiac disease is summarized.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Normal Hemodynamic and Echocardiographic Changes with Pregnancy Normal Hemodynamic Changes During normal pregnancy, plasma volume, erythrocyte volume, and cardiac output increase substantially over baseline values (Fig. 31-1 (Figure Not Available) ; Table 31-1 ). Many of the original studies on the hemodynamic changes of pregnancy were based on right heart catheterization with Fick or thermodilution cardiac output data. Thus, these studies included small numbers of patients with evaluation of only a few time points during pregnancy.[1] [2] The more recent use of Doppler cardiac output measurement techniques has greatly increased our understanding of the magnitude and timing of cardiac output changes during pregnancy.[3] [4] [5] [6] Overall, cardiac output increases progressively during pregnancy by as much as 45% over baseline values.[5] [7] [8] [9] A consistent finding using noninvasive Doppler measurements is that a definite increase in cardiac output occurs as early as 10 weeks of gestation. Some studies suggest that maximum cardiac output is reached at 24 weeks' gestation, with no further increases in later pregnancy Figure 31-1 (Figure Not Available) Plasma and erythrocyte volumes increase during pregnancy. (From Pitkin PM: Clin Obstet Gynecol 1976;19:489–513.)

TABLE 31-1 -- Normal Anatomic and Hemodynamic Changes of Pregnancy Anatomic Aortic root Left ventricle

Slight increase in diameter (2–3 mm) Slight increase in end-diastolic dimension and slight decrease in end-

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Left atrium Hemodynamic Cardiac output

Stroke volume Heart rate Blood pressure Systemic vascular resistance Pulmonary artery pressure Left ventricular end-diastolic pressure

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systolic dimension Slight increase in size Increased beginning in first trimester; maximum increase (at term) of 45% over baseline value Increased Increased by 25%–30% Unchanged Decreased Unchanged Unchanged

(Fig. 31-2) . Other studies ( Fig. 31-3 and Fig. 31-4 ) show a continued increase in cardiac output throughout pregnancy, with increases in stroke volume accounting for much of the first-trimester increase, followed by a continued increase in heart rate (and thus cardiac output) in the last two trimesters. On average, heart rate increases by 25% to 30% over baseline values during pregnancy (Fig. 31-5) . [6] The underlying mechanism of the increase in cardiac output with pregnancy is presumably hormonal, but the exact sequence of events remains unclear. [10] Recent data suggest that an increase in venous tone during pregnancy contributes to preload augmentation.[4] In addition, a decrease in aortic stiffness reduces afterload.[6] The fall in systemic vascular resistance allows blood pressure to increase only slightly despite an increased stroke volume (see Fig. 31-5) . Some studies suggest that pregnancy is associated with an increased wall stress[11] however, this view is challenged by other studies that suggest that wall stress decreases by about 30%. [5] [12] Left ventricular contractility appears to be depressed in pregnancy, based on measurement of the afterload-adjusted velocity of circumferential fiber shortening.[11] [12] Left ventricular systolic performance is maintained, despite this possible decrease in contractility, because of the altered loading conditions of pregnancy. Pulmonary pressures also remain normal during pregnancy,[13] suggesting a similar decrease in pulmonary vascular resistance to balance the increased

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blood flow volume. Diastolic filling pressures in both the right and the left heart also remain normal in pregnancy.[14] Technical Aspects of Doppler Cardiac Output Measurements Doppler measurement of cardiac output in pregnancy is based on the same principles as in nonpregnant patients. Stroke volume (SV) is calculated from the cross-sectional area (CSA) of flow multiplied by the velocity time integral (VTI) of flow at that site: 681

Figure 31-2 Increase in cardiac output from the nonpregnant state throughout pregnancy. P-P, prepregnancy; PN, postnatal. (From Hunter S, Robson SC: Br Heart J 1992;68:540–543.)

SV = CSA × VTI Typically, cross-sectional area is assumed to be circular and is calculated from a two-dimensional echocardiographic diameter measurement recorded with the ultrasound beam perpendicular to the flow diameter. The velocity time integral is measured by either pulsed or continuous wave Doppler ultrasonography, with the Doppler beam aligned parallel to the flow stream. As in nonpregnant patients, it is critical that (1) diameter be measured accurately, (2) the Doppler beam be aligned parallel to the direction of blood flow, and (3) diameter and velocity data be obtained almost simultaneously from the same intracardiac site. In addition, this method assumes that flow is laminar with a relatively flat (or blunt) flow-velocity profile, and that flow fills the anatomic cross-sectional area. Whereas these assumptions appear to be warranted in nonpregnant patients according to numerous studies validating this approach[15] (see Chapter 26) , the potential effect of the altered flow conditions during pregnancy warrants re-evaluation. Specific concerns in pregnant patients include the possibility that the flow profile may not be blunt or may be asymmetric, given the higher flow volumes. Possible changes in cross-sectional flow areas during pregnancy may also affect these measurements. Validation of cardiac output measurements in pregnancy has been performed by several groups of investigators using either of two basic Doppler approaches (Table 31-2) . Some investigators have applied the technique of measuring ascending aortic flow with a continuous wave

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Doppler probe from a suprasternal approach.[16] [17] The cross-sectional area of flow is calculated from a carefully recorded A-mode aortic diameter (Fig. 31-6) measured at the sinotubular junction, the narrowest segment of the aorta, since the highest flow velocity (as obtained with continuous wave Doppler) will correspond to the smallest flow area. Doppler cardiac outputs calculated with this method correlated well with simultaneous thermodilation cardiac outputs in pregnant women undergoing right heart catheterization for clinical indications.[16] Of note, Figure 31-3 Hemodynamic changes during pregnancy and post partum. (From Mabie WC, DiSessa TG, Crocher LG, et al: Am J Obstet Gynecol 1994;170:849–856.)

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Figure 31-4 Serial changes in heart rate (A), stroke volume (B), and cardiac output (C) recorded using Doppler echocardiography in a series of 89 women with no cardiac disease and a normal pregnancy. (Data from Easterling TR, Benedetti TJ, Schmucker BC, Millard SP: Obstet Gynecol 1990;76:1061– 1069.)

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Figure 31-5 Sequential changes in mean arterial pressure (A) and a total peripheral resistance (B) in 89 women with no cardiac disease and a normal pregnancy. (Data from Easterling TR, Benedetti TJ, Schmucker BC, Millard SP: Obstet Gynecol 1990;76:1061–1069.)

serial studies in pregnant women suggest that aortic root diameter increases during pregnancy,[18] [19] so that repeat aortic diameter measurements are needed at each time point. This contrasts with the situation in nonpregnant adults in whom both left ventricular outflow tract (LVOT) and aortic diameters tend to remain relatively constant over time. Other investigators have measured cardiac output in

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TABLE 31-2 -- Validation of Doppler Cardiac Output Measurements in Pregnancy Standard Gestational Doppler of Author n Age Method Reference r Easterling 23 Third CWD TD 0.93 [16] et al trimester A-mode Ao Robson et 15 Nonpregnant PD asc Fick 0.93 [22] al Ao 2D Aoleaflets Ao Doppler 0.96 Robson et 40 Pregnant [22] al Nonpregnant MV vs. MV 0.96 PA PA 0.97

Regression Equation SEE (L/min) (L/min) Dop = 1.07 TD - 0.58

Fick = 1.0 Dop + 0.8 0.4

Ao = 1.02 0.37 MV - 0.96 Ao = 0.97 0.47 PA + 0.40 MV = 0.92 0.34 PA + 0.62 Lee et al 16 Pregnant LVOT TD 0.94 TD = 0.74 0.64 [20] LVOT + 1.91 Ao, aorta; asc, ascending; CWD, continuous wave Doppler; Dop, Doppler; LVOT, left ventricular outflow tract; MV, mitral valve; PA, pulmonary artery; PD, pulsed Doppler; SEE, standard error of estimate; TD, thermodilution; 2D, two-dimensional; Fick, Fick method of cardiac output measurement. pregnant women using standard clinical cardiac ultrasonography systems.[7] [20] [21] [22] LVOT diameter is measured from a two-dimensional parasternal long-axis view; LVOT flow is recorded via an apical approach using pulsed Doppler echocardiography, with the sample volume positioned just proximal to the aortic valve plane.[23] This method correlates well with simultaneous Fick cardiac outputs in nonpregnant patients.[15] In a group of pregnant women, internal 684

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Figure 31-6 Doppler measurement of cardiac output based on a continuous wave Doppler recording of the velocity time integral [v(t)] in the ascending aorta, heart rate (HR), and an A-mode aortic diameter (D) for calculation of cross-sectional area (CSA) at the sinotubular junction. Stroke volume (SV) and cardiac output (CO) are calculated as shown. (From Easterling TR, Watts HD, Schmucker BC, Benedetti TJ: Obstet Gynecol 1987;69:845–850. Reprinted with permission from The American College of Obstetricians and Gynecologists.)

consistency between Doppler cardiac outputs measured from diameter and flow data across the aortic, mitral, and pulmonic valves was demonstrated. [24]

Reproducibility, in addition to accuracy, is critical for the application of these methods in following individual patients during the course of pregnancy. Several studies suggest that both these methods can be performed reproducibly with an acceptable degree of recording and measurement variability in pregnant patients, with a coefficient of variation of 5% to 8%.[16] [24] [25] Numerous studies on the reproducibility of Doppler cardiac output measurements have been reported in nonpregnant patients as well. Although there is still concern that these methods have been validated against invasive standards in only small numbers of pregnant women, the data should still accurately reflect hemodynamic changes over time (if not absolute values) both in individuals and in groups of patients. Compared with the two-dimensional pulsed wave Doppler approach, the advantage of the A-mode continuous wave method is that a smaller, less expensive, dedicated instrument can be used for cardiac output measurements. Although optimal results require careful data acquisition, focused education and training of appropriate individuals allow more widespread application of this technique. Potential disadvantages include (1) the possibility of a nonperpendicular measurement of aortic root diameter (resulting in overestimation of cardiac output); (2) a nonparallel intercept angle between the Doppler beam and the direction of aortic flow (resulting in underestimation of cardiac output); and (3) failure to recognize abnormal aortic flow conditions (e.g., aortic stenosis or regurgitation) that invalidate the Doppler method. When any of these problems are suspected, a standard clinical echocardiographic examination should be performed to resolve the difficulty. M-mode and Two-Dimensional Echocardiographic Changes The increased cardiac output of pregnancy is reflected in changes in left

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ventricular dimensions, volumes, and geometry (Table 31-3) . M-mode studies show that left ventricular end-diastolic dimension increases slightly (by 2 to 3 mm on average) and end-systolic dimension is unchanged, so that there is a slight increase in fractional shortening during pregnancy.[19] [26] [27] [28] These changes in left ventricular diastolic dimension correlate with increased preload due to changes in systemic venous tone.[4] Left ventricular wall thickness also increases slightly, with a corresponding increase in calculated left ventricular mass. Similar changes in right ventricular dimensions have been noted. With two-dimensional echocardiography, a slight increase in end-diastolic volume and in ejection fraction is seen, with little change in end-systolic volume. [8] [19] , [26] [29] [30] [31] These findings are consistent with the altered loading conditions of an increased end-diastolic volume and decreased systemic vascular resistance and do not imply an increase in left ventricular contractility. There are conflicting data on the changes in contractility with pregnancy.[5] [12] [14] , [26] There have been few studies evaluating left ventricular geometry in normal pregnancy; however, no dramatic changes in ventricular shape have been observed. Several investigators have found consistent increases in aortic and LVOT diameters during pregnancy, with the magnitude of this change averaging 1 to 2 mm.[18] [32] Even this small average change is significant for accurate cardiac output calculations, and given the wide range of values, some individuals have more pronounced changes in outflow tract geometry. Left atrial anteroposterior dimension increases by about 4 mm, with the maximum change seen at term compared with a study performed several weeks post partum.[19] Changes in atrial dimension in the peripartum period are associated with changes in serum atrial natriuretic peptide levels.[33] A small increase in mitral annulus diameter has been documented in conjunction with a much larger change in tricuspid annulus diameter.[19] A small pericardial effusion is seen on echocardiography in as many as 25% of healthy pregnant women, with a higher prevalence in women with preeclampsia. [33] Doppler Flows The increases in annular diameters partially compensate for the increased

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transvalvular volume flow of pregnancy, 685

TABLE 31-3 -- Normal Echocardiographic Measurements in Pregnancy (M Changes) Measurement Modality Aortic root M-mode A-mode LVOT (cm2 ) 2D area LA dimension 2D (mm) M-mode M-mode LV EDD M-mode (mm) M-mode M-mode M-mode M-mode 2D LV ESD (mm)

M-mode

Mean ± SD 30 ± 12 25 ± 2 3.5 ± 0.3 38 ± 4 36 37 47 ± 4 46 ± 3 51 ± 3 48 49 52 ± 4 32

M-mode 29 ± 3 2D 33 ± 4

Gestational Comparison Time of Age Value Comparison Third tri 28 ± 3 2 mo pp Term

24 ± 4

10 wk

Term

3.2 ± 0.3

2 mo pp

Term

34 ± 5

2 mo pp

Term Term Term

31 33 48 ± 4

Preconception 24 wk pp 12 wk pp

24–32 wk

43 ± 3

Third tri

50 ± 4

Nonpregnant controls 2 mo pp

Third tri Term Term

45 47 50 ± 3

Preconception 24 wk pp 2 mo pp

Term

32

24 wk pp

Term

30 ± 2

Term

34 ± 5

Nonpregnant controls 2 mo pp

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PWT (mm)

M-mode 10 ± Term 9±1 12 wk pp 1 M-mode 7 ± 1 Third tri 6±1 2 mo pp 2D 8 ± 1 Term 7±1 2 mo pp LV mass (gm) M-mode 175 ± Term 135 ± 25 12 wk pp 37 M-mode 203 Term 157 24 wk pp M-mode 183 Term 120 Preconception M-mode 186 ± Term 151 ± 34 2 mo pp 39 FS (%) M-mode 40 ± Term 33 ± 7 12 wk pp 7 35 ± 5 2 mo pp M-mode 30 ± Term 5 LV EDV 2D 108 ± Term 102 ± 13 2 mo pp (mL) 14 LV ESV (mL) 2D 44 ± Term 44 ± 7 2 mo pp 10 EF (%) 2D 60 ± Term 57 ± 4 2 mo pp 4 RV (mm) M-mode 20 ± Third tri 18 ± 1 2 mo pp 1 M-mode 19 ± 24–32 wk 15 ± 2 Nonpregnant 3 controls Mitral annulus 2D 24 ± Third tri 21 ± 4 2 mo pp (mm) 5 Tricuspid 2D 27 ± Third tri 18 ± 3 2 mo pp annulus (mm) 3 EDD, end-diastolic dimension; EDV, end-diastolic volume; EF, ejection ESD, end-systolic dimension; ESV, end-systolic volume; FS, fractional shor LA, left atrial; LV, left ventricular; LVOT, left ventricular outflow tract; pp partum; PWT, posterior wall thickness; RV, right ventricular; tri, trimester. but increases in transvalvular flow velocities are also seen[21] (Table 31-4) . Both the maximum aortic and LVOT flow velocity increase by

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approximately 0.3 m per second compared with the nonpregnant state. Less dramatic changes in transmitral velocities are seen with an increase in E velocity of only 0 to 0.1 m per second and an increase in A velocity of only 0.1 to 0.2 m per second. However, the TABLE 31-4 -- Normal Doppler Flow Velocities in Pregnancy Measurement Modality Aorta (m/s) CWD LVOT (m/s)

PD

Mitral E (m/s) MV-tips

Mitral A (m/s) MV-tips

E/A

Heart rate (bpm)

Cardiac output (L/min)

MV-tips

Flow Velocity 1.4 ± 0.2 1.3 ± 0.1 0.7 ± 0.2 0.9 ± 0.1 0.6 ± 0.1 0.6 ± 0.1 1.5 ± 0.2 1.3 ± 0.3 84 ± 10

Gestational Comparison Time of Age Value Comparison Term 1.1 ± 0.2 12 wk pp

89 ± 15 87 77 ± 10 6.5 ± 1.5

Term

1.0 ± 0.1

12 wk pp

Third tri

0.8 ± 0.1

2 mo pp

6–12 wk

0.8 ± 0.1

12 wk pp

Third tri

0.5 ± 0.1

2 mo pp

24–27 wk

0.5 ± 0.1

12 wk pp

Term

1.8 ± 0.2

12 wk pp

Third tri

1.6 ± 0.4

2 mo pp

Third tri

70 ± 16

2 mo pp

32–35 wk Term Term Term

69 ± 12 69 70 ± 7 4.3 ± 0.6

12 wk pp 24 wk pp 2 mo pp 2 mo pp

7.6 Term 5.0 24 wk pp CWD, continuous wave Doppler; MV, mitral valve; PD, pulsed Doppler; partum; tri, trimester.

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relative increase in E and A velocities being unequal, the E/A ratio changes from the normal pattern in young women (higher E than A with an E/A ratio of >1.5) to a pattern of equalized or reversed E/A velocities (E/A ratio of <1.0) later in pregnancy. Peak pulmonary venous A wave velocity, but not duration, also increases during pregnancy.[6] Postpartum Changes

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Interestingly, the estimated magnitude of changes in hemodynamics and cardiac anatomy with pregnancy depends on whether the values obtained during pregnancy are compared to postpartum values or to values obtained in the same patient before the onset of pregnancy. It is often difficult to obtain data in the prepregnant time period (since women typically present to the physician after the onset of pregnancy), but a few studies have followed women prospectively starting from the prepregnant state. These studies found hemodynamic and anatomic changes of greater magnitude than studies that compared values obtained during pregnancy with postpartum data. This suggests that at least some of the changes of pregnancy may persist into the postpartum period or may be permanent. Although in the postpartum period hemodynamic and anatomic changes return toward baseline rapidly over 6 to 12 weeks (Fig. 31-7) ,[7] [34] [35] the postpartum baseline level may be different from the prepartum baseline level. Specifically, aortic and left ventricular dimensions, while remaining within normal adult limits, may remain larger than the prepregnant values in that individual. Analysis of these data is complicated by the small number of subjects studied, by the possibly confounding effects of breastfeeding or other factors, and by the measurement variability of the techniques. Further studies are needed, because if there are significant, persistent changes after pregnancy, perhaps adult normal values not only should be indexed for body size and gender, but also should consider parity in women. Normal Valvular Regurgitation As in nonpregnant patients, small degrees of valvular regurgitation are often found on Doppler echocardiography.[36] [37] [38] It is unlikely that these small regurgitant leaks are audible on auscultation or account for the presence of a murmur in pregnant patients. Early studies suggested an abnormally high prevalence of tricuspid regurgitation in pregnant women.

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[38]

With the recognition of the extremely high prevalence of small amounts of tricuspid, mitral, and pulmonic regurgitation in normal individuals, it is now apparent that the prevalence of physiologic degrees of valvular regurgitation in pregnant women is similar to that in nonpregnant normal adults. Similarity of Hemodynamic Changes with Exercise and During Pregnancy It is notable that many of the hemodynamic changes of pregnancy are similar to the normal changes seen with exercise. The increase in heart rate and cardiac output and decrease in systemic vascular resistance are analogous to changes seen at a moderate level of physical exertion. In addition, the changes in cardiac anatomy seen with pregnancy are similar to those seen with repetitive activity in physically conditioned individuals. Specifically, the increases in left ventricular end-diastolic dimensions, volume, and left ventricular mass, with normal diastolic filling Figure 31-7 Changes in heart rate and cardiac output after normal delivery. (From Hunter S, Robson SC: Br Heart J 1992;68:540–543.)

patterns, are analogous to the changes seen with regular physical activity in nonpregnant women and in men. Presumably, these changes represent a similar hemodynamic response to a chronic elevation in volume flow rate. In contrast, the increase in aortic root dimension observed in pregnant women by several groups of investigators has not been seen with physical conditioning, suggesting that the mechanism of this effect is related to physical changes in the vessel wall, possibly mediated by hormonal effects.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Doppler Echocardiographic Evaluation of Hemodynamics in Pregnancy Positional Hemodynamic Changes The effect of positional changes on hemodynamics can be readily evaluated with Doppler echocardiography. Orthostatic 687

changes from sitting to standing positions are similar to the changes seen in nonpregnant individuals, with no significant differences between early and late pregnancy.[31] When a pregnant patient changes from a supine to a standing position, heart rate increases, stroke volume and cardiac output decrease, and systemic vascular resistance rises, while mean arterial pressure is maintained. During pregnancy, the supine position is associated with compression of the inferior vena cava by the gravid uterus, resulting in a decrease in venous return to the right atrium and a decline in stroke volume and cardiac output.[21] This supine decrease in cardiac output can be reversed (or prevented) by placing the patient in a left lateral decubitus position. One implication of this physiologic change is that diagnostic echocardiographic studies should be performed with the pregnant patient in a left lateral decubitus position whenever possible. If optimal imaging requires a supine position, the length of time the patient is positioned on her back should be limited. Peripartum Period Dramatic changes in loading conditions occur in the peripartum period related to the effects of (1) uterine contractions, (2) the pain associated with labor and delivery, (3) anesthetic medications, and (4) the immediate blood loss associated with delivery (Fig. 31-8) . Although all these normal physiologic changes are well tolerated by healthy women, they can result in

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acute decompensation in women with underlying heart disease. Despite the acute blood loss associated with delivery, stroke volume and cardiac output actually rise after delivery of the placenta (by about 10%)[34] and remain elevated for about 24 hours.[29] [34] Over the next several days to 2 weeks, cardiac output declines by about 25% to 30% compared with the immediately prepartum value, related to a decrease in both heart rate and intravascular volume. During labor, uterine contractions result in an acute increase in both heart rate and intravascular volume as uterine blood is forced into the circulating blood pool. The magnitude of the increase in cardiac output during Figure 31-8 Changes in cardiac output and stroke volume during normal labor. (From Hunter S, Robson SC: Br Heart J 1992;68:540– 543.)

contractions increases as labor progresses, with an augmentation of as much as 20% in cardiac output with each contraction.[29] [39] There are also mild increases in pulmonary and left ventricular pressures, which may be accentuated in patients with decreased left ventricular compliance (e.g., those with aortic stenosis or left ventricular hypertrophy). The volume changes associated with cesarean section and delivery are even greater than those associated with vaginal delivery, so there is often little hemodynamic advantage to this mode of delivery in patients with heart disease.[40] The hemodynamic effects of pain include increased heart rate and systemic vascular resistance. In patients with cardiac disease, the hemodynamic effects of pain may lead to a decline in cardiac output. The negative effects of pain can be eliminated by appropriate anesthesia. However, anesthesiarelated changes in preload and afterload also affect cardiac function, especially in heart disease patients. Thus, the choice of anesthetic agent and route of administration depends on the specific cardiovascular concerns in an individual patient.[40] Exercise Physiology Exercise physiology in pregnant women is similar to that in nonpregnant women except that the basal values are altered by pregnancy. For example, resting heart rate and stroke volume are larger at rest than in the nonpregnant state. With exercise, heart rate and cardiac output rise

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appropriately.[41] [42] Exercise studies in pregnant women at 32 weeks' gestation showed a higher exercise heart rate, higher maximal oxygen consumption, and high arteriovenous oxygen difference compared to 3 months post-partum.[43] Conditioned women have a greater cardiac output than sedentary women for any given heart rate, as is seen in nonpregnant, physically conditioned individuals.[44] [45] [46] [47] [48] However, the cardiovascular effects of aerobic conditioning are most evident during strenuous (not mild or moderate) exercise in pregnant women.[49] Systemic Diseases Doppler echocardiography is a useful tool for examining the hemodynamic changes associated with systemic diseases in pregnant patients. For example, in hyperthyroid pregnant women, the increased heart rate, elevated cardiac output, and decreased systemic vascular resistance can be documented, and the resolution of these changes with therapy can be monitored.[50] Echocardiographic evaluation of the effects of beta-agonist tocolysis,[51] pheochromocytoma,[52] sickle cell disease,[53] and renal artery stenosis[54] have also been reported.

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Pregnancy-Induced Hypertension and Preeclampsia Hemodynamics Pregnancy-induced hypertension is defined as an increase in systolic blood pressure from baseline ≥ 30 mm 688

Hg, a diastolic increase ≥ 15 mm Hg, systolic blood pressure ≥ 140 mm Hg, or diastolic blood pressure ≥ 90 mm Hg. Preeclampsia is defined as hypertension after the 20th week of pregnancy and proteinuria > 300 mg per 24 hours. Eclampsia is the onset of convulsions in a woman with preeclampsia. In a prospective study of 400 primigravida women, gestational hypertension developed in 24 and preeclampsia in 20 women.[55] The hemodynamics of pregnancy-induced hypertension and preeclampsia are complex and not fully understood.[56] [57] [58] [59] [60] Most likely, preeclampsia is a heterogeneous disease with different hemodynamic subsets.[61] Early in the disease course, cardiac output is elevated; later in the course, elevated systemic vascular resistance is seen in association with clinical decompensation. For any given cardiac output, mean arterial pressure is elevated in preeclamptic compared with normotensive pregnant women[9] [18] [55] (Fig. 31-9) . Central venous and pulmonary capillary wedge pressures tend to be normal except in decompensated patients with pulmonary edema. In preeclamptic patients with pulmonary edema, central venous and pulmonary wedge pressures can be discrepant to the point that invasive hemodynamic monitoring is needed. Pulmonary artery pressures in preeclampsia typically remain normal. However, because serum oncotic pressure is reduced even more than normal in preeclamptic pregnant patients, interstitial fluid in the lungs and pulmonary edema can occur at relatively low left atrial and

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pulmonary wedge pressures. Echocardiographic Findings In the few studies that have compared cardiac structure in preeclamptic versus normotensive pregnant patients, Figure 31-9 Cardiac output (CO), mean arterial pressure (MAP), and systemic vascular resistance (SVR) in 35 preeclamptic patients and 18 normotensive patients. (From Easterling TR, Watts HD, Schmucker BC, Benedetti TJ: Obstet Gynecol 1987;69:845–850. Reprinted with permission from The American College of Obstetricians and Gynecologists.)

TABLE 31-5 -- Echocardiographic Findings in Preeclampsia Author/Year EDD (mm) Kuzniar (1983) Thompson (1985) Veille (1984) ESD (mm) Kuzniar (1983) Thompson (1985) EDV (ml) Kuzniar (1983) ESV (ml) Kuzniar (1983) FS (%) Kuzniar (1983) Thompson (1985) Veille (1984) Ao-Root Easterling (1991) LV mass

Normal Pregnant Women Women with PIH

P value

51.4 ± 2.2 45.0 ± 2.3 50 ± 4

49.2 ± 3.4 44.0 ± 5.1 48 ± 4

.01 NS NS

33.8 ± 2.6 28.7 ± 1.9

32.3 ± 3.8 29.8 ± 4.7

NS NS

128.5 ± 14.4

115.2 ± 18.8

.01

46.9

42.5

NS

35 ± 3 36 ± 5 32 ± 4

35 ± 4 34 ± 4 37 ± 7

25.0 ± 0.2

27.3 ± 1

NS NS <.02 .01

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Thompson (1985) 147 ± 12 157 ± 16 <.01 Veille (1984) 105 ± 14 117 ± 20 <.05 PIH, pregnancy-induced hypertension. For remaining abbreviations, see Table 31-4 . Kuzniar et al: Am J Obstet Gynecol 1983;146:400–405 (25 normals, 42 PIH). Thompson et al: Am J Obstet Gynecol 1985;155:994–999 (11 normals, 14 PIH). Veille et al: Am J Obstet Gynecol 1984;150:443–449 (17 normals, 23 PIH). Easterling et al: Obstet & Gynecol 1991;78:1073–1077 (89 normals, 9 PIH). few or no differences have been found in left ventricular dimensions, volumes, fractional shortening, or left ventricular mass (Table 31-5) . Aortic root dimension appears to be slightly greater in preeclamptic than in normotensive pregnant patients and tends to be inversely related to total peripheral resistance.[18] Impact on Prognosis and Treatment Plans Doppler cardiac output measurements and calculation of systemic vascular resistance in patients with pregnancy-induced hypertension and preeclampsia may allow tailoring of medical therapy on the basis of hemodynamic subsets.[62] For example, hypertension related to a high cardiac output might respond to beta-blocker therapy, whereas elevated systemic vascular resistance might respond to vasodilator therapy. Importantly, maternal hemodynamics affect fetal growth: high-resistance hypertension is associated with lower birth weights.[63] Women at risk of preeclampsia can be identified based on an elevated cardiac output (>7.4 L/min by Doppler echo) before 24 weeks' gestation. In a double-blind randomized trial of women with an elevated cardiac output early in pregnancy, atenolol decreased the incidence of preelampsia (1/28 vs. 5/28, P = .04) but increased the risk of a low birth weight infant (P = .02).[64]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Heart Disease in Pregnancy Overall, few pregnant women (<0.2%) have significant heart disease given the low prevalence of heart disease in 689

women of childbearing age in the general population. The prevalence of specific types of heart disease in pregnancy reflects both the geographic distribution of these diseases and the patterns of health care in the overall population.[65] For example, in the United States, the prevalence of rheumatic valvular disease in young women has decreased, whereas that of surgically treated congenital heart disease with survival to adulthood is increasing. The clinical impact of heart disease in pregnancy is greater than the prevalence of significant heart disease would suggest, because a much larger number of patients are referred for echocardiographic evaluation for suspected cardiac disease. The most common symptoms and signs prompting a suspicion of cardiac disease are (1) evaluation of a murmur, (2) evaluation of congestive heart failure symptoms, and (3) a history of pre-existing heart disease. It is important that the normal hemodynamic changes of pregnancy be distinguished from pathologic abnormalities when these patients are evaluated. The echocardiographic diagnosis of significant heart disease in a pregnant woman can affect patient management in several ways.[66] [67] [68] [69] First, the cardiac diagnosis may have important prognostic implications (morbidity and morality) for both mother and fetus. Second, special or more intensive monitoring of the mother or fetus, or both, may be needed during pregnancy or in the peripartum period. Third, surgical or medical intervention may be needed either during or after pregnancy. Finally, the risk of congenital heart disease in the fetus may be increased, suggesting

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the need for fetal echocardiographic evaluation. Pulmonary Vascular Disease Elevated pulmonary artery pressures may be due to primary pulmonary hypertension, secondary to left-sided heart disease, or due to congenital heart disease with intracardiac shunting. Elevated pulmonary pressures of any cause are associated with poor maternal and fetal outcomes. When an intracardiac shunt is present and there is equalization of pulmonary and systemic vascular resistance, the result is a condition termed Eisenmenger's syndrome.[70] Women with Eisenmenger's syndrome have mixing or arterial and venous return to the heart resulting in cyanosis, arterial oxygen desaturation, and polycythemia. In a review of pulmonary vascular disease in pregnancy, the group of 73 women with Eisenmenger's syndrome had a maternal mortality rate of 36%, the group of 27 women with primary pulmonary hypertension had a maternal mortality rate of 30%, and the group of 25 women with secondary pulmonary hypertension had a maternal mortality rate of 56%.[71] The neonatal survival rate was about 88% in all groups, with all maternal deaths occurring within 35 days after delivery. Doppler echocardiographic measurement of pulmonary pressures allows identification of women with pulmonary hypertension, quantitation of disease severity, and evaluation of the response to therapy with nifedipine or nitric oxide.[72] [73] The major limitation of Doppler data in this setting is that only pressures, not vascular resistance, can be assessed. Congenital Heart Disease Noncyanotic Patients with No Prior Surgical Procedures

The most common congenital defect newly diagnosed during pregnancy is an atrial septal defect (Fig. 31-10) . [74] , [75] These patients are usually asymptomatic but have a prominent "flow murmur," prompting a request for echocardiography. Two-dimensional echocardiographic and Doppler diagnosis of atrial septal defects in pregnancy is straightforward, so that contrast echocardiography is not needed (and should be avoided) for detection of the interatrial shunt in pregnant women. Given the increased cardiac output and ventricular volumes of pregnancy, evaluation of the shunt ratio can be problematic in borderline cases. At least in theory, the decreased systemic vascular resistance of pregnancy might result in

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increased systemic blood flow without affecting pulmonary blood flow (a decreased pulmonic-to-systemic shunt ratio). However, accurate definition of the shunt ratio is not necessary during pregnancy, since pregnancy is well tolerated with an excellent fetal outcome, regardless of the size of the left-to-right shunt. If necessary, the patient can be reevaluated post partum before a final decision is made regarding the need for surgical closure of the defect.[76] Ventricular septal defects in noncyanotic adults are typically small and associated with a loud systolic murmur. On Doppler examination, a highvelocity jet from left to right ventricle is seen with normal chamber dimensions and function. This lesion is also well tolerated, except for an increased risk of endocarditis, and further evaluation or treatment is rarely needed. Pregnancy does not significantly alter the echocardiographic findings. Occasionally, a patient with a previously undiagnosed patent ductus arteriosus presents during pregnancy. The classic continuous machinerylike murmur may or may not be appreciated on auscultation if the murmur is soft. With two-dimensional imaging, the patent ductus itself is often difficult to visualize in adults, so a directed Doppler examination is essential when this diagnosis is suspected. Diastolic flow reversal in the pulmonary artery is seen with both color flow imaging and pulsed wave Doppler techniques. When a patent ductus arteriosus is not suspected a priori, the findings of left atrial or left ventricular enlargement in excess of the expected changes of pregnancy (due to the left-to-right shunt and volume overload) or of diastolic flow reversal in the descending thoracic aorta (in the absence of significant aortic regurgitation) should prompt a careful search for this possible diagnosis. Congenitally corrected transposition of the great arteries, also known as ventricular inversion, most often is associated with a normal physiologic pattern of blood flow through the heart and may first be recognized during pregnancy. However, associated defects are common, including ventricular septal defects, pulmonic stenosis, complete heart block, and regurgitation of the systemic atrioventricular 690

Figure 31-10 Calculation of the pulmonic to systemic shunt ratio in a 26-year-old pregnant woman with an atrial septal defect. The pulmonic

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flow rate is calculated as the product of the pulmonary artery (PA) cross-sectional area using a parasternal pulmonary artery diameter measurement (A), and the velocity time integral (VTI) in the pulmonary artery recorded with pulsed Doppler (B). Systemic flow is calculated as the product of the cross-sectional area of the left ventricular (LV) outflow tract using a parasternal long-axis diameter measurement (C), and the velocity time-integral in the left ventricular outflow tract recorded from an apical approach using pulsed Doppler (D). In this example, the calculated Qp/Qs was 1.5 to 1. Ao, aorta; LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract.

valve. Outcome during pregnancy depends on the associated defects in patients with congenitally corrected transposition. Published summaries of the outcome of pregnancy in a total of 87 women with 118 pregnancies show a live birth rate of 83%.[77] [78] [79] Complications during pregnancy included congestive heart failure, increased cyanosis, endocarditis, stroke, and myocardial infarction. Other well-tolerated types of noncyanotic congenital heart disease seen in pregnant patients who have had no prior surgical procedures include mild pulmonic stenosis and Ebstein's anomaly of the tricuspid valve.[80] Ebstein's anomaly may occur as an isolated anomaly with varying degrees of tricuspid regurgitation or may be associated with an atrial septal defect, resulting in cyanotic heart disease. In women with noncyanotic Ebstein's anomaly, pregnancy is well tolerated. [81] [82] Despite varying degrees of tricuspid regurgitation, no maternal deaths, strokes, heart failure, or arrhythmias were reported in 111 pregnancies in 44 women with Ebstein's anomaly. [83] Noncyanotic Patients with Prior Surgical Procedures

An increasing number of patients who have undergone previous surgical procedures for congenital heart disease are surviving to adulthood. When these patients become pregnant, echocardiographic evaluation is requested by the primary care physician to detect any residual structural or functional cardiac abnormalities, to evaluate for long-term complications of the surgical procedure, and to optimize patient management during pregnancy and in the peripartum period. Since data on maternal and fetal outcome 691

in this patient population are limited, evaluation and management are based on an individualized approach in each patient.

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In patients with previous surgical procedures that completely correct the congenital abnormality, outcome in pregnancy is similar to that in normal women. For example, patients with a previous atrial or ventricular septal defect closure or patent ductus arteriosus ligation are expected to have normal cardiac anatomy and function, with a corresponding normal echocardiographic examination. [76] When residual mild abnormalities are present after corrective surgery for congenital heart disease, maternal outcome is also likely to be similar to that in normal subjects, with the proviso that the echocardiographic examination should be directed toward potential residual abnormalities or late complications. For example, patients with surgical repair of tetralogy of Fallot may have recurrent or residual right ventricular outflow tract obstruction, ventricular septal defect, a false aneurysm of the pulmonary outflow tract, or pulmonic insufficiency.[84] Patients with a previous aortic coarctation repair may have residual or recurrent stenosis.[85] [86] Even when restenosis is not present, these patients are at risk for late systemic hypertension related to hyperdynamic left ventricular systolic function, which may present initially as exerciseinduced hypertension.[87] Women with a repaired coarctation and a residual gradient of less than 20 mm Hg can have successful pregnancies, with one study reporting 29 births for 36 pregnancies. [88] With complex congenital heart disease and palliative or partially corrective surgical procedures, residual or recurrent anatomic and functional cardiac abnormalities occur commonly, resulting in an increased maternal risk. Echocardiographic evaluation is especially valuable in these patients both before pregnancy to assess the potential risk and during pregnancy to monitor cardiovascular function. With complex congenital heart disease, arrhythmias are a frequent cause of morbidity and mortality.[89] Survival after Fontan repair is now 60% at 10 years, so that some women undergoing this procedure will reach childbearing age and may become pregnant. [90] Maternal survival has been documented, but fetal outcome is uncertain.[91] Of seven pregnancies in six women after Fontan repair, there were three spontaneous abortions, three therapeutic abortions, and only one liveborn child. In another series of 33 pregnancies in women with a Fontan repair, there were only 15 (45%) live births; however, there were no significant maternal complications and no deaths.[92] [93] Pregnancy in patients with a previous Mustard interatrial baffle repair (Fig.

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31-11) for transposition of the great arteries has been reported in 16 women who had a total of 23 pregnancies.[94] [95] [96] Maternal outcome was excellent, with no deaths or significant complications. However, all these patients were asymptomatic before pregnancy and had an excellent baseline functional status. Specifically, none had significant baffle leaks or obstruction, significant systemic atrioventricular valve regurgitation, or systemic ventricular systolic dysfunction. In patients with significant functional cardiac abnormalities, maternal outcome is dependent on the specific underlying abnormalities; for example, patients with systemic ventricular dysfunction are at risk for heart failure during pregnancy. Thus, echocardiographic evaluation in patients with an interatrial baffle is directed toward evaluation of the interatrial baffle (which may require transesophageal imaging), evaluation of systemic and venous ventricular function, detection and quantitation of systemic atrioventricular (tricuspid) valve regurgitation, and assessment of any other residual or acquired abnormalities. Cyanotic Heart Disease

Eisenmenger's physiology (Fig. 31-12) is characterized by equalization of pulmonary and systemic vascular pressures in association with a large intracardiac communication such as a ventricular septal or atrioventricular canal defect.[96] During pregnancy and in the peripartum period, the decrease in systemic vascular resistance, in the setting of irreversible pulmonary hypertension, can result in increased right-to-left shunting and decreased pulmonary blood flow, with subsequent cardiovascular collapse due to hypoxia and hypotension.[97] [98] Maternal mortality is extremely high (between 30% and 70% in different series) and only 15% of infants are born at term, so pregnancy should be avoided in these patients. [70] [99] Of note, there may not be a tricuspid regurgitant jet of adequate signal strength for estimating pulmonary artery systolic pressure in patients with Eisenmenger's physiology. The presence of pulmonary hypertension must then be inferred from the findings of a large, nonrestrictive intracardiac communication, a short time to peak velocity in the pulmonary artery, midsystolic notching on the pulmonic valve M-mode, and the pattern of ventricular septal motion. If severe pulmonary hypertension is not clearly established, other diagnostic tests should be considered in view of the grave prognosis associated with this condition. Rarely, a patient with no previous cardiac diagnosis presents during pregnancy with Eisenmenger's physiology.

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Cyanotic congenital heart disease without Eisenmenger's physiology also connotes high maternal mortality and morbidity.[97] [98] [100] In 822 pregnancies in 416 cyanotic women, the rate of cardiovascular complications was 32%, with one maternal death. Fetal outcome was also suboptimal; only 43% of pregnancies resulted in live births, 37% of which were premature. Factors that predict a poor outcome include functional status before pregnancy, arterial oxygen saturation, and blood hemoglobin. Other studies suggest that maternal outcome is also strongly related to the degree of right ventricular pressure overload.[101] Thus, echocardiographic evaluation should include estimates of pulmonary systolic pressure, as well as definition of the anatomic abnormalities and ventricular function. In a series of 41 pregnancies in 15 women with cyanosis after partial repair for complex pulmonary atresia, there were only 8 healthy children. Although there were no maternal deaths in this series or in a smaller study, the incidence of maternal complications was high, with complications including pulmonary embolism, heart failure, and arrhythmias.[102] [103]

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Figure 31-11 This 23-year-old pregnant woman had a history of transposition of the great arteries with a previous Mustard interatrial baffle. The apical fourchamber view (A) shows a porcine valve (arrow) in the systemic atrioventricular valve position with the transposed ventricles. Transesophageal imaging from a high esophageal position (B) shows the atrial baffle with no significant obstruction or leak. Several months post partum, the patient developed a new systolic murmur, and Doppler examination (C) showed acute prosthetic regurgitation related to degenerative changes of the valve leaflets. IVC, inferior vena cava.

693

Figure 31-12 (color plate.) Endocardial cushion defect with a large ventricular septal defect, atrial septal defect, and Eisenmenger's physiology in a 19-year-old pregnant woman with no previous cardiac diagnosis. A modified four-chamber view (A) shows the atrial and ventricular septal defects (arrow) and the common atrioventricular valve. Color flow imaging (B) shows severe atrioventricular valve regurgitation (arrow). A diastolic frame in the same view (C) shows flow from both atria into both ventricles. The tricuspid regurgitant jet velocity (TR-Jet) (D) is elevated to 5 m per second, confirming severe pulmonary hypertension. Despite relatively stable hemodynamics during pregnancy and delivery

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with careful hemodynamic monitoring, the patient had abrupt hemodynamic collapse 48 hours post partum and died. RV, right ventricle; LV, left ventricle.

Valvular Heart Disease Valvular Stenosis

In a pregnant patient, stenosis of a semilunar valve is usually due to a congenitally abnormal valve.[104] Mild to moderate stenosis of the pulmonic valve is well tolerated, and severe pulmonic stenosis is rare in adults. In contrast to patients with pulmonic valve stenosis, those with aortic valve stenosis, even if asymptomatic before pregnancy, may decompensate during pregnancy. Anatomically, these valves are often unicuspid with a small central orifice. Patients with a previous surgical commissurotomy may have significant restenosis [104] one study estimated that about 20% of such patients require reoperation at a mean interval of 13 (range, 3 to 26) years after the initial procedure.[105] Thus, depending on the patient's age at the initial operation, restenosis may be diagnosed during pregnancy. As stroke volume increases across the stenotic valve with pregnancy, an increase in the pressure gradient measured by Doppler echocardiography is seen. However, calculation of valve area with the continuity equation still provides accurate assessment of stenosis severity (Fig. 31-13) . Some patients may become symptomatic during pregnancy owing to the increased metabolic demands in 694

Figure 31-13 Aortic valvular aortic stenosis in a 25-year-old pregnant woman who underwent an aortic valve commissurotomy 10 years previously. The parasternal long-axis view shows a congenitally abnormal aortic valve (arrow) with reduced systolic opening. The maximum jet across the aortic valve, recorded with continuous wave Doppler from a high right parasternal position, shows a maximum velocity of 5.0 m per second. There was mild to moderate coexisting aortic regurgitation. Aortic valve area, calculated by the continuity equation, was 1.0 cm2 . This patient was managed with placement of a pulmonary artery catheter and arterial line at the time of delivery. Because of fetal presentation, the patient underwent a cesarean section with epidural anesthesia, which was tolerated well. Ao, aorta; LA, left atrium; LV, left ventricle.

the setting of a limited ability to increase stroke volume across the valve.[104] [106] These patients may present with angina during pregnancy even though

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they were asymptomatic in the prepartum period. Reduced diastolic ventricular compliance secondary to left ventricular hypertrophy can also lead to congestive heart failure. Even when aortic stenosis patients remain physiologically compensated during pregnancy, any superimposed hemodynamic alteration can lead to acute decompensation. For example, the high cardiac output and heart rate associated with a viral or bacterial infection may result in acute pulmonary edema due to a combination of an increased valve gradient and a shortened diastolic filling time. The role of echocardiography in pregnant patients with aortic stenosis is to accurately delineate disease severity so that monitoring and therapy during pregnancy and in the peripartum period can be optimized (Fig. 31-14) . In some patients, the severity of stenosis may worsen during pregnancy, being possibly related to the hormonal and metabolic changes of pregnancy. Most pregnant women with aortic stenosis can be managed medically, but balloon aortic valvuloplasty or valve replacement during pregnancy has been required in rare cases. [106] [107] [108] [109] [110] [111] Rheumatic mitral valve stenosis is often diagnosed initially during pregnancy (Fig. 31-15) . If mitral stenosis is moderate in severity or if disease progression has been gradual, the patient may not have noted symptoms or exercise limitation before the pregnancy. Early in pregnancy, the increased transmitral volume flow rate and the shortened diastolic filling time due to the increase in heart rate result in further elevation of left atrial pressures. This may result in pulmonary edema, depending on the severity of mitral valve obstruction. Since it is often difficult to appreciate the diastolic murmur of mitral stenosis in pregnant dyspneic patients, mitral stenosis should be considered in the differential diagnosis of all pregnant patients with heart failure or pulmonary congestion. Echocardiography reliably differentiates mitral stenosis from other causes of heart failure (e.g., cardiomyopathy or diastolic dysfunction) and will distinguish cardiac from noncardiac causes of respiratory distress. Echocardiographic measures of mitral stenosis severity, including twodimensional valve area, Doppler gradients, and pressure half-time valve area, remain valid in pregnancy, so that echocardiographic evaluation allows optimization of patient monitoring and therapy. Usually, patients can be managed medically during pregnancy using beta blockers to improve diastolic filling, even with severe mitral stenosis, although decompensation may require invasive monitoring in an intensive care unit setting.[112] In some severe cases, maternal or fetal complications may

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necessitate mechanical relief of stenosis severity during pregnancy, preferably with percutaneous balloon valvuloplasty.[113] , [114] Echocardiography is then valuable in assessing the likelihood of complications and the expected result of percutaneous mitral valvuloplasty. [115] [116] [117] If the latter is performed, echocardiographic monitoring (either transthoracic or transesophageal) allows fluoroscopy time to be minimized. [118] [119]

Valvular Regurgitation

Pathologic valvular regurgitation in pregnancy may be due to a congenital abnormality (bicuspid aortic valve), previous bacterial endocarditis, rheumatic disease (Fig. 31-16) , or myxomatous valve disease or may be associated with more complex congenital heart disease (Fig. 31-17) . Standard two-dimensional and echocardiographic methods for detection and evaluation of valvular 695

Figure 31-14 Hemodynamic responses in a patient with severe valvular aortic stenosis showing increased vascular return associated with uterine contractions. BP, blood pressure; EKG, electrocardiogram; FHR, fetal heart rate; HR, heart rate; PAP, pulmonary artery pressure. (From Easterling TR, Chadwick HS, Otto CM, Benedetti TJ: Obstet Gynecol 1988;72:113–118. Reprinted with permission from The American College of Obstetricians and Gynecologists.)

regurgitation are applicable to the pregnant patient. Physiologically, it is plausible that pregnancy may result in a decrease in regurgitant severity due to the afterload reduction of decreased systemic vascular resistance. This potentially beneficial physiologic effect may be counterbalanced, to some extent, by the hormonal and vascular changes of pregnancy. Increased aortic root dimensions may increase aortic regurgitant severity, whereas increased laxity of valve tissues may lead to an increase in mitral regurgitant severity. Valvular regurgitation may be well tolerated during pregnancy by some patients. Other patients develop signs and symptoms of congestive heart failure with pulmonary congestion, decreased exercise tolerance, orthopnea, and paroxysmal nocturnal dyspnea. Decompensation can occur in patients with chronic valvular regurgitation because of either (1) the increased cardiac output demands of pregnancy or (2) worsening of the

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underlying valvular abnormality (e.g., chordal rupture in a patient with myxomatous mitral valve disease). Echocardiographic evaluation can distinguish between these two possibilities and can help optimize therapy in the decompensated patient. Quantitation of valvular regurgitant severity and evaluation of left ventricular systolic function may be confounded by the anatomic and hemodynamic changes of pregnancy. In patients with severe regurgitation, decreased systemic vascular resistance due to pregnancy can result in an apparent decrease in regurgitant severity and improvement in left ventricular systolic function. In these patients, surgical intervention may be inappropriately delayed. Conversely, left ventricular dimensions may be slightly larger than in the nonpregnant state, resulting in misdiagnosis in a patient with only moderate regurgitation. In either case, postpartum reevaluation of regurgitant severity and ventricular function will provide accurate data for clinical decision making. Prosthetic Heart Valves

The increased heart rate and stroke volume associated with normal pregnancy affect Doppler evaluation of velocities and pressure gradients across prosthetic valves. Thus, the volume flow rate should be taken into consideration when evaluating prosthetic valves in pregnant women. The alterations in loading conditions may also affect the accuracy of the pressure half-time method.[120] The outcome of pregnancy is significantly affected by the presence of a prosthetic heart valve.[121] [122] [123] [124] With mechanical valves, the risks of valve thrombosis (8% to 9%), embolic events (3% to 5%), serious bleeding (5%), heart failure (28%), and maternal death (4% to 8%) are high[125] even with careful monitoring of anticoagulation. With a bioprosthetic valve, there is less risk of maternal death (0 to 5%), but accelerated valve degeneration during pregnancy results in a high rate of heart failure (35%) and urgent repeat replacement of the valve in the early postpartum period (35%). [122] The effect of pregnancy in accelerating valve degeneration is underscored by the observation that women with prosthetic heart valves and more 696

Figure 31-15 (color plate.) Rheumatic mitral stenosis in a 39-year-old

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pregnant Samoan woman. Color flow imaging in the apical fourchamber view (A) shows rheumatic mitral stenosis with proximal flow acceleration and a high-velocity jet (arrow). The pulsed wave Doppler tracing (B) shows a mean gradient of 10 mm Hg and a mitral valve area of 1.2 cm2 by the pressure half-time method (D). Pulmonary artery systolic pressure was estimated to be 40 mm Hg on the basis of the tricuspid regurgitant jet velocity of 2.8 m second (C) and mild dilation of the inferior vena cava. The patient did well throughout pregnancy and delivery and was followed on medical therapy. LA, left atrium; LV, left ventricle; RA, right atrium.

than one pregnancy have a lower 10-year graft survival rate for bioprosthetic valves (17%) than women with only one pregnancy (55%).[126] Echocardiography plays a critical role in identifying valve dysfunction and in assessing valve degeneration during pregnancy (see Fig. 31-11) . A baseline Doppler echocardiographic study in the prepartum period or early in pregnancy is needed for accurate assessment of changes later in pregnancy. Cardiomyopathies The risk of pregnancy in a patient with a known cardiomyopathy is related to the severity of the underlying disease.[127] In familial types of cardiomyopathy (hypertrophic and some forms of dilated cardiomyopathy), the genetic implications of the diagnosis also need to be taken into consideration. Thus, echocardiography is used to confirm or exclude the diagnosis in patients considering pregnancy who are at risk for an inherited cardiomyopathy, and to assess disease severity in patients with a known cardiomyopathy.[128] Pregnancy in patients after cardiac transplantation has also been described,[129] although maternal (10% mortality) and fetal outcomes are poor.[130] Peripartum cardiomyopathy[127] [131] presents in late pregnancy or post partum with clinical signs and symptoms of heart failure (Fig. 31-18) (Figure Not Available) . The diagnosis typically is established by echocardiography in the appropriate clinical setting. Echocardiographic monitoring of disease severity, especially left ventricular systolic function, helps optimize patient management. Other Heart Diseases in Pregnancy Marfan's Syndrome

Pregnancy in patients with Marfan's syndrome is associated with an increased risk of aortic dissection (Fig. 31-19) . Initial series suggested a

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very high risk: of 32 women 697

Figure 31-16 (color plate.) A 21-year-old black woman with rheumatic mitral valve disease who presented with severe mitral regurgitation in the first trimester of pregnancy. The parasternal long-axis view (A) shows rheumatic mitral valve disease with commissural fusion and diastolic doming (arrow) with marked left atrial (LA) and left ventricular (LV) enlargement. Color flow imaging in the apical four-chamber view (B) shows severe mitral regurgitation. After delivery of a healthy infant, the patient underwent surgical mitral valve repair. Intraoperative transesophageal echocardiography (C) confirmed severe mitral regurgitation. The surgical repair involved a commissurotomy, placement of an annuloplasty ring (arrows), and lateral posterior leaflet fixation (D). The mitral regurgitation resolved and there were no further clinical symptoms. Ao, aorta; RA, right atrium; RV, right ventricle.

with Marfan's syndrome and at least one pregnancy, 20 (63%) suffered an acute aortic dissection and 16 (50%) died during pregnancy.[132] Subsequent series suggested a maternal mortality rate of only 1%, especially when aortic diameter is only mildly increased.[133] [134] However, in a recent study of 91 pregnancies in 36 women with Marfan's syndrome, 4 of 36 (11%) had dissection related to pregnancy and 2 others required aortic surgery following delivery for a total aortic complication rate of 17%.[135] The mechanism of aortic dissection in pregnant women with Marfan's syndrome presumably relates to (1) the underlying defect in aortic wall structure, (2) normal structural changes in the aortic wall with pregnancy, and (3) the increased stroke volume and left ventricular dP/dt of pregnancy. Gestational hypertension may further aggravate the risk of dissection.[136] With careful echocardiographic evaluation of aortic root dimensions and geometry, together with a review of the patient's family history and consultation between the cardiologist and geneticist,[137] women with Marfan's syndrome can be counseled about the potential risks prior to pregnancy, especially since the risk of dissection during pregnancy appears to be directly related to the degree of aortic root dilation. However, it is notable that some Marfan's patients suffer aortic dissection with only mildly increased aortic root dimensions.[135] [138] Treatment with beta blockade[139] , [140] 698

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Figure 31-17 (color plate.) Cleft mitral valve and atrial septal defect in a pregnant patient with a cardiac murmur. A modified four-chamber view (A) shows the atrial septal defect in an ostium primum position (arrow), with color flow imaging (B) showing a prominent flow stream across this region. A parasternal short-axis view (C) shows a cleft anterior mitral valve leaflet (arrows), and color flow imaging in a long-axis view (D) shows mild to moderate mitral regurgitation. Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Figure 31-18 (Figure Not Available) Onset of peripartum cardiomyopathy in relation to time of delivery with data derived from previously reported series including 347 patients. (From Homans DC: N Engl J Med 1985;312:1432–1437. Reprinted by permission of The New England Journal of Medicine. Copyright 1985, Massachusetts Medical Society.)

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Figure 31-19 This 22-year-old black woman was referred to the high-risk obstetrics center at 8 months of pregnancy for evaluation of possible Marfan's syndrome. Standard (A) and high (B) long-axis parasternal views show mild aortic (Ao) root dilation with relative preservation of the sinuses of Valsalva. Although the patient did meet numerous clinical criteria for Marfan's syndrome, the degree of aortic root enlargement was mild. There were no complications during pregnancy or delivery. LA, left atrium; LV, left ventricle.

ade[139] [140] and careful peripartum anesthetic management[141] may improve the prognosis in pregnant Marfan's patients. Some authors have even suggested prophylactic aortic root replacement when pregnancy is planned, if aortic root dilation is present.[142] [143] Successful surgical repair during pregnancy of aortic dissection in Marfan's syndrome has been reported.[144] Aortic Dissection

There is an increased risk of aortic dissection in pregnancy, even in women without Marfan's syndrome. Echocardiography is often the initial diagnostic test requested in these patients. Prompt recognition and surgical intervention can be lifesaving.[145] Ischemic Heart Disease

Clinical manifestations of coronary artery disease are rare during pregnancy owing to the low prevalence of atherosclerotic coronary artery narrowing in

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women of childbearing age. In women aged 15 to 44 years, the incidence of myocardial infarction unrelated to pregnancy is 5.0 per 100,000 womenyears and the rate of cerebrovascular events is 10.7 per 100,000 womenyears.[146] Occasional cases are recognized, however.[147] A literature review of 125 cases of myocardial infarction in pregnancy found the highest incidence in multigravida women older than 33 years of age. Myocardial infarction tended to occur the third trimester, often during labor and delivery.[148] Only 43% of the myocardial infarctions were due to atherosclerosis, 21% were thrombotic without evidence of underlying atherosclerosis. A total of 165 were due to coronary dissection and in 29% coronary anatomy was normal, suggesting the possibility of coronary spasm.[146] Diagnosis of myocardial infarction after delivery should be based on troponin I levels, as there is a twofold increase in myoglobin and creatinine kinase myocardial band in normal women within 30 minutes of delivery.[149] Thrombolytic therapy is contraindicated in pregnancy and the early postpartum period, so the optimal clinical approach to revascularization is percutaneous balloon angioplasty with or without placement of an intracoronary stent, although coronary bypass grafting surgery during pregnancy also has been described.[150] [151] [152] [153]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Monitoring in Pregnant Patients In addition to monitoring disease severity and cardiovascular hemodynamics in pregnant patients, both transthoracic and transesophageal [118] echocardiography have been used to monitor diagnostic and therapeutic procedures. One of the advantages of echocardiographic monitoring during pregnancy is the avoidance of exposure to ionizing radiation. Echocardiographic monitoring in pregnant women has been reported for electrophysiologic testing,[154] pacer implantation,[155] and percutaneous balloon mitral valvuloplasty.[156]

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Impact of Echocardiography: Common Clinical Presentations During Pregnancy Pulmonary Edema and Heart Failure in the Third Trimester and Peripartum Period In the pregnant patient with acute respiratory distress, the initial differential diagnosis is between a cardiac and a noncardiac cause such as acute pulmonary embolism, pneumonia, or an acute viral syndrome. An echocardiographic study in these situations helps demonstrate normal cardiac anatomy and function, allowing attention to be focused on potential noncardiac causes of the illness 700

TABLE 31-6 -- Respiratory Distress in Pregnancy: Echocardiographic Differential Diagnosis Pathophysiology Cardiac ↓ LV systolic function

LV diastolic function LV pressure overload Impaired cardiac filling

Examples Peripartum cardiomyopathy Congenital heart disease Dilated cardiomyopathy Hypertension Aortic stenosis Aortic stenosis Hypertension Mitral stenosis Pericardial disease

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LV volume overload Noncardiac Capillary "leak" Infection Pulmonary vascular obstruction ↓ Pulmonary blood flow LV, left ventricular.

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Aortic regurgitation Mitral regurgitation Preeclampsia Adult respiratory distress syndrome Pneumonia Viral syndrome Pulmonary embolus Eisenmenger's syndrome

such as pneumonia or adult respiratory distress syndrome associated with pyelonephritis. Conversely, if there is a cardiac cause, it can be quickly identified and evaluated, permitting appropriate therapeutic interventions. Of the cardiac conditions encountered in pregnant patients with pulmonary edema in the third trimester or in the peripartum period (Table 31-6) , the most prevalent are mitral valve stenosis and peripartum cardiomyopathy. On physical examination, the diastolic rumbling murmur of mitral stenosis is difficult to appreciate and the patient herself is often unaware of a heart condition. The added hemodynamic burden of pregnancy may result in a previously asymptomatic patient presenting with "sudden" and "unexplained" pulmonary edema. It is not unusual for the echocardiogram (ordered for other reasons) to be the first clue that valvular obstruction is present. A patient with peripartum cardiomyopathy may present with the insidious onset of heart failure symptoms, or the condition may be more abrupt in onset. In the latter case, it is likely that the patient has unrecognized heart failure symptoms that can be elicited in retrospect after the onset of pulmonary edema. The degree of left ventricular systolic dysfunction is variable. Typically, clinical symptoms are first noted between 1 month ante partum and 1 month post partum. [127] [157] Echocardiographically, peripartum cardiomyopathy is indistinguishable from other forms of dilated cardiomyopathy. Evaluation of the Pregnant Patient with a Cardiac Murmur

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A systolic murmur is a common finding during pregnancy, being reported in as many as 80% of women in some series.[158] This murmur typically is a "flow" murmur caused by the increased volume flow rate of pregnancy. Depending on its location and timing, it most often originates from the pulmonic valve, although some flow murmurs of pregnancy may be due to high flow across the aortic valve. With the normal murmur of pregnancy, Doppler echocardiography shows no abnormal flow patterns, although antegrade velocities are increased, as expected in pregnancy. One study of 103 women with no previous cardiac history referred for evaluation of a murmur during pregnancy found that 79% had a benign murmur on physical examination, and all of these individuals had normal results on Doppler echocardiogram.[158] Benign ejection murmurs were soft and mid-systolic. Even in the 14% with a loud or long ejection murmur, most had normal Doppler study results, with abnormalities seen in only three patients (one mitral valve prolapse with mild mitral regurgitation, one nonobstructive hypertrophic cardiomyopathy, one bicuspid aortic valve). In contrast, in the 7% of patients with a pansystolic, late systolic, or diastolic murmur, all had abnormal echocardiographic results. This group included three ventricular septal defects, one large atrial septal defect, one atrial septal defect in conjunction with rheumatic mitral regurgitation, one mitral valve prolapse, and one nonobstructive hypertrophic cardiomyopathy. Although it is likely that the prevalence of specific cardiac diagnoses will vary with the population base, this study clearly demonstrates the importance of careful patient selection in requesting echocardiography for evaluation of a murmur in pregnancy. To minimize the inappropriate use of echocardiography in pregnant women, one approach is to limit echocardiographic evaluation to pregnant women with a murmur only if they have (1) a history of underlying heart disease, (2) definite cardiac symptoms, (3) a grade 3/6 or greater systolic murmur, or (4) a diastolic murmur. Use of these criteria will avoid unnecessary echocardiography. Conversely, it is critically important to perform an echocardiographic examination in patients with pathologic or possibly pathologic murmurs. Many cases of previously undiagnosed congenital heart disease, valvular stenosis, and valvular regurgitation are recognized during pregnancy. In addition to the prognostic information obtained by having the correct cardiac diagnosis, the echocardiographic data resulted in significant changes in patient management. Such changes included recommendation of endocarditis prophylaxis at delivery for structural heart disease, surgical

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closure of an atrial septal defect post partum, and genetic counseling in patients with inherited diseases in the study described earlier.[158] Like other clinical guidelines, these criteria are not absolute and, given the negligible risk of echocardiography, it is preferable to err on the side of performing echocardiographic studies in normal women than to miss a case of significant heart disease in a pregnant patient. When a pathologic murmur is present, it is incumbent on the echocardiographer to make sure the referring physician is aware of the significance of this finding and to ensure appropriate assessment of maternal and fetal risk. In view of the multidisciplinary nature of care for pregnant women with heart disease and the impact of maternal heart disease on both mother and fetus, referral to a maternal-fetal specialist in a high-risk obstetrics clinic is 701

needed for optimal care, particularly in patients with hemodynamically significant lesions. This consideration also applies to nonpregnant women with heart disease in whom appropriate counseling regarding the risks of pregnancy and contraceptive options is needed either to avoid unnecessary anxiety and delay in starting a family (if the maternal-fetal risk is low) or to avoid a high-risk complicated pregnancy (when the maternal-fetal risk is high). Communication with the maternal-fetal specialist is often initiated by the echocardiographer. Mitral Valve Prolapse Because a diagnosis of mitral valve prolapse is common in young women, concern is often raised that this diagnosis may affect the risk or management of pregnancy; some series report a history of mitral valve prolapse in as many as 1.2% of all pregnancies.[159] No echocardiographic changes regarding the presence or degree of mitral prolapse[159] and no increase in maternal risk have been seen in pregnant patients with this diagnosis. [160] [161] Many of these women have only minor abnormalities of leaflet anatomy or motion without significant valvular dysfunction. Thus, echocardiography plays an important role in reassuring both patient and referring physician that the risk of pregnancy is not affected by this diagnosis and that the management of pregnancy and the peripartum period can be considered routine, other than the need for endocarditis prophylaxis. In the patient with significant functional mitral valve disease— myxomatous leaflets and mitral regurgitation—echocardiography allows

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assessment of the degree of regurgitation and the left ventricular response to chronic volume overload. Palpitations and Arrhythmias in Pregnancy Most women experience an increased awareness of their heartbeat with occasional premature ventricular and atrial beats during pregnancy. Significant arrhythmias, associated with hypotension, dizziness, or shortness of breath, most often occur in patients with known underlying heart disease or a history of arrhythmias. The onset of symptomatic arrhythmia during pregnancy warrants echocardiographic evaluation, as in the nonpregnant patient, to evaluate for structural heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Limitations of Echocardiography and Alternative Approaches Echocardiography often provides all the information needed for patient management in pregnant women with heart disease, but in some situations other diagnostic approaches or imaging modalities may be needed. If transthoracic imaging is inadequate because of poor ultrasound tissue penetration, transesophageal echocardiography is appropriate and can be safely performed during pregnancy. Other useful imaging procedures in patients with congenital and valvular heart disease include radionuclide ventriculography, magnetic resonance imaging, computed tomographic imaging, and angiographic evaluation in the catheterization laboratory. In pregnant patients, the use of ionizing radiation with some of these techniques needs to be considered in the overall risk-benefit analysis of whether evaluation is needed during pregnancy or can be safely postponed to the postpartum period. When direct and repeated measurements of pulmonary pressures, left ventricular filling pressures, and cardiac output are needed, invasive monitoring with an indwelling right heart catheter is the procedure of choice. In patients with significant heart disease, invasive monitoring may be needed in the peripartum period to allow maintenance of optimal loading conditions under the changing volume and hemodynamic conditions of labor, delivery, and anesthesia.

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Section 7 - Other Vascular and Systemic Diseases

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Chapter 32 - Hypertension Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy John S. Gottdiener MD Joseph A. Diamond MD Robert A. Phillips MD, PhD

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Clinical and epidemiologic studies have convincingly demonstrated the independent predictive value of echocardiographically measured left ventricular hypertrophy (LVH) for cardiovascular morbidity and mortality. [1] [2] [3] [4] [5] [6] [7] [8] Hypertension affects over 20% of the American

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population (60% of African Americans older than 60 years of age).[9] Given the wealth of information provided by cardiac ultrasonography, it is tempting to apply echocardiography widely to define pathophysiology in individual patients. Although echocardiography is unquestionably informative, however, its routine use in all patients with hypertension could impose enormous costs that are not justified by clinical benefit. These reasons are all compelling enough to review the role of echocardiography in the evaluation of patients with hypertension. Pathologic findings in hypertension include increased LV wall thickness, increased cardiac weight, perivascular and myocardial fibrosis, and increased myocyte diameter.[10] Of note, diabetes mellitus in combination with hypertension is associated with a higher risk of congestive heart failure[11] and myocardial infarction[12] than occurs with either disease alone. Comparing autopsy findings in patients with hypertension, those with diabetes, and those with both diseases, it was found that heart weight and fibrosis are greatest in diabetic hypertensive hearts.[10] Moreover, findings of congestive heart failure are associated with the degree of myocardial fibrosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Studies in Hypertension Concentric versus Eccentric Hypertrophy The strong clinical relationship between congestive heart failure and hypertension initially suggested to clinicians the existence of end-stage hypertensive cardiomyopathy, characterized by a poorly contractile, dilated left ventricle; however, this finding has not been proved in human patients with hypertension uncomplicated by coronary artery disease. In studies of cardiac anatomy and function in hypertensive subjects using echocardiography, Figure 32-1 Left ventricular (LV) architecture characterized by relation of wall thickness to cavity size. LVDD, LV diastolic cavity dimension in diastole alone and after indexing (LVDDI) for body surface area; LVH, LV hypertrophy. (From Gottdiener JS, Reda DJ, Materson BJ, et al: J Am Coll Cardiol 1994;24:1492–1498, with permission from the American College of Cardiology.)

concentric LVH (Fig. 32-1) has been the usual cardiac finding.[13] [14] [15] [16] [17] [18] With concentric LVH there is an increase in LV weight, a relatively uniform increase in septal and free wall thickness, and a normal or slightly increased cavity size. This pattern, associated with pressure overload from hypertension or aortic stenosis, results from increased thickness of myocardial cells owing to addition of sarcomeres in parallel.[19] By convention, concentric LVH is defined as a ratio of the combined thickness of the septum and free wall to cavity dimension in diastole greater than 0.45. Systolic function, measured by ejection phase indices such as fractional shortening or ejection fraction, typically is normal or enhanced. Most clinical echocardiography studies have used previously treated patients with hypertension, whereas population-based cohorts usually include a mix of subjects with untreated hypertension as well as those with treated hypertension. In a study of newly identified untreated patients,[20] an

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increase in relative wall thickness, without increases in LV weight (i.e., concentric remodeling), was more common than concentric hypertrophy. In eccentric hypertrophy (see Fig. 32-1) , the LV cavity dilates, wall thickness remains normal, and relative wall thickness remains less than 0.45. This pattern is usually associated with volume overload, but it can occur in association with hypertension. Eccentric hypertrophy is caused by cell elongation from addition of sarcomeres in series. Myocardial Composition in Left Ventricular Hypertrophy and Congestive Heart Failure Myocytes constitute approximately 75% of the heart mass; the remaining 25% of the heart mass is cardiac interstitium composed of the coronary vasculature, fibroblasts, macrophages, and mast cells. In hypertensive heart disease, myocytes hypertrophy and interstitial components undergo hyperplasia, hypertrophy, and remodeling. [21] [22] [23] Increases in myocyte and interstitial mass that occur as the heart hypertrophies adversely alters ventricular and vascular performance, creating a substrate for 707

increased cardiovascular morbidity and mortality. Excess collagen production by fibroblasts increases total interstitial and periarteriolar fibrosis, which reduces ventricular compliance. Echocardiographically derived parameters (pixel intensity, skewness, kurtosis, and the broad band of echoes about the distribution) have been shown to correlate with histologically assessed collagen volume in patients with hypertension and LVH.[24] Vascular smooth muscle cells undergo hyperplasia and hypertrophy, resulting in medial hypertrophy, coronary artery wall remodeling, and an increased ratio of coronary wall thickness to lumen diameter.[25] These structural changes decrease vasodilator capacity. Although the precise structural changes that lead to decompensated systolic and diastolic function from compensated LVH are not currently known, myocardial fibrosis likely plays an important role. As part of the hypertrophic response, cardiac fibroblasts undergo a phenotypic change, assuming a myofibroblast configuration. Stimulated myofibroblasts proliferate and increase production of extracellular matrix proteins, including fibronectin, laminin, and collagen I and III. This increase results in progressive fibrosis. Many of these processes are controlled by integrins, which are cell surface receptors that mediate the cell's ability to interact

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with its environment.[26] Progressive fibrosis of the heart is a major component of the remodeling process in hypertensive heart disease and leads to LV systolic dysfunction (systolic congestive heart failure [CHF-S]) through impaired myocyte contractility, oxygenation, and metabolism. Several experimental studies suggest that this process may be reversible, including a study of hypertensive patients, which showed that angiotensin-1 receptor blockade with losartan results in decreased plasma levels of growth factors including endothelin-1, basic fibroblast growth factor, and platelet-derived growth factor.[27] This finding may help to explain the positive survival impact of angiotensin converting enzyme inhibitors, and it may suggest positive benefits of angiotensin receptor blockers in patients with CHF-S.[28] [29] Myocyte hypertrophy may decrease the efficiency of excitation-contraction coupling, leading to decreased efficiency of contraction and development of CHF.[30] Disproportionate Septal Thickening Echocardiography studies have shown disproportionate septal thickening in 6% to 18% of hypertensive patients,[31] [32] suggesting overlap of the cardiac manifestations of hypertension with those of hypertrophic cardiomyopathy in which asymmetric septal hypertrophy (e.g., a ratio of septal to free wall thickness ≥ 1:3) is a prominent feature. The echocardiographic findings in most patients with hypertensive hypertrophy, however, differ substantially from those of hypertrophic cardiomyopathy.[33] [34] Although localized increases in midanterior septal thickness measurements may result in septal-to-free wall ratios exceeding the criterion of 1:3, commonly used to describe asymmetric septal hypertrophy, most hypertension patients with disproportionate septal thickening do not have the substantial increases in wall thickness or the extensive distributions of asymmetric hypertrophy of the LV wall characteristic of hypertrophic cardiomyopathy. Because right ventricular (RV) muscle is commonly thickened in patients with hypertensive LVH,[35] [36] [37] it is possible that inclusion of RV muscular structures may have contributed to the apparent thickness of the midanterior ventricular septum in earlier studies using M-mode echocardiography without two-dimensional (2D) guidance. Even using 2D guidance to acquire echocardiographic data, M-mode recordings made without inspection of the simultaneously acquired 2D images still can lead to incorrect measurements. Nonetheless, a 2D echocardiography study[38] of patients with hypertension and unusually thickened LV walls did find patterns of hypertrophy that overlapped those in patients with hypertrophic cardiomyopathy.

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Hypertensive Hypertrophic Cardiomyopathy of the Elderly The term hypertensive hypertrophic cardiomyopathy of the elderly has been used to describe substantial increases in LV wall thickness, exaggerated systolic function, and impairment of diastolic LV filling, particularly in elderly women.[39] In fact, the echocardiogram in such patients usually differs substantially from that in patients with hypertrophic cardiomyopathy. The original description by Topol et al[39] of elderly white women with marked increase in relative wall thickness, small cavity size, and systolic hyperfunction is consistent with more recent observations[40] of "inappropriate hypertrophy," that is, hypertrophy in excess of that which would be predicted by the loading conditions of the ventricle. Specifically, such patients have lower wall stress than normal, exaggerated systolic function, small LV cavity, and marked increases in relative wall thickness. Pearson et al[41] also found that such patients had long-standing hypertension and were predominantly female, but mostly African American. On Doppler imaging, these patients had obstruction localized to the LV outflow tract, although midventricular obstruction also has been described.[42] Late peaking of the systolic Doppler waveform in the midventricle and LV outflow tract[41] and systolic anterior motion of the mitral valve[43] have been noted, similar to patterns seen in genetically transmitted hypertrophic cardiomyopathy.[42] Also similar to genetically transmitted hypertrophic cardiomyopathy has been the presence of provocable obstruction with nitroglycerin on Doppler examination.[44] The Framingham Study[45] also found a similar pattern of cardiac hypertrophy in elderly women, but not men, with systolic hypertension, and others[40] have suggested that patients with exaggerated hypertrophic responses may have a neurohormonal drive to hypertrophy. Importantly, these patients may fail to decrease, or actually increase, LV mass despite adequate lowering of blood pressure with drugs. Prevalence of Left Ventricular Hypertrophy in Hypertension The reported prevalence of LVH in hypertension has varied widely from about 20% to 49% depending on 708

demographic and hemodynamic characteristics of the patient population. The geometric pattern of LVH varies as well. Eccentric LVH is more common in younger subjects and those with volume overload.[46]

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With aging, eccentric LVH may change to concentric LVH as a consequence of age-associated increases in peripheral vascular resistance. African-American men in hypertensive studies have been shown to have a greater proportion of concentric LVH than do whites,[18] [47] possibly related to less pronounced nocturnal decline in blood pressure in African American than white patients.[48] Men are more likely to have eccentric LVH, whereas women are more likely to have concentric LVH. [45]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Left Ventricular Hypertrophy and Risk A principal use of echocardiography in cardiovascular epidemiologic studies has been the identification of LVH, a discrete variable based on selection of a partition value of LV mass. As surrogate end points of risk, abnormalities of diastolic,[49] [50] [51] [52] [53] [54] [55] [56] [57] electrophysiologic,[6] [8] [58] [59] , and systolic function[60] [61] [62] [63] [64] [65] [66] [67] [68] have been associated with the presence of LVH. The importance of LVH in the morbidity of hypertensive disease has been underscored by the number of electrocardiographic and echocardiographic studies that have convincingly demonstrated its importance as an independent predictor of morbidity and mortality. [3] [5] , [59] [69] Not only does LVH as a dichotomous variable predict adverse outcome, but the magnitude of LV mass as a continuous variable also is associated with cardiovascular risk, even with values for LV mass within the "normal range." In the Framingham Study, it was shown[4] that for each 50 g/m increase in LV mass (corrected for height) there was a relative risk for mortality of 1.73, even in subjects free of clinically apparent cardiovascular disease. It also was demonstrated that this risk was independent of blood pressure, age, antihypertensive treatment, and other cardiovascular risk factors. It has been reported[5] that individuals with a higher relative wall thickness at any value of LV mass, including values below the partition value for LVH (i.e. concentric remodeling)[5] [70] have greater risk of cardiovascular events. During a 10-year follow-up of hypertension patients it was shown[5] that the incidence of a cardiovascular event was 30% in patients with concentric LVH, 25% in those with eccentric LVH, 15% in those with concentric remodeling, and only 9% in those with normal LV mass and geometry (Fig. 32-2) (Figure Not Available) . Others have suggested that the prognostic importance of concentric remodeling may not be independent of LV mass.[71] Importantly, there is an association of LVH with complex ventricular arrhythmia, a possible precursor of sudden death in hypertensive patients, even in patients without coronary artery disease on angiography.[8] In

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patients with reversible myocardial perfusion defects on thallium scintigraphy, both LVH and inducible ischemia are independently associated with ventricular arrhythmia. [58] Although there is comorbidity between hypertension, LVH, and coronary artery disease, LVH is nonetheless associated with an increase in mortality even in the absence of Figure 32-2 (Figure Not Available) Relation of left ventricular (LV) architecture, LV hypertrophy (LVH), and outcome. Increased mortality (top) and morbidity (bottom) are associated with increased relative wall thickness (>0.45) even in the absence of increased LV mass (<125 g/m2 ), that is, concentric remodeling. (From Koren MJ, Devereaux RB, Casale PN: Ann Intern Med 1991;114:345–352, with permission.)

coronary disease on angiography. Studying an inner-city cohort of 785 patients, Ghali et al[69] found that LVH on echocardiography, using LV mass corrected for body surface area, was associated with an even higher risk ratio for all-cause death in patients without coronary artery disease (4.14; 95% confidence limits, 1.77 to 9.71) than in patients with the disease (2.14; 95% confidence limits, 1.24 to 3.68), even when adjusted for age, gender, and hypertension.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Relationship of Left Ventricular Mass to Body Size, Age, and Gender: What's Normal? The heart is no exception from other body organs in that its size is proportionate to that of the body.[72] [73] Numerous studies of population cohorts have demonstrated the relationship between echocardiographic measurements, height, and weight.[74] [75] [76] [77] [78] [79] Moreover, echocardiographic dimensions and LV mass decrease with starvation,[72] [73] [80] [81] , and they increase with refeeding.[80] , [82] Hence, in order to assess whether individual echocardiographic dimensions, including derived LV mass, differ from normal values, some sort of adjustment for body 709

size is desirable. One commonly used adjustment is to divide (normalize) LV mass by body surface area; however, echocardiographic studies of normal subjects from infancy through old age have shown that cardiac dimensions are not linearly related to body surface area.[74] [75] Moreover, variance in body weight may reflect more than allometric (physiologic growth) factors. Specifically, obesity both increases blood pressure[83] [84] and is a strong stimulus for LVH,[85] [86] greater than blood pressure itself.[18] [87] Therefore, normalization of LV mass by body surface area, which is computed using body weight, tends to flatten the contribution of obesity to LV mass and LVH.[85] [88] For that reason, independent groups of investigators have suggested using height for allometric indexation.[85] [88] The Framingham group[85] has developed norms for LV mass indexed by height alone, whereas studies from the Cornell group[89] have suggested that normalization is better accomplished by dividing by height to the power of 2.7. In the elderly there may be different relationships between height and LV mass. In the Cardiovascular Health Study,[90] height added nothing to a statistical model of LV mass that used body weight once other covariates

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including systolic blood pressure, prevalent disease, and diastolic blood pressure were taken into account. A possible explanation for this observation is that height in the elderly may reflect disease as well as allometric influences, probably from vertebral compression with aging. An additional option for normalizing LV mass to body size is the use of fatfree mass,[87] [91] which may be determined by measurement of bioelectric impedance.[92] The application of LV mass indexed to fat-free body mass in one study[93] resulted in markedly lower LVH prevalence values in obese subjects compared with LV mass criteria indexed by height or by weight.[2] [7]

Although advancing age has been associated with increases in LV mass,[75] [94] [95] this increase may be the result of concomitant disease rather than an effect of aging per se.[95] [96] Effects of gender on LV mass are somewhat problematic.[75] [97] Echocardiographic studies have shown greater LV mass in men than women.[13] [74] [75] , [77] [98] Moreover, gender-based difference in LV mass appears to begin at puberty (DeSimone, personal communication). It is uncertain, however, whether the differences in LV mass represent an independent effect of gender, or the effect of gender differences in lean body weight, itself an important descriptor of LV mass.[77] [96] Greater lean body weight in men may account for greater LV mass in men than in women. [96] The effect of gender on LV mass seems to be minor, even taking total body weight into account.[75] [76] [77] Using indexation of LV mass by fat-free body mass, gender differences in normal values for LV mass no longer exist.[93] Hence, the determination of abnormal LV mass in individual patients, or groups of patients, undergoing clinical echocardiographic evaluation may be complicated by uncertainty about what is abnormal. Nonetheless, LV mass has generally been "corrected" for body size (height or body surface area) and presented as gender-specific values. Table 32-1 (Table Not Available) summarizes normal values for LV mass using these various approaches.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Demographic and Physiologic Descriptors of Left Ventricular Hypertrophy in Hypertension Although elevated blood pressure is considered to be an important factor promoting increases in LV mass and LVH, it has become clear that only a portion of the observed variance in LV mass is accounted for by blood pressure. Other clinical descriptors that have been implicated as contributing to LVH include obesity, age, race, dietary sodium intake, insulin resistance, and other neurohormonal factors such as adrenergic factors and the reninangiotensin system (Table 32-2) .[47] [57] [78] [85] , [86] [95] , [99] [100] [101] [102] [103] [104] [105]

Obesity In one study of normal subjects and patients with hypertension [100] obesity was associated with eccentric LVH consequent to LV cavity dilation. LV mass was not higher in lean hypertensive subjects than in lean normotensive subjects. Hammond et al[77] also found that increased LV mass with obesity was a consequence of LV cavity dilation but not increased wall thickness. In the Framingham Study,[85] [86] which used echocardiography in a large population-based cohort, obesity measured by body mass index or by skinfold thickness was associated with substantial increases in the prevalence of LVH in men. Although both hypertension and obesity were independently associated with LV mass and wall thickness, the associations were additive but not synergistic. More recently, Liebson et al[47] noted that in patients with mild hypertension and virtual absence of LVH on electrocardiogram (ECG), body weight and body mass index were important predictors of LV wall thickness, mass, and hypertrophy. Eccentric dilated hypertrophy was the most common pattern (52%) of LVH, followed by concentric LVH (33%). We evaluated 692 male veterans with mild-moderate hypertension and a high prevalence (63% using Framingham criteria) of LVH. LV mass, LVH

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prevalence (Fig. 32-3) , LV wall thickness, and LV cavity volume all were greater in obese and overweight hypertensive men than in hypertensive subjects of normal weight. Moreover, despite the importance of obesity in the cohort, even lean hypertensive subjects with mild-moderate hypertension had a high prevalence of LVH, in contrast to a previous study. [100] Also, relative wall thickness was equally increased in all adiposity groups. Hence, concentric hypertrophy is common even in obese men with mild-moderate hypertension. Moreover, we found that obesity amplified the slope relationship of systolic blood pressure with LV mass (Fig. 32-4) . Therefore, there appears to be a synergistic effect of obesity and hypertension on LV mass and hypertrophy. Age Studies have differed in their findings on the independence of the relationship between age and LV mass.[47] , [78] [86] , [95] [103] Our findings supported those of the Treatment 710

TABLE 32-1 -- Normal Values for Left Ventricular Mass (Not Available) Data from: Gardin J, Henry W, Savage D, et al: J Clin Ultrasound 1979;7:439– 447. Devereux RB, Lutas EM, Casale PN, et al: J Am Coll Cardiol 1984;4:1222–1230. Hammond IW, Devereux RB, Aldermann MA: J Am Coll Cardiol 1986;7:639–650. Byrd BF, Wahr D, Wang YS, et al: J Am Coll Cardiol 1985;6:1021– 1025. Levy D, Savage DD, Garrison RJ, et al: Am J Crdiol 1987;59:956–960. Koren MJ, Devereuz RB, Casale PN: Ann Int Med 1991;114:345–352. DeSimone G, Daniels SR, Devereux RB, et al: J Am Coll Cardiol 1992;20:1251–1260. Kuch B, Hense HW, Gneiting B, et al: Circulation 2000;102:405–410, with permission.

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Cardiovascular Health Study, Gottdiener J (personal communication).

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TABLE 32-2 -- Factors That Affect Left Ventricular (LV) Mass Demographic and physiologic variables Age Race Gender Body size Hemodynamic workload Blood pressure Vascular resistance or impedance LV inotropy and geometry Stress Exercise Physiologic Nonhemodynamic factors Renin-angiotensin system Parathyroid hormone Genetic susceptibility Growth hormones Salt intake of Mild Hypertension Study (TOMHS)[47] and Hammond et al[101] in suggesting that in patients with established hypertension, the relationship of LV mass to age is not independent of blood pressure. Moreover, in the Cardiovascular Health Study, an epidemiologic study of almost 6000 community-based men and women older than 65 years of age, Gardin et al [106] found that after adjustment for other covariates, age was only weakly associated with LV mass.

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Although elderly normotensive subjects do not have higher LV mass than do younger subjects,[107] wall thickness is greater, and the Doppler ratio of early to late diastolic filling (E/A ratio) is decreased. In the Systolic Figure 32-3 Prevalence of left ventricular hypertrophy (LVH) according to body weight category determined from body mass index (weight/height2 ) in patients with established hypertension. Indexing of LV mass by body surface area (Cornell criteria) results in lower prevalence of LVH. * P< .05 versus normal weight. †P < .05 versus overweight. (From Gottdiener JS, Reda DJ, Materson BJ, et al: J Am Coll Cardiol 1994;24:1492–1498, with permission from the American College of Cardiology.) Figure 32-4 Effect of obesity on relation between systolic blood pressure and left ventricular (LV) mass. Body weight categories are the same as in Figure 32-3. (From Gottdiener JS, Reda DJ, Materson BJ, et al: J Am Coll Cardiol 1994;24:1492–1498, with permission from the American College of Cardiology.)

Hypertension in the Elderly Program (SHEP) study,[51] elderly subjects with isolated systolic hypertension had greater LV mass and relative wall thickness than age-matched normotensive control subjects. The distribution of echocardiographic LV mass was reported in a cohort of 5201 participants in the Cardiovascular Health Study who were 65 years of age and older.[106] After adjustment of LV mass for body weight, there was a modest increase in LV mass with age, less than 1 g per year increase in age for both genders. Also, greater LV mass in men persisted after adjustment for body weight, although adjustments for lean body mass were not performed. Race The prevalence and severity of hypertension is greater in African Americans than whites,[108] [109] and ECG studies have suggested a greater prevalence of LVH as well.[110] [111] However, using echocardiographic LVH as a reference standard, Lee et al[111] found that the specificity of ECG criteria for LVH, not adjusted for race, is lower for African Americans than whites. In addition, most echocardiographic studies have failed to show higher LV mass in African Americans.[18] , [47] [101] , [102] [112] [113] In evaluating patients differing substantially in number or in characteristics from previous studies, we found no racial difference in LV mass or LVH

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prevalence on echocardiogram.[18] Interestingly, the prevalence of LVH on ECG (Fig. 32-5) was two- to sixfold greater in African Americans based on the ECG criteria used.[114] African Americans did have greater septal wall, posterior wall, and relative wall thickness than did whites, as has been noted by others.[101] [102] In addition, LV mass, body size, and chest wall configuration, as well as other factors that can differ by race, may affect ECG characteristics, which contribute to ECG diagnoses of LVH. In a more recent study, race-based differences in ECG prevalence of LVH persisted even after taking these factors into account.[115]

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Figure 32-5 Influence of race on prevalence of left ventricular hypertrophy (LVH): Echocardiographic (ECHO) versus various electrocardiographic criteria (Minnesota codes, Romhilt-Estes, Sokolow). Despite statistically insignificant difference in LVH prevalence on echocardiogram, markedly greater prevalence of LVH is present on electrocardiogram in African-American men with established hypertension with all criteria used (P < .05 all comparisons).

Hemodynamic Workload In the past, the increase in LV mass seen in subjects with mild-moderate hypertension was considered to be passively related to the increase in cardiac workload imposed by hypertension.[14] [18] [77] [86] Usually blood pressure, or systemic resistance in part calculated from blood pressure, is used to quantify hemodynamic workload. However, an increasing body of research has shown that although the relation between casual blood pressure and LV mass is significant, the magnitude of that relation is relatively small. Although this relation may be improved somewhat using ambulatory blood pressure recording for 24 hours, the correspondence with LV mass is still relatively weak.[116] [117] [118] [119] Although systolic blood pressure averaged over 30 years[120] is also a better predictor of LV mass and wall thickness than casual systolic blood pressure, the variance of LV mass is still largely related to factors other than blood pressure. Even using 30-year average systolic blood pressure, there is only a modest correlation between LV mass index and systolic pressure. Interestingly, of the three structural components on the echocardiogram used to calculate LV mass (septal wall thickness, posterior wall thickness, and LV diastolic cavity dimension), wall thicknesses, but not LV diastolic cavity dimension, is

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statistically correlated with systolic blood pressure. Besides patients with hypertension, normotensive subjects may have LVH. [16] [121] In addition to clinical studies indicating that factors other than blood pressure contribute to LV mass, several animal studies have indicated a dissociation between LV mass and blood pressure.[122] [123] In the spontaneously hypertensive rat, a genetic model of hypertension in which both hypertension and LVH occur spontaneously, LV mass increases before an increase in blood pressure.[124] [125] It also has been shown that subhypertensive doses of norepinephrine result in LVH despite a failure to elevate blood pressure.[126] Additionally, some studies have suggested that drugs administered to produce uniform lowering of blood pressure do not produce uniform changes in LV mass, either in experimental animals or in humans.[127] For example, sympatholytic agents such as α-methyldopa have been shown to produce decreases in LV mass, whereas a vasodilator (hydralazine) used in doses to produce equal reductions of blood pressure failed to reduce LV mass. These data would suggest that both LV mass and blood pressure respond to a common, perhaps adrenergic stimulus in hypertension. Of note, a genetic contribution to LVH is suggested by the finding of increased LV mass in normotensive children of hypertensive parents.[128] [129] Of interest, the finding of relatively high LV mass in normotensive children is predictive of the subsequent development of sustained hypertension.[130] Hence, although blood pressure and LV mass may be covariables, elevation of blood pressure may not be the primary cause of LVH. In normotensive persons, enhanced augmentation of systolic pressure by reflected waves, a process associated with aging of the arterial tree, elevates wall stress and is associated with increased LV mass.[131] Of interest, arterial reflected waves may be greater with shorter aortic length, found in individuals of short stature.[132] [133] [134] Population studies have shown a relationship between short stature and adverse cardiovascular outcome.[135] [136] [137] In a preliminary report,[138] short stature was independently associated with increased LV wall thickness and concentric remodeling in population-based elderly individuals, perhaps providing some mechanistic explanation for the epidemiologic associations. Other hemodynamic factors associated with increased mass are volume, which obviously directly increases LV mass, and intrinsic contractility of the ventricle. An intrinsically hypercontractile ventricle requires less wall thickening to overcome wall stress. Thus, an inverse relation exists between

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LV mass and intrinsic myocardial contractility.[139] [140] The poor relation between blood pressure and LV mass does not necessarily indicate the absence of hemodynamic stimuli to LV muscle hypertrophy. In a study using echocardiography to express LV hemodynamic load in hypertension patients as "total load" (product of systolic blood pressure and endocardial surface area) and as "peak meridional force" (product of systolic blood pressure and LV cross-sectional area), Ganau et al[139] found better correlation of LV mass with total load (r = 0.68) and with peak meridional force (r = 0.70) than with systolic blood pressure (r = 0.45). Furthermore, the theoretically "optimal" LV mass, that is, the LV mass which would produce normal peak stress, was better correlated with end-diastolic volume (r = 0.72) than with systolic blood pressure (r = 0.46), indicating the relative importance of LV preload to LV mass. Moreover, the close relationship (r = 0.76) of actual and theoretically optimal LV mass suggested that LVH was usually appropriate to hemodynamic load. The findings of the Framingham Study,[120] which found no relationship between LV diastolic dimension and systolic blood pressure but a significant relationship between systolic blood pressure and wall thickness are consistent with the data of the Cornell group[141] in suggesting that hemodynamic stress is a stimulus to hypertrophy. To summarize, increased afterload manifested by elevations of systolic blood pressure results in increases of LV wall thickness. However, in some patients, compensatory decreases in LV preload are sufficient to maintain LV mass at normal values (concentric remodeling). In others, volume 713

overload prevents this response, resulting in increases in LV mass that are disproportionate to the pressure overload.

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Stress Reactivity, Behavior, and Left Ventricular Hypertrophy Given the absence of hypertension at rest in some individuals with LVH, it is reasonable to consider the relationships between LV mass and elevations of blood pressure with physical or mental activity, that is, stress reactivity. Exercise Stress We hypothesized that elevation of systolic or diastolic blood pressure to above predicted normal ranges with exercise may indicate a propensity for the future development of sustained hypertension.[121] In 39 normotensive men (average age 45 ± 9; range 34 to 71 years) echocardiography LVH (LV mass index > 134 g/m2 ) was present in 14 of 22 men with an exercise systolic blood pressure of 210 mm Hg or greater but in only one individual with a lower exercise blood pressure. Of note, there was a linear relation (Fig. 32-6) (Figure Not Available) between the maximum systolic blood pressure achieved during exercise and the LV mass index (r = 0.65; P < .0001). The increase in LV mass in association with exercise reactivity was characterized primarily by an increase in posterior wall and intraventricular septal thicknesses rather than an increase in LV internal dimension. This pattern of concentric hypertrophy is similar to that seen in individuals with established hypertension. Additionally, the subjects with enhanced exercise blood pressure reactivity also had greater left atrial size Figure 32-6 (Figure Not Available) Relationship between maximum systolic blood pressure during exercise and left ventricular (LV) mass in normal subjects, hypertensive patients, and patients with aortic stenosis. The horizontal dotted line indicates the partition value of 210 mm Hg or determination of exaggerated systolic pressure response to exercise. The coefficient correlation is 0.65; P > .0001. BP, blood pressure. (From Gottdiener JS, Brown J, Zoltick J, et al: Ann Intern Med 1990;112:161–166, with permission.)

consistent with an adverse effect of increased LV mass on LV filling. Based on this data the estimate of LVH prevalence in a population of

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healthy men is approximately 4%, which is comparable to the value of 3.1% detected in normotensive subjects by Hammond et al.[141] Based on screening of 582 normotensive men, Polonia et al[142] found 60 normotensive men with an exaggerated systolic blood pressure response to exercise. In these 60 subjects, LVH was present on echocardiogram in 52%, most of whom had eccentric hypertrophy and normal diastolic LV function on Doppler imaging. In contrast, patients with established hypertension had predominantly concentric LVH and abnormal diastolic function. There was a significant correlation between LV mass and peak exercise blood pressure, but not blood pressure during milder levels of physical activity, supporting the relationship between exercise pressor reactivity and LV mass in normotensive subjects. The finding in the Muscatine Study of normal children[130] that subsequent magnitude of LV mass was predicted by exercise but not resting blood pressure also is consistent with the hypothesis that exercise pressor reactivity is a predictor rather than a consequence of increased LV mass. Similarly, in the Framingham cohort, Lauer et al[143] found significantly higher LV mass and prevalence of LVH in normotensive men and women with an exaggerated blood pressure response to exercise than in control subjects (Fig. 32-7) . This difference was reduced, but not eliminated, by adjustment of LV mass for age, resting systolic blood pressure, and body mass index. Race-based differences in blood pressure reactivity to exercise, that is, higher systemic vascular resistance during exercise in AfricanAmerican than in white men,[144] may also affect studies of exercise reactivity and LV mass. Increased LV mass in normotensive subjects with a hypertensive response to exercise has also been noted [145] using threedimensional (3D) echocardiography. Psychologic Reactivity to Stress Psychologic reactivity to stress refers to the hemodynamic and neuroendocrine changes produced in response to behavioral stress.[146] Because the magnitude of such changes usually cannot be inferred from resting (baseline) data, reactivity measurements often contribute unique information on the physiologic functioning of the individual. Several sources suggest that LV mass in humans correlates better with blood pressure during mental challenge than during resting conditions. Devereux et al[147] showed that the strongest correlations of LV mass and LV wall thickness with blood pressure occurs during workplace activity.

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Furthermore, psychologic job strain is correlated with increased LV mass in working men.[148] These studies suggest that LV mass either reflects the integrated effects of daily hemodynamic load on the heart, best indicated by blood pressure recorded during work stress, or that the response of blood pressure to work stress is a marker for a common pathophysiologic substrate underlying LVH. The notion that psychologic stress may produce LVH 714

Figure 32-7 Afterload-independent left ventricular (LV) function displayed as a relation of LV midwall (right) or endocardial (left) fractional shortening to end-systolic stress in hypertensive patients. When endocardial fractional shortening is used, many patients are above the 95% confidence interval of the normal relation (parallel dotted lines), suggesting enhanced contractility. With midwall fractional shortening, few patients exceed the confidence limits while many are below them, which is consistent with depressed contractility. SEE, standard error of estimate. (From De Simone G, Devereaux RB, Roman MJ, et al: J Am Coll Cardiol 1994:23;1444–1451, with permission from the American College of Cardiology.)

in the absence of sustained hypertension is supported by the studies of Julius and Brant.[149] Hindquarter compression in dogs produced transient, neurogenic elevation of peripheral arterial resistance and mean blood pressure (average, 25 mm Hg). Although sustained elevations of blood pressure did not occur, concentric LVH nonetheless was evident as early as 3 weeks, progressing to a 28% increase over baseline values at 9 weeks. Additionally, studying cynomolgus monkeys, Kaplan et al[150] found an association between increased cardiac reactivity to psychologic stress and cardiac mass, but only in animals with resting blood pressure greater than the sample median. Studies of the relationship between psychologic reactivity and LV mass in humans have had mixed results. One study found that blood pressure reactivity to mental stress was predictive of subsequent increase in LV mass among borderline hypertensive subjects during a 2-year follow-up.[151] Moreover, in normotensive young men, Manuck[152] noted an association between LV mass indexed by body surface area and diastolic blood pressure response to mental stress tasks. We examined[153] laboratoryinduced hemodynamic responses to exercise, cold, and mental stress as well as 24-hour ambulatory blood pressure measures as predictors of LV

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mass in 36 healthy normotensive subjects. Systolic blood pressure responses to mental stress (r = 0.42; P < .01) and cold pressor (r = 0.34; P < .05) were significantly related to LV mass. After adjusting for body size, the mental stress-induced systolic blood pressure responses were the only significant predictors of LV mass index (r = 0.32; P < .05). Exercise systolic blood pressure responses were associated with LV mass index in men (r = 0.63; P = .02) but not in women. Multivariate regression analyses revealed that systolic blood pressure during mental stress was significantly predictive of LV mass index independently of covariates. Hemodynamic responses elicited during laboratory tasks may therefore reveal important information about the pathophysiologic processes involved in the development of cardiac end-organ damage. In contrast, Rostrup et al[154] found no association between reactivity to mental or cold pressor stress and either LV wall thickness or LV mass. On multivariate analysis, the only significant predictors of wall thickness were resting systolic blood pressure and plasma epinephrine, and only systolic blood pressure predicted LV mass or LV mass indexed by height. Body weight, ordinarily a robust predictor of LV mass was not predictive in this study, possibly because LV mass was indexed by height and because of the apparent lack of obesity in their cohort. Failure of the expected diurnal decrease in systolic and diastolic blood pressure during nighttime hours also may be associated with a higher LV mass at any level of casual or 24-hour blood pressure.[155] [156] The relationship between nocturnal pressure and LV mass suggests that diurnal blood pressure variation may be a marker of sympathetic or other neurohumoral pathophysiology, rather than simply being due to a greater hemodynamic stress because of persistently elevated blood pressures during nighttime hours.

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Nonhemodynamic Factors It is surprising that although in vitro and in vivo animal models demonstrate an excellent relationship between LVH and mechanically imposed afterload, there is poor correspondence of blood pressure to LVH in hypertensive patients. However, blood pressure measurements fail to 715

provide an accurate measure of integrated blood pressure over time in any given subject, and systolic blood pressure is an incomplete measure of the actual impedance to LV ejection. Additionally, impedance to ejection is not the only hemodynamic stressor experienced by the left ventricle. Theoretic and experimental observations in humans have indicated that, in fact, inotropic properties of the left ventricle and LV geometry as well as blood pressure are important in describing ideal LV mass.[139] Nonetheless, nonhemodynamic factors remain an important consideration in the pathogenesis of LVH in human hypertension including neurohumoral factors, genetic susceptibility, neurobehavioral aspects, diet (particularly salt intake), and the interaction of hypertension with other pathologic processes such as atherosclerosis and diabetes mellitus. However, it remains unproved whether humoral factors mediate right ventricle hypertrophy and LVH in response to hemodynamic overload of the ventricle, or if elevation of blood pressure and cardiac hypertrophy are both secondary responses to a primary neuroendocrine disorder. Supporting a role of the adrenergic system as the mediator of cardiac hypertrophy has been the finding that subhypertensive doses of norepinephrine are capable of inducing LVH.[126] Additionally, it has been demonstrated that serum from animals with LVH may induce hypertrophy of cardiac myocyte in vitro.[157] In human hypertensive subjects, an association between LV muscle mass and plasma norepinephrine has been described,[158] but only in patients with LVH and abnormally elevated norepinephrine.

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Further support for a neurohumoral stimulus for LVH, independent of blood pressure, are the findings of several studies that cardiac hypertrophy in humans and in animals may not be reversed by vasodilators such as hydralazine and minoxidil or by diuretics despite blood pressure reduction equal to that produced by drugs that result in regression of LVH, such as αmethyldopa or calcium inhibitor drugs.[159] [160] [161] [162] The failure of LVH to regress has been considered to result from reflex adrenergic or reninangiotensin system activation. However, it should be noted that virtually every antihypertensive drug has been shown in at least some studies to produce regression of LVH in hypertensive patients. Additionally, there is a complex interaction of direct and reflex effects of drugs, involving not only blood pressure reduction but renal and endocrine responses. LV mass also may be affected by reflex changes in heart rate because the increase in preload accompanying longer diastolic filling periods during bradycardia may act as a hemodynamic stimulus to hypertrophy. Hence, bradycardia and increases in LV cavity size produced by beta-blocker drugs may be expected to limit, or even abolish, reductions of LV mass, which might be expected with blood pressure reduction, despite decreases in LV wall thickness.[163] However, the importance of the adrenergic stimuli in development of LVH has been questioned.[164] Cardiac and vascular structural changes, seen in renovascular hypertension and hyperaldosteronism, are not observed in patients with essential hypertension or pheochromocytoma.[165] Furthermore, only a minority of patients with pheochromocytoma has LVH, although pheochromocytoma is characterized by extraordinarily high levels of norepinephrine. [166] Genetic Susceptibility Epidemiologic and basic science research in the mid to late 1990s indicated that genetic factors are important for the development of LVH, independently of hypertension. Given the role of the renin-angiotensin system in LVH, genetic regulation of this system has been of particular interest. Insertion or deletion polymorphism in the intron 16 (noncoding region) of the gene for angiotensin converting enzyme (ACE) has been well studied.[167] [168] [169] [170] [171] [172] [173] [174] The homozygous genotype for the deletion (DD) is associated with electrocardiographic evidence of LVH,[167] particularly in normotensive men, supporting the concept that this association is independent of hemodynamic factors. The homozygous DD genotype has been associated with increased LV mass on echocardiogram

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in untreated hypertensive patients,[168] with concentric remodeling of the LV, a geometric pattern associated with increased cardiovascular risk,[169] and with the development of LVH following renal transplantation.[172] In normotensive athletes the DD genotype was predictive of the magnitude in physiologic increases in LV mass as part of a physical training program.[174] Epidemiologic evidence for genetic influence on LV mass includes offspring studies that suggest that LV mass in children of hypertensive parents is elevated independently of blood pressure.[175] [176] Also, a large population study of siblings showed familial disposition of LVH.[177] A study of monozygotic twins, however, showed that genetic influences on LV mass can be modified by environmental factors.[178] Renin-Angiotensin System Because angiotensin I and angiotensin II may stimulate myocardial protein synthesis and the renin-angiotensin system has been established as playing a role in some forms of hypertension, it is reasonable to suspect a direct link between the renin-angiotensin system and myocardial hypertrophy. The role of the plasma renin-angiotensin-aldosterone axis in hypertensive end-organ pathophysiology has been extensively explored. Experimental and human studies have linked plasma renin activity to degree of LVH,[123] [179] [180] but this finding is not universally accepted. [164] The product of renin activity, angiotensin I, is the substrate for angiotensin converting enzyme. Expression and regulation of the ACE gene and, thus, angiotensin II levels, may modulate development of LVH. This finding is supported by in vitro studies in which local release of angiotensin II in response to the mechanical stretch is a necessary permissive factor for induction of the hypertrophic growth response.[181] Although there is ample evidence that angiotensin II is involved in the hypertrophic response, it is apparently not necessary for it, which was shown in a study in which LVH developed in mice in response to pressure overload despite "knockout" of the angiotensin II type 1 receptor.[168] Aldosterone, 716

the synthesis of which is partially controlled by angiotensin II levels, appears to regulate cardiac fibroblast metabolism and growth.[22] These observations may explain why elevated plasma renin levels confer a greater risk for myocardial infarction in patients with hypertension.[182] Animal studies of LVH regression in the spontaneously hypertensive rat

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have documented a parallel reduction of plasma renin activity and LV mass in animals treated with propranolol or α-methyldopa, but an increase was shown in both parameters in animals treated with minoxidil at a dose that produces a similar blood pressure reduction.[159] Although these studies were not sufficient to demonstrate a direct link between angiotensin and LVH, angiotensin converting enzyme–inhibiting drugs have prevented the development of cardiac hypertrophy in both spontaneously hypertensive rats[183] and salt-sensitive, salt-resistant Dahl rats[183] [184] Additionally, numerous clinical studies using echocardiography[163] [185] [186] [187] [188] [189] [190] [191] have shown that angiotensin converting enzyme inhibitors have produced reductions of LV mass as well as mean blood pressure. However, echocardiographic studies in patients with high renin versus low renin forms of hypertension have failed to show differences of LV mass.[65] Even though the relation between renin-angiotensin activation and LV mass is uncertain, LV performance in hypertensive subjects appears to be worse in high renin subgroups.[192] Of note, a high renin profile also has been associated with a greater risk of myocardial infarction in patients with hypertension.[182] Although the mechanisms for these associations remain uncertain, it has been well documented that angiotensin has potent vasoconstrictive effects. Hence, these patients may have altered coronary reactivity with a propensity toward infarction as well as accelerated atherosclerosis, perhaps related to smooth muscle hyperplasia.[193] [194] Growth Hormones Hormones and factors that regulate general growth also may be involved in myocardial hypertrophy. For example, marked increases in LV mass may occur in persons with acromegaly as a result of elevated growth hormone and insulin-like growth factor 1 (IGF-1).[195] IGF-1 levels are higher in hypertensive patients with LVH than in hypertensive patients without LVH. [196] In utero, insulin is a trophic factor, which causes macrosomia.[197] Insulin levels and the degree of insulin resistance may independently modulate LV mass in normotensive and borderline hypertensive subjects.[98] [198] This process may occur because insulin resistance leads to increased levels of intracellular calcium, possibly as a result of decreased Na+ , K+ ATPase activity. Elevated intracellular calcium may be an important stimulus for myocardial actin and myosin protein synthesis,[194] which now appears to be caused by the stimulus of calcineurin. This ionic hypothesis [199] may also explain the association between parathyroid hormone levels and LV mass in hypertensive persons.[123]

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Parathyroid Hormone There are important relationships between intracellular calcium metabolism and myocardial protein synthesis. Several studies have described the role of intracellular calcium both as a mediator of myocardial trophic stimuli and in the induction of proto-oncogenes that direct protein synthesis.[194] Although calcium metabolism is regulated in part by parathyroid function, it has not been established that parathyroid gland abnormality plays a role in the relation between intracellular calcium, myocardial protein synthesis, or arteriolar smooth muscle contraction and resistance. However, relations between parathyroid function, parathyroid hormone, and hypertension have been described in some studies,[200] [201] although hypercalcemia per se has not been associated with LVH. In a clinical study LV mass on echocardiogram and ambulatory blood pressure both were associated with plasma renin activity and with parathyroid hormone even after adjustment for mean 24-hour blood pressure.[123] This result occurred even though parathyroid hormone level did not exceed the normal range in any patient and there was no relation between serum ionized calcium and LV mass index. Salt Intake Although the interaction among salt intake, salt excretion, and blood pressure in hypertension has been well appreciated, relations between LV mass and sodium metabolism independent of blood pressure have been less well studied. Experimental studies have indicated a role for sodium intake in LVH. Despite failure to reverse hypertension, sodium restriction in rats with induced renal hypertension may produce reductions in heart weight.[202] In a clinical study, sodium excretion predicted not only increased LV mass consequent to an increase in LV volume (as might be expected with sodium-related volume overload) but also was a strong predictor of increased posterior and relative wall thickness. In fact, sodium excretion was a stronger predictor than all the other nonhemodynamic determinants, including body mass index, hematocrit, and serum epinephrine.[203] Further work is needed, however, to determine the independence of sodium intake from systolic blood pressure in the induction of LVH in hypertensive patients.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Correlates of Left Ventricular Hypertrophy Myocardial Infarction It has been recognized in epidemiologic studies that patients with hypertension and LVH suffer a worse outcome with acute myocardial infarction than might otherwise be expected.[204] Although this result may be related to acceleration of atherosclerosis by hypertension, the presence of LVH may increase the extent of myocardial necrosis.[205] [206] The increased extent of myocardial infarction may occur from both increased oxygen demand of hypertrophic myocardium and decreased oxygen supply consequent to impaired subendocardial perfusion. Hence, the echocardiographic finding of LVH in patients with known ischemic coronary disease should indicate 717

particular risk for increased morbidity and mortality following myocardial infarction. Prediction of Subsequent Hypertension Although ventricular hypertrophy seems to be a consequence of hypertension, the reverse may also be true; that is, hypertension may be of cardiogenic origin. Longitudinal evaluation of young hypertensive patients has shown initially normal systemic vascular resistance with normal or increased cardiac output but gradual decline in cardiac output and increase in systemic resistance during 20 years of follow-up.[207] The predictive value of echocardiographic LV mass for subsequent elevation of blood pressure in initially normotensive individuals has been established in children[130] [208] as well as adults.[209] [210] [211] Left Ventricular Systolic Function

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The hypertrophic response to pressure and volume overload has been considered adaptive because an increase in functioning muscle mass seemingly preserves cardiac function despite increasing hemodynamic load.[212] [213] [214] With mechanical pressure overload, the cardiac response is characterized primarily by an increase in LV wall thickness. This increase in wall thickness can moderate or even prevent an increased afterload according to the Laplace relation Tension = Pr / 2h where P is LV pressure, r is LV internal radius, and h is wall thickness. Presumably, at some point, LVH becomes maladaptive and systolic failure occurs. However, cardiac hypertrophy is often accompanied by alterations of myocardial perfusion even before systolic failure. Such alterations include subendocardial ischemia, decreased coronary flow reserve, and increased coronary vascular resistance. However, mechanical pressure overload models of LVH may not be entirely pertinent to essential hypertension in which the pathogenesis of both hypertension and LVH may be considerably more complex than increased systemic resistance alone. Echocardiographic studies of LV function at rest in hypertensive patients generally disclose normal or even increased ejection fraction despite the presence of LVH.[18] [60] [61] [62] [63] [64] [65] It has been suggested that exaggerated LV function in some patients may be the result of low afterload related to the marked decreases in end-systolic stress owing to excessive increases in LV wall thickness.[66] Rather than being a favorable prognostic feature, supranormal ejection fraction is associated with greater peripheral target organ damage than is lesser hypertrophy and lower (but still normal) ejection fraction. It is important to note, however, that both fractional shortening, obtained readily from end-diastolic and end-systolic cavity measurements of the LV chamber minor axis between endocardial surfaces, and ejection fraction, derived from the same parameters, are affected by loading conditions of the left ventricle.[215] [216] [217] Hence, according to the Laplace equation, in which wall tension describes afterload, either a decrease in cavity size, increase in wall thickness, or decrease in systolic blood pressure can decrease afterload and result in normal or even increased fractional shortening, despite the presence of myocardial dysfunction. Left Ventricular Diastolic Function

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The importance of diastolic function in hypertension and LVH is underscored by epidemiologic studies showing that systolic function is commonly preserved, particularly in elderly individuals with congestive heart failure,[218] [219] [220] and that abnormalities of diastolic function may predict the development of heart failure. [221] Reports in the late 1980s and early 1990s suggested that diastolic abnormalities occur early in the course of hypertension and precede detectable hypertrophy. [222] [223] [224] [225] More recent studies challenge the notion that diastolic abnormalities are the first sign of hypertensive heart disease; these studies suggest that diastolic abnormalities do not precede structural changes but rather occur simultaneously. In general, diastolic function is inversely related to LV mass in patients with hypertension[226] [227] [228] and regression of LV mass with calcium channel blockers, beta blockers, and ACE inhibitors is often,[162] [229] [230] [231] [232] [233] [234] [235] but not always,[236] associated with improved LV diastolic function. In the HARVEST study,[237] young patients with stage I hypertension had significantly greater LV mass and more concentric remodeling than did normotensive subjects. There was no significant difference in Doppler mitral inflow velocity (E/A) ratio, however, a marker of diastolic dysfunction. Experimental data suggest that a diastolic abnormality in the absence of frank hypertrophy indicates that the heart is beginning to hypertrophy in response to hemodynamic or nonhemodynamic stimuli. Numerous echocardiographic studies have evaluated diastolic LV filling in hypertensive patients with and without LVH.[49] [52] [53] [54] [57] [238] [239] [240] [241] [242] Importantly, it has been shown in experimental animals that abnormalities of diastolic function may accompany increases in either the fibrous[243] or muscular components[244] of hypertrophy (Fig. 32-8) . Additionally, LVH may be associated with diastolic dysfunction in the absence of elevated systolic pressure.[56] Complicating the use of Doppler techniques for evaluation of diastolic function in patients with hypertension has been the complex effects of structural cardiac alterations on parameters of diastolic filling. Moreover, Doppler parameters are sensitive to loading conditions of the ventricle, left atrial pressure, heart rate, as well as passive and active diastolic properties of the LV chamber and myocardium. [245] [246] [247] Additionally, compensatory reflex changes that are autonomically mediated may moderate the effects of loading on diastolic filling patterns. In normal subjects studied over a short time interval,[246] [247] autonomic blockade with

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propranolol and atropine substantially altered the effects of decreases in preload (passive tilt) and increases in afterload (handgrip) on Doppler diastolic filling patterns.

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Figure 32-8 Example of a normal tissue Doppler velocity profile sampled from the basal septum from the apical four-chamber view (left). Note two systolic peaks (S1, isovolumic contraction; S2, peak systolic shortening velocity) and two diastolic peaks (Em, peak early diastolic myocardial relaxation velocity; Am, late diastolic myocardial velocity associated with atrial contraction).

Left Atrial Size Although most echocardiographic studies in hypertension have focused on structural and functional alterations of the left ventricle, effects on the left atrium also are important. Left atrial size is of clinical relevance for the occurrence of atrial fibrillation,[248] stroke,[249] [250] and congestive heart failure. In an early echocardiographic study of hypertension, Savage et al[60] found increased left atrial dimension in 5% (compared with increased LV mass in 51%) of patients even though mean left atrial size was not increased for the group in comparison with normal subjects. Notably, left atrial dimension was weakly (r = .20; P < .05) correlated with systolic blood pressure, as was LV mass (r = .23; P < .01). In elderly patients with systolic hypertension studied as part of the Systolic Hypertension in the Elderly Program (SHEP), left atrial enlargement on echocardiogram was present in 51% of patients, but also in 30% of age-matched, normotensive control subjects. [51] This finding is consistent with the established relationship between left atrial size and age in both normotensive and hypertensive subjects.[60] There were weak but significant relationships in the SHEP study between left atrial size and LV mass indexed by body surface area (r = .20) and relative wall thickness (r = .31). In the Framingham study of a free living cohort,[251] blood pressure and LV mass were both correlated with left atrial enlargement on echocardiogram, although on multivariable analysis most of the variance in left atrial dimension was explained by LV mass. In hypertensive men, we found that obesity contributed to left atrial size independently of LV mass, age, height, or blood pressure.[252] Moreover, there was no relation between LV mass and left atrial size in hypertensive patients of normal weight; such a relation

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did exist in obese patients. Treatment of hypertension also reduced left atrial size, although drugs differ in their effects. In a trial of single drug therapy,[253] the greatest reduction in left atrial size was associated with hydrochlorothiazide. Right Ventricular Hypertrophy Although extensive studies have been reported on the relation between LVH and systemic arterial pressure overload, the response of the right ventricle to hypertension has not been extensively studied. It has been shown that measurement of RV wall thickness by echocardiography is feasible[254] and correlates well with autopsy measurements.[255] It should be noted, however, that measurements made from the epigastric window, reflecting the body of the right ventricle, are thicker than those made from the left parasternal window, which record the thickness of the anterior RV wall near the outflow tract.[35] The RV wall thickness is increased in patients with RV overload[254] as well as in patients with LVH consequent to hypertension or aortic stenosis.[35] [37]

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Because RV pressure overload does not ordinarily accompany arterial hypertension, determination of the presence of right ventricular hypertrophy (RVH) in patients with systemic hypertension[37] can be considered a test of the hypothesis that ventricular hypertrophy may be dissociated from pressure overload. We performed 2D echocardiographic targeted M-mode echocardiography in patients with systemic overload of the left ventricle (systemic hypertension and aortic stenosis) to determine the prevalence of increased RV wall thickness and its association with the clinical and hemodynamic descriptors in patients with echocardiographic evidence of increased LV wall thickness.[35] It was found that average RV wall thickness in hypertensive patients of (7 ± 2 mm) and in patients with aortic stenosis (6 ± 2 mm) was significantly greater than that in normal subjects and in patients with dilated cardiomyopathy who did not have LV pressure overload. Of note, the magnitude of increase in RV wall thickness was not associated with pulmonary hypertension. There was a linear relationship (r = 0.76; P < .005) between LV and RV wall thickness measured echocardiographically (Fig. 32-9) . These data suggest that the hypertrophic response of cardiac ventricular muscle is not dependent on a sustained pressure overload of that ventricle.

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Although the mechanism of the hypertrophic response of the "nonstressed" ventricle is unclear, the presence of RVH in the absence of RV pressure overload supports the hypothesis of disassociation between pressure overload and hypertrophy. This study does not exclude ventricular interdependence,[256] however, from either syncytial transmission of force or transmission of hemodynamic stress across the intraventricular septum as a possible mechanism of RVH in left-sided overload.

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Effects of Antihypertensive Therapy in the Heart Left Ventricular Mass Pharmacologic Therapy

Although antihypertensive therapy has been shown to reduce LV mass and LVH,[187] [257] some studies indicate Figure 32-9 Relationship between right ventricular (RV) and left ventricular (LV) wall thickness in patients with LV pressure overload. (From Gottdiener JS, Gay JA, Maron BJ, Fletcher RD: J Am Coll Cardiol 1985;6:550–555, with permission from the American College of Cardiology.)

that not all drugs are equally effective in reducing LV mass, even with comparable reduction of blood pressure.[159] [162] [258] , [259] In particular, it has been suggested that diuretics and vasodilators may be ineffective in decreasing LV mass because of their failure to inhibit neurohumoral mechanisms responsible for LVH.[159] However, much of the literature on LV mass regression has been based on uncontrolled, short-term and nonrandomized studies with only one or two therapeutic limbs and relatively small numbers of patients. [187] Moreover, the influence of other covariates known to affect LV mass, such as obesity, the magnitude of weight loss, the extent of systolic blood pressure reduction, race, plasma renin, sodium excretion, and physical activity have often not been evaluated.[18] [62] Although diuretics are effective and inexpensive drugs advocated by the Joint National Committee on Hypertension[260] for the initial therapy of mild-moderate hypertension, some studies[261] [262] [263] [264] [265] [266] have suggested that diuretics are either completely ineffective for reduction of LV mass or produce only small decreases in LV mass, disproportionate to

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their effects on blood pressure. Moreover, studies in animals and humans [261] [267] [268] [269] [270] have provided a theoretical basis for ineffective regression of LVH with diuretics, in contrast to that produced by other drugs. According to this theory, beta blockers, angiotensin converting enzyme inhibitors, calcium blockers, and centrally acting alpha blockers reduce blood pressure and interfere with postulated neurohormonal mechanisms of hypertrophy. Although effective in lowering blood pressure, diuretics and peripheral vasodilators either produce no inhibition of these mechanisms or result in their reflex activation.[271] Therefore, despite reduction of blood pressure, diuretics and peripheral vasodilators might be expected to be associated with no decrease or even an increase in LV mass. Despite these considerations, a recent meta-analysis[272] and published literature reviews[261] [273] have suggested that diuretics can in fact produce decreases in LV mass.[274] [275] [276] [277] [278] Although many studies of LV mass reduction have been criticized for methodologic limitations,[261] [262] [263] [264] [265] [266] [267] [268] [269] [270] [271] [272] [273] [274] [275] [276] [277] [278] [279] including short duration, lack of controls, small sample sizes, and uncertain blinding, the Treatment of Mild Hypertension Study (TOMHS) avoided these methodologic shortcomings. TOMHS was a double-blind, placebocontrolled trial of 844 patients with mild hypertension and a low prevalence of LVH, randomized to nutritional-hygienic intervention in combination with one of five classes of active antihypertensive drugs or placebo. Echocardiographic evaluation over 4 years showed decreased LV mass for all treatment groups including placebo and chlorthalidone.[186] LV mass decreased more in the chlorthalidone treatment group (P = .03) than in the placebo only group, based on longitudinal analyses adjusted for baseline LV mass.[280] The Veterans Affairs Trial of Monotherapy in Mild-Moderate Hypertension was a placebo-controlled, titration trial of monotherapy, employing six active drugs and placebo to test the comparative efficacy of different classes of drugs for the lowering of diastolic blood pressure.[281] One objective of this study was to use echocardiography to assess the response of LV mass and its structural components over the 2-year period of antihypertensive monotherapy. Because the mechanisms responsible for 720

LVH, and presumably its regression, are multifactorial,[18] the echocardiographic data were analyzed with adjustment for potentially

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contributory factors in addition to drug selection, such as body weight, the magnitude of blood pressure reduction, race, and age, using appropriate statistical methods.[163] Patients with mild-moderate hypertension (diastolic blood pressure 95 to 109 mm Hg) were randomly allocated to treatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, prazosin, or placebo in a double-blinded trial in which medications were titrated to achieve a goal diastolic blood pressure of 90 mm Hg. Echocardiograms in 510 patients at 8 weeks, 259 at 1 year, and 153 at 2 years were evaluated for changes in LV mass, statistically adjusting for covariates including blood pressure, body weight, race, and age. At 2 years, only hydrochlorothiazide was associated with reduction of LV mass (−38.5 ± 10.8 g; P = .002). The effect of hydrochlorothiazide persisted even after adjustment for covariates (-32.3 g; 95% confidence interval [CI] -52.5 to 12.2 g), caused by decreased wall thickness. LV mass increased with atenolol (26.9 ± 11.7 g; P = .036). After adjustment for covariates the increase was 16.4 g, with a CI of 36.8 to -3.9 g (Fig. 32-10) (Figure Not Available) . Hydrochlorothiazide proved efficacious in another relatively large monotherapy comparison. We evaluated 134 patients with mild-moderate hypertension in an 18-center, double-blind, diastolic blood pressure titration comparison of isradipine (a dihydropyridine calcium blocker) with hydrochlorothiazide.[282] At 6 months, the decrease in LV mass of −11 ± 5 g with isradipine was significantly less than that achieved (−43 ± 7 g) with hydrochlorothiazide, although comparable decreases in septal and posterior wall thickness occurred with both drugs. By study design, the magnitude of decrease in diastolic blood pressure was equivalent with both drugs, although the extent of decrease in systolic blood pressure on 24-hour ambulatory blood pressure recording was greater with hydrochlorothiazide. Nonetheless, on multiple regression analysis selection of drug remained a significant predictor of LV mass reduction, even after adjustment for systolic blood pressure, race, age, weight, and gender. In patients with isolated systolic hypertension, a diuretic-based regimen supplemented as needed with beta blocker was associated with reduction of LV mass.[283] Although studies may differ with respect to efficacy of LV mass reduction with many drugs, virtually all studies have demonstrated efficacy of angiotensin converting enzyme inhibitors whether used as monotherapy or in combination with other therapy. Moreover, some studies suggest that the

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magnitude of LV mass reduction with angiotensin converting enzyme inhibitors[284] and following valve replacement in aortic stenosis[167] may be related to the angiotensin converting enzyme genotype. Nonpharmacologic Therapy

Nonpharmacologic therapies for hypertension have also been associated with reduction of LV mass. In TOMHS[186] a "nutritional-hygienic" intervention including weight loss was associated with reduction of LV mass, which was not enhanced by the addition of any of several types of Figure 32-10 (Figure Not Available) Comparative effects of monotherapy on left ventricular (LV) mass reduction in hypertensive men at 12 months of therapy. (From Gottdiener JS, Reda DJ, Massie BM, et al: Circulation 1997;95:2007–2014, with permission.)

single drug therapy. In another study[285] a greater trend in LV mass reduction was seen with weight loss than with drug therapy of hypertension, despite better reduction of blood pressure with drugs. Additionally, McMahon et al[286] demonstrated greater reduction of LV mass with weight reduction than with metoprolol. Moreover, salt restriction also has been associated with reduction of LV mass on echocardiogram.[186] [287] [288] Although exercise has been successful in reducing blood pressure in hypertensive patients, it has been associated with increased LV mass on echocardiography,[289] secondary to increased LV cavity size with no change in wall thickness. This pattern of increase in LV mass, accompanied by preservation of diastolic LV function was considered to be consistent with physiologic hypertrophy. Left Ventricular Function Systolic Function

Loss of contractile protein with LV mass reduction during antihypertensive therapy might, in principle, have 721

adverse effects on LV systolic function, particularly if increases in blood pressure toward initial levels or higher were to occur without "protection" from the previously elevated LV mass. Clinical studies that have evaluated ejection phase indices of LV function with echocardiography, however, have not demonstrated adverse effects of LV mass reduction on systolic

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function during or after antihypertensive therapy. [97] [163] , [187] [228] [290] Studies employing ejection phase indices, such as velocity of circumferential fiber shortening, fractional shortening, and ejection fraction, might not have been capable of detecting myocardial impairment because these indices are highly load dependent. The tendency for LV function to increase during the initial stages of therapy may in fact reflect the effects of reduced afterload. [97] Other studies that measured relationships of endocardial fractional shortening to end-systolic stress may also have overestimated myocardial contractility for reasons previously discussed. However, an evaluation of midwall fractional shortening relationships with end-systolic stress in patients with substantial reductions of LV mass during treatment also failed to disclose adverse effects.[231] Diastolic Function

Conceivably, reduction of LV mass might be associated with adverse effects on diastolic LV function, which could happen if reduction of LV mass occurred without reduction in connective tissue mass. Then, with reduction of total LV mass, a relative increase in the collagen to LV weight ratio could result in decreased diastolic distensibility of the left ventricle. However, studies using Doppler echocardiography have failed to disclose worsened diastolic function with LVH regression.[187] [239] [291] , [292] Indeed, several studies have shown improvement in diastolic indices of LV filling on Doppler echocardiography.[239] [291] Left Ventricular Fibrosis Regression On a cautionary note, all hypertensive agents may not be equally effective in regression of the increased myocardial fibrosis that accounts for part of the LVH response to hypertension. In a rat model of LVH reduction of blood pressure and LV mass, zofenopril, nifedipine, and labetalol given in equipotent doses for reduction of blood pressure all produced regression of LVH,[293] whereas only nifedipine and zofenopril regressed myocardial fibrosis. In a human study using endomyocardial biopsy to compare the effects of lisinopril with hydrochlorothiazide, [294] angiotensin converting enzyme inhibition with lisinopril was associated with regression of fibrosis and improvement in diastolic function, whereas hydrochlorothiazide was not. Notably, regression of LV mass occurred with diuretic but not with angiotensin converting enzyme inhibitor, possibly related to previous optimal blood pressure control in all patients in combination with added reduction of preload in association with diuretic.

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Clinical Outcome Although reduction of LV mass with treatment of hypertension does not produce adverse effects on surrogate measures of outcome such as LV function, there are no prospective, controlled trials that test whether the reduction of LV mass is beneficial independently of reduction of blood pressure. However, in an analysis of a cohort of hypertensive patients receiving drug therapy, Verdecchia et al[295] showed that regression of LVH was associated with reduction in clinical events independently of the magnitude of blood pressure decrease. Moreover, in the Framingham study [296] reduction of ECG features of LVH also were independently associated with reduced risk for cardiovascular disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Methods and Technical Considerations in the Evaluation of Hypertension Technical Limitations Although echocardiography provides information on cardiac function and structure unavailable by any other means and is free of known risks or significant discomfort, the technique confers substantial technical problems in data acquisition and interpretation. To optimize accuracy and reproducibility, careful methods need to be applied in training, acquisition, and interpretation of echocardiogram data. Using echocardiography to quantitate cardiac volumes, function, and LV mass requires accurate identification of interfaces between the cardiac blood pool and walls. Additionally, measurement of LV free wall thickness (needed in quantitation of LV mass) necessitates recognition of the often subtle interface between epicardium and pericardium. Primary echocardiographic measurements of wall thickness and chamber size may be obtained from the "ice-pick" view of 2D targeted M-mode echocardiography, which provides linear dimensions, or from tracing chamber and wall areas on still-frame 2D echocardiograms. The linear dimensions obtained from M-mode echocardiography may fail to adequately represent true cardiac chamber volume particularly when there are distortions in cardiac geometry. Although area measurements from 2D echocardiography still-frames provide greater image sampling of cardiac structures than ice-pick M-mode dimensions, still-frames (even of technically optimal studies) suffer from image degradation, with generally greater uncertainty in identification of cardiac borders than with M-mode echocardiography. With either means of echocardiographic display, using primary echocardiographic data to obtain cardiac volumes requires mathematic algorithms that rely on assumptions of cardiac geometry. Meticulous alignment of the ultrasound beam in reference to the proper anatomic axes is also required. Variations of angulation of the manually

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directed echocardiography sector between serial examinations results in variability of primary echocardiography measurements. Because the algorithms for LV volume estimation either 722

TABLE 32-3 -- Comparison of One-, Two-, and Three-Dimensional Echocardiographic Mass Determination with Magnetic Resonance Imagin End-diastole End-systole P Regression P Regressi Comparison r SEE VALUE Equation r SEE VALUE Equation 1D Echo0.725 25.6 .018 1D Echo- 0.788 28.7 .007 1D Echo Penn = Penn vs. Penn = 1.35 (MR MRI 0.99 (MRI) + 4.0 - 19.2 2D Echo-AL 0.694 24.2 .030 2D Echo- 0.717 28.2 .030 2D Echo vs. MRI AL = 0.86 AL = 1.1 (MRI) + (MRI) + 32.4 14.1 2D Echo-TE 0.687 21.8 .030 2D Echo- 0.710 24.5 .020 2D Echo TE = 0.9 vs. MRI TE = 0.76 (MRI) + (MRI) + 13.0 27.7 3D Echo0.882 10.4 .001 3D Echo- 0.908 10.8 .001 3D Echo PSR = 0. PSR vs. PSR = 0.72 (MRI) + MRI (MRI) + 13.2 32.2 MRI, magnetic resonance imaging; 1D Echo-Penn, M-mode echocardiographic method (Penn convention); 2D Echo-AL, two-dimension echocardiographic area-length method; 2D Echo-TE, two-dimensional echocardiographic truncated-ellipsoid method; 3D Echo-PSR, threedimensional echocardiographic polyhedral surface reconstruction method.

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square or cube primary echocardiography measurements, errors in

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measurement of primary variables result in proportionate magnification of errors in calculation of LV volumes and mass. Under some circumstances, any geometric model of LV volume may not be true to actual LV geometry. For example, the "bullet" formula for LV volumes (V = 5/6 AL; A = LV short-axis area, L = LV long-axis area) assumes a bullet shape of the LV, which does not exist in the case of LV aneurysm. Use of Simpson's rule (method of discs), which uses integral calculus to segment an irregular LV contour into multiple cylinders, is preferable. However, a technical tradeoff is made because apical views of the LV must be used. Apical views, which image the LV endocardium in lateral (poor) resolution, generally result in overestimation of LV cavity volume, whereas the parasternal short-axis view required by the bullet formula images the LV endocardium mostly in axial (good) resolution. Although one may select the algorithm appropriate to each subject and use it on subsequent examinations, intervening clinical events, such as apical myocardial infarction, may make this difficult. Hence, the sources of variability in echocardiographic studies separated by several years may be substantial. M-mode versus Two-Dimensional Measurements Controversy exists regarding specific measurement techniques used to determine LV mass, with some investigators[297] suggesting that enhanced reproducibility and accuracy may be obtained using planimetry of 2D echocardiography still-frames, whereas probably a larger experience has been obtained with the use of the M-mode and then subsequently 2D targeted M-mode recordings. [64] [141] , [187] [298] [299] Although both approaches have their merits, large quantities of normal as well as diseased population data have been obtained using 2D targeted M-mode recordings, and these techniques have been used by us in two large echocardiography core laboratory studies in hypertension (Table 32-3) . The principal advantage of 2D targeted M-mode recording is that it allows more certain identification of interfaces defining the endocardial and epicardial margins of the LV posterior wall, providing ready calculation of LV mass based on certain geometric assumptions. A theoretical disadvantage is imposed by the selection of essentially three measurements for LV mass calculation, but the distribution of muscle mass in the left ventricle is neither homogeneous nor conforms exactly to the geometric models used. Although 2D echocardiography, by providing multiple planes of image with essentially full visualization of LV walls and cavity, offers theoretical advantages for

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computation of LV mass, many of these advantages are lost by the uncertainty imposed on measurements by the generally vague cardiac borders seen on still-frame images. Additionally, subtle differences in regional LV wall thickness that can be appreciated qualitatively are difficult to measure on 2D echocardiography because of resolution difficulties, principally in lateral and azimuthal image planes. Distorted Left Ventricular Geometry Because patients with distorted LV geometry may not meet the assumptions necessary for the measurement of cardiac volumes using 2D targeted M-mode echocardiography, [300] it has been suggested that 2D echocardiography may provide improved accuracy and reproducibility of LV mass measurement. In addition, a good quality M-mode echocardiogram from the parasternal location may not be obtainable in all patients. However, some adequate 2D echocardiography images may be obtainable from an apical echocardiography window. Algorithms for Left Ventricular Mass Measurement Although 2D echocardiograms obtained from the apical window provide more complete interrogation of the left ventricle than do parasternal images, lateral resolution limitations of apical images require that wall thickness be measured from parasternal short-axis images. Because the position of the transducer on the chest wall is relatively fixed, however, the circular cross-sectional image obtained from this window cannot be iterated from base to apex to create a LV "shell" volume, which would represent LV mass. Hence, even 2D algorithms for estimation of LV mass use the parasternal window to calculate an average LV wall thickness, which can then be applied to either bullet or apical window disc method algorithms for LV volumes to obtain LV mass. Unfortunately, however, LV wall thickness is not uniform even in normal ventricles, and following myocardial infarction substantial segmental thinning of the LV wall can occur. Hence, problems in the estimation of LV mass imposed by distorted LV geometry following myocardial infarction are not completely solved by substituting 2D echocardiography for 2D targeted M-mode methods. Additionally, a principal disadvantage of 2D targeted M-mode echocardiography for the estimation of LV mass is failure to obtain technically adequate parasternal window recordings, either because of

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unacceptable obliquity of the echo sector to the LV long axis or because of inadequate definition of LV wall and cavity interfaces. If adequate apical window 2D echocardiograms are obtainable in such patients, reasonable quantitative estimation of LV volumes and ejection fraction may be obtained; however, as noted earlier, LV mass estimation remains problematic. It is easy to improperly align (Fig. 32-11) the echo sector relative to anatomic axes or improperly place the M-mode cursor during 2D targeted recording of the left ventricle. Such errors of acquisition technique can result in large error and variation in the measurement of LV mass. As shown in Fig. 32-12 a "true" LV mass calculation of 227 g may vary between 181 g to 448 g based on beam angulation errors. Paper versus Tape Recording of Two-Dimensional Targeted M-mode Data Paper strip chart recorders allow high-quality recordings of large numbers of contiguous beats, facilitating 724

Figure 32-11 Distortion produced in parasternal short-axis images by inappropriate angulation of the echo beam (B and C) through the heart. A, Correct angulation and nondistorted, orthogonal short axis.

close examination and measurement. Gray scale range and recording speed of paper strip chart recording is excellent, allowing identification of potential structural interfaces with high temporal resolution. However, storage of lengthy strip chart recordings is cumbersome, and strip chart recorders are expensive, often adding more than $10,000 to the cost of an ultrasonograph. Additionally, paper is expensive, potentially environmentally toxic, and permits recording of only a portion of the echocardiographic examination because real-time 2D images still require other recording formats such as videotape, or more recently, optical disc. Hence, many laboratories have abandoned paper strip chart recording, and videotape is used to record all components of the echocardiographic examination. Moreover, videotape is readily converted into digital format for archiving, whereas paper recording is not.

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Videotape M-mode recording appears to provide more restricted gray-scale display than does paper strip recording, limiting choices of structural interfaces. Moreover, only about two to four beats per screen can be displayed at recording speeds of 50 mm per second, making side by side comparison of multiple beats difficult. Additionally, the images on videoscreen are difficult to measure directly without the aid of electronic calipers, and multiple measurements are more visually fatiguing from video than from paper strip chart. Given these differences, it is by no means certain that measurements made from videotape are interchangeable with those made from paper recording. Hence, for assessment of long-term sequential changes in cardiac dimensions, studies recorded years ago on paper may not be comparable to those recorded more recently on videotape. To compare these two methods we measured 48 echocardiograms performed one to two apart in 24 patients with hypertension.[301] For any given patient the studies were performed by the same sonographer using the same machine, and all studies were read in a core laboratory by a single reader. The paper and tape strip chart segments were of the same beats obtained from targeted 2D echocardiography. Although LV mass measured from the paper recording was highly correlated with that on tape (r = 0.80), LV mass was significantly higher on paper (254 ± 60 g) than on tape (232 ± 66 g, P = .0008). Measurements of septal and posterior wall thickness were greater on tape than on paper; measurements of LV diastolic dimension did not differ (Fig. 32-13) . Although Figure 32-12 Effects of beam angulation errors on two-dimensional targeted M-mode measurements of left ventricular (LV) mass.

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Figure 32-13 Systematic differences in left ventricular mass (LVM), septum, and posterior wall measurements based on whether recording was done on strip chart paper or videotape. Reproducibility did not differ between recording formats. * P < .05.

the intertest error of LV mass was the same for both recording methods

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(about 11%), the width of the 95% confidence limits for LV mass, determined from the test-retest variability, was somewhat greater (13 g) for paper than tape. Although tape has a smaller gray scale range than paper, the decrease in potentially ambiguous interfaces may in fact have resulted in less test-retest variability. Moreover, systematic differences between the two recording methods indicate that they cannot be used interchangeably. Possible Public Health Applications The problem of inherent variability in the measurement of LV mass affecting clinical use of echocardiography may be approached statistically. It is possible to derive an estimate of the probability that LVH is present for any given value of LV mass (Fig. 32-14) . This calculation is based on the z-statistic, using similar methods employed to determine the probability that hypertension is present for any given level of ambulatory blood pressure.[302] If the cutoff for LVH is 125 g/m2 , (95th percentile for LV mass), a subject with an LV mass index greater than 110 g/m2 has at least a 20% chance of having actual LVH. Because of the prognostic implications of LVH, one could consider that intensive treatment for LV mass reduction should begin when there is at least a 20% probability that LVH is present. Similarly, if LV mass is less than 110 g/m2 , the risk of a cardiovascular event in a patient with stage I hypertension is low; therefore, initiation or intensity of treatment would be determined by the presence or absence of other risk factors (Fig. 32-15) . Three-Dimensional Echocardiography More recently, 3D echocardiography (Fig. 32-16) (Figure Not Available) using a polyhedral surface reconstruction algorithm has Figure 32-14 Estimated probability that an observed left ventricular (LV) mass index (LV mass/body surface area) obtained by either Mmode or three-dimensional echocardiography is greater than 125 g/m2 Standard deviation is 17.4 g/m2 for M-mode and 6.8 g/m2 for three-dimensional (assuming a body surface area of 1.7 m2 ).

been employed by King et al[303] [304] to measure LV mass. This method has the advantage of reducing dependence on geometric models. In an in vitro validation study[303] in which excised sheep and pig left ventricles were imaged in a water bath using 3D echocardiography, the correspondence of echocardiographic LV mass to LV weight was excellent (r = .995; standard

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error of the estimate [SEE] = 2.91 g). Moreover, in normal human subjects [303] [304] LV mass on 3D echocardiography was more closely related (r = .90) to that determined on magnetic resonance imaging (MRI) than LV mass measured by either 2D echocardiographic bullet formula (r = .71) or 2D guided M-mode echocardiography (r = .73). Additionally, interobserver variability was better with 3D echocardiography than with other echocardiographic techniques. In a comparison study of 3D echocardiography, using a magnetic tracking system with cardiac MRI, Chuang et al[305] found correlations of MRI with 2D echocardiography for measurement of LV mass in 45 patients of .84 to .92 based on the 2D method used. The SEE was at best 22.5 g (22.5 to 30.8). In contrast, the correlation with Figure 32-15 Strategy for risk stratification and antihypertensive therapy options based on left ventricular (LV) mass determination in a patient with hypertension. ABPM, ambulatory blood pressure monitoring; CV, cardiovascular; 2D, two-dimensional.

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Figure 32-16 (Figure Not Available) Three-dimensional echocardiographic method of left ventricular mass determination from nonparallel, nonintersecting short-axis cross sections. Different views are used to assemble three-dimensional reconstruction. (From Moore CR, Krakoff LR, Phillips RA: Hypertension 1997;29:1109–1113, with permission.)

3D echocardiography was 0.99 and the SEE was only 6.9 g. Moreover, interobserver variation for 3D echocardiography was 7.6% compared with 17.7% for 2D echocardiography.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in Epidemiologic Studies There is a significant learning curve present, even for clinically experienced sonographers, in recording technically adequate echocardiographic studies for the assessment of LV mass, particularly in older subjects. In a Framingham analysis of M-mode echocardiograms performed in over 6000 subjects aged 17 to 90 years, the ability to record acceptable quality echocardiograms in subjects older than 60 years rose from a minimum of 28% during the first 5 months of the study to a maximum of 74% to 81% during studies 2 years later.[306] Additionally, in the Cardiovascular Health Study, older subjects within the cohort were less likely to have measurable and interpretable studies than were younger subjects. Hence, echocardiography "dropouts" were not randomly distributed, leading to the possibility of bias in data interpretation. 2D echocardiographic measurements were even more problematic than 2D guided M-mode. Field Center Differences In previous large echocardiography trials, major differences in echocardiographic quality have existed between field centers. For example, in a 15-center Veterans Administration hospitals trial of antihypertensive monotherapy, the percentage of readable echocardiograms for LV mass varied from approximately 30% to 85% (Fig. 32-17) . This rate was not due to differences between centers in the proportion of easy or difficult patients. Although the use of suboptimal equipment in some cases contributed to poor studies, the intercenter differences existed mostly because of variation in technical performance. Importantly, extensive previous clinical experience in echocardiography was no guarantee of high-quality echocardiograms for research purposes. Cardiac Sonographer Training Cardiac sonographers, including experienced and clinically capable individuals, have been trained to use subtle eye-hand coordination to obtain

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optimum images pertinent Figure 32-17 Differences in technical adequacy ("readability") of echocardiograms for estimation of left ventricular mass in multicenter clinical trial of hypertension therapy.

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to clinical diagnosis. Although the examination generally contains common structured and repetitive elements, a good sonographer focuses on clinical questions that have been previously identified on the order form or modifies the examination technique to develop and fine-tune findings as they are encountered. Unfortunately, many of the useful habits of experienced sonographers in clinical practice are counterproductive in obtaining studies suitable for the estimation of LV mass or for Doppler evaluation of diastolic LV performance. For example, sonographers commonly seek to obtain a panoramic view of the aorta, left atrium, and left ventricle in the parasternal long-axis view. Although this image may be aesthetically pleasing and clinically informative, it usually results in angulation of the LV long axis so that targeted M-mode recordings of the left ventricle at the tips of the mitral valve record elongated LV dimensions that easily can be 10 mm greater than the true value. Cubing this error, as is done in the computation of LV mass from the 2D targeted M-mode recording, results in enormous error. Moreover, the 2D parasternal shortaxis cross-sectional images would be elliptic instead of circular. Hence, 2D echocardiographic calculation of LV mass using these distorted parasternal short-axis images would also produce substantial error. To obtain a circular cross-sectional image in the parasternal short-axis view, relatively high echocardiographic windows are sometimes required, which may not provide as clear or inclusive images. This strategy is counterintuitive for many sonographers, and it is difficult to teach. Echocardiography Reliability The use of echocardiography in the management of hypertension is dependent on the accuracy of echocardiography in detection of clinically important abnormality (e.g., LVH, LV systolic and diastolic dysfunction). Equally important in a chronic disease like hypertension is the ability of the test to reliably measure serial changes in quantitative parameters of disease. Hence, if therapy is targeted to regression of increased LV mass,

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echocardiography must be able to detect increases in LV mass associated with increased risk, or decreases in LV mass of the magnitude that would occur with effective antihypertensive therapy. However, estimation of LV mass requires certain geometric assumptions and arithmetic manipulation of primary echocardiographic measurements whether 2D or 2D targeted M-mode echocardiography is used. Because the acquisition of echocardiographic data is heavily operator interactive, minor variation in echocardiography technique may result in obtaining images that are not consistent with the geometric assumptions for calculation of LV mass. Moreover, slight differences in echocardiographic signal controls or guidance of the M-mode cursor may alter the ability to detect echocardiographic interfaces. Additionally, alterations in heart rate, autonomic tone, and loading conditions[50] [245] [247] and minor differences in placement of the Doppler sample volume[307] may substantially affect measurement of diastolic filling velocities. Hence, although echocardiography has been useful in clinical trials to study many subjects, its value for sequentially measuring LV mass and diastolic function in a single patient may be questioned. In one study[308] of the temporal variability of echocardiography for measurement of LV mass and function in hypertension patients, the width of the CI for LV mass was 59 g. Decreases in LV mass in clinical trials[272] have generally been substantially smaller; for example, an average of 21 g with diuretics (95% CI, -6 to -49 g) and an average of 45 g with angiotensin converting enzyme inhibitors (95% CI, -66 to -23 g). Some of the variability in sequential echocardiographic assessment of LV mass may result from a large number of sites contributing echocardiograms and using equipment that provides less satisfactory images than what is available with modern state-of-the-art instruments. However, more recent studies of test-retest reliability also have shown substantial variability. In one study[309] of 261 subjects who had repeat echocardiograms in 16 centers, with central reading, the test-retest variability was 65 g, similar to that in the previously discussed study. Even in another study[310] in which a single highly experienced reader evaluated and corrected virtually all of the readings, 95% test-retest reliability was still ± 35 g. Hence, changes in LV mass greater than that value would be required to infer either worsening or improvement of LV mass in an individual patient. Although measurement of LV mass with 2D echocardiography may be more reproducible than 2D targeted M-mode in normal subjects and

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patients with distorted LV contour,[297] [300] [311] it has not been demonstrated that it is sufficiently reproducible for the clinical measurement of sequential change in LV mass in hypertensive patients of varying echogenicity. In the future, however, clinical application of 3D echocardiographic reconstruction may provide substantially improved reproducibility of LV mass measurement.[304] Although the test-retest reliability of ejection fraction determination with 2D targeted M-mode echocardiography has been excellent with a width of the 95% CI of 4.5 units,[308] the temporal variability of early and late peak diastolic velocities was so poor as to preclude their serial use. Left Ventricular Hypertrophy Regression or Regression to the Mean? Given the large confidence width for measurement of LV mass, one could argue that serial echocardiography during treatment should be reserved for patients with markedly increased LV mass. A decrease in LV mass with treatment of greater than 59 g could then be taken to represent a true therapeutic effect. However, selecting patients with values for LV mass of any given value above (or for that matter, below) the population mean can result in subsequent determinations reflecting regression to the mean. Therefore, values higher than "true" values for LV mass on an initial determination tend to decrease on subsequent measurement (Fig. 32-18) . Hence, given the large measurement variability, any treatment choice is likely to show benefit if only patients with particularly 728

Figure 32-18 Regression to the mean as applied to measurement of left ventricular (LV) mass when only patients exceeding a given partition value are selected for follow-up examination. Ht, height; LVH, LV hypertrophy; LVM, LV mass. (From Gottdiener J: J Am Soc Echocardiogr 1996;9:585–590.)

high values for LV mass are selected. Of course, patients with particularly low values for LV mass are likely to show "worsening," that is, increase in LV mass, with subsequent measurement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Recommendations for Echocardiography in Hypertension Studies Two-Dimensional Guided M-mode Echocardiography: Selection of Beats for Measurement Parasternal short-axis views of the left ventricle in which the M-mode cursor traverses the center of a circular cross-sectional image at or just below the tips of the mitral leaflets need to be obtained, often using echocardiography windows higher than might otherwise be used in clinical practice (Table 32-4) . Proper cephalad-caudad orientation of the sector can be identified by minimal motion of mitral valve structures (presumably distal mitral tips or chordae tendineae) and absence of structures consistent with the bases of the papillary muscles. Eccentric cross-sectional images need to be excluded. Arbitrarily, we exclude images in which the estimated eccentricity (ratio of vertical midsectional chord to horizontal midsectional chord) is greater than 1.1. Attempts should be made to select beats with optimal definition of the posterior wall epicardial-pericardial interface, defined by visual extension into diastole of the anterior aspect of the small systolic posterior free space. It's helpful for the sonographer performing the study to inspect the recording and make preliminarily measurements to ensure that the appropriate interfaces are indeed present. Special care is required to exclude RV muscular structures (e.g., moderator band, crista supraventricularis) from the RV aspect of the septum by selecting beats where these structures do not abut against the septum within the path of the M-mode cursor. Additionally, small LV tendons traverse the anterior portion of the LV cavity in close proximity to the anterior septal segment. It is equally important to identify these tendons and exclude them from the septal and LV cavity measurements. Failure to identify confounding RV or LV structures can result in substantial overestimation of septal wall thickness, and in the case of LV tendons, underestimation of LV cavity dimension.

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Beat Averaging, Respiratory Control Cardiac dimensions on echocardiogram may differ over the respiratory cycle. Presumably these phasic respiratory changes result from increases in cardiac filling produced by negative intrathoracic pressures during inspiration. However, respiration also alters the position of the heart relative to the placement of the echo transducer. This alteration can produce measurement error because of anatomic translation and rotation of the heart, which may also be phasic with respiration. With 2D guided M-mode echocardiography, even though the transducer is held in a stationary position on the chest wall, the LV dimension may decrease as the ventricle "scans" the M-mode cursor because of LV rotation around the long axis and LV horizontal translation across the cursor. Vertical translation, ventricular rotation around the short axis, and tilting of the long axis relative to the cursor can create additional variability. It is difficult to know how much "respiratory variation" in cardiac dimensions may in fact represent positional artifact that is associated with respiration and how much is related to hemodynamic alterations during respiration. It has been a common practice to average multiple beats (3 to 10, or so) to reduce respiratory and other variability. Unfortunately, averaging sequential beats may contaminate LV dimensions obtained from anatomically "true" images with those reflecting positional artifact. However, using M-mode echocardiography recorded simultaneously on a videotape split-screen with the parasternal short-axis real-time image showing the M-mode TABLE 32-4 -- Recommendations for Echocardiography in Hypertensive Patients Parameter 2D guided M-mode

Recommendations Select circular cross-sectional beats (eccentricity ≤ 1.1) Use proper cephalad-caudal orientation Use posterior wall epicardial-pericardial interface Exclude right ventricular structures Beat averaging Use end-expiration during quiet respiration Patient position Use optimal (usually left lateral) position Transducer frequency Use highest frequency that provides adequate tissue penetration Imaging depth Use shallowest depth at which all measured components are displayed

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2D, two-dimensional.

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cursor placement, it is possible to select the anatomically "best" beats that minimize positional artifact. Only M-mode echocardiography beats corresponding to noneccentric short-axis images with the cursor traversing the center of the ventricular cavity are used, which requires adequate length of recording. Often, 30 or more beats of good quality tracing during quiet respiration may be required to obtain 3 to 5 "best" images with appropriate cursor placement and adequate wall and cavity interfaces. Alternatively, one may record the echocardiogram only during "gently held" expiration or continuously using a respiratory trace to permit selection of end-expiratory beats during quiet respiration. However, many patients have difficulty complying with even careful instructions, suspend breathing at end-tidal volume, and perform an unwanted Valsalva maneuver or exaggerate the depth of respiration. This situation often degrades echocardiography quality by shifting the window, and it likely produces undesired physiologic effects that disrupt the basal state. Additionally, the use of respiration markers, such as devices inserted into the nose or sensors that encircle the thorax, may be intrusive and cumbersome. Hence, it has been our practice to record the echocardiogram during quiet respiration. However, care is taken to record adequate numbers of beats with simultaneous 2D images. Patient Position In general patients need to be positioned in left lateral recumbency in order to optimize imaging of the left ventricle and also to help standardize the method for obtaining these images. However, optimal echocardiographic windows differ substantially between patients. Moreover, the echocardiographic window does not remain constant in a given patient over time. Hence, strict adherence to recording and reproducing patient position and transducer placement between patients, and on serial examinations, is not practical. Transducer Frequency Endocardial definition may be affected by transducer frequency and focal

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length. Hence, imaging should be performed with the highest frequency transducer that provides adequate tissue penetration. In obese individuals and subjects with a large chest diameter, a lower transducer frequency (2.5 MHz) is usually necessary. Imaging Depth It is helpful to image the left ventricle in the most magnified presentation, that is, at the shallowest display depth that contains all components of the image needed to be measured. This approach is of particular importance when the echocardiographic images are digitized for offline analysis. Use of greater display depths than necessary results in the desired portions of the image being represented by fewer pixels than if the display depth were adjusted so that the portions of the image required for analysis filled as much of the display screen as possible. The resulting lower pictorial information content increases the possibility of measurement error. Additionally, frame rates may be slower at deeper display depths, potentially resulting in blurred endocardial definition. Another reason for using maximum magnification is to minimize the effects of hand tremor in measurement of structures with either hand or electronic calipers. Hand tremor is not proportional to image size. Hence, any given amount of unintended hand motion results in a proportionately larger error with smaller images.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Use of Echocardiography in Patients with Hypertension The value of echocardiography as a research tool in hypertension is uncontested. In a relatively short time it has defined the cardiac structural and functional effects of hypertension, determined the prevalence of LVH and LV remodeling, determined the cardiac effects of antihypertensive therapy, and, in epidemiologic studies, provided fundamental insights into the relationships between blood pressure, genetic susceptibility, and LV mass. Although it has been suggested that treatment choices in individual patients should be guided by echocardiographic findings,[312] the value of echocardiography in the clinical management of hypertension is unproved. Potential Impact on Clinical Management The benefits of echocardiography depend on its value in affecting treatment decisions and in early identification and intervention in patients at risk who would not otherwise be treated (Table 32-5) . Moreover, demonstration of value requires that the impact of echocardiography on clinical decisions is accompanied by improvement in patient outcome.[315] Importantly, any consideration of the usefulness of echocardiography is contingent on its reliability for assessment of target measures such as LV mass. However, little information is available on the impact of echocardiographic data on physician behavior or on patient outcomes in hypertension. Before formulating strategies for using echocardiography in the management of hypertension, it is helpful to specifically consider which echocardiographic assessments are likely to be of value and then consider clinical situations in which the findings of those assessments might influence clinical decision making. For example, pertinent echocardiographic assessments might include quantitation of LV mass, determining the presence or absence of LVH, assessment of LV architecture (e.g., relative wall thickness, concentric remodeling), and

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measurement of LV systolic and diastolic function. Because of the comorbidity of hypertension and coronary artery disease, regional wall motion abnormality also is an appropriate goal of echocardiography in the evaluation of patients with hypertension. Hypertension accelerates coronary atherosclerosis, and with LVH there is more extensive myocardial necrosis in 730

TABLE 32-5 -- Hypothetical Impact of Echocardiography on Clinical Management Clinical Subset Established hypertension

Borderline hypertension "White-coat" hypertension

Hemodynamic profile

High risk for

Echocardiographic Target Finding LV mass or LVH No LVH

LV mass or LVH

Possible Impact Diurectics, vasodilators OK Unequivocal Neurohormonal blockade (ACE inhibitors),? calcium blockers Pesistent Change drugs LVH with therapy No LVH Follow closely

Equivocal or mild LVH Unequivocal LVH Cardiac output and High total peripheal output-low resistance resistance High resistancelow output Regional wall RWMA

Nutritional Rx

Drug Rx Beta blocker, diuretics, calcium blockers ACE inhibitors, vasodilators Prior infarct—?

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motion abnormality present (RWMA) RWMA and ↓ LV function

stress test

?angiography; drug selection— "antiischemic" antihypertensive drugs Hypertension in Valvular disease, Mitral Avoid vasodilators, the elderly LV architecture annular diuretics; ? avoid calcification calcium blockers LV outflow tract Aortic dynamic gradient stenosis ↑ ↑ relative Avoid diuretics; wall avoid vasodilators, ? thickness, beta blockers small LV cavity, LV outflow tract obstruction LV, left ventricular; LVH, left ventricular hypertrophy; Rx, therapy; ACE, angiotensin converting enzyme. the distribution of the infarct-related artery[206] and worse clinical outcome [204] than would otherwise occur. Another targeted echocardiographic assessment in elderly patients with hypertension is age-related degenerative valvular disease, principally aortic stenosis, which may have clinical interactions with hypertensive LVH. Also, inappropriately small LV cavity size and markedly thickened LV walls (hypertensive hypertrophic cardiomyopathy) may contribute to orthostatic hypotension in older patients, particularly with usage of diuretics or vasodilators. Hence, echocardiography may be of particular importance in the management of hypertension in the elderly. Another way to look at the potential application of echocardiography in clinical hypertension is to consider how the findings might effect management of certain clinical subsets or hemodynamic profiles. Table 325 summarizes this potential strategy. The results of assessment of LV mass and architecture, according to this schema, could have clinical impact on

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management choices in established hypertension, "white coat hypertension," and borderline hypertension. For example, marginally elevated blood pressure, or intermittently elevated blood pressure in the physician's office in the presence of concentric remodeling or clear-cut LVH, might result in drug therapy with agents believed to be effective for reduction of LV mass. In contrast, the absence of cardiac abnormality might suggest the feasibility of close follow-up, perhaps coupled with nutritional-hygienic management (e.g., weight loss, exercise, salt restriction). Some investigators have suggested that the hemodynamic profile may differ in hypertension.[313] Conceivably, patients with elevated blood pressure consequent to increased cardiac output but normal or low peripheral resistance may be appropriately treated with beta blockers, whereas those with elevated resistance but normal or low cardiac output might be more appropriately managed with vasodilators. It is important to emphasize, however, that this schema that outlines ways in which echocardiography may impact the management of hypertension is theoretical. There are few data to prove that the use of echocardiography would in fact have impact on physician behavior,[314] and there is no data to suggest it would affect patient outcome. Economic Cost Assuming one echocardiogram (even at a relatively modest charge in some regions of $500) is performed yearly for each of 20 million Americans with established hypertension, the yearly cost for echocardiography alone would be $10 billion. Costs would be even higher if patients with borderline hypertension were studied. Moreover, if the results of echocardiography resulted in inappropriate use of more costly medication than would be otherwise required, adverse effects of echocardiography on health care economics could be still greater. "Targeted" or "limited" echocardiograms have been advocated as a way to make echocardiography economically feasible for the evaluation of hypertension patients.[314] Black et al[314] estimated that the cost for echocardiography could be reduced to about $146, compared with complete exams costing 2 to 3 times as much. In contrast, the cost for electrocardiography was $68. However, it is important to distinguish the actual cost of an examination from the laboratory charges. For example, the sonographer may require an additional half hour to perform a "full" exam, and an additional 10 minutes of physician reading time may be obligated. Assuming sonographer labor costs at $30 per hour and physician labor cost

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at $130 per hour, the actual savings in labor would be only $37. Most other costs (equipment, disposables, space, insurance) would not be materially reduced by a limited exam. Hence, in our laboratory, as well as others, a "limited" examination would not result in a threefold cost savings. Naturally, omitting color flow, pulsed, and continuous wave Doppler would substantially reduce allowable charges from most federal and private reimbursement plans. Hence, reimbursement for a "limited" echocardiogram could be reduced to the amounts described. However, in this age of capitation and other changes in health 731

care reimbursement, reimbursements may not differ between "full" and "limited" studies. Potential Economic Benefit In contrast, if echocardiography in fact permits more effective treatment of hypertension and allows the identification of prehypertensive subjects at risk for morbidity and mortality of hypertensive disease, substantial cost savings could be incurred, as well as improvement in patient welfare.

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Chapter 33 - Echocardiographic Findings in Acute and Chronic Pulmonary Disease Selwyn P. Wong MD Catherine M. Otto MD

The pulmonary circulation is interposed between the right and left ventricles, resulting in interdependency of cardiac and pulmonary function in health and disease. The cardiac manifestations of pulmonary disease are mainly, but not exclusively, directed toward the right heart, and therefore the role of echocardiography in pulmonary disease is based on examination of the right heart.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Basic Principles The burden of pulmonary disease on the right ventricle is related to elevations in pulmonary artery pressure[1] resulting in an increased pressure load on the ventricle. The response of the right ventricle is dependent on the severity and time course of that elevation.[2] It is now recognized that the right heart has a vital role in normal circulatory function[3] [4] [5] [6] and that the diagnosis and treatment of dysfunction resulting from pulmonary disease is clinically important.[7] [8] Right Heart Anatomy and Blood Supply The right ventricle has a complex geometry. It is pyramidal in shape and can be divided into an inflow and an outflow tract (Fig. 33-1) . The inflow tract is made up of the tricuspid valve, papillary muscles, chordae tendineae, and trabeculated myocardium. The outflow tract consists of the infundibulum. The base of the pyramid is the inflow region and the interventricular septum and the anterior and posterior aspects of the free wall form the three faces. The free wall is attached to the interventricular septum anteriorly and posteriorly, with the interposed septum forming a convex bulge in the right ventricular cavity, giving the cavity a crescentic shape in cross section as it wraps around the left ventricle (Fig. 33-2) . The crista supraventricularis is a muscle bundle that separates the inflow and outflow zones. The right ventricle has prominent trabeculations and a large muscle bundle (the moderator band) running from the septum to the free wall. These features aid in distinguishing the right ventricle from the left ventricle. The muscle mass of the right 740

Figure 33-1 (color plate.) Right ventricular endocardial surface. The surface is reconstructed from a three-dimensional echocardiogram and

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demonstrates the pyramidal shape of the chamber. The inflow region forms the base of the pyramid, with the three faces composed of the interventricular septum and anterior and posterior free walls.

ventricle is approximately one sixth that of the left ventricle. The thin free wall and crescentic shape of the right ventricle impart to the chamber a high degree of compliance with the ability to accommodate large volumes and filling pressures.[7] The right atrium is thin-walled and lies superior and medial to the right ventricle. The trabeculated appendage is broad based and triangular in shape, and the body of the atrium has relatively smooth walls. Also visible on echocardiography are the crista terminalis running from the inferior to the superior vena cava, the valve of the coronary sinus, and embryologic remnants including the eustachian valve (valve of the inferior vena cava) and the Chiari network (a vestige of the right valve of the sinus venosus). Blood flow to the right ventricle myocardium is predominantly from the right coronary artery, which supplies the posterior right lateral of the free wall and the inferior one third of the septum through its marginal branches and the anterior free wall through the conus branch. The left anterior descending artery supplies the remainder of the septum and also provides small branches to the right ventricular free wall. Unlike flow to the left ventricle, right ventricular wall perfusion is biphasic, occurring in both diastole and systole.[3] Right Ventricular Physiology The role of the right ventricle is the delivery of oxygen-deficient venous blood to the gas exchange membranes of the pulmonary circulation. Under normal conditions, the vascular impedance of the pulmonary circulation is low, with resistance of the circulation one tenth that of the systemic circulation. Thus, a perfusion gradient of just 5 mm Hg is required to drive blood through the pulmonary circulation. [2] This relatively low hemodynamic requirement allows the thin-walled right ventricle to pump blood at the same rate and volume as the thick-walled left ventricle. In addition, pressure overload on the right ventricle is normally prevented by the ability of the pulmonary vascular bed to accommodate large changes in blood flow (e.g., with exercise) with little change in pressure. This is achieved by the recruitment of vessels in the poorly perfused upper lung and distention of compliant vessels elsewhere.[9] Despite these minimal hemodynamic requirements, acute impairment of right ventricular function

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can lead to circulatory collapse.[10] Right ventricular contraction involves contraction of the spiraling muscle fibers that make up the ventricular wall followed by movement of the free wall toward the interventricular septum with flattening of the free wall and expulsion of blood by passive compression of the right ventricular chamber.[11] From canine experiments, it has been estimated that the free wall and septum contribute equal degrees of energy to right ventricular function.[12] The normal right ventricle increases systolic output principally by increasing end-diastolic volume. This is unlike left ventricular systolic output, in which an increase is dependent on a pressure increase that is generated by the Figure 33-2 (color plate.) Right and left ventricular endocardium. The surfaces are reconstructed from a three-dimensional echocardiogram. The convex bulge of the interventricular septum into the right ventricle imparts a crescentic shape to that chamber as it wraps around the left ventricle (the left ventricular surface is displayed as a mesh).

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left ventricular chamber. Both ventricles are able to use the respective alternate mechanisms, in the face of abnormal loading conditions or injury, to maintain systolic output; however, these secondary mechanisms are less efficient for each ventricle. [4] Right ventricular performance is influenced by the contractile state of the myocardium and extrinsic factors, including loading conditions, left ventricular performance, pericardial constraint, coronary perfusion, function of the interventricular septum, and intrapericardial pressure.[3] In the setting of pulmonary disease, it is the alteration of loading conditions that is the greatest influence on the right heart. The left ventricle influences right ventricular performance due to ventricular interdependence defined as the forces transmitted from one ventricle to the other through the myocardium and pericardium, that are independent of circulatory and neurohormonal effects.[13] This interdependence results from the ventricles being encircled by common muscle fibers, sharing a septal wall, and being constrained by the pericardium. The existence of this entity has been demonstrated by studies

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in which the circulatory connections between the ventricles are disrupted and then showing that increasing the volume or pressure in one ventricle leads to an increase in pressure in the other ventricle.[13] During diastole, acute distention of either ventricle alters the compliance and geometry of the opposite chamber by changing the configuration of the shared interventricular septum, which alters filling in diastole of the opposite ventricle. Systolic interdependence also is in part due to the interventricular septum. Although the septum is considered to be functionally part of the left ventricle, it is displaced rightward into the right ventricular cavity in systole and so has an important role in right ventricular ejection. Transfer of forces via the free walls contributes to ventricular interdependence and affects the whole heart.[13] The restraining effect of the normal pericardium also contributes to diastolic ventricular interdependence. The normal pericardium accommodates only a 20% acute increase in cardiac volume before constraint leads to an increase in ventricular filling pressures.[4] A result of the pulmonary and systemic circulations lying in series is the backwards transmission of elevated left ventricular filling pressure through the pulmonary circulation, thus augmenting right ventricular afterload.[14] This is the most common mechanism of right ventricular failure and is distinct from the afterload elevation caused by primary pulmonary disease. Pathophysiologic Response of the Right Ventricle Dysfunction of the right heart can be due to pressure overload, volume overload, or ischemia. Differentiation between the response to these three mechanisms is an important part in distinguishing right ventricular dysfunction from primary cardiac rather than pulmonary disease. The development of pulmonary disease causes alterations in the pulmonary vasculature that lead to pulmonary arterial hypertension with the hemodynamic consequence being right ventricular pressure overload. Right Ventricular Pressure Overload

The thin-walled right ventricle is highly sensitive to increases in afterload and poorly constructed to compensate for acute changes. The ability of the right ventricle to increase systolic pressure acutely is dependent on increasing end-diastolic volume (preload). This mechanism fails when an acute rise in pulmonary vascular resistance requires a mean pulmonary artery pressure of about 40 mm Hg to perfuse the pulmonary bed, with rapid right ventricular failure ensuing[4] and causing total circulatory collapse through failure of left ventricular filling. [15]

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Chronic elevation in right ventricular pressure is better tolerated through the compensatory mechanisms of increased preload, geometric alteration, and right ventricular hypertrophy. Right-sided chamber enlargement can be massive and incorporate alteration of shape to an ellipsoid shape similar to that of the left ventricle. If compensatory mechanisms are inadequate, there is progression to pump failure. Tricuspid regurgitation usually develops early, with severe regurgitation a reliable sign of late right ventricular failure.[2] Right Ventricular Volume Overload

In contradistinction to pressure overload, pure volume overload is well tolerated by the right ventricle. The compliant right ventricle tolerates the increased load through dilation, hypertrophy, and augmentation of right ventricular systolic function with the maintenance of a normal ejection fraction. Ventricular interdependence can result in detrimental consequences to the left ventricle when there is displacement of the interventricular septum into the left ventricular cavity impairing left ventricular systolic and diastolic function, and by septal hypertrophy compromising left ventricular compliance. Right Ventricular Ischemia

Detailed description of coronary disease involving the right ventricle is beyond the scope of this chapter. Clinically right ventricular infarction almost always occurs in the setting of inferior left ventricular infarction with the damaged right ventricle acting as a passive conduit.[10] [16] The clinical setting should distinguish right ventricular infarction from the right ventricular abnormalities induced by pulmonary disease. (See Chapter 12.)

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Approach The echocardiographic examination in pulmonary disease is based on the examination of the right heart and in particular the assessment of rightsided chamber size, shape, function, and hemodynamics. Newer ultrasonographic techniques focus on specific pulmonary structures. Leftsided chamber alterations are usually secondary. Echocardiographic Views of the Right Heart

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The complex three-dimensional shape of the right heart and the position of the right ventricle beneath the sternum preclude complete right heart examination from any one transthoracic window, and examination from multiple windows is required. The transthoracic examination is even more difficult in the setting of pulmonary disease that involves an increase in lung volume, with this tissue being interposed between the ultrasound probe and target structures, reducing image quality. Transthoracic Views

The best views for specific right heart and pulmonary structures are listed in Table 33-1 . The right ventricular inflow view is obtained from anterior and medial angulation of the transducer from the standard parasternal long-axis view. Structures visible in this view are the free and diaphragmatic right ventricular walls, the anterior and posterior tricuspid leaflets, and the right atrium with the orifice of the inferior vena cava (Fig. 33-3) . Associated structures are the coronary sinus orifice adjacent to the tricuspid annulus, eustachian valve at the

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TABLE 33-1 -- Optimal Transthoracic Views for Visualizing Right Heart and Pulmonary Structures View Parasternal long-axis right ventricular inflow

right ventricular outflow

Parasternal short-axis base short-axis midventricular level Apical four-chamber

Subcostal long-axis

short-axis

Structure Right ventricle Interventricular septum Right ventricular free wall (anterior and posterior) Tricuspid valve leaflets (anterior and septal) Inferior right atrium Proximal right ventricular outflow tract Right ventricular outflow tract Pulmonary valve Main pulmonary artery Main pulmonary artery and bifurcation Right atrium Right ventricle Interventricular septum Right atrium Tricuspid valve leaflets (posterior and septal) Interventricular septum Right ventricle Right ventricular free wall (lateral) Right ventricle Right ventricular free wall Interventricular septum Tricuspid valve Right atrium Right ventricular outflow tract

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Pulmonary valve Tricuspid valve Right atrium Inferior vena cava Figure 33-3 Right ventricular inflow view from a transthoracic echocardiogram. ATVL, anterior tricuspid valve leaflet; CS, coronary sinus; EV, eustachian valve; IVC, inferior vena cava; PTVL, posterior tricuspid valve leaflet; RA, right atrium; RV, right ventricle.

inferior vena caval orifice, Chiari network (a vestige of the right valve of the sinus venosus), tricuspid annulus, and tricuspid chordae. This view allows a good window for Doppler interrogation of a tricuspid regurgitation jet. Clockwise rotation of the probe to an orthogonal plane produces images in the parasternal short-axis view. At the base of the heart, the right atrium, interatrial septum, the septal and anterior tricuspid leaflets, right ventricular outflow tract, pulmonary valve, and main pulmonary artery and its bifurcation can be seen (Fig. 33-4) . Forward Figure 33-4 Basal parasternal short-axis transthoracic view. This view demonstrates the right ventricular outflow tract (RVOT), pulmonary valve, and proximal pulmonary arteries in a patient with primary pulmonary hypertension. The main pulmonary artery (MPA) is dilated, measuring 3.2 cm in diameter. A small jet of pulmonary regurgitation is seen by color Doppler echocardiography (color plate). AoV, aortic valve; LPA, left pulmonary artery; PR, pulmonary regurgitation; RPA, right pulmonary artery.

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Figure 33-5 Mid-parasternal short-axis transthoracic view. This view is at the level of the mitral valve in a patient with primary pulmonary hypertension and demonstrates the right ventricle in short-axis. The right ventricle (RV) is hypertrophied and severely dilated. The left ventricle (LV) is relatively small. IVS, interventricular septum.

and regurgitant flow through the pulmonary valve can be inspected in this

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view. At a mid-short-axis level (toward the middle of the left ventricle), right ventricular size, shape, and function in the free wall is visible (Fig. 33-5) . Geometry and motion of the right ventricle, right atrium, and septum are well seen from the apical four-chamber Figure 33-6 Apical four-chamber transthoracic view during (A) diastole and (B) systole. This patient has severe pulmonary hypertension with accompanying right ventricular and right atrial enlargement. The moderator band is seen running from the ventricular septum to the free wall. The leftsided chambers are compressed. Note the obvious bowing of the interatrial septum toward the left atrium, indicating right atrial pressure greater than left atrial pressure. There is paradoxical motion of the interventricular septum with systolic motion toward the right ventricle, which is typical of severe right ventricular pressure overload. LV, left ventricle; PTVL, posterior tricuspid valve leaflet; RA, right atrium; RV, right ventricle; STVL, septal tricuspid valve leaflet.

view (Fig. 33-6) . Doppler interrogation of tricuspid flow is often optimal in this view (Fig. 33-7) . The tricuspid annulus is well seen and located more apically than that of the mitral valve. In this view, the septal and posterior tricuspid valve leaflets are visualized, as is the moderator band, which can be seen traversing the right ventricle near the apex. An altered appearance of the interatrial septum with bowing toward the left (indicating right atrial pressure superior to left) may be the initial sign of right heart disease. The coronary sinus can be seen to enter the right atrium by posterior angulation of the transducer. Inspection of the right heart may be improved by moving the transducer medially from the true apex. The subcostal window may be of particular value in patients with increased lung volume (Fig. 33-8) . Of particular importance are visualization of the inferior vena caval dimensions in the assessment of right atrial pressure and Doppler assessment of hepatic venous flow. Transesophageal Views

With the use of a multiplane probe, the standard four-chamber midesophageal view with 0 degrees of rotation displays the interatrial septum, the right atrium, the right ventricular size, shape, and systolic function, and the septal and anterior tricuspid leaflets ( Table 33-2 ; Fig. 339 ). A long-axis view (90-degree rotation) in this position displays the right ventricular outflow tract and pulmonary valve in the far field (Fig. 33-10) .

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Turning the probe toward the right side brings into view the inflow tract of the right ventricle and tricuspid valve, and further 744

TABLE 33-2 -- Optimal Transesophageal Views for Visualizing Right Heart and Pulmonary Structures View High esophageal (0 degrees) short-axis (30–45 degrees) Midesophageal (four-chamber, 0 degrees)

Structure Right ventricular outflow tract Right atrium Right ventricle Right ventricular free wall Interventricular septum Tricuspid valve leaflets (anterior and septal) Right atrium Long-axis (90–120 degrees) Pulmonary valve Right ventricular outflow tract Right atrium Transgastric: short-axis (0 degrees) Right ventricle long-axis (90 degrees) Right atrium Tricuspid valve Right ventricle rightward angulation shows the right atrium, interatrial septum, and cava. From a high esophageal position, a basal short-axis view shows the right ventricular outflow tract with the pulmonary valve and long-axis views of the main pulmonary artery and its bifurcation (0-degree rotation)—the aortic valve lies posterior to the pulmonic valve and is seen in the short-axis view. Additionally, the right pulmonary artery can be seen in cross section posterior to the ascending aorta when imaged in the long-axis view. Further rotation to the right shows the right pulmonary artery as it goes on to course behind the superior vena cava (and superior to the left atrium). The left pulmonary

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Figure 33-7 (color plate.) Tricuspid regurgitation on color flow Doppler echocardiogram. Severe tricuspid regurgitation (TR) is demonstrated in this apical four-chamber transthoracic view. The mosaic-colored jet of regurgitation fills more than two thirds of the dilated right atrium. The right ventricle (RV) is severely dilated, with the right ventricular apex extending beyond the left ventricular apex. LV, left ventricle. Figure 33-8 Subcostal four-chamber transthoracic view. This patient with primary pulmonary hypertension had image quality from parasternal and apical windows that was poor, but the subcostal window gave rise to good images. There is hypertrophy of the right ventricular free wall and dilation of the right ventricle (RV) and atrium (RA). The interatrial septum (IAS) is bowed to the left. There is a small pericardial effusion anteroapically. Pericardial effusions are not uncommonly seen in patients with primary pulmonary hypertension. LV, left ventricle; PE, pericardial effusion.

artery is less reliably imaged beyond the basal short-axis view described but may be seen by imaging in a vertical plane directed laterally. A standard transgastric position can display the right-sided structures in short (0-degree rotation) and long Figure 33-9 Midesophageal four-chamber transesophageal view at 0 degrees rotation. This view demonstrates the right heart structures in a horizontal plane. ATVL, anterior tricuspid valve leaflet; LA, left atrium; LV, left ventricle; RV, right ventricle; STVL, septal tricuspid valve leaflet.

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Figure 33-10 High-esophagus transesophageal view. This view demonstrates the right ventricular outflow structures. AoV, aortic valve; PV, pulmonary valve; RV, right ventricle; RVOT, right ventricular outflow tract.

(90-degree rotation) axis by turning of the probe rightward (Fig. 33-11) . Qualitative and Quantitative Evaluation of Right Heart Function Right Ventricular Volume, Mass, and Ejection Fraction

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The quantitative analysis of right ventricular volume is limited by the nongeometric shape and technical difficulty in echocardiographic examination related to location of Figure 33-11 Transgastric long-axis transesophageal view. The right ventricle is severely dilated in this patient with biventricular failure. ATVL, anterior tricuspid valve leaflet; CT, chordae tendineae; PM, papillary muscle; PTVL, posterior tricuspid valve leaflet; RA, right atrium; RV, right ventricle.

the chamber. The best geometric models for calculating right ventricular volumes are derived from biplane imaging and an area-length equation, as follows: Volume = c × area {1} × length {2} where c is a constant depending on the geometric model and {1} and {2} are orthogonal views of the right ventricle. Geometric shapes that have been studied in children or in vitro include the ellipsoid, pyramids with square or triangular bases, and the parallelepiped (a six-faced polyhedron whose faces are parallelograms lying in pairs of parallel planes).[17] [18] [19] None of these geometric formulas are of sufficient simplicity and accuracy to be used clinically, however. In practice, measurement of right ventricular volume in adult patients is difficult because of the constraints of complete right ventricular imaging in two orthogonal planes. Two-dimensional measurements of volume using a single plane and applying the modified Simpson's rule for an ellipsoid shape uses the software on current echocardiographic machines.[20] This method is analogous to left ventricular volume measurement and displays varying accuracy depending on ventricular geometry. The assumption of an ellipsoid right ventricular shape is more valid in cor pulmonale patients than in normal subjects. No geometric formula has been developed for right ventricles distorted by the pressure load of pulmonary hypertension and the added volume load of subsequent tricuspid regurgitation. Other techniques that have had modest results include the use of echocardiographic contrast to aid visualization in right ventricular volume quantification [21] and online automated border detection,[22] but such methods do not overcome the limitation of geometric assumptions on the shape of the ventricle.

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Several investigators have quantified right ventricular volumes using threedimensional echocardiography and reconstruction in animal models, in vitro or in vivo with validation by magnetic resonance imaging.[23] [24] [25] [26] [27] [28] [29] Although three-dimensional analysis offers accurate volume measurement without the need for geometric assumptions, the need for border tracing and extensive data analysis limits the clinical usefulness of this technique. Intracardiac ultrasonography is a further research technique described for the accurate quantification of right ventricular volumes and ejection fraction.[30] In the clinical setting, semiquantification of right ventricular volumes is usually sufficient. Right ventricular dilation is described as mild (enlarged, but area less than left ventricular area), moderate (right ventricular area equal to left ventricular area), or severe (right ventricular area greater than left ventricular area).[31] Similarly, right ventricular shape description is semiquantitative and limited to a description of the deviation from the normal crescentic shape to a more spherical conformation. The thickness of the right ventricular free wall is best assessed by M-mode measurement but can be difficult because of interposed structures and adherent fat (Fig. 33-12) . Normal thickness in adults is 5 mm or less. The presence of right ventricular hypertrophy suggests right ventricular pressure overload.

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Figure 33-12 Right ventricular hypertrophy demonstrated by an Mmode tracing. The thickness of the right ventricular (RV) free wall at end-diastole is 0.86 cm. IVS, interventricular septum; LV, left ventricular.

The quantitative echocardiographic assessment of right ventricular systolic function using ejection fraction is limited by the problems in measuring right ventricular volume. Furthermore, the heavily trabeculated right ventricular endocardial surface makes tracing of this border in end-systole difficult. However, assessment of right ventricular function by echocardiography in patients with pulmonary disease plays an important part in clinical decisions, the monitoring of therapy, and prognosis. Echocardiography

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Figure 33-13 Severe pressure overload of the right ventricle with paradoxical interventricular septal motion. The parasternal short-axis views show a right ventricle that is hypertrophied and dilated. There is leftward ventricular septal shift and reversal of the normal curvature. A, The reversal of septal curvature is maximal at end-systole, as shown by the large arrow. B, There is near restoration of normal septal curvature at end-diastole. LV, left ventricle; RV, right ventricle; RVH, right ventricular hypertrophy.

provides additional hemodynamic information over nuclear modalities and, unlike contrast ventriculography, is noninvasive. Functional assessment includes description of endocardial myocardial thickening or endocardial motion in the right ventricular free wall (i.e., hyperkinetic, normal, hypokinetic, akinetic). The motion of the interventricular septum is important in cases of pulmonary disease causing right heart disease. Initial pressure overload of the right ventricle decreases septal motion. Increased right ventricular pressure leads to flattening of the interventricular septum throughout the cardiac cycle with further elevation eventually leading to a concave septal configuration that is maximal at end-systole. This paradoxical septal motion gives the impression that the septum predominantly supports right ventricular rather than left ventricular function (Fig. 33-13) . In contrast, predominant volume overload results in a D-shaped left ventricle from early diastole and the septum may move back to its normal configuration in systole (Fig. 33-14) . Other methods of assessing right ventricular function use newer echocardiographic techniques. Tricuspid annular velocity at the free wall is an example of an older concept measured by newer techniques of either pulsed wave[32] or color[33] Doppler tissue imaging. Velocity reflects longaxis shortening. Since the apex is relatively fixed and rotation about the long axis is minimal, this velocity also reflects contraction of the right ventricle. [32] Compared with values in normal subjects or patients with anterior infarction, reductions in peak systolic and peak diastolic tricuspid annular velocities were found in 38 patients with inferior infarction, especially if the right ventricle was involved. Tricuspid motion was also reduced as compared with normal subjects.[34] Additionally, reduced excursion of 747

Figure 33-14 Severe volume overload of the right ventricle (RV). The

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parasternal short-axis views show a D-shaped left ventricle (LV). In right ventricular volume overload, the maximal leftward shift of the interventricular septum occurs during late diastole (A) rather than late systole (B).

the tricuspid annular plane was reported as an independent predictor of survival in patients with severe reduction of left ventricular ejection fraction and heart failure.[35] A second new technique is color kinesis, which encodes endocardial motion by color. This requires pixels to be classified as blood or myocardium. During diastole the pixels of transition are color-coded and color overlays are added frame by frame to map the endocardial motion.[36] The use of color kinesis in right ventricular regional function analysis has been described in one study in which patients with pressure overload or heart failure exhibited significantly decreased endocardial motion along the right ventricular free wall. Additionally, if mixed pressure/volume overload was present, a markedly increased ventricular septal motion compensated for any decreased right ventricular free wall motion.[37] The pulmonary valve has reduced motion in the presence of elevated pulmonary arterial pressure. M-mode examination of the valve classically shows mid-systolic notching. Estimation of Pulmonary Pressures

Cardiac sequelae of pulmonary disease are manifested largely through elevation in the pulmonary artery pressure. Hence, in the echocardiographic assessment of such patients, the ability to measure pulmonary pressures is paramount, and Doppler echocardiography is an accurate and reliable noninvasive tool for this purpose. Additionally, Doppler examination (spectral and color) should be used for the interrogation of each valve. In clinical practice, the most useful assessment of pulmonary pressures is that of systolic pulmonary artery pressure using the velocity of the tricuspid regurgitant jet together with an estimate of right atrial pressure. The advantages of this technique are its ease of acquisition and its reliability and reproducibility (Table 33-3) . Right Atrial Pressure

In patients with pulmonary disease, right atrial pressure reflects dysfunction of the right ventricle. The best estimate of mean right atrial pressure in nonventilated patients[38] is from measurement of the segment of the inferior

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vena cava diameter adjacent to the right atrium in the subcostal view (Fig. 33-15) . The measurement incorporates examination during quiet respiration and forced inspiration ("sniff")[38] [39] [40] (Table 33-4) . The estimation of right atrial pressure is used together with the right TABLE 33-3 -- Right Atrial Pressure Estimation from Inferior Vena Caval Diameter Inferior Vena Caval Diameter Small (<1.5 cm) Normal (1.5 to 2.5 cm) Dilated (>2.5 cm) Dilated inferior vena cava and hepatic veins

Diameter Change with Inspiration Collapse >50% decrease <50% decrease No change

Right Atrial Pressure Estimate, mm Hg 0–5 5–10 10–15 >20

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Figure 33-15 Mean right atrial pressure estimate. The inferior vena cava (IVC) is seen in long-axis from a subcostal window. The diameter of the vessel is measured adjacent to the right atrium during (A) quiet respiration and (B) forced inspiration or "sniff." The caval diameter is dilated during quiet respiration, and decreases by less than 50% on forced inspiration, giving an estimated mean right atrial pressure of 10 to 15 mm Hg.

ventricular-to-right atrium pressure gradient to estimate pulmonary artery systolic pressure. Tricuspid Regurgitant Velocity

The estimation of the pulmonary artery systolic pressure is the most important common clinical echocardiographic measurement in patients with pulmonary disease. The right ventricular-to-right atrium pressure gradient is obtained by measuring the velocity (VTR ) of the tricuspid

regurgitant jet using continuous wave Doppler (Fig. 33-16) and incorporating the velocity into the Bernoulli equation. The addition of the mean right atrial pressure (RAP) gives an estimate of right ventricular systolic pressure, which, in the absence of pulmonic stenosis, is assumed as equal to the pulmonary artery systolic pressure (PAPsystolic ):

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PAPsystolic = 4(VTR )2 + RAP A tricuspid regurgitant jet suitable for measurement is present in more than 90% of subjects, even if the degree of regurgitation is modest.[41] This method has been well validated compared with invasive measures of pulmonary artery pressure (correlation r-values, 0.95–0.97; SE estimate, TABLE 33-4 -- Comparison of Doppler Methods of Pulmonary Artery Pressure Estimation Pulmonary Artery Pressure Ease of Method Estimated Acquisition Sensitivity Tricuspid regurgitation Systolic +++ ++++ Pulmonary Mean ++++ + acceleration time Right ventricular Mean + + ejection time Pulmonary Diastolic ++ + regurgitation Isovolumic relaxation Systolic + ++ time

Specificity ++++ +++ + ++ +++

4.9–7.0 mm Hg).[41] [42] [43] [44] The normal velocity of the tricuspid regurgitant jet ranges from 2.0 to 2.5 m per second. Values of pulmonary artery systolic pressure in health and disease are listed in Table 33-5 . Several technical factors are important to the reliability of this technique. These include the parallel alignment of the ultrasound beam to the tricuspid regurgitant jet, careful inspection with multiple angulation in several windows to yield the regurgitant jet with the highest velocity (usually the apical or right ventricular inflow views), and avoidance of misinterpretation of mitral regurgitation velocity as tricuspid regurgitation velocity (tricuspid regurgitation is usually of longer duration, with a slower upstroke and later systolic peak). The presence of pulmonic stenosis requires adjustment of the measured right ventricular systolic pressure to estimate pulmonary artery pressure.

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The right ventricular-to-pulmonary artery pressure difference, estimated from the velocity of the pulmonary stenotic jet, is subtracted from the right ventricular systolic pressure: PAPsystolic = [4(VTR )2 + RAP] − [4(VPS )2 ] where PAPsystolic is systolic pulmonary artery pressure, VTR is peak velocity of the tricuspid regurgitant jet, RAP is

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Figure 33-16 Pulmonary artery systolic pressure estimate from the velocity of the tricuspid regurgitant jet. The jet velocity is measured by continuous wave Doppler echocardiography from the apical window in a patient with severe pulmonary hypertension. The peak velocity is severely elevated (5.1 m/sec). From the modified Bernoulli equation (4 × [peak velocity]2 ) the systolic pulmonary artery pressure is estimated as 104 mm Hg plus mean right atrial pressure.

estimated right atrial pressure, and VPS is peak velocity of the pulmonary stenotic jet.

In ventilated patients or if inferior vena caval visualization is suboptimal, the mean right atrial pressure must be estimated from nonechocardiographic methods (jugular venous pressure, central venous pressure).[38] Pulmonary Artery Velocity Curve

The time to peak velocity in the pulmonary outflow tract (also called acceleration time) is a Doppler method that estimates the mean pulmonary artery pressure. In comparison to the left ventricle, ejection from the right ventricle has slower acceleration, a longer time from onset of flow to peak flow, and a rounder velocity curve (Fig. 33-17) . With increased pulmonary pressure, the right ventricular ejection pattern approximates more a leftsided ejection pattern. In addition, there is asymmetry of the pulmonary artery velocity curve with a shortened time to peak velocity. The absolute time that best predicts TABLE 33-5 -- Normal Values for Doppler Indices of Pulmonary Artery Pressure

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Pulmonary Normal Artery Range, Pulmonary * Pressure mm Hypertension, Echocardiographic * Measured mm Hg Method of Estimation Hg Systolic 15–30 >30 Tricuspid regurgitation jet velocity Diastolic 3–12 Pulmonary regurgitation jet velocity Mean 9–16 >20 Pulmonary acceleration time (AcT) Right ventricular ejection time (RVET) AcT/RVET

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Normal Range 2.0 ± 0.2 m/sec † 1.5 ± 0.2 m/sec ‡ 137 ± 24 msec § 304 ± 38 msec § 0.45 ± 0.05 §

* Data from Davidson CJ, Fishman RF, Bonow RO: Cardiac catheterization. In Braunwald E (ed): Heart Disease: A Textbook of Cardiovascular Medicine, vol 1, 5th ed. Philadelphia, W.B. Saunders, 1997, pp 177–204. † Data from Berger M, Haimowitz A, Van Tosh A, et al: J Am Coll Cardiol 1985;6:359–365. ‡ Data from Berger M, Hecht SR, Van Tosh A, Lingam U: J Am Coll Cardiol 1989;13:1540–1545. § Data from Kitabatake A, Inoue M, Asao M, et al: Circulation 1983;68:302–309.

elevated mean pulmonary pressure (greater than 20 mm Hg) is unclear but is in the region of 100 msec,[45] [46] although it may be as low as 80 msec.[44] A logarithmic relationship between the time to peak velocity and the mean pulmonary artery pressure has been described.[46] [47] [48] With severe pulmonary hypertension, a mid-systolic notch may be present in the deceleration slope of the pulmonary artery Doppler flow profile (see Fig. 33-17) . This notch is analogous to the mid-systolic notch seen in Mmode examination of the pulmonary valve. The notch may be secondary to transient elevation of pulmonary artery pressure above right ventricular pressure due to a decrease in pulmonary artery compliance and an increase in main pulmonary artery size, impedance, and transmission time of the velocity wave. The presence of a mid-systolic notch in the pulmonary outflow Doppler profile is highly specific for pulmonary hypertension.

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The pulmonary artery acceleration time is easily measured in most patients, including those with chronic lung disease. Reliability of the method is less than when using the tricuspid regurgitant jet velocity, however.[49] There is 750

Figure 33-17 Pulmonary artery flow patterns. A to C, Schematic drawings of the patterns of pulmonary artery flow recorded by spectral Doppler according to the degree of pulmonary arterial hypertension. When mean pulmonary pressure is normal (A), the Doppler profile is symmetrical. Moderate elevation of the pulmonary arterial pressure (B) results in an asymmetrical Doppler envelope and a decreased time to peak velocity (or acceleration time). As the degree of hypertension increases (C), the time to peak velocity further shortens and may be accompanied by a mid-systolic notch in the flow profile with severe pulmonary hypertension (see text). Denoted are the site of measurements for the pre-ejection period (PEP), right ventricular ejection time (RVET) and acceleration time (AT). D to F, Spectral Doppler echocardiographic recordings from the proximal pulmonary artery corresponding to the patterns drawn in parts A to C.

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heavy dependence on the position of the Doppler sample volume because acceleration and velocities are higher along the inner edge of curvature of the pulmonary artery. Because the curvature is three-dimensional, positioning of the sample volume in the middle of the vessel in the imaged plane may not avoid overestimation of velocity by sampling adjacent to the vessel wall in the orthogonal nonimaged plane. Furthermore, the short absolute time interval of acceleration time lends itself to high measurement error and lower reproducibility. Right Ventricular Outflow Tract Flow Velocity Profile

Mean pulmonary arterial pressure can be estimated by measurement of the time to peak velocity in the right ventricular outflow tract similar to the use of pulmonary artery acceleration times.[47] [48] Pulmonary Regurgitation Velocity

The diastolic pulmonary artery pressure can be reasonably estimated by adding the right atrial pressure to the diastolic gradient between the pulmonary artery and right ventricle (Fig. 33-18) . This gradient is

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estimated from the pulmonary regurgitant flow velocity by means of the simplified Bernoulli equation and correlates closely to that obtained at catheterization. [50] Many patients with pulmonary hypertension have some degree of pulmonic regurgitation, as do up to 40% of the healthy population. [41] Right Isovolumic Relaxation Time and Ventricular Ejection Times

The right ventricular isovolumic relaxation time is the interval between pulmonic valve closure and tricuspid valve opening. This time increases with pulmonary hypertension and can be related using nomograms derived from pediatric populations. In adults, pulmonic valve closure is difficult to ascertain, and the short time interval lends itself to measurement variability and error. Right ventricular ejection time shortens with increasing pulmonary hypertension. In contrast, the right ventricular pre-ejection time lengthens with increasing pulmonary arterial pressure. Although neither time is useful alone, the ratio of pulmonary acceleration time to total right ventricular ejection time or pre-ejection time can be used to estimate mean pulmonary artery pressure[46] [51] with correlation to mean pulmonary pressure similar or better than acceleration time alone. Again, the short values of these time intervals render them impractical for general clinical use.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Cor Pulmonale: The Right Heart in Pulmonary Disease Cor pulmonale refers to the adaptive mechanisms by which the right heart responds to the hemodynamic burden invoked by disease of the lung, thorax, or pulmonary circulation. The hemodynamic burden increases the pressure load on the right ventricle, and the adaptive mechanisms are principally chamber enlargement and hypertrophy. Cor pulmonale does not refer to right heart disease that is secondary to left heart disease or to congenital Figure 33-18 (color plate.) Assessment of pulmonary artery diastolic pressure using the pulmonary regurgitant jet. The velocity at end-diastole is elevated at 1.98 m/sec corresponding to an estimated pulmonary artery diastolic pressure of approximately 16 mm Hg.

cardiac abnormalities. Nearly any chronic lung disease, and neuromuscular disorders or thoracic cage abnormalities that ultimately lead to pulmonary hypertension, can cause cor pulmonale. When the adaptive mechanisms cannot compensate for the hemodynamic burden, right ventricular failure ensues. The pulmonary hypertension that results from pulmonary disease is termed secondary pulmonary hypertension. Both primary and secondary pulmonary hypertension are causes of cor pulmonale. The causes of secondary pulmonary hypertension have been well established, but the mechanisms by which pulmonary hypertension develops have not. Secondary pulmonary hypertension due to pulmonary disease is related to the increased resistance to flow through the pulmonary vascular bed in a variety of ways (Table 33-6) . A combination of mechanisms, including vascular bed obliteration or destruction in parenchymal lung diseases, hypoxic pulmonary vasoconstriction, and the structural changes in the vessel walls from chronic vasoconstriction likely result in the secondary

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hypertension of pulmonary disease.

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TABLE 33-6 -- Etiology of Cor Pulmonale Pathology Parenchymal pulmonary disease Disease of the airways Interstitial lung disease

Disease of pulmonary vasculature Disease of the arterial wall Thromboembolic disorders

Diseases of chest wall or neuromuscular apparatus

Specific Diseases Chronic bronchitis, emphysema, cystic fibrosis Cryptogenic fibrosing alveolitis, connective tissue diseases, sarcoidosis, pneumoconiosis, scleroderma, malignant infiltration, radiation, eosinophilic granuloma Primary pulmonary hypertension Thromboembolism, tumor embolism, primary thrombotic disorders Sleep apnea, kyphoscoliosis, neuromuscular disease, pleural fibrosis

In patients with chronic lung disease, cor pulmonale is associated with an increased morbidity and functional status,[52] and frank right ventricular failure predicts increased mortality.[15] Echocardiographic Features of Acute Cor Pulmonale In the setting of acute cor pulmonale, a normal right ventricle faces a sudden increase in afterload. In response, there is an increase in right ventricular preload with chamber to maintain adequate right ventricular pressure to perfuse the pulmonary bed. The echo findings are as follows: 1. Pulmonary hypertension. In addition to elevation of the pulmonary artery pressures, the pulmonary artery flow may be biphasic, with reduction of flow in mid-systole. [53] The right ventricle that is

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2.

3. 4. 5.

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unconditioned to pressure elevation can generate only a limited increase in pulmonary pressure and the acutely elevated mean pulmonary arterial pressure will rarely exceed 40 mm Hg. [54] If the acute increase in afterload is devastating, the failing right heart will be unable to generate adequate pressure, and measurements of pulmonary pressures will be low.[53] Hence, the presence of low pulmonary arterial pressures may be a premorbid finding. Right ventricular enlargement. The compliant right ventricle has great capacity to increase in size, even in the setting of acute elevation in pulmonary resistance, and may enlarge to twice the volume of the left ventricle.[53] Septal flattening and paradoxical septal motion. Right ventricular hypokinesis. This is an important sign that indicates failure of the right ventricle in the face of the acute afterload increase. Diastolic left ventricular impairment. The acute right ventricular dilation within the stiff pericardium must be associated with a proportional reduction in left ventricular diastolic dimension, and left ventricular filling is impaired.[55]

Echocardiographic Features of Chronic Cor Pulmonale In chronic cor pulmonale, the slower time course of afterload increase allows for adaptations in the right heart. 1. Pulmonary hypertension. The degree of elevation of pulmonary arterial pressures may be severe, as right ventricular dilation and hypertrophy can enable the generation of systemic, or even suprasystemic, pulmonary artery pressures.[56] 2. Right ventricular enlargement. Dilation occurs in response to pressure overload. In addition, chronic dilation with consequent tricuspid regurgitation places a volume load on the right ventricle, further increasing any dilation. 3. Right ventricular hypertrophy. In chronic cor pulmonale, right ventricular thickness averages 10 mm, which matches the average thickness in the left ventricular wall. Thickening may be more pronounced at the apex.[53] 4. Interventricular septal flattening and abnormal motion. 5. Right ventricular hypokinesis. Free wall hypokinesis indicates a failing right ventricle.[57] 6. Diastolic left ventricular impairment. Chronic right ventricular pressure overload distorts early diastolic left ventricular geometry,

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delaying the left ventricular filling phase. The functional diastolic impairment of the left ventricle is closely correlated to pulmonary hypertension levels.[58]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in Clinical Pulmonary Disease This section discusses specific pulmonary diseases in which echocardiography has a role in diagnosis, management, and prognosis. Not every pulmonary disease is discussed, but any such disease of sufficient severity can cause cor pulmonale. Parenchymal Lung Disease Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease causes an estimated 70,000 deaths per year in the United States and is the most common pulmonary disease resulting in right ventricular dysfunction.[59] Up to 40% of patients with chronic obstructive pulmonary disease have cor pulmonale at autopsy. [9] This lung disease causes mild elevation in the peak pulmonary artery systolic pressure that is typically in the range of 40 to 50 mm Hg. Patients with cor pulmonale from chronic obstructive pulmonary disease usually have advanced airway obstruction with a forced expiratory volume in one second of less than 1 L.[15] The quality of echocardiographic image acquisition is impaired in patients with chronic bronchitis or emphysema due to the presence of expanded lung volumes causing decreased ultrasound tissue penetration. The feasibility of obtaining the relevant hemodynamic parameters 753

in such patients has reportedly varied. Adequate tricuspid regurgitation velocity was obtained in only 24% to 30% in some early studies from the late 1980s,[47] [48] whereas other studies reported measurable tricuspid regurgitant velocities in most patients.[60] [61] The use of agitated saline contrast enhances detection of the tricuspid regurgitant jet.[62] [63] Pulmonary flow velocities are more easily obtained and can be satisfactorily measured

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in most patients with chronic airways disease from the traditional echocardiographic windows.[47] [64] The subcostal approach may confer additional diagnostic power in patients with hyperexpanded lungs.[65] [66] Accurate pulmonary artery Doppler and two-dimensional echocardiographic measurements were obtained in 52 of 59 patients with chronic airways disease by imaging from a left oblique subcostal window. [65] The current quality of echocardiographic equipment and clinical familiarity with the examination of patients with chronic obstructive pulmonary disease should allow the accurate assessment of pulmonary pressure in the majority of patients. Right ventricular wall thickness is difficult to measure by echocardiography in patients with chronic obstructive pulmonary disease because of the difficulties in imaging the free wall, and measurements correlate poorly to autopsy-derived right ventricular weight.[67] Imaging limitations and the nongeometric shape of the right ventricle limit the echocardiographic assessment of right ventricular function to qualitative descriptions. The measurement of pulmonary arterial pressure in patients with chronic obstructive pulmonary disease provides high prognostic value. In 175 patients with chronic obstructive lung disease and moderate to severe airway obstruction, the mean pulmonary artery pressure was assessed by catheterization. Survival rates after 4 and 7 years were significantly lower in the subgroup with a mean pulmonary artery pressure greater than 20 mm Hg and in patients older than 60 years of age. [68] In an echocardiographic study of 166 patients with advanced chronic obstructive pulmonary disease treated with long-term oxygen therapy, multivariate analysis showed right ventricular systolic pressure to be independently predictive of mortality. In this study, right ventricular systolic pressure higher than 35 mm Hg, age greater than 70 years, and forced expiratory volume in 1 second lower than 30% of the predicted value were associated with shortened survival.[69] A pulmonary acceleration time less than 100 msec identifies pulmonary hypertension (mean pulmonary artery pressure > 20 mm Hg),[46] [70] with a sensitivity of 71% and a specificity of 94%. The presence of cor pulmonale in patients with chronic obstructive pulmonary disease confers a worsened prognosis.[71] [72] In the early stages of the chronic pulmonary disease, there may be no evidence of structural effects on the right heart. However, the ability of the right ventricle to maintain normal systolic function by hypertrophy despite chronic pressure overload is limited. Thus, dilation and then frank systolic failure ensue. In a

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Veterans Administration trial, patients with obstructive pulmonary disease and an episode of right heart failure had a 4-year mortality rate of 73%. [73] Right ventricular systolic dysfunction is common (59%) in chronic obstructive pulmonary disease patients undergoing assessment for lung transplantation.[74] Atherosclerotic-like lesions in enlarged central pulmonary arteries are a more recent echocardiographic finding reported in approximately half of 25 patients with chronic obstructive pulmonary disease studied by transesophageal echocardiography. The lesions were present even in the absence of significant pulmonary hypertension and did not have a close relationship with the severity of pulmonary dysfunction. [75] Intravenous contrast echocardiography with perflenapent emulsion has been reported as safe in stable ambulatory patients with chronic airway obstruction despite the abnormal pulmonary vascular architecture.[76] Interstitial Lung Disease

Interstitial lung disease causes thickening and fibrosis of the alveolar walls with disruption of the alveolar-capillary unit. The incidence of pulmonary hypertension in patients with interstitial lung disease is high, although the degree of elevation in pulmonary arterial pressures is moderate until late in the disease.[1] Significant cor pulmonale usually is a very late occurrence.[15] The degree of pulmonary hypertension correlates with the degree of hypoxia. As with chronic obstructive pulmonary disease, the pulmonary artery pressure is an important predictor of survival in patients with interstitial disease.[77] However, in patients with scleroderma (especially with the CREST variant), pulmonary hypertension predominates and can be severe, even without significant parenchymal lung involvement. [78] Pulmonary Vascular Diseases Diseases of the pulmonary vasculature cause an anatomic obstruction of the pulmonary vascular bed with consequent elevation in right ventricular afterload. The severity of cor pulmonale and pulmonary hypertension are generally greater than in parenchymal lung disease. The two most common pulmonary vascular conditions are primary pulmonary hypertension in which the cause for elevation in vascular resistance is unknown and pulmonary thromboembolic disease. Less common pulmonary vascular causes of an increase in pulmonary vascular resistance are pulmonary vasculitis, high altitude, and pulmonary veno-occlusive disease.

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Primary Pulmonary Hypertension

Primary pulmonary hypertension is a devastating but rare disease, with an estimated median survival of 2.8 years.[79] The criteria for diagnosis includes a mean pulmonary artery pressure of greater than 25 mm Hg at rest or 30 mm Hg or greater with exercise. The average mean pulmonary artery pressure in patients with primary pulmonary hypertension is 60 mm Hg, and the severity of pressure elevation correlates with functional class. [79] Furthermore, 754

pulmonary artery and right atrial pressures (and cardiac index) correlate closely with mortality. The echocardiographic findings in primary pulmonary hypertension, in addition to the elevated pressure measurements, include enlargement of the right atrium and right ventricle with a small or normally sized left ventricle. The ratio of interventricular septum to left ventricular posterior wall thickness may be increased. The severity of findings is associated with higher pulmonary arterial and mean right atrial pressures, lower cardiac index, and impaired exercise capacity.[80] Elevated right ventricular pressures during diastole may cause motion of the interventricular septum toward the left, impacting on left ventricular diastolic function through impairment of left ventricular filling.[81] The invasive assessment of pulmonary artery pressures in patients with primary pulmonary hypertension carries higher than usual risk. Thus, noninvasive assessment by echocardiography is especially important in allowing serial examination, which is of clinical use particularly in the monitoring of response to therapy in patients treated with calcium channel blockers[82] or prostacyclin.[83] [84] [85] As assessed by echocardiography, a 12week infusion of prostacyclin showed beneficial effects on right ventricular size, curvature of the interventricular septum, and maximal tricuspid regurgitant jet velocity.[80] Lack of improvement in echocardiographic parameters may identify patients requiring transplantation. Given the difficulties in quantifying right ventricular systolic function, alternative approaches have been suggested, including a Doppler right ventricular index (defined as the sum of isovolumic contraction and isolvolumic relaxation times, divided by ejection time). The index is a measure of global right ventricular function. In one study, the Doppler

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index was retrospectively measured in 53 patients. The index was significantly higher in patients with primary pulmonary hypertension compared with normal subjects (0.84 ± 0.2 vs. 0.28 ± 0.04). The Doppler index was one of two independent predictors of outcome within a multivariate model (the second was treatment with calcium channel blockers). [86] However, the short absolute values of the times used in the index confer a high degree of measurement error. The differentiation of chronic pulmonary thromboembolism from primary pulmonary hypertension using noninvasive Doppler ultrasonographic techniques based on differences in the pulmonary artery pressure waveform has been reported in one study. Pulmonary artery systolic pressure was measured using continuous wave Doppler measurement of tricuspid regurgitant velocity (assuming a right atrial pressure of 0) and diastolic pressure from the pulmonary regurgitant velocity. The pulse pressure was normalized by systolic pressure or mean pressure to established indices. Normalized pulse pressures were higher in chronic pulmonary thromboembolism than in primary pulmonary hypertension (by systolic pressure, 0.82 ± 0.05 vs. 0.63 ± 0.10, P < 0.01; by mean pressure, 1.65 ± 0.30 vs. 0.94 ± 0.25, P < 0.01). Using optimal cut-off values, the normalized pulse pressures had sensitivities of 0.95 and specificities of 1.00 for the differentiation of the two conditions. The difference is likely due to the central major occlusive site in chronic pulmonary thromboembolism rather than the peripheral occlusion in primary pulmonary hypertension.[87] The expanding field of intravascular ultrasonography has particular clinical value in the minority of cases of pulmonary hypertension in which the cause is unclear.[88] The actual cause in many patients with pulmonary hypertension of uncertain cause is chronic thromboembolism. Intravascular ultrasonography is superior to angiography for demonstration of walladherent thrombus [89] and residual thrombus after thrombolysis in both dogs[90] and humans.[91] , [92] Intravascular ultrasonography can also be used for visualizing the presence of thrombus in veins. An important clinical advantage of intravascular ultrasonography over other imaging modalities of the pulmonary circulation is avoidance of intravenous contrast agents. This is particularly important in the seriously ill patient. In addition, the imaging of small pulmonary arteries (1.5 to 3 mm diameter) and the quantification of area, diameter, and vessel wall thickness by intravascular ultrasonography corresponds well to anatomic measurements.[93] Similarly, assessment of vessel wall motion and reactivity is possible,[88] making intravascular ultrasonography an invaluable research tool in the study of

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pulmonary hypertension and its treatment. Pulmonary Thromboembolic Disease

Acute pulmonary embolism is the third most common cardiovascular emergency (behind myocardial ischemia and stroke)[94] and has an inhospital mortality rate of up to 30% if untreated. Chronic pulmonary embolism is an important cause of secondary pulmonary hypertension (and may exacerbate primary pulmonary hypertension). The role of echocardiography in pulmonary embolism is the aiding of diagnosis and management decisions, and monitoring of hemodynamic responses to therapy. The hemodynamic effects of pulmonary embolism are dependent on the rate at which vascular obstruction occurs. Acute Pulmonary Embolism

In patients without preceding cardiopulmonary disease, acute pulmonary vascular obstruction places a sudden increase in afterload on the right ventricle that is proportional to the degree of obstruction of the vascular bed.[54] There is dilation and an increase in filling pressure of the right ventricle in response to the increased afterload. The echocardiographic findings are of right ventricular dilation (in 50% to 100%),[57] [95] [96] right ventricular free wall hypokinesis (in 40%)[97] with sparing of the apex,[98] abnormal interventricular septal motion, tricuspid regurgitation, and elevated pulmonary artery and right atrial pressures. A 25% to 30% obstruction of the vascular bed is necessary to cause an increase in pulmonary artery pressure and for the echocardiographic findings to be manifested.[54] Therefore, results of the echocardiographic examination may be normal with a smaller pulmonary embolic event. In the acute setting, a normal right ventricle can rarely generate a mean pulmonary artery pressure greater than 40 mm Hg, thus massive pulmonary embolism (30% to 755

40% vascular obstruction) can result in right ventricular failure and cardiogenic shock with mean pulmonary arterial pressures of just 20 to 40 mm Hg.[96] Patients with pre-existing cardiopulmonary disease are able to generate higher pulmonary pressures acutely, and a lesser degree of obstruction is needed to increase the pressure. [99]

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In acute pulmonary embolism, echocardiography should be used to provide additional information to the diagnostic imaging modalities. Transthoracic echocardiography can rarely (4%) visualize pulmonary intravascular or intracardiac thrombus[97] but is able to detect the indirect consequences. In a review of 11 studies (8 transthoracic echocardiography and 3 transesophageal echocardiography) in pulmonary embolism, the presence of right ventricular dilation or an elevation in tricuspid regurgitant velocity, or both, gave diagnostic power for pulmonary embolism similar to transthoracic (sensitivity 67%, specificity 89%) and transesophageal (sensitivity 70%, specificity 81%) echocardiography. However, the overall prevalence of pulmonary embolism in these studies was only 46% in the transthoracic echocardiography group and 71% in the transesophageal echocardiography group with a large embolic burden.[100] Transesophageal echocardiography was found to have a high sensitivity (97%) and specificity (86%) in visualizing central pulmonary emboli in patients with proven severe emboli,[101] but the prevalence of central emboli in the study was low (approximately 60%). Imaging with transesophageal echocardiography may differentiate old from fresh thrombus (floating, protruding, elongated, and so on, with acute thrombus).[102] However, transesophageal echocardiography visualizes the left pulmonary artery less well than the right and is semi-invasive, thus it is a less desirable investigation in patients with respiratory compromise. In patients with proven embolism, the pulmonary artery pressure at rest measured by transthoracic echocardiography may differentiate subacute from acute massive pulmonary embolism.[95] Tricuspid regurgitant jet velocity was reported as significantly lower in patients with acute massive pulmonary embolism than in patients with subacute massive pulmonary embolism (3.0 ± 0.4 m per second vs. 4.2 ± 0.6 m/sec, P < 0.001). In addition, patients with subacute disease were correctly identified by a right ventricular free wall thickness greater than 5 mm, tricuspid regurgitant jet velocity greater than 3.7 m per second, and the occurrence of both a dilated right ventricular cavity with normal interventricular septal motion or an inspiratory collapse of the inferior vena cava, or both. Impact of Echocardiography on Clinical Management

The particular value of echocardiography in thromboembolic disease is the assessment of hemodynamically unstable patients with suspected pulmonary embolism. Echocardiography can provide additional or confirmatory diagnostic information or assess for other causes for

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circulatory instability. The assessment of right ventricular dysfunction by echocardiography can identify patients with pulmonary embolism who may benefit from treatment. The benefits of acute thrombolytic therapy in addition to anticoagulation have been limited to patients with abnormal right ventricular wall motion.[57] [97] [103] Spontaneous fibrinolysis leads to progressive reduction in right heart enlargement, with a normal pattern returning in 12 to 20 days.[96] Thrombolytic treatment causes a more rapid resolution of the echocardiographic abnormalities within 24 hours.[57] [104] Thrombolysis is indicated in pulmonary embolism with the presence of right heart failure or systemic hypotension and if there is echocardiographic right ventricular dysfunction.[105] Embolectomy should be considered if thrombolysis is contraindicated or fails.[106] Echocardiographic markers predict mortality following pulmonary embolism. The most important parameter is right ventricular hypokinesis, [104] [107] which, if present at baseline, independently predicts an increased mortality rate at 2 weeks and 3 months (twofold increase). [97] Elevated pulmonary artery systolic pressure (>50 mm Hg) at the time of diagnosis also predicts the presence of pulmonary hypertension at 1 year.[108] Acute Respiratory Distress Syndrome The syndrome of acute respiratory distress is defined by the presence of severe hypoxemia and carries with it mortality rates of 40% to 60%.[109] Although there is microvascular obstruction and some increase in the right ventricular pressure load, acute cor pulmonale with echocardiographic features is seen in less than 10% of patients with the acute respiratory distress syndrome.[53] Furthermore, acute echocardiographic changes are usually delayed for up to 2 weeks, probably coinciding with the progressive destruction of pulmonary tissue.[53] Thoracic Surgery Lung Transplantation

The preoperative role of echocardiography in lung transplantation candidates includes the identification of patients with cardiac contraindications to transplantation (poor left ventricular function and significant coronary artery disease).[110] Right ventricular function is less

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important. Because the right ventricles of lung transplantation candidates often are subject to chronic pulmonary hypertension, right ventricular systolic dysfunction is common. Early concerns regarding the ability of right ventricles to recover after transplantation were avoided by the performing of heart-lung transplantation instead of lung transplantation alone. However, right ventricular recovery after single lung transplantation was first demonstrated in the early 1990s in patients with pulmonary hypertension and some degree of right ventricular dysfunction[111] [112] and in patients with severe preoperative right ventricular dysfunction.[113] In the latter study, improved right ventricular systolic function occurred early and was sustained throughout the follow-up period in 13 of the 14 patients. Echocardiographic examination 756

revealed improvements in septal motion and pulmonary hemodynamics with reversal of right heart dilation and dysfunction. Two subsequent studies including patients with right ventricular dysfunction and severe pulmonary hypertension reported a variable improvement in right ventricular function despite improvement in pulmonary pressures. [114] [115] In one study, improvement was less in patients with modest pulmonary hypertension preoperatively, leading the authors to surmise that the degree of reduction in pulmonary pressure and any intrinsic myocardial disease may be important.[114] In both studies, the persistence of right ventricular dysfunction was associated with a poorer outcome. The perioperative monitoring of right ventricular function by transesophageal echocardiography during lung transplantation surgery can assist decision making on the need for cardiopulmonary bypass.[110] Transesophageal echocardiography also enables direct visualization of the vascular anastomoses during and after the operation. The right pulmonary artery anastomosis is reported to be visible in 100% of cases in separate studies.[116] [117] However, there is disparity regarding visualization of the left pulmonary arterial anastomoses (71%[117] and 0%[116] ). Important stenoses that have been initially diagnosed by Doppler measurement across the suture line are reported.[117] The pulmonary venous anastomoses are almost always visible by transesophageal echocardiography. [116] [117] The diameter of the vein and mean pulmonary venous velocity are greater in the allograft than native lung.[118] Transesophageal echocardiography can also identify severe stenosis or thrombosis in the pulmonary veins, contributing to graft failure with such abnormalities described in 29% of patients undergoing

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lung transplantation.[119] A further mechanical complication of lung transplantation amenable to echocardiographic examination is right ventricular outflow tract obstruction in patients with severe right ventricular hypertrophy. Obstruction is caused by the acute decrease in right ventricular size resulting from the dramatic decrease in pulmonary vascular resistance in the immediate posttransplantation period.[120] Lastly, echocardiography also has a role in the detection of intracardiac shunting that can also cause postoperative hypoxemia in lung transplant patients.[121] Lung Volume Reduction Surgery

Lung volume reduction surgery provides either a bridge to lung transplantation or a definitive therapy for advanced chronic obstructive lung disease. The role of echocardiography in patient selection primarily is based on measurement of pulmonary pressures. Severe pulmonary hypertension (mean pulmonary artery pressure greater than 35 mm Hg or systolic pulmonary artery pressure greater than 45 mm Hg) is considered a contra-indication to lung reduction surgery.[122] Rest and stress transthoracic echocardiography has been described in two studies to assess for coronary disease in candidates for lung volume reduction surgery and, despite poor ultrasound windows, was feasible in almost all patients. Stress echocardiography provided an excellent negative predictive value for adverse cardiac events in the perioperative period.[123] [124]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Differentiation of Pulmonary Heart Disease from Primary Cardiac Disease The echocardiographic findings in pulmonary disease almost exclusively affect the right heart and manifest mainly through increased right ventricular afterload. However, the most common cause of right heart abnormalities is primary cardiac disease, not pulmonary disease, although disease of both organ systems may coexist. Thus if echocardiographic abnormalities attributable to pulmonary disease are present, the possibility of the abnormalities being caused in whole or part by a cardiac disorder should be considered. Right Ventricular Pressure Overload Any pulmonary diseases of sufficient severity can cause secondary pulmonary hypertension. Similarly, secondary pulmonary hypertension can be caused by any left heart disease that sufficiently increases left heart filling pressures to cause passive and reactive elevation in pulmonary artery pressures.[4] Secondary pulmonary hypertension may be due to an increase in left atrial pressure alone (e.g., mitral valve disease, cor triatriatum, atrial myxoma) or in combination with elevation in left end-diastolic pressure (left ventricular systolic or diastolic dysfunction from any cause). Pulmonary veno-occlusive disease (considered here as a primary cardiac disease) causes secondary pulmonary hypertension by a similar physiologic pathway. Thus, the finding of pulmonary hypertension, irrespective of the presence of significant pulmonary disease, should be accompanied by examination for left ventricular dysfunction, mitral valve pathology, and other causes of left atrial pressure elevation. A significant degree of left heart disease is generally required to cause secondary pulmonary hypertension. In the absence of left heart disease, pulmonary disease alone should not cause elevation in left atrial and ventricular filling pressures (except in severe right ventricular hypertrophy with diastolic motion of the interventricular septum into the left ventricular chamber, impairing filling).

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Increased right ventricular afterload can also be caused by any obstruction to the pulmonic valve or right ventricular outflow tract (e.g., subpulmonic web, pulmonary stenosis, tumor), although these are rare in adults. Right ventricular systolic pressure (and possibly right atrial pressure) will be elevated without pulmonary hypertension. There will be an increase in the forward flow velocities across the right ventricular outflow tract and pulmonary valve. Right Ventricular Volume Overload Chronic right ventricular volume overload leads to dilation and hypertrophy of the right ventricle and augmentation 757

of systolic function, consequences similar to the chronic right ventricular pressure overload of pulmonary disease. In patients with such echocardiographic findings, examination should be made for the presence of primary cardiac conditions causing volume overload, including left-toright cardiac shunts, valve regurgitation, and high cardiac output states. The left-to-right cardiac shunts include atrial septal defects, ruptured sinus of Valsalva aneurysm to the right atrium, coronary artery fistulae to the right atrium, partial anomalous pulmonary venous drainage, and a defect between the left ventricle and right atrium (Gerbode's defect). Color and pulsed wave Doppler echocardiography should be used to examine for the presence of such intracardiac shunts. The most common shunt is the atrial septal defect, which accounts for 30% of adult congenital heart disease and is commonly first diagnosed in adulthood. Severe regurgitation of the pulmonic or tricuspid valves from any cause can result in right ventricular volume overload. Severe valve regurgitation can result from right ventricular dilation due to severe pulmonary disease but will have an accompanying elevation in pulmonary arterial pressures. Lastly, high output states (e.g., beriberi heart disease from thiamin deficiency, thyrotoxicosis) can cause right ventricular volume overload, even in the absence of structural cardiac disease. In the absence of severe left ventricular dysfunction, however, pulmonary hypertension is not a feature of these diseases. Right Ventricular Systolic Dysfunction

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Right ventricular systolic dysfunction can be a cardiac consequence of pulmonary disease and usually carries with it a poor prognosis. The most common cause of right ventricular systolic failure, however, is as a consequence of chronic left ventricular dysfunction and secondary pulmonary hypertension.[4] Distinguishing the cause of the right ventricular systolic dysfunction by echocardiography is dependent on the clinical context of examination and the presence of left ventricular dysfunction. Right ventricular systolic dysfunction can also occur as a consequence of a primary decrease in contractile state of the right ventricular myocardium. In nonischemic cardiomyopathy, the left ventricle is also invariably involved. Isolated right ventricular infarction is rare (<3% of all infarctions). The importance of right ventricular involvement in approximately one third of inferior left ventricular infarctions is well described.[10] Echocardiography demonstrates involvement of the affected free wall with hypokinesis or akinesis and improvement or recovery of function in the majority of patients if the acute event is survived.[125]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Schulman DS, Matthay RA: The right ventricle in pulmonary disease. Cardiol Clin

1992;10:111–135. 2. Lee FA: Hemodynamics of the right ventricle in normal and disease states. Cardiol

Clin 1992;10:59–67. 3. Hines R: Right ventricular function and failure: A review. Yale J Biol Med

1991;64:295–307. 4. Barnard D, Alpert JS: Right ventricular function in health and disease. Curr Probl

Cardiol 1987;12:417–449. 5. Baker B, Wilen M, Boyd C, et al: Relation of right ventricular ejection fraction to

exercise capacity in chronic left ventricular failure. Am J Cardiol 1985;54:596–599. 6. Polak J, Holman L, Wynne J, Colcucci W: Right ventricular ejection fraction: An

indicator of increased mortality in patients with congestive heart failure associated with coronary disease. J Am Coll Cardiol 1983;2:217–224. 7. Dell'Italia LJ: The right ventricle: Anatomy, physiology, and clinical importance.

Curr Probl Cardiol 1991;16:653–720. 8. Matthay RA, Berger HJ: Cardiovascular function in cor pulmonale. Clin Chest Med

1983;4:269–295. 9. Fishman AP: Chronic cor pulmonale. Am Rev Respir Dis 1976;114:775–794. 10. Kinch JW, Ryan TJ: Right ventricular infarction. N Engl J Med 1994;330:1211–

1217.

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11. Rushmer RF, Thal W: The mechanics of ventricular contraction: A

cinefluorographic study. Circulation 1951;4:219–228. 12. Fixler DE: Hemodynamic alterations during septal or right ventricular ischemia in

dogs. Am Heart J 1977;93:210–215. 13. Satamore WP, Dell'Italia LJ: Ventricular interdependence: Significant left

ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis 1998;40:289–308. 14. Dell'Italia LJ, Starling MR, Crawford MH: Right ventricular infarction:

Identification by hemodynamic measurements before and after volume loading and correlation with noninvasive techniques. J Am Coll Cardiol 1984;4:931–939. 15. Weidemann HP, Matthay RA: Cor pulmonale. In Braunwald E (ed): Heart Disease:

A Textbook of Cardiovascular Medicine, vol 2, 5th ed. Philadelphia, W.B. Saunders, 1997, pp 1604–1625. 16. Berger PB, Ryan TJ: Inferior myocardial infarction. High-risk subgroups.

Circulation 1990;81:401–411. 17. Levine RA, Gibson TC, Aretz T, et al: Echocardiographic measurement of right

ventricular volume. Circulation 1984;69:497–505. 18. Helbing WA, Bosch HG, Maliepaard C, et al: Comparison of echocardiographic

methods with magnetic resonance imaging for assessment of right ventricular function in children. Am J Cardiol 1995;76:589–594. 19. Saito A, Ueda K, Nakano H: Right ventricular volume determinations by two-

dimensional echocardiography. J Cardiogr 1981;11:1159. 20. Wilson NJ, Neutze JM, Rutland MD, Ramage MC: Transthoracic

echocardiography for right ventricular function late after the Mustard operation. Am Heart J 1996;131:360–367. 21. Tokgozoglu SL, Caner B, Kabakci G, Kes S: Measurement of right ventricular

ejection fraction by contrast echocardiography. Int J Cardiol 1997;59:71–74. 22. Oe M, Gorcsan JR, Mandarino WA, et al: Automated echocardiographic measures of right ventricular area as an index of volume and end-systolic pressure-area relations to assess right ventricular function. Circulation 1995;92:1026–1033. 23. Jiang L, Siu SC, Handschumacher MD, et al: Three-dimensional

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echocardiography. In vivo validation for right ventricular volume and function. Circulation 1994;89:2342–2350. 24. Jiang L, Handschumacher MD, Hibberd MG, et al: Three-dimensional

echocardiographic reconstruction of right ventricular volume: In vitro comparison with two-dimensional methods. J Am Soc Echocardiogr 1994;7:150–158. 25. Ota T, Fleishman CE, Strub M, et al: Real-time, three-dimensional

echocardiography: Feasibility of dynamic right ventricular volume measurement with saline contrast. Am Heart J 1999;137:958–966. 26. Papavassiliou DP, Parks WJ, Hopkins KL, Fyfe DA: Three-dimensional

echocardiographic measurement of right ventricular volume in children with congenital heart disease validated by magnetic resonance imaging. J Am Soc Echocardiogr 1998;11:770–777. 27. Shiota T, Jones M, Chikada M, et al: Real-time three-dimensional echocardiography for determining right ventricular stroke volume in an animal model of chronic right ventricular volume overload. Circulation 1998;97:1897–1900. 758

28. Vogel M, Gutberlet M, Dittrich S, et al: Comparison of transthoracic three

dimensional echocardiography with magnetic resonance imaging in the assessment of right ventricular volume and mass. Heart 1997;78:127–130. 29. Munoz R, Marcus E, Palacio G, et al: Reconstruction of 3-dimensional right

ventricular shape and volume from 3 orthogonal planes. J Am Soc Echocardiogr 2000;13:177–185. 30. Vazquez de Prada JA, Chen MH, Guerrero JL, et al: Intracardiac

echocardiography: In vitro and in vivo validation for right ventricular volume and function. Am Heart J 1996;131:320–328. 31. Otto CM: Echocardiographic evaluation of left and right ventricular systolic

function. In Otto CM (ed): Textbook of Clinical Echocardiography, 2nd ed. Philadelphia, WB Saunders, 2000, pp 120–121. 32. Alam M, Wardell J, Andersson E, et al: Characteristics of mitral and tricuspid annular velocities by pulsed wave doppler tissue imaging in healthy subjects. J Am Soc Echocardiogr 1999;12:618–628.

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33. Kukulski T, Hubbert L, Arnold M, et al: Normal regional right ventricular function

and its change with age: A Doppler myocardial imaging study. J Am Soc Echocardiogr 2000;13:194–204. 34. Alam M, Wardell J, Andersson E, et al: Right ventricular function in patients with

first inferior myocardial infarction: Assessment by tricuspid annular motion and tricuspid annular velocity. Am Heart J 2000;139:710–715. 35. Ghio S, Recusani F, Klersy C, et al: Prognostic usefulness of the tricuspid annular

plane systolic excursion in patients with congestive heart failure secondary to idiopathic or ischemic dilated cardiomyopathy. Am J Cardiol 2000;85:837–842. 36. Vignon P, Mor-Avi V, Weinert L, et al: Quantitative evaluation of global and

regional left ventricular diastolic function with color kinesis. Circulation 1998;97:1053–1061. 37. Vignon P, Weinert L, Mor-Avi V, et al: Quantitative assessment of regional right

ventricular function with color kinesis. Am J Respir Crit Care Med 1999;159:1949– 1959. 38. Jue J, Chung W, Schiller NB: Does inferior vena cava size predict right atrial

pressures in patients receiving mechanical ventilation? J Am Soc Echocardiogr 1992;5:613–619. 39. Abaci A, Kabukcu M, Ovunc K, et al: Comparison of the three different formulas

for Doppler estimation of pulmonary artery systolic pressure. Angiology 1998;49:463–470. 40. Pepi M, Tamborini G, Galli C, et al: A new formula for echo-Doppler estimation of

right ventricular systolic pressure. J Am Soc Echocardiogr 1994;7:20–26. 41. Yock PG, Popp RL: Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70:657–662. 42. Berger M, Haimowitz A, Van Tosh A, et al: Quantitative assessment of pulmonary

hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985;6:359–365. 43. Currie PJ, Seward JB, Chan KL, et al: Continuous wave Doppler determination of

right ventricular pressure: A simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750–756.

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44. Stevenson JG: Comparison of several noninvasive methods for estimation of

pulmonary artery pressure. J Am Soc Echocardiogr 1989;2:157–171. 45. Kosturakis D, Goldberg SJ, Allen HD, Loeber C: Doppler echocardiographic

prediction of pulmonary arterial hypertension in congenital heart disease. Am J Cardiol 1984;53:1110–1115. 46. Kitabatake A, Inoue M, Asao M, et al: Noninvasive evaluation of pulmonary

hypertension by a pulsed Doppler technique. Circulation 1983;68:302–309. 47. Torbicki A, Skwarski K, Hawrylkiewicz I, et al: Attempts at measuring pulmonary

arterial pressure by means of Doppler echocardiography in patients with chronic lung disease. Eur Respir J 1989;2:856–860. 48. Tramarin R, Torbicki A, Marchandise B, et al: Doppler echocardiographic

evaluation of pulmonary artery pressure in chronic obstructive pulmonary disease. A European multicentre study. Working Group on Noninvasive Evaluation of Pulmonary Artery Pressure. European Office of the World Health Organization, Copenhagen. Eur Heart J 1991;12:103–111. 49. Chan KL, Currie PJ, Seward JB, et al: Comparison of three Doppler ultrasound

methods in the prediction of pulmonary artery pressure. J Am Coll Cardiol 1987;9:549–554. 50. Masuyama T, Kodama K, Kitabatake A, et al: Continuous-wave Doppler

echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation 1986;74:484–492. 51. Jiang L, Stewart WJ, King ME, Weyman AE: An improved method for estimation

of pulmonary artery pressure using Doppler velocity time intervals. J Am Coll Cardiol 1984;3:613. 52. Weitzenblum E, Loiseau A, Hirth C, et al: Course of pulmonary hemodynamics in

patients with chronic obstructive pulmonary disease. Chest 1979;75:656–662. 53. Jardin F, Dubourg O, Bourdarias JP: Echocardiographic pattern of acute cor

pulmonale. Chest 1997;111:209–217. 54. McIntyre K, Sasahara A: The hemodynamic response to pulmonary embolism in

patients without prior cardiopulmonary disease. Am J Cardiol 1971;28:288–294. 55. Valtier B, Dubourg O, De Lassence A: Left and right intracardiac Doppler blood

flow analysis in patients with severe acute pulmonary embolism. Am Rev Respir Dis 1993;147:A-609.

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56. McIntyre K, Sasahara A: The ratio of pulmonary arterial pressure to pulmonary

vascular obstruction: Index of preembolic cardiopulmonary status. Chest 1977;71:692–697. 57. Come PC, Kim D, Parker JA, et al: Early reversal of right ventricular dysfunction

in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator. J Am Coll Cardiol 1987;10:971–978. 58. Schena M, Clini E, Errera D, Quadri A: Echo-Doppler evaluation of left ventricular

impairment in chronic cor pulmonale. Chest 1996;109:1446–1451. 59. Rich S: Pulmonary hypertension. In Braunwald E, Zipes DP, Libb P (eds): Heart

Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001. 60. Laaban JP, Diebold B, Zelinski R, et al: Noninvasive estimation of systolic

pulmonary artery pressure using Doppler echocardiography in patients with chronic obstructive pulmonary disease. Chest 1989;96:1258–1262. 61. Globits S, Burghurber OC, Koller J, et al: Effect of lung transplantation on right

and left ventricular volumes and function measured by magnetic resonance imaging. Am J Respir Crit Care Med 1994;149:1000–1004. 62. Himelman RB, Stulbarg M, Kircher B, et al: Noninvasive evaluation of pulmonary

artery pressure during exercise by saline-enhanced Doppler echocardiography in chronic pulmonary disease. Circulation 1989;79:863–871. 63. Himelman RB, Struve SN, Brown JK, et al: Improved recognition of cor

pulmonale in patients with severe chronic obstructive pulmonary disease. Am J Med 1988;84:891–898. 64. Migueres M, Escamilla R, Coca F, et al: Pulsed Doppler echocardiography in the

diagnosis of pulmonary hypertension in COPD. Chest 1990;98:280–285. 65. Ferrazza A, Marino B, Giusti V, et al: Usefulness of left and right oblique

subcostal view in the echo-Doppler investigation of pulmonary arterial blood flow in patients with chronic obstructive pulmonary disease: The subxiphoid view in the echoDoppler evaluation of pulmonary blood flow. Chest 1990;98:286–289. 66. Zompatori M, Battaglia M, Rimondi MR, et al: Hemodynamic estimation of

chronic cor pulmonale by Doppler echocardiography: Clinical value and comparison with other noninvasive imaging techniques. Rays 1997;22:73–93.

mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005

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67. MacNee W: Pathophysiology of cor pulmonale in chronic obstructive pulmonary

disease (part one). Am J Respir Crit Care Med 1994;150:833–852. 68. Weitzenblum E, Hirth C, Ducolone A, et al: Prognostic value of pulmonary artery

pressure in chronic obstructive pulmonary disease. Thorax 1981;36:752–758. 69. Dallari R, Barozzi G, Pinelli G, et al: Predictors of survival in subjects with chronic obstructive pulmonary disease treated with long-term oxygen therapy. Respiration 1994;61:8–13. 70. Burghuber OC, Brunner CH, Schenk P, Weissel M: Pulsed Doppler

echocardiography to assess pulmonary artery hypertension in chronic obstructive pulmonary disease. Monaldi Arch Chest Dis 1993;48:121–125. 759

71. Klinger JR, Hill NS: Right ventricular dysfunction in chronic obstructive

pulmonary disease: Evaluation and management. Chest 1991;99:715–723. 72. Traver GA, Cline MG, Burrows B: Predictors of mortality in chronic obstructive

pulmonary disease: A 15-year follow-up study. Am Rev Respir Dis 1979;119:895– 902. 73. Renzetti A, McClement J, Litt B: The Veterans Administration cooperative study

of pulmonary function. Am J Med 1966;41:115–129. 74. Vizza CD, Lynch JP, Ochoa LL, et al: Right and left ventricular dysfunction in

patients with severe pulmonary disease. Chest 1998;113:576–583. 75. Russo A, De Luca M, Vigna C, et al: Central pulmonary artery lesions in chronic obstructive pulmonary disease: A transesophageal echocardiography study. Circulation 1999;100:1808–1815. 76. Kitzman DW, Wesley DJ: Safety assessment of perflenapent emulsion for

echocardiographic contrast enhancement in patients with congestive heart failure or chronic obstructive pulmonary disease. Am Heart J 2000;139:1077–1080. 77. Bishop J, Cross K: Physiologic variables and mortality in patients with various

categories of chronic respiratory disease. Bull Eur Physiopathol Respir 1984;20:495– 500.

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78. Ungerer RG, Tashkin DP, Furst D: Prevalence and clinical correlates of pulmonary

arterial hypertension in progressive systemic sclerosis. Am J Med 1983;75:65–74. 79. D'Lonzo GE, Barst RJ, Ayres SM: Survival in patients with primary pulmonary

hypertension: Results from a national prospective registry. Ann Intern Med 1991;115:343–349. 80. Hinderliter AL, Willis PW IV, Barst RJ, et al: Effects of long-term infusion of

prostacyclin (epoprostenol) or echocardiographic measures of right ventricular structure and function in primary pulmonary hypertension. Primary Pulmonary Hypertension Study Group. Circulation 1997;95:1479–1486. 81. Louie EK, Rich S, Levitsky S, Brundage BH: Doppler echocardiographic

demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol 1992;9:84–90. 82. Rich S, Kaufmann E, Levy PS: The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. N Engl J Med 1992;327:76– 81. 83. Jones DK, Whigenbottam TW, Wallwork J: Treatment of primary pulmonary

hypertension with intravenous epoprostenol (prostacyclin). Br Heart J 1987;57:270. 84. Rubin LJ, Mendoza J, Hood M: Treatment of primary pulmonary hypertension

with continuous intravenous prostacyclin (epoprostenol). Ann Intern Med 1990;112:485. 85. Barst RJ, Rubi LJ, McGoon MD: Survival in primary pulmonary hypertension with

long-term continuous intravenous prostacyclin. Ann Intern Med 1994;121:409. 86. Yeo TC, Dujardin KS, Tei C, et al: Value of a Doppler-derived index combining

systolic and diastolic time intervals in predicting outcome in primary pulmonary hypertension. Am J Cardiol 1998;81:1157–1161. 87. Nakayama Y, Sugimachi M, Nakanishi N, et al: Noninvasive differential diagnosis

between chronic pulmonary thromboembolism and primary pulmonary hypertension by means of Doppler ultrasound measurement. J Am Coll Cardiol 1998;31:1367– 1371. 88. Gorge G, Ge J, Baumgart D, et al: In vivo tomographic assessment of the heart and

blood vessels with intravascular ultrasound. Basic Res Cardiol 1998;93:219–240. 89. Ricou F, Nicod PH, Moser KM, Peterson KL: Catheter-based intravascular

ultrasound imaging of chronic thromboembolic pulmonary disease. Am J Cardiol

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1991;67:749–752. 90. Tapson VF, Davidson CJ, Gurbel PA, et al: Rapid and accurate diagnosis of

pulmonary emboli in a canine model using intravascular ultrasound imaging. Chest 1991;100:1410–1413. 91. Gorge G, Erbel R, Schuster S, et al: Intravascular ultrasound in diagnosis of acute

pulmonary embolism. Lancet 1991;8741:623–624. 92. Gorge G, Schuster S, Ge J, et al: Intravascular ultrasound in patients with acute

pulmonary embolism after treatment with intravenous urokinase and high-dose heparin. Heart 1997;77:73–77. 93. Pandian NG, Weintraub A, Kreis A, et al: Intracardiac, intravascular, two-

dimensional, high-frequency ultrasound imaging of pulmonary artery and its branches in humans and animals. Circulation 1990;81:2007–2012. 94. Dalen JE, Alpert JS: Natural history of pulmonary embolism. Prog Cardiovasc Dis

1975;17:259–270. 95. Kasper W, Geibel A, Tiede N, et al: Distinguishing between acute and subacute

massive pulmonary embolism by conventional and Doppler echocardiography. Br Heart J 1993;70:352–356. 96. Jardin F, Dubourg O, Gueret P, et al: Quantitative two-dimensional

echocardiography in massive pulmonary embolism: Emphasis on ventricular interdependence and leftward septal displacement. J Am Coll Cardiol 1987;10:1201– 1206. 97. Goldhaber SZ, Visani L, De Rosa M: Acute pulmonary embolism: Clinical

outcomes in the international cooperative registry (ICOPER). Lancet 1999;353:1386– 1389. 98. McConnell MV, Solomon SD, Rayan ME, et al: Regional right ventricular

dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996;78:469–473. 99. McIntyre K, Sasahara A: Determinants of right ventricular function and

hemodynamics after pulmonary embolism. Am J Cardiol 1974;65:534–543. 100. Kline JA, Johns KL, Colucciello SA, Israel EG: New diagnostic tests for

pulmonary embolism. Ann Emerg Med 2000;35:168–180.

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101. Wittlich N, Erbel R, Eichler A, et al: Detection of central pulmonary artery

thromboemboli by transesophageal echocardiography in patients with severe pulmonary embolism. J Am Soc Echocardiogr 1992;5:515–524. 102. Chan RKM, Johns JA, Calafiore P: Clinical implications of morphological

features of central pulmonary artery thromboemboli shown by transoesophageal echocardiography. Br Heart J 1994;72:58–62. 103. Wolfe MW, Lee RT, Feldstein ML, et al: Prognostic significance of right

ventricular hypokinesis and perfusion lung scan defects in pulmonary embolism. Am Heart J 1994;127:1371–1375. 104. Goldhaber SZ, Haire WD, Feldstein ML: Alteplase versus heparin in acute

pulmonary embolism: Randomized trial assessing right ventricular function and pulmonary embolism. Lancet 1993;341:507–511. 105. Goldhaber SZ: Pulmonary embolism. N Engl J Med 1999;339:93–104. 106. Meyer G, Tamisier D, Reynaud P, Sors H: Acute pulmonary embolectomy. In

Goldhaber SZ (ed): Cardiopulmonary Diseases and Cardiac Tumors. (Braunwald E [ed]: Atlas of Heart Diseases, vol 3). Philadelphia, Current Medicine, 1995, p 61. 107. Ribeiro A, Lindmarker P, Juhlin-Dannfelt A, et al: Echocardiography Doppler in

pulmonary embolism: Right ventricular dysfunction as a predictor of mortality rate. Am Heart J 1997;134:479–487. 108. Ribeiro A, Lindmarker P, Johnsson H, et al: Pulmonary embolism: One-year

follow-up with echocardiography Doppler and five-year survival analysis. Circulation 1999;99:1325–1330. 109. Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med

2000;342:1334–1349. 110. Myers BF, Patterson MD: Lung transplantation: Current status and future

prospects. World J Surg 1999;23:1156–1162. 111. Scuderi LJ, Bailey SR, Calhoon JH, et al: Echocardiographic assessment of right

and left ventricular function after single-lung transplantation. Am Heart J 1994;127:636–642. 112. Kramer MR, Valantine HA, Marshall SE, et al: Recovery of the right ventricle

after single-lung transplantation in pulmonary hypertension. Am J Cardiol 1994;73:494–500.

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113. Ritchie M, Waggoner AD, Davila-Roman VG, et al: Echocardiographic

characterization of the improvement in right ventricular function in patients with severe pulmonary hypertension after single-lung transplantation. J Am Coll Cardiol 1993;22:1170–1174. 114. Schulman LL, Leibowitz DW, Anandarangam T, et al: Variability of right

ventricular functional recovery after lung transplantation. Transplantation 1996;62:622–625. 115. Katz WE, Gasior TA, Quinlan JJ, et al: Immediate effects of lung transplantation

on right ventricular morphology and function in patients with variable degrees of pulmonary hypertension. J Am Coll Cardiol 1996;27:384–391. 760

116. Michel-Cherqui M, Brusset A, Liu N, et al: Intraoperative transesophageal

echocardiographic assessment of vascular anastomoses in lung transplantation: A report on 18 cases. Chest 1997;111:1229–1235. 117. Hausmann D, Daniel WG, Mugge A, et al: Imaging of pulmonary artery and vein

anastomoses by transesophageal echocardiography after lung transplantation. Circulation 1992;86:II251–258. 118. Ross DJ, Vassolo M, Kass R, et al: Transesophageal echocardiographic

assessment of pulmonary venous flow after single lung transplantation. J Heart Lung Transplant 1993;12:689–704. 119. Leibowitz DW, Smith CR, Michler RE, et al: Incidence of pulmonary vein

complications after lung transplantation: A prospective transesophageal echocardiographic study. J Am Coll Cardiol 1994;24:671–675. 120. Gorcsan JD, Reddy SC, Armitage JM, Griffith BP: Acquired right ventricular

outflow tract obstruction after lung transplantation: Diagnosis by transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:324–326. 121. Suriani RJ: Transesophageal echocardiography during organ transplantation. J

Cardiothorac Vasc Anesth 1998;12:686–694. 122. Payne DK, Markewitz BA, Owens MW: Surgical treatment of chronic obstructive

pulmonary disease. Am J Med Sci 1999;318:89–95.

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123. Bossone E, Martinez FJ, Whyte RI, et al: Dobutamine stress echocardiography for

the preoperative evaluation of patients undergoing lung volume reduction surgery. J Thorac Cardiovasc Surg 1999;118:542–546. 124. Bach DS, Curtis JL, Christensen PJ, et al: Preoperative echocardiographic

evaluation of patients referred for lung volume reduction surgery. Chest 1998;114:972–980. 125. Bellamy GR, Rasmussen HH, Nasser FN, et al: Value of two-dimensional

echocardiography, electrocardiography, and clinical signs in detecting right ventricular infarction. Am Heart J 1986;112:304–309.

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761

Chapter 34 - Echocardiographic Findings in Systemic Diseases Characterized by ImmuneMediated Injury Carlos A. Roldan MD Bruce K. Shively MD

The connective tissue diseases are chronic inflammatory states caused by autoimmunity. These diseases are more common in women than in men (with the exception of human leukocyte antigen B-27–related arthropathies), usually manifest from the second through the fifth decade, and cause significant morbidity and mortality. Although the heart is not the principal target organ of these diseases, cardiovascular involvement is common and may have serious consequences. The cardiac structures usually affected are the valves, pericardium, and myocardium. Less often, the coronary arteries, great vessels, and conduction system are involved (Table 34-1) . Estimates of the prevalence of cardiac involvement vary widely because of differences in study populations and methods of cardiac evaluation. Although autoimmune injury probably underlies the cardiac complications of connective tissue disease, the evidence is incomplete, and the exact immune mechanisms are unknown.

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Echocardiography in patients with connective tissue diseases is usually indicated to evaluate exertional dyspnea or fatigue, chest discomfort, cerebral or systemic embolism, or a murmur detected incidentally. A normal echocardiogram usually rules out a significant cardiac cause of these syndromes, with the exception of chest discomfort, which may result from coronary artery disease or from pericarditis without pericardial effusion. Conversely, an abnormal result usually identifies the cause of the patient's presenting problem and the severity of cardiac involvement and may help guide therapy. Certain echocardiographic findings are specific to particular connective tissue diseases (Table 34-2) . Echocardiographic techniques are applied frequently in the assessment of patients with connective tissue diseases. The most important parameters are the assessment of left ventricular systolic function and the identification of previous myocardial infarction; estimation of left atrial pressure; identification and estimation of the severity of accompanying pulmonary hypertension and right heart failure; examination of the left ventricle for thrombus or thrombotic potential; identification of clinically significant diastolic dysfunction; assessment of the hemodynamic severity of valvular regurgitation; detection of tamponade physiology in a patient with pericardial effusion; and detection of pericardial constriction. Detailed explanations of these applications of echocardiography are discussed in other chapters; useful guidelines are given in Table 34-3 .[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]

Echocardiography has tremendous untapped potential 762

TABLE 34-1 -- Cardiac Involvement in Connective Tissue Diseases Disease Type of Involvement Systemic lupus Libman-Sacks vegetations erythematosus

Leaflet fibrosis

Frequency (%) * Comments 10–30 These valve masses are characteristic of lupus valve disease 10–50 Leaflet calcification is

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Rheumatoid arthritis

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Valvular regurgitation (mild or worse) Pericarditis

10–40

Asymptomatic effusion Myocarditis/cardiomyopathy

2–20 1–20

10–50

Coronary disease: atherosclerotic nonatherosclerotic

25 <5

Myocardial infarction

<10

Diastolic dysfunction † Pulmonary hypertension

15–35 5–15

Cardioembolism Pericarditis

5–20 ≤10

uncommon Valve stenosis i rare (<3%) Antinuclear antibodies in pericardial fluid are diagnostic b not always present Associated with cellular antigen Ro and La antibody

Coronary arterit rarely clinically diagnosed Libman-Sacks vegetations can embolize to the coronary arterie Causes: interstitial lung disease, vasculitis, and thromboembolis Occurs in patien with active disease, high rheumatoid fact level, and nodul disease;

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pericardial fluid can have rheumatoid fact Asymptomatic effusion Leaflet fibrosis

Valve granulomas

<5

Valve regurgitation, ≥ mild Myocarditis/cardiomyopathy

<5 <10

Coronary disease: atherosclerotic

nonatherosclerotic

Ankylosing spondylitis

30–40 ≤30

Myocardial infarction Diastolic dysfunction Pulmonary hypertension Proximal aortitis/valvulitis Aortic regurgitation, ≥ mild Subaortic bump

Conduction system disease

20–30

Rare

Leaflet fibrosis indistinguishabl from that of systemic lupus Unique to this disease Amyloid deposition is a rare cause Similar to the general population In postmortem series, coronary arteritis ranges from 11–20%

5–15 ≤25 Unknown 25–60 Characteristic o the disease 10–40 10–40 Decreases anterior mitral leaflet mobility and causes regurgitation ≤50 Extension of aortic

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root/annulus sclerosis into the proximal septum and atrioventricular node Diastolic dysfunction 20–50 Pericarditis <15 Asymptomatic effusion Unknown Myocarditis/cardiomyopathy <15 Uncertain if pericarditis or myocarditis is related to the primary disease Scleroderma Coronary disease: atherosclerotic <20 nonatherosclerotic >50 Intramyocardial or small vessel coronary artery disease Myocarditis/cardiomyopathy 10–50 Most commonly related to recurrent intramyocardial ischemia/necros Diastolic dysfunction 15–40 Pulmonary hypertension ≤50 Caused by pulmonary fibrosis, vasculitis, and le heart disease Pericarditis 5–40 Asymptomatic effusion 15–25 Valve disease (any type) <10 Polymyositis or Myocarditis/cardiomyopathy 25 Myocarditis is dermatomyositis more common i

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Mixed connective tissue disease

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Pericarditis

5–25

Asymptomatic effusion Pulmonary hypertension Hyperkinetic heart syndrome Coronary artery disease Myocardial infarction Pulmonary hypertension

5–25 Rare Rare

patients with peripheral myositis More frequent in children and in overlap syndrom

Unknown Unknown ≤80 Causes are simil to those of other connective tissu diseases Pericarditis 20–40 Asymptomatic effusion 15–30 Myocarditis/cardiomyopathy <5

* Variability of rates is related to differences in patient population characteristics, study design, and diagnostic methods. † Defined by Doppler echocardiographic criteria.

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TABLE 34-2 -- Echocardiographic Features of Valve Lesions in Selected Conditions Affected Disease Structures Systemic MV, AoV lupus leaflets, erythematosus rarely

Characteristic Lesions Libman-Sacks vegetations: masses usually <1 cm in diameter, with

Functional Sequelae Mild to moderate MR or AR are

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chordae, TV and PV; spares annuli

Rheumatoid arthritis

Ankylosing spondylitis

Rheumatic

heterogeneous echo reflectance (but not calcified) and with irregular borders; usually rounded shape. Attached to leaflet with a broad base. No independent motion. Lesions are usually located at leaflet base on atrial side of MV and aortic side of AoV. Diffuse leaflet sclerosis common; calcification uncommon and mild. Rheumatoid nodules: masses usually <0.5 cm in diameter, with homogeneous soft tissue echo reflectance and irregular border; usually rounded shape. Any location on leaflet; leaflet sclerosis generally mild or absent.

common, but stenosis is rare. Potential embolic source.

More than mild MR or AR is rare; stenosis not reported. Rupture of a nodule may lead to severe valve regurgitation. Not associated with cardioembolism. Mild to Sclerosis, stiffness, and Proximal dilatation of Ao root extends moderate AR or aorta, annulus and to the annulus. AoV leaflet MR are AoV, base sclerosis is generally mild. common. of anterior Subaortic bump: a localized Stenosis not reported. thickening of base of mitral anterior mitral leaflet due to leaflet; downward extension of Ao posterior MV leaflet, root and annular sclerosis. mitral annulus and chordae spared 90% MV leaflet edges and Leaflet edge MV, AoV leaflets, rarely annuli and chordae; spares TV and PV

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fusion and chordal shortening produce a tethered mitral leaflet motion; analogous doming motion of the aortic cusps may be seen. If fusion predominates, stenosis results; if leaflet retraction predominates, regurgitation results. Degenerative MV and Sclerosis is concentrated at Annular disorders AoV annuli base of leaflets and annulus, calcification and leaflets; with progressive extension predominates for MV, with spares toward leaflet tip. When leaflet sclerosis chordae localized, sclerosis may less common appear masslike. and usually limited to posterior leaflet. MR rarely more than mild, and stenosis is subclinical. AoV leaflet sclerosis and fusion lead to stenosis, and leaflet distortion leads to AR, almost always mild. Infective Usually MV Acute: mass with Valve heart disease

involvement of MV and/or AoV; 10% TV and/or PV; annuli of valves and aortic root spared

chordae are most affected; with severe disease, sclerosis extends toward base of leaflet and may involve papillary muscles. Extensive calcification may occur. When localized, sclerosis may appear masslike, but very high echo reflectance is unlike other lesions, except degenerative. AoV cusp edges are affected in a similar pattern.

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endocarditis

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and AoV, but TV in IV drug users; PV very infrequently involved

homogeneous soft tissue reflectance and irregular borders; size and shape are highly variable, usually with narrow base, often pedunculated. Lesions almost always exhibit motion independent of underlying structure and almost always oscillatory. MV and TV lesions prolapse into atria in systole, AoV and PV lesions prolapse into outflow tracts in diastole. Lesions usually attached to distal third of leaflet. With AoV disease, additional vegetations may occur on anterior mitral leaflet and chordae. Chronic: localized thickening and/or increased reflectance of leaflet or chordae. Lesion is not necessarily distal on leaflet. Fibrous tissue reflectance and calcification are common. Rounded masses generally <0.5 cm in diameter, with homogeneous soft tissue echodensity; frequently multiple and located on leaflet edge.

regurgitation is common and frequently severe; stenosis involving native valves is rare. Cardioembolism is common.

Mild or no Seen on valve MV and regurgitation; AoV nidus for leaflets, infective sparing endocarditis or annuli and cardioembolism. chordae; rare on TV or PV AR, aortic regurgitation; AoV, aortic valve; MR, mitral regurgitation; MV, mitral valve; PV, pulmonary valve; TV, tricuspid valve. Thrombotic disorders

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TABLE 34-3 -- Echocardiographic Data Useful in Diagnosing Connective Tissue Diseases Diagnosis Myocardial infarction

Diastolic dysfunction

Left atrial pressure estimation

Severe mitral regurgitation

Echocardiographic Data Regional akinesis with wall thinning and increased reflectance (transmural myocardial infarction). Regional hypokinesis or akinesis alone is less specific when ejection fraction <40%. Wall motion abnormality should fit epicardial coronary artery distribution.[1] [2] Left atrial dilation and left atrial hypertension coupled with normal or high left ventricular ejection fraction and normal or low diastolic volume. [3] [4] [5]

Comment Reduced left ventricular ejection fraction still may be ischemic in absence of these findings.

Mild degrees of diastolic dysfunction may produce transmitral A > E, but clinical importance not clear. When left atrial hypertension develops in middle-aged or older patients, E > A (see below). When the ejection fraction is When ejection fraction reduced (<40% as a rule of is normal and the thumb) and if patient is older than patient is <40 years 55 and has a transmitral E/A ratio old, specificity of these >2, E deceleration time <150 findings is unknown. msec, or pulmonary venous Left atrial hypertension systolic fraction <30%, then by these techniques is pulmonary wedge pressure is very strongly related to a likely to be >15 mm Hg.[4] [5] [6] poor prognosis in dilated cardiomyopathies. Mitral regurgitation jet area >6 All methods are limited 2 cm or jet area/atrial area >40% in regurgitant lesions

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or jet width at origin >5.5 mm.[7]

Aortic regurgitation jet height at origin/outflow tract diameter >65% or pressure half-time <200 msec.[8] Right atrial If the inferior vena cava collapses pressure >50% with normal inspiration, or estimation inferior vena cava systolic peak velocity is >50% of diastolic velocity, then right atrial pressure is likely to be ≤10 mm Hg. If collapse is <50% and systolic peak velocity <50% of diastolic, then right atrial pressure is likely to be >10 mm Hg.[9] Pulmonary Systolic tricuspid valve pressure artery pressure gradient is calculated as = 4V2 estimation (where V is maximal tricuspid regurgitation velocity), then added to estimated right atrial pressure. Pulmonic valve gradient is assumed to be 0. [10] Tamponade Right atrial inversion time index >0.3, right ventricular diastolic collapse, inspiratory increase in isovolumic relaxation time of >85% and decrease in E wave of >40%. Right atrial pressure estimation is usually but not always elevated.[11] [12] Constriction Biatrial dilation with normal ventricular volumes and systolic function, diastolic septal displacement, usually coupled with findings of left and right

with eccentric jets. Assessment of jet width is limited with transthoracic echocardiography.

Severe aortic regurgitation

May not be valid in diseases leading to marked respiratory changes in intrathoracic pressure or positive pressure ventilation.

Values above 30 to 35 mm Hg are abnormal.

The echocardiographic diagnosis of tamponade is especially important when clinical syndrome is incomplete or atypical.

No single finding has high specificity. Pericardial thickening must be demonstrated by magnetic resonance

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atrial hypertension and inspiratory decrease in E wave >30% and hepatic venous diastolic flow reversal.[13] [14]

imaging for diagnosis of constriction. Differentiation from restrictive cardiomyopathy requires additional data. A, late diastolic flow velocity; E, early diastolic flow velocity. to provide fundamental information about the connective tissue diseases. In addition to providing data on the prevalence of cardiac lesions, longitudinal studies using serial echocardiograms are likely to clarify the natural history of cardiac disease and the influence of therapy and other factors on disease outcome. Increased application of transesophageal echocardiography is almost certain to result in upward revision of current prevalence estimates of valvular involvement in patients with these diseases. Accurate characterization of valve morphology by transesophageal echocardiography may advance our understanding of the pathogenesis and prognostic significance of these lesions.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Systemic Lupus Erythematosus Background Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that usually affects the musculoskeletal and mucocutaneous systems and frequently causes fatigue, myalgia, arthralgia or arthritis, photosensitivity, and serositis. Kidney, central nervous system, and cardiovascular disease are less common but are important causes of morbidity and mortality. The most important forms of cardiac involvement in SLE are valve disease and pericarditis, with coronary artery disease, myocarditis (in the acute inflammatory stage or as a dilated cardiomyopathy), and pulmonary hypertension less commonly detected. Vascular thrombosis and embolism occur in patients with SLE because of hypercoagulability, vasculitis, or heart disease. Overall, cardiovascular disease is the third most common cause of death of SLE patients, after infections and renal disease.[15] Associated Cardiovascular Involvement Valve Disease

Valve disease in SLE can be subdivided into Libman-Sacks vegetations (i.e., noninfected valve masses) and 765

Figure 34-1 (Figure Not Available) Mitral valve Libman-Sacks vegetation and valve thickening in a patient with systemic lupus erythematosus. This transesophageal fourchamber view shows an irregular mass (arrow) of heterogeneous echodensity on the atrial side of the basal posterior mitral leaflet. Diffuse thickening predominantly of the middle and tip portions of the anterior (aml) and posterior (pml) mitral leaflets is also noted. Moderate mitral regurgitation was present. LA, left atrium; LV, left ventricle; RV, right ventricle. (From Roldan CA, Shively BK, Lau CC, et al: J Am Coll Cardiol 1992;20:1127–1134.)

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leaflet fibrosis. More than one half of SLE patients probably have abnormal valves, but the degree of anatomic and functional abnormality is usually mild to moderate and clinically silent.[16] [17] Infrequently, even mild disease may be complicated by cardioembolism or hemodynamically significant regurgitation due to acute immune-mediated valvulitis or infective endocarditis. [18] [19] [20] The pathogenesis of valve disease in SLE is still not completely defined. Current data suggest that subendothelial deposition of immunoglobulins and complement lead to an increased expression of alpha-3 beta-1 integrin on the endothelial cells, increased amount of collagen IV, laminin, and fibronectin, proliferation of blood vessels, inflammation, thrombus formation, and finally fibrosis.[21] A role for antiphospholipid antibodies (i.e., IgG and IgM anticardiolipin antibodies, lupus anticoagulant, and a false-positive result for the Venereal Disease Research Laboratory [VDRL] test) has been proposed.[22] However, their primary pathogenic role is still debatable because patients with valve disease can have low levels of antibodies; those with normal valves have elevated antibodies; and those without antibodies have valve disease.[16] [23] The data also do not demonstrate an association of valve disease with duration, activity, severity, and therapy of SLE.[17] [24] [25] [26] In 1924, Emanuel Libman and Benjamin Sacks first reported mass lesions on the valves of patients with SLE.[27] They described cauliflower-like fibrous masses 2 to 4 mm in diameter that were located on any of the four cardiac valves. Active vegetations have central fibrinoid necrosis with fibroblastic proliferation and fibrosis, surrounded by mononuclear and polymorphonuclear cellular infiltration, small hemorrhages, and platelet thrombus. Healed masses have central fibrosis, minimal or no inflammatory cell deposition, and no or hyalinized and endothelialized thrombus. Active, healed, and mixed masses can be seen in the same valve. SLE patients frequently have diffuse leaflet fibrosis. Affected leaflets show replacement of the normal spongiosum and endothelial layers by postinflammatory fibrous tissue and infrequently by calcification. Almost all patients with Libman-Sacks vegetations have accompanying leaflet fibrosis, but fibrosis is more prevalent than Libman-Sacks vegetations among unselected SLE patients.[24] [27] [28] The basis for the difference in these two patterns of valve injury is unknown. Echocardiographic studies have shown that Libman-Sacks vegetations are usually less than 1 cm in diameter, vary in shape, have irregular borders,

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and have heterogeneous echodensities. The broad-based growths rarely move independently of the underlying valve structure. Lesions are usually attached to the basilar portion of the aortic and mitral valve leaflets, on the atrial side of the mitral valve, and on the aortic side of the aortic cusps[16] [17] [22] (Fig. 34-1) (Figure Not Available) (Fig. 34-2) (Figure Not Available) (Fig. 34-3) (Fig. 34-4) (Figure Not Available) (Fig. 34-5) . The lesions are rarely seen on the right heart valves (Fig. 34-6) . Echocardiographic studies estimate the prevalence of Libman-Sacks vegetations among patients with SLE as less than 10% by transthoracic echocardiography and up to 30% by transesophageal echocardiography.[16] [17] [22] , [29] Libman-Sacks vegetations are frequently accompanied by mild valve regurgitation but are otherwise usually clinically silent. Significant complications such as severe regurgitation resulting from recurrent or acute valvulitis, leaflet Figure 34-2 (Figure Not Available) Mitral valve Libman-Sacks vegetation and valve thickening in a patient with systemic lupus erythematosus. This transesophageal tangential portion of a four-chamber view shows a large mass (arrowhead) with heterogeneous echodensity on the atrial side of the basal posterior mitral leaflet. Associated diffuse thickening of both mitral leaflets is seen, and there was also mild mitral regurgitation. aml, anterior mitral leaflet; LA, left atrium; LV, left ventricle; pml, posterior mitral leaflet. (From Roldan CA, Shively BK, Lau CC, et al: J Am Coll Cardiol 1992;20:1127–1134.)

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Figure 34-3 Mitral valve Libman-Sacks vegetations and thickening in a patient with systemic lupus erythematosus. This transesophageal fourchamber view shows two masses (arrowheads) with heterogeneous echodensity on the atrial side of the base and midportions of the posterior mitral leaflet. A third mass (arrow) is seen on the tip portion of the anterior mitral leaflet. Associated diffuse thickening, predominantly of the middle and tip portions of both mitral leaflets, is also demonstrated. Mild mitral regurgitation was detected. aml, anterior mitral leaflet; LA, left atrium; LV, left ventricle; pml, posterior mitral leaflet.

perforation including bioprosthetic leaflets, and noninfective mitral valve chordal rupture; infective endocarditis; or cardioembolism occur in up to 20% of patients with valve disease.[16] [17] [19] [26] Infective endocarditis can mimic, accompany, or trigger a flare of SLE and can lead to severe valve dysfunction, heart failure, and septic death. Similarly, a flare of SLE can

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mimic endocarditis (pseudo-infective Figure 34-4 (Figure Not Available) Aortic valve Libman-Sacks vegetation in a patient with systemic lupus erythematosus. This transesophageal view, longitudinal to the left outflow tract, shows a mass (arrow) of irregular borders and heterogeneous echodensity at the base of the noncoronary cusp (ncc) and posteromedial aortic root wall. No aortic regurgitation was seen. aml, anterior mitral leaflet; LA, left atrium; LV, left ventricle; pml, posterior mitral leaflet; rcc, right coronary cusp. (From Roldan CA, Shively BK, Lau CC, et al: J Am Coll Cardiol 1992;20:1127–1134.)

Figure 34-5 Aortic valve Libman-Sacks vegetations and thickening in a patient with systemic lupus erythematosus. This transesophageal view longitudinal to the outflow tract demonstrates two well-defined small masses on the vessel side of the aortic right and noncoronary cusps (arrowheads). Mild localized thickening at the base of the right coronary cusp (rcc), the tip of the noncoronary cusp (ncc), and the tip of the anterior mitral leaflet (aml) is also noted (arrows). No aortic or mitral regurgitation was detected. LA, left atrium; LV, left ventricle; pml, posterior mitral leaflet.

endocarditis). A low white blood cell count, elevated antiphospholipid antibodies, and negative or low C-reactive protein indicates active SLE. Echocardiographic characteristics associated with significant complications have not been identified. In a serial transesophageal echocardiographic study, Libman-Sacks vegetations were observed to resolve and reappear over time, independently of SLE disease duration, severity, activity, or therapy.[26] Of importance, the effect on valve masses of long-term anticoagulation in patients with antiphospholipid antibodies is controversial.[30] The leaflet fibrosis (i.e., increased thickness and echocardiographic reflectance) accompanying Libman-Sacks vegetations may cause reduced leaflet mobility, but valve stenosis is rare (<3%). In a transesophageal study, 48% of unselected SLE patients had abnormal leaflets, defined as leaflet thickness greater than 3 mm in a patient younger than 60 years of age.[16] Transthoracic echocardiographic studies generally report a lower frequency of valve thickening. Shadowing caused by intense leaflet scarring is observed in 12% of patients. Annular, subvalvular, and right heart involvement is rare. Rheumatic and SLE valve disease have similar immunopathogenesis. Therefore, except for elevation of antistreptolysin antibodies in rheumatic carditis, acute rheumatic and SLE endocarditis can have similar clinical and serologic markers. In their chronic states, the echocardiographic

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characteristics of these two conditions may also overlap.[16] [26] [31] This uncertainty is likely to continue unless a specific hematologic or other marker for SLE valve disease or previous rheumatic fever is found. In patients older than 60 years of age, the pattern of valve scarring characteristic of SLE may be partially obscured by combination with changes due to aging.[32] The echocardiographic 767

Figure 34-6 Pulmonic valve Libman-Sacks vegetation and thickening in a patient with systemic lupus erythematosus. This transesophageal view longitudinal to the right outflow tract (RVOT) and pulmonary artery (PA) demonstrates a mass with soft tissue density on the tip, vessel side, of the anterior pulmonic leaflet (apl), and localized thickening of this leaflet basal portion (arrow). Mild pulmonic regurgitation was present. Ao, aorta; lpl, left pulmonic leaflet; LV, left ventricle.

appearances of Libman-Sacks, thrombotic, and infective vegetations may overlap[30] [33] [34] (see Table 34-2) . Pericarditis

As many as 50% of SLE patients suffer at least one episode of symptomatic pericarditis.[35] [36] Most episodes are acute, uncomplicated, and associated with transient increases in pleuritis, serositis, and overall SLE disease activity. Cardiac tamponade and constrictive pericarditis are uncommon (<2%), but acute pericarditis and cardiac tamponade can be the initial manifestation of SLE. Because an effusion is usually, but not always, present, the diagnosis of pericarditis rests on manifestations of the clinical syndrome, not the echocardiogram. Pericardiocentesis in patients with symptomatic pericarditis typically yields serosanguineous or exudative fluid containing a low complement level and antinuclear antibodies. The latter component has not been described in effusions due to other causes. Pericardial biopsy demonstrates immune complex deposition, indicating autoimmune injury.[37] An effusion without accompanying signs and symptoms of pericarditis in a SLE patient probably results from mild pericarditis or another process such as nephrotic syndrome or uremia. Asymptomatic effusions are common incidental findings in SLE patients, occurring in as many as 20% of those hospitalized with active disease. [17] [22] , [38] , [39]

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Echocardiography is essential for the evaluation of suspected SLE pericarditis to assess the size of an effusion and look for signs of tamponade physiology (see Table 34-3) . Tamponade is uncommon in SLE pericarditis, but the high morbidity rate of this complication and the potential for an atypical clinical presentation mandate careful evaluation. [40] Echocardiographic interpretation must be tempered with the recognition that evidence of tamponade may appear at any time after the study is performed because of unpredictable increases in effusion volume. As in tamponade from any cause, echocardiographic indicators of tamponade, even without demonstrable right atrial hypertension or circulatory compromise, should prompt intensive monitoring or therapy. Serial echocardiograms after drainage or during anti-inflammatory drug therapy help to follow changes in the size of the effusion and detect recurrence of tamponade. Rarely, constrictive or infectious pericarditis may complicate SLE pericarditis.[41] [42] Echocardiography is an effective screening method when constriction is under consideration as a late sequela of SLE pericarditis (see Table 34-3) . Echocardiography is insensitive for the detection of mild or moderate pericardial thickening. Cardiac magnetic resonance imaging is preferred for assessing pericardial thickness and is an important confirmatory test when the echocardiogram suggests constriction.[43] Myocardial Disease

Left ventricular systolic or diastolic dysfunction in SLE can result from atherosclerotic coronary artery disease, coronary arteritis, or small vessel vasculitis, but postmyocarditis dilated cardiomyopathy (i.e., primary SLE cardiomyopathy) and severe valve disease must also be considered. In unselected SLE patients, the overall prevalence of a reduced resting left ventricular ejection fraction is probably less than 20%.[16] [22] [21] [44] However, approximately one third of SLE patients in a study demonstrated an exercise-induced fall or subnormal rise in ejection fraction.[45] Diffuse left ventricular hypokinesis as a consequence of SLE cardiomyopathy is uncommon, but when associated with active disease may indicate acute myocarditis and could respond favorably to steroid or cytotoxic therapy. An association of cellular antigen Ro (SSA) and La (SS-B) antibodies and myocarditis has been established, but their primary pathogenic role is still undefined.[46] [47] The evaluation of the SLE patient with a reduced ejection fraction should include coronary angiography. Coronary artery disease cannot be excluded

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by echocardiography, because certain types of ischemic myocardial injury (e.g., chronic ischemia, nontransmural infarction) may produce a left ventricular appearance indistinguishable from that of SLE cardiomyopathy. When the echocardiographic evaluation indicates previous myocardial infarction, coronary angiography is required to clarify the patient's treatment options and prognosis.

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In young SLE patients with normal systolic function and no pericardial or valve disease, diastolic dysfunction has been reported in 15% to 35% of SLE patients by Doppler echocardiography. They demonstrated prolongation of the isovolumic relaxation time of 104 ± 18 msec (vs. 74 ± 13 msec in normal subjects), reduced peak early diastolic filling velocity (E) to 69 ± 19 cm per second (vs. 83 ± 17 cm per second), reduced ratio of early to late diastolic flow velocity (E/A) to 1.15 ± 0.53 (vs. 1.47 ± 0.35), and prolonged mitral pressure half-time to 74 ± 14 msec (vs. 65 ± 8 msec; P < .02 for all). [48] In these studies, ventricular filling abnormalities occurred more frequently in patients with active disease than in those with inactive SLE (64% vs. 14%). Recent series of young patients with active SLE and normal coronary arteries demonstrated a high prevalence of abnormal left ventricular Doppler filling variables suggestive of diastolic dysfunction and reversible, fixed, and mixed myocardial perfusion defects. [49] [50] These results could reflect subclinical SLE myocardial disease. Thrombotic Diseases

Patients with SLE are subject to intracardiac thrombosis and cerebral or systemic embolism due to hypercoagulability. Enough data are now available to support the procoagulant and possible vascular inflammatory properties of antiphospholipid antibodies (i.e., anticardiolipin antibodies and lupus anticoagulant).[21] [22] [23] [51] [52] Echocardiography is used frequently to identify a source for cardioembolism in patients with SLE. In patients with or without antiphospholipid antibodies, substrates of high embolic potential are Libman-Sacks or thrombotic vegetations.[51] Postmortem and transthoracic echocardiographic series of SLE patients frequently identify Libman-Sacks vegetations as a probable cause of cardioembolism.[53] , [54] As for the general population, other substrates with high embolic potential are acute anterior myocardial infarction, reduced left ventricular ejection fraction

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(<35% as a rule of thumb), and atrial fibrillation. If substrates of high potential are not identified, transesophageal echocardiography is a reasonable next step to evaluate the presence and extent of SLE valve disease and other possible sources such as atrial stasis, aortic atheroma, and probably patent foramen ovale or interatrial septal aneurysm. Coronary Artery Disease

Autopsy studies show a 25% prevalence of coronary atherosclerosis in patients with SLE, although clinically evident disease is less common.[16] [24] [28] [35] [36] [55] , The improved longevity of SLE patients has led to an increased incidence of coronary artery disease. Although traditional risk factors including obesity have been associated with coronary artery disease, other factors such as long-standing SLE (>12 years) and prolonged steroid therapy (>14 years) lead to sustained hypercholesterolemia (level >200 mg/dL). Patients with inactive SLE have high levels of VLDL and triglycerides and low levels of high-density lipoprotein. These abnormalities are worse in patients with active SLE.[55] [56] Antiphospholipid antibodies have also been associated with coronary artery disease. They produce peroxidation of low-density lipoprotein and endothelial dysfunction leading to vasoconstriction and thrombosis by release of platelet-derived growth factor and thromboxane A2 and decreased production of prostacyclin and prostaglandin I.[56] In SLE patients, angina, myocardial infarction, and left ventricular dysfunction may also result from coronary arteritis or embolization to a coronary artery.[57] Coronary arteritis should be suspected in a young patient with an acute coronary syndrome, especially if accompanied by active SLE and evidence of vasculitis affecting other organs. Coronary embolism or in situ thrombosis are rare but warrant consideration when myocardial infarction occurs with no anginal prodrome or in association with a cardioembolic substrate or an underlying procoagulant state such as elevated antiphospholipid antibodies. [35] [36] [55] [56] [57]

The echocardiographic detection of myocardial infarction is summarized in Table 34-3 . Dobutamine echocardiography is useful for detection and for risk stratification of patients with suspected or known coronary artery disease and arthritis precluding exercise testing. Newly suspected coronary artery disease may warrant coronary angiography because of the relative youth of these patients and the need for accurate risk stratification, and to guide choices of SLE treatment, such as steroids, immunosuppressives, or both if coronary arteritis is suspected.

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Pulmonary Hypertension

Pulmonary hypertension occurs in 5% to 14% of SLE patients. The most common causes include interstitial lung disease, vasculitis, and thromboembolism. Myocardial and valve disease should also be considered. Doppler echocardiography is valuable in the diagnosis, assessment of severity, and follow-up of SLE-associated pulmonary hypertension.[58] [59]

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Rheumatoid Arthritis Background Rheumatoid arthritis is a chronic autoimmune disease characterized by symmetric arthritis, potentially involving any synovial joint but usually affecting the metacarpophalangeal and proximal interphalangeal joints and wrists. In this disease, the patient's serum contains rheumatoid factor, a group of IgM or IgG antibodies directed against autologous IgG. Nonarthritic manifestations of rheumatoid arthritis include rheumatoid nodules, systemic vasculitis, glomerulonephritis, pulmonary fibrosis, and several cardiovascular diseases: pericarditis, valve disease, myocarditis, coronary arteritis, aortitis, and cor pulmonale. Clinically apparent heart disease occurs in as many as 25% of patients with rheumatoid arthritis and is more likely in patients with long-standing disease; active extra-articular, erosive polyarticular, and nodular disease; systemic vasculitis; and high serum titers of rheumatoid factor. Heart 769

disease is the third leading cause of death in patients with rheumatoid arthritis. [60] [61] Associated Cardiovascular Involvement Pericarditis

Echocardiographic studies have shown pericardial effusions in as many as 50% of rheumatoid arthritis patients, but symptomatic pericarditis is unusual.[61] [62] [63] Episodes of pericarditis tend to occur in patients with active arthritis, high serum levels of rheumatoid factor, rheumatoid nodules, an erythrocyte sedimentation rate greater than 55 mm per hour, and positive antinuclear antibodies. Immunoflurescent staining of the biopsied pericardium reveals deposits of IgG, IgM, C3, and C1q, indicating

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autoimmune injury.[64] The pericardial effusion is exudative and bloody with a low glucose level, and it may contain rheumatoid factor.[65] [66] As with SLE pericarditis, tamponade and constriction are rarely reported.[67] [68] The role of echocardiography in the diagnosis and management of rheumatoid effusions parallels its role in SLE pericarditis[69] [70] (see Table 34-3) . Valve Disease

Estimates of the prevalence of valve disease in rheumatoid arthritis are highly variable. A few early echocardiographic studies reported prevalence rates of nonspecific valve abnormalities as high as 30%.[63] [71] [72] Valve disease is probably more common in patients with erosive polyarticular and nodular disease, systemic vasculitis, and high serum titers of rheumatoid factor. Valve disease in rheumatoid arthritis occurs as leaflet fibrosis and valve granulomas. The leaflet fibrosis is indistinguishable from that seen in SLE. In contrast, valve granulomas appear to be unique to rheumatoid arthritis. [73] [74] These granulomas or nodules can also be seen on valve rings, papillary muscle tips, and atrial or ventricular endocardium. Histologically, the granulomas resemble subcutaneous rheumatoid nodules, containing a central portion of fibrinoid necrosis surrounded by a mononuclear infiltrate and sometimes by Langhans cells and giant cells. It is thought that these nodules result from a process of focal vasculitis. On an echocardiogram, rheumatoid valve nodules usually appear as small (<0.5 cm2 ), spheroid masses with homogeneous reflectance, usually appearing singly and on any portion of the leaflet. The adjacent leaflet appears normal or shows mild sclerosis. This picture is unlike that of Libman-Sacks vegetations ( see Table 34-2 ; compare Fig. 34-1 (Figure Not Available) Fig. 34-2 (Figure Not Available) Fig. 34-3 Fig. 34-4 (Figure Not Available) Fig. 34-5 with Fig. 34-7 (Figure Not Available) Fig. 34-8 Fig. 34-9 (Figure Not Available) ). Rheumatoid valve disease is almost always mild and asymptomatic, and it is less likely than SLE valve disease to result in clinically significant valve dysfunction. However, two unusual forms of acute valve regurgitation in rheumatoid arthritis have been described. In the first form, acute mitral or aortic valvulitis has been complicated by severe valve regurgitation that required valve replacement. [75] [76] [77] In the second form, acute severe valve

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Figure 34-7 (Figure Not Available) Mitral valve disease in a patient with rheumatoid arthritis. This transesophageal two-chamber view of a 63-year-old man with rheumatoid nodular disease demonstrates a small nodular mass (arrowhead) with homogeneous echodensity at the tip and chordal junction of the posterior mitral leaflet (pml). Associated mild thickening of the tips of the anterior and posterior mitral leaflets is noted. Mild mitral regurgitation was seen. This mitral valve mass is suggestive of a rheumatoid nodule. aml, anterior mitral leaflet; LA, left atrium; LV, left ventricle. (From Roldan CA: In Braunwald E [ed]: Atlas of Heart Diseases, vol 6. Philadelphia, Current Medicine, 1996, pp 1–32.)

regurgitation has complicated "rupture" of a valve granuloma.[75] [78] Myocardial Disease

Some patients with rheumatoid arthritis have nonspecific myocarditis, myocardial granuloma formation, or cardiac amyloidosis.[74] Evidence of present or past myocarditis is revealed at autopsy in as many as 30% of patients, but decreased systolic function by echocardiography is seen less commonly. [79] Mild diastolic dysfunction is common but may be caused by hypertrophy as well as coronary artery disease.[80] An echocardiographic description of myocardial granulomas has not been published. The echocardiographic features of amyloidosis due to rheumatoid arthritis appear to be the same as for amyloidosis of other types but may coexist or mimic rheumatoid constrictive pericarditis (see Chapter 29) . Coronary Artery Disease

Patients with rheumatoid arthritis are prone to atherosclerotic coronary disease and coronary arteritis. Coronary obstructive lesions are more likely to be caused by atherosclerosis, because rheumatoid arthritis afflicts older men with a greater frequency than other connective tissue diseases. In addition to older age at the onset of the disease and male sex, high disease activity as reflected by 770

Figure 34-8 Aortic valve disease in a patient with rheumatoid arthritis. This transesophageal view longitudinal to the outflow tract shows a localized nodularity with increased echoreflectance on the midportion of the noncoronary cusp (ncc) (arrow). The appearance of the noncoronary and right coronary cusps is normal. Thickening and sclerosis of the posteromedial aortic root wall is noted (arrowheads). Aortic valve regurgitation was not demonstrated. aml, anterior mitral leaflet; LA, left atrium; rcc, right coronary cusp.

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serologic markers of inflammation and steroid therapy and subclinical arteritis predispose these patients to atherosclerosis and increased cardiovascular mortality.[81] Therefore, the overall prevalence of atherosclerotic coronary artery disease in patients with rheumatoid arthritis is probably higher than in age-matched control subjects. Coronary vasculitis occurs as part of rheumatoid disease, but, unlike atherosclerosis, this disease affects the small or medium-sized intramyocardial arteries and spares the epicardial vessels. Although it is described in patients at postmortem examination, its clinical detection is rare.[82] Patients with coronary arteritis generally present with unstable angina or myocardial infarction. The indications for echocardiography and coronary angiography are generally the same as in ischemic heart disease. In addition to conventional therapy, steroids and other immunosuppressive therapy are of benefit in managing coronary arteritis. Pulmonary Hypertension

Pulmonary hypertension with normal pulmonary venous pressure may occur in rheumatoid arthritis because of several processes: interstitial fibrosis, pulmonary vasculitis, and obliterative bronchiolitis.[83] The prevalence of this disease is unknown but probably low. The mortality rate is high within 1 year of diagnosis. Prompt diagnosis is vital. Lung biopsy or bronchoalveolar lavage may confirm pulmonary vasculitis and bronchiolitis obliterans, both of which are frequently responsive to immunosuppressive therapy. Dyspnea in a patient with rheumatoid arthritis is an indication for echocardiographic screening for pulmonary hypertension. Pulmonary hypertension may not be accompanied by clinical or echocardiographic evidence of cor pulmonale, especially if the pulmonary artery pressure is less than 50 mm Hg. If pulmonary hypertension is identified, echocardiography should also be used to rule out left atrial hypertension or a potential cause of same (e.g., left ventricular dysfunction, mitral valve disease). In the absence of a left heart basis for pulmonary hypertension, the search for a treatable pulmonary cause should be pursued, as discussed previously. When pulmonary hypertension presents with symptoms potentially caused by right heart failure (e.g., exertional dyspnea, fatigue, peripheral edema), echocardiography is useful to assess the severity of right ventricular dysfunction and tricuspid regurgitation and to estimate right atrial and

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pulmonary artery pressure (see Table 34-3) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Ankylosing Spondylitis Background Ankylosing spondylitis and the other HLA-B27-related arthropathies are autoimmune diseases characterized by inflammation of the vertebral and sacroiliac joints. Arthritis of other joints, uveitis, and proximal aortitis and aortic valvulitis are common. Other complications are rare, and although arthritis may be disabling, the overall prognosis is good. Figure 34-9 (Figure Not Available) Aortic valve disease in a patient with rheumatoid arthritis. This transesophageal aortic valve short-axis view from a 42-year-old woman with high rheumatoid factor shows irregular nodules with increased echoreflectance at the bases (arrowheads) of the left (lcc) and right (rcc) coronary cusps. The appearance of the cusps is otherwise normal. Mild aortic valve regurgitation was detected. LA, left atrium; ncc, noncoronary cusp; RA, right atrium; RVOT, right ventricular outflow tract. (From Roldan CA: In Braunwald E [ed]: Atlas of Heart Diseases, vol 6. Philadelphia, Current Medicine, 1996, pp 1–32.)

Associated Cardiovascular Involvement Aortitis and Valve Disease

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Among patients with ankylosing spondylitis, the prevalence rates of ascending aorta and aortic valve disease have varied widely, but aortitis and aortic regurgitation are commonly clinically important. Evidence of present or past inflammation is found in all layers of the aortic wall, and the process leads to dilation, fibrosis, and calcification.[84] , [85] The reason for selective injury of the proximal aorta is unknown. Aortic regurgitation is generally mild to moderate and results from the combination of dilation of the aortic root and annulus and thickening with retraction of the aortic cusps. Hemodynamically significant regurgitation is usually caused by

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acute valvulitis or supervening infective endocarditis.[86] [87] The mitral valve may become abnormal when aortic root fibrosis extends downward into the anterior mitral leaflet. This often results in localized fibrotic thickening at the base of the anterior mitral leaflet, a condition called "subaortic bump." [84] In several echocardiographic studies, including a recent transesophageal series, aortic root thickening, increased stiffness, and dilation were seen in 60%, 60%, and 25% of patients, respectively. Aortic valve thickening seen in 40% of patients manifested mainly as nodularities of the aortic cusps. Mitral valve thickening seen in one third of patients manifested predominantly as basal thickening of the anterior mitral leaflet, forming the characteristic subaortic bump. Valve regurgitation seen in almost half of patients was moderate in one third of them. Aortic root disease and valve disease were related to duration of the disease Figure 34-10 Aortic root and aortic and mitral valve disease in a patient with ankylosing spondylitis. This transesophageal view longitudinal to the outflow tract in a 31-year-old man shows marked thickening of the posteromedial aortic root (arrowheads) extending to the basal portion of the noncoronary cusp (ncc) and into the base and midportions of the anterior mitral leaflet ("subaortic bump," arrow). Mild thickening of the right coronary cusp (rcc) tip and mild aortic root dilation are also noted. Moderate aortic regurgitation was demonstrated. aml, anterior mitral leaflet; AoR, aortic root; LA, left atrium; LV, left ventricle. Figure 34-11 Aortic root and aortic and mitral valve disease in a 43year-old man with ankylosing spondylitis. This transesophageal view longitudinal to the outflow tract demonstrates severe sclerosis of the aortic root (AoR) predominantly of the posteromedial wall (arrowheads) extending to the base of the anterior mitral leaflet (aml) to form the subaortic bump (arrow). Moderate aortic root dilation is present. The noncoronary (ncc) and right (rcc) coronary cusps show mild localized thickening of their middle and tip portions. Moderate aortic regurgitation was demonstrated. LA, left atrium; LV, left ventricle.

but not to its activity, severity, or therapy[88] [89] [90] [91] ( Fig. 34-10 Fig. 34-11 Fig. 34-12 Fig. 34-13 (Figure Not Available) ). Conduction Abnormalities

Atrioventricular and intraventricular conduction blocks occur with a greater

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than expected frequency in patients with ankylosing spondylitis.[88] [92] [93] Their reported prevalence rates, as for aortic root and valve disease, have been widely variable but are at least 20%. Echocardiographic studies have demonstrated an association of conduction abnormalities with aortic root thickening and subaortic bump, suggesting a role for extension of aortic root fibrosis into the proximal septum and atrioventricular node.[88] [94] Occasionally, third-degree heart block requires permanent pacemaker implantation. Myocardial and Pericardial Disease

The frequency of myocardial and pericardial disease in patients with ankylosing spondylitis is probably not different from the frequency in the general population. One study of 28 patients with ankylosing spondylitis found left ventricular systolic dysfunction in one fifth.[95] These data have not been replicated, and bias in patient selection may account for the results. Brewerton et al,[96] in a postmortem study, demonstrated a high frequency of increased connective tissue in the left ventricular wall and by echocardiography showed a high prevalence of abnormalities suggestive of diastolic dysfunction. These abnormalities consisted of a prolongation of time from minimum left ventricular dimension to mitral valve opening 772

Figure 34-12 Aortic root and mitral valve disease in a 41-year-old man with ankylosing spondylitis. This transesophageal view longitudinal to the outflow tract demonstrates sclerosis of the aortic root walls (small arrows) extending into the anterior mitral leaflet (aml) base and forming a large subaortic bump (arrow). Decreased mobility of the anterior mitral leaflet is noted and mild mitral regurgitation was seen. The aortic valve cusps appear normal, and no aortic regurgitation was detected. LA, left atrium; LV, left ventricle; ncc, noncoronary cusp; pml, posterior mitral leaflet; rcc, right coronary cusp.

(32 vs. 10 msec) and prolongation of the isovolumic relaxation time (91 vs. 68 msec). Crowley et al[97] compared 59 ankylosing spondylitis patients (mean age 42 years) with no clinical heart disease to 44 age- and gendermatched healthy volunteers. Twelve patients (20%) showed evidence of diastolic filling abnormalities consisting of prolongation of the isovolumic relaxation time (>86 msec), reduced E peak velocity (<36 m per second), increased A peak velocity (>65 m per second), reduced E/A ratio (<0.9),

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reduced ejection fraction slope (<2.4 m/sec2 ), and prolonged E deceleration time (>204 msec). In both studies, these abnormalities were unrelated to age, disease duration, or disease activity. In another study of ankylosing spondylitis in patients younger than 45 years and without cardiovascular symptoms, radionuclide ventriculography demonstrated decreased left ventricular filling rate and increased time to peak filling.[98] These studies suggest that primary subclinical myocardial disease associated with abnormal left ventricular filling abnormalities may occur in patients with ankylosing spondylitis. Pericardial disease in patients with ankylosing spondylitis is thought to be rare. In one series of 222 patients, only 2 cases (1%) of clinical pericarditis were described. Echocardiographic studies have reported incidentally detected small pericardial effusions more commonly.[99]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Scleroderma Background In scleroderma, excessive connective tissue accumulates in the blood vessels, skin, joints, skeletal muscle, and multiple organs, including the heart. Thickening of the skin and Raynaud's phenomenon affect more than 90% of patients. In the diffuse type, there is symmetric fibrosis of the skin of the face, trunk, and extremities, with frequent involvement of internal organs. In the limited cutaneous type, the skin changes are limited to the extremities and face; internal organs are generally spared. This latter type is associated with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal hypomotility, sclerodactyly, and telangiectasia). The limited cutaneous type is more commonly associated with pulmonary hypertension. Cardiovascular disease occurs in as many as 50% of scleroderma patients. [100] Coronary artery disease, myocarditis, and pericarditis occur, as well as pulmonary and systemic hypertension-related heart disease. Arrhythmias and conduction abnormalities are less frequent. Overall, heart disease is the third major cause of death, after pulmonary and kidney disease.[101] Associated Cardiovascular Involvement Coronary Artery Disease

In scleroderma, the intramyocardial coronary arteries and arterioles become narrowed or occluded by two mechanisms: (1) intimal inflammation and fibrosis due to an immune-mediated arteritis or (2) abnormally increased Figure 34-13 (Figure Not Available) Aortic root disease and mitral "subaortic bump" in a patient with ankylosing spondylitis. This transesophageal view longitudinal to the outflow tract of a 55-year-old man demonstrates marked thickening of the proximal aortic root predominantly of the posteromedial wall (arrowheads) that extends 1 cm into the basal portion of the anterior mitral leaflet, producing the characteristic subaortic bump (arrow). Decreased mobility of the anterior mitral leaflet (aml) and

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mild mitral regurgitation were noted. The appearance of the aortic cusps is normal and no aortic regurgitation was detected. LA, left atrium; LV, left ventricle; ncc, noncoronary cusp; pml, posterior mitral leaflet; rcc, right coronary cusp. (From Roldan CA: In Braunwald E [ed]: Atlas of Heart Diseases, vol 6. Philadelphia, Current Medicine, 1996, pp 1–32.)

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vasoconstriction due to an immune-mediated endothelial dysfunction or increased mast cell degranulation of vasoactive substances such as histamine, prostaglandin D2 , and leukotrienes C4 and D4 . Intramyocardial coronary arterial spasm analogous to Raynaud's phenomenon can occur.[102] [103] Vasospasm of the epicardial coronary arteries is rarely seen. For unknown reasons, angina is unusual. Because of predominant involvement of the intramyocardial coronary arteries, the echocardiographic findings typical of transmural myocardial infarction (see Table 34-3) are often not seen. Instead, patients with sclerodermal coronary artery disease usually present with left ventricular diastolic or global systolic dysfunction. Occasionally, a transmural myocardial infarction due to epicardial coronary vasospasm can occur, and its echocardiographic diagnosis relies on the same findings as those of atherosclerotic disease. The cold pressor test with simultaneous myocardial perfusion scanning and echocardiographic evaluation frequently demonstrates transient wall motion abnormalities corresponding to perfusion defects.[104] In certain studies, as many as 70% of scleroderma patients have reversible, fixed, or both types of perfusion scan abnormalities and angiographically unremarkable epicardial coronary arteries, but reduced resting coronary flow reserve because of intramyocardial vessel disease.[105] [106] [107] Myocardial Disease

Clinically apparent scleroderma-associated myocarditis is common but frequently unrecognized. Pathologic evidence of present or past myocarditis is found in most patients.[100] [108] Myocarditis is more common in patients with diffuse cutaneous involvement, anti-Scl70 antibodies, peripheral myopathy, and age older than 60 years.[108] [109] In echocardiographic studies, a reduced left ventricular ejection fraction has been found in some asymptomatic patients, but it is more commonly seen in patients with clinically evident heart disease.[110] [111] [112] Associated right

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ventricular dysfunction is reported commonly for patients with left ventricular dysfunction. Reduced ejection fraction on echocardiography (with or without cardiac symptoms) is associated with reduced survival.[101] The mortality rate is high (80% at 1 year) for those who develop clinical left ventricular failure. Doppler echocardiographic parameters similar to those used in other connective tissue diseases have suggested the presence of reduced left ventricular compliance in some scleroderma patients.[113] , [114] Ultrasonic videodensitometric analysis of the myocardium in patients with scleroderma younger than 50 years of age who do not have hypertension or diabetes, demonstrates low cyclic variation indexes that may represent primary myocardial fibrosis or microvascular disease rather than changes related to aging or hypertension.[103] Left ventricular potentials on signal averaged electrocardiography, septal infarction pattern (Q waves in V1 and V2 ), complex ventricular arrhythmias, or conduction abnormalities on electrocardiography have been noticed with increased frequency in patients with scleroderma.[115] Septal infarction patterns are associated with fixed septal or anteroseptal perfusion abnormalities thought to represent septal fibrosis. Echocardiographic data on septal wall motion in these patients have not been reported. Pulmonary Hypertension and Cor Pulmonale

Interstitial lung disease and resultant pulmonary hypertension are a major feature of scleroderma. Pulmonary fibrosis can occur in as many as 80% and pulmonary hypertension in as many as 50% of patients. Pulmonary hypertension secondary to inflammatory vasculopathy or pulmonary vasospasm is less common and is associated with the limited cutaneous type. Abnormal pulmonary function tests, abnormal lung uptake of gallium and technetium-99m Sestamibi, and radiographic abnormalities often precede cor pulmonale on echocardiography. Pulmonary hypertension is associated with a 50% mortality rate at 8 years.[116] Techniques for the echocardiographic diagnosis of pulmonary hypertension and cor pulmonale are summarized in Table 34-3 . Pericarditis

Clinically evident pericardial disease occurs in 5% to 15% of scleroderma patients and manifests as pericardial effusion, acute pericarditis, and rarely as cardiac tamponade or pericardial constriction.[100] [117] Pericardial disease

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is more common in patients with a diffuse form than a limited cutaneous form of the disease and may be associated with antiphospholipid antibodies [100] [117] [118] (Fig. 34-14) (Figure Not Available) . The pericardial effusion is usually an exudate, although without evidence of autoantibodies, immune complexes, or complement depletion. The application of echocardiography to the management of effusions was discussed previously (see Table 34-3) . Valve Disease

Published data suggest that scleroderma rarely causes valve disease. Unreplicated reports have described small masses similar to Libman-Sacks vegetations (one with probable embolization), aortitis and aortic regurgitation, and an increased frequency of mitral valve prolapse[119] [120] [121] [122] (see Fig. 34-14) (Figure Not Available) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Polymyositis and Dermatomyositis Background Polymyositis and dermatomyositis are clinically similar diseases characterized by autoimmune-mediated skeletal muscle inflammation leading to symmetric proximal muscle weakness. Unlike polymyositis, dermatomyositis is accompanied by a rash on the face, neck, chest, and extensor surfaces of the extremities. Overlap syndromes frequently occur in which features of dermatomyositis or polymyositis are combined with other connective tissue diseases such as SLE, rheumatoid arthritis, and scleroderma. Rarely, 774

Figure 34-14 (Figure Not Available) Mitral valve disease in a 72-year-old woman with scleroderma. Transthoracic long parasternal (A) and four-chamber (B) echocardiographic views show an irregular, highly reflectant nodularity in the midportion of the anterior mitral leaflet (aml) (arrowheads). Mild regurgitation was demonstrated. In spite of the patient's age, no degenerative changes were detected in the mitral or aortic valve. Thus, the valve abnormality is most likely related to scleroderma, probably immune-mediated valve disease. Anterior and posterior pericardial effusion (pe) can be seen in the long parasternal view. LA, left atrium; LV, left ventricle. (From Roldan CA: In Braunwald E [ed]: Atlas of Heart Diseases, vol 6. Philadelphia, Current Medicine, 1996, pp 1–32.)

polymyositis or dermatomyositis can be associated with antiphospholipid antibody syndrome. Myocarditis and pericarditis appear to be associated with polymyositis and dermatomyositis. Atherosclerotic coronary artery disease, conduction disorders, valve dysfunction, and pulmonary hypertension are uncommon and may be coincidental because of the high frequency of risk factors for heart disease and the advanced age of these patients.[123] [124] [125]

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Associated Cardiovascular Involvement Myocardial Disease

In postmortem series, as many as 50% of patients with polymyositis or dermatomyositis show histologic evidence of active or healed myocarditis, and approximately 10% to 20% of them have dilated cardiomyopathy.[126] [127] The clinical prevalence of myocarditis is unknown. Postmortem series of patients with myocarditis report a 25% to 45% rate of clinical myocarditis or heart failure. Patients with myocarditis frequently have active skeletal muscle myositis; as many as 50% of those with peripheral myositis, as indicated by uptake of technetium-99m pyrophosphate, also have myocardial uptake. [128] Limited prospective data, including two echocardiographic studies, suggest that few patients with polymyositis or dermatomyositis manifest wall motion abnormalities or a decreased left ventricular ejection fraction during the course of their disease.[129] [130] [131] Diastolic dysfunction has not been reported. An occasional patient with polymyositis or dermatomyositis develops findings of a hyperdynamic circulatory 775

state accompanied by an elevated ejection fraction on echocardiography. The pathogenesis of this hyperkinetic heart syndrome is unknown, and patients are usually minimally symptomatic. Echocardiographic criteria for the diagnosis include an increased mean velocity of circumferential fiber shortening, fractional shortening, stroke volume, and cardiac output.[132] Pericarditis

The prevalence of pericardial disease in polymyositis and dermatomyositis patients is low. Pericarditis is more frequent in patients with the overlap syndrome and in children. Echocardiographic series have shown an up to 25% prevalence of small and asymptomatic pericardial effusions. Cardiac tamponade and constriction are rare.[123] [124] [133]

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Mixed Connective Tissue Disease Background Mixed connective tissue disease is an overlap syndrome with features of SLE, rheumatoid arthritis, scleroderma, and polymyositis. This disease is characterized by high titers of antibodies to nuclear ribonucleoprotein; patients also have speckled antinuclear antibodies and rheumatoid factor. Typical clinical features of this disease include Raynaud's phenomenon, hand edema, polyarthritis, sclerodactyly, interstitial pulmonary fibrosis, myositis, and esophageal hypomotility. Associated Cardiovascular Involvement Pulmonary Hypertension

Pulmonary hypertension is a frequent and prognostically grave complication of mixed connective tissue disease, occurring in as many as 80% of patients. It most frequently affects patients with disease features of scleroderma. Pulmonary fibrosis and proliferative vasculitis of the small and medium-sized pulmonary arteries have been described as causes.[134] [135] After the diagnosis of pulmonary hypertension is suspected, echocardiography is essential to the diagnosis and follow-up of these patients in a manner analogous to that described for other diseases (see Table 34-3) . Pericarditis

Pericardial disease is common, but most patients have asymptomatic, small pericardial effusions on echocardiography. Clinical pericarditis is uncommon. Nuclear ribonucleoprotein-immune complexes are found in the pericardial fluid.[136] [137] [138] [139] Valve and Myocardial Disease

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No data associating specific forms of valve disease with mixed connective disease have been reported. Myocarditis with left ventricular systolic dysfunction and heart failure has been rarely described.[140] [141] [142] Limited data on left ventricular diastolic function show abnormalities similar to those described for other connective tissue diseases.[143]

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Chapter 35 - Echocardiography in the Evaluation of Cardiac Disease Due to Endocrinopathies, Renal Disease, Obesity, and Nutritional Deficiencies Marcus F. Stoddard MD

A variety of endocrine disorders, renal diseases, nutritional deficiencies, and obesity may adversely alter cardiac function and structure and affect cardiovascular morbidity and mortality. These disorders may impair systolic and diastolic function, cause valvular regurgitation or stenosis, and lead to ventricular hypertrophy and dilation. Although the cardiac manifestations of these disorders are nonspecific, their detection may have clinical relevance and a significant impact on patient management. Echocardiography plays an important role in the timely detection of cardiac abnormalities from these diverse disease entities, particularly in asymptomatic patients. In addition, considerable concern has arisen over a possible link between the use of diet medications and valvular heart disease. As a result, echocardiography is increasingly being performed in virtually anyone who has used diet medications. Limited information exists on the natural history or treatment of diet medication-related valvular heart disease. If properly employed, however, echocardiography is likely to play an important role when anorexigen-induced valvulopathy is being considered.

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Endocrinopathies and Heart Disease Diabetic Heart Disease Systolic Dysfunction and Diabetes

The presence of a dilated cardiomyopathy specifically due to diabetes mellitus was first suggested by Rubler et 780

TABLE 35-1 -- Echocardiographic Findings in Diabetes Mellitus Diastolic Dysfunction ↓ Peak early filling velocity ↓ E/A ratio ↑ % Atrial contribution ↑ Pressure half-time

Structural Systolic Dysfunction Abnormalities ↑ LV pre-ejection Left ventricular period hypertrophy ↓ LV ejection time Left ventricular enlargement ↓ Shortening fraction Abnormal myocardial acoustics ↓ Velocity circumferential FS

↑ Isovolumetric relaxation time ↑ Rapid filling phase E/A, early to atrial velocity ratio; FS, fiber shortening; LV, left ventricular. al[1] in 1972. At postmortem examination, cardiac enlargement,

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hypertrophy, and fibrosis were seen in four adult diabetic patients with histories of congestive heart failure unexplained by coronary artery, hypertensive, valvular, or alcoholic heart disease. The existence of a diabetic dilated cardiomyopathy characterized by four-chamber enlargement and impaired systolic function was initially met with skepticism. Subsequent studies confirmed the existence of diabetic cardiomyopathy distinct from atherosclerotic or hypertensive heart disease. [2] [3] [4]

Systolic dysfunction in diabetic patients may consist of prolongation of the left ventricular pre-ejection period, shortened left ventricular ejection time, decreased ejection fraction and stroke volume, and increased left ventricular end-systolic volume.[5] [6] [7] The factors accounting for diabetic cardiomyopathy are unknown but may relate to diabetic microangiopathy of the coronary circulation, duration of diabetes, and type of diabetes.[8] [9] Diastolic Dysfunction and Diabetes

Several studies confirm an association between diabetes mellitus and diastolic dysfunction. Diastolic function is more likely to be impaired in diabetic patients with overt nephropathy, autonomic neuropathy, or retinopathy,[10] [11] [12] [13] but diastolic dysfunction may occur in diabetic patients with uncomplicated disease. [14] [15] [16] Compared with the impairment of systolic function, impairment of diastolic function appears to be an earlier sign of diabetic cardiomyopathy. In addition, diastolic dysfunction as determined by Doppler echocardiography may occur after only a few years of diabetes mellitus.[17] Diastolic dysfunction in diabetes may consist of impaired left ventricular relaxation, increased compliance, or both conditions. Myocardial hypertrophy, interstitial collagen accumulation, and fibrosis occur in diabetic cardiomyopathy and may partially account for increased compliance.[1] [18] Experiments implicate an abnormal reuptake of calcium into the sarcoplasmic reticulum in diabetes,[19] possibly accounting for impaired left ventricular relaxation. Diastolic dysfunction in diabetes may manifest as prolongation of the isovolumetric relaxation time, reduced early diastolic filling, and increased atrial contribution to diastolic filling.[20] [21] Importantly, left ventricular diastolic dysfunction determined by Doppler echocardiography in type II diabetic subjects adversely reduces maximal exercise capacity and tolerance.[22] [23] Echocardiographic Findings in Diabetes

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The structural and functional cardiac abnormalities that may occur in persons with diabetes mellitus have been well characterized by means of echocardiography (Table 35-1) . In diabetic persons, as compared with control subjects, pulsed Doppler echocardiography of mitral valve inflow has shown decreased peak early inflow velocity, decreased peak early to peak late filling velocity (E/A) ratio, increased pressure half-time, and increased atrial contribution to filling (Fig. 35-1) (Figure Not Available) .[14] [15] [16] [24] , Prolongation of the isovolumetric relaxation time in diabetic patients has been demonstrated using continuous wave Doppler echocardiography (Fig. 35-2) (Figure Not Available) .[16] These abnormalities most likely reflect impairment in left ventricular relaxation and Figure 35-1 (Figure Not Available) Individual values of peak atrial to peak early filling velocity (A/E) ratio of young insulin-dependent diabetic patients (D) without retinopathy, nephropathy, or coronary artery disease are compared with those of normal control subjects (C). Abnormal filling is common in these young diabetic patients despite lack of other end-organ disease. (From Paillole C, Dahan M, Paycha F, et al: Am J Cardiol 1989;64:1010–1016.)

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Figure 35-2 (Figure Not Available) Individual values of isovolumetric relaxation time (IRT) for diabetic (D) and control (C) subjects. IRT is frequently prolonged in diabetic patients despite lack of other end-organ disease. (From Paillole C, Dahan M, Paycha F, et al: Am J Cardiol 1989;64:1010–1016.)

occur in approximately 30% of asymptomatic young diabetic persons without ischemic, hypertensive, or valvular heart disease.[14] Abnormalities of diastolic filling can be further unmasked in diabetic patients with normal diastolic filling at rest by performance of isometric hand-grip exercise Doppler echocardiography. [25] Digitized M-mode echocardiography of the left ventricular wall in diastole have shown prolongation of the rapid filling phase in more than 50% of young insulin-dependent diabetic patients.[26] Several studies have demonstrated left ventricular systolic dysfunction in diabetic patients.[5] [6] [7] [10] [11] [12] [18] , [24] In diabetic patients with long-term, complicated disease, systolic time intervals are frequently abnormal and include prolongation of left ventricular pre-ejection period and shortening of ejection time.[5] [7] [10] [11] Shortening fraction derived by M-mode echocardiography may be decreased in diabetic patients with long-standing disease.[18] [24] In young asymptomatic diabetic patients, abnormalities of left

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ventricular shortening fraction and velocity of circumferential fiber shortening measured by M-mode echocardiography may become evident immediately after exercise.[27] Left ventricular hypertrophy is a feature of diabetes mellitus and can be assessed by M-mode and two-dimensional echocardiography.[18] [24] Abnormal myocardial acoustic properties characterized by a reduction in the cyclic variation of ultrasound-integrated backscatter can be detected in asymptomatic diabetic patients and may reflect early subclinical cardiomyopathic changes attributable to collagen deposition in the heart (Fig. 35-3) (Figure Not Available) .[28] Clinical Utility

Preventive cardiology depends on detection of disease in its earliest stages coupled with effective treatments. In persons with diabetes mellitus, echocardiography may be useful in the early detection of left ventricular diastolic dysfunction.[14] [15] [16] [17] [25] To appropriately apply Doppler echocardiography to assess left ventricular diastolic function, a comprehensive approach must be employed and attention to detail is needed (see Chapter 6) . Abnormal systolic function may be unmasked at an early stage in the disease by stress echocardiography[27] ( see Chapter 13 and Chapter 14 ). Importantly, systolic and diastolic dysfunction in diabetes mellitus may be reversible or preventable with glycemic control (Fig. 35-4) (Figure Not Available) .[20] [21] The clinical utility of echocardiography in myocardial tissue characterization in the diabetic patient awaits further study but appears promising.[28] Thyroid Disease and Heart Disease Systolic Function and Thyroid Disease

Impairment of left ventricular systolic function is a well-documented feature of chronic hypothyroidism.[29] [30] [31] [32] [33] [34] [35] Myocardial contractility is depressed by hypothyroidism, possibly because of alterations in contractile protein isoforms. This process may lead to the development of dilated cardiomyopathy and congestive heart failure.[32] Hyperthyroidism has a multifaceted effect on the cardiovascular system. Enhanced resting left ventricular contractile function is a consistent finding in hyperthyroidism.[34] [36] [37] [38] During exercise, however, selected subjects with hyperthyroidism display a paradoxical decline or blunted increase in left ventricular ejection fraction, stroke volume, heart rate, and cardiac

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output.[34] [36] [39] Kahaly et al[40] demonstrated impaired cardiopulmonary exercise capacity in patients with hyperthyroidism, which was reversible in the euthyroid state. In addition, hyperthyroidism is associated with cardiomegaly and congestive heart failure. Importantly, a striking reversal of congestive heart failure and dilated cardiomyopathy due to hyperthyroidism may occur after induction of a euthyroid state.[37] For example, Umpierrez et al[41] showed an increase in mean left ventricular ejection fraction from 28% before to 55% after becoming euthyroid in patients with hyperthyroidism. Diastolic Function and Thyroid Disease

Left ventricular diastolic dysfunction is an associated feature of hypothyroidism. M-mode and Doppler echocardiographic 782

Figure 35-3 (Figure Not Available) Comparison of myocardial acoustic properties from the left ventricular septum and posterior wall in control subjects and diabetic patients assessed by ultrasonic backscatter indexes (cyclic variation in dB and delay). Diabetic patients show an altered magnitude and delay of cyclic variation of backscatter consistent with a myopathic process despite the presence of normal ventricular size and function. ** P < .01 and * P < .05 versus control subjects; error bars are SD. (From Perez JE, McGill JB, Santiago JV, et al: J Am Coll Cardiol 1992; 19:1154–1162.)

indexes are consistent with impaired relaxation in hypothyroidism.[42] [43] Importantly, impaired relaxation may be reversed by thyroid hormone replacement.[42] [43] Left ventricular relaxation assessed by Doppler echocardiography is enhanced by hyperthyroidism,[44] [45] which may normalize after treatment induces a euthyroid state. Structural and Pericardial Disease

Pericardial effusion is a manifestation of hypothyroidism. The incidence of pericardial effusion in hypothyroidism varies with severity of disease and occurs in 30% to 80% of patients with advanced, severe disease[46] [47] [48] [49] and in 3% to 6% of patients with mild disease.[50] Cardiac tamponade due to pericardial effusion from hypothyroidism is rare.[51] Histologic studies have demonstrated myofibrillar swelling and interstitial edema and fibrosis in the cardiac tissue of patients with hypothyroidism. Asymmetric septal hypertrophy may occur as a feature of hypothyroidism but appears to be rare.[52] An association between Graves' disease and mitral valve prolapse

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has been reported. [53] [54] A prevalence as high as 16.5% of mitral valve prolapse in patients with Graves' disease has been found.[54] The basis for this association is unknown; however, recent studies suggest a possible autoimmune-mediated mechanism[55] or potential genetic linkage between Graves' hyperthyroidism and mitral valve prolapse. [56] Echocardiographic Findings in Thyroid Disease

M-mode, two-dimensional, and Doppler echocardiography have been used to demonstrate impaired left ventricular systolic function in patients with hypothyroidism (Table 35-2) . Several studies have shown prolongation of the pre-ejection period and reduction of the shortening fraction, ejection fraction, velocity of circumferential fiber shortening, and systolic ejection force.[29] [30] [31] [32] [33] [34] [35] Hyperthyroidism enhances cardiac sensitivity to beta agonists and augments resting left ventricular ejection fraction and rate, and velocity of circumferential fiber shortening, as assessed by twodimensional, Doppler, and M-mode echocardiography,[38] [39] respectively. However, stress echocardiography may demonstrate a blunted response in left ventricular ejection fraction, stroke volume, and cardiac output.[39] Impaired diastolic function of hypothyroid patients is manifested by prolongation in isovolumetric relaxation time and reduction in early diastolic posterior wall thinning rate.[42] These abnormalities can be assessed by Doppler and M-mode echocardiography. Enhanced diastolic function of hyperthyroidism is manifested by a shortening of isovolumetric relaxation time and deceleration time and an increase of early diastolic deceleration rate, as assessed by Doppler echocardiography.[44] Two-dimensional echocardiography is an excellent 783

Figure 35-4 (Figure Not Available) Individual and mean data values of peak atrial to peak early filling velocity (A/E) ratio in non-insulin-dependent diabetic patients before and 1 and 6 months after glycemic control by insulin treatment. A significant reduction in A/E ratio occurs during treatment, consistent with improved diastolic filling. (From Hiramatsu K, Ohara N, Shigematsu S, et al: Am J Cardiol 1992;70:1185–1189.)

technique to diagnose pericardial effusion in hypothyroidism. The diagnosis of hypothyroidism can be easily missed in some medical conditions such as Down's syndrome, and the finding of pericardial effusion by echocardiography may lead to the correct diagnosis of thyroid

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dysfunction (Fig. 35-5) . [57] Clinical Utility

The cardiac abnormalities seen in patients with hypothyroidism are potentially reversible. M-mode, two-dimensional, TABLE 35-2 -- Echocardiographic Findings in Thyroid Disease Hypothyroidism DIASTOLIC SYSTOLIC DYSFUNCTION DYSFUNCTION ↑ LV pre-ejection period ↑ Isovolumetric relaxation time ↓ Shortening fraction ↓ Posterior wall thinning rate ↓ LV ejection fraction ↓ Velocity circumferential FS Hyperthyroidism ENHANCED SYSTOLIC FUNCTION ↑ LV ejection rate

ENHANCED DIASTOLIC FUNCTION ↓ Isovolumetric relaxation time ↑ Velocity ↓ Early filling circumferential FS deceleration time ↑ LV ejection fraction ↑ Early filling deceleration rate FS, fiber shortening; LV, left ventricular.

STRUCTURAL ABNORMALITIES LV enlargement Pericardial effusion 30–80% (advanced disease) 3–6% (mild disease) STRUCTURAL ABNORMALITIES LV enlargement Mitral valve prolapse

and Doppler echocardiography are useful for detecting and assessing the severity of cardiac abnormalities associated with hypothyroidism. An accurate diagnosis of heart failure in the setting of hypothyroidism may be problematic because of nonspecific symptoms. Echocardiographic findings of cardiac dysfunction would support the diagnosis of heart failure and potentially affect the specific selection of medical therapy. Pericardial tamponade in hypothyroidism is difficult to recognize and easily confused with heart failure.[51] Both may present with dyspnea, tachycardia, jugular

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venous distention, enlarged cardiac silhouette, and peripheral edema. The diagnosis of cardiac tamponade is facilitated by the use of echocardiography. In patients with hyperthyroidism, attributing exercise limitations to primary cardiac disease may be challenging on the basis of resting cardiac function, which is typically enhanced. However, exercise echocardiography may be useful in unmasking a blunted improvement in systolic function with exercise and aid in treatment.[34] [36] , [39] Acromegalic Heart Disease Ventricular Hypertrophy and Acromegaly

Cardiovascular complications are a major cause of morbidity and mortality from acromegaly. Left ventricular hypertrophy occurs in many patients with acromegaly and contributes to the morbidity and mortality from this disease. [58] [59] [60] [61] [62] [63] The development of left ventricular hypertrophy in acromegaly is partially explained by the association of hypertension with this disease.[64] [65] However, left ventricular hypertrophy may occur in a significant proportion of acromegalic patients in the absence of hypertension. [58] [59] [60] [61] [62] [63] [64] [65] In addition, left ventricular mass has been shown to increase with short-term growth hormone hypersecretion [66] [67] and to regress after effective chronic pharmacologic therapy.[68] Pathologic studies on acromegalic hearts show extensive interstitial fibrosis. Ultrasonographic tissue characterization in uncomplicated acromegalic patients demonstrates an abnormal increase in echoreflectivity. [69] The type of left ventricular hypertrophy is typically concentric.[58] [59] , [61] Although asymmetric septal hypertrophy may develop in acromegaly, its reported prevalence 784

Figure 35-5 Transthoracic two-dimensional parasternal long-axis (A) and four-chamber (B) views demonstrating a large pericardial effusion (PE) with compression of the right ventricle (RV) and right atrium (RA) due to confirmed cardiac tamponade by invasive evaluation. This patient was a 26-year-old man with Down's syndrome who presented with dyspnea. Profound hypothyroidism was confirmed after the echocardiographic findings of pericardial effusion. LV, left ventricle; LA, left atrium.

among patients with this condition is highly variable.[58] [59] [60] [61] [62] Some studies have reported a rare association [58] [59] , [61] and others have described a frequent association[60] [62] between asymmetric septal hypertrophy and

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acromegaly. In addition to concentric wall thickening, left ventricular diastolic chamber enlargement develops in acromegaly and may occur in the absence of other associated diseases such as hypertension, coronary artery disease, and diabetes mellitus.[58] [59] [61] , [62] The reported incidence of an increased left ventricular mass in patients with acromegaly is 38% to 81%.[58] [59] [60] [61] [70] The development of right ventricular hypertrophy in persons with acromegaly has also been described.[71] Diastolic Dysfunction and Acromegaly

Given the frequent association of acromegaly with left ventricular hypertrophy, hypertension, premature coronary artery disease, and diabetes mellitus, it is not surprising that diastolic dysfunction often occurs in those with acromegaly [70] [71] [72] [73] (Table 35-3) . Prolongation of isovolumetric TABLE 35-3 -- Echocardiographic Findings in Acromegaly Structural Abnormalities Concentric LV hypertrophy (>50%) Asymmetric septal hypertrophy (variable frequency)

Diastolic Dysfunction (>50%) ↓ Peak early filling velocity ↓ E/A ratio ↑ Early filling deceleration time ↑ Isovolumetric relaxation time Abnormal SVC flow

LV enlargement Increased LV mass (38–81%) RV hypertrophy E/A, early to atrial velocity; LV, left ventricular; RV, right ventricular; SVC, superior vena cava. relaxation time and abnormal left ventricular diastolic filling, characterized by reduction of early filling and augmentation of atrial contribution to filling, occur in most acromegalic patients, even in the absence of hypertension, diabetes mellitus, or coronary artery disease.[70] [71] [72] , [74] Disease duration and increased left ventricular mass are important factors in the severity of impaired left ventricular filling.[72] Abnormalities of right ventricular filling similar to those of the left ventricle also occur.[67] [71] Systolic Function and Acromegaly

In the absence of long-standing, severe acromegaly complicated by

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hypertension, coronary artery disease, or diabetes mellitus, left ventricular systolic dysfunction in acromegalic patients appears uncommon.[58] [59] [60] [61] [62] [70] [71] , In patients with short-term acromegaly uncomplicated by hypertension, coronary artery disease, or diabetes mellitus, left ventricular systolic function, as assessed by shortening fraction, stroke volume, and cardiac output, typically is enhanced.[75] However, prolonged untreated acromegaly may lead to dilated cardiomyopathy and heart failure.[76] Acromegaly is characterized by excessive apoptosis of myocytes and nonmyocytes, which correlates with the extent of impairment in ejection fraction and disease duration, possibly explaining acromegalic cardiomyopathy. [76] Echocardiographic Findings in Acromegaly

Echocardiography is well suited to delineate the protean cardiac manifestations of acromegaly (see Table 35-3) . M-mode and twodimensional echocardiographic findings include concentric left ventricular hypertrophy,[58] [59] [61] , [67] [74] 785

septal hypertrophy that may simulate hypertrophic cardiomyopathy,[60] [62] right ventricular hypertrophy,[71] and left ventricular dilation.[58] [59] [61] [63] Pulsed Doppler echocardiography of transmitral valve velocities in these patients shows a reduction of peak early filling velocity and E/A ratio and an increase in peak atrial filling velocity and deceleration time of early filling.[67] [71] [72] , [74] Abnormalities of transtricuspid valve Doppler velocities similar to those of the mitral valve are a feature of acromegaly.[67] , [71] Isovolumetric relaxation time, assessed by Doppler echocardiography, is prolonged in acromegalic patients.[67] [71] [74] Pulsed Doppler echocardiography has shown abnormal superior vena caval flow, characterized by a decrease in peak forward diastolic velocity and an increase in peak flow velocity reversal during atrial contraction.[71] These findings are consistent with biventricular diastolic dysfunction, possibly reflecting impaired ventricular relaxation. Clinical Utility

Acromegaly frequently leads to heart disease, which may be asymptomatic. Clinical studies have demonstrated that suppression of growth hormone release by octreotide acetate, a long-acting somatostatin synthetic peptide analog, in acromegalic patients significantly reduces left ventricular

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hypertrophy and reduces abnormalities of isovolumetric relaxation time and left and right ventricular filling.[77] [78] The echocardiographic evaluation of cardiac size and function in patients with acromegaly is of value to assess ventricular hypertrophy and cardiac dysfunction. Prolongation of isovolumetric relaxation time is the most sensitive echocardiographic finding of cardiac involvement in acromegaly and may be useful in the evaluation in the subclinical stage of the disease.[74] Ventricular hypertrophy and dysfunction are important indicators for aggressive treatment to control growth hormone levels as a means of improving heart disease in patients with excessive growth hormone.[68] [75] [77] , [78] Hyperparathyroidism and Heart Disease Cardiac Calcification

The major cause of death in primary hyperparathyroidism patients is cardiovascular disease.[79] [80] [81] Hypercalcemia due to primary hyperparathyroidism may induce calcification of coronary arteries,[82] valves,[83] [84] [85] and myocardium.[83] [84] [85] [86] Aortic valve calcification occurs in 46% to 63% of primary hyperparathyroidism patients, and mitral valve or submitral annulus calcification has been reported in 33% to 49% of these patients.[83] [84] [85] Aortic and mitral stenosis may result from primary hyperparathyroidism.[83] [84] Myocardial calcific deposits have been reported in 62% to 74% of patients with primary hyperparathyroidism.[83] [84] [85] Myocardial calcification mainly involves the interventricular septum and may result in third-degree heart block.[83] [84] Structure and Function in Hyperparathyroidism

Left ventricular hypertrophy is a common feature of primary hyperparathyroidism and may be caused by an excessive serum concentration of parathyroid hormone or elevated extracellular calcium concentration.[84] [85] [86] [87] [88] Partial regression of left ventricular hypertrophy may occur 6 months to 1 year after parathyroidectomy in these patients.[84] [85] , [87] [88] Primary hyperparathyroidism is associated with hypercontractile function and may be a cause of hypertrophic cardiomyopathy.[86] A reduced transmitral valve E/A ratio by pulsed Doppler echocardiography has been reported in patients with primary hyperparathyroidism and suggests that left ventricular diastolic dysfunction may be a feature of this disease.[89] [90] Echocardiographic Findings in Hyperparathyroidism

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Two-dimensional echocardiography is useful for determining the extent of myocardial and valvular calcification in patients with primary hyperparathyroidism (Table 35-4) . The presence and severity of aortic or mitral stenosis can be assessed by Doppler echocardiography. M-mode and two-dimensional echocardiographic methods are useful for evaluation of possible hypertrophic cardiomyopathy.[86] Clinical Utility

Echocardiography helps identify left ventricular hypertrophy and valvular stenosis in patients with primary hyperparathyroidism. Parathyroidectomy may promote regression of myocardial hypertrophy.[84] Adrenal Diseases and Heart Disease Cushing's Syndrome and Echocardiographic Features

Cushing's syndrome is caused by excessive secretion of adrenocortical hormones. Left ventricular hypertrophy frequently occurs in patients with this syndrome and is partially attributable to associated hypertension. An echocardiographic TABLE 35-4 -- Echocardiographic Findings in Primary Hyperparathyroidism Structural Valvular Disease Abnormalities Aortic valve calcification Myocardial calcification (46–63%) (62–74%) Mitral valve/annulus LV hypertrophy calcification (33–49%) Asymmetric septal hypertrophy Aortic stenosis Mitral stenosis LV, left ventricular.

Enhanced Systolic Function ↑ LV ejection fraction

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study showed left ventricular hypertrophy and asymmetric septal

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hypertrophy in 75% of patients with Cushing's syndrome.[91] Asymmetric septal hypertrophy in this syndrome is common and severe, with interventricular septal thickness ranging from 1.6 to 3.2 cm and the ratio of septal to posterior wall thickness ranging from 1.33 to 2.67.[91] Primary Hyperaldosteronism and Echocardiographic Features

Left ventricular wall thickening without asymmetric septal hypertrophy is a feature of primary hyperaldosteronism.[91] , [92] Several investigators have reported concentric left ventricular hypertrophy in primary hyperaldosteronism,[93] [94] [95] evidence of diastolic dysfunction as reflected by reduced mitral valve peak early filling velocity and E/A ratio, and increased atrial contribution to filling.[94] [95] Clinical Utility

Regression of left ventricular hypertrophy in Cushing's syndrome after surgical treatment frequently occurs and may be dramatic.[91] Echocardiographic findings of severe left ventricular hypertrophy or hypertrophic cardiomyopathy without obvious cause should raise the clinical suspicion of glucocorticoid excess, possibly from Cushing's syndrome. Regression of left ventricular hypertrophy may occur after surgical excision of an aldosterone-producing tumor in patients with primary hyperaldosteronism.[95]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

End-Stage Renal Disease and Heart Disease Uremic Cardiomyopathy Congestive heart failure commonly occurs in patients with end-stage renal failure.[96] The pathogenesis of heart failure in uremic patients is complex and multifactorial and may include anemia, electrolyte and acid-base abnormalities, volume overload, hypertension, coronary artery disease, and uremic toxins. Although some studies have reported normal left ventricular function in patients with uremia,[97] [98] many support the presence of a specific uremic cardiomyopathy.[99] [100] [101] [102] [103] The features of uremic cardiomyopathy include cardiac enlargement, impaired left ventricular systolic function, and ventricular hypertrophy. In addition, after renal transplantation systolic function improves, left ventricular volume decreases, and left ventricular hypertrophy regresses, independent of blood pressure control.[104] Secondary hyperparathyroidism is a suspected cause of left ventricular systolic dysfunction due to uremia.[102] Structural and Valvular Heart Disease in Renal Disease Calcification of the myocardium, valves, or cardiac skeleton is found in most patients with end-stage renal disease and is caused by derangements in calcium and phosphorus metabolism.[105] [106] [107] [108] [109] Calcification of the aortic valve has been reported in 28% to 31% of patients with end-stage renal disease.[108] [109] Mitral annular calcification has been described in 10% to 36% of patients on dialysis. [107] [108] A recent study using transesophageal echocardiography with enhanced two-dimensional resolution has shown that calcification may also occur in "atypical" areas such as the base of both mitral leaflets and intervalvular fibrosa.[110] Aortic valve regurgitation is a feature of renal failure and is explained by valvular calcification[109] [111] it occurs in 13% of renal failure patients.[109] Mitral regurgitation may occur in 38% of renal failure patients and may be caused by mitral annular calcification or left ventricular dilation.[109]

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Tricuspid and pulmonic insufficiency occur with the same frequency as do mitral and aortic regurgitation, respectively, in patients with chronic renal failure.[109] [112] However, the mechanism of right-sided valvular regurgitation consists of increased pulmonary artery pressures from mitral regurgitation as opposed to valvular calcification.[109] , [113] Calcific aortic and mitral stenoses are important valvular abnormalities of renal failure. Occasionally, aortic and mitral stenoses may rapidly progress in patients with chronic renal failure, possibly because of associated secondary hyperparathyroidism.[114] Pericardial disease from renal failure may manifest as pericardial effusion, pericardial thickening, or cardiac tamponade.[106] Concentric left ventricular hypertrophy or asymmetric septal hypertrophy may be seen in renal failure patients with or without associated systemic hypertension.[115] [116] [117] [118] In renal failure patients with secondary hyperparathyroidism, eccentric left ventricular hypertrophy may occur, characterized by left ventricular dilation and normal wall thickness. [119]

Diastolic Function and Renal Disease Left ventricular diastolic dysfunction as assessed by Doppler echocardiography is associated with renal failure and may persist after renal transplantation. [120] [121] Echocardiographic Findings in Renal Disease Structural or valvular abnormalities of the heart detectable by echocardiography occur in most patients with end-stage renal disease and may include atrial or ventricular dilation; concentric hypertrophy; asymmetric septal hypertrophy; mitral annulus calcification; aortic and mitral valve calcification; myocardial calcification; aortic, mitral, tricuspid, and pulmonic valvular regurgitation; aortic and mitral valve stenosis; and pericardial effusion ( Fig. 35-6 and Fig. 35-7 , Table 35-5 ).[99] [100] [101] [102] [103] [105] [106] [107] [108] [109] [111] [112] [113] [114] [115] [116] [119] Despite the many echocardiographic features of end-stage renal disease, none are diagnostic of a specific structural or valvular abnormality or of cardiomyopathy due to renal failure. Hemodialysis is a commonly used treatment in patients with end-stage renal disease. An acute reduction in intravascular volume is associated with hemodialysis. It is not unanticipated that this treatment would significantly alter loading conditions. Left ventricular end-diastolic diameter derived by

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M-mode echocardiography may decrease on average by 4 mm after hemodialysis.[122] The decrease in left ventricular end-diastolic diameter after hemodialysis 787

Figure 35-6 Transthoracic two-dimensional parasternal long-axis view in a patient with chronic renal failure demonstrating associated mitral annular calcification (MAC), pericardial effusion (PE), a calcified aortic valve (arrow), and hypertrophy of the septal (SW) and posterior (PW) left ventricular walls.

results from a decrease in early filling without a compensatory increase in atrial contribution to filling, as assessed by transmitral valve Doppler echocardiography. [122] The influence of hemodialysis on systolic function, as assessed by M-mode or two-dimensional echocardiography, or both methods, is complex and may be influenced by dialysate composition,[123] dialysis-induced changes in serum Figure 35-7 Two-dimensional short-axis (A) and continuous wave (B) Doppler echocardiography of the mitral valve in a patient with chronic renal failure demonstrating mitral stenosis from encroachment upon the mitral orifice by mitral annular calcification (MAC). The planimetered mitral orifice area (A) was 2.77 cm2 , and the peak gradient by modified Bernoulli equation was 10 mm Hg. IW, inferoposterior wall; PE, pericardial effusion; SW, septal wall.

TABLE 35-5 -- Echocardiographic Findings in Renal Disease Structural Valvular Disease Abnormalities Aortic valve calcification Concentric LV (28–31%) hypertrophy Mitral annular calcification Eccentric LV hypertrophy (10–36%) Aortic regurgitation (13%) LV enlargement Mitral regurgitation (38%) Asymmetric septal hypertrophy

Systolic Dysfunction ↑ LV ejection fraction

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Aortic stenosis Mitral stenosis Tricuspid regurgitation Pulmonic insufficiency

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Atrial enlargement Pericardial effusion Pericardial thickening Myocardial calcification

LV, left ventricular. electrolytes,[124] left ventricular mass,[125] and previous treatment with a beta antagonist.[125] Systolic function after hemodialysis, as assessed by echocardiographically derived shortening fraction, left ventricular ejection fraction, velocity of circumferential fiber shortening, or ratio of fractional shortening to end-systolic stress, may be enhanced,[123] [124] [125] [126] depressed, [125] [126] or unchanged.[122] [123] [127] Doppler echocardiographic findings of diastolic dysfunction in patients with renal failure include reduced transmitral peak early filling velocity and E/A ratio and prolonged isovolumetric relaxation time.[120] [121] Ultrasonic backscatter of myocardium in renal failure is increased, reflecting cardiac calcification (Fig. 35-8) (Figure Not Available) .[128] Clinical Utility Echocardiography is a useful noninvasive method of evaluating patients with end-stage renal disease who present 788

Figure 35-8 (Figure Not Available) Illustration of ultrasonographic videodensitometric analysis of myocardium in end-stage renal disease. Left panels show digitized two-dimensional echocardiographic images of the left ventricle (parasternal long-axis view) of a control subject, a hypertensive patient, and a dialysis patient. The graph on right demonstrates variation in echocardiographic intensity in the region of interest placed at the posterior wall level during one cardiac cycle divided into 12 frames for the control (closed circle), hypertensive (open rectangle) and dialysis (closed triangle) groups. Time 0 is end-diastolic frame and time 4 is endsystolic frame. (From Di Bello V, Panichi V, Pedrinelli R, et al: Nephrol Dial Transplant 1999;14:2184–2191.)

with cardiovascular symptoms. An accurate diagnosis of the cause of congestive heart failure in renal failure patients on the basis of clinical assessment is challenging. Congestive heart failure in renal disease patients is frequently multifactorial and could be diagnosed on the basis of

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congestive cardiomyopathy, inadequate ventricular hypertrophy, valvular regurgitation, or stenosis. Pericardial effusion with secondary cardiac tamponade could simulate congestive heart failure. M-mode, twodimensional, and Doppler echocardiography are useful in the diagnosis of the many structural and valvular abnormalities that may cause heart failure in the renal failure patient. Echocardiography is useful for predicting survival in chronic dialysis patients.[129] Echocardiographic assessment of left ventricular size and function is a significantly better predictor of prognosis than clinical evaluation or electrocardiographic findings.[129] Patients on dialysis with abnormal left ventricular systolic function and dilated left ventricular cavities have a poor prognosis, with one study reporting a mean survival of 7.8 months in such patients.[129] A prospective study using serial echocardiography has shown that improvement in renal failure-related cardiac abnormalities (e.g., left ventricular hypertrophy and systolic dysfunction) 1 year after the patient starts dialysis is associated with an improved cardiac outcome over a mean follow-up period of 41 months.[130] Thus, serial echocardiography adds prognostic information beyond the initial study, a potentially important application of echocardiography in the evaluation of patients with end-stage renal disease. Systemic hypotension induced by hemodialysis is occasionally serious or life threatening. In patients with dialysis-induced hypotension refractory to conventional therapy, echocardiography helps assess potential causes of hypotension after dialysis, such as intravascular volume depletion, impaired systolic function, or a hyperdynamic state with secondary intraventricular obstruction. Patients with impaired early left ventricular filling and a short duration of early filling are at higher risk for hemodynamic instability during hemodialysis and may be identified prospectively by Doppler echocardiography.[131] In the preoperative evaluation for renal transplantation, echocardiography is useful for predicting patient and renal graft survival.[132] M-mode echocardiographically derived increased left ventricular end-systolic diameter (≥4.0 cm) and a decreased shortening fraction (<20%) are predictive of a reduced chance of patient survival (Fig. 35-9) (Figure Not Available) . [132] Decreased graft survival in renal transplant patients is predicted by elevated end-systolic diameter (Fig. 35-10) (Figure Not Available) .[132]

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Figure 35-9 (Figure Not Available) Survival curves for diabetic patients with immunohematologic and cardiac (i.e., left ventricular end-systolic diameter >4.0 cm, shortening fraction <20%, and/or coronary artery disease) risk factors. Echocardiographic parameters are useful for prediction of reduced patient survival. (From Weinrauch LA, Delia JA, Monaco AP, et al: Am J Med 1992;93:19–28.)

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Obesity and Heart Disease Systolic Function in Obesity Congestive heart failure is a frequent cause of death in morbidly overweight persons.[133] [134] Long-standing obesity is associated with preclinical and clinical left ventricular hypertrophy, dilation,[135] [136] [137] [138] [139] [140] and impaired systolic function.[138] [141] [142] [143] [144] [145] [146] These abnormalities of left ventricular structure and function may occur in the absence of hypertension or coronary artery disease. These findings are consistent with the notion of an obesity cardiomyopathy.[139] Obesity is accompanied by increases in circulatory blood volume and cardiac output, which are proportional Figure 35-10 (Figure Not Available) Survival curves of renal allografts in diabetic patients with immunohematologic and cardiac (i.e., elevated end-systolic diameter) risk factors. Echocardiographic elevated end-systolic diameter predicted decreased graft survival. (From Weinrauch LA, Delia JA, Monaco AP, et al: Am J Med 1992;93:19–28.) Figure 35-11 (Figure Not Available) Correlation of left ventricular (LV) mass versus change in LV ejection fraction (LVEF) during exercise (i.e., LV exercise response) in morbidly obese subjects. Increasing LV mass is associated with a decreasing LV exercise response. (From Alpert MA, Singh A, Terry BE, et al: Am J Cardiol 1989;63:1478–1482.)

to excess body weight.[140] [142] The high-output state of morbid obesity occurs primarily from increases in adipose tissue blood flow. Resting heart rate is minimally affected, but stroke volume is increased. Systolic function curves or indexes, such as the stroke work index to left ventricular enddiastolic pressure or pre-ejection period to left ventricular ejection time ratio, however, may be reduced in obese patients, consistent with depressed myocardial systolic function.[143] [145]

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Reduced left ventricular ejection fraction and attenuation of the normal increase in ejection fraction with exercise may occur in morbidly obese persons.[145] In such individuals, increased left ventricular mass is associated with an attenuation of the normal increase in left ventricular ejection fraction during exercise (Fig. 35-11) (Figure Not Available) .[145] Weight reduction in subjects with obesity is associated with improvement in systolic function.[138] [146] [147] [148] Diastolic Function in Obesity Abnormalities of left ventricular filling have been reported in asymptomatic, otherwise healthy obese persons.[149] [150] Prolongation of isovolumetric relaxation time occurs in obesity.[148] [151] These findings may be noted in the absence of systolic dysfunction and are consistent with left ventricular diastolic dysfunction. It is possible that impaired left ventricular relaxation, compliance, or both occur in obese patients because of the associated left ventricular hypertrophy. Weight reduction is associated with improvement in left ventricular diastolic filling and isovolumetric relaxation.[146] [147] [152] Structural Abnormalities in Obesity Compared with normal-weight control subjects with similar blood pressure, obese patients show an increase in 790

Figure 35-12 (Figure Not Available) Correlation of LV mass versus percentage over ideal body weight in morbidly obese subjects. Increasing severity of obesity is associated with greater LV mass. (From Alpert MA, Singh A, Terry BE, et al: Am J Cardiol 1989;63:1478–1482.)

left atrial diameter, aortic root diameter, left ventricular end-diastolic diameter, septal and posterior wall thickness, and left ventricular mass.[137] Obesity causes eccentric hypertrophy (i.e., left ventricular dilation and normal or mildly increased wall thickness). The eccentric hypertrophy in obesity is accounted for by chronic increased intravascular volume.[137] This partially explains the association between increasing left ventricular mass and severity of obesity (Fig. 35-12) (Figure Not Available) . [149] Inadequate hypertrophy of the left ventricular wall to normalize wall stress in the face of a dilated cavity occurs in some obese persons and may account for impaired myocardial systolic function.[139] Weight loss induces significant

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reductions in left ventricular end-diastolic diameter, end-systolic wall stress, and left ventricular mass.[149] [150] [153] , [154] Anorexigen Use, Valvulopathy, and Pulmonary Hypertension in Obesity Obesity is associated with serious cardiovascular health risks, such as heart disease, stroke, and systemic hypertension. Appetite-suppressant medications or anorexigens with diverse mechanisms of action are used in the treatment of obese subjects to promote weight reduction. Concerns have recently emerged, however, about the potential association of valvular heart disease and the use of specific anorexigens, which alter serotonin metabolism. Connolly et al[155] in 1997 reported 24 obese individuals with echocardiographic findings of pathologic mitral or aortic regurgitation who had been treated with fenfluramine and phentermine. Structural abnormalities by echocardiography in these cases included aortic or mitral leaflet thickening, diastolic doming of the anterior mitral leaflet and immobility of the posterior mitral leaflet, shortening and thickening of chordae tendineae, and retraction of aortic valve leaflets.[155] Furthermore, histopathologic findings available for three of these subjects included fibrotic endocardial changes of valve leaflets and chordae tendineae, which were indistinguishable from the features of carcinoid or ergotamine valvulopathy.[155] [156] Based on pooled data from five echocardiographic surveys, the Food and Drug Administration (FDA) reported an alarming prevalence of 33% of at least mild aortic or mitral regurgitation in subjects after the use of anorexigens, namely fenfluramine or dexfenfluramine with or without phentermine.[156] However, subsequent studies employing matched control subjects and blinding of echocardiographic interpretations have shown a considerably lower prevalence of aortic valvular regurgitation in association with the use of anorexigens when the FDA criteria were met.[158] [159] [160] Some studies[160] [161] have shown no association between anorexigen use and valvular heart disease, particularly when duration of treatment was less than 3 months. None of these studies have shown a specific association between moderate or severe mitral regurgitation and the use of diet medications.[161] [162] In addition, aortic or mitral valvular regurgitation that meets the FDA criteria when present appears not to progress and may regress in obese subjects after cessation of the use of fenfluramine or dexfenfluramine.[163] [164] [165] Ideally, quantitative measures, such as effective regurgitant area and flow rate by proximal isovelocity surface area, should

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be employed to assess regurgitation severity. A prospective epidemiologic study has shown a significantly greater risk for primary pulmonary hypertension in obese subjects treated with anorexigens as compared with control subjects.[166] The use of appetite suppressants, including dexfenfluramine or fenfluramine, for longer than 3 months showed an odds ratio of 23 (95% CI, 6.9–77) for primary pulmonary hypertension in obese individuals.[166] Echocardiography is a useful modality to estimate peak pulmonary artery systolic pressure and should play an important role in the noninvasive estimation of pulmonary artery pressure in obese subjects when pulmonary hypertension on the basis of anorexigen use is suspected. However, Weyman et al[167] have shown that peak pulmonary systolic pressure, estimated by echocardiography, is greater than 35 mm Hg in nearly one third of otherwise normal obese individuals. These data suggest caution when ascribing mild elevation of pulmonary artery systolic pressure to anorexigen use in obese subjects. Echocardiographic Findings in Obesity The M-mode and two-dimensional echocardiographic features of chronic obesity consist of aortic root, left atrial, and left ventricular enlargement and eccentric hypertrophy (Table 35-6) . [137] [150] Although stroke volume, as assessed by pulsed Doppler and two-dimensional echocardiography, is increased in obese persons, this change is accounted for by left ventricular dilation. [151] M-mode echocardiographically derived left ventricular shortening fraction and two-dimensionally determined ejection fraction may be reduced in morbid obesity (Fig. 35-13) .[138] [146] [147] [152] The Doppler echocardiographically derived pre-ejection period to left ventricular ejection time ratio is increased in obesity.[151] The pulsed Doppler-derived isovolumetric relaxation time may be prolonged in obesity.[148] [151] Transmitral valve Doppler indexes of diastolic filling may be abnormal for these patients and show decreased 791

TABLE 35-6 -- Echocardiographic Findings in Obesity Structural Abnormalities Systolic Dysfunction Diastolic Dysfunction Eccentric LV hypertrophy ↓ LV ejection ↑ Isovolumetric

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fraction relaxation time ↓ Shortening fraction ↓ E/A ratio

LV enlargement ↑ LV mass ↑ Left atrial size ↓ PEP/LVET ratio ↑ Aortic root diameter E/A, early to atrial velocity; LV, left ventricular; PEP/LVET, preejection to left ventricular ejection time. peak early filling velocity,[149] increased peak atrial filling velocity,[148] [149] reduced peak early to atrial filling velocity ratio,[146] [147] [148] [149] [150] increased atrial contribution to filling, [147] and reduced deceleration rate of early filling. [147] [148] [149] These findings may be more commonly seen if obesity is morbid, of long duration, and associated with eccentric hypertrophy (Fig. 35-14) (Figure Not Available) .[149] [150] [152] Clinical Utility The echocardiographic findings of obesity are nonspecific. However, echocardiography is useful in the assessment of obese patients with congestive heart failure. Appraisal of left ventricular systolic function, diastolic filling, chamber size, and hypertrophy may help guide medical therapy. Substantial weight reduction by the morbidly obese may improve left ventricular systolic function, decrease chamber size, and reduce left ventricular mass.[138] [147] [153] [154] Echocardiography may be of benefit in obese subjects with suspected aortic or mitral valvulopathy on the basis Figure 35-13 Transesophageal two-dimensional short-axis view of the left ventricle at the papillary muscle level in a patient with obesity cardiomyopathy. A, Eccentric hypertrophy. B, Reduced systolic function. The anterolateral wall was the best-contracting segment (arrows).

of anorexigen use. However, attempting to apply the FDA criteria for valvulopathy, which are based solely on the presence of at least mild aortic or mitral regurgitation, is simplistic and not clinically helpful. Isolated aortic or mitral regurgitation in the presence of an otherwise structurally normal valve as assessed by echocardiography may well be a normal

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variant. In addition, pre-existing conditions, such as rheumatic disease, prior to the use of anorexigens may also explain valvulopathy and should be considered. The presence of aortic or mitral valvular thickening unexplained by other causes in combination with at least mild aortic regurgitation or at least mild mitral regurgitation, respectively, should be present before a diagnosis of anorexigen-induced valvulopathy can be entertained. In addition, data from Weyman et al[167] suggest caution when attributing mild elevation of pulmonary artery systolic pressure as estimated by echocardiography to anorexigen use in obese subjects. Technical issues in the performance and interpretation of echocardiography in obese subjects are important. Body habitus in these patients may make acquisition of adequate transthoracic views challenging. Subcostal views complement standard approaches and should be employed. Transesophageal echocardiography should be considered whenever necessary to circumvent limitations of transthoracic echocardiography.

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Nutritional Deficiencies and Heart Disease Vitamin and Trace Element Deficiencies and Heart Disease Beriberi Heart Disease

Severe thiamine deficiency persisting for at least 3 months is the cause of a clinical syndrome called beriberi. Heart 792

Figure 35-14 (Figure Not Available) Correlation of left ventricular mass to height index (LVM/HT) with peak E and A wave velocities, E/A ratio, and E wave deceleration half-time. All indexes of diastolic function become increasingly impaired as LVM/HT increases. (From Alpert MA, Lambert CR, Boyd TE, et al: Am Heart J 1995;130:1068–1073.)

disease in beriberi patients is characterized by biventricular failure and marked edema[168] [169] [170] associated with a high cardiac output and arteriolar vasodilation. Right ventricular failure may predominate, but significant elevation of left ventricular end-diastolic and pulmonary capillary wedge pressures may occur. The disease has been virtually eliminated in the United States, but it can be seen in alcoholic persons who become thiamine deficient. The hemodynamic abnormalities are reversible with thiamine therapy but may not respond to inotropic agents or diuretics. The possibility of thiamine deficiency and beriberi heart disease should be considered in cases of refractory congestive heart failure presumed to result from alcoholic cardiomyopathy. Keshan Heart Disease

A dilated cardiomyopathy characterized by myocardial fibrosis and necrosis has been described in China.[171] Selenium and vitamin E deficiency may be important in the development of Keshan heart disease. Suspected cases of selenium deficiency and cardiomyopathy similar to this

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disease have been reported in the United States.[172] Keshan disease is preventable by selenium supplementation in the diet. Other Vitamin Deficiencies and Heart Disease

Vitamin C deficiency may cause scurvy and heart abnormalities. The manifestations of cardiac involvement in scurvy may include dyspnea, chest pain, sudden death, PR interval prolongation, and ST-segment abnormalities. The direct effects of vitamin A, vitamin D, or niacin deficiency on heart muscle in humans have not been established. Protein and Calorie Malnutrition Kwashiorkor and Heart Disease

Protein-calorie malnutrition leads to kwashiorkor. The heart disease seen in this condition is characterized by atrophy of cardiac muscle fibers, interstitial edema, vacuolization of myocardial fibers, and low-output congestive heart failure. Although the condition is rare in developed nations, it may contribute to heart disease in patients with chronic illnesses or anorexia nervosa. Echocardiography and Nutritional Deficiencies

Few studies of the echocardiographic features of heart disease due to nutritional deficiencies have been reported and the findings tend to be nonspecific. Echocardiographic features of beriberi cardiomyopathy or selenium deficiency cardiomyopathy include left ventricular enlargement and decreased indexes of systolic function (Table 35-7) . Left ventricular diameter and mass, as assessed by M-mode echocardiography, are decreased in protein-calorie malnutrition. Left ventricular systolic dysfunction is common in protein-calorie malnutrition and manifested by a decrease in shortening fraction, mean velocity of circumferential fiber shortening, systolic time interval, and cardiac index.[173] Clinical Utility

Nutritional deficiencies may adversely affect cardiac structure and function and increase cardiovascular morbidity 793

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TABLE 35-7 -- Echocardiographic Findings in Nutritional Deficiencies Beriberi Heart Disease (Thiamine Deficiency) LV enlargement ↓ LV ejection fraction RV enlargement

Keshan Heart Disease (Selenium Deficiency) LV enlargement ↓ LV ejection fraction

Kwashiorkor (ProteinCalorie Malnutrition) ↓ LV mass ↓ LV end-diastolic diameter

Segmental LV wall motion ↓ Shortening fraction abnormality ↓ Velocity circumferential fiber shortening ↓ Cardiac index LV, left ventricular; RV, right ventricular.

and mortality. Appropriate nutritional replacement may reverse cardiac abnormalities caused by nutritional deficiencies. Echocardiography may be useful for the noninvasive documentation of cardiac involvement when heart disease due to nutritional deficiency is suspected.

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797

Chapter 36 - Aging Changes Seen on Echocardiography Kiran B. Sagar MD Abraham C. Parail MD

Cardiovascular disease remains the leading cause of morbidity and mortality in the elderly, who represent the most rapidly growing demographic group in the United States. As their number and proportion of the population increase, knowledge about the normal morphologic and physiologic changes that accompany aging and the ability to discriminate between normal and pathologic states become increasingly important issues. This chapter delineates the echocardiographic changes associated with normal aging and disease and describes their roles in the diagnosis and management of cardiovascular disease in the older patient.

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Normal Changes in Cardiovascular Structure Left Ventricular Mass Several echocardiographic and necropsy studies, evaluating large numbers of healthy subjects without a history of systemic hypertension, cardiovascular, or valvular disease, have shown relatively mild increases in left ventricular (LV) wall thickness and cardiac mass concomitant with increasing age.[1] [2] [3] [4] [5] [6] [7] Despite a progressive hypertrophic increase in LV wall thickness starting in the third decade of life, however, aging does not produce wall thickness that exceeds the upper limit of normal (≤11 mm). The classic echocardiographic study of aging by Gerstenblith et al[2] used M-mode echocardiography in assessing 105 male, normotensive subjects ranging in age from 25 to 84 years. An age-related increase in LV wall thickness from 8.7 mm in men under 44 years of age to 10.7 mm in men over 65 was demonstrated. Similarly, Gardin et al[1] studied 136 adults (78 men and 58 women, 20 to 97 years of age) who showed no evidence of cardiovascular disease. When patients were stratified into six age groups, statistically significant (P < .01) and progressive changes were found, especially when the oldest group (>70 years) was compared with the youngest group (21–30 years). The mean septal thickness and LV free-wall thickness increased from 9.8 and 10.1 mm, respectively, in the youngest group to 11.8 mm (for both) in the oldest group, an increment of 20% and 18%, respectively. An estimated 15% increase in LV mass was observed; however, between these extremes in age, wall thickness showed only minimal changes, such that the mean values for septal and free-wall thickness increased by only 0.3 mm for each decade between the third and seventh decades. A study by Pearson et al[3] of 53 healthy normotensive subjects (21 men and 32 women, 25–75 years of age) demonstrated that posterior wall thickness

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(10 mm vs. 8 mm, P < .05) was significantly greater in elderly than in younger subjects. These results supported previous investigations. In each of these echocardiographic studies, LV end-diastolic and endsystolic cavity dimensions showed little or no changes with increasing age. The increases in LV mass associated with aging resulted largely from increases in wall thickness rather than cavity enlargement. The Cardiovascular Health Study,[6] involving a cohort of 5201 men and women over 65 years of age, investigated the effects of age, gender, hypertension, and coronary heart disease (CHD) on LV mass and systolic function in the elderly. LV mass adjusted for body weight increased modestly with age (P < .001), increasing less than 1 g/y for men and women. After adjusting for body weight, LV mass was significantly greater in men than in women, and greater in participants with clinical CHD compared with participants with neither CHD nor hypertension (P < .001).

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TABLE 36-1 -- Distribution of Mean Left Ventricular Mass, WeightAdjusted Left Ventricular Mass, and Blood Pressure Among Obese and Nonobese Participants by Disease Status

Parameter Nonobese Patients LV mass (g)

Neither Clinical Heart Disease nor Clinical CHD Hypertension Hypertension MEN WOMEN MEN WOMEN MEN WOMEN 188.2 135.6 P

Weight-adjusted LV mass 195.4 148.3 (g) Systolic BP (mm Hg) 132.7 138.7

165.7 131.0 P

156.7 116.4 P

P

P

172.7 139.6

161.1 120.2

P

146.0 145.2

121.0 119.2 P

Diastolic BP (mm Hg)

69.2 68.1

75.0 71.2

67.2 P 64.8 P

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Obese Patients LV mass (g) 197.6 160.0 198.8 152.9 172.6 132.2 Weight-adjusted LV mass 179.3 140.8 186.5 139.0 157.7 121.1 (g) Systolic BP (mm Hg) 134.7 138.8 144.4 143.4 124.2 120.7 Diastolic BP (mm Hg) 70.9 68.6 75.7 71.5 69.4 67.4 BP, blood pressure; CHD, coronary heart disease; LV, left ventricular. Adapted from Gardin JM, Siscovick D, Anton-Culver H: Circulation 1995;91:1739–1748. Reproduced with permission. Copyright 1995 American Heart Association. P < 0.001. P < 0.01. P < 0.05 for nonobese versus obese participants. All comparisons were performed separately for each age-disease group combination.

The weight-adjusted LV mass and blood pressure values for obese and nonobese participants are listed by disease status in Table 36-1 (see also Chapter 32) . Weight-adjusted LV mass was significantly higher for men (P < .001) and for subjects with CHD than for other groups. Participants with hypertension had significantly higher LV mass than those without hypertension or clinical CAD. LV mass increased with age (P < .001), but as seen in Figure 36-1 , after adjusting for weight, the age effect was small. The minimal effect of age in this study may reflect the highly truncated age range; no subjects were younger than 65 years. Gardin et al[6] developed reference equations for calculating the expected LV mass of men or women, in grams: LV mass (men) = 16.6 [weight (kg)]0.51 LV mass (women) = 13.9 [weight (kg)]0.51 If the ratio of observed-to-expected LV mass is between 0.69 and 1.47, the patient's LV mass should not be considered larger than expected for his or her body weight. Chamber Dimensions

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The influence of aging on LV cavity dimensions are shown in Table 36-2 and Figure 36-2 . There is a minor decrease or no change seen in LV internal dimensions with age. [1] A significant increase in the aortic root and left atrial dimensions occurs with age, specifically when the oldest group (>70 years) is compared with the youngest group (21–30 years).[1] [2] [3] [4] [8] Changes in aortic and left atrial dimensions are outlined in Figure 36-3 and Figure 36-4 and Table 363 . It is important to consider these age-related changes when taking echocardiographic measurements of the size of the left atrium to make quantitative statements about the effect of various diseases such as hypertension and coronary artery disease. Cardiac Valves Aging is associated with morphologic changes of the cardiac valves, most prominently on the aortic and mitral valves and is presumably related to increased ventricular systolic pressure.[7] [8] [9] [10] A review of necropsy data of 765 patients revealed that all indexed mean valve circumferences increased progressively throughout adult life, although this trend was greater for semilunar than for atrioventricular valves. The mean circumference of the aortic valve surpassed that of the pulmonic valve in the fourth decade and approached that of the mitral valve.[7] Krovetz[10] Figure 36-1 Bar graph shows weight-adjusted mean left ventricular (LV) mass displayed by sex (women on left, men on right for each age group) and disease status group across 5-year age intervals. Data are computed using the lower age end point and the mean weight for each age category (65–69, 70–74, 75–79, 80–84, 85+ years). Weight-adjusted LV mass was significantly associated with sex, disease status, and age. Of interest, within each age group the magnitude of the sex effect exceeded that of the effect of the disease (e.g., clinical coronary heart disease [CHD], hypertension [HTN]). (From Gardin JM, Siscovick D, Anton-Culver H: Circulation 1995;91:1739–1748.)

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TABLE 36-2 -- Mean Values of Echocardiographic Parameters for Three Age Groups Group I (25–

Group II

Group III

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Parameter Mitral valve E-F slope (mm/sec) Aortic root, diastole (mm) LV wall thickness (mm) Systolic Diastolic Systolic/m2 Diastolic/m2

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44 yr) 102.3 ± 3.7 (52) 30.9 ± 0.6 (45)

(45–64 yr) 79.0 ± 3.8 (35) * 32.0 ± 0.6 (34)

(65–84 yr) 67.1 ± 5.2 (18) † 32.9 ± 0.8 (17) ‡

15.4 ± 0.5 17.6 ± 0.7 18.8 ± 0.6 (33) (15) (12) * 8.7 ± 0.3 (33) 9.8 ± 0.5 (16) 10.7 ± 0.5 (13) * 7.6 ± 0.3 (33) 9.2 ± 0.3 (15) 10.0 ± 0.4 † (12) † 4.3 ± 0.1 (33) 5.0 ± 0.2 (16) 5.7 ± 0.2 (13) *

†§

LV dimension (mm) Systolic

34.4 ± 1.1 32.1 ± 0.89 32.1 ± 1.4 (37) (17) (11) Diastolic 51.8 ± 1.03 50.8 ± 1.3 51.2 ± 1.4 (37) (17) (11) 17.3 ± 0.5 16.7 ± 0.5 16.8 ± 0.6 Systolic/m2 (37) (17) (11) 26.0 ± 0.5 26.4 ± 0.6 27.0 ± 0.7 Diastolic/m2 (37) (17) (11) Fractional shortening of the 0.34 ± 0.01 0.36 ± 0.01 0.37 ± 0.02 minor semiaxis (37) (17) (11) VCF (circ/sec) 1.17 ± 0.04 1.23 ± 0.04 1.30 ± 0.08 (37) (17) (11) LV, left ventricular; VCF, velocity of circumferential fiber shortening. Adapted from Gerstenblith G, Frederiksen J, Yin FCP: Circulation 1977;56:273–277. * P < 0.01 as compared with group I. The number of subjects is given in parentheses next to the mean and standard error of the mean. † P < 0.001 as compared with group I. ‡ P < 0.05 as compared with group I. § P < 0.05 as compared with group II.

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reviewed published reports of aortic annulus size measured at autopsy. When corrected for body surface area, the aortic annulus size was found to increase with age in both men and women after 20 years of age.[10] Aging is also associated with thickening and calcification of the aortic and mitral valves. Calcific deposits are common in the bases of the aortic cusps, at the margins of closure on the atrial aspect of the mitral leaflets, and in the mitral valve annulus.[7] [8] [9] [10] [11] [12] [13] [14] [15] [16] Many elderly patients have calcific deposits in the aortic valve cusps, the mitral valve annulus, and the epicardial coronary arteries; this triad of calcific deposits is known as the "senile calcification syndrome."[8] Sahasakul et al[9] demonstrated that the mean thickness found at various sites of the aortic and mitral valves, as measured in 200 autopsy specimens, increased significantly (P < .001) with age. In subjects over 60 years of age, the valves were more than twice the thickness of those under 20 years.[9] Figure 36-2 Left ventricular (LV) end-diastolic and end-systolic dimensions in millimeters versus age in years. For each age group the mean and 95% prediction intervals for normal values are depicted. (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

Mitral annular calcification (MAC) is a degenerative process that increases with age and occurs more frequently in women than in men (Fig. 36-5) .[7] [8] In a prospective study of 976 unselected elderly persons in a long-term health care facility (mean age, 82 ± 8 years; range, 62–103 years), conducted with technically adequate M-mode and two-dimensional (2D) echocardiograms of the mitral valve, MAC was detected in 402 (57%) of 714 women and 124 (47%) of 262 men.[14] The prevalence of MAC with increasing age in elderly men and women is shown in Table 36-4 .[14] The amount of calcium may vary from a few spicules to a large mass located behind the posterior leaflet, often forming a ridge or ring that encircles the mitral valve. Calcification Figure 36-3 Aortic root dimension in late diastole is plotted in millimeters versus age in years. The mean value for each age group is depicted by a circle plotted at the mean age in the age group. The

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bracket and shaded area on either side of the circle represents the interval for normal values for a subject with a body surface area (BSA) of 1.8 m2 . The 95% prediction intervals are also shown for subjects with BSA values of 1.4 m2 (dotted lines) and 2.2 m2 (solid lines). (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

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Figure 36-4 Left atrial dimension in late diastole in millimeters versus age in years. For each age group the mean and 95% prediction intervals for normal values are depicted. (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

may interfere with normal cyclic changes in annular size and, in conjunction with mechanical stretching of the leaflets, can cause mitral regurgitation, which is usually mild.[16] [17] MAC may restrict leaflet motion, but actual calcification of leaflets and mitral stenosis is rare.[15] , [17] Although the annular calcium is covered with a layer of endothelium, ulceration of the lining can expose underlying calcific deposits, which may serve as a nidus for platelet aggregation and subsequent thromboembolism. [14] In patients with endocarditis associated with MAC, the avascular nature of the annulus predisposes to periannular and myocardial abscesses. Calcific deposits in the aortic valve are common in elderly persons and may lead to valvular aortic stenosis. In an autopsy series, calcific deposits on the aortic valves were found in 22 (55%) of 40 patients between 90 and 103 years of age.[18] In a prospective 2D echocardiographic study of subjects 62 years and older, a calcified aortic valve was detected in 22 (18%) of 119 men and 67 (19%) of 354 women.[19] Calcific aortic stenosis was observed in 12% of the elderly; it was mild in 10% (Doppler-derived peak gradient < 25 mm Hg), moderate in 6% (peak gradient 20 to 49 mm Hg), and severe in 2% (peak Doppler gradient > 30 mm TABLE 36-3 -- Data Describing the Left Ventricular Outflow Tract and Aortic Valve in Different Age Groups Age Group (yr)

55–71

75–76

80–81

85–86

P Value

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Parameter (n=76) (n=197) (n=155) (n=124) Left ventricular 19.9±2.3 † 18.5±2.6 17.9±2.7 17.8±3.0 outflow tract diameter (mm) Peak velocity in left 101±17 90±19 90±20 93±25 ventricular outflow tract (cm/sec) Peak velocity across 126±27 127±53 131±53 143±55 aortic valve (cm/sec) 0.82±0.11 0.76±0.19 0.75±0.20 0.71±0.21 Velocity ratio ‡ 2.56±0.63 2.07±0.72 1.91±0.74 1.77±0.75 Aortic valve area (cm2 ) Adapted from Lindroos M, Kupari M, Heikkila J, et al: J Am Coll Cardiol 1993;21:1220–1224.

*

0.000

0.000

0.002 0.001 0.000

* Significance (P) values refer to comparison between age groups with the KruskalWallis test. † Data are presented as mean value±standard deviation. ‡ Velocity ratio is equal to the peak velocity in the left ventricular outflow tract divided by the peak velocity across the aortic valve.

Hg). The frequency of aortic stenosis increases with age. Lindroos et al[20] reported the prevalence of aortic valve abnormalities detected by echocardiography in 552 older subjects. Mild calcification was found in 40% and severe calcification in 13% of subjects. Critical aortic stenosis (aortic valve area < 0.8 cm2 ) existed in 2.2%, and aortic regurgitation, mostly mild, was found in 29% of subjects. LV outflow and aortic flow velocities also change with age (see Table 363) . There is a statistically significant decrease in LV outflow tract diameter and velocity while aortic valve area also decreases with age. In contrast, aortic velocity increases with age.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Normal Changes in Left Ventricular Function Systolic Function Previous studies evaluating age-associated changes in cardiovascular function have demonstrated that resting LV systolic function is maintained with advancing age.[21] [22] [23] [24] [25] Noninvasive investigations using Mmode echocardiography in healthy elderly subjects screened for cardiovascular disease have consistently revealed that LV ejection fraction, percentage of fractional shortening, and cardiac output are preserved with aging. [21] [23] Animal model studies indicate that contractile function is maintained with aging. Lakatta et al[22] demonstrated in isolated rat papillary muscle that resting tension, peak active isometric tension, and maximal rate of tension development were similar in young and senescent cardiac muscle. Similarly, Yin et al[23] showed that contractile function in the intact dog heart is not altered with age. LV systolic function has also been evaluated by Doppler aortic-flow velocity parameters. Gardin et al[24] studied the relationship between age and Doppler aortic-flow velocity measurements in 97 healthy adults (45 men and 52 women, 21 to 78 years of age) who were carefully screened for cardiac disease by history, cardiac examination, electrocardiography, chest radiography, and M-mode and 2D echocardiography. Multiple linear regression analysis showed that the aortic peak flow velocity, aortic average acceleration, and aortic flow velocity integral were all significantly lower in subjects 61 to 70 years of age than in those 21 to 30 years of age (all P < .001). This 801

TABLE 36-4 -- Prevalence of Mitral Annular Calcification

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Age (yr) Men Women 7/35 (20) * 62–70 4/22 (18) * 71–80 13/42 (31) 40/116 (34) 81–90 44/75 (59) 146/226 (65) 91–100 19/22 (86) 56/63 (89) 101–103 3/3 (100) Adapted from Aronow WS, Koenigsberg M, Kronzon J, et al: Am J Cardiol 1987;59:181–182. * Number affected per total number, with the percentage affected given within parentheses.

study concluded that the age-related decrease in aortic peak velocity and aortic flow velocity integral resulted partly from the increases in aortic root diameter that occurred with aging. Pearson et al[3] demonstrated similar results in a study involving 53 healthy subjects. These observations are relevant to differentiating the normal aging heart from certain pathologic states. For example, patients with dilated cardiomyopathy have markedly reduced aortic peak flow velocities, flow velocity integrals, and average acceleration parameters compared with normal subjects.[25] These age-dependent changes must be kept in mind when using Doppler aortic flow parameters in evaluating LV performance. Diastolic Function Unlike the preserved systolic function, age-related alterations in LV diastolic function have been demonstrated in the healthy elderly population. [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] Earlier investigators using Mmode echocardiography revealed a decrease in the E–F slope (closing velocity of the mitral valve) and E/A ratio (ratio of early-to-late diastolic flow velocity).[34] Later studies using Doppler echocardiography showed that aging is associated with changes in mitral Doppler flow velocity.[35] [36] [37] [38] There is a progressive increase in end-diastolic transmitral flow velocity (A) and a decrease in the E/A ratio. Gardin et al[34] studied the relationship between age and pulsed Doppler transmitral flow velocity measurements in 66 adults between 21 and 78

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years of age who were without evidence of cardiovascular disease. These researchers demonstrated that aging is associated with progressive decreases in early diastolic transmitral peak flow velocity (E) and early diastolic deceleration. They detected progressive increases in A and mitral A/E (Fig. 36-6) . These findings concur with a study by Miyatake et al,[35] which reported that the ratio of peak velocity in the atrial contraction phase to the peak velocity in the rapid filling phase showed a significant increase with aging (r = 0.82, P < .001). Pearson et al[3] reported a doubling of the percentage of atrial contribution (37% vs. 19%, P < .0001) and a halving of ratio of peak early to peak atrial (E/A) velocity (0.85 vs. 1.77, P < .01), which was similar to the atrial contribution found by Arora et al[33] with the use of radionuclide angiography (36% for a mean age of 75 years; 16% for a mean age of 26 years). The preponderance of data demonstrates that normal aging is associated with alterations in LV diastolic performance: an age-related decline in early diastolic LV filling, with a compensatory, increased contribution of atrial systole to maintain adequate resting ventricular filling volume. Because congestive heart failure increases in prevalence with age and an estimated 40% of adult patients with cardiac failure have symptoms resulting from diastolic LV dysfunction, it is essential to define and detect LV diastolic dysfunction in order to provide appropriate therapy (see Chapter 6) . The availability of reference Doppler diastolic indices may provide an alternative modality for the identification of LV dysfunction in the elderly. Using the original Framingham Figure 36-5 Mitral annular calcification in left parenteral long-axis (top) and short-axis (bottom) views. Ao, aortic root; LA, left atrium; LV, left ventricle; MAC, mitral annular calcification.

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Figure 36-6 Doppler mitral flow velocity recordings from a young 32-yearold normal subject (top) and an older 82-year-old normal subject (bottom). The peak velocity in early diastole (E) is lower and the late diastolic velocity (A) is higher in the older subject than in the younger subject.

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Heart Study population, Sagie et al[39] established reference values for various Doppler parameters (Table 36-5) based on a large cohort of rigorously defined healthy subjects (26 men and 88 women between 70 and 87 years of age). This study demonstrated that TABLE 36-5 -- Mean and Percentile Values of Doppler Diastolic Filling Indices for 114 Study Subjects Over 70 Years of Age Lower Median Upper Percentiles Percentiles Percentiles Diastolic Indices Mean 5% 10% 50% 75% 90% 95% E-velocity (m/sec) 0.44 0.25 0.26 0.41 0.51 0.69 0.76 A-velocity (m/sec) 0.59 0.38 0.43 0.56 0.68 0.80 0.84 E/A (ratio) 0.76 0.48 0.52 0.70 0.86 1.05 1.21 E/A TV1 (ratio) 1.36 0.79 0.90 1.33 1.57 1.76 1.94 AFF (ratio) 0.40 0.29 0.32 0.40 0.44 0.49 0.52 AT (sec) 0.06 0.02 0.03 0.05 0.07 0.08 0.09 DT (sec) 0.14 0.09 0.10 0.14 0.16 0.19 0.23 AFF, atrial filling fraction; AT, acceleration time; DT, deceleration time; A-velocity, peak velocity A; E-velocity, peak velocity E; E/A, ratio of early-to-late peak velocities; E/A TV1, ratio of early-to-late timevelocity integrals. Modified from Sagie A, Benjamin EJ, Golderisi M, et al: J Am Soc Echocardiogr 1993;6:570–576. 87% of the elderly population had peak velocity E/A ratios of less than 1.0, 75% had values less than 0.86, and 25% had values less than 0.62. Because healthy, younger subjects frequently have peak velocity E/A ratios greater than 1.0, it may be inappropriate to apply reference values based on younger subjects to elderly populations for assessment of diastolic LV dysfunction. The exact mechanisms responsible for these age-related diastolic alterations are not fully known, but multiple factors have been postulated. Normal physiologic and morphologic changes of aging that could contribute to the decreased early diastolic filling include prolonged isovolumic relaxation secondary to delayed calcium uptake by the sarcoplasmic reticulum; increased ventricular stiffness from quantitative and qualitative changes in the myocardial collagen and fibrous tissue content; sclerosis of the mitral

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leaflets with subsequently prolonged diastolic closure time; and an increase in LV wall thickness, and an increase in afterload. As the elderly population increases, recognition of the normal ageassociated changes in cardiovascular structure and function becomes imperative for assessing cardiac disease in the elderly. Aging changes seen in the normal older population are summarized in Table 36-6 . Response to Stress and Exercise Exercise capacity declines with age because of a blunted heart rate response to the stress.[21] The stroke volume and cardiac output, however, are maintained because of a larger increase in LV end-diastolic volume and a decrease in end-systolic volume during exercise.[21] [40]

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Clinical Value of Echocardiography in the Older Population Left Ventricular Hypertrophy Data from the Framingham study indicate that LV hypertrophy determined from M-mode echocardiographic mass is an independent predictor of mortality and morbidity from coronary heart disease and stroke.[41] [42] [43] Since echocardiographic LV mass is the gold standard for diagnosing LV hypertrophy, it is important to define 803

TABLE 36-6 -- Summary of Aging Changes Seen on Echocardiography Parameter Left ventricular mass Left ventricular dimensions Left atrial size Aortic root size Left ventricular systolic function Left ventricular diastolic function (E/A) Mitral annular calcification Aortic valve calcification or stenosis ↑, increase; ↓, decrease.

Change ↑ Normal ↑ ↑ Normal ↓ ↑ ↑

normal limits for age, body weight, and gender, according to criteria established by Gardin et al.[6] Inter- and intraobserver variability in the measurement of LV mass should be defined for each echocardiographic laboratory.

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Congestive Heart Failure Heart failure is a common problem in the elderly. Many elderly persons with heart failure have normal or only slightly reduced LV systolic function. [44] Proper definition and accurate detection of LV diastolic dysfunction are needed to provide appropriate treatment for patients with congestive heart failure. Because Doppler echocardiography is commonly used to assess LV diastolic dysfunction, it is important to know the reference values for Doppler indices of diastolic function in the elderly. The reference values established by Sagie et al[39] should be used. In the Cardiovascular Health Study, Gardin et al[45] examined patterns of LV diastolic filling in several subgroups of elderly subjects. As demonstrated in other studies, peak early velocity on transmitral Doppler examination decreased, peak late velocity increased, and the early-to-late velocity ratio decreased with advancing age and hypertension. In multivariate analyses, congestive heart failure caused by LV systolic dysfunction was associated with an increase in early and late diastolic velocities as well as an increase in the early-to-late velocity ratio compared with age-matched normal subjects. This difference is likely related to an increase in early left atrial-to-LV pressure difference.[45] Diagnosis of Coronary Artery Disease LV segmental wall motion abnormalities indicating coronary artery disease are as accurate in the elderly as they are in younger patients. Wall motion abnormalities affect a high percentage of the older population, including almost 2% of those without overt coronary disease, 43% of patients with hypertension alone, and 18% of patients with coronary disease who are living in the community.[6] Because this prevalence of coronary artery disease is high among older women, the prevalence of wall motion abnormalities is also high. Stress echocardiography is safe and accurate for diagnosis of ischemic disease in the elderly ( see also Chapter 13 and Chapter 14 ). In a preliminary study of 93 patients over 65 years of age (mean, 72 years), including 34 patients with acute myocardial infarction, dobutamine-stress echocardiography (DSE) was performed without any complication; it had a sensitivity of 85% and a specificity of 94%. The peak dose of dobutamine was not significantly different from that administered in patients younger than 61 years (authors' unpublished data, 2001). Hiro et al,[46] in a study that examined results and safety of DSE in the elderly, found no significant

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difference in the prevalence of positivity between age groups but found more frequent asymptomatic hypotension and ventricular arrhythmias in subjects older than age 75 years. Valvular Heart Disease There is a high prevalence of aortic valve disease among the elderly. [47] [48] In 35 patients with ejection systolic murmur, nonsignificant aortic stenosis (peak gradient < 20 mm Hg) was found in seven, significant aortic stenosis (peak gradient > 30 mm Hg) in seven, and mitral regurgitation in seven.[44] Aronow and Kronzon[48] reported the prevalence of aortic stenosis to be 12% for 721 patients with a mean age of 82 ± 8 years. Severe aortic stenosis affected 2%, moderate aortic stenosis affected 6%, and mild stenosis affected 2% of these patients.[48] Otto and Pearlman[49] demonstrated that Doppler echocardiography was cost-effective for the diagnosis of aortic stenosis in the elderly. The incidence of mitral valve prolapse and MAC also is higher in this group of patients. Mitral valve prolapse is a common cause of isolated mitral regurgitation in the elderly.[4] Previous analyses have shown that aortic valvular stenosis is associated with adverse cardiovascular outcomes. The echocardiographic diagnosis of aortic sclerosis, in the absence of hemodynamically significant valvular obstruction, has also been found to be associated with significant cardiovascular morbidity and mortality. Otto et al[50] found an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The clinical factors associated with degenerative calcific aortic valve disease are also similar to the risk factors for atherosclerosis; factors include advanced age, male gender, present smoking, and hypertension.[51] Thromboembolism Cardiogenic embolism is the presumed cause of ischemic strokes in 20% of patients. Potential cardiac sources of emboli more specific to the elderly are arteriolosclerotic intra-aortic debris and MAC. Both of these represent arteriolosclerosis, which is more prevalent in the elderly. In the previously cited analysis by Otto that examined the association of aortic valve sclerosis with cardiovascular mortality and morbidity, the risk of stroke, when adjusted for age and gender, was increased by 30%.[50] The rates of other cardiogenic embolic phenomena such as those associated with LV

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thrombus, left atrial thrombus, vegetation, atrial myxoma, and paradoxical emboli, are the same as for younger subjects. Amyloidosis

804

Senile amyloidosis is a frequent postmortem finding in patients over 80 years of age. It is an infrequent cause of heart failure and syncope. Echocardiographic criteria for the diagnosis of amyloidosis include increased myocardial echogenicity and wall thickness, myocardial speckle, increased atrial septal thickness, and thickened valves (see Chapter 28) . These criteria however, have not been validated in the elderly, who may have thickened valves due to aging, and the characteristics of amyloid protein are different from those of the primary amyloidoses.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Cost-Effectiveness of Echocardiography Echocardiography is cost-effective compared with other noninvasive and invasive imaging techniques. Otto and Pearlman[49] developed a noninvasive diagnostic approach and tested it prospectively in 77 patients with symptomatic aortic stenosis. They reported a sensitivity of 98%, a specificity of 89%, and a total error rate of 3.9%. They concluded that this approach could have resulted in cost savings between 24% and 34% compared with an invasive diagnostic approach. Although their study did not specifically target the older population, presumably a similar diagnostic approach could be applied to the elderly. Although LV function, pericardial disease, and coronary disease can be evaluated with other noninvasive imaging techniques such as nuclear imaging and magnetic resonance imaging, echocardiography is the least expensive. No data are available to determine the cost-benefit ratio and outcome analysis of echocardiography in the elderly population. Echocardiography, however, appears to be cost effective in the elderly because a correct diagnosis allows optimizing therapy and enhancing clinical decision making. Echocardiography differentiates normal aging changes from pathologic changes. Additional studies are needed to define changes in the right ventricle and to assess the impact of echocardiography on the management of elderly patients.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

806

Chapter 37 - Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Edmond W. Chen MD Rita F. Redberg MD

Cerebrovascular Ischemia Stroke, a sudden development of a focal neurologic deficit, remains the third leading cause of death in the United States. There were 600,000 strokes that resulted in 280,000 deaths and over 1 million hospitalizations, in 1997 alone. [1] With 4.4 million survivors today, the medical and social costs are estimated to range between $15 and $30 billion annually.[2] Five percent to 13% of strokes occur in patients younger than 45 years of age[3] up to 40% of strokes occur in patients without occlusive cerebrovascular disease; and it is estimated that the source is of cardiac origin in 15% to 20%.[4] Another 30% to 40% (100,000 to 200,000 per year) are in the category of stroke of undetermined cause, also known as cryptogenic stroke. [5] [6] An increasing number of echocardiographic findings have been found in this group of cryptogenic stroke patients and in patients with embolic stroke (Table 37-1) . Cardiac tumors can be a source of emboli, but the most commonly implicated sources are thrombi from the left atrial appendage or left ventricle, left atrial spontaneous contrast, atrial septal aneurysm associated with a patent foramen ovale (PFO), thrombi traversing a PFO (i.e.,

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paradoxical emboli), valve vegetations (infected or sterile), fibrinous mitral valve strands, protruding aortic atheroma of the aortic arch and ascending aorta, and emboli associated with mitral and aortic prostheses. Echocardiography is most helpful in defining the cause of cerebrovascular ischemia in patients without occlusive cerebrovascular disease. This chapter discusses indications for, clinical value of, and the limitations of transthoracic, transesophageal, and contrast echocardiography in this setting; particular emphasis is placed on the utility and insights provided by transesophageal echocardiography (TEE) in cases of stroke and the impact of echocardiography on patient management.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transthoracic Echocardiography Indications As with other diseases, the work-up for an embolic event includes taking the patient's history, performing a TABLE 37-1 -- Stroke Occurrence by Type Type of Stroke Atherosclerotic thrombosis Lacunae Embolism Hemorrhage Vascular Indeterminate

Occurrence (%) 20 5–10 20 10–20 5 35–40

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physical examination, and obtaining an electrocardiogram (ECG), often followed by a carotid duplex ultrasound. If significant carotid stenosis is identified, some centers proceed with magnetic resonance angiography, with or without cerebral angiography and endarterectomy. In the search for a cardiac source of emboli, the history and physical examination can be helpful in deciding which patients should undergo an echocardiogram. In the group without occlusive cerebrovascular disease, findings in the history, such as myocardial infarction, congestive heart failure, rheumatic heart disease, prosthetic valve replacement, or atrial fibrillation or flutter, become more conclusive when combined with findings from an echocardiographic examination for the source of embolus.

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[7]

Similarly, the yield of data is augmented if there are findings in the physical examination that suggest left ventricular dyskinesia, cardiac enlargement, left-sided valvular regurgitation, mitral stenosis, or a midsystolic or late systolic click. An ECG examination showing features of atrial fibrillation, transmural myocardial infarction, or left atrial enlargement increases the probability for a cardiac source of emboli. If there is no evidence of cardiac disease indicated by the history, physical examination, or ECG, the yield of findings from a transthoracic echocardiogram (TTE) for the identification of a source of lesions usually is less than 1%.[7] [8] [9] [10] [11] A pooled analysis of 13 studies found that TTE yielded a source incidence of 0.7% in patients with no cardiac history; in patients with clinical cardiac abnormalities, the yield increased to 13%.[12] In a review of 280 patients between 19 and 96 years of age who underwent TTE for assessing suspected systemic emboli, Come et al[7] found a 35% incidence of abnormalities that might have predisposed patients to systemic embolism and a 4% incidence of lesions that were possibly or probably responsible for emboli. If patients were classified according to clinically evident cardiovascular disease, the incidence of findings in the group with cardiovascular disease was 47% TABLE 37-2 -- Echocardiographic Evaluation of Cardiac Source of Embolus

Left ventricular thrombus Vegetation, mitral or aortic (>10 mm) Myxoma

H&P Factors that Increase the Likelihood of this Finding Mitral valve disease, atrial fibrillation CAD, history of myocardial infarction Fever, weight loss, changing murmurs Systemic symptoms

Possible Source of Embolus Patent foramen ovale

No specific

Probable Source of Embolus Left atrial thrombus

Atrial septal aneurysm No specific

Best Age Diagnostic Group Test Any TEE age >50 yr TTE Any age Any age

TEE (preferred)/TTE TTE/TEE

<55 yr TTE with contrast <55 yr TEE

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Left atrial size >4.0 cm Aortic atheroma Prostheses, mitral or aortic Rheumatic mitral valve disease Mitral annular calcification Atrial septal defect

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Mitral value disease, decreased LV compliance CAD, advanced age Varied History of rheumatic fever Advanced age

Any age >60 yr Any age Any age >55 yr

TTE TEE TEE TTE TTE

No specific or decreased exercise tolerance No specific

<40 yr TEE (preferred)/TTE Any TEE Fibrinous valve strands age Mitral valve prolapse Atypical CP, early Any TTE systolic murmur age Vegetation (<10 mm) Fever Any TEE age (preferred)/TTE LV aneurysm CAD >50 yr TTE Dilated Fatigue, reduced exercise Any TTE cardiomyopathy tolerance age H&P, history and physical; CAD, coronary artery disease; CP, chest pain; LV, left ventricular; TTE, transthoracic echocardiography; TEE, transesophageal echocardiography. for abnormalities that might have predisposed to systemic embolism and 4% for lesions possibly or probably responsible for emboli. In the group without cardiovascular disease, the rates were 14% and 0%, respectively. In another study of 138 patients with one or more recent episodes of focal cerebral ischemia, in whom a cardiac mechanism was suspected or no probable mechanism of ischemia was identified, intracardiac thrombus was found in 9 patients (6.5%); 32 patients (23.2%) had other cardiac disorders, possibly related to the ischemic event; and the remaining 97 patients (70.3%) had study results that were normal or added nothing to the clinical findings. Two-dimensional (2D) echocardiography was of limited value in assessing patients with no clinical cardiac disease or hypertension only; it was more valuable for patients known to have cardiac disease, especially

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atrial fibrillation.[9] Routine echocardiography can be considered in the evaluation of patients suspected of cerebral embolism, although the yield is low.[12] [13] Transthoracic echocardiography, in particular, is not recommended for patients in whom there are no findings suggesting cardiac disease. However, some experts consider echocardiography to be indicated for patients younger than 45 to 55 years of age who have experienced an embolic event.[14] This may be because younger patients are less likely to have extracardiac causes of embolus, which are usually associated with the degenerative process of aging. Many of the findings associated with cerebrovascular ischemia in this age group, such as PFO, spontaneous echocardiographic contrast (SEC), and atrial septal aneurysm, are best seen by TEE. However, the utility of TEE has not been established, and it is not clear that any of these findings are actually a cause of embolism or whether these findings mandate specific treatment (Table 37-2) . For older patients (>65 years), a growing body of data implicates atheromas in the aorta as a source of embolic events, which may increase the yield of TEE findings in this group as well. Findings and Techniques Left Atrial Size

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Transthoracic echocardiography is an excellent method to evaluate left atrial size. The left atrial diameter can be measured in the parasternal longaxis and short-axis views by M-mode or directly from the 2D image (online or offline), using commercially available measurement packages. Normally, the left atrial diameter is less than 4.0 cm. Measurements of left atrial diameter should be made at end-systole, from leading edge to leading edge. M-mode echocardiography has been shown to predict angiographic left atrial area,[15] but it has limitations that compromise accurate volume estimates. Two-dimensional apical imaging correlates well with cinecomputed tomographic measurements of atrial volume.[16] [17] [18] The left atrium is best imaged in the two- and four-chamber apical views, with the patient in steep left recumbency, and with suspended respiration. Atrial volume can then be calculated by a single-plane area-length method from each view or by using the biplane method of discs. Normal left atrial

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volume is approximately 36 mL, or 20 mL/m2 . This volume is increased in athletes.[17] The atrial appendage, especially in enlarged atria, can sometimes be visualized in the apical views. Occasionally, a particularly large thrombus can be seen in the enlarged left atrium by TTE (Fig. 37-1) . The sensitivity of TTE for the detection of left atrial thrombus is 25% to 57% overall and 63% to 83% for left atrial cavity thrombus. Specificity is 94% to 99%, as confirmed at surgery. Most thrombi occur, however, in the left atrial appendage, which is a posterior structure, and the sensitivity of TTE for detecting left atrial appendage thrombi drops to 0% to 16%. An enlarged left atrium, particularly in a patient Figure 37-1 Left atrial thrombus seen in four-chamber apical view on TTE. This 78-year-old woman had severe congestive cardiomyopathy with a giant left atrium and was in atrial fibrillation. There was no intrinsic mitral valve disease. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

with atrial fibrillation, may have an intra-atrial thrombus, suggesting the need for TEE to better visualize left atrial appendage thrombus or the need for presumptive anticoagulation. Mitral Annular Calcification

Despite a number of studies that have suggested an association between mitral annular calcification and stroke,[8] [11] [19] [20] [21] [22] [23] [24] the role of mitral annular calcification in stroke remains unclear. In an analysis of Mmode echocardiograms in 1159 members of the Framingham study, Benjamin et al[25] contended that mitral annular calcification was an independent risk factor for stroke, especially embolic stroke. This association was maintained in subjects without atrial fibrillation, congestive heart failure, or clinically apparent coronary artery disease. These authors postulated that the mechanism may be calcific emboli or that the mitral annular calcification may serve as a nidus for thrombus.[25] In another prospective study of 2148 subjects, patients with mitral annular calcification were more likely to suffer a cerebrovascular event, with a risk ratio of 2.6 (P = .001). This risk was further increased in the presence of mitral stenosis and atrial fibrillation[24] however, the Stroke Prevention in Atrial Fibrillation (SPAF)-II trial of 568 patients failed to find such an association. [26] A more recent prospective cohort study of 657 patients with

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mitral annular calcification identified by 2D echocardiography showed no increased incidence of stroke.[27] Mitral annular calcification is easily detected by TTE. Using 2D criteria, it is best identified in the same views in which the mitral valve is seen: the parasternal long-axis and short-axis views, as well as the two- and fourchamber apical views. Mitral annular calcification is visually defined as increased echodensity in the mitral annulus, which is a C-shaped structure and distinct from the mitral valve. Annular calcification occurs posteriorly, may extend toward the base of the heart, and can appear to infiltrate the myocardium. Extensive mitral annular calcification can obscure visualization of the thin mitral valve leaflets and can cause decreased mitral valve excursion, although usually not severe mitral stenosis. Mitral annular calcification can be graded as mild, moderate, or severe. Autopsy studies reveal this condition in approximately 10% of patients. [28] [29] It is associated with obesity, elevated systolic blood pressure, aging, aortic stenosis, and hypertrophic obstructive cardiomyopathy. It is found predominantly in elderly women, with an incidence of 12% in women over 70.[28] Mitral annular calcification occurs earlier in renal dialysis patients, and it may be associated with the presence of aortic atheroma as well.[30] [31] Left Ventricular Wall Thickness

Left ventricular mass index has been identified as an independent risk factor for carotid atherosclerosis in normal and hypertensive subjects.[32] Roman et al[32] studied a group of 486 adults without cardiovascular disease, using 809

echocardiography to determine left ventricular mass and carotid ultrasound for measurement of common carotid artery dimensions and detection of carotid atherosclerosis. Patients with left ventricular hypertrophy were twice as likely to have carotid atheroma (35% vs. 18%; P < .01). As with left atrial size, left ventricular mass can be measured by M-mode echocardiography or 2D planimetry. Left Ventricular Wall Motion

Transthoracic echocardiography is an excellent method for evaluating left ventricular wall motion abnormalities in most patients. Exceptions are

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patients with technically difficult echocardiographic windows, those with chronic obstructive pulmonary disease, or very obese patients. The anterior septum and inferior wall are well seen in the parasternal long-axis view; the anterior, anteroseptal, posterior, lateral, and septal walls are seen in the parasternal short-axis view; the inferoseptal, septal, lateral, apical, and anterolateral walls are seen in the four-chamber apical view; and the inferior and anterior walls are visualized in the two-chamber apical view. Regional wall motion abnormalities are an indicator of ischemic heart disease. The identification of wall motion abnormalities, particularly of an aneurysm, greatly increases the likelihood of finding an associated left ventricular thrombus. Left Ventricular Thrombus

Transthoracic echocardiography also is the best imaging modality for detecting intracardiac thrombus in the left ventricle. These masses generally are seen in the setting of wall motion abnormalities, particularly anterior and apical, or cardiomyopathy. Identification of an aneurysm in the apical view necessitates a careful search by the echocardiographer for the presence of apical thrombi. Thrombi are visually defined as a distinct mass of echoes in the left ventricular cavity that are seen clearly throughout the cardiac cycle in at least two different echocardiographic views. They appear as irregular sessile or mobile structures that are contiguous with the endocardium in an area of abnormal wall motion, such as ischemic or infarcted myocardium (Fig. 37-2) . Thrombi are best seen in the four-chamber apical view by TTE, because the transducer is closest to the cardiac apex in this view. Identification of thrombi can be made more certain by using off-axis views that are directed toward or across the apex. In some cases, the transducer may be directed inferiorly or caudally across the apical impulse location. We call this maneuver the "backhanded" apical view. In this process, it is best to use a high-frequency transducer (3.5 or 5 MHz). This view combined with the use of a higher-frequency transducer increase the examiner's ability to detect apical thrombus. Ventricular thrombus should be associated with a wall-motion abnormality in the same location. Rarely, thrombi may form in the left ventricle, in the setting of transient ischemia or coronary spasm, with normal wall motion seen by echocardiography. Thrombi also are seen in patients with dilated cardiomyopathies secondary to ischemic Figure 37-2 Left ventricular apical thrombus seen in the two- (left) and

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four-chamber (right) views in TTE from a 56-year-old man with ischemic cardiomyopathy. The thrombus appears as a cap adherent to the apex. (Courtesy of Ray Stainback, MD.)

or nonischemic causes. These patients have diffuse hypokinesis, generally with an ejection fraction of less than 30%, and the thrombus is most often found in the apical third of the left ventricle. Flow patterns in the left ventricle can predict thrombus formation after myocardial infarction. An abnormal Doppler-flow pattern is highly associated with the formation of thrombus. In a study of 62 patients, no patient with a normal Doppler-flow pattern seen within 24 hours of myocardial infarction went on to develop a thrombus.[33] In this study, oral anticoagulation did not prevent the formation of thrombus, although it did decrease significantly the incidence of peripheral embolization in patients with left ventricular thrombus. The incidence of embolization from ventricular thrombus in dilated cardiomyopathy is approximately 1% to 4% per year.[4] [34] [35] [36] [37] The independent risk factors for stroke are low ejection fraction, older age, and the absence of aspirin or anticoagulation therapy. Thrombi that are protruding and mobile are most likely to embolize.[38] In the latest consensus recommendation for the management of chronic heart failure, the panel did not endorse routine anticoagulation, emphasizing that "in the absence of definitive trials, it is not clear how anticoagulants should be prescribed in patients with heart failure."[35] The European Society of Cardiology, while acknowledging the lack of data in this area, suggested that anticoagulation "may be advisable in selected patients with large hearts and a low ejection fraction."[39] Echocardiography is useful in this setting to identify thrombi and to target patients who may benefit from anticoagulation.[4] [19] [34] [37] , [38] , [40] Patients known to be at high risk for embolization, such as those in atrial fibrillation or those with a history of previous embolization, should also undergo anticoagulation therapy. Definitive recommendations addressing the need for anticoagulation therapy for patients with dilated cardiomyopathy and normal sinus rhythm await results of clinical trials such as WATCH and WARCEF (see "Studies in Progress"). In cases of anterior myocardial infarction, embolic risk is greatest in the first 3 months after the infarction.[41] [42] [43] [44] [45] [46] After that period, the clot has organized and is less of an

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810

embolic risk, and 40% of clots resolve spontaneously.[47] More recent data suggest an increased incidence of stroke long after the initial infarction. In the Survival and Ventricular Enlargement (SAVE) trial, 2231 patients with left ventricular dysfunction following an episode of myocardial infarction were prospectively followed for a mean of 42 months.[48] During the study, 4.6% of these patients experienced strokes, with an estimated 5-year rate of stroke of 8.1%.[48] Presently, anticoagulation therapy is recommended following myocardial infarction in patients unable to take aspirin, patients with persistent atrial fibrillation, and patients with left ventricular thrombus. The American College of Cardiology and American Heart Association Task Force on acute myocardial infarction considers anticoagulation therapy a class II indication in patients with extensive wallmotion abnormalities, paroxysmal atrial fibrillation, or severe left ventricular dysfunction, with or without congestive heart failure.[49] Chronic anticoagulation therapy in patients with left ventricular dysfunction or dilated cardiomyopathy remains controversial.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transesophageal Echocardiography Indications Transesophageal echocardiography offers higher resolution imaging than TTE because the adjacent, airless imaging pathway allows the use of 5- to 7.5-MHz probes. This TABLE 37-3 -- Transthoracic versus Transesophageal Echocardiography in Evaluation of Cardiac SOE in Patients with Cerebral Ischemia

Studies Cujec[51]

No. Patients 63

Mean Yield Age ± of SD Yield TEE (Range of TTE n in yr) n (%) (%) 63 ± 15 -0 -0 (18– 87)

de Belder

131

—

[52]

— Pearson[56]

79

59 (17– 84)

+9 (14) +26 (41)

72 (55)

92 (70)

Patients with Clinical Findings Heart Seen by Disease n TEE Only (%) ASA/PFO— 24 (38) 2 LAA thrombus—1 Myxoma MV—2 PFO—18 53 (40)

SEC—27 Vegetation— 2 12 (15) 45 ASA/PFO— (57) 9 -7 (19) -15 LASEC—13 (39)

41 (52)

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Comess[59]

66

Lee[55]

50

Pop[57] †

72

Hofmann

153

[54]

+5 (12) +30 LA clot—6 (73) 62 -6 (30) -18 — (60) +9 (19) +35 (76) 63 ± 13 0 26/50 LA/LAA (Except (52) clot—5 MAC) (20– LA/LV 82) SEC—9 MV strands—11 60 -0 (0) -5 (9) LAA thrombus—2 +6 (32) +6 LAA mass— (32) 1 Ao dissection— 1 MVP—1 42 -20 -49 Intracardiac (19) (46) masses (16– +35 +39 60) (76) (88)

46 (70)

29 (58)

19 (26)

46 (30)

84 (cerebral ischemia) 50 (peripheral embolus) 19 (retinal ischemia) Ao, aorta; ASA, atrial septal aneurysm; LA, left atrium; LAA, left atrial appendage; MV, mitral valve; MVP, mitral valve prolapse; SEC, spontaneous echo contrast; LV, left ventricle; MAC, mitral annular calcification; PFO, patent foramen ovale.

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* All patients had transient ischemic attack or cerebrovascular accident unless otherwise noted. -, patients without cardiovascular disease; +, patients with cardiovascular disease. † TEE showed thoracic aortic plaque in 32 patients (44%).

advantage becomes particularly evident when studying structures close to the probe, such as the left atrium (and left atrial appendage) and thoracic aorta. All series that compare TTE with TEE show that the latter is superior for identifying potential sources of arterial emboli (Table 37-3) . [10] [14] , [50] [51] [52] [53] [54] [55] [56] [57] For example, Pearson et al,[10] in a study of 79 patients, found that the yield of potential sources of embolism rose from 15% to 57% when comparing TTE with TEE in patients known to have preexisting cardiac disease, and from 19% to 39% in those patients without pre-existing cardiac disease. The data for the effect of age on the usefulness of TEE in evaluating emboli are evolving. As stated previously, patients with no cardiac disease have an extremely low likelihood of positive findings on TTE, generally less than 1%. Even though TEE is superior to TTE in identifying potential sources of emboli in patients without known cardiac disease, overall yield is increased to only 1.6% in a pooled analysis.[32] Thus, patients with a history of ischemic stroke and who are under 45 to 55 years of age tend to have a low overall yield as well. Although some authorities recommend TEE evaluation of embolic events as the initial diagnostic test for patients younger than 45 to 55 years of age with no other heart disease,[3] [14] others do not recommend such an approach.[12] In any case, this age group is less likely to have occlusive cerebrovascular disease. Findings best visualized by TEE, such as PFO, atrial septal aneurysm, atrial septal defect, and spontaneous contrast, have been associated with embolic events in this group of patients. All comparative studies show a higher 811

TABLE 37-4 -- Grading of Aortic Plaques Class Characteristics

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I II III IV

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Normal intima Minimal intimal thickening Raised irregular plaque <5 mm Complex protruding plaque with ≥5 mm thickness, ulceration, or calcified density

yield of diagnostic findings by TEE; what remains unclear is whether these possible and probable sources of embolism are truly responsible for ischemic events. This enigma is complicated by studies that have found occlusive carotid vascular disease and probable or possible cardiac sources of emboli in the same patients. Lee et al[55] studied 50 consecutive hospitalized patients with recent transient ischemic attacks or embolic strokes using TTE and TEE (Table 37-4) . Potential sources of emboli were found only by TEE in approximately half (52%) of these patients. The most common possible source of emboli in this study was the presence of highly mobile filamentous strands on the mitral valve.[14] The investigators postulated that these strands might represent a fissured surface of fibrosis that could serve as a nidus for thrombus formation. The next most common possible source was SEC,[9] followed by left atrial clot[58] and PFO.[4] [55] In the largest prospective study that looked at the value of TEE in assessing cerebral ischemia, Comess et al[59] studied 145 consecutive patients with TEE and carotid ultrasound. In 45% of patients, atrial septal aneurysm, interatrial shunt, and SEC were the abnormalities most commonly found. During a mean follow-up of 18 months, recurrent cerebral ischemia was more commonly found in patients with positive TEE findings, particularly those with atrial septal aneurysm, interatrial shunt, and left atrial thrombus. [59]

Data from the Significance of Transesophageal Echocardiography in Prevention of Recurrent Strokes (STEPS) registry of 805 patients (18 to 95 years of age; mean, 59 years) showed a higher yield of abnormal findings by TEE in patients with otherwise unexplained embolic events. Abnormal findings on TEE that may have been a source of emboli were noted in 85% of patients in atrial fibrillation and 50% of patients in normal sinus rhythm. [60]

These echocardiographic findings, which are associated with stroke in

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younger patients, are all best seen by TEE. Transesophageal echocardiography also is superior to TTE in identifying a cause for embolic events in patients with plaque in the thoracic aorta. Older patients are most likely to belong in this group, particularly those without other sources of embolism, who have a history of coronary artery disease or peripheral vascular disease. Patients in whom left atrial thrombus is suspected as the source of emboli, such as patients with mitral valve disease or those in atrial fibrillation, should also undergo TEE. Yields are increased by TEE for patients with native or prosthetic valves who are suspected of having endocarditis. Selected groups of younger patients, older patients, and patients with mitral or aortic valvular disease may have increased yield from a TEE study for sources of emboli. Findings and Techniques Left Atrial Appendage Thrombus

Left atrial appendage evaluation is now an integral part of a complete TEE, especially in patients suspected of cardioembolic event.[61] Most left atrial thrombi occur in the left atrial appendage. Because the left atrium and its appendage are posterior structures lying in the far field of the image, the appendage is poorly visualized on TEE, so that TEE is necessary to look for a left atrial appendage thrombus. Transesophageal echocardiography has the advantages of higher frequency transducers and closer proximity to the left atrium. The sensitivity for detection of left atrial cavity and appendage thrombi by TEE is 90% to 95%, with a specificity of 95% to 100%. The left atrial appendage can be visualized in the basal transverse and longitudinal planes. Multiplane imaging optimizes views of the left atrial appendage. We often are able to see this structure most clearly at 30-degree rotation of the image plane. The appendage is easily recognized by its characteristic triangular structure (Fig. 37-3) . It is important to be familiar with the appearance of a normal left atrial appendage, because the appendage is traversed by pectinate muscles along its length. When one is familiar with the normal ridgelike appearance of the left atrial appendage, a thrombus is more easily recognized. Thrombus may be recognized by identifying a mobile or sessile, irregularly shaped, gray, textured density that is clearly separate from the lining of the atrial appendage (Fig. 37-4) . It is a clearly defined echo-dense intracavitary mass, acoustically distinct from the endocardium. Commonly associated echocardiographic features are increased left atrial size and SEC.

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Left atrial appendage thrombi occur most often in patients who are in atrial fibrillation, although 5% to 10% of left atrial thrombi are seen in patients who are in normal sinus rhythm and are without mitral valve disease. The Figure 37-3 Normal left atrial appendage (LAA)(asterisk) seen in a multiplane basal short-axis TEE view. Note the typical crescentic structure of the LAA and its normal ridged lining. The arrow identifies the left superior pulmonary vein (LSPV). There is a normal fibrous structure that separates the LAA and LSPV, which is nicknamed the "warfarin ridge" because it can be mistaken for a left atrial clot.

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Figure 37-4 A 47-year-old woman with atrial fibrillation who underwent TEE prior to planned cardioversion. A, Pulsed Doppler sampling in the left atrial appendage shows a low-velocity fibrillatory pattern associated with stasis and thrombi. B, TEE view of the left atrium showing chamber enlargement, spontaneous contrast, and left atrial appendage thrombus. (Courtesy of Ray Stainback, MD.)

incidence of left atrial thrombus identified by TEE in patients with systemic emboli ranges from 5% to 17% in reported series, with the incidence increasing in series in which a higher percentage of the patients studied had mitral stenosis or atrial fibrillation. A complete evaluation of the left atrial appendage also includes evaluation of its velocity and flow pattern ( see Chapter 38 , Fig. 38-5 ). This can be done by placing a pulsed-Doppler sample volume in the left atrial appendage approximately 1 cm from the orifice, where normal left atrial appendage flow has been characterized. In a TEE study of left atrial flow in 109 patients, the forward left atrial appendage contraction wave was measured as 46 ± 18 cm/s, followed by a retrograde filling wave of 46 ± 17 cm/s in sinus rhythm. In 40% of patients in sinus rhythm, additional forward and retrograde velocities of 23 ± 10 and 22 ± 11 cm per second, respectively, were seen. In contrast, atrial fibrillation was associated with reduced forward and retrograde flows in an irregular pattern. [62] Reduced antegrade appendage flow velocity is associated with a higher incidence of left atrial thrombus. Mugge et al[63] pointed out the usefulness of left atrial appendage function in assessing embolic risk. The association

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between atrial appendage thrombus in this structure and embolic stroke has been established, as has the association between appendage dysfunction and the tendency to form thrombus. The study demonstrated a strong association between atrial appendage thrombus and SEC in the atrial cavity and with embolic events if the appendage flow velocity fails to exceed 25 cm per second.[63] In the SPAF-III TEE substudy, 37% of the 382 patients showed flow velocity reduced to 20 cm per second or less, which was associated with a higher incidence of left atrial thrombus (17% compared with 5% in patients with higher velocity, P < .001).[64] Subsequent analysis of TEE findings of 721 patients in the SPAF-III study supported the above finding. Multivariate analysis found antegrade flow velocity of <20 cm per second (relative risk 2.6, P = .02) to be associated with left atrial appendage thrombus.[65] If left atrial appendage thrombus is seen by TEE, the patient should undergo anticoagulation therapy. Any correctable causes of left atrial dysfunction should be evaluated. For example, if the patient is in atrial fibrillation, cardioversion should be considered, as discussed in Chapter 33 . If the patient has mitral valve disease, consideration of treatment— mitral valvuloplasty or surgery—is warranted (see Chapter 19) . Spontaneous Echocardiographic Contrast

Spontaneous echocardiographic contrast in the left atrium is a dramatic finding on echocardiography. It is defined as the presence of dynamic, smokelike, swirling echoes.[66] To optimize detection of SEC, a highfrequency transducer (≥5 MHz) should be used, and the entire left atrial cavity and appendage should be carefully imaged in a basal short-axis view and a four-chamber view. The gain and compression settings need to be optimized to avoid missing low-amplitude echoes. Spontaneous echocardiographic contrast is seen best with higher gains and can be differentiated from white-noise artifact by the characteristic swirling motion (Fig. 37-5) . To maximize detection of intermittent left atrial SEC, sufficient time should be allowed for imaging. Because it depends on transducer frequency and gain settings of the instrument, SEC is difficult to quantitate. If frequencies higher than 5 MHz are used, low-intensity contrast can be seen in normal subjects without mitral regurgitation who have normal or slightly reduced cardiac output. If gain settings are too low or if there is bright light in the examination setting (e.g., in the operating room), spontaneous contrast can be missed. This finding is best seen using a 5-MHz or greater frequency transducer, with the gain set high enough to create uniform low-level background noise throughout the atrium.

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Spontaneous echocardiographic contrast can be seen by Figure 37-5 TEE, four-chamber view, showing spontaneous contrast filling the dilated left atrium of this 70-year-old woman with rheumatic mitral stenosis. (Courtesy of Ray Stainback, MD.)

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TTE[67] but is more frequently identified by TEE, reported in up to 20% of patients undergoing TEE in some centers.[68] This increased detection of SEC by TEE was confirmed in a larger study of 400 consecutive TEE patients, in whom SEC in the left atrium was seen in 19%. SEC was not seen in any patient by TTE in this study.[69] Spontaneous echocardiographic contrast can be found in the left atrial appendage, right atrium, left ventricle, or descending aorta. In all these sites, SEC generally is associated with a low-flow state and increased thrombotic risk,[68] [69] [70] [71] [72] [73] [74] although there are rare reports of SEC in patients with no significant cardiac abnormalities. SEC is thought to represent increased echogenicity because of the aggregation of blood cells at low shear rates. A number of reports correlated local coagulation or systemic hematologic abnormalities, or both, such as anticardiolipin antibody, sedimentation rate, and fibrinogen levels, with an increased incidence of SEC.[74] [75] [76] [77] In the SPAF-III study, plasma fibrinogen greater than 35 mg/dL (P < .001) was associated with the identification of any SEC; however, dense SEC was associated only with age in the multivariate model.[74] Furthermore, SEC can be found in the left atrium in conditions associated with stasis of blood in the left atrium, such as atrial fibrillation, left atrial thrombus, and enlarged left atrium secondary to mitral stenosis. Its incidence is increased in the setting of acute myocardial infarction even with normal sinus rhythm.[78] In one report of TEE studies of 1288 patients in normal sinus rhythm, SEC was seen in 2% of the patients. The presence of SEC was associated with a higher prevalence of stroke in patients with SEC when compared with controls, 83% versus 56%, P = 0.02.[79] Spontaneous echocardiographic contrast is also associated with age and mitral regurgitation.[66] However, SEC is not seen in patients with severe mitral regurgitation (unless the left atrium is very large), probably because

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the mitral regurgitant jet agitates the left atrial blood pool. The absence of spontaneous contrast in mitral regurgitation appears to be associated with decreased embolic risk.[80] [81] In a large TEE study, mitral regurgitation was an independent predictor of the absence of SEC.[66] In this study of 400 patients, Black et al[66] found SEC in 19%, 95% of whom showed atrial fibrillation or mitral stenosis. In mitral stenosis and in nonvalvular atrial fibrillation, SEC was the only independent predictor of embolism, or stroke, or both. In another study, SEC was found to carry a relative risk ratio of 10.6 for mitral stenosis patients in atrial fibrillation compared to those without SEC. In a study of 47 patients with mitral stenosis in sinus rhythm, Bernstein et al[82] found that SEC did not predict clinical events but was a predictor of more severe stenosis (i.e., it was a marker of stasis). Right atrial SEC is seen in conditions that promote stasis of right atrial blood, including atrial fibrillation and an enlarged right atrium, as in cor pulmonale. It is less likely to be seen in patients with severe tricuspid regurgitation. Left ventricular SEC is seen in states of low flow, such as cardiomyopathy and left ventricular aneurysm.[38] Descending aortic SEC has been associated with severe left ventricular dysfunction leading to reduced cardiac output and low flow in the descending aorta. It also may be seen in the false lumen of patients with aortic dissection.[83] Atrial Septum

Structures and findings in the atrial septum generally are better identified and characterized better by TEE than by other methods. Atrial Septal Aneurysm.

Atrial septal aneurysm has been identified in 1% of all patients in a large autopsy study[84] it is seen in 0.2% of all TTE readings[85] and in 3% to 8% of all TEE readings.[86] In a population-based sample of 363 subjects in Olmsted County, Minnesota, the prevalence of atrial septal aneurysm found on TEE was 2.2%.[87] An atrial septal aneurysm appears as a redundant, highly mobile membranous portion of the atrial septum and is defined as a billowing or localized outpouching greater than 11 mm from the plane of the septum, with a base of 1.5 cm.[88] It is associated with atrial septal defects or PFO in up to 77% of cases.[55] [87] [89] The speculation is that atrial septal aneurysm may be a remnant, perhaps, of a healed atrial septal defect. The best view for identifying an atrial septal aneurysm by TTE is the

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parasternal short-axis view at the level of the atria. It also may be visualized in the four-chamber apical view or in the subcostal view. The best view for identifying an atrial septal aneurysm by TEE is the basal longitudinal view at the level of the atrial septum, or the four-chamber view using the transverse plane at the level of the midesophagus. To define an atrial septal aneurysm, measurements of the total excursion of the localized bulging of the septum primum should be made. If the bulging occurs consistently into either atrium, excursion should be measured from the maximal point of the bulging to an imaginary line connecting the nonaneurysmal segments of the septum primum at the base of the aneurysm. The distance between the maximal extent of aneurysmal bulging and this imaginary line is considered the excursion distance. If there is cardiorespiratory variation in the excursion of the aneurysm, the maximal distance of excursion into either atrium should be added to determine the total phasic excursion. One group recently proposed a classification scheme based on the direction of bulging. They suggested that each subtype may have different clinical correlates[90] however, this scheme awaits further validation. An association between atrial septal aneurysm and stroke was first suggested in 1985, in a case report of a 34-year-old woman.[91] Atrial septal aneurysm is found more often in patients with stroke than in those referred for TEE for other reasons (15% vs. 4%).[56] Schneider et al studied first 23 and then 40 patients with this entity using TEE. [88] [89] More than 83% had an associated patent foramen; in 52%, there was a history of cerebrovascular accident; and in 27%, TTE did not reveal the redundant interatrial septum. Identification of multiple fenestrations and thrombi within the aneurysm could be achieved only by TEE. The authors concluded that evidence of interatrial septal aneurysm should be sought by TEE in cases of unexplained stroke and, if found, treated with anticoagulation therapy. They speculated that the mechanism of 814

embolization might be primary thrombus formation within the aneurysm and paradoxical embolization through an interatrial communication. Nevertheless, the association of atrial septal aneurysm with stroke remains unclear. Recently, in the Stroke Prevention Assessment of Risk in a Community (SPARC) study of 363 subjects with a history of cerebral embolism, atrial septal aneurysm was more frequently identified (7.9% vs.

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2.2% of controls, odds ratio [OR] 3.65, P = .002); and, in 86% of the patients with atrial septal aneurysm, TEE failed to identify other potential causes.[87] In a prospective study of 42 patients with a history of atrial septal aneurysm, however, who were identified from 846 patients who had undergone cardiac surgery, no association was shown between stroke and atrial septal aneurysm. During the mean follow-up of 69.5 months, no patient demonstrated any cerebrovascular or embolic event.[92] Lipomatous Hypertrophy.

It may be difficult to appreciate lipomatous hypertrophy by TTE because the atrial septum sits in the far field of the image, where beam-spread artifact often obscures the details of the septum. On TEE, the entity appears as a characteristic dumbbell-shaped interatrial septum that involves the septum primum and venous portions but always spares the foramen ovale (Fig. 37-6) . In some cases, this entity can be mistaken for a tumor, but its sessile behavior, location, and fatty nature identify it as benign. It is more common with aging and may be associated with diabetes. There is no specific treatment indicated (except to avoid surgery for tumor). Lipomatous hypertrophy of the interatrial septum has been associated with arterial embolization and pulmonary emboli,[93] as well as with arrhythmias and sudden death.[94] Most descriptions of this abnormality are single case reports, and the entity awaits further study. Contrast Technique.

Contrast is useful for identifying a PFO or atrial septal defect. The saline contrast technique requires a three-way stopcock and sterile normal saline. A syringe containing 3 mL of normal saline and Figure 37-6 Lipomatous septal hypertrophy (arrows) seen in a horizontal plane four-chamber TEE view of the atrial septum. Note the dumbbell-shaped appearance of the septum with the thin portion of the fossa ovalis separating the two lipomatous areas of septum, an incidental finding in a 68-year-old man undergoing vascular surgery. Figure 37-7 Set-up for a saline contrast injection. A three-way stopcock is attached to a 20-gauge Intracath in the patient's antecubital vein with two syringes attached. A saline and air mixture is then added, agitated until milky white, and vigorously injected during echocardiographic imaging.

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0.1 mL of air is attached to one part of the stopcock, and an empty syringe is attached to the other stopcock; the third port is attached to a catheter (e.g., Intracath) placed in the antecubital vein. Contrast is then agitated by passing it forcefully between the two syringes until it has an opalescent appearance (Fig. 37-7) . A vigorous bolus injection is made into the antecubital vein while the atrial septum is being visualized. Massaging and elevating the upper arm can facilitate arrival of the bolus of contrast medium into the heart, as can the use of at least a 20-gauge catheter. Increased quantities of saline (up to 10 mL) can be used if the contrast effect is inadequate, particularly in larger patients. Contrast is seen passing from the right to the left atrium if there is a patent communication and right atrial pressure exceeds left atrial pressure. New transpulmonary contrast agents are becoming available. Their efficacy compared with saline in identification of intracardiac shunts is not yet determined. Atrial Septal Defect.

Atrial septal defects can be a route for paradoxical emboli. Defects are identified on 2D echocardiography using the same views as previously described for identifying atrial septal aneurysm. As with other findings in the atrial septum, identifying atrial septal defects is readily increased by the use of TEE[95] [96] and is particularly applicable for detecting sinus venosus defects.[97] Atrial septal defects may be suspected or identified using 2D echocardiography and should be confirmed by Doppler echocardiography (Fig. 37-8) and by the use of contrast. An atrial septal defect is identified by a negative contrast effect (Fig. 37-9) , the lack of contrast resulting from blood flow across the atrial septal defect, thus "washing out" the contrast from the right atrium. Although there may be a transient rise in right atrial pressure during early systole, the contrast injection can be reliably performed during the resting state and during provocative maneuvers that transiently raise right atrial pressure above left atrial pressure, such as Valsalva's maneuver or a cough. The appearance of contrast in the left atrium provides only a qualitative assessment of interatrial shunting; the actual shunt fraction cannot be measured by this technique. Other 815

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Figure 37-8 (color plate.) This 44-year-old woman was evaluated for decreasing exercise tolerance and a murmur. TTE showed right-sided chamber enlargement. A, Biatrial multiplane TEE view at 119 degrees shows dropout of the atrial septum and an enlarged right atrium. B, Color flow Doppler in longitudinal view confirms the flow across the secundum atrial septal defect.

echocardiographic indicators, however, such as right-chamber enlargement, suggest a hemodynamically significant left-to-right shunt (see Chapter 40) . Patent Foramen Ovale.

Patent foramen ovale has been associated with cryptogenic stroke. It occurs in approximately 25% of all adult hearts as a consequence of the failure of the septum secundum to fuse to the septum primum over the foramen ovale. The foramen ovale is a one-way valve allowing flow from the right to the left atrium. In fetal life, the foramen ovale serves as a conduit for highoxygen, high-glucose blood to reach the fetal heart and brain and usually closes within several hours of birth because of increased pulmonary resistance. Visualization of the foramen ovale requires imaging directly over the interatrial septal foraminal area. The foramen lies within the thin portion of the fossa ovalis. Contrast or color Doppler allows identification of a PFO. The atrial septum should be visualized and carefully aligned in the fourchamber apical view. After contrast is injected, the echocardiogram should be closely observed for opacification of the right atrium with contrast and then for passage of microbubbles from the right atrium Figure 37-9 Saline contrast injection in the patient seen in Figure 37-8 shows a negative contrast effect secondary to left-to-right flow across the atrial septal defect.

Figure 37-10 This 48-year-old man had a history of transient ischemic attacks. Longitudinal plane TEE biatrial view saline contrast injection shows opacification of the right atrium and multiple microbubbles passing into the left atrium, consistent with a patent foramen ovale.

into the left atrium. A PFO is defined as the passage of more than three microbubbles from the right atrium to the left atrium within the first three cardiac cycles after opacification of the right atrium with contrast (Fig. 37-

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10) . If no bubbles pass with spontaneous respiration, during which there is reversal of atrial pressure gradient in early systole, the injections should be repeated while the patient is asked to perform Valsalva's maneuver. The patient should be asked to release the Valsalva strain as the right atrium begins to opacify. With a successful Valsalva maneuver, the atrial septum can be seen to bow transiently from right to left, indicating raised right atrial pressure. Inspiration during this maneuver may cause increased impedance secondary to lung expansion and thereby decrease the echocardiographic image quality or ever alter the imaging plane, and the echocardiographer should be prepared for this. If patients cannot perform Valsalva's maneuver, they may be asked to cough. Transesophageal echocardiography has increased the detection rate for PFO.[10] In a study of 238 patients that compared the value of transthoracic and transesophageal color Doppler and contrast echocardiography for detecting a PFO, a PFO was detected by contrast TEE in 22%, whereas only 8% were detected by contrast TTE. A PFO was detected in 50% of patients under 40 years of age and with otherwise unexplained ischemic stroke. A higher sensitivity is exhibited by TEE than for TTE for detecting PFO, and PFOs are observed in significant numbers in younger patients with embolic events.[53] There have been numerous studies linking the presence of PFO with stroke, particularly in younger patients, defined as younger than 40 years,[98] 45 years,[99] or 55 years of age,[100] and in all cryptogenic stroke patients.[101] Lechat et al[100] found the prevalence of PFO to be significantly higher in a group of patients under 55 years of age with stroke (40%) than in an agematched control group (10%). The prevalence of PFO in this younger stroke group is as high as 40% to 74% in reported series.[52] [102] Because PFOs are a common finding and their size and permeability vary greatly, as presumably would their embolic risk, several studies have sought to define echocardiographically 816

characteristics of "high-risk" PFO. Characteristics include larger PFOs and right-to-left shunting.[103] [104] [105] [106] One study of PFO in patients with cerebral ischemia showed increased separation between the septum primum and septum secundum, increased mobility of the foramen ovale membrane,

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and defects of larger size (2.8 vs. 0.7 cm) than in patients without ischemia. Patients with these findings had a 12.5% recurrence rate of cerebral ischemia at 24 months (P = .05).[103] The same group later reported that in 101 patients with a PFO and a history of stroke, those who had PFO at rest and membrane mobility greater than 6.5 mm had a recurrent stroke rate of 16.3% compared to those with PFO only with maneuvers and mobility less than 6.5 mm (4.3%, P = .05).[106] In another contrast TEE study of 74 consecutive patients referred for ischemic stroke, 23 patients had PFO. Separating patients into those with strokes of determined origin versus cryptogenic strokes showed that the PFO dimension was significantly larger in patients with cryptogenic stroke than in those with an identifiable cause of stroke (2.1 to 1.7 vs. 0.57 ± 0.78 mm; P < .01). The number of microbubbles crossing the interatrial septum was also greater in patients with cryptogenic stroke than in those with an identifiable cause of stroke (13.9 ± 10.7 vs. 1.6 ± 0.8; P < .0005). The authors concluded that patients with cryptogenic stroke have larger PFOs with more extensive right-to-left interatrial shunting than patients with stroke of determined cause and that TEE is useful for identifying these characteristics.[104] When magnetic resonance and computed tomography imaging data of 95 patients with a history of ischemic stroke, who had undergone TEE, were analyzed, one study found that patients with larger PFOs had more abnormal findings. For example, superficial infarcts occurred more frequently in patients, who had PFOs 2 mm or longer, than in patients with no PFO or PFOs 2 mm or shorter (50% vs. 21%, P = 0.02). [107] Because approximately 25% to 30% of the normal population have PFO, other investigators have suggested caution in interpreting this finding as a cause of cerebral ischemia.[14] [108] [109] There are several reasons for the difficulties in extrapolating from the finding of a PFO by echocardiography or autopsy to the likelihood that this entity is responsible for a stroke. A PFO is a one-way valve that opens when right atrial pressure exceeds left atrial pressure, either transiently, such as during a Valsalva maneuver, coughing, or sneezing, or in conditions that cause chronically elevated right atrial pressure. For a stroke to occur, there must be a thrombus on the right side of the heart, presumably originating from a deep venous thrombosis, which happens to be passing through the heart at the same time that right atrial pressure is elevated. If there is not chronic right-sided pressure elevation, the investigator must postulate that the patient had a transient right-sided pressure elevation at the exact time of transit of the thrombus. Further complicating the interpretation of this echocardiographic finding, echocardiography detects a patent foramen of only 5 to 15 µm, the size of

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the microbubbles injected as contrast media, but a thrombus must be approximately 1 mm to cause a clinical event. A number of studies, however, found an association with deep venous thromboses and with embolic events in patients with PFO, providing a potential source for paradoxical embolism.[110] [111] In a study of 227 patients, 56 were noted to have interatrial shunting. Fifty-three of the 56 patients underwent venography of the lower limbs. Five (9.5%) patients were noted to have acute deep venous thrombosi, of which four were clinically silent. The authors recommended phlebography for patients with PFO and embolic event.[111] If a PFO is identified in a patient with cerebrovascular ischemia, anticoagulation therapy with warfarin or aspirin has been suggested.[112] Unfortunately, existing data are largely derived from small retrospective series and heterogeneous populations. Because of the common occurrence of PFO in the population, causal relationship is difficult to establish. The true recurrence rate is unknown at this time, and as such, effects of potential therapeutic benefits from drugs, devices, or surgery are difficult to measure. In the Lausanne Stroke Study, 140 consecutive patients with clinical evidence of cerebral embolism and PFO were followed for a mean period of 3 years.[113] Only 8 patients had a recurrent infarct (1.9% per year). In the French Study Group on Patent Foramen Ovale and Atrial Septal Aneurysm of 132 patients with PFO or atrial septal aneurysm, with mean followup of 22.6 months, only 8 patients had a stroke, yielding an actuarial risk of 2.3% at 2 years.[114] Using decision analysis, Nendaz and colleagues found that even when modeling the recurrence rate at 0.8% per year based on reported rates in the community, any therapeutic option may be potentially beneficial.[115] Although surgical closure has demonstrated some success,[116] [117] it is unclear when a surgical approach may be indicated. Similarly, although remaining transcatheter devices seem safe, the larger issue of whether PFO is the real culprit remains. In the largest transcatheter PFO surgical closure study of 63 patients, followed for a mean period of 2.6 years, 14% of the patients had residual shunting and 4 patients had recurrent embolic events; two strokes occurred in the setting of suboptimal device performance. Risk of recurrence was 3.2% per year.[118] Until data from randomized controlled studies are available, the evidence suggests the use of anticoagulation or antiplatelet therapy in patients with cerebral embolism for whom the only potential cause may be a patent

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foramen ovale. There is some evidence, although mostly anecdotal, to suggest that surgical closure of the PFO is indicated in these patients to prevent recurrent embolization, but this procedure cannot be recommended with certainty at this time. Chiari's Network

Chiari's remnant is a remnant of the right venous valve from fetal life. It runs from the inferolateral part of the right atrium and extends onto the atrial septum in the region of the lower portion of the limbus of the fossa ovalis. Also known as Chiari's network, it is a fenestrated, filamentous structure that typically has an undulating appearance in real-time imaging (Fig. 37-11) . When not fenestrated, it is known as the eustachian valve or valve of the inferior vena cava, a normal structure. This structure can be seen in the right atrium by TTE in the four-chamber 817

Figure 37-11 Basal TEE view at 45 degrees showing the filamentous Chiari's network in the right atrium.

apical view and is even better visualized by TEE. It is easily identified in the bicaval (90-degree) view of the right atrium and can also be seen by looking at the basal short-axis view in the horizontal plane. These structures are normal variants and should be differentiated from right atrial clots. Chiari's networks may retain their role from fetal life, when they facilitated flow from the inferior vena cava across the PFO. Data on Chiari's network is limited, but in one study of 1436 patients who underwent TEE, Chiari's network was present in 2% of the patients. It was more frequently associated with PFO (83% vs. 28% control, P < .001) and atrial septal aneurysm (24%). Chiari's network was significantly more common in patients with unexplained embolic events than in patients evaluated for other indications (4.6% vs. 0.5%, P < .001).[119] Mitral Valve Strands

Several TEE studies have identified mitral valve strands in a high proportion of patients with a history of systemic embolism. The reported prevalence ranges widely, from 2% to 41%.[54] [120] [121] [122] [123] [124] [125] In a

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cohort of 1475 randomly selected subjects in Olmsted County, Minnesota, mitral valve strands were identified in 47% of patients, of whom 98% had no prior history of stroke.[126] The true prevalence, however, remains unknown. Mitral valve strands appear as small, fine threadlike material arising from the atrial surface of the mitral valve and have motion independent of the valve. In the literature, the term valve strand is often used interchangeably with Lambl's excrescence or valve excrescence. Unfortunately, there is no uniform definition of this entity. Valve strands are more commonly associated with the mitral valve but can occur on the atrial side of the tricuspid valve and on the ventricular side of the aortic valve. They have also been identified on prosthetic valves.[127] The histology of mitral valve strands is unknown. They may represent degenerative changes of the leaflet because they are associated with calcified or thickened mitral valves. They may also represent thrombi, fibrin strands, torn chordae, or redundant leaflets. Gross examination of a mitral valve that had filamentous strands seen by TEE revealed the strands to be consistent with a Lambl's excrescence.[54] The role of mitral valve strands in cerebral embolism remains in question. A number of retrospective studies suggested a potential association with embolic events.[54] [120] [121] , [123] [124] In one study, 9% of patients 50 years of age or younger had mitral valve strands as the only identified cardiac abnormality; however aortic atheroma were not routinely investigated.[123] In the French Study of Aortic Plaques in Stroke, 284 patients with a history of stroke were prospectively followed for 2 to 4 years. Mitral valve strands were found in 22.5% of the 284 case patients compared with 12.1% of the controls. The presence of mitral valve strands was associated with an increased risk of stroke, with an odds ratio of 2.2 (P = .005). Further analysis, however, showed a lack of increase in recurrence of stroke.[124] In another prospective TEE study, patients with mitral valve strands were prospectively followed clinically as well as with repeat TEE. The prevalence of valve strands appeared similar in the both normal subjects and patients with a history of stroke, with a reported prevalence of up to 47% of the subjects. Not only was there no association with future embolic events, TEE findings of valve strands persisted unchanged over time.[125] Thus, the contribution of mitral valve strands in embolic stroke is likely small. Intracardiac Tumors

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Cardiac tumors are rare, with an incidence of 0.001% to 0.28% in autopsy series.[128] They can, however, be a source of embolus. Cardiac metastases occur in 2% to 20% of patients with malignancies, most commonly lung or breast cancer. The most common primary cardiac tumors are myxomas, 80% of which occur in the left atrium, attached to the fossa ovale by a stalk. They can usually be recognized with TTE by their typical location and appearance (Fig. 37-12) . Myxomas often contain cysts and may have dermal elements such as bone, giving them a calcified appearance. Transesophageal echocardiography, however, has the advantages of better localizing the stalk, more clearly defining the characteristic heterogeneous appearance and mobility, and identifying any involvement of or any damage to the mitral valve (Fig. 37-13) .[129] [130] These advantages are invaluable in planning the surgical Figure 37-12 This patient is a 62-year-old woman with symptoms of weight loss and syncope. TTE showed large left atrial myxoma that prolapsed through mitral valve in the parasternal long-axis view.

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Figure 37-13 A 30-year-old woman whose physical examination was remarkable for a diastolic rumble and tumor plop. She underwent TEE prior to myxoma resection. Biatrial longitudinal view (A) and biatrial horizontal view (B) show left atrial myxoma with a heterogeneous appearance; it is attached to the interatrial septum. (Courtesy of Ray Stainback, MD.)

approach because these tumors, once identified, should always be removed in view of their embolic potential—highly mobile tumors with broad bases of attachment have much higher embolic potential than the wellencapsulated variety. Lambl's Excrescences and Papillary Fibroelastomas

Myxomas also occur on valves, but valve tumors are most often fibroelastomas.[131] [132] Papillary fibroelastomas are rare, accounting for 7% to 8% of nonmalignant cardiac tumors. They usually are discovered at autopsy, with an autopsy incidence of 0.002% to 0.33%, although the detection rate in their premorbid stage is higher with increasing use of echocardiography. They have a characteristic appearance on echocardiography and are commonly attached to a left-sided valve. They

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are usually found in older patients (>60 years), although they have been reported in patients ranging from 3 to 86 years of age. The literature is confusing because of a profusion of names for the same entity; cardiac papilloma, papillary fibroma, giant Lambl's excrescence, and papillary endocardial tumor have all been used to describe what is properly called a papillary fibroelastoma. Some reports differentiate Lambl's excrescences from papillary fibroelastomas by composition and location; Lambl's excrescences lack the rich acid mucopolysaccharide matrix and smooth muscle cells that are found in papillary fibroelastomas, which occur along the line of valve closure at contact points, and are more likely to occur in multiples (Fig. 37-14) . [133] Papillary fibroelastomas have "multiple papillary fronds" and can appear like a sea anemone attached to the endocardial surface of the valves by a small pedicle. They rarely exceed 1 cm in diameter. Lambl first described them, in 1856, as small filiform projections on the cusps of aortic valves. These tumors can form a nidus for platelet and fibrin aggregation and lead to systemic or neurologic emboli. They are most commonly identified on the valves as left-sided valvular structures much more commonly than as right-sided structures. They have also been found on the chordae and papillary apparatus, left ventricular septum, left ventricular outflow tract, left ventricular free wall, and the left atrium. [134] [135] Clinical manifestations include such conditions as cerebral embolism,[136] myocardial infarction,[137] sudden death,[138] pulmonary embolism,[139] and syncope.[140] In one striking case, a 3.5-year-old child presented with acute embolic stroke. Evaluation, which included echocardiography, revealed papillary fibroelastoma as the only potential source.[141] A review of echocardiograms at the Mayo Clinic from 1980 to 1995 found 54 patients with an echocardiographic diagnosis of papillary fibroelastomas; 17 of these patients were confirmed by pathologic diagnosis. They represented 0.019% of all patients who underwent echocardiographic evaluation during this period of time. Transesophogeal echocardiography was more helpful in identifying the condition than was TTE. Most of the tumors (81.5%) were found on the valvular endocardium, usually on the left side. Despite the association with valvular surfaces, valvular dysfunction is uncommon. The echocardiographic finding included small pendunculated tumors (usually <1.5 cm), with a refractive appearance and intratumuoral echolucency. Embolic events were observed

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in 20% of these patients. Surgical resection in this study was curative, with no new embolic events occurring at follow-up.[134] In another series of 15 patients at St. Elizabeth Hospital in New York, 9 patients had a history of stroke, with 4 of them having another potential source of embolism. In none of the patients with an embolic event was there a right-sided finding of papillary fibroelastoma. The authors recommended surgical excision in symptomatic patients only.[135] Anticoagulation therapy has been recommended when asymptomatic papillary fibroelastomas are identified; surgical excision is recommended for patients with a history of embolic events. These recommendations are not based on data from clinical trials. Valvular Vegetation

Acute bacterial endocarditis with deposition of vegetative material on one of the cardiac valves is another possible Figure 37-14 Small mass seen attached to the mitral valve consistent with Lambl's excrescence.

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Figure 37-15 This 44-year-old man with a history of intravenous drug use who presented with fever and cerebral and peripheral emboli underwent aortic valve replacement. A, TEE parasternal short-axis view showing a mobile 14-mm mass on the aortic valve. B, Parasternal long-axis view showing aortic vegetation. Ao, aortic valve; LA, left atrium; LV, left ventricle. (Courtesy of Elizabeth Ryan, MD.)

source of cardiac embolus (see Chapter 21) . The incidence of systemic embolization is observed in 22% to 50% of cases, with up to 65% of these events involving the central nervous system.[142] Most embolic events are observed during the first 2 to 4 weeks of therapy.[143] Early diagnosis and treatment are the keys to prevention of complications. Endocarditis should be suspected on clinical grounds in a patient with a history of fever, weight loss, high sedimentation rate, fatigue, and a new or changing murmur. Echocardiography is useful for identifying vegetations. Localization of

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vegetations to the precise cusp of attachment is possible by M-mode echocardiography, but only masses larger than 5 mm in diameter can be detected by M-mode methods.[144] Even when 2D imaging supplanted Mmode echocardiography as the imaging mode of choice, there was still suboptimal sensitivity.[145] This sensitivity was improved when TEE was used in the study of endocarditis.[146] In the early 1990s, several studies examined the difference in sensitivity between TTE and TEE.[147] [148] [149] [150] [151] Although specificity for both TTE and TEE is high (98% to 100%), the sensitivity of TTE is 44% to 60% for vegetation, and the sensitivity of TEE is 88% to 100%.[13] [142] Endocarditis is defined in these studies as a mass on a valve with characteristics that are highly suggestive of a vegetation. Characteristics include the location, shape, and texture of the mass; its characteristic motion; and accompanying abnormalities (Fig. 37-15) . Vegetations usually appear gray, with a lower level of reflectance than normal valve leaflets, as is seen for example in liver tissue. They are found on the upstream side of the valve (i.e., on the atrial side of the mitral and ventricular side of the aortic valve) at the point of turbulent flow, where a regurgitant or stenotic jet hits the valve or wall. Vegetations appear as lobulated, amorphous, and mobile structures. The mobility may be chaotic, may have an orbiting motion (around the valve), or may have fine vibrations imparted by contact with a jet. Echocardiographic characteristics that make a mass unlikely to be a vegetation include high reflectivity, high-contrast appearance (i.e., appears white not gray), well-defined borders, stringy appearance with a narrow base of attachment, and lack of associated valvular regurgitation. These guidelines apply to TTE and TEE images. In a study of TTE for the diagnosis of endocarditis, a group at Duke University[152] looked at the site, size, mobility, shape, and attachment of vegetations. There was high interobserver agreement on the presence and location of vegetations but less agreement on the size, mobility, and shape. Vegetation size was helpful in predicting emboli, with vegetations larger than 10 mm more likely to embolize (>50% vs. 42%). Generally, findings from TTE were not helpful in predicting complications. In one study in which 57 patients with acute infective endocarditis underwent both TTE and TEE, neither modality helped predict embolic complications.[153] In a similar study using TEE, Mugge et al[154] also found that the only

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echocardiographic finding predictive of embolic events was the size of the vegetation mass. They found a stronger association between vegetation size and embolic events than in the Duke study. This association was particularly true for mitral valve vegetations, perhaps owing to the increased sensitivity of transesophageal imaging. In this study, vegetations larger than 10 mm were more likely to embolize (46% vs. 20%; P <.001). Other researchers also have found that the size of the vegetation is related to the chance of embolization.[152] [155] [156] [157] Vegetations on the mitral valve are thought to have the highest embolic risk for cerebrovascular events. Rohmann et al,[155] using an innovative approach, performed serial TEE in 83 patients. They found that prognosis was much worse if a vegetation was enlarged or did not change during 4 to 8 weeks of therapy than if the vegetation shrank with therapy. These differences included incidence of valve replacement (45% vs. 2%), embolic events (45% vs. 17%), abscess formation (13% vs. 2%), and mortality (10% vs. 0%; all P < .05).[155] In the UCSF Echo Laboratory, these data have encouraged a strategy of watchful waiting in the case of patients with large vegetations but without embolic events or signs of congestive heart failure. After 7 days of therapy, TEE is repeated, the vegetations are remeasured, and therapy is planned according to the results. Even using this abbreviated time scale, decreases in vegetation size have been observed. The widespread adoption of this shortening of Rohmann's protocol, although promising, must await further verification. The American Heart Association (AHA) consensus panel now recommends routine echocardiography in patients suspected of infective endocarditis. In particular, TEE is indicated in patients with moderate to high risk for infective endocarditis such as large or mobile vegetations, valvular insufficiency, suggestion of perivalvular extension, or secondary valvular dysfunction, or if the patients are difficult to image with TTE.[13] [142] A recent study found the use 820

of TEE is cost-effective, even in patients with suspected intravascularassociated staphylococcal bacteremia.[158] Intraoperative Transesophageal Echocardiography

Neurologic sequelae from cardiopulmonary bypass surgery are increasingly recognized as common. In particular, stroke is a reported complication that

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occurs in 2% to 6% of procedures.[159] [160] There are several insights from TEE studies that show promise for reducing this serious complication. Atheromatous aortic plaque is one of the most important risk factors for embolic events during cardiac surgery. One possible explanation could be that placement of the aortic cannula may dislodge the plaque; this is especially likely for a mobile and protruding atheroma. Other maneuvers that may dislodge the aortic atheroma during cardiopulmonary bypass surgery are overaggressive palpation, aortic cross-clamping, anastomosis of proximal vein grafts to the ascending aorta, and the "sandblast" effect of high-pressure cannula flow against the aortic wall. Intraoperative TEE monitoring allows identification of plaque location, and the anesthesiologist or cardiologist can guide the surgeon in placement of the aortic cannula to avoid plaque. Guidance of cannula placement by TEE has been more accurate than direct palpation in identification of aortic atheroma in the operating room.[161] There is evidence that intraoperative TEE guidance to avoid atheroma during cannula placement can decrease the risk of stroke. [162] Katz et al[162] reported a case of intraoperative TEE monitoring during cardiopulmonary bypass in which a mobile atheroma was seen to disappear as the cannula was inserted into the arch in the region of the atheroma. The patient awoke with a neurologic deficit. Other techniques that have been used in an attempt to reduce embolic events during cardiopulmonary bypass surgery include hypothermic circulatory arrests, a long aortic cannula, and aortic arch débridement in patients at high risk for emboli, as determined by TEE.[161] [163] Aortic arch endarterectomy, however, has recently been found to be associated with a higher risk of intraoperative stroke.[164] Epiaortic surface imaging may be even more accurate than TEE in identifying aortic plaque[164] because it allows the most precise localization of plaque and avoids the shadowing that can obscure imaging in the anterior portion of the aorta, particularly if multiplane TEE is not available. TABLE 37-5 -- Prevalence of Complex Atheroma Detected by TEE in Case-Control Studies Studies Tunick[167] Amarenco

Plaque Thickness ≥5 mm ≥4 mm

Control Patient Cases (N) (N) (%) 122 122 27 250 250 14.4

Control (%) 9 2

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[168]

Jones[169] Stone[170] Di Tullio[171] Ferrari[172] Di Tullio[173]

≥5 mm ≥5 mm ≥5 mm ≥4 mm ≥4 mm

215 49 106 418 152 1312 (Total)

202 57 114 698 152 1595 (Total)

21.4 32.7 26 25.6 22.4

3.5 7 13 5 2.6

Thoracic Aortic Atheroma

Atheromatous changes in the thoracic aorta are now recognized as an important risk factor for embolic events. Because of their location, TEE is by far the imaging modality of choice.[165] To image the descending aorta, it is best to start from the transgastric view. The TEE probe should be rotated 180 degrees from the transgastric view and withdrawn slowly into the esophagus. The depth of field can be adjusted to 4 to 6 cm because the descending aorta is quite close to the esophagus. This magnifies the image and facilitates identifying intimal thickening and plaque. The distance of the probe tip from the incisors should be annotated every 5 cm and at any point where there is an abnormality. Biplane or multiplane probes should be used for imaging, whenever possible. To examine the aortic arch, the probe should be rotated anteriorly at approximately 20 cm from the incisors. This structure is best imaged with bi- or multiplane technology. It is best to image the arch at the conclusion of the TEE examination because many patients experience reflex gagging at this insertion level, and the probe can then be withdrawn after completion of aortic arch imaging. Atherosclerotic plaque often involves the arch and descending thoracic aorta. The atherosclerotic changes are commonly graded from I to IV (see Table 37-4) . Atheroscerotic changes in the aorta are common in the general population. In an autopsy series of 500 consecutive patients, ulcerated plaques were detected in 5% of the patients with no history of cerebrovascular disease. In patients with a history of stroke, however, the prevalence of plague at this site was 26%. In patients who had cerebral infarcts without hemorrhage, the prevalence was 28%.[166] In case-control studies of patients with a history of stroke who underwent TEE, the prevalence ranges from 14% to 33%. On

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the other hand, ulcerated plaques are only seen in 5% of the control patients in these studies (Table 37-5) . [167] [168] [169] [170] [171] [172] [173] In studies in which any significant aortic atheroma in patients with a history of ischemic stroke is considered, the prevalence is approximately 27%.[167] [169] [170] [171] [172] [173] The prevalence of significant aortic arch disease is approximately 14%.[168] [174]

Since the embolic potential of aortic atheromas was first described by Tunick and Kronzon in 1990,[175] numerous papers have documented an association between atheromatous changes in the aorta and systemic emboli.[167] [168] [169] [170] [171] [172] [173] Atheromas at highest risk for embolization are those that protrude 4 mm or more into the aortic lumen or are pedunculated and have freely mobile components (Fig. 37-16) . Amarenco 821

Figure 37-16 This 70-year-old man was undergoing coronary artery bypass grafting. A, Horizontal plane TEE view of the descending aorta shows a large aortic atheroma protruding into the aortic lumen. Intimal thickening and irregularity are also noted. B, Longitudinal TEE view of the same plaque.

et al,[168] using TEE in a prospective case-control study of 250 patients over 60 years of age, discovered a higher incidence of plaque 4 mm or thicker in the ascending aorta and proximal arch in patients with no known explanation for stroke, compared with a control group of cerebrovascularaccident patients with known or possible causes of stroke (28% vs. 8%). After adjustment for atherosclerotic risk factors, the odds ratio for ischemic stroke among patients with such plaques was 9.1. Plaques 4 mm or thicker in the aortic arch were not associated with atrial fibrillation or stenosis of the extracranial internal carotid artery. In contrast, plaques that were 1 to 3.9 mm thick were frequently associated with carotid stenosis of 70% or greater. These results confirm a strong, independent association between atherosclerotic disease of the aortic arch and the risk of ischemic stroke, especially for thick plaques.[168] Not only does aortic plaque pose an apparent risk factor for the first stroke but thoracic aortic atheroma 4 mm or thicker predicts recurrent events. In a follow-up study of 331 patients admitted for stroke, originally described by Amarenco et al,[168] the incidence of recurrent stroke was 11.9 per 100 person-years in patients with atheroma 4 mm or thicker compared with

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those whose aortic-wall thickness was 1 to 3.9 mm and less than 1 mm (P < .001). After adjusting for other potential risk factors for stroke, the presence of aortic plaques 4 mm or thicker was found to be an independent predictor of recurrent stroke.[174] In a smaller study, Dressler et al also noted a high recurrent stroke rate of 38% in 1 year.[176] Interestingly, in the SPAFIII substudy, complex aortic atheroma independently predicted increased risk of stroke.[177] Complex aortic atheroma independently predicted risk of recurrence, also at 12% per year.[178] In addition, patients with complex aortic atheroma are at risk for vascular embolic events. In a prospective TEE study of the risk of vascular events in patients with protruding aortic atheromas, 42 of 521 patients had protruding atheromas and no other source of emboli. They were followed for up to 2 years and compared with a control group without atheromas, matched for age, gender, and hypertension. In 42 patients with atheromas, 14 (33%) had 19 vascular events (five brain, two eye, four kidney, one bowel, seven lower extremity) during follow-up; in 42 control patients, 3 (7%) had vascular events (two brain and one eye). Univariate analysis identified only protruding atheromas as significantly correlating with events, and multivariate analysis showed that only protruding atheromas independently predicted events.[179] In the French Study of Aortic Plaques in Stroke, the incidence of vascular events was 26 per 100 person-years of follow-up. [174] In a follow-up study of echocardiographic correlates of vascular events, the same group noted with interest that ulceration did not increase the risk of vascular events. The lack of calcification markedly increased the risk of subsequent vascular events (relative risk of 10.3, P < .001). The authors postulated that the lack of calcification may be associated with plaques that are vulnerable.[180] Pathophysiologically, limited evidence suggests embolic strokes probably result from thromboembolic occlusion by the mobile elements in these complex aortic plaques. In a pathologic and TEE study, the mobile elements seen on TEE intraoperatively appeared on pathologic examination to be thrombi. For identification of thrombus, TEE had a sensitivity of 91% and a specificity of 90%.[181] In a separate pathologic and TEE study, again the mobile elements seen intraoperatively in the aorta were associated with thrombosis that was confirmed pathologically.[182] In 1998, Freedberg et al described a case report of a patient with protruding atheroma who died of an embolic phenomenon. For the first time, emboli from these atheroma were visualized in transit on TEE.[183] Together these studies provide a pathologic basis for thromboembolism in patients with aortic atheromas.

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A high risk of embolic events related to invasive procedures also has been shown in patients with aortic atherosclerosis, particularly those patients with pedunculated aortic plaques.[184] [185] In one study of patients with aortic arch disease and atheroma 5 mm or thicker, 17% of the 59 patients suffered an embolic event following cardiac catheterization through the femoral approach compared with 3% of controls (P = .01). Similarly, 5 of 10 patients who underwent placement of intra-aortic balloon pump experienced an embolic event compared with 0 events in 12 controls (P = .02).[185] If possible, TEE examination of the thoracic aorta in selected patients should be performed before invasive aortic procedures such as leftheart catheterization and intra-aortic balloon pulsation. If pedunculated plaque or mobile thrombus is identified, invasive aortic procedures should be undertaken only with the understanding of an increased embolic risk in these patients. Some operators prefer to perform left-heart catheterization from the arm, using the Sones technique in these high-risk patients—for whom TEE is key in identification—if angiography is indicated. Because aortic atherosclerosis seen by TEE is a marker for coronary artery disease, [186] [187] patients at high risk for emboli often are the ones who need invasive procedures. The treatment of atheromatous plaque is not well defined. Earlier reports of peripheral embolization in patients on warfarin raised concerns about the safety of anticoagulation in these patients.[188] The increasing use of warfarin in clinical practice, however, has thus far been found to be safe. Perhaps the largest controlled experience with warfarin is in the area of atrial fibrillation. In SPAF-III, as discussed earlier, patients with complex aortic plaques in the setting of atrial fibrillation have a fourfold increased rate of stroke (P = .005). The use of warfarin 822

decreased the risk by as much as 75% (P = .02).[178] A number of recent uncontrolled studies have all found a lower incidence of stroke with the use of warfarin.[172] [176] [189] The lack of randomized controlled data made rational treatment difficult. As it turns out, atheromatous lesions are dynamic in nature. Montgomery et al performed serial TEE examinations in patients with significant atheromatous disease of the aorta. No intervention was prescribed. During a 20-month period, 7 of the 10 patients with severe atherosclerotic aortic disease developed a new mobile lesion. The same number of patients showed resolution of a previously documented mobile lesion. Of note, only one clinical embolic event was documented in these

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patients.[190] The need for better clinical data is clear. Until outcome data are available, the use of anticoagulation therapy, although safe, should be reserved for patients with a history of otherwise unexplained embolic event and high-risk echocardiographic features. This is an area of continued study. Percutaneous Valvuloplasty

An embolic rate of 4% is associated with percutaneous balloon mitral valvuloplasty (see Chapter 19) . The embolic event can occur during the procedure or in the first few days after the procedure and is associated with a highly calcified valve. This feature can be identified echocardiographically, and echocardiography may serve to influence the occurrence or course of the procedure.[191] Mitral Valve Prolapse

Mitral valve prolapse is another common finding that is purportedly associated with emboli in some studies. It is defined echocardiographically if two of the following four criteria are present: (1) superior displacement of any part of the mitral leaflets above the annulus 2 mm or more in the parasternal long-axis view; (2) marked superior displacement (>3 mm) of the bellies of the anterior and posterior mitral leaflets above the annulus, with the coaptation point at or above the annular plane in the four-chamber apical view; (3) increased mitral leaflet thickness (>5 mm); and (4) pathologic mitral regurgitation. Ischemic neurologic events were previously thought to be highly correlated with mitral valve prolapse, especially in patients under 45 years of age. [192] [193] Some of these studies, however, were done using M-mode criteria for mitral valve prolapse. By these criteria, 7% to 21% of a healthy population were defined as having mitral valve prolapse. Since then, there has been more accurate definition of mitral valve prolapse using 2D criteria. Using the currently accepted criteria for mitral valve prolapse, the association between mitral valve prolapse and ischemic neurologic events is no longer seen. Earlier studies found mitral valve prolapse in up to 40% of younger patients with stroke or transient ischemic attack, but Gilon et al found mitral valve prolapse in only 1.9% to 2.7% of younger patients, using accepted 2D criteria. Furthermore, this case-control study of 213 patients 45 years of age or younger suggested that mitral valve prolapse was not associated with an increased incidence of stroke.[194] In a population-based

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cohort study of 1079 residents of Olmsted County, Minnesota, patients with echocardiographic diagnosis of mitral valve prolapse between 1975 and 1989, without prior stroke or transient ischemic attack, were followed until the development of their first stroke. Patients with mitral valve prolapse had a twofold increase of incidence of stroke (standardized morbidity ratio, 2.1; 95% confidence interval, 1.3 to 3.2). After adjustment of risk factors such as age, diabetes, congestive heart failure, atrial fibrillation, and mitral valve replacement, however, no association between mitral valve prolapse and stroke was seen. Of note, the mean age at initial stroke was 78 years of age.[195] In subsequent follow-up of 49 patients with mitral valve prolapse and a history of ischemic stroke, no increased incidence of recurrent stroke was identified.[196] More recently, in the offsprings of the Framingham Heart Study, mitral valve prolapse was seen in 2.4% of 3491 subjects. The natural history, as in other studies, was benign, with no increase in ischemic stroke risks.[197]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Studies in Progress Warfarin Antiplatelet Recurrent Stroke Study The Warfarin Antiplatelet Recurrent Stroke Study (WARSS)[198] is a randomized, double-blind, multicenter study funded by the National Institute of Neurological Disease and Stroke. It enrolled 2206 patients from 1993 to 1998. The average age of patients enrolled was 63 ± 11 years; 41% were female and the population was ethnically diverse. Patients all underwent TTE and were randomized to warfarin or aspirin and followed for recurrent embolic events for a minimum of 2 years. Results showed no difference in recurrent stroke or death for either of the two treatment arms. For major secondary outcomes, there was no difference in recurrent stroke or death or major hemorrhage. Subgroup analysis showed no difference when analyzed by race, ethnicity, gender, or baseline stroke subtype. Overall, the result favored aspirin, with an 11% benefit over warfarin; however, this difference was not statistically significant (www.conferencecapture.com/cc/aan; accessed July 26, 2001). Patent Foramen Ovale in Cryptogenic Stroke Study The Patent Foramen Ovale in Cryptogenic Stroke Study (PICSS)[198] is a substudy of WARSS. The study focuses on 500 patients with cryptogenic stroke. This subset of patients undergoes TEE for identification of PFO. This group is followed separately and may be randomized in future trials for surgical or percutaneous closure of the PFO. Results will be available in 2002. Warfarin-Aspirin Reduced Cardiac Ejection Fraction Study Warfarin-Aspirin Reduced Cardiac Ejection Fraction Study (WARCEF) [199] is a randomized, double-blind,

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823

multicenter study with a target enrollment of 2860 and mean follow-up of 3 years. Patients with low ejection fractions are randomized to warfarin or aspirin. The primary outcome is death, recurrent stroke, or intracerebral hemorrhage. Warfarin and Antiplatelet Therapy in Chronic Heart Failure Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) [199] is a randomized, multicenter study of patients with a history of congestive heart failure and low ejection fraction. The patients are randomized to warfarin, aspirin, and clopidogrel. Primary outcome includes death, stroke, and myocardial infarction.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Attribution of Embolic Events to a Cardiac Source Approximately 20% of strokes are thought to result from a cardiac source of embolism, and 40% are of undetermined origin, but an increasing number in the latter category have been associated with the various echocardiographic findings discussed in this chapter. Despite the strong association between echocardiographic findings of a source of embolus and stroke, it remains difficult to show a true cause-and-effect association. The scientific difficulty was demonstrated in a paper by Sansoy et al.[200] This group at the University of Virginia compared two groups of patients, one group undergoing echocardiography who had embolic events versus an age-matched group undergoing echocardiography but with no history of embolic events. It was observed that the incidence of echocardiographic findings believed to be cardiac sources of emboli, such as left ventricular thrombus and left atrial appendage thrombus and PFO, were similar in these two groups. This observation led the authors to question whether the finding of a cardiac thrombus in a patient with stroke is unrelated to the cause of the stroke. Because we must make medical decisions with the best data we have available, the findings of a probable source of embolus by echocardiography in a patient with embolic events is strong enough evidence to mandate anticoagulation therapy, preferably with warfarin. The finding of a possible source of embolus by echocardiography in a patient with embolic events, based on currently available data, also suggests a benefit from anticoagulation with aspirin or warfarin, preferably aspirin. More definitive recommendations for this group can be made when the results of large, randomized trials such as WARSS are available.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Influence of Echocardiographic Evaluation on Patient Management Several studies have examined how echocardiographic evaluation of patients with embolic events influences patient management. In the Value of Transesophageal Echocardiography (VOTE) study, 847 of the 3001 patients underwent TEE because of a history of cerebrovascular accident or transient ischemic attack; TEE led to a change in clinical management of 27% of patients and a change in drug regimen for 15.7% in this group. This was a higher percentage of change in drug regimen (14.1%) but a lower percentage of change in clinical management (38.5%) than for the group as a whole. The data suggested that TEE is useful for determining the management of patients with cerebrovascular ischemia, particularly in establishing pharmacologic therapy.[201] In the Significance of Transesophageal Echocardiography in the Prevention of Recurrent Stroke (STEPS) study, 242 patients with unexplained cerebral ischemia underwent TEE and were followed for 1 year. Recurrent stroke occurred in 17 of 132 (13%) of the patients in the aspirin group versus 5 of 110 (5%) of the patients receiving warfarin (P <.02). The TEE findings again played a major role in determining the pharmacologic therapy.[189] In support of the above findings, McNamara and his colleagues [202] performed a cost-effectiveness analysis on the value of echocardiography in the clinical management of stroke. In their analysis, the indication for anticoagulation therapy was limited to only left atrial or left atrial appendage thrombus. Interestingly, they found that TTE alone or in sequence with TEE was not cost-effective compared with TEE alone. Because of their findings, they recommended TEE in all patients with new stroke.[202] These studies together suggest that more changes in patient management are made as a result of TEE than as a result of TTE. This difference is no doubt related to the greater number of findings made on TEE than on TTE.

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The important question of how these changes in patient management affect patient outcome measures, such as rate of recurrent embolization and mortality, however, remains to be answered. This question is now being addressed in several clinical trials, of which the results will be available in the next few years.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Good medical judgment based on best available evidence should guide the work-up and management of systemic embolism. We have outlined a simple approach to the echocardiographic evaluation of patients who present with a suspected embolic event (Fig. 37-17) . Echocardiography is often recommended in patients suspected of a cardioembolic stroke. [12] [13] , [203] This recommendation is particularly strong for groups that have a possible contraindication to anticoagulation and if it is important to define precisely the risks and benefits of anticoagulation. Conversely, the recommendation for echocardiography is weakened for patients who would be anticoagulated regardless of echocardiographic findings. Both the AHA Echocardiography Task Force and the Canadian Task Force on Preventive Health Care considered echocardiography to be not useful in cases where findings of the echocardiogram do not alter management, particularly in anticoagulation.[12] [13] At this time, anticoagulation for many of the associated echocardiographic findings are 824

Figure 37-17 Echocardiographic evaluation of patients with a systemic embolic event. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

not supported by clear clinical data.[204] The results of randomized clinical trials will help further refine the management and work-up of patients with embolic events.

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829

Chapter 38 - The Role of Echocardiography in Atrial Fibrillation and Flutter Aneesh V. Tolat MD Warren J. Manning MD

Technologic advances in two-dimensional and Doppler ultrasonography have led to the emergence of echocardiography as an integral tool in the evaluation and management of patients with cardiac rhythm disturbances. Transthoracic and transesophageal echocardiography (TEE) provide detailed information about cardiac anatomy and function. Patients with ventricular tachyarrhythmias are routinely referred for echocardiographic examination for identification of suspected structural heart disease.[1] [2] [3] [4] Echocardiography may also play a role in the localization of bypass tracts in Wolff-Parkinson-White syndrome[5] and in the choice of optimal pacemaker type, lead position, and settings in patients with hemodynamic compromise related to rhythm disturbances.[6] In addition, serial echocardiographic assessment of ventricular function has led to the recognition of tachycardia-induced cardiomyopathy as a distinct clinical syndrome.[7] In addition to ventricular arrhythmias, echocardiography provides useful information in the evaluation and management of patients with atrial arrhythmias, particularly atrial fibrillation. In this chapter, we review the detailed structural and functional information derived from transthoracic

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echocardiography and TEE and how these data assist in the evaluation and management of patients with atrial fibrillation and flutter.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Assessment of Atrial Anatomy and Function Left Atrial Anatomy Transthoracic echocardiography has long been recognized as a reliable and reproducible method to assess the anatomy of the body of the left atrium. M-mode echocardiography[8] [9] [10] allows for the measurement of left atrial dimension in the parasternal long- or short-axis orientations. Overall, this unidimensional index correlates well with angiographically derived left atrial area and volume[9] [10] but may be disproportionately erroneous in disease states associated with asymmetric atrial dilation, such as mitral valve disease. [11] [12] Transthoracic two-dimensional imaging provides more accurate assessment about atrial anatomy. The left atrium is well seen from both the parasternal and the apical windows. In our laboratory, we typically measure the major dimension or length (L) of the left atrium in the apical four-chamber view during ventricular systole to complement the M-mode dimension (D1 ) from the parasternal long-axis window. Measurement of left atrial width from the parasternal short axis (D2 ) then facilitates calculation of left atrial volume using an ellipsoid model[11] [12] Echocardiographically derived left atrial volumes correlate well with angiographic volume.[10] In situations in which there is focal atrial asymmetry, such as distortion of the left atrium from an extrinsic structure (e.g., mediastinal tumor, hiatal hernia, or descending thoracic aortic aneurysm), accurate calculation of left atrial volume may be improved by using a Simpson Rule approach. Transesophageal echocardiography is a well tolerated but moderately

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invasive diagnostic imaging technique that allows for superior visualization of posterior structures such as the left atrium and atrial appendage. Although 830

Figure 38-1 Transthoracic echocardiographic image taken from the apical four-chamber view obtained with a 5 MHz imaging transducer. Note the thrombus (arrow) along the posterior wall of the left atrium in this patient with rheumatic mitral stenosis. LV, left ventricle; RA, right atrium.

TEE may be used to assess the body of the left atrium from orientations analogous to transthoracic imaging,[13] its greatest advantage is in evaluation of the anatomy and function of the left atrial appendage. Identification of Left Atrial Thrombi Anatomic imaging of the body of the left atrium may be readily obtained from transthoracic two-dimensional echocardiography, but identification or exclusion of left atrial and left atrial appendage thrombi are best reserved Figure 38-2 Transesophageal echocardiographic image taken in the horizontal plane using a 5 MHz imaging transducer. A, 15 mm thrombus (arrow) near the mouth of the left atrial appendage; B, 4 mm thrombus (arrow) at the tip of the left atrial appendage. (From Manning WJ, Reis GJ, Douglas PS: Br Heart J 1992;67:171.)

for TEE. The sensitivity of transthoracic echocardiography for the detection of left atrial thrombi (Fig. 38-1) has been estimated at only 39% to 63%,[14] [15] [16] with very limited success for identifying thrombi in the left atrial appendage. Even with modified views,[17] visualization of the left atrial appendage may be accomplished in less than 20% of patients.[18] Recent preliminary data suggest improved left atrial appendage assessment with newer echocardiographic technology,[19] but this approach requires further validation. Imaging of the left atrial appendage is readily accomplished with monoplane, biplane, or multiplane TEE (Fig. 38-2) . The normal length and neck width of the adult left atrial appendage in the horizontal and vertical imaging planes are 28 ± 5 mm and 16 ± 5 mm, respectively.[20] Left atrial

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appendage anatomic indexes are dependent on imaging plane, with greater neck width and cross-sectional area when observed at a 135-degree imaging plane as compared with a 45-degree or 90-degree plane, consistent with its shape idealized as a special ungula of a right circular cylinder.[21] Multiple lobes and trabeculations are common[21] (see Fig. 38-2) . The accuracy of monoplane TEE for the identification of left atrial thrombi has been reported by several investigators. Aschenberg et al[18] were among the first to report on preoperative monoplane TEE for atrial thrombi. Among 21 consecutive patients presenting for routine mitral valve replacement, 6 patients had TEE evidence of left atrial thrombi. All six thrombi were confirmed at surgery and no additional thrombi were seen on direct inspection. Mügge et al[22] subsequently reported on 12 patients with atrial thrombi detected by monoplane TEE who were referred for cardiac surgery. All thrombi were confirmed on direct inspection. Similarly, Olson et al[23] performed monoplane TEE in 20 patients immediately prior to mitral valve replacement or mitral valve repair. They prospectively identified all three atrial thrombi seen at surgery, including two in the left atrium and one in 831

Figure 38-3 Transesophageal echocardiographic image depicting normal right atrial appendage (RAA) in the horizontal imaging plane (A) and another patient with a right atrial thrombus (arrow) in the vertical plane (B).

the right atrium. Finally, in the largest monoplane TEE series, Hwang et al [24] reported on more than 200 patients with rheumatic mitral valve disease undergoing monoplane TEE within 3 days of valve surgery. Sensitivity and specificity for detection of atrial thrombus were 93% and 100%, respectively. Over the past decade, monoplane TEE technology has largely been supplanted by biplane (pediatric probe) and multiplane (adult probe) imaging. The additional imaging planes offered by the latter two technologies offers superior visualization of the left atrial appendage. In our experience of nearly 200 consecutive patients undergoing monoplane, biplane, or multiplane intraoperative TEE immediately prior to mitral valve surgery, TEE sensitivity and specificity for left atrial thrombi were 100% and 99%, respectively.[25] We have found both biplane and multiplane TEE

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to be superior to monoplane imaging. For the left atrial appendage, clinically relevant differences between biplane and multiplane imaging are less certain. We have yet to encounter a situation in which an atrial appendage thrombus was "missed" during vertical (90-degree) plane imaging but was seen during the intermediate viewing angles afforded by multiplane technology. Such a situation has been reported by others,[26] however, and we therefore recommend multiplane imaging whenever it is available. Right Atrial Anatomy The right atrium has not been as well studied by either transthoracic echocardiography or TEE. As is the case with the left atrium, twodimensional transthoracic imaging provides a reasonably comprehensive assessment of right atrial volume. The primary transthoracic window is the apical four-chamber view, with right atrial area estimated using a lengthdiameter ellipsoid formula. Parasternal short-axis and subxiphoid windows provide complementary data. The right atrial appendage is rarely appreciated from transthoracic approaches, but biplane (Fig. 38-3) and multiplane TEE (135-degree) readily allow for visualization of this structure. In our experience, monoplane TEE is quite inferior for the evaluation of the right atrial appendage. Care must be taken to avoid mistaking normal structures (such as the eustachian valve or Chiari network) for thrombi.[27] Transthoracic and TEE sensitivity and specificity data for identification of right atrial thrombi are relatively sparse. Schwartzbard et al[28] reported on 20 patients with TEE evidence of right atrial thrombus, including 7 confirmed at surgery. Transthoracic echocardiography identified thrombus in only 6 patients (30%). All right atrial appendage thrombi were missed by surface echocardiography. Atrial Mechanical Function In addition to providing information about atrial anatomy, echocardiography is a powerful tool for evaluation of atrial systolic performance. The atria are traditionally believed to have two primary functions: as passive conduits or reservoirs for oxygenated blood passing from the vena cava or lungs to the ventricles and as booster pumps to augment passive diastolic ventricular filling. Prior to the advent of echocardiography, assessment of atrial mechanical

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function had been limited to invasive catheter-based techniques,[29] which are impractical for serial assessments. M-mode echocardiographic assessment of mitral valve motion can be used in patients with cardiac arrhythmias and was first described by Gabor and Winsberg.[30] Normal anterior mitral leaflet excursion is 13 mm,[31] with depressed excursion seen with mitral stenosis, low cardiac output, and in association with atrial mechanical dysfunction. With the development of two-dimensional guided pulsed Doppler technology, transmitral Doppler spectra have become recognized as an accurate technique for quantifying atrial mechanical function. In the absence of 832

Figure 38-4 Spectral display of transmitral pulsed Doppler echocardiographic flow velocity. A, atrial filling wave; E, early filling wave; ECG, electrocardiogram. The time scale (top) is measured in milliseconds. (From Manning WJ, Silverman DI, Katz SE, et al: J Am Coll Cardiol 1993;22:222, with permission from the American College of Cardiology.)

aortic insufficiency, left ventricular filling may be divided into passive and active phases. The initial (early, or E) wave in the transmitral Doppler flow profile represents passive ventricular filling, and the final (atrial, or A) wave represents active filling during atrial systole (Fig. 38-4) . This transmitral Doppler flow profile can be influenced by a number of factors, including heart rate, loading conditions, and sample volume position. The most common indexes of interest include peak A wave velocity, percentage of A wave filling, and peak and percentage E/A ratios. Peak E and A wave velocities vary considerably with sample position. In our laboratory, we generally assess the transmitral profile at its maximum (between the tips of the mitral leaflets). In addition to the previously described quantitative indexes of transmitral Doppler data, the transmitral Doppler profile may also be used to calculate atrial ejection force, defined as that force which the atrium exerts to propel blood into the left ventricle.[32] The atrial ejection force is based on newtonian mechanics and is proportional to the mitral orifice area and the square of the peak A wave velocity. As with more traditional E wave and A wave indexes, atrial ejection force may be dependent on loading parameters, although this subject remains to be more completely studied. If

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calculation of atrial ejection force is desired, a pulsed Doppler sample position at the level of the mitral annulus would be geometrically more appropriate. Left Atrial Appendage Function Since the left atrial appendage is a "blind pouch," volumetric ejection must equal inflow during each cardiac cycle. Pollick and Taylor[33] noted that patients with sinus rhythm who were free of atrial thrombus had a characteristic contractile left atrial appendage apex and a noncontractile base. Two-dimensional TEE guided pulsed Doppler has allowed for further characterization of left atrial appendage systolic performance. The pulsed Doppler profile taken at the mouth of the left atrial appendage displayed characterizing ejection and filling phases (Fig. 38-5A) . In a healthy adult population, peak left atrial appendage ejection and filling velocities are 46 ± 18 cm per second and 46 ± 17 cm per second, respectively.[34] Investigators have subsequently characterized left atrial appendage flow patterns as having four distinct morphologic types (see Fig. 38-5) : type I, sinus; type II, flutter (regularized saw-tooth); type III, fibrillatory (irregular saw-tooth) with ejection velocity greater than 0.2 m per second; and type IV, stagnant/absent flow with peak ejection velocity of 0.2 m per second or less. In rare instances, there may be a discontinuity between the body of the atrium and appendage[35] [36] with sinus pattern on transmitral flow but a fibrillatory pattern in the appendage. As compared with anatomic indexes, which appear to be dependent on imaging plane, Doppler indexes of atrial appendage ejection and inflow are independent of imaging plane.[21] Spontaneous echocardiographic contrast, a marker for stasis, is typically seen with type III or IV appendage flow, whereas left atrial appendage thrombi are most commonly seen with type IV flow.[37] [38] As with transmitral Doppler data, left atrial appendage flow velocities are dependent on Doppler sample position and loading conditions.[39] Right atrial appendage function has not been well studied and remains to be defined.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography and Atrial Fibrillation Prevalence of Atrial Fibrillation Atrial fibrillation is a common arrhythmia, with an overall prevalence of 0.4% in the United States[40] and responsible for more than 180,000 hospital admissions annually.[41] Its prevalence increases sharply with increasing age and is found in up to 4% of persons over 60 years of age.[42] Preliminary data from the Framingham Heart Study suggest that an increased E/A was associated with an increased risk for the subsequent development of atrial fibrillation.[42] In an earlier Framingham Heart Study, the presence of chronic atrial fibrillation was associated with a near doubling of both overall and cardiovascular mortality. [43] Atrial flutter is a far less common sustained arrhythmia. Analogous 833

Figure 38-5 Spectral display of pulsed Doppler echocardiographic flow velocity with the sample volume at the mouth of the left atrial appendage. A, Patient in sinus rhythm. B, Patient with atrial fibrillation with active appendage ejection. C, Patient with atrial fibrillation with minimal atrial appendage mechanical function. The vertical calibration markings for each represent 0.2 m/sec intervals.

detailed epidemiologic studies are not available. Symptoms and Clinical Impact Atrial fibrillation is characterized by a lack of organized atrial mechanical and electrical activity. This condition promotes stasis of blood within the atria and increases the risk of thrombus formation. Thromboembolism associated with atrial fibrillation is believed to account for nearly half of all cardiac sources of emboli. In addition to the risk of thrombus formation,

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loss of organized atrial mechanical activity impairs the atrium's ability to act as a "booster" pump, and thus impairs ventricular filling (and consequently cardiac output).[44] The mechanical function of the atria appears to be less severely impaired in atrial flutter, but thrombus formation remains a concern, particularly among patients with alternating atrial fibrillation and flutter or flutter in the setting of mitral stenosis or left ventricular systolic dysfunction. Important clinical issues related to atrial fibrillation include the following: 1. Thromboembolism, including cerebral and other systemic emboli and pulmonary emboli. These events are likely due to the migration of thrombi formed within the atria during the period of atrial fibrillation or may relate to new thrombus formation after conversion to sinus rhythm. Most atrial thrombi reside in the left atrial appendage (a structure best visualized by TEE). TEE evidence of spontaneous echocardiographic contrast and depressed atrial appendage ejection velocity are markers for increased risk for both thrombus formation and for clinical thromboembolism. 2. Hemodynamic decompensation, which may include depressed cardiac output, congestive heart failure, fatigue, and pulmonary edema. Decompensation is particularly common among patients with a noncompliant ventricle. Such a situation may occur with normal aging and with left ventricular hypertrophy related to systemic hypertension or aortic stenosis. This hemodynamic deterioration is particularly common in the setting of a rapid ventricular rate, during which the diastolic filling period is preferentially shortened. 3. Palpitations, most commonly associated with atrial fibrillation with a rapid (>100 per minute) ventricular response. Patients with controlled ventricular rates (<100 per minute) are often asymptomatic. 4. Tachycardia-induced cardiomyopathy, which may occur in patients with poorly controlled rapid ventricular rates. Atrial Size and Atrial Fibrillation Left atrial enlargement is common among patients with atrial fibrillation, particularly those with mitral valve disease or systemic hypertension. Data suggest that left atrial enlargement decreases the likelihood that long-term maintenance of sinus rhythm will be maintained.[45] [46] Aronow et al[47] studied 588 patients and found that an enlarged left atrium was present in 57% of patients with chronic atrial fibrillation as compared with only 8% of those with sinus rhythm. Data from the Framingham Heart Study suggest

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that among those without a history of atrial fibrillation, left atrial enlargement is among the strongest predictors for the subsequent development of nonvalvular atrial fibrillation.[43] Several groups have reported that left atrial size increases with progressive duration of atrial fibrillation. [48] [49] [50] While atrial fibrillation promotes further left atrial enlargement, there are data suggesting that cardioversion 834

and maintenance of sinus rhythm may reverse this process. Using M-mode techniques, DeMaria et al[31] reported a decrease in left atrial size within 1 hour of cardioversion. We studied a group of 21 patients with atrial fibrillation of 5 months' duration.[51] Patients with persistent sinus rhythm had significantly smaller left atria 3 months after cardioversion as compared with precardioversion data. In contrast, the group of patients who reverted to atrial fibrillation had no change in left atrial size. Similarly, Gosselink et al[52] reported on atrial size in 41 patients with chronic atrial fibrillation undergoing precardioversion and 6-month postcardioversion echocardiography. They found both left and right atrial volumes decreased among patients with persistent sinus rhythm, with no change in the group who reverted to atrial fibrillation. Finally, Van Gelder et al[53] reported on 120 patients with chronic atrial fibrillation who were cardioverted and remained in sinus rhythm for at least 6 months. Significant regression of both left and right atrial size was documented (except in patients with mitral stenosis). These data strongly suggest that restoration of sinus rhythm may reverse the process of progressive left and right atrial enlargement but do not exclude the possibility that atrial growth may affect maintenance of sinus rhythm and thus select for patients who demonstrate such reversal. Since atrial enlargement may be deleterious, and cardioversion to sinus rhythm may prevent or reverse such dilation, we believe that avoidance of cardioversion should not be based on an absolute left atrial size. If the duration of atrial fibrillation is brief, an attempt at cardioversion should be made for all initial presentation of nonvalvular atrial fibrillation. Patients with chronic (>1 year) atrial fibrillation, rheumatic mitral valve disease, and prominent left atrial enlargement (>6.0 cm), however, are far less likely to be maintained in sinus rhythm after conversion.[54]

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Detection of Atrial Thrombi in Atrial Fibrillation Atrial fibrillation is believed to be responsible for almost half of cardiogenic thromboembolism. Several large, multicenter, randomized studies have now confirmed the beneficial effect of chronic anticoagulation (International TABLE 38-1 -- Characteristics of Patients at Risk for Atrial Thrombi *

Total number Age (yr)

Left No Left Entire Atrial Atrial P Group Thrombus Thrombus Value 70 463 533 † 71.6 ± 70.7 ± 71.7 ± 13.2 .55 13.0 14.0 45.9 54.3 44.4 .16 60.0 64.3 59.1 .49 4.4 ± 9.3 5.8 ± 15.4 3.9 ± 8.0 .18 8.3 28.9 7.3 .003

Gender (% female) First episode of AF (%) Duration of AF (wk) History of thromboembolism (%) Left atrial SEC (%) 48.0 85.5 36.9 .0001 Left atrial dimension (cm) 4.6 ± 0.7 4.7 ± 0.7 4.6 ± 0.7 .29 Mitral regurgitation (0–3 +) 1.3 ± 0.9 1.2 ± 0.6 1.3 ± 0.9 .35 Left ventricular dysfunction 40.9 60.7 38.1 .002 (%) AF, atrial fibrillation; SEC, spontaneous echocardiographic contrast. * Data presented are mean value ± SD. † TEE could not be completed in six patients. Data for these six are excluded.

Normalized Ratio [INR] 2.0 to 3.0) in patients with atrial fibrillation[55] [56] [57] [58] [59] for clinical stroke prevention. Since transthoracic echocardiography is so limited for the assessment of atrial thrombi,[14] [15] [16] data on the prevalence of left atrial thrombi was not available until the introduction of TEE. Among patients presenting with atrial fibrillation of greater than 2 days' or of unknown duration, we found atrial thrombi in 13%,[60] [61] of which more than 92% were left atrial thrombi and nearly all

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of these involved the left atrial appendage. These data are similar to those reported by others,[62] [63] [64] but higher than the approximately 6% incidence of clinical thromboembolism following cardioversion without anticoagulation.[65] [66] [67] [68] This apparent discrepancy can be explained by the fact that some thrombi may not migrate and some embolic events may be clinically silent.[69] Patients at particularly high risk for atrial thrombi (Table 38-1) included those with rheumatic mitral valve disease, depressed left ventricular systolic function, recent thromboembolism,[70] and TEE evidence of severe left atrial spontaneous echocardiographic contrast and complex aortic debris.[71] Duration of atrial fibrillation and left atrial dimension are not predictive of left atrial thrombi.[60] [61] In contrast to data suggesting that moderate or worse mitral regurgitation is protective against clinical thromboembolism,[72] [73] we have found that mitral regurgitation is not protective against left atrial thrombi (see Table 38-1) among those with new onset atrial fibrillation.[60] Immediate cardioversion is generally advocated for patients with atrial fibrillation of less than 24 hours' duration,[74] under the assumption that the prevalence of atrial thrombi in this group was very low. This common teaching was challenged when Stoddard et al[75] reported a 14% prevalence of atrial thrombi among patients with atrial fibrillation of less than 3 days' duration and a prevalence of 27% in those with a duration 3 days or more in a predominantly male population. In contrast, we found an incidence of clinical thromboembolism following cardioversion (without antecedent TEE or prolonged warfarin anticoagulation) of less than 1% among patients with atrial fibrillation of less than 2 days' duration.[76] Thus, prolonged warfarin or screening TEE are likely not needed in this group (unless they have a history of thromboembolism, severe left ventricular dysfunction, or mitral 835

stenosis). Although we perform cardioversion of atrial fibrillation of less than 48 hours' duration without prolonged warfarin or screening TEE, we do initiate therapeutic anticoagulation at presentation (rather than delaying anticoagulation until the patient has been in atrial fibrillation for 48 hours). As might be expected, atrial thrombi are more common among patients with atrial fibrillation who present with acute thromboembolism. In our experience, residual left atrial thrombi are found in more than 40% of these

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patients.[77] Right atrial thrombi appear to be far less common among patients with atrial fibrillation and represent less than 5% of all atrial thrombi.[60] [61] [78] Right atrial spontaneous echocardiographic contrast is distinctly unusual. It is seen in only 10% of patients with atrial fibrillation[60] but is highly predictive for right atrial thrombi. Chronic Atrial Fibrillation and Predictors of Thromboembolism

Compared with patients who present with new-onset atrial fibrillation and undergo TEE prior to cardioversion, risk factors of thromboembolism differ in patients with chronic atrial fibrillation. Left ventricular systolic dysfunction is among the strongest independent predictors of thromboembolism in patients with chronic atrial fibrillation.[70] The TEE substudies of the Stroke Prevention in Atrial Fibrillation Investigators Committee (SPAF) III study[71] have extended echocardiographic indexes known to be associated with thromboembolism to include dense spontaneous echocardiographic contrast, depressed (<20 cm/s) left atrial appendage ejection velocity, left atrial thrombus, and complex aortic plaque. Importantly, the SPAF-III data suggest that these TEE indexes may identify high- and low-risk subgroups from among clinically high-risk patients (age, female gender, systemic hypertension, left ventricular dysfunction, prior thromboembolism).[71] [79] Guidance of Early Cardioversion

Cardioversion of atrial fibrillation is performed in an effort to improve cardiac function, relieve symptoms, and decrease the risk of thrombus formation. Unfortunately, successful cardioversion is associated with an approximately 6% incidence of clinical thromboembolism among patients who are not systematically anticoagulated for several weeks prior to cardioversion.[65] [66] [67] [68] Since atrial thrombi are poorly detected by conventional transthoracic echocardiography, conventional care of patients with atrial fibrillation of unknown or prolonged (>2 days') duration had demanded that these patients receive several weeks of anticoagulation before cardioversion, followed by several weeks of anticoagulation after cardioversion while atrial mechanical function recovers.[80] [81] Although no randomized and only two prospective studies[62] [67] have been reported, 3 to 4 weeks of warfarin therapy appears to decrease the risk of an embolic event following cardioversion to less than 1.6%.[62] [67] [68] Use of warfarin, however, carries a risk of major (2%) and minor (10-20%) hemorrhagic

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complications.[62] [80] In addition, many patients develop a subtherapeutic INR during the month leading to cardioversion. For these individuals, the warfarin dose is increased and the "1-month clock" restarted. Finally, conventional therapy leads to a delay in cardioversion for the majority of patients who do not have an atrial thrombus, and a second hospitalization is needed later for cardioversion. Rationale and Advantages

The risks and benefits of a TEE-guided approach to cardioversion are summarized in Table 38-2 . A TEE-guided approach to early and safe cardioversion has several advantages over traditional strategies for hospitalized patients with atrial fibrillation. Currently, up to 8 weeks of oral anticoagulation are recommended with cardioversion,[74] [80] [81] including 3 to 4 weeks before and after cardioversion. This period of anticoagulation exposes patients to a significant risk of a hemorrhagic complication[62] [80] by doubling the exposure of systemic anticoagulation. For unclear reasons, the atrial fibrillation population appears to be at increased risk of hemorrhagic complications during the second month of anticoagulation.[62] Early cardioversion offers physiologic advantages over traditional therapy. A shorter duration of atrial fibrillation prior to cardioversion is among the strongest predictors for long-term maintenance of sinus rhythm.[46] Almost 60% of patients hospitalized for atrial fibrillation at our hospital[60] [61] have been in atrial fibrillation for less than 1 month. For these individuals, traditional treatment of 3 to 4 weeks of anticoagulation prior to cardioversion serves to more than double the total period of atrial fibrillation prior to cardioversion. Early cardioversion may also lead to a more rapid return to normal atrial function. The time required for return of atrial mechanical function is directly related to the duration of atrial fibrillation prior to cardioversion.[81] [82] Patients with atrial fibrillation less than 2 weeks prior to cardioversion appear to have complete return of atrial TABLE 38-2 -- Benefits and Risks of Transesophageal Echocardiography (TEE)-Guided Cardioversion Benefits Shorter initial duration of atrial fibrillation Enhanced recovery of atrial mechanical function More rapid resolution of symptoms of congestive heart failure

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Increased likelihood that sinus rhythm will be maintained(?) Greater success of pharmacologic cardioversion(?) No need to return for elective cardioversion after 1 month of warfarin anticoagulation Shorter total duration of atrial fibrillation Fewer hemorrhagic complications Lower cost for warfarin medication and monitoring Fewer thromboembolic events than conventional therapy(?) More cost-effective than conventional therapy Identify high-risk population that requires lifelong warfarin regardless of clinical risk factors(?) Risks TEE "misses" clinically relevant thrombi that subsequently migrate and cause stroke/thromboembolism Morbidity associated with TEE Cost of TEE

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mechanical function within 24 hours of cardioversion, whereas those with atrial fibrillation of 2 to 6 weeks require a week and those with atrial fibrillation for more than 6 weeks require up to 3 weeks. With elimination of a transthoracic echocardiogram, a TEE approach to guide early cardioversion also appears to have cost savings.[83] Finally, a TEE approach may also reduce the incidence of thromboembolism after cardioversion. The "costs" of the TEE approach include the morbidity of TEE, cost of TEE, and risk that TEE will not be adequate to identify atrial thrombi, which subsequently migrate and cause clinical events. Current Data

We reported on our experience with a TEE-guided approach (Fig. 38-6) to early cardioversion among 533 patients with atrial fibrillation of unknown or prolonged duration who underwent precardioversion TEE in the absence of prolonged chronic anticoagulation.[60] [61] [78] Seventy-six

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Figure 38-6 Schematic of the transesophageal echocardiographic protocol. AF, atrial fibrillation; CV, cardioversion; PTT, partial thromboplastin time. (From Manning WJ, Silverman DI, Keighley CS, et al: J Am Coll Cardiol 1995;25:1356.)

atrial thrombi were identified in 70 patients (13%). Of the 463 without TEE evidence of thrombi, 413 (89%) were successfully cardioverted to sinus rhythm, all without prolonged anticoagulation, and 1 (0.2%; 95% CI, 0 to 0.8%) experienced a clinical thromboembolic event. The one adverse event occurred in an elderly woman with mild mitral stenosis who presented 1 week after cardioversion with a brachial artery embolus. She had been therapeutically anticoagulated between TEE and presentation with the adverse event.[61] None of the 70 patients with atrial thrombi were cardioverted, but five (7%) died during the index hospitalization. Repeat TEE to document resolution of atrial thrombi was recommended for all with atrial thrombi, with cardioversion only after documentation of thrombus resolution. Other prospective studies using a similar anticoagulation regimen have shown similar results. Stoddard et al[64] reported on 82 patients scheduled for elective cardioversion of atrial fibrillation. Atrial thrombi were identified in 837

13% of patients. Sixty-six of 71 patients without atrial thrombi underwent successful cardioversion and no patient experienced a clinical embolic event. The pilot study data from the Assessment of Cardioversion Using Transesophageal Echocardiography (ACUTE) trial reported no thromboembolic complications among 47 patients treated with an anticoagulation strategy similar to ours.[62] Finally, data from the 1222patient, multicenter, randomized ACUTE trial were recently reported,[64] [84] which demonstrated "equivalence" for the TEE and the conventional approaches. The ACUTE trial directly compared conventional therapy of 4 weeks of warfarin with a strategy of anticoagulation followed by TEE and early cardioversion if no atrial thrombi are seen. While these reports are encouraging, several adverse events have occurred among patients with a "negative" TEE for atrial thrombi who have undergone early cardioversion using monoplane TEE or in the absence of

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systemic anticoagulation. [85] Many underwent electrical cardioversion several days or weeks following TEE with no anticoagulation during this interval. For these patients, it is impossible to exclude the possibility that atrial thrombi may have formed either between the TEE and cardioversion, or even after cardioversion. Impaired atrial mechanical function,[86] impaired atrial appendage function,[87] [88] or new spontaneous contrast[64] [88] have all been documented following cardioversion. As in our original report[78] we strongly recommend that all patients being considered for multiplane TEE-guided early cardioversion be anticoagulated with intravenous heparin or a therapeutic dose of warfarin at the time of TEE, continuing through cardioversion, and that warfarin anticoagulation be continued for at least 1 month after cardioversion. Multiplane TEE should be performed (without transthoracic echocardiography) immediately prior to cardioversion to adequately visualize the atria and appendages and to exclude the presence of atrial thrombi. Heightened vigilance for thrombi is necessary if there is prominent spontaneous echo contrast or poor (<0.2 m per second) atrial appendage ejection velocity. If a thrombus is seen on TEE, cardioversion should be deferred and the patient maintained on warfarin for 4 weeks followed by repeat TEE to document thrombus resolution prior to cardioversion.[89] Patients with right atrial appendage thrombi should be treated in a similar manner. If the atrial appendage cannot be adequately "cleared" of thrombus, the patient should be treated conservatively with 3 to 4 weeks of therapeutic warfarin prior to cardioversion. Although not directly supported by clinical trials, it is our clinical practice to treat patients with atrial fibrillation who have TEE evidence of atrial thrombi with "lifelong" warfarin (INR, 2.0 to 3.0) even after resolution of thrombus has been documented and cardioversion to sinus rhythm has been achieved. We believe such an approach is prudent given that the overall recurrence rate of atrial fibrillation is high, and these patients have already selected themselves as being at increased risk for atrial thrombus formation. Resolution of Atrial Thrombi

The use of several weeks of anticoagulation prior to cardioversion results in a reduction of cardioversion-related thromboembolism from 6% to less than 1%. The mechanism by which warfarin conveys this beneficial effect had been presumed to be thrombus organization and adherence to the atrial endocardium, thus reducing the likelihood of postcardioversion migration. [90] Consistent with this hypothesis, several investigators have reported that

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atrial thrombi in patients with rheumatic mitral valve disease may not resolve even after several months of warfarin.[90] [91] [92] In nonrheumatic, new-onset atrial fibrillation, a different mechanism appears responsible. We have found that after 4 weeks of warfarin, almost 85% of atrial thrombi have completely resolved[93] (Fig. 38-7) . Similar data have been reported by Corrado et al.[63] These data support the hypothesis that the mechanism of warfarin's benefit is related to thrombus resolution or silent migration and prevention of new thrombus formation (rather than thrombus organization). Although randomized data are not available, we interpret these data as supportive of the need for follow-up TEE examination for documentation of thrombus resolution prior to cardioversion.[89] Mechanism of Thromboembolism after Cardioversion Although usually occurring within 72 hours, thromboembolism has been reported up to 10 days following successful cardioversion in patients with maintained sinus rhythm.[94] Such adverse events have classically been attributed to migration of left atrial thrombi that were present at the time of cardioversion.[74] TEE has documented the new appearance of, or more pronounced, spontaneous left atrial contrast following electrical cardioversion.[64] [88] In addition, more depressed left atrial appendage ejection velocity is common after spontaneous or electrical cardioversion. [87] [88] , These findings have led to the hypothesis that atrial thrombi may form after cardioversion due to atrial injury or stunning. Indeed, left ventricular "stunning" as a result of electrical cardioversion has been previously described,[95] [96] and relatively impaired atrial mechanical function has been seen after electrical (as compared with pharmacologic) cardioversion.[82] [97] Finally, in rare instances, there may be a discontinuity between the body of the atrium and the appendage[35] [36] with a sinus pattern on the surface electrocardiogram and transmitral Doppler echocardiogram but a fibrillatory pattern in the appendage. Premature discontinuation of warfarin may thereby lead to new thrombus formation. These data all emphasize the importance of warfarin anticoagulation during the pericardioversion period. For patients who are not considered candidates for out-of-hospital warfarin, we recommend therapeutic anticoagulation with heparin for at least 24 hours after cardioversion. Assessment of Return of Atrial Mechanical Function After Cardioversion The noninvasive nature of echocardiography makes it the ideal modality for the serial assessment of atrial function

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Figure 38-7 Serial transesophageal echocardiographic studies showing the left atrium and left atrial appendage viewed in the vertical plane with a 5 MHz biplane probe. The thrombus (arrow) is in the body of the left atrium, closely associated with the mitral annulus in the posterior portion of the left atrium. A, Initial study demonstrating a mobile 12 mm thrombus. B, Thrombus persists but is smaller after 1 week of warfarin therapy. C, After 3 weeks of warfarin, the thrombus continues to be seen (arrow). D, Complete resolution of thrombus is seen after 5.5 weeks of warfarin. (From Collins LJ, Silverman DI, Douglas PS, Manning WJ: Circulation 1995;93:162, with permission. Copyright 1995 American Heart Association.)

after cardioversion. DeMaria et al[31] reported serial M-mode data of anterior mitral leaflet excursion before and after cardioversion among 35 patients with atrial fibrillation of 14 months' duration. One hour after cardioversion, prominent mitral "A" waves were found in 94% of their study group, although anterior leaflet excursion was less than that seen in normal subjects (7.5 mm vs. 13 mm). These early data suggested that atrial mechanical contraction was reduced after cardioversion despite normal atrial depolarizations on electrocardiography. Two patients had no discernible atrial anterior mitral leaflet motion, and both of these patients reverted to atrial fibrillation within 1 week. These investigators also found an increased left ventricular end-diastolic dimension, with unchanged endsystolic dimension, consistent with an improvement in left ventricular ejection fraction. Orlando et al[98] also used M-mode echocardiography to evaluate atrial function after cardioversion. Five hours after cardioversion, 4 of their 15 patients (27%) had no mitral A wave. In their experience, neither the presence of an A wave nor its amplitude correlated with longterm maintenance of sinus rhythm. Pulsed Doppler echocardiography permits serial noninvasive evaluation of flow across the mitral valve and is thus ideally suited to assess atrial systolic function. Transmitral Doppler spectra accurately reflect the left atrial contribution to total left ventricular filling. As reported by van Gelder et al[99] and Viswanahan et al,[100] these temporal changes in transmitral Doppler spectra parallel improvements in left ventricular ejection fraction [100] and peak oxygen consumption.[99] Shapiro et al[86] reported transmitral Doppler data from

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839

a group of patients with atrial fibrillation of 2 days' duration or less. Peak A wave velocities immediately after cardioversion were similar to those in a control (sinus) population. In contrast, patients with a duration of atrial fibrillation of greater than 1 year prior to cardioversion had significantly smaller A wave amplitude after cardioversion. We performed serial transmitral pulsed Doppler examination in 21 patients undergoing elective cardioversion, with a duration of atrial fibrillation of 5 months.[51] Over 3 months of follow-up, there were significant increases in both peak A wave velocity and percent atrial contribution to total left ventricular filling (Fig. 38-8) . Neither index returned to normal until 3 weeks after cardioversion. Additional studies have confirmed that transmitral Doppler data are not predictive of the long-term maintenance of sinus rhythm.[98] [101] Thus it appears that return of atrial mechanical function is not sufficient to allow for premature discontinuation of postcardioversion anticoagulation. Recently, atrial compartment surgery, or the MAZE procedure, has received considerable interest as an approach to prevent recurrent atrial fibrillation. Shyu et al[102] studied 22 patients with chronic atrial fibrillation who underwent atrial compartment operations. Over 70% of their group had no transmitral A wave 1 week after surgery, despite sinus rhythm on the surface electrocardiogram. Even after 2 months, 40% of their patients had not regained evidence of A waves. Of note, right atrial Figure 38-8 Serial transmitral pulsed Doppler inflow velocity profiles from an individual patient. Note the progressive increase in peak A wave velocity during the observation period. For each spectrum, the vertical calibration markings indicate 0.2 m per second flow velocity. (From Manning WJ, Leeman DE, Gotch PJ, Come PC: J Am Coll Cardiol 1989;13:620. Reprinted with permission from the American College of Cardiology.)

mechanical function appeared to recover more rapidly than left atrial mechanical function. Studies of atrial mechanical function in patients with atrial fibrillation of an intermediate (3-day to 4-week) duration had been previously limited by the relative scarcity of such patients. This was due to the recommendation that patients with atrial fibrillation of more than 2 days' duration receive anticoagulation for 3 to 4 weeks prior to cardioversion. Our TEE cardioversion trial allowed us to evaluate atrial function among patients with this intermediate duration of atrial fibrillation. We found that both the

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immediate peak A velocity and the percentage A wave filling were significantly lower (Fig. 38-9) in the groups with atrial fibrillation of moderate (>2 up to 6 weeks) and prolonged (>6 weeks) duration as compared with the patients with atrial fibrillation of only brief (≥2 weeks) duration.[81] This depression in peak A velocity persisted until at least 1 week following cardioversion. In addition, 1 week after cardioversion, both peak A velocity and percentage A wave filling were depressed in the group with atrial fibrillation of prolonged duration as compared with the group with atrial fibrillation of moderate duration. As compared with 3-month postcardioversion data, full recovery of atrial mechanical function was achieved within 24 hours for patients with brief (<2 weeks) duration, within 1 week for patients with moderate (2 to 6 weeks) duration, and within 1 month for patients with prolonged (>6 weeks) duration of atrial fibrillation. Twenty-seven 840

Figure 38-9 Comparison of transmitral pulsed Doppler peak A-wave velocity among patients with brief (<2 weeks), moderate (2–6 weeks), and prolonged (>6 weeks) atrial fibrillation immediately after, at 24 hours, and at 1 week after cardioversion. *P < .05 vs. brief duration. †P < .05 vs. moderate duration. (From Manning WJ, Silverman DI, Katz SE, et al: J Am Coll Cardiol 1994;23:1537.)

patients (45%) reverted to atrial fibrillation during follow-up. Those reverting to atrial fibrillation had a longer duration prior to cardioversion (10.2 vs. 5.3 weeks; P = .04). There were no differences in left atrial dimension, patient age, mode of cardioversion, peak A wave velocity, or percentage of A wave filling among patients who reverted to atrial fibrillation compared with those with sustained sinus rhythm. Evidence of Electrical Injury to the Atria Left ventricular myocardial injury as a result of electrical cardioversion has been previously described.[95] [96] TEE data acquired with electrical cardioversion have shown new or more pronounced spontaneous left atrial contrast following electrical cardioversion[64] [88] as well as depressed left atrial appendage ejection velocity.[88] We reported on transmitral Doppler data from 33 patients with atrial fibrillation of less than 5 weeks' duration following elective electrical or pharmacologic (primarily quinidine or procainamide) cardioversion using transmitral Doppler examination.[97]

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Immediately following cardioversion, patients who underwent electrical cardioversion demonstrated lower peak A wave velocity as compared with those who were cardioverted pharmacologically (Fig. 38-10) . This depression in atrial systolic function was also present at the 24-hour study but had resolved at 1 week. Similarly, Mattioli et al[103] randomized 64 patients with atrial fibrillation (duration 1 day to 6 months) to either directcurrent shock or pharmacologic cardioversion. They found that the recovery of atrial mechanical function occurred sooner with pharmacologic cardioversion. Finally, Pollak and Falk[104] performed electrical cardioversion in 37 patients receiving sotalol or placebo. They found relatively depressed atrial function among the group receiving sotalol as compared with those receiving placebo. Spontaneous Echo Contrast Spontaneous echo contrast, or "smoke," refers to the presence of dynamic smokelike echoes in a cardiac cavity and is occasionally seen by transthoracic echocardiography in the left atrium in patients with mitral stenosis and atrial fibrillation. More commonly, spontaneous echo contrast is identified on transthoracic imaging of the left ventricular apex with a high-frequency transducer in patients with an apical aneurysm. Spontaneous echo contrast likely represents stasis of blood within the cavity, but it may also reflect alterations in blood components such as platelets, red cells, and fibrinogen. Black et al[105] found an association between spontaneous echo contrast and erythrocyte aggregation in low shear rate conditions. Aspirin and warfarin therapy do not appear to affect the presence of left atrial spontaneous echo contrast.[105] At least mild spontaneous echo contrast may be seen in over half of patients with atrial fibrillation,[60] [71] [78] and in over 80% of patients with atrial fibrillation and left atrial appendage thrombi.[60] Among patients with nonvalvular atrial fibrillation, Chimowitz et al[106] found that left atrial spontaneous echo contrast was associated with an increased risk of stroke. Black et al[105] found that spontaneous echo contrast by TEE was an independent predictor of left atrial thrombus among patients with suspected cardioembolism. Although unproved, it seems likely that recovery of atrial mechanical function would decrease or abolish spontaneous echo contrast. SPAF-III TEE data[71] suggest that warfarin anticoagulation decreases the risk of thromboembolism in patients with spontaneous echo contrast.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography and Atrial Flutter Sustained atrial flutter is far less common then atrial fibrillation. As a result, there are fewer data regarding atrial function at baseline and following cardioversion. It has generally been accepted that the relatively preserved atrial mechanical function (Fig. 38-11) with atrial flutter results in a lower risk of thromboembolism (as compared with atrial fibrillation). In a retrospective review, Arnold Figure 38-10 Comparison of transmitral peak A wave velocity among patients who underwent pharmacologic and electrical cardioversion. (From Manning WJ, Silverman DI, Katz SE, et al: Am J Cardiol 1995;75:626, with permission from Excerpta Medica Inc.)

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Figure 38-11 M-Mode echocardiographic image depicting motion of the anterior mitral leaflet (arrows) corresponding to flutter waves on the electrocardiogram in a patient with atrial flutter.

et al[68] reported on 122 patients with atrial flutter at the time of cardioversion, including 74% who were not receiving anticoagulation. No patient experienced a clinical thromboembolic event. These data would support the concept that patients with atrial flutter do not require anticoagulation prior to cardioversion. However, there have been reports of atrial thrombus identified during TEE study among patients with atrial flutter[107] [108] and postcardioversion thromboembolism. A limitation of interpreting the literature on atrial flutter is the definition of the arrhythmia. For many studies,[68] a patient is defined as having atrial flutter if it is the

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rhythm during the intervention or period of observation (e.g., at the time of TEE or cardioversion). Many patients may have alternating periods of atrial fibrillation and flutter, making clinical distinction of pure atrial flutter difficult. Irani et al[109] performed TEE in 47 consecutive patients with atrial flutter (and without atrial fibrillation by history or Holter monitoring). They found that 11% of patients had left atrial thrombus, and 31% had spontaneous echo contrast, values similar to those found in patients with atrial fibrillation. Similar to our findings for atrial fibrillation, [60] [61] , [78] moderate or severe mitral regurgitation was not protective against thrombus formation for this group. Jordaens et al[110] studied 22 patients with atrial flutter with serial transmitral Doppler echocardiography after cardioversion. Analogous to data on atrial fibrillation, they found that 20% of patients had Doppler evidence of atrial standstill immediately after cardioversion. There was a progressive increase in peak A wave velocity and percentage of A wave filling over a 6-week period. Based on these data, our recommendation is to treat patients with atrial flutter who have periods of atrial fibrillation ("atrial flutter-fibrillation") in the same manner as those with isolated atrial fibrillation. When it is certain that a patient has sustained atrial flutter, particularly for a short period of time, it may be reasonable to cardiovert without anticoagulation, although individualized risk-benefit considerations are most appropriate. We would generally treat conservatively patients who had atrial flutter in the setting of rheumatic mitral valve disease, a history of thromboembolism, or left ventricular systolic dysfunction, with shortterm anticoagulation and screening TEE or several weeks of anticoagulation prior to attempted cardioversion.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Current and Future Areas of Investigation As the ability of echocardiography to provide detailed structural and functional information about the heart continues to grow, so likely will its role in the evaluation and optimal management of patients with atrial fibrillation. Among the areas of current and future investigation are 1. Improved methods of assessment of atrial mechanical function, such as measurement of atrial ejection force. 2. Randomized prospective studies to further define the safety of TEE to guide early cardioversion among patients with atrial fibrillation, as in the ACUTE Trial. 3. Randomized trials to examine the need for repeat TEE prior to cardioversion among patients with a thrombus on initial TEE. 4. Clinical studies examining TEE risk stratification for aspirin or warfarin in patients with chronic atrial fibrillation. 5. Assistance in localization of structural abnormalities and foci of abnormal electrical activity, including assistance in radiofrequency ablation of arrhythmic foci. 6. Identification of clinical or echocardiographic indexes that predict recurrence of atrial fibrillation or identify a group at low risk for thromboembolism so as to minimize postcardioversion anticoagulation. 7. Anatomic and Doppler descriptions of right atrial appendage in health and disease.

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Section 8 - Echocardiography in Adult Congenital Heart Disease

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Chapter 39 - General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease A. Rebecca Snider MD

Two-dimensional (2D) echocardiography has had a major impact on our ability to diagnose complex congenital heart defects. With this technique, one can image detailed structural anatomy even more precisely than with cardiac catheterization in most patients. The echocardiographic approach to the diagnosis of complex congenital heart disease is very logical and systematic, requiring a basic knowledge of how cardiac chambers are identified on the 2D echocardiogram. In this chapter, we review (1) the echocardiographic approach to segmental analysis of the heart, (2) the echocardiographic features used to determine the morphology of the cardiac chambers and great vessels, and (3) the echocardiographic appearance of the more frequently encountered forms of complex congenital heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Approach to Segmental Analysis of the Heart General Considerations The echocardiographic approach to the diagnosis of complex congenital heart disease involves a segmental analysis of the heart.[1] [2] [3] [4] [5] [6] In this type of analysis, one can think of the heart as being much like a house. To describe a house completely, one must say where the rooms or chambers are located on each floor. For the "cardiac house," this description includes where each atrium is on the ground floor, where the ventricles are on the second story, and where each great artery is positioned at the top 846

TABLE 39-1 -- Summary of Segmental Approach to Cardiac Diagnosis Atrial situs: describes location of atria Solitus: morphologic RA on right Inversus: morphologic RA on left Ambiguus: undifferentiated atria Asplenia: bilateral right-sidedness Polysplenia: bilateral left-sidedness Bulboventricular loop: describes location of ventricles d-Loop: morphologic RV on right l-Loop: morphologic RV on left Ventriculoarterial connections: describes connections of great arteries Concordant: Ao arising from LV, PA from RV

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Discordant (transposition): Ao arising from RV, PA from LV Double-outlet right ventricle Double-outlet left ventricle Single outlet from heart Aortic atresia Pulmonary atresia Truncus arteriosus Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. of the house. In addition, a complete description of the house should include the location of the staircases that connect the floors. For the cardiac house, this description includes atrioventricular and ventriculoarterial connections. In this approach, if the atria are not correctly identified, the entire house comes tumbling down.[7] Thus, the approach to echocardiographic diagnosis of the patient with complex congenital heart disease begins with a determination of the atrial situs (Table 39-1) . The word situs refers to the topology or spatial position of the structure. In atrial situs solitus, the morphologic right atrium is on the right and the morphologic left atrium is on the left. In situs inversus, the morphologic right atrium is on the left and the morphologic left atrium is on the right. In situs ambiguus, the atria do not differentiate into right and left atria; instead, both atria can have features of (1) a morphologic right atrium, a condition called asplenia, or (2) a morphologic left atrium, a condition called polysplenia. [2] [6] , [8] The next step in the diagnosis of complex congenital heart disease is determination of the bulboventricular loop (see Table 39-1) . This loop describes the locations of the ventricles. In a d-loop (dextro loop), the morphologic right ventricle is on the right and the morphologic left ventricle is on the left. In an l-loop (levo loop), the morphologic right ventricle is on the left and the morphologic left ventricle is on the right. These definitions of d- and l-loop apply regardless of the atrial situs. Thus, concordant or normal connections between the atria and ventricles (morphologic right atrium to morphologic right ventricle, morphologic left atrium to morphologic left ventricle) occur when there is situs solitus with a d-loop or situs inversus with an l-loop. Discordant or abnormal connections (morphologic right atrium to morphologic left ventricle, morphologic left

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atrium to morphologic right ventricle) occur when there is situs solitus with an l-loop or situs inversus with a d-loop. [1] [2] , [5] In general, the convexity of the aorta points to the position of the right ventricle and thus helps indicate the bulboventricular loop.[2] The definitive indicator of the bulboventricular loop, however, is the relative positioning of the ventricular inlets or atrioventricular valves. Thus, in a d-loop the tricuspid valve is to the right of the mitral valve, and in an l-loop the tricuspid valve is to the left of the mitral valve.[9] [10] In most cardiac defects the inflow and trabecular portions of the right ventricle are on the same side relative to the components of the left ventricle, so that determination of the bulboventricular loop is straightforward (i.e., tricuspid valve to the right indicates d-loop, tricuspid valve to the left indicates l-loop). In some rare complex malformations discussed in detail later in this chapter, the inflow and trabecular portions of the right ventricle can be located on different sides of the left ventricular inflow (e.g., in certain forms of crisscross hearts). The spatial locations of the trabecular and outflow portions of the ventricles alone do not indicate the bulboventricular loop; their final spatial position is determined by the degree of apical rotation in the ninth week of gestation. Normally, the cardiac apex pivots to the hemithorax opposite the bulboventricular loop.[4] [11] In the early embryogenesis of the normal heart, the apex is oriented to the right (following initial rightward loop formation), but it subsequently rotates to the left as the primitive ventricular cavity develops into the left ventricle. Thus, in a normal d-loop the apex pivots to the left hemithorax; in a "normal" l-loop (i.e., one in the setting of situs inversus) the apex pivots to the right hemithorax. When the atrial situs and the loop are alignment concordant, apical pivoting is usually complete. Failure of complete apical pivoting is commonly associated with discordant atrioventricular connections. Partial pivoting in either concordant or discordant atrioventricular connections leads to a sagittally oriented ventricular septum and mesocardia. Rotational anomalies of the cardiac apex cause the ventricular septum and greater ventricular mass to be grossly displaced in space, whereas the inlet relationships of the ventricles are preserved. Abnormal rotation can occur either in the frontal plane, along the longitudinal axis, or in both patterns. The resultant possible spatial relationships of the chambers and septal orientation are listed in Table 39-2 .[11] Rotational anomalies of the cardiac apex also can cause the semilunar valves to be altered in their spatial relationships. An understanding of these apical

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TABLE 39-2 -- Rotational Anomalies of the Cardiac Apex Normal Heart Apex displaced 30 to 60 degrees from a vertical direction in the frontal plane Ventricular septum tilted so that its anterior edge is leftward and superior to its posterior edge Superoinferior Ventricles Abnormal tilting of the apex in the frontal plane Resultant horizontal ventricular septum and superior right ventricle Crisscross Ventricles Abnormal apical rotation along the longitudinal axis Dextroversion Lack of apical pivoting in situs solitus, d-loop Resultant abnormal positioning of the apex to the right Preservation of the relationship between the great arteries

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rotational abnormalities and the resultant changes in the plane of the ventricular septum, the positioning of the greater ventricular mass, and the positioning of the great arteries is an essential component of the echocardiographic approach to segmental analysis of complex cardiac defects. If the echocardiographer does not understand the effects that rotational anomalies of the apex have on the standard imaging planes, imaging artifacts can be created easily and incorrect assessments made of the adequacy of chamber size. In most congenital cardiac defects, there is harmony between the situs (topology) and alignment (connections) information[12] which means that situs concordance nearly always predicts alignment concordance, and situs discordance nearly always predicts alignment discordance. For example, situs solitus with an l-loop (discordant situs information) almost always predicts discordant atrioventricular connections or alignments (right atrium on the right connected to left ventricle on the right). The rare and notable exception to this rule is the heart with crisscross atrioventricular relations (discussed later). In this case, knowledge of the atrial situs and the

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bulboventricular loop might be wrongly predictive of the alignment or connections of these segments. In other words, there is disharmony between the situs and alignment information. The final step in the diagnosis of complex congenital heart disease is a description of the great artery connections (see Table 39-1) . In normal or concordant connections, the pulmonary artery arises from the morphologic right ventricle and the aorta arises from the morphologic left ventricle. Normally, the aortic valve is situated posterior and to the right of the pulmonic valve. Transposition is a discordant ventriculoarterial connection in which the aorta arises from the morphologic right ventricle and the pulmonary artery arises from the morphologic left ventricle.[2] [5] [6] Classically, the old definition of transposition was based on spatial relations of the great arteries, that is, that transposition is present when the aortic valve and ascending aorta are anterior to the pulmonary valve and main pulmonary artery.[8] The more current definition of transposition proposed by Van Praagh et al[2] [5] and used in this chapter is based on the ventriculoarterial connections and not the spatial interrelationships. The literal Latin root meaning of the word transposition is from trans (across) and positio (placement). Thus, the great arteries are literally "placed across" the ventricular septum, with the aorta arising from the morphologic right ventricle and the pulmonary artery arising from the morphologic left ventricle.[13] The old definition of transposition based on the anteroposterior relations of the great arteries has been largely abandoned because of the existence of transposition with a posterior aortic valve and an anterior pulmonic valve in 11% of autopsy-proved cases of transposition with dextrocardia.[14] Likewise, when the ventricles are severely rotated, normally connected great arteries can have an anterior aortic valve and a posterior pulmonic valve.[13] Other types of great artery connections include double-outlet right ventricle, double-outlet left ventricle, and single outlet from the heart. Three common forms of single outlet from the heart include truncus arteriosus, aortic atresia, and pulmonary atresia. In Van Praagh's system of nomenclature, any great artery relationship that is neither normally crossed nor transposed is referred to as being malposed.[5] [15] [16] Thus, for the heart with both great arteries arising from the right ventricle, with the aortic valve anterior and to the right of the pulmonic valve, the preferred nomenclature is double-outlet right ventricle connection with d-malposed great artery relationships (not double-outlet right ventricle and transposition, which would be two mutually exclusive types of

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connections). Although this is the terminology used throughout this chapter, there is no single agreed upon system of nomenclature for congenital heart disease. Clarity in the description of cardiac anatomy is undoubtedly the most important focus for the echocardiographer, and several approaches to cardiac nomenclature are available to allow one to accomplish this goal. Definition of Cardiac Chambers from the Two-Dimensional Echocardiogram Before we review how cardiac chambers are identified on the echocardiogram, one of the largest controversies in cardiac nomenclature needs to be addressed: the definition of a ventricle. Anderson et al[6] [17] proposed a rule of 50% for determining whether a cardiac chamber is a ventricle. This rule states that a chamber is a ventricle if it receives 50% or more of an inlet. The inlet consists of the fibrous ring of the atrioventricular valve and need not always include a patent atrioventricular valve with wellformed valve leaflets. For example, in hypoplastic left heart with aortic and mitral atresia, the fibrous ring of the mitral valve contains an imperforate membrane and is situated over the small left ventricle. Thus, this small leftsided chamber is a ventricle because it receives 100% of an inlet (even though there is no antegrade flow across the inlet). A chamber need not have an outlet to be a ventricle. Thus, the left ventricle in double-outlet right ventricle is a ventricle because it receives the mitral valve even though it does not have an outlet. The rule of 50% has also been used to define the ventriculoarterial connections. Thus, if 50% or more of a great artery arises above a chamber, the great artery is defined as being connected to that chamber.[6] [17] Application of the rule of 50% requires definitions for chambers that are not ventricles. According to the original descriptions,[6] [17] rudimentary chambers are chambers that receive less than 50% of an inlet and therefore do not qualify to be ventricles. There are two types of rudimentary chambers. An outlet chamber is one that has less than 50% of an inlet but 50% or more of an outlet or great artery. A trabecular pouch is a chamber that has less than 50% of an inlet and less than 50% of an outlet.[17] More recently, chick embryo studies by de la Cruz et al[18] have shown that the trabeculated portions of the ventricles are the original developmental components. The inlet and outlet components form from the trabeculated component during and after looping; thus, the apical components are the oldest parts of the ventricles and form the basis for subsequent

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development. These and other observations form the basis for the belief by some investigators that chambers in the ventricular mass that possess 848

a trabeculated portion of a ventricle should be considered ventricles regardless of whether they have an inlet or outlet component.[19] Anderson has suggested that when such small chambers lack an inlet, they be called rudimentary ventricles.[20] Anatomic Landmarks on the Septal Surfaces

To diagnose complex congenital heart disease, one must know how cardiac chambers are identified on the 2D echocardiogram (Table 39-3) . The cardiac chambers are largely defined by the anatomic landmarks on their septal surfaces.[21] The morphologic right atrium has a septal surface that receives the tendinous insertion of the eustachian valve and has the limbus of the fossa ovalis. The eustachian valve crosses the floor of the right atrium from the orifice of the inferior vena cava and inserts into the septum primum (the lower portion of the atrial septum adjacent to the atrioventricular valves). This tendinous insertion is along the lower border of the fossa ovalis and is called the inferior limbic band (Fig. 39-1) (Figure Not Available) .[3] [4] [21] The left atrial septal surface has the flap valve of the fossa ovalis. This is the septum primum tissue that covers the foramen ovale and seals it closed after birth (Fig. 39-2) . [21] The flap valve can be seen on the 2D echocardiogram protruding into the left atrium in the fetus when the foramen ovale is open; after birth, however, the flap valve is usually difficult to identify on the transthoracic 2D echocardiogram. With the use of high-frequency transesophageal imaging transducers, the flap valve can be imaged in a large proportion of patients. In cases in which the flap valve is tightly adherent to the left atrial septal surface and therefore cannot be visualized as a separate structure on the 2D echocardiogram, other methods for identification of the left atrium must be used. The morphologic right ventricle is the chamber whose septal surface has prominent muscle bundles crossing from the septum to the parietal free wall (Fig. 39-3) . The largest of the septoparietal muscle bundles is the moderator band. In addition, the septal surface of the right ventricle receives chordal insertions from the tricuspid valve septal leaflet.[3] [4] [21]

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TABLE 39-3 -- Definition of Cardiac Chambers from Two-Dimensional Echocardiography Right Atrium Tendinous insertion of eustachian valve Short, stout appendage Usually receives drainage of inferior vena cava, superior vena cava, and coronary sinus Left Atrium Flap valve of fossa ovalis Long, finger-like appendage Usually receives drainage of pulmonary veins Right Ventricle Septoparietal muscle bundles Atrioventricular valve chordal insertions into septum Tricuspid valve Left Ventricle Smooth septal surface Mitral valve Figure 39-1 (Figure Not Available) Subcostal four-chamber view from a normal patient showing the anatomic features of the morphologic right atrium (RA). The morphologic RA has a septal surface that receives the tendinous insertion of the eustachian valve. In this view the eustachian valve can be seen crossing the floor of the RA from the orifice of the inferior vena cava to its insertion into the septum primum. LA, left atrium; LV, left ventricle. (From Snider AR, Bengur AR: Twodimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 501.)

The morphologic left ventricle is the chamber whose septal surface is smooth. There are no septoparietal free wall muscle bundles and the mitral valve normally has no chordal insertions into the septum (see Fig. 39-3) .[3] [4] [21]

Additional Features of the Cardiac Chambers

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Another useful anatomic feature for identifying the ventricles is that the atrioventricular valve always belongs to Figure 39-2 Subcostal sagittal view from a normal patient. The flap valve (arrow) of the foramen ovale is seen on the atrial surface of the left atrium (LA). The flap valve of the foramen ovale is an anatomic marker of the morphologic LA. AO, aorta; RA, right atrium; RPA, right pulmonary artery.

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Figure 39-3 Apical four-chamber view from a normal subject. The morphologic right ventricle (RV) has prominent muscle bundles traversing from the septal surface to the parietal free wall and an atrioventricular valve closer to the cardiac apex. The morphologic left ventricle (LV) has a smooth septal surface and an atrioventricular valve farther from the cardiac apex. Note the pulmonary veins draining to the morphologic left atrium (LA). RA, right atrium.

the appropriate ventricle. Thus, the tricuspid valve is always found in the morphologic right ventricle and the mitral valve is always found in the morphologic left ventricle. The tricuspid valve is closer to the cardiac apex (see Fig. 39-3) , has three leaflets, and has chordal insertions into the ventricular septum. The mitral valve is farther from the cardiac apex, is a fish-mouth bicuspid valve, and has chordal insertions only into two papillary muscles in the left ventricle (see Fig. 39-3) .[21] Systemic and pulmonary venous return can help identify the atria. The pulmonary veins usually drain to the morphologic left atrium; however, this is not a constant feature of the left atrium, because the pulmonary veins can drain anomalously. If three or more pulmonary veins drain by separate orifices to a chamber and there is no evidence of a pulmonary venous confluence, that chamber is most likely a morphologic left atrium. The inferior vena cava usually drains to the morphologic right atrium. This relationship is constant in most cases except in patients with situs ambiguus (discussed later). The superior vena cava usually drains to the morphologic right atrium; however, this relationship is not constant, as it can drain to either or both atria.[3] [4] [17] The morphology of the atrial appendages can help identify the atria.[3] The

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right atrial appendage is short and stout, resembling "Snoopy's" nose, and the left atrial appendage is long and finger-like, resembling "Snoopy's" ear (Fig. 39-4) . Also, the abdominal situs may provide helpful information for determining the atrial situs.[3] [4] [21] For example, in most patients with atrial situs solitus, there is also abdominal situs solitus. Thus, subcostal views of the abdomen show that the inferior vena cava is to the right of the spine, the descending aorta is to the left of the spine, the stomach bubble is on the left, and the liver is on the right (Fig. 39-5) . Likewise, in most patients with atrial situs inversus, there is also abdominal situs inversus. Subcostal views of the abdomen show that the inferior vena cava is usually to the left of the spine and the descending aorta is usually to the right. The stomach bubble is on the right and the liver is on the left. In atrial situs ambiguus the liver may be to the right, to the left, or transverse. The stomach bubble can be on either side or in the midline. Several types of anomalies of systemic venous drainage often are present and suggest the diagnosis of situs ambiguus. These anomalies are discussed in detail later in this chapter. When the atrial and abdominal Figure 39-4 Transesophageal echocardiogram from a normal patient showing several basal short-axis transverse views. Top, The aortic valve (AO) is seen in cross section. Middle, The transducer has been rotated rightward to image the right atrial appendage (RAA) and the main pulmonary artery (MPA), which is anterior and to the left of the AO. Note that the RAA is short and stout and resembles "Snoopy's" nose. Bottom, The transducer has been rotated leftward to image the left main coronary artery (LMCA), the left anterior descending coronary artery (LAD), and the left atrial appendage (LAA). Note the long, finger-like appearance of the LAA, which resembles "Snoopy's" ear. The arrow indicates a prominent pulmonary vein shelf, which is a normal structure and should not be mistaken for a thrombus. L, left coronary cusp; LA, left atrium; N, noncoronary cusp; R, right coronary cusp; RA, right atrium; RV, right ventricle.

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Figure 39-5 Subcostal short-axis view from a patient with atrial and abdominal situs solitus. Note that the liver is on the patient's right. The inferior vena cava (IVC) is to the right of the spine and the descending aorta (DAO) is to the left of the spine.

situs are discordant (atrial situs solitus with abdominal situs inversus or vice versa), the incidence of severe, complex congenital heart disease is

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high. Defects with atrioventricular and ventriculoarterial discordance are frequent in this setting. [4] Evaluation of the Patient with Dextrocardia The term dextrocardia simply indicates that the heart is located primarily in the right chest and implies that Figure 39-6 Diagrammatic representation of the types of dextrocardia. In dextroposition (in situs solitus), the entire heart is shifted to the right chest, either because of a space-occupying mass in the left chest or because of absence of the normal lung volume filling the right chest. Usually, the alignment of the major axis of the heart is normal (pointed toward the left) or rotated slightly vertically; however, the entire heart is shifted to the right of midline or to the retrosternal area. The parasternal long- and short-axis views are obtained with the usual orientation of the plane of sound but with the transducer positioned just to the right of the sternum. The apical views are also obtained with the usual orientation of the plane of sound but with the transducer positioned just to the right of the lower sternal border. In dextroversion (in situs solitus), there is failure of apical pivoting. The cardiac apex is to the right of midline and the atria are usually in their normal positions or shifted slightly to the right. The major axis of the heart is aligned from the left shoulder toward the right hip. The parasternal long-axis view is obtained with the plane of sound oriented in the mirror-image direction of normal. Because the atria are usually normally positioned and the great arteries arise normally from the ventricles, the parasternal short-axis view is obtained with a normal orientation of the plane of sound. In mirror-image dextrocardia or situs inversus totalis, the heart is located in the mirror-image position of normal. Both atria are usually entirely to the right of the sternum, and the cardiac apex is usually in the right fifth or sixth intercostal space at the anterior axillary line; hence, the major axis of the heart is aligned between the left shoulder and right hip. The parasternal long-axis view is obtained from the right second or third intercostal space with the plane of sound oriented in a mirror-image direction of normal (from left shoulder to right hip). The parasternal short-axis view is obtained from the same transducer location with the plane of sound also oriented in the mirror-image direction of normal (from right shoulder to left hip). The apical views are obtained with the transducer positioned in the right fifth or sixth intercostal space in the anterior axillary line and with the plane of sound oriented in a mirrorimage direction of normal. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

one of three conditions is present (Fig. 39-6) .[14] , [22] First, dextrocardia can occur because the heart is displaced into the right chest, either because of a space-occupying mass in the left chest or because of absence of the normal lung volume filling the right chest. This form of dextrocardia is commonly called dextroposition. Second, dextrocardia can occur because of failure of

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pivoting of the cardiac apex to the left. This condition is known as dextroversion and is frequently associated with atrioventricular discordance.[4] Third, dextrocardia can occur with abnormal atrial situs (i.e., situs inversus or situs ambiguus). The most common condition in this category is situs inversus totalis, in which the heart is located in the mirrorimage position of normal. When a patient is referred with a diagnosis of dextrocardia,[23] the echocardiographic examination is begun from the subcostal position rather than from the parasternal window, the routine starting position. From the subcostal four-chamber view, patients with dextroposition have the morphologic right atrium and right ventricle to the right of the morphologic left atrium and left ventricle. Usually, the alignment of the major axis of the heart is normal (pointed toward the left) or rotated slightly vertically; however, the entire heart is shifted to the right of midline or to the retrosternal area. In patients with dextroversion the morphologic right atrium is to the right of the morphologic left atrium; however, the major axis of the heart is aligned from the left shoulder toward the right hip.[22] In this condition the cardiac apex is to the right of midline and the atria are usually in their normal positions or shifted slightly to the right (Fig. 39-7) . In dextrocardia with atrial situs inversus, the morphologic left atrium is 851

Figure 39-7 Subcostal four-chamber views from a patient with dextroversion of the cardiac apex. Top, The left-sided ventricle has a smooth septal surface and is therefore the morphologic left ventricle (LV). The LV gives rise to a vessel that arches and is therefore the aorta (AO). Bottom, The plane of sound has been tilted far anteriorly. The right-sided ventricle has a prominent moderator band in its apical portion and is therefore a morphologic right ventricle (RV). The RV gives rise to a vessel that dives posteriorly and is therefore a pulmonary artery (PA). Other echocardiographic views showed that this patient had atrial situs solitus; therefore, the atrioventricular and ventriculoarterial connections are normal. The only abnormality in this heart is failure of pivoting of the cardiac apex to the left. LA, left atrium.

to the right of the morphologic right atrium, and both atria are usually entirely to the right of the sternum ( Fig. 39-8 and Fig. 39-9 ). The cardiac apex is usually in the right fifth or sixth intercostal space at the anterior axillary line; therefore, the major axis of the heart is aligned between the left shoulder and right hip.[22]

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In dextrocardia with atrial situs inversus, the parasternal long-axis view is obtained from the right second or third intercostal space with the plane of sound oriented in a mirror image of normal (from left shoulder to right hip). The parasternal long-axis view has only anteroposterior and superoinferior directions and does not display the right-to-left orientation of cardiac structures. Thus, on the video monitor, cardiac structures appear to be oriented in a normal fashion, and only the examiner knows that the images were obtained in a mirror-image plane. The parasternal short-axis views are obtained from the same transducer location with the plane of sound also oriented in the mirror-image direction of normal (from right shoulder to left hip). Unlike the parasternal long-axis view, the parasternal short-axis view displays the right-to-left orientation of cardiac structures. Thus, on the video monitor, in patients with dextrocardia and atrial situs inversus, the parasternal short-axis view appears to be a backward version of normal. It is important that the examiner not "correct" the image by using the leftright invert button. Inverting the images to make the views appear "normal" is contrary to the accepted guidelines for 2D image orientation and leads to confusion in understanding the spatial anatomy. In dextrocardia with situs inversus, the apical views are obtained with the transducer positioned in the right fifth or sixth intercostal space and with the plane of sound oriented in a mirror-image direction of normal. Like the parasternal short-axis view, the apical four-chamber view in dextrocardia with situs inversus appears to be backward.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiographic Features of Frequently Encountered Complex Congenital Cardiac Defects All possible concordant and discordant connections are listed in Table 394 . The following discussion covers Figure 39-8 Subcostal coronal views from a patient with atrial situs inversus, l-loop, and normal great vessels. This patient had total anomalous pulmonary venous return to the upper portion of the inferior vena cava (IVC) and a hypoplastic right lung. Top, The right and left pulmonary veins (RPV and LPV) can be seen connecting to a common pulmonary vein that drains below the diaphragm and connects to the upper IVC. Note that the RPVs are considerably smaller than the LPVs because of diminished drainage from the hypoplastic right lung. Bottom, The plane of sound has been tilted anteriorly to image the subcostal four-chamber view. Note that the heart is in the right chest with the apex to the right. The left-sided atrium receives the superior vena cava (SVC) and the IVC (top) and is therefore the morphologic right atrium (RA). The RA connects to a ventricle on the left that has an atrioventricular valve closer to the apex. These findings indicate that the left-sided ventricle is the morphologic right ventricle (RV) and that there is l-looping. LA, left atrium; LV, left ventricle.

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Figure 39-9 Subcostal views from the same patients as in Figure 39-8 . Top, The plane of sound has been tilted farther than that in Figure 39-8 in order to image the posterior great artery. Note that the morphologic left ventricle (LV) on the patient's right gives rise to a vessel that arches and is therefore the aorta (AO). Bottom, The plane of sound has been tilted even farther anteriorly to image the anterior great artery. Note that the morphologic right ventricle (RV) on the patient's left gives rise to a vessel that crosses from left to right anterior to the AO. This vessel is a normally connected pulmonary artery (PA). LA, left atrium; RA, right atrium.

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the anatomy of these and other frequently encountered complex congenital defects. Associated lesions that should alert one to the diagnosis are also discussed. Atrioventricular Concordance and Ventriculoarterial Discordance or Simple Transposition of the Great Arteries In the most common form of transposition the morphologic right atrium on the patient's right is connected TABLE 39-4 -- Possible Segmental Connections AV Connection Concordant Concordant Discordant Discordant

VA Connection Concordant Discordant Discordant Concordant

Defect Normal heart d-Transposition l-Transposition Isolated ventricular inversion Anatomically corrected malposition AV, atrioventricular; VA, ventriculoarterial.

to the morphologic right ventricle on the patient's right, which in turn is connected to the aorta. On the patient's left the morphologic left atrium is connected to the morphologic left ventricle, which is connected to the pulmonary artery. This defect is called situs solitus, d-loop, d-transposition, or simply d-transposition. The "d" in the third term is used to describe the spatial relations of the aortic and pulmonic valves. The mirror image of this defect is situs inversus, l-loop, l-transposition. In more than 80% of cases the aortic valve spatially is located to the right of the pulmonary valve; hence, the use of the "d." Other spatial relationships are possible. In a small percentage of cases the aortic infundibulum and valve may be to the left of the pulmonary valve. This spatial relationship is frequently found in patients with d-transposition and a large ventricular septal defect, and it is often referred to as situs solitus, dloop, l-transposition. In this nomenclature the "l" in the third term refers to the spatial position of the aorta (to the left). In another small percentage of patients the aortic valve may be directly anterior to the pulmonary valve. The echocardiographic diagnosis of transposition of the great arteries is based on demonstrating an abnormal connection of the right ventricle to the aorta. Although the spatial relationships of the great arteries may provide supportive evidence of the diagnosis, they should never be used as the sole

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diagnostic criteria. The connections between the ventricles and great arteries can be seen in multiple echocardiographic views; however, the subcostal views are particularly useful for complete segmental analysis of the heart (Fig. 39-10) (Figure Not Available) . The anatomic and echocardiographic features of dtransposition are well known and are not reviewed in detail in this chapter. These features include (1) complete subaortic muscular infundibulum, (2) pulmonary valve-mitral valve fibrous continuity, (3) parallel spatial alignment of the outflow tracts and great arteries, (4) straight muscular septum, and (5) posterior angulation of the posterior great artery.[23] [24] [25] Associated Defects Ventricular Septal Defect.

Ventricular septal defects occur in about 33% of patients with dtransposition. Most of these defects are in the outlet septum and are associated with an overriding pulmonary artery. In this situation, anterior displacement of the infundibular septum results in a narrowed right ventricular infundibulum, discontinuity of the infundibular septum and the trabecular septum, and a malaligned-outlet ventricular septal defect.[26] Although the pulmonary artery overrides the ventricular septum, more than 50% of the pulmonary artery is committed to the left ventricle and there is pulmonary-mitral continuity. In patients with a malaligned-outlet ventricular septal defect, tricuspid valve abnormalities are frequent, occurring in 65% of patients in one series.[27] The types of tricuspid valve anomalies that occur are chordal attachments to the infundibular septum or ventricular septal crest, overriding of the tricuspid annulus, straddling tricuspid valve with chordal attachments into the left ventricle, tricuspid valve tissue protruding through the ventricular 853

Figure 39-10 (Figure Not Available) Subcostal views in coronal body planes from a patient with d-transposition of the great arteries. Top, View obtained by tilting the transducer posteriorly to image the inlets of the ventricles. The eustachian valve can be imaged in the morphologic right atrium (RA) and the pulmonary veins can be seen draining to the morphologic left atrium (LA). Middle, The plane of sound has been tilted slightly anteriorly to image the midportion of the heart. The smooth-walled morphologic left ventricle (LV) on the patient's left (d-loop) gives rise to a posterior vessel that bifurcates and is therefore the pulmonary artery (PA). Bottom, The plane of sound has been tilted far anteriorly. The morphologic right ventricle (RV) on the

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patient's right gives rise to the aorta (AO). (From Snider AR, Bengur AR: Twodimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 497.)

septal defect and causing subpulmonary obstruction, and cleft anterior leaflet of the tricuspid valve. The anterior displacement of the infundibular septum causes subaortic narrowing and produces a long, oblique course from left ventricle to aorta. These anatomic features make intraventricular repair extremely difficult and favor repair with an arterial switch procedure, closure of the ventricular septal defect, and resection of subaortic muscle, if necessary.[26] After closure of the ventricular septal defect, the right ventricle always becomes smaller, and right ventricular outflow gradients that were of minor significance preoperatively may become significant. The subaortic narrowing seen in patients with d-transposition and a malaligned-outlet ventricular septal defect may lead to the development of coarctation and interruption of the aorta. In one review of 129 pathologic specimens with d-transposition, 17% had right ventricular outflow obstruction and 7% had associated aortic arch obstruction as well. Anatomic narrowing of the subaortic region was found only in association with a malaligned-outlet ventricular septal defect. Aortic arch obstruction was present in 44% of specimens with a malaligned-outlet ventricular septal defect and in only 3% of specimens with an intact ventricular septum.[28] Other types of outlet ventricular septal defects occur less commonly in patients with d-transposition. Outlet ventricular septal defects can occur with posterior displacement of the infundibular septum, left ventricular outflow tract narrowing, and posterior malalignment between infundibular septum and trabecular septum.[26] In these cases, muscular subpulmonary obstruction is nearly always present. Because of the posterior deviation of the infundibular septum, a direct route from left ventricle to aorta is present, and patients with this defect are good candidates for repair by way of intraventricular rerouting from left ventricle to aorta.[26] Coarctation of the aorta is not associated with this type of ventricular septal defect. Another type of outlet ventricular septal defect that occurs very infrequently in patients with d-transposition is a subarterial (subaortic)

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ventricular septal defect in which the infundibular septum is hypoplastic or absent, but not displaced.[26] In patients with this defect, the aorta is frequently to the left and anterior. [26] Perimembranousinlet ventricular septal defects are commonly found in patients with d-transposition. This type of defect is also associated with tricuspid valve abnormalities of the type described earlier for a malaligned-outlet defect. In one series, 100% of patients with inlet ventricular septal defect had tricuspid valve abnormalities.[27] Other types of defects found with d-transposition are isolated muscular defects and perimembranous trabecular defects. Left Ventricular Outflow Tract Obstruction.

Obstruction to the pulmonary outflow occurs in patients with dtransposition with or without a ventricular septal defect. With an intact ventricular septum, dynamic subpulmonary obstruction is common, either before or after an intra-atrial baffle procedure. This dynamic obstruction is caused by a prominent systolic bulging of the ventricular septum into the left ventricular outflow tract.[29] On the short-axis views the left ventricle is thin walled and crescent shaped. Only minimal pressure gradients are detected by pulsed or continuous wave Doppler techniques. With significant fixed anatomic obstruction and an intact ventricular septum, the left ventricular pressure increases and the left ventricle becomes spherical and thick walled. The most common forms of fixed pulmonary 854

stenosis in this setting are fibrous subpulmonary diaphragm, fibromuscular ridge, and valvular stenosis (usually a bicuspid pulmonary valve).[30] Subpulmonary stenosis occurs more commonly in association with a ventricular septal defect, and certain types of subpulmonary stenosis are specific for certain types of ventricular septal defect. For example, posterior deviation of the infundibular septum occurs with malaligned-outlet ventricular septal defect,[26] whereas accessory tricuspid leaflet tissue bowing into the left ventricular outflow tract tends to occur with perimembranous-inlet defects.[27] Atrioventricular Discordance and Ventriculoarterial Discordance or lTransposition of the Great Arteries l-Transposition of the great arteries is a condition in which there is both

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atrioventricular and ventriculoarterial discordance; therefore, in situs solitus the morphologic right atrium on the patient's right is connected to the morphologic left ventricle on the patient's right, which in turn is connected to the pulmonary artery. On the left the morphologic left atrium is connected to the morphologic right ventricle, which is connected to the aorta.[31] This defect is called situs solitus, l-loop, l-transposition, or simply l-transposition. The "l" in the third term is used to describe the spatial relations of the aortic and pulmonic valves. In most cases the aortic valve is to the left; hence the use of the "l." Because of the presence of discordant connections at two levels, the circulation is hemodynamically correct (systemic venous blood flows to the pulmonary artery and pulmonary venous blood flows to the aorta); some investigators have called this defect corrected transposition of the great arteries. This terminology is not used in this chapter because of the confusion it creates in distinguishing this defect from surgically corrected d-transposition. The mirror-image situation is situs inversus, d-loop, d-transposition. As with d-transposition, the echocardiographic diagnosis of l-transposition is based on demonstrating abnormal connections between the right ventricle and aorta and also between the atria and the ventricles (Fig. 39-11 (Figure Not Available) and Fig. 39-12 ). The spatial relationships of the great arteries may provide supportive evidence of the diagnosis, but these are never used as the sole diagnostic criteria. In l-transposition the aortic valve is usually supported by a complete muscular infundibulum and is therefore located more superiorly than the pulmonary valve (see Fig. 39-11) (Figure Not Available) . In most cases the muscular infundibulum of the left ventricle is absorbed so that the pulmonary valve is wedged deeply in the heart between the two atrioventricular valves. Direct valvular continuity exists between the posterior cusp of the pulmonary valve and the anterior leaflet of the mitral valve; however, indirect continuity also exists with the tricuspid valve on the left via the central fibrous body and membranous septum.[31] With a slight tilting of the plane of sound in the parasternal longaxis view, "continuity" of the pulmonary valve to both atrioventricular valves can be shown. As in d-transposition, the ventricular outflow tracts and great arteries in ltransposition exit the heart in a parallel Figure 39-11 (Figure Not Available) Subcostal coronal views from a patient with situs solitus, l-loop, l-transposition of the great arteries, a large ventricular septal defect, and severe subvalvular and valvular pulmonary stenosis. Top, View obtained with the transducer tilted posteriorly to image the inlets of the heart. The pulmonary

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veins can be seen draining to the left-sided atrium, indicating that it is the morphologic left atrium (LA) and there is atrial situs solitus. Middle, The plane of sound has been tilted anteriorly. The right-sided ventricle has a smooth septal surface and a shape suggesting that it is the morphologic left ventricle (LV). The LV gives rise to a vessel that bifurcates into two branches and is the pulmonary artery (PA). These findings indicate an l-loop with l-transposition. Note the severe subvalvular and valvular pulmonary stenosis and the poststenotic dilation of the PA. There is an outlet ventricular septal defect. Bottom, The plane of sound has been tilted far anteriorly. The ventricle on the left side is triangular in shape and has prominent septal-parietal free wall muscle bundles, indicating that it is the morphologic right ventricle (RV). The RV gives rise to a vessel that arches and is the aorta (AO). RA, right atrium. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 507.)

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Figure 39-12 (color plate.) A, Apical four-chamber view from a patient with atrial situs solitus, l-loop, and l-transposition of the great arteries. Note that the ventricle on the left has a prominent moderator band and an atrioventricular valve closer to the cardiac apex. These findings indicate that the leftsided ventricle is the morphologic right ventricle (RV) and there is an l-loop. The leftsided tricuspid valve in this patient is much more apically displaced than is normal because of associated Ebstein deformity of the valve. B, Color Doppler examination from the same view shows a tricuspid regurgitation jet (red flow area) with a wide proximal diameter indicating a large regurgitant orifice. Note the massive left atrial (LA) dilation caused by the physiologic mitral regurgitation. LV, left ventricle; RA, right atrium. (From Snider AR, Serwer GA, Ritter SB: Echocardiography in Pediatric Heart Disease, 2nd ed. St. Louis, Mosby–Year Book, 1997, p. 322.)

fashion rather than wrapped around each another. Unlike the normal heart or the heart with d-transposition, however, the right ventricle is usually not anterior to the left ventricle in l-transposition. Typically, the ventricles are positioned side by side and the ventricular septum is oriented in a straight line perpendicular to the frontal plane through the thorax (Fig. 39-13) . In some cases the ventricles are arranged in a superoinferior fashion, the morphologic right ventricle being superior (Fig. 39-14) . The unusual spatial relationships of the ventricles, ventricular septum, and great arteries can lead to unusual and often confusing echocardiographic images (especially in the parasternal views). Associated Defects

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Tricuspid Valve Abnormalities.

Abnormalities of the left-sided tricuspid valve occur in about 90% of patients with l-transposition of the great arteries.[31] The common Figure 39-13 A, Parasternal short-axis view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with partial apical pivoting. The ventricle on the left has a prominent moderator band and is the morphologic right ventricle (RV). Note that the ventricles are positioned side by side, with the septum oriented perpendicular to the frontal body plane. This arrangement of the ventricular mass and septum is due to lack of complete apical pivoting, which commonly occurs in hearts with atrioventricular discordance. B, Parasternal short-axis view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with complete apical pivoting. The apex has pivoted completely to the side opposite the loop and thus points to the right hemithorax. As a result, the ventricular septum is oriented in a plane the mirror image of normal. C, Subcostal coronal view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with complete apical pivoting. The apex has completely rotated to the side opposite the loop. Note the left atrioventricular valve positioned closer to the cardiac apex, indicating that it is a tricuspid valve. The plane of the ventricular septum is the mirror image of normal. LA, left atrium; LV, left ventricle; RA, right atrium.

malformation is an Ebstein-type deformity in which the origin of the valve leaflet is displaced downward so that the basal attachments of the leaflets are from the systemic ventricular wall below the annulus fibrosus. Typically, the anterior leaflet is the least malformed and the septal and posterior leaflets are the most malformed. Occasionally, the valve leaflets are fused together and poorly demarcated. The chordae tendineae may be shortened, irregular, and thickened so that they hinder valve motion. All these anatomic features result in some loss in the size of the functioning right ventricle (the "atrialized" portion of right ventricle is between the annulus and the displaced valve) and a tricuspid valve incapable of closing properly (tricuspid regurgitation).[32] [33] [34] In patients with l-transposition, deformities of the tricuspid valve other than Ebstein malformation occur and lead to the development of tricuspid regurgitation (physiologic mitral regurgitation). Deformities such as deficient valve leaflet tissue, thickened valve leaflets, dilation of the annulus fibrosus, abnormal papillary muscles, and 856

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Figure 39-14 Top, Subcostal coronal view from a patient with situs solitus, l-loop, and l-transposition and superior-inferior arrangement of the ventricles. The left atrium (LA) communicates by way of a straddling and overriding tricuspid valve to a superiorly positioned right ventricle (RV). Note the horizontal position of the ventricular septum and the inferiorly positioned, smooth-walled left ventricle (LV). Bottom, Parasternal view through the inflow tracts of both ventricles. The two atrioventricular valves are seen in the same view aligned parallel, indicating that this patient does not have crisscross atrioventricular relations. RA, right atrium.

shortened chordae tendineae that insert directly into the ventricular wall may all occur and contribute to valvular dysfunction.[33] In patients with ltransposition and a ventricular septal defect (usually perimembranous inlet), chordae can insert through the ventricular septal defect into the morphologic left ventricle (straddling tricuspid valve). Uncommonly, obstruction to right ventricular inflow can occur in patients with l-transposition. This obstruction usually takes the form of a stenosing membrane or ring just above the tricuspid valve. On the 2D echocardiogram a supratricuspid stenosing ring appears as a thin, linear echo just above the left-sided tricuspid valve. Medially, the ring inserts into the left atrial surface just above the crux of the heart, and laterally it inserts into the free wall of the left atrium below the appendage.[35] Ventricular Septal Defect.

Ventricular septal defect occurs in about 70% of patients with ltransposition[31] and is usually perimembranous in location. In ltransposition, ventricular septal defects are frequently accompanied by other malformations (i.e., perimembranous inlet defects are associated with tricuspid valve straddle; anterior outlet defects are associated with mitral valve straddle). Left Ventricular Outflow Tract Obstruction.

Left ventricular outflow tract obstruction occurs in approximately 40% of patients with l-transposition. Usually, the stenosis is subvalvular—either a subvalvular diaphragmatic ring or an aneurysm of fibrous tissue protruding into the left ventricular outflow tract.[36] This fibrous tissue can originate from the membranous septum, mitral valve, tricuspid valve, or pulmonary valve. Right Ventricular Outflow Tract Obstruction.

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Right ventricular outflow obstruction is rare in patients with l-transposition, occurring in only about 10% of patients. [35] Subaortic stenosis can occur in patients with an outlet ventricular septal defect and anterior and leftward displacement of the infundibular septum. Most patients with l-transposition and subaortic stenosis also have aortic coarctation; however, aortic coarctation can occur without subaortic stenosis.[35] Atrioventricular Discordance with Ventriculoarterial Concordance Isolated Ventricular Inversion

Isolated ventricular inversion is a term first used in 1966 to describe the rare congenital cardiac malformation of ventricular inversion without transposition of the great arteries (i.e., atrioventricular discordance and ventriculoarterial concordance).[37] Because isolated ventricular inversion causes a physiologic state identical to that of complete transposition of the great arteries, most patients with this defect are symptomatic in infancy with cyanosis and congestive heart failure. On the 2D echocardiogram, patients with isolated ventricular inversion have atrioventricular discordance.[38] In the usual situation, there is atrial situs solitus and lbulboventricular loop (Fig. 39-15) (Figure Not Available) . The ventriculoarterial connections are normal. Thus, a posterior aorta usually arises from a right-sided morphologic left ventricle and is in fibrous continuity with the right-sided mitral valve (Fig. 39-16) (Figure Not Available) . An anterior pulmonary artery arises from the left-sided morphologic right ventricle and is separated from the left atrioventricular valve by a persistent subpulmonary conus. The normal relationships of the great arteries to one another (aortic valve rightward, posterior, and inferior to the pulmonary valve; great arteries coiled around each other) create a "circle-sausage" appearance in the short-axis views. Anatomically Corrected Malposition

Another rare defect with atrioventricular discordance and ventriculoarterial concordance is anatomically corrected malposition.[5] The echocardiographic techniques described previously are used to diagnose atrioventricular discordance (morphologic right atrium connected to morphologic left ventricle) and ventriculoarterial concordance (aorta arising from morphologic left ventricle).[39] In anatomically corrected malpositions, however, there is an 857

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Figure 39-15 (Figure Not Available) Apical four-chamber view showing normal atrial situs and discordant atrioventricular connections in a patient with isolated ventricular inversion. The pulmonary veins can be seen draining to the left-sided atrium, suggesting that this chamber is the morphologic left atrium (LA); therefore, there is atrial situs solitus. The left-sided ventricle has a prominent septoparietal muscle bundle and an atrioventricular valve closer to the cardiac apex. These features show that this chamber is the morphologic right ventricle (ARV); therefore, there is ventricular inversion. The right-sided morphologic left ventricle (ALV) has no septoparietal muscle bundles and has an atrioventricular valve farther from the cardiac apex. A, apex; R, right; RA, right atrium. (From Snider AR, Enderlein MA, Teitel DR, et al: Isolated ventricular inversion: Two-dimensional echocardiographic findings and a review of the literature. Pediatr Cardiol 1984;5:28.)

abnormal relationship between the aorta and the atrioventricular canal, such that mitral-aortic fibrous continuity does not occur (there is usually bilateral conus). In addition, although the great vessels arise above the correct chamber, the aortic valve is anterior to the pulmonary valve and the great vessels exit the heart in a parallel fashion. Univentricular Atrioventricular Connection Nomenclature and Definitions

Considerable controversy exists surrounding the definition, classification, and nomenclature for various forms of complex congenital heart defects; however, there is no greater controversy than that surrounding the nomenclature of hearts with a large dominant ventricle and a small rudimentary ventricular chamber that lacks an inflow. Terms used to describe these hearts include single ventricle, double-inlet ventricle, univentricular heart, and univentricular atrioventricular connection, among others. The debate started with the use in classic descriptions of the term "single ventricle."[19] As pointed out by Van Praagh et al,[19] the hearts in this category nearly always possess two ventricular chambers; therefore, the term "single ventricle" is inaccurate. In the late 1970s and early 1980s, Anderson et al[40] [41] [42] [43] attempted to clarify the confusion surrounding the terminology and classification of these hearts. They used the term univentricular heart of the left ventricular type to describe hearts in which the dominant chamber was morphologically a left ventricle and the rudimentary chamber had morphologic features of the trabecular portion of the right ventricle, and the term univentricular heart of the right ventricular type to describe hearts in which the dominant chamber was morphologically a right ventricle and the

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rudimentary chamber had morphologic features of the trabecular portion of the left ventricle. These authors introduced a new definition for what constitutes a ventricle and introduced terms to define rudimentary chambers in the heart that were not by definition ventricles.[40] [41] [42] Their proposed nomenclature was based on the following observations: The ventricles of the normal heart possess inlet, trabecular, and outlet Figure 39-16 (Figure Not Available) Subcostal coronal views from the same patient as in Figure 39-15 (Figure Not Available) . These views show discordant atrioventricular connections and normal relationships between the great arteries and the ventricles. Top, The aorta (Ao) and aortic arch can be seen arising from the rightsided ventricle, which the four-chamber view in Figure 39-15 (Figure Not Available) has shown to be the morphologic left ventricle (ALV). Bottom, With even more anterior tilting of the transducer, the anteriorly positioned pulmonary artery (PA) and its bifurcation can be seen arising from the left-sided morphologic right ventricle (ARV). In addition, the great vessels are normally coiled around each other ("circle sausage" appearance). A subaortic ventricular septal defect also can be seen. I, inferior; R, right; RA, right atrium. (From Snider AR, Enderlein MA, Teitel DR, et al: Isolated ventricular inversion: Two-dimensional echocardiographic findings and a review of the literature. Pediatr Cardiol 1984;5:28.)

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portions.[42] The inlet portion extends from the atrioventricular annulus to the insertions of the papillary muscles and need not contain a perforate atrioventricular valve. The outlet portion supports the semilunar valve, and the trabecular portion extends from the inlet and outlet portions to the ventricular apex. In the normal heart the inlet and outlet portions of the morphologic left ventricle are in fibrous continuity. In the morphologic right ventricle, these two portions are separated from one another by the crista supraventricularis. In the normal heart, each trabecular zone receives its own inlet; however, all the atrioventricular inlets can be committed to one trabecular portion, which is the classic definition of single ventricle.[40] [42]

As discussed earlier, Anderson et al then proposed that a chamber must have 50% or more of an inlet portion to be classified as a ventricle. A chamber need not have an outlet portion to be a ventricle (the left ventricle in

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Figure 39-17 Diagrammatic representation of the anatomic features used to diagnose the type of univentricular heart on two-dimensional echocardiography. The drawings represent parasternal short-axis projections. In single ventricle of the left ventricular (LV) type, the trabecular septum (stippled) and rudimentary chamber (RC) are anterior to the atrioventricular valves. The trabecular septum runs to the acute or obtuse margin of the heart and not to the crux of the heart (black circle). Thus, there is no intervening septum at the crux of the heart between the atrioventricular valves. Most often, the RC is at the left basal aspect of the heart (l-loop); however, it can also be located less frequently at the right basal aspect of the heart (d-loop). Most commonly, the ventriculoarterial connections are discordant with the aorta (AO) arising from the RC and the pulmonary artery (PA) arising from the main ventricle (depicted in the diagram); however, any ventriculoarterial connection is possible. In single ventricle of the right ventricular (RV) type, the RC and trabecular septum are posterior to the atrioventricular valves. The trabecular septum courses to the crux of the heart and there is usually left atrioventricular valve atresia (shown). Most commonly, the ventriculoarterial connections are double outlet from the main ventricle (shown); however, any ventriculoarterial connection is possible.

double-outlet right ventricle has only inlet and trabecular portions). Chambers receiving less than 50% of an inlet were termed rudimentary chambers. Rudimentary chambers possessing an outlet portion were termed outlet chambers, whereas those with only a trabecular zone were called trabecular pouches. Subsequently, Van Praagh and others argued that this definition of a ventricle was arbitrary and that the use of the term "univentricular heart" was misleading, because these hearts really possess two ventricular chambers.[18] [19] These investigators suggested that the hearts in question be described in terms of their basic embryologic abnormality (abnormal atrioventricular connection), and thus preferred the continued use of terms such as double-inlet left ventricle and tricuspid atresia. In 1984, Anderson et al[20] (in response to arguments against their definition of a ventricle) introduced the term univentricular atrioventricular connection to describe hearts in which both inlets 859

(whether patent or not) were primarily committed to one dominant ventricle. They described the small ventricular chamber that is present in almost all of these hearts as a rudimentary ventricle because it lacked the inlet portion.

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This short review of the controversy surrounding the nomenclature and classification of univentricular atrioventricular connection was undertaken not to support one point of view but to explain and clarify as many of the existing schools of thought as possible. Readers must choose their own preferred nomenclature, but it is important that they understand the meaning and derivation of all terms used in the medical literature to avoid confusion and misunderstanding. Throughout this chapter, the approach to the echocardiographic diagnosis of univentricular heart is based on the definitions and classification proposed by Anderson et al.[40] [41] [42] The distinction made in using the term "univentricular atrioventricular connection" is appreciated; however, the term "univentricular heart" often is used instead (with the realization that there are two ventricular chambers) because it is simpler and less cumbersome. Also, the terms "outlet chamber" and "trabecular pouch" continue to be used occasionally because they are in widespread use and are understood by everyone. Also, these terms, in a simple and economic use of words, convey additional information concerning the inlet and outlet connections of the chamber. Anatomic Findings

In the most common type of univentricular heart, all atrioventricular connections are committed to a chamber with a left ventricular trabecular pattern. In this case the rudimentary chamber has a right ventricular trabecular pattern and is located anterosuperiorly in the ventricular mass. This defect has been called double-inlet left ventricle, single ventricle of the left ventricular type, and univentricular heart of the left ventricular type. Conversely, all atrioventricular connections can be committed to a chamber with right ventricular trabecular pattern. In this situation the rudimentary ventricle contains a left ventricular trabecular portion and is located posteriorly in the ventricular mass. This defect is known as univentricular heart of the right ventricular type. In rare cases, neither right nor left ventricular trabecular portions are well formed and a single chamber is present with indeterminate trabecular pattern. This defect has been called univentricular heart of the indeterminate type without rudimentary chamber.[41] [42] Another important point in the morphology and echocardiographic diagnosis of univentricular heart is the nature of the septum that separates the main ventricle from the rudimentary chamber. Because the ventricles are considered to possess inlet, trabecular, and outlet portions, the septum separating them can be considered to possess inlet, trabecular, and outlet portions. Both inlets are committed to only one chamber; hence, by

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definition, the inlet septum is absent in the univentricular heart. The septum separating the ventricle from the rudimentary chamber must be the trabecular septum. The position and orientation of the trabecular septum in the ventricular mass is a key feature in the echocardiographic diagnosis of the univentricular heart.[42] Figure 39-18 Parasternal long-axis view from a patient with a univentricular heart of the left ventricular type and discordant ventriculoarterial connections. In this view the small outlet chamber (OC) can be seen anterior to the main left ventricle (LV). In this patient the pulmonary artery (PA) arose from the LV and the aorta (AO) arose from the OC. There was no pulmonary stenosis and the bulboventricular foramen was restrictive (1.4 cm2 /m2 ). LA, left atrium. Echocardiographic Diagnosis of the Type of Univentricular Heart

In univentricular heart of the left ventricular type the rudimentary chamber is located anterior to the main ventricle and is separated from this chamber by an anterior trabecular septum (Fig. 39-17) . Because the trabecular septum is an anterior structure, it is well visualized in the parasternal longand short-axis views.[43] [44] [45] In the parasternal long-axis view (Fig. 39-18) the rudimentary ventricle is seen anteriorly and separated from the main chamber by the trabecular septum. The outlet foramen or ventricular septal defect is seen connecting the main left ventricle and the rudimentary right ventricle. With this view alone it is not possible to distinguish a univentricular heart of the left ventricular type from a ventricular septal defect with a large left ventricle. This distinction is not possible because the parasternal long-axis view allows visualization of only one atrioventricular connection. Also, because the parasternal long-axis view has only anteroposterior and inferosuperior orientations, it is not possible to determine whether the rudimentary chamber is at the right or left basal aspect of the heart. When the transducer is rotated into the parasternal short-axis view, the distinction between univentricular heart of the left ventricular type and ventricular septal defect with a large left ventricle is immediately apparent. In univentricular heart of the left ventricular type, both atrioventricular valves lie posterior to the trabecular septum (Fig. 39-19) . Because these valves usually do not have the anatomic features of the normal tricuspid and mitral valves, we refer to them as the right and left atrioventricular valves. There is no intervening inlet septum between the two atrioventricular valves; therefore, these valves may actually touch one

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another when they open in diastole ("kissing" atrioventricular valves). In addition, 860

Figure 39-19 Parasternal short-axis view from a patient with a univentricular heart of the left ventricular type and ventriculoarterial discordance. The right and left atrioventricular valves are both committed to the left ventricle (LV). There is no septum intervening between the valves. Note the outlet chamber (OC) situated anteriorly. Both atrioventricular valves are posterior to the trabecular septum. The trabecular septum lies between the OC and the LV.

both atrioventricular valves are in fibrous continuity with the posterior great artery. From the parasternal short-axis view, one can determine whether the rudimentary right ventricle lies to the right or left basal aspect of the heart. Most commonly, the rudimentary right ventricle lies to the left (l-loop) and the trabecular septum courses obliquely and somewhat posteriorly from the right and anterior cardiac border to the acute margin of the heart. When the rudimentary chamber lies to the right (d-loop), the trabecular septum courses obliquely and somewhat posteriorly from the left anterior cardiac border to the obtuse margin of the heart (see Fig. 39-19) . From the parasternal short-axis views, one can easily understand why the rudimentary chamber and trabecular septum cannot be visualized in the four-chamber views in patients with univentricular heart of the left ventricular type. The four-chamber views are posterior planes that pass through both atrioventricular valve inlets and the crux of the heart; therefore, these planes lie posterior to the trabecular septum and rudimentary chamber (Fig. 39-20) . In an echocardiographic study of 57 patients with double-inlet left ventricle,[46] all patients had atrial situs solitus and normal systemic and pulmonary venous return. An l-loop was present in 63% and a d-loop in 37%. Shiraishi and Silverman[47] reported finding atrial situs inversus in 2 of 42 patients with double-inlet left ventricle and 2 atrioventricular valves. In their series, l-loop occurred in 74% and d-loop in 26%. In univentricular heart of the right ventricular type the rudimentary chamber possesses the left ventricular trabecular portion and is thus located posteriorly (see Fig. 39-17) . Likewise, the trabecular septum runs

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posteriorly to the crux of the heart. In the parasternal long- and short-axis views, visualization of the atrioventricular connections anterior to the trabecular septum is diagnostic of univentricular heart of the right ventricular type (Fig. 39-21) . The rudimentary chamber can be located posteriorly and to the right or posteriorly and to the left. Because the rudimentary chamber is posterior and the trabecular septum extends to the crux of the heart, portions of these two structures normally can be seen in the apical and subcostal four-chamber views. If a single chamber is present in the heart with no evidence of a trabecular septum or rudimentary chamber in any echocardiographic view, the diagnosis of univentricular heart of indeterminate type can be made. Echocardiographic Evaluation of Ventriculoarterial Connections

With the univentricular heart, any ventriculoarterial connection can occur, including concordant connections, Figure 39-20 Subcostal coronal views from a patient with univentricular heart of the left ventricular type and discordant ventriculoarterial connections. Top, The transducer has been tilted posteriorly to image the inlets of the heart. This view is a posterior plane passing through both atrioventricular valve inlets and the crux of the heart; therefore, this plane lies posterior to the trabecular septum and rudimentary chamber. Note the "kissing" atrioventricular valve with no intervening ventricular septum oriented to the crux of the heart. Both atrioventricular valves empty into the large posterior left ventricle (LV). Bottom, The transducer has been tilted anteriorly to image the outflow tracts. The LV is connected to a posterior pulmonary artery (PA). A small rightward and anterior outlet chamber (OC) gives rise to an anterior and rightward aorta (AO). Note that many of the echocardiographic features of transposition of the great vessels are seen. The great vessels are aligned parallel and the posterior PA has a posterior sweep. The bulboventricular foramen in this patient was of good size. LA, left atrium; RA, right atrium.

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Figure 39-21 Parasternal long-axis (top) and short-axis (bottom) views from a patient with univentricular heart of the right ventricular type. The main right ventricle (RV) is anterior to a small rudimentary left ventricle (LV). Top, Both great arteries arise from the RV, with the pulmonary artery (PA) located posterior to the aorta (AO). There is muscular subvalvular pulmonary stenosis. Bottom, Both atrioventricular valves (arrows) can be seen

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emptying into the RV anterior to the trabecular septum and rudimentary LV.

discordant connections, double outlet from the main or outlet chambers, and single outlet from the heart. Certain combinations of univentricular heart and ventriculoarterial connections, however, are commonly associated with one another and thus deserve mention. A high percentage of patients with univentricular heart of the left ventricular type have discordant ventriculoarterial connections: the aorta arises from the rudimentary right ventricle or outlet chamber and the pulmonary artery arises from the main left ventricle. In this situation the great vessels are parallel and exhibit the characteristic echocardiographic features of transposition (parallel alignment of the great arteries in long-axis views, posterior sweep of the posterior pulmonary artery in long-axis views, double circles in short-axis views) (see Fig. 39-20) . In the report of 57 patients with double-inlet left ventricle referred to previously,[46] transposition of the great arteries was present in 86% (13 with d-loop and 36 with l-loop). The great arteries were normally related in the remaining 14%, all of whom had a d-loop (so-called Holmes heart). In univentricular heart of the left ventricular type with absent right atrioventricular connection, the bulboventricular loop is usually to the right and the ventriculoarterial connections are most often concordant.[40] [41] [42] In univentricular heart of the right ventricular type, the ventriculoarterial connections are usually double outlet from the main chamber or single outlet from the heart with pulmonary atresia. In univentricular heart of indeterminate type and no outlet chamber, the connections can only be double outlet or single outlet from the main chamber.[42] Echocardiographic Evaluation of Atrioventricular Connections Double-Inlet Connections.

In the most common situation, univentricular heart exists with a doubleinlet atrioventricular connection in which both atria connect with the dominant ventricle by way of two separate atrioventricular valves or, less commonly, by way of a common atrioventricular valve. In the series of 50 patients with double-inlet ventricle reported by Shiraishi and Silverman,[47] double-inlet connection occurred with two atrioventricular valves in 88% and with a common atrioventricular valve in only 12%. It is of note that all the patients in this series with double inlet by way of a common atrioventricular valve had echocardiographic features of situs ambiguus. Also of note was the finding of a stenotic atrioventricular valve in 30% of

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patients with two separate atrioventricular valves. Most often, the stenotic valve was the left atrioventricular valve. On echocardiographic examination of patients with double-inlet left ventricle by way of two atrioventricular valves, the atrioventricular valves can be seen in short-axis and four-chamber views, both situated posterior to the trabecular septum (see Fig. 39-20) . There is no intervening inlet septum and both valves are in continuity with the posterior great artery. Univentricular hearts of the right ventricular type also can have doubleinlet connection by way of two atrioventricular valves. Usually the valves lie side by side and anterior to the trabecular septum.[42] Univentricular hearts of indeterminate type usually have a double-inlet connection, but this connection is generally via a common atrioventricular valve rather than by separate right and left atrioventricular valves. Absence of an Atrioventricular Connection.

Many hearts with atresia of an atrioventricular valve have absence of the connection rather than an imperforate valve. In absent connection the floor of the atrium is entirely muscular and is separated from the main ventricle by the atrioventricular sulcus.[42] This situation is quite distinct from those in which an imperforate membrane or connection sits above a tiny ventricular chamber. For example, in patients with univentricular heart of the left ventricular type and absent right atrioventricular connection, the apical and subcostal four-chamber views show the right and left atria above the main ventricle (Fig. 39-22A) (Figure Not Available) . There is no small chamber situated beneath the atretic right connection and no evidence of a septum oriented to the crux of the heart. The rudimentary chamber and trabecular septum are located anteriorly and have no connection to the blind-ending right atrium. [41] [42] In tricuspid atresia with an imperforate membrane and two separate ventricles, the right atrium can be seen in the four-chamber views situated directly above and connected to a small 862

Figure 39-22 (Figure Not Available) A, Apical four-chamber view from a patient with univentricular heart of the left ventricular type with an absent right atrioventricular connection. The right atrium (RA) and the left atrium (LA) both sit above the large left ventricle (LV). There is no small chamber beneath the atretic right connection and no evidence of a septum oriented to the crux of the heart. B, Apical four-chamber view from a patient with tricuspid atresia with an imperforate membrane and two separate ventricles. The connection between the RA and right ventricle (RV) is present, but the tricuspid valve is imperforate. The ventricular septum courses to the crux of the heart

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between the RV and LV, with the ventricular septal defect shown by the arrow. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 495.)

right ventricular chamber (see Fig. 39-22B) (Figure Not Available) . Here, the connection between the right atrium and right ventricle is present, but the tricuspid valve is imperforate. The ventricular septum courses to the crux of the heart between the right and left ventricles. The same diagnostic approach applies to the distinction between hypoplastic left heart with mitral atresia and univentricular heart of the right ventricular type with absent left atrioventricular connection. Straddling Valves.

In univentricular hearts an inlet portion can override or straddle the trabecular septum, whether it is located anteriorly or posteriorly. The degree of commitment of the straddling valve to its own trabecular zone or to the trabecular zone of a chamber already receiving an inlet determines whether the heart is classified as biventricular or univentricular.[42] In some instances the straddling inlet appears equally committed to both chambers on the 2D echocardiogram, and a definite diagnosis cannot be made. In these cases the position of the small chamber and septum may suggest the most likely diagnosis. Echocardiographic Evaluation of Interventricular Communication

In hearts with univentricular atrioventricular connection the communication between the main and rudimentary ventricles has been referred to by several terms, including ventricular septal defect, bulboventricular foramen, and outlet foramen. Bevilacqua et al[46] described the morphology of the ventricular septal defect in 46 patients with double-inlet left ventricle. In 24 patients the defect was separated from the semilunar valves and completely surrounded by muscle (muscular defect), and it tended to enter the rudimentary chamber inferiorly and apically. In 19 patients the defect was adjacent to the anterior semilunar valve (subaortic defect), and it was associated with hypoplasia of the infundibular septum in 5 patients and posterior malalignment of the infundibular septum (with or without hypoplasia) in 14. The remaining 3 patients had multiple muscular defects. Although further anatomic subsets of defects (e.g., midmuscular, atrioventricular canal types) can be distinguished on the pathologic examination, these subtypes were not recognized reliably on

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echocardiographic examination. The ventricular septal defect was restrictive in 47%. Only 21% of subaortic defects were restrictive, whereas 67% of muscular defects were restrictive. In patients with double-inlet left ventricle and transposition a restrictive ventricular communication resulted in an increased incidence of subaortic stenosis and/or aortic arch obstructions. The defect can be stenotic at birth or can become restrictive. In patients with transposition and pulmonary stenosis the defect was rarely stenotic; however, in transposition without pulmonary stenosis a restrictive ventricular septal defect was significantly more common. These are the same patients previously reported to develop subaortic stenosis after pulmonary artery banding.[48] [49] It is likely that subaortic stenosis develops in these patients not because of the pulmonary artery banding procedure but because the initial size of the defect places them at risk for developing a restrictive interventricular communication, and consequently subaortic stenosis. The pressure gradient across a restrictive outlet foramen can be estimated from several views using Doppler echocardiography; however, several studies suggest that direct measurement of the size of the foramen is a better indicator of obstruction.[47] [50] Situs Ambiguus The association of splenic abnormalities with complex cardiac defects and abdominal heterotaxy is well described. Traditionally, 863

these syndromes have been referred to as asplenia and polysplenia because each appears to be somewhat distinct in regard to the associated cardiac abnormalities, clinical features, and outcomes.[51] [52] [53] For example, Van Mierop et al[54] [55] described the association of right atrial isomerism with asplenia syndrome, noting the presence of bilateral sinoatrial nodes and two morphologic right atrial appendages in these hearts. Similarly, they observed left atrial isomerism with two morphologic left atrial appendages in hearts with polysplenia syndrome.[56] Noting that the status of the spleen was not always a reliable marker of these two syndromes, Van Mierop et al [57] preferred to use the bronchial branching pattern as a more consistent indicator of the diagnosis. In Phoon and Neill's[51] comprehensive review of asplenia, however, some examples of asplenia associated with bilateral bilobed lungs, interrupted inferior vena cava, and other features more

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commonly associated with polysplenia were described. These researchers concluded that although asplenia is clearly a syndrome of relative right isomerism and polysplenia a syndrome of relative left isomerism, some overlap exists between the two syndromes, making all the currently used terminology (e.g., asplenia, polysplenia, situs ambiguus, bilateral rightsidedness, bilateral left-sidedness) somewhat unsatisfactory. Although recent observations in patients with these syndromes suggest that they represent a continuum of congenital defects (both cardiac and extracardiac), there are several associated anomalies whose presence might suggest one or the other diagnosis.[4] [51] [58] [59] [60] [61] [62] [63] [64] For example, bilateral superior venae cavae, each draining to the ipsilateral atrial cavity, are commonly found in both asplenia and polysplenia; however, drainage of the left-sided superior vena cava to the coronary sinus is encountered nearly always with polysplenia. Anomalies of the systemic veins that drain the abdomen are also common.[61] In asplenia syndrome the inferior vena cava and aorta tend to be on the same side of the spine, either to the right or to the left (Fig. 39-23) (Figure Not Available) .[56] In polysplenia syndrome the inferior vena cava is frequently interrupted. In these cases, lower systemic venous return is by way of the azygous or hemiazygous vein, and the hepatic veins drain directly into one or both atria (Fig. 39-24) .[56] [61] [62] Anomalous pulmonary venous return also is common in situs ambiguus. In asplenia syndrome, total anomalous pulmonary venous return is nearly always present (in more than 80% of cases) and can be of any type. When the veins enter the cardiac atrium directly (rather than by way of a common pulmonary vein), they tend to drain to the smooth intercaval portion of the atria near the midline and are connected by a narrow confluence.[61] In polysplenia syndrome the pulmonary veins enter one atrium in a normal fashion in one third of cases. In over 50% of cases, however, the right veins enter the right-sided atrium and the left veins enter the left-sided atrium.[56] The anatomy of the cardiac chambers and great vessels is extremely variable in situs ambiguus, but a few common associations deserve mention. In asplenia syndrome, atrioventricular septal defects and single ventricle are common. Most often, the single ventricle is not the classic double-inlet left ventricle; instead, a very rudimentary septum is present between the two ventricles.[51] The great arteries Figure 39-23 (Figure Not Available) Subcostal short-axis (top) and sagittal (bottom) views from a patient with asplenia syndrome. The inferior vena cava (IVC) is on the same side of the spine as the descending aorta (DAO). Note that the IVC is anterior to

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the DAO. This abnormality of systemic venous drainage is commonly present in patients with asplenia syndrome. A, anterior; Ao, aorta; R, right; V, vertebral body. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 505.)

are frequently transposed and there is a high incidence of severe pulmonary stenosis or atresia. In polysplenia syndrome, atrial septal defects, ventricular septal defects, and double-outlet right ventricle are often encountered. Transposition of the great arteries and severe pulmonary stenosis are uncommon in polysplenia syndrome.[56] [60] Crisscross Hearts The term crisscross heart has been used to describe the rare abnormality in which the systemic and pulmonary venous streams cross at the atrioventricular level without mixing. The right-sided atrium connects to the left-sided ventricle and the left-sided atrium connects to the right-sided ventricle. This defect is believed to occur as a result of a differential rate of development of the right ventricular 864

Figure 39-24 (color plate.) Color Doppler examinations from a patient with polysplenia syndrome and an interrupted inferior vena cava. A, In the subcostal cross-sectional view, the descending aorta flow is seen in red (flow toward the transducer) because the transducer is situated in the abdomen and pointed slightly superiorly toward the patient's head. A large venous structure (blue flow area) is seen posterior and to the left of the descending aorta in the abdomen. This posterior structure represents a large hemizygous vein through which the lower body systemic venous drainage returned to a left-sided superior vena cava. Flow in the hemizygous vein is seen in blue because the flow is directed away from the transducer and toward the patient's head. B, In the subcostal long-axis view, flow in the descending aorta is again seen in red, indicating flow down the aorta toward the transducer. Flow in the hemizygous vein (located posterior to the aorta) is seen in blue, indicating flow away from the transducer toward the heart. (From Snider AR, Serwer GA, Ritter SB: Echocardiography in Pediatric Heart Disease, 2nd ed. St. Louis, Mosby–Year Book, 1997, p. 568.)

sinus and infundibulum. As a result, the ventricles appear to have rotated around their longitudinal axis (clockwise rotation when viewed from the apex in d-loop ventricles) without concomitant motion of the atria and

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atrioventricular valve annuli, producing actual crossing of the inflow tracts. The defect can be found with concordant or discordant atrioventricular connections. A ventricular septal defect is invariably present, and discordant ventriculoarterial connections are common. Associated defects can be expected.[65] On 2D echocardiography, the diagnosis should be suspected when a parallel arrangement of the atrioventricular valves and ventricular inflow regions cannot be found in the four-chamber views.[65] [66] [67] [68] [69] In the most posterior subcostal four-chamber view the left-sided atrium can be seen communicating by way of an atrioventricular valve to the right-sided ventricle. In the usual situation the left-sided atrium is a morphologic left atrium connected to a right-sided morphologic left ventricle. The left ventricle is posterior, inferior, and rightward. The posterior mitral valve is oriented from posterosuperior to anteroinferior (Fig. 39-25) .[64] As the plane of sound is tilted further anteriorly, the connection from the rightsided atrium to the left-sided ventricle can be seen. In the usual situation the right-sided morphologic right atrium is connected to a morphologic right ventricle that is anterior, superior, and leftward. The anterior and superior tricuspid valve is oriented from right to left and from posterior to anterior. Although part of the tricuspid valve and right ventricular sinus extend to the left of the mitral valve, the annulus of the tricuspid valve is to the right of the annulus of the mitral valve. In this plane a distal portion of the mitral valve leaflets can often be seen in cross section inferior to the longitudinal section through the tricuspid leaflets. With even further tilting of the plane of sound anteriorly, the entire anterior ventricle and its outflow portion can be visualized. In the usual situation this anterior and superior ventricle is a morphologic right ventricle that gives rise to a transposed aorta. Associated defects are common in crisscross hearts. Ventricular septal defects are invariably present and usually occur in the inlet septum. Subvalvular and valvular pulmonary stenosis commonly occur. In most cases of crisscross heart, there is hypoplasia of the right ventricle. The degree of underdevelopment of the right ventricular sinus is directly related to the angle between the long axes of the atrioventricular valves and the degree of ventricular rotation. Straddling mitral valve is also commonly encountered in crisscross hearts. In these cases the ventricles appear to have rotated through a greater angle, thus allowing alignment of the mitral valve and infundibulum.[12] [70]

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Although the ventricles in crisscross hearts are often arranged in a superiorinferior relationship, the terms "crisscross" heart and "superior-inferior ventricles" are not synonymous, and care should be taken not to confuse these entities on the echocardiographic examination. Superior-inferior ventricles represent a distinct entity characterized by a malpositioning of the ventricles with a horizontal ventricular septum.[71] The defect is believed to occur as a result of an abnormal tilting of the cardiac apex in the frontal plane. In a study of 17 patients with superior-inferior ventricles, Hery et al [71] found crisscross relationships of the atrioventricular valves in 41% of the patients. Most patients (59%) did not have crisscross relationships. Crisscross heart is one of the few congenital defects in which knowledge of the atrioventricular connections or alignments is wrongly predictive of the ventricular spatial position. For example, knowledge of the atrial situs and the bulboventricular loop indicates the atrioventricular connections, which in turn usually correspond to the situs or position of the ventricles. Thus, the usual form of crisscross heart (right-sided morphologic right atrium to left-sided morphologic right ventricle to left-sided aorta) can be described as atrial situs solitus, d-loop, and l-transposition of the great arteries.[67] Without further explanation, one would assume from this nomenclature that 865

Figure 39-25 Subcostal coronal views from a patient with a crisscross heart and dextrocardia. Top, The plane of sound is tilted far posteriorly. The pulmonary veins drain to the left-sided atrium, suggesting that this is a morphologic left atrium (LA). The morphologic LA is connected to a smoothwalled ventricle that has the anatomic features of a morphologic left ventricle (LV). The LV is located posteriorly, inferiorly, and rightward. The posterior mitral valve is oriented from posterosuperior to anteroinferior. Middle, The plane of sound has been tilted anteriorly so that the connections from the right-sided atrium to the left-sided ventricle can be seen. The right-sided atrium receives the drainage of the superior vena cava (SVC) and has other features suggesting that this chamber is a morphologic right atrium (RA). The anterior and superior tricuspid valve (arrows) is oriented from right to left and from posterior to anterior. A cross-section of the distal portion of the mitral valve leaflets can be seen inferior to the longitudinal section through the tricuspid valve leaflets. This view provides direct visualization of the crisscross arrangement of the atrioventricular valves. Bottom, Further tilting of the transducer shows that the left-sided ventricle has features of a morphologic right ventricle (RV) and gives rise to the leftward and anterior aorta (AO). Note that the morphologic RV is anterior, superior, and leftward.

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the atrioventricular alignments or connections are concordant and that the morphologic right ventricle is to the right of the morphologic left ventricle. It is suggested, therefore, that in the rare instances in which there is disharmony between the situs and alignment information, both should be stated. The previously mentioned heart would then be referred to as atrial situs solitus, d-loop ventricles with crisscross connections, and ltransposition of the great arteries.[12] [67]

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868

Chapter 40 - Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Mary Etta E. King MD

Caring for adults with congenital heart disease who have not had prior surgical intervention is a fascinating lesson in the natural history of congenital anomalies of the heart. It can also be a remarkable tribute to the tolerance, adaptation, and perseverance of the patient in the face of longstanding cardiac disability. In managing adults with unoperated congenital heart disease, three clinical subgroups emerge: patients with mild or slowly progressive defects who do not require intervention; patients who have eluded previous diagnosis and are still amenable to surgical correction; and patients with abnormalities that are deemed inoperable. It is the task of the cardiologist to evaluate each patient thoroughly to determine optimal management. Echocardiography has been a major boon to cardiologists in diagnosing and evaluating the anatomic and physiologic status of the adult with congenital heart disease. The technique is not without challenge or difficulty, however. Cardiac enlargement and hypertrophy as well as associated scoliosis cause chest wall deformities that limit transthoracic ultrasound access. Congenital or acquired pulmonary disease and cardiac malpositions lend additional

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impediment to surface echocardiographic imaging. Transesophageal echocardiography is useful in circumventing some of these difficulties and plays a major adjunctive role in evaluating and managing the adult with congenital heart disease.[1] [2] It has been said that "chance favors the prepared mind." Thus, the likelihood of an accurate diagnosis with any of these technologies requires a clear understanding of congenital heart defects and the expected sequelae and complications. This chapter includes the clinical features and echocardiographic evaluation and management of congenital heart defects that are encountered in the adult patient without the benefit of previous surgical intervention. Discussion includes valvular abnormalities, disorders affecting the left ventricular outflow tract and aorta, septal defects and shunt lesions, and complex congenital abnormalities most frequently encountered. The relative frequency of these anomalies in the unoperated adult is shown in Table 40-1 .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Valvular Abnormalities Bicuspid Aortic Valve The congenitally bicuspid aortic valve is the most frequent of all congenital heart defects, occurring in approximately 1% to 2% of the U.S. population. [3] Morphologically, the bicuspid valve may have two equal cusps with a single central commissure, or the cusps may be disparate TABLE 40-1 -- Congenital Heart Defects in the Unoperated Adult Most Common Bicuspid aortic valve

Less Common Ventricular septal defect

Discrete subaortic stenosis Pulmonic stenosis Patent ductus arteriosus

Rare Double-outlet right ventricle Complete transposition

Ebstein's anomaly Coarctation of the Tetralogy of Fallot Truncus arteriosus aorta Coronary arteriovenous fistula Tricuspid atresia Atrial septal Sinus of Valsalva aneurysm Univentricular heart defect Corrected transposition

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Figure 40-1 Echocardiographic views from a patient with a bicuspid aortic valve and a chronic aortic dissection. The parasternal long-axis view (top) demonstrates the markedly dilated proximal ascending aorta

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with a suggestion of an intimal flap (arrow). At surgical repair, the transesophageal echocardiography showed a bicuspid aortic valve (bottom left) and confirmed an intimal tag in the dilated aortic root (bottom right). Ao, aorta; AoV, aortic valve; Asc Ao, ascending aorta; LV, left ventricle.

in size, with an eccentric commissure and the larger cusp containing a raphe. Functionally, a bicuspid valve may be nonstenotic and nonregurgitant, which is especially true in the adolescent and young adult, of whom as many as one third have no significant functional impairment.[4] Progression of stenosis is common, however, even in valves with mild dysfunction. By the age of 60 years, 53% of bicuspid valves are stenotic, and by the age of 70 years, 73% become significantly stenotic. Of individuals older than 40 years who require aortic valve replacements, about 30% have a congenitally abnormal aortic valve.[5] The mechanism of progressive valvular dysfunction appears to be a "wear and tear" process leading to fibrosis and calcification. Congenitally bicuspid aortic valves have a known association with abnormalities of the aorta. Aortic coarctation occurs in a small percentage of patients with bicuspid aortic valves. Aortic dissection is another abnormality recognized for its association with a bicuspid aortic valve (Fig. 40-1) . Reported studies have shown that 5% to 9% of patients with dissecting aneurysms of the aorta also have a bicuspid aortic valve. Pathologic study of the aorta in these patients revealed changes consistent with cystic medial necrosis. [4] [5] [6] [7] Poststenotic dilation of the ascending aorta has long been recognized in congenital aortic stenosis, presumably caused by mechanical impingement of a jet lesion eccentrically directed by the domed leaflets. The ascending aorta may be dilated, however, even in functionally normal bicuspid valves, raising the possibility of a common developmental defect affecting both the valve and the aortic root. Another group of malformations associated with a bicuspid aortic valve is Shone's complex. This complex comprises several levels of inflow or outflow obstruction to the left heart: supramitral ring, congenital mitral stenosis, discrete subaortic membrane, bicuspid aortic valve, and coarctation. Whereas most patients with this "left heart blight" have received evaluation and treatment as children, milder forms may be seen in the adult population, prompting careful assessment of the mitral valve structure and subaortic region in the adult with a bicuspid aortic valve.

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Infectious endocarditis is a significant problem for patients with congenital aortic stenosis (see Chapter 21) . Unfortunately, it may be the presenting symptom for a patient with a previously undiagnosed bicuspid aortic valve. Natural history studies of young adults with congenital aortic stenosis found a 35-fold higher incidence of endocarditis in that group than in the general population.[8] [9] A slightly higher incidence was seen in those patients with aortic regurgitation. Progression of valvular infection to the surrounding aortic root may occur if there is a delay in diagnosis and treatment or in the presence of a particularly invasive microorganism. Echocardiographic Evaluation

The distinctive echocardiographic features of the congenitally bicuspid aortic valve include systolic doming in the parasternal long-axis views and the demonstration of a single commissural line with two functional valve cusps 870

in the parasternal short-axis views. Particular care must be taken to assess the valve in systole as well as in diastole. In patients with asymmetric leaflets and a prominent raphe, the valve may appear tricuspid in diastole; however, the elliptical "football" shape of the systolic orifice indicates that the raphe is not a functional commissure. The valve leaflets often are thickened and fibrotic, more so with increasing age. When extensive calcification occurs, doming may no longer be noted and the morphology of the cusps in the short-axis views may be difficult to distinguish from calcific stenosis of a tricuspid aortic valve. Valvular stenosis should be evaluated with pulsed and continuous wave Doppler imaging exactly as one would a stenotic tricuspid aortic valve. Because of the eccentric nature of the stenotic jet in congenital aortic stenosis, Doppler sampling from the right parasternal window may detect the highest systolic velocities and should always be attempted in addition to the usual apical and suprasternal notch sampling. Serial aortic valve areas should be routinely calculated by the continuity equation in addition to peak and mean gradients. The development of left ventricular dysfunction may mask progression of stenosis if valve gradients alone are used to assess the severity of stenosis.[10] Valvular regurgitation is frequently present and may be the predominant functional abnormality in the adolescent and young adult. Careful

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echocardiographic inspection of the valve leaflets may give an indication of whether Figure 40-2 Transesophageal echocardiographic images from a patient with a bicuspid valve and severe aortic insufficiency. A, An aortic valve in cross section demonstrates the typical elliptic orifice of a bicuspid valve in systole. B, A long-axis view of the left ventricular outflow tract (Lvot) shows that prolapse and malcoaptation of the right coronary leaflet is the cause of the patient's significant aortic insufficiency, shown in C (color plate). Ao, aorta.

regurgitation is caused by fibrosis and retraction of the commissural margins of the leaflets, cusp prolapse, aneurysmal enlargement of the root and valve annulus or valvular destruction secondary to endocarditis. Color flow Doppler imaging readily detects the regurgitant flow and can be used to semiquantitate the degree of aortic insufficiency. Serial assessment of the effect of regurgitation on ventricular size and function should be performed just as described for a regurgitant trileaflet aortic valve ( see Chapter 17 and Chapter 18 ). The subvalvular left ventricular outflow tract and the mitral valve should be carefully investigated for congenital anomalies. Associated coarctation must be excluded, and the size and shape of the ascending aorta should be serially followed. Transesophageal echocardiography may be useful if valve morphology is difficult to determine transthoracically and if such information would guide a surgical attempt at valve repair (Fig. 40-2) . Additionally, more accurate aortic and pulmonary annular dimensions can be measured if a pulmonary autograft (Ross procedure) is planned or to guide the choice of a mechanical valve. Evaluation of endocarditis and aortic root abscess are also indications for a transesophageal study. Quantitative functional assessment of the valve usually is more accurate from the transthoracic approach, although transgastric views may allow adequate Doppler alignment for valve gradients. Management

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Confirmation of the presence of a bicuspid aortic valve and echo-Doppler determination of the severity of stenosis and regurgitation assist in clinical

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management decisions. Even the patient with a functionally normal bicuspid aortic valve should receive endocarditis prophylaxis for dental work, invasive procedures, and vaginal delivery. Periodic cardiologic follow-up is also important given the progression of valve dysfunction with age. Patients with mild to moderate degrees of stenosis or insufficiency require more regular surveillance. Development of chest pain, syncope, congestive heart failure, left ventricular hypertrophy with strain, significant arrhythmia or having a mean Doppler gradient of greater than 50 mm Hg are indications for further investigation and consideration of balloon valvuloplasty or surgical valvotomy or valve replacement. In the young adult with supple valve leaflets, balloon valvuloplasty has shown success in relieving significant aortic stenosis.[11] Aortic insufficiency, however, generally increases by at least one grade after percutaneous balloon dilation, limiting the usefulness of this procedure in a patient with combined stenosis and more than mild insufficiency.[12] With newer expertise in surgical aortic valve repair, current indications for surgical intervention in the adolescent and young adult with a bicuspid aortic valve may undergo closer scrutiny. Concerns about valve replacement and anticoagulation in young adults may be unnecessary if initial enthusiasm for aortic valve repair or the Ross procedure is maintained.[13] [14] The Ross procedure involves translocation of the patient's native pulmonary valve into the aortic position and replacement of the pulmonary valve with an aortic homograft. The premature calcification and degeneration that have plagued the homograft and heterologous bioprosthetic aortic valves are not a problem when the patient's own pulmonary valve is used in the aortic position. Some enlargement of the neoaortic annulus and sinuses is observed in the immediate postoperative period, which does not appear to progress with longer follow-up.[14] The long-term outcome of the aortic homograft in the place of the translocated pulmonary valve is uncertain, but intermediate follow-up has shown reasonable durability, with a 9% failure rate and a 12% incidence of dysfunction in a large series of patients. The rate of freedom from dysfunction for older children and adults was 87% at 8 years. Use of a pulmonary autograft was associated with lower rates of failure and dysfunction.[15] Pulmonary Stenosis Congenital valvular pulmonary stenosis is a common anomaly that has a

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slightly higher prevalence in women. This anomaly generally follows a benign course with increasing age. Children and adolescents with mild pulmonary stenosis (peak gradient < 25 mm Hg) have less than a 5% chance of requiring valvotomy during childhood and essentially no need for intervention in adulthood. Those with more moderate degrees of stenosis (peak gradient of 25 to 50 mm Hg) have only a 20% likelihood of requiring intervention.[16] Pulmonary valve morphology in the adult usually involves a supple but thickened valve with commissural fusion or a bicuspid valve. Calcification is rarely seen even in older patients. Poststenotic dilation of the main and left pulmonary arteries is common. Pulmonary insufficiency is frequently present, but it is usually mild.[17] Valvular stenosis is usually an isolated finding; however, acquired infundibular stenosis, supravalvular stenosis, branch pulmonary stenoses, and atrial septal defect are occasionally associated. Abnormalities of the pulmonary valve and pulmonary artery are part of several genetic syndromes such as Noonan's syndrome, Williams' syndrome, trisomies 13 through 15 and 18, and congenital rubella. Because of the benign nature of this lesion, patients with pulmonary stenosis are likely to escape detection during childhood and first come to medical attention during their adult years. Echocardiographic Evaluation

Recording diagnostic two-dimensional images of the pulmonary valve in adults can be difficult because of the frequent interference of overlying lung tissue. Positioning the patient in a high left lateral decubitus position and imaging during held expiration, however, may improve the ability to visualize the valve leaflets and the pulmonary artery. Apical or subcostal views of the right ventricular outflow tract also are useful in assessing the adult with pulmonary stenosis. Leaflet thickening may actually enhance echocardiographic visualization of the valve, and the presence of poststenotic dilation of the mid or distal portion of the main pulmonary artery often is a clue to previously unsuspected valvular pathology. Classic valvular stenosis causes systolic doming of the leaflets (Fig. 40-3) (Figure Not Available) . Pulsed wave Doppler demonstrates an increase in systolic velocity that begins at the valvular level, and continuous wave Doppler allows estimation of the peak and mean transvalvular gradient. Color flow mapping distinctly delineates the turbulent jet of high-velocity flow into the main pulmonary artery. Because of the horizontal substernal course of the right ventricular outflow tract, accurate peak Doppler flow velocities sometimes are difficult to obtain from the parasternal approach. Sampling

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of the highest peak systolic velocity may be more accurate from the apical or subxiphoid approach. In older patients, long-standing valvular obstruction leads to significant right ventricular hypertrophy including the infundibular portion of the ventricle. Dynamic infundibular obstruction thus adds to the right ventricle–pulmonary artery gradient over time. Doppler flow patterns from sampling within the infundibulum typically demonstrate the dagger-shaped, late-peaking systolic signal characteristic of dynamic obstructions. Management

In general, the adult with mild valvular pulmonary stenosis (peak systolic gradient < 35 mm Hg) requires 872

Figure 40-3 (Figure Not Available) Parasternal long-axis echocardiographic view of the right ventricular outflow tract in a patient with valvular pulmonary stenosis. The valve leaflets are thickened and dome into the pulmonary artery in systole. There is poststenotic dilation of the main pulmonary artery. PA, pulmonary artery. (Modified from Liberthson RR: Congenital heart disease in the child, adolescent, and adult. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1125, with permission. Copyright 1989, Little, Brown and Company.)

no specific intervention. Although bacterial endocarditis is uncommon in isolated valvular pulmonary stenosis, antibiotic prophylaxis is still recommended as appropriate for low- or intermediate-risk cardiac lesions. [18] Decisions regarding intervention in patients with peak gradients between 35 and 50 mm Hg should be individualized, but balloon or surgical valvotomy is not generally indicated for the asymptomatic individual without significant right ventricular hypertrophy. In individuals with peak gradients greater than 50 mm Hg, percutaneous balloon valvotomy or surgical valvotomy should be considered. Balloon valvotomy is rapidly becoming the treatment of choice for this group of patients. Echocardiographic evaluation is quite helpful, both for determining which patient is most likely to respond favorably and to follow the results of the dilation. A small pulmonary annulus and markedly thickened, cartilaginous leaflets predict a poor response to dilation. In addition, the patient who has acquired significant infundibular hypertrophy may demonstrate a high postprocedural gradient. Regression of hypertrophy, however, occurs in a large percentage of patients after removal of the valvular component of obstruction and thus does not constitute a contraindication to balloon

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valvuloplasty.[19] In such cases with apparent residual obstruction, reassessment of Doppler gradients is recommended over the following 6 months before proceeding to a second valvuloplasty or surgical valvotomy. Mitral Valve Anomalies Patients with congenital anomalies of the mitral valve usually present with the clinical findings of mitral insufficiency. Thus, when patients are referred for echocardiographic evaluation of the severity of mitral regurgitation and suitability for mitral valve repair, one of several congenital problems in mitral valve structure may be found. A cleft in the anterior leaflet occurs either as an isolated abnormality or as part of a complex involving defects in the atrioventricular septum. A double-orifice mitral valve results from abnormal fusion of the embryonic endocardial cushions. Patients with this anomaly may have two equal orifices or one large mitral orifice and a smaller vestigial one. Functionally, the doubleorifice mitral valve can be stenotic or regurgitant. A parachute mitral valve has abnormal attachments of the valve leaflets to the papillary muscles. Classically, one large centrally placed papillary muscle is present with all chordae from both leaflets converging on this muscle; however, a variation of this pattern occurs in which two papillary muscles are present but with all or most of the chordal attachments devoted to one papillary muscle. Although this arrangement often creates significant inflow obstruction in infancy and childhood, the coexistence of redundant leaflet tissue and chordae and strategically placed commissures and clefts may produce a valve that functions with minimal obstruction. A variety of other minor aberrant arrangements of the papillary muscles may be noted echocardiographically in adults that may contribute to inadequate coaptation of the mitral leaflets during systole. For example, it is common to find an additional posterior papillary muscle with chordal attachments creating a bifid appearance of the posterior leaflet. A papillary muscle on the high lateral or anterolateral wall (the papillary muscle of Moulaert) may have chordal attachments from the anterior leaflet, resulting in a triangular mitral valve orifice. [20] Echocardiographic Evaluation

Echocardiographic assessment of congenital mitral anomalies uses all the usual windows for evaluating the mitral valve. The parasternal short-axis view defines the number of leaflets, a single or double orifice, the presence of a cleft, and the number and location of the papillary muscles (Fig. 40-4) . Long-axis or off-axis views may be needed to follow the chordal

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attachments to their respective papillary muscles. Pulsed, continuous wave, and color Doppler all are important to assess the functional significance of these structural anomalies. Doppler quantification of the severity of mitral stenosis and regurgitation is discussed in Chapter 20 . Abnormal flow patterns created by any of the congenital mitral valve lesions predispose to the development of infectious endocarditis. Mitral anomalies are sometimes first detected when the adolescent or young adult is referred for an echocardiographic search for valvular vegetations. Management

Management of congenital mitral stenosis or regurgitation in the adolescent and adult follows the same clinical guidelines as that in acquired mitral abnormality. With the 873

Figure 40-4 Parasternal short-axis echocardiographic views of the left ventricle at the mitral valve level. Left, Parachute mitral valve with anterior and posterior leaflets inserting on the posteromedial papillary muscle. A small anterolateral papillary muscle is present (arrowhead) but does not receive any valvular attachments. Center, Double-orifice mitral valve. There is a discrepancy in orifice size, with the medial orifice (double arrows) being larger than the lateral (single arrow) orifice. Right, Cleft anterior leaflet from a patient with a partial atrioventricular canal defect. The two portions of the anterior leaflet (arrowheads) are attached to the interventricular septum.

increasing success of mitral valve repair, delaying surgical treatment in order to avoid a prosthetic valve has become less necessary. Preoperative or intraoperative transesophageal echocardiography determination of exact leaflet anatomy and the mechanism of valve dysfunction has been a key factor in predicting successful plastic repair. [21] Transesophageal echocardiography features of interest include the presence and degree of calcification or fibrosis, adequacy and mobility of individual leaflets, site and direction of the regurgitant jet, and presence of leaflet clefts and papillary muscle anomalies. Tricuspid Valve Anomalies Ebstein's malformation of the tricuspid valve is a relatively rare congenital cardiac malformation with a wide variability in natural history. The anomaly described by Ebstein consists of apical displacement of the septal

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and posterior tricuspid leaflets associated with an enlarged anterior leaflet that is variably bound to the right ventricular free wall. The septal or posterior leaflet may be rudimentary or dysplastic. Downward displacement of the functional valve orifice creates an enlarged right atrium and an atrialized portion of the right ventricle. The true right ventricle is frequently hypoplastic and functionally impaired. The infundibular portion of the right ventricle and the pulmonary artery may be mildly underdeveloped. An atrial septal defect or patent foramen ovale is present in the majority of patients.[22] The clinical presentation of this anomaly ranges from severe cyanosis in the newborn to mild tricuspid insufficiency or arrhythmia in the adult. The latter finding may be secondary to marked right atrial enlargement or to tachyarrhythmias in conjunction with Wolff-ParkinsonWhite syndrome, which is found in 10% to 15% of patients with Ebstein's anomaly.[23] The "Ebsteinoid" valve can be functionally obstructive and is variably regurgitant. Diagnosis in the adolescent or adult is commonly made during echocardiographic evaluation of clicks and murmurs heard on auscultation or as a part of clinical investigations for the cause of tachyarrhythmias. Occasionally, a patient with unexplained cyanosis or paradoxical embolization is found to have Ebstein's anomaly. Echocardiographic Evaluation

Echocardiography is ideally suited for the anatomic delineation of the tricuspid valve leaflets. The parasternal inflow view of the right heart, when properly aligned, demonstrates the apical displacement of the posterior leaflet and the elongated sail-like anterior leaflet arising normally from the tricuspid annulus. The apical four-chamber plane is optimal for defining the origin of the septal leaflet, the degree of adherence of the anterior leaflet to the free wall, and the size of the true right ventricle (Fig. 40-5) . Attention should be directed to the relative sizes and contractility of the atrialized and the true right ventricle. Color flow Doppler detects tricuspid insufficiency, which may be severe or can be present as multiple eccentric regurgitant jets through commissures in the funnel-like valve orifice. Inflow obstruction is rarely manifested as an elevated transvalvular gradient; instead, the displaced valve leaflets provide a resistance to forward flow that elevates systemic venous pressure and drives flow right to left across the atrial communication. Careful two-dimensional imaging of the interatrial septum and color Doppler interrogation should demonstrate an atrial septal communication in most patients. Agitated saline contrast injection may be necessary if imaging is suboptimal or the shunt is not apparent by color Doppler. Transesophageal echocardiography provides additional

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information about leaflet origins and chordal attachments, as well as better direct imaging of the interatrial septum in adults with difficult transthoracic studies. In some individuals with Ebstein's malformation, late development of clinical heart failure occurs as a result of left ventricular dysfunction.[24] When the left ventricular cavity is significantly distorted by the enlarged right heart chambers, calculation of left ventricular volumes and ejection fraction by the simpler echocardiographic methods is difficult. Qualitative estimation of left ventricular function or a Simpson's rule formulation, however, can provide useful clinical information regarding left ventricular performance. Management

Patients with Ebstein's malformation frequently remain asymptomatic, leading full and active lives despite marked 874

Figure 40-5 Apical four-chamber echocardiographic view in a patient with Ebstein's malformation of the tricuspid valve. The view has been modified to best demonstrate the tricuspid leaflets in diastole. There is marked enlargement of the right atrium (RA) and atrialized right ventricle (at RV), with the true right ventricle composed only of the area between the valve leaflets and the apex. The tricuspid annulus is shown (x), and the origin of the septal leaflet is displaced apically (arrowheads). The anterior leaflet is elongated but not tightly bound to the right ventricular free wall.

structural abnormality of the tricuspid valve apparatus and right atrial enlargement. Although some centers have suggested that tricuspid valve repair should be recommended in the asymptomatic patient if the cardiothoracic ratio is greater than 65%,[23] most centers would restrict intervention to those with progressive cyanosis, severe tricuspid insufficiency, left or right ventricular failure, paradoxical embolization, or intractable arrhythmias. Surgical repair of the abnormal tricuspid valve is preferred to valve replacement if the anatomy is favorable. Good results have been reported [25] [26] when there is sufficient size and mobility of the anterior leaflet to permit it to serve as a monocusp valve after plication of the right atrium and atrialized right ventricle. Echocardiographic assessment of the size and mobility of the leaflets, the degree of displacement, and the function of the right ventricle is critical for the

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selection of patients most suitable for valve repair. A numeric scoring system has been proposed for preoperative echocardiographic assessment of suitability for valve repair (Fig. 40-6) (Figure Not Available) . Patients with an echocardiographic index less than 5 are good candidates for a monocusp valve repair.[27]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Left Ventricular Outflow Tract and Aorta Subaortic Stenosis Subaortic obstruction in the adult occurs in several forms. A discrete form, the subaortic membrane, seems to be a developmental anomaly that is rarely seen in neonates but does appear in older children and young adults. It has been postulated that turbulent flow in the left ventricular outflow tract stimulates the growth of "rest" tissue in the region of the membranous septum, creating the discrete outflow obstruction.[28] [29] [30] Discrete subaortic stenosis is usually formed by a thin fibrous membrane attached circumferentially or along a portion of the circumference of the left ventricular outflow tract. It may lie immediately adjacent to the base of the aortic leaflets or be attached more distally near the junction of the muscular and membranous portion of the interventricular septum. Occasionally the entire circumferential structure is composed of muscle, creating a muscular subaortic collar. In older patients, what began as a discrete membrane may be complicated by the development of muscular subaortic hypertrophy. The muscular hypertrophy obscures the thinner membrane, thus masking the true pathophysiology of the obstructive process. Long-segment tubular narrowing of the left ventricular outflow tract is seen more commonly in children, usually requiring surgical attention before the adult years. As previously mentioned, discrete subaortic stenosis may occur in association with other obstructive lesions affecting the left heart— supramitral ring, bicuspid aortic valve, and coarctation. In addition, aortic valve endocarditis occurs frequently because of the abnormal flow patterns created by the subaortic narrowing. Subaortic membranes also are found as part of a complex that includes a perimembranous ventricular septal defect and an obstructive muscle bundle in the right ventricle.[31] With increasing Figure 40-6 (Figure Not Available) Score of echocardiographic features in Ebstein's anomaly. Assigning the score shown for each of the features listed provides a means of estimating whether tricuspid valve repair or valve replacement is required. Scores

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of 5 or higher are highly predictive of the need for valve excision and replacement. RA, right atrium; RV, right ventricle. (Adapted from Shiina A, Seward JB, Tajik AJ, et al: Circulation 1983;68:542.)

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age, the ventricular septal defect may close spontaneously, leaving the patient with a discrete obstruction of the left ventricular outflow tract and a muscular collar in the right ventricle. Late development of discrete subaortic stenosis has been described in patients with complete or partial atrioventricular canal defects, especially after surgical repair.[32] Echocardiographic Evaluation

Echocardiographic detection of a subaortic membrane is typically made in the parasternal long-axis views of the left ventricular outflow tract where a linear structure protrudes from the left surface of the interventricular septum and the base of the anterior mitral leaflet is tented up by the tension of the circumferential membrane (Fig. 40-7) . In some cases, the membrane is difficult to visualize unless the ultrasound beam is directly incident to the plane of the obstructing membranes. Low parasternal or apical long-axis views are thus more likely to detect the fine linear structure. When the membrane originates immediately beneath the aortic valve, its detection requires appreciation of subtle abnormality in the excursion of the aortic cusps and observation of a persistent echo in systole when the aortic cusp opens into the sinus of Valsalva. Unexplained turbulence and increased flow velocities by Doppler across an apparently normal aortic valve also are a clue to the presence of a high discrete subaortic membrane. Systolic flow acceleration by pulsed or color Doppler occurs proximal to the aortic valve. Aortic insufficiency is commonly found in these patients as a result of long-standing subaortic flow disturbance or from infectious endocarditis. Initial and serial assessment of outflow tract pressure gradients by Doppler is important, because Figure 40-7 Parasternal long-axis echocardiographic view of the left ventricle (LV) from a patient with discrete subaortic stenosis, ventricular septal defect, and aortic valve prolapse. The discrete subaortic membrane is shown as a linear density protruding from the upper left septal surface (arrow). The anterior aortic sinus is distorted and has prolapsed into the perimembranous ventricular septal defect immediately below it (arrowhead). Ao, aorta; LA, left atrium.

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progression of both the severity of obstruction and the degree of aortic insufficiency is well described in younger patients.[33] As with other lesions, transesophageal echocardiography may be helpful in the patient with limited transthoracic access to delineate the exact nature of left ventricular obstruction. This approach is particularly useful in cases with mixed or multiple-level obstruction. Both midesophageal views of the subaortic area and transgastric images of the left ventricular outflow tract are useful for obtaining diagnostic information. Management

Surgical excision of the circumferential membrane is recommended for patients with symptoms, left ventricular hypertrophy with strain, or a significant outflow gradient. Controversy still exists regarding surgical intervention in the asymptomatic patient with lower gradients. Some have argued that resection of the membrane preserves the aortic valve from further trauma and reduces or prevents progressive aortic insufficiency.[34] [35] Others have found that subaortic stenosis follows a less predictable course, with stenosis and regurgitation remaining trivial over many years.[36] The frequent need for reoperation and the development of aortic insufficiency despite surgical excision[37] indicate caution in recommending surgical intervention in the asymptomatic patient with only a mild hemodynamic abnormality. Close clinical and echocardiographic follow-up is warranted, and endocarditis prophylaxis is essential. When surgical excision is indicated, intraoperative transesophageal echocardiography can be helpful to monitor the success of membrane removal and detect complications such as mitral valve perforation or iatrogenic creation of a ventricular septal defect. Percutaneous balloon dilation has been attempted in patients with discrete fibrous membranes.[38] [39] Selection criteria for optimal success include a thin discrete membrane less than 3 mm in width, a sufficient distance between the membrane and aortic valve to permit a subaortic chamber, and the absence of more than grade 2 aortic insufficiency. Intermediate followup has shown a substantial reduction in gradient that persists over 5 years in 48% of patients, with no significant change in the degree of aortic insufficiency.[40] In one series, patients older than 13 years of age had the lowest rate of recurrent stenosis after balloon dilation; however, potential damage to the mitral and aortic valves and incomplete relief of obstruction dictates a cautious approach in applying this technique. Certainly in adults with acquired secondary muscular outflow obstruction, percutaneous dilation is unlikely to produce the desired results.

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Supravalvular Aortic Stenosis Supravalvular aortic stenosis is an uncommon lesion that may not become clinically apparent until older childhood or adolescence. Obstruction occurs as either a discrete membrane at the sinotubular junction, an "hourglass" deformity, or a diffuse hypoplasia of the entire ascending aorta (Fig. 40-8) (Figure Not Available) . The hourglass deformity is 876

Figure 40-8 (Figure Not Available) The three major types of supravalvular aortic stenosis. Left, Discrete infolding of the aorta at the sinotubular junction produces an hour-glass deformity. Center, Membranous weblike obstruction. Right, Diffuse tubular hypoplasia of the ascending aortic root. (From Maizza AF, Ho SY, Anderson RH: J Heart Valve Dis 1993;2:74.)

encountered most frequently, constituting 66% of cases of supravalvular obstruction, whereas diffuse hypoplasia (20%) and discrete membranous stenosis (10%) are less common.[41] Obstruction at the supravalvular level occurs as an isolated abnormality or part of an inherited syndrome. Williams' syndrome is one such inherited abnormality associated with mild mental retardation, failure to thrive, characteristic "elfin" facies, and multiple peripheral pulmonary stenoses. A familial autosomal dominant form of supravalvular aortic stenosis also occurs unassociated with mental retardation.[42] Some supravalvular stenoses are incidental findings associated with a systolic murmur and no gradient, whereas others are progressively obstructive lesions. The aortic valve leaflets are often normal; however, in some patients the cusps are distorted by the supravalvar constriction or incorporated into the stenosing ring. When progressive obstruction and failure of normal aortic growth occurs, left ventricular hypertrophy and the typical symptoms of aortic stenosis appear. Echocardiographic Evaluation

Echocardiographic detection of supravalvular stenosis relies on careful inspection of the sinotubular junction and proximal ascending aorta, which is possible with cranial angulation in right or left parasternal windows, or from suprasternal notch views. The diameter of the normal aorta at the sinotubular junction equals or slightly exceeds that of the aortic annulus. The tubular portion of the ascending aorta should never be smaller than the aortic annulus.[43] Echo-Doppler study should determine the type of supravalvular lesion and

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the severity of stenosis. Because routine echocardiographic study in adults often does not include the ascending aorta above the sinuses of Valsalva, missing the correct diagnosis on initial study is very possible. The impetus to look specifically for this lesion may be a high-velocity turbulent flow detected by continuous wave Doppler across an otherwise normal aortic valve. Accurate assessment of the supravalvular gradient by Doppler is best determined from the right parasternal or suprasternal window rather than from the cardiac apex. Doppler estimates of the severity of stenosis may overestimate the true degree of obstruction because of the phenomenon of pressure recovery seen in tubular or long-segment stenoses. Gradients for discrete membranous forms are more likely to be accurate.[44] Imaging of the proximal branch pulmonary arteries should be attempted in patients with Williams' syndrome, although associated branch stenoses of the pulmonary arteries may be too distal for echocardiographic detection. Management

The decision for surgical intervention for supravalvular aortic stenosis is made according to the same indications as for valvular obstruction— significant outflow gradient with left ventricular hypertrophy or symptoms. The morphology of the supravalvular narrowing dictates the type of repair required, varying from patch aortoplasty to partial root replacement. A good relief of obstruction for this lesion should be possible with low mortality and without a need for reoperation.[45] [46] Abnormalities of the aortic valve leaflets may persist after repair of the root and need clinical and echocardiographic surveillance. Associated branch pulmonary stenoses may require balloon dilation or surgical arterioplasty. Sinus of Valsalva Aneurysms Congenital aneurysms of the aortic sinuses of Valsalva are thought to result from a weakness in the aortic media at its junction with the annulus fibrosus. A small diverticulum or finger-like protrusion extends most commonly from the right or noncoronary sinus. Because the aortic sinuses are almost entirely intracardiac, the aneurysms extend into regions of the heart that lie adjacent to the affected aortic sinus. For aneurysms of the right coronary sinus, the right ventricle and right atrium are common termination sites. Aneurysms of the noncoronary sinus usually enter the right atrium.[47] Over time, the aneurysm may enlarge to become a "windsock," potentially causing obstructive problems in the right ventricular outflow tract or tricuspid valve. Rarely, sinus of Valsalva

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aneurysms burrow into the interventricular septum, causing atrioventricular conduction defects. [48] Protrusion into the left ventricular outflow tract may create outflow tract obstruction.[49] Congenital sinus of Valsalva aneurysms come to clinical attention most typically in adolescence and young adulthood when the protruding structure ruptures into the receiving chamber. Acute rupture of a large aneurysm causes retrosternal or epigastric pain and severe dyspnea from congestive heart failure. By contrast, perforation of a small aneurysm may go unnoticed until a continuous murmur is heard by auscultation or chronic congestive heart failure from the long-standing volume overload brings the patient to medical attention. Coronary artery compression by a sinus of Valsalva aneurysm is an interesting though unusual mode of presentation. [50]

Echocardiographic Evaluation

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Sinus of Valsalva aneurysms may be an incidental finding on echocardiographic study, but they are discovered more often during echoDoppler evaluation of a continuous murmur with the suspected diagnosis of patent ductus arteriosus or coronary artery fistula.[51] [52] Parasternal longand short-axis views of the aortic sinuses demonstrate the finger-like windsock extending from the base of the sinus toward the site of termination (Fig. 40-9) . The originating sinus may be somewhat enlarged, but the native morphology of the root and valve is usually not significantly distorted. It is important to determine that the aneurysm originates from the aortic sinus above the plane of the aortic valve in order to distinguish this lesion from the more common aneurysm of the membranous interventricular septum. Delineation of a normal coronary artery origin and lumen size distinguishes the sinus of Valsalva aneurysm from a coronary artery fistula. Acquired aortic fistulas after endocarditis can be differentiated because they lack the extended aneurysmal channel seen with a sinus of Valsalva aneurysm. Color flow Doppler demonstrates continuous turbulent flow within the aneurysm and into the receiving chamber. In patients with a significant left-to-right shunt, left atrial and left ventricular enlargement reflect the size of the volume overload, and right-sided chamber enlargement occurs when the aneurysm communicates with the right atrium. Mild aortic insufficiency is expected from distortion of the aortic cusp and root enlargement is expected from long-standing volume

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overload. Severe aortic insufficiency should raise the suspicion of aneurysm rupture into the left ventricular Figure 40-9 (color plate.) Parasternal short-axis echocardiographic images of the aorta (Ao) at the base of the heart. A, Aneurysm of the right coronary sinus of Valsalva shown as a narrow "windsock" protruding into the right atrium (RA) (arrows). B, Color flow Doppler image demonstrates turbulent flow filling the narrow channel and creating a shunt from the aorta into the right atrium.

outflow tract or secondary endocarditis affecting the aortic valve leaflets. Management

Small unruptured aneurysms found incidentally can be followed expectantly. Larger aneurysms or those that are adversely affecting surrounding structures should be electively excised. Ruptured sinus of Valsalva aneurysms require surgical closure to prevent late congestive symptoms caused by volume overload and to decrease the susceptibility to infectious endocarditis. Coarctation of the Aorta Coarctation of the aorta in the adolescent and adult is most often discovered during investigation of hypertension found in the course of routine physical examination. Weak or absent femoral pulses, left ventricular hypertrophy on the electrocardiogram, or a systolic murmur in the back or through collaterals in conjunction with the hypertension results in a referral to the echocardiographic laboratory or cardiologist's office for definitive diagnosis. The anatomic lesion found most commonly in adults is a discrete ridge or diaphragm narrowing the aortic lumen just below the left subclavian artery and opposite the ductus arteriosus or ligamentum arteriosum. Poststenotic enlargement of the descending thoracic aorta is usually present. Rarely, the coarctation lies more distally in the thoracic or abdominal aorta. Functionally, patients seen 878

as adults are usually asymptomatic, because the degree of obstruction created by the coarctation is mild or moderate, or collateral vessels bypass a

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more severe stenosis. About 50% of patients with adult coarctation have a bicuspid aortic valve. [53] Other structural defects of the left heart such as discrete subaortic membranes or mitral valve anomalies occasionally are present, and a small ventricular septal defect or residual patency of the ductus arteriosus may coexist. Cerebrovascular accidents from ruptured berry aneurysms, aortic dissection, and endocarditis or endarteritis also complicate the natural history of adult coarctation of the aorta. Echocardiographic Evaluation

Echocardiographic diagnosis of coarctation relies on two-dimensional visualization of the anatomy of the aortic arch and Doppler detection of flow disturbance in the descending aorta (Fig. 40-10) . Although the aorta can be imaged in part from a variety of parasternal views, suprasternal notch or right parasternal windows provide the best access to the region of interest. Because the site of coarctation can be difficult to visualize, patient positioning maneuvers that optimize the suprasternal view are important. In the long-axis view of the aortic arch, the brachiocephalic vessels should be identified and traced distally if possible. Just beyond the left subclavian artery, a shelf of infolded tissue narrows the aortic lumen. The thoracic aorta distal to the coarctation is often dilated from the systolic jet through the stenotic area. Color flow Doppler detects a narrowed flow stream at Figure 40-10 A, Suprasternal long-axis echocardiographic view of the aortic arch depicts tubular narrowing of the transverse arch with discrete coarctation at the isthmus (arrow). B (color plate), Doppler color flow mapping shows aliasing and turbulence beginning at the site of discrete obstruction (arrow). C, Continuous wave Doppler signal was obtained in the descending thoracic aorta and illustrates a high peak velocity in systole (3 m per second) with a gradient that persists during early diastole (arrowheads). D, Pulsed wave Doppler signal obtained from the descending abdominal aorta. There is blunting of the systolic upstroke and turbulent continuous flow during diastole (arrowheads) indicative of significant obstruction to flow located more proximally in the aorta. Asc Ao, ascending aorta.

the point of coarctation and systolic flow acceleration, with continuation of flow into diastole in cases of significant obstruction. In fact, when twodimensional imaging is indistinct, the color flow turbulence may alert the sonographer to the site of obstruction. Continuous wave Doppler in patients

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with discrete obstruction shows a typical pattern of increased systolic flow velocity and a continued gradient in diastole. Doppler gradients (∆P) estimated from the peak systolic velocity (V2 ) of the continuous wave

Doppler signal usually overestimate the catheter-measured gradient. Better correlations have been shown when the velocity proximal to the coarctation (V1 ) is included in the Bernoulli equation [∆P = 4(V2 2 − V1 2 )] or when both the peak systolic velocity and pressure half-time of the diastolic gradient are considered.[54] [55] Long-segment narrowing of the aorta without discrete obstruction causes acceleration of flow, giving high peak velocities by continuous wave Doppler. Conversion of these velocities into systolic gradients mistakenly predicts significant coarctation. The lack of a diastolic gradient helps to distinguish flow acceleration from true obstruction. Doppler flow patterns in the descending abdominal aorta are extremely useful in detecting upstream obstruction.[56] Patients with tubular narrowing but without a discrete obstruction demonstrate a normal pattern of abdominal aortic flow—rapid systolic upstroke, relatively laminar flow signal, and no continuation of flow into diastole. With coarctation, the flow profile has a delay in the systolic upstroke, turbulence in systole, and variable degrees of diastolic antegrade flow (see Fig. 40-10) . Routinely including the Doppler profile of abdominal aortic flow in the clinical examination is an excellent method to 879

screen for unsuspected coarctation. Adults with coarctation may have considerable tortuosity of the transverse arch, making both visualization and alignment for accurate Doppler detection of gradient impossible. In such cases, a high degree of suspicion is generated by abnormal flow in the abdominal aorta, directing a more diligent search from off-axis views or with a stand-alone continuous wave Doppler probe. Although Doppler flow patterns are relatively easy to obtain in most adults with coarctation, direct imaging of the anatomy of the arch and descending aorta may be limited. Alternative imaging modalities often are necessary to further define the exact details of the obstruction and to guide decisions for management. Transesophageal echocardiography can detect the site and configuration of the obstruction. Long-axis views allow quantitation of lumenal narrowing; however, Doppler gradients are difficult to obtain because the affected region of the aorta generally lies perpendicular to the interrogating Doppler beam.[57] Magnetic resonance imaging is an accurate

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noninvasive imaging tool for displaying complete arch anatomy, and newer applications allow velocity mapping as well.[58] [59] Angiography may be required in the older adult to assess the degree of collateral development as well as coronary anatomy if surgical repair is planned. Management

Hypertension, a significant pressure gradient between the upper and lower extremities, and a reduction in luminal diameter of greater than 50% are indications for intervention in the adult with coarctation. Some centers recommend percutaneous balloon dilation for discrete lesions in adolescents and young adults, finding good relief of the gradient, improvement in hypertension, and a low rate of restenosis.[60] [61] [62] Small saccular aneurysms may occur at the dilation site either acutely or on later follow-up. Although some of these aneurysms have been surgically repaired, serial follow-up of others has shown no progression in size and no rupture or dissection. The long-term outcome of these iatrogenic aneurysms is uncertain, however. Intravascular echocardiography performed immediately after dilation can demonstrate the intimal tear that routinely occurs during balloon angioplasty.[63] , [64] Transthoracic echocardiographic evaluation after angioplasty is helpful in assessing residual gradient and restenosis, but it cannot detect reliably the presence of small aneurysms. Repeat magnetic resonance imaging or angiography is needed for follow-up evaluation of this complication. The use of balloon-expandable intravascular stents has been recently applied in the treatment of aortic coarctation.[65] Early and intermediate follow-up suggests excellent relief of stenosis without a significant incidence of stent migration, fracture, restenosis or thromboembolic complications.[66] With increasing age, diminished pliability of aortic tissue increases the possibility of a more extensive aortic tear or rupture after balloon angioplasty; therefore, patients older than 30 years may be managed more safely surgically. Surgical repair of coarctation in the adult can be accomplished with low operative mortality and good intermediate outcome. [67] Attention to the degree of collateral formation is important to ensure adequate perfusion during cross-clamping and to prevent spinal cord injury. Prosthetic bypass grafts or other alternatives to mobilization and end-to-end anastomosis may be required in adults with less elastic tissue. Residual hypertension is common after late repair of coarctation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Septal Defects and Shunt Lesions Atrial Septal Defects After the bicuspid aortic valve, atrial septal defects are the most common congenital lesion found in adolescents and adults, constituting nearly 22% of adult congenital heart defects.[68] The ostium secundum defect is the most frequent (75%) followed by the ostium primum type (20%) and the sinus venosus defect (5%).[68] A very rare form of atrial septal communication is the coronary sinus septal defect in which the roof of the coronary sinus is partially or completely absent, allowing left-to-right shunt from the left atrium into the coronary sinus and thence into the right atrium. A patent foramen ovale, the fetal communication between the overlapping layers of the primum and secundum portions of the atrial septum, persists in 10% to 18% of adults as determined by echocardiographic contrast injection and as many as 25% to 30% of patients in autopsy series.[69] [70] Because of failure of fusion of the two septal layers, the flap of septum primum covering the fossa ovalis may open transiently with changes in the transatrial pressure gradient, allowing the passage of flow in either direction. Additionally, this thin membranous layer may have multiple small perforations or develop into a septal aneurysm with or without an atrial shunt. Improved detection of atrial defects and more aggressive investigation in patients with cerebrovascular events has generated great interest regarding the association of patent foramen ovale, atrial septal aneurysm, and cryptogenic stroke.[71] [72] [73] A large multicenter trial is currently under way to examine prospectively the exact nature of the relationship between patent foramen ovale and stroke. It is clear, however, that the potential for a right-to-left embolus exists when there is any form of communication in the interatrial septum (see Chapter 37) . Patients with shunting at the atrial level are usually asymptomatic until middle to late adult years. If their cardiac anomaly has not been diagnosed

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during childhood by the physical findings of a widely split second heart sound and pulmonic flow murmur, detection may occur by routine chest xray findings of cardiomegaly and pulmonary plethora. Beginning in the fourth or fifth decades of life, symptoms of fatigue, dyspnea on exertion, and atrial arrhythmia develop. Right or left ventricular failure and paradoxical embolization also may be the mode of presentation in older patients with atrial septal defects. Endocarditis is quite rare, most often seen in patients with accompanying mitral valve anomalies.

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Figure 40-11 (Figure Not Available) (color plate.) Series of apical four-chamber echocardiographic views from a patient with a large ostium primum atrial septal defect. A, Large defect in the inferior portion of the atrial septum (arrow). B, Doppler color flow mapping readily detects the passage of flow through the defect (arrow and arrowhead). C, After IV injection of agitated saline, a positive contrast effect is observed as opacified blood from the right atrium (RA) crosses from right to left (arrows). D, Shunting of unopacified blood from the left atrium (LA) creates a negative contrast effect in the right atrium (arrows). LV, left ventricle; RV, right ventricle. (From Levine RA, et al: Echocardiography: Principles and clinical application. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1555. Copyright 1989, Little, Brown and Company.) Echocardiographic Evaluation

Patients with atrial septal defects require echocardiographic assessment of the anatomic abnormality of the atrial septum, the hemodynamic effect of shunt flow, and the presence of any associated defects. Imaging of the interatrial septum is best performed with subxiphoid views when these are available. The true apical four-chamber view is unreliable because falsepositive septal dropout often occurs in the midatrial septum. An off-axis four-chamber view obtained by sliding midway between the apical and subxiphoid views, however, yields a more perpendicular interface between the interrogating ultrasound beam and the interatrial septum. Parasternal short-axis and right parasternal views are supplemental windows for imaging the atrial septum. The septum primum covering the fossa ovalis is thinner than either the superior portions of the septum or the region near the crux of the heart. Mobility of the septum primum or aneurysmal deformity (>1-cm deviation from the plane of the basal septum) raises the suspicion of a patent foramen ovale. True atrial septal defects should have a distinct edge visible at the blood-tissue interface. All aspects of the atrial septum

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should be inspected, including the superior rim, with visualization of the superior vena caval entry. Right parasternal views are especially helpful for imaging this area. When the atrial defect can be imaged directly, measurement of its dimensions in orthogonal planes and its size relative to the entire atrial septal length should be made. Pulsed and color flow Doppler add additional diagnostic power to the transthoracic examination. In any of the views mentioned earlier, the passage of flow across an apparent atrial defect further confirms the presence of an interatrial communication (Fig. 40-11) (Figure Not Available) . When right heart pressures are normal, a clear stream of flow occurs in late systole with accentuation in diastole. Elevation of right heart pressures decreases the trans-septal pressure gradient, and shunt flow then may be difficult to distinguish from other low-velocity atrial flows. Contrast echocardiography plays an important diagnostic role in cases in which the imaging and Doppler findings are equivocal. With rapid IV injection of 5 mL of agitated saline (or saline mixed with a small amount of the patient's blood), highly reflective microbubbles appear in the right atrium and right ventricle. Contrast passes into the left atrium and left ventricle within three to five cardiac cycles in the presence of an interatrial communication (see Fig. 40-11) (Figure Not Available) . Even when leftto-right shunting is predominant, there is a period of transient right-to-left shunting during which contrast can pass into the left atrium. The right-toleft pressure gradient can be augmented by having the patient cough or perform a Valsalva maneuver. A negative contrast effect occurs with leftto-right shunts when unopacified blood enters the densely opacified right atrium. Negative contrast is a less reliable diagnostic feature, however, because flow from the inferior vena cava or coronary sinus may create the same appearance. Sensitivities of 92% to 100% have been reported for detection of atrial septal defects by transthoracic contrast echocardiography.[74] [75] It has been suggested 881

that injection from the leg improves the sensitivity of the contrast technique, because the eustachian valve tends to direct inferior vena caval flow across the fossa ovalis. [76] Transthoracic echocardiographic study also helps to define the hemodynamic effects of shunt flow. Right atrial and right ventricular

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enlargement and dilation of the main pulmonary artery are expected with shunts of 1.5:1 or greater. The pulmonary veins are prominent, but the left atrium is usually normal in size unless there is associated mitral regurgitation or left ventricular failure. The interventricular septum in the cross-sectional views of the left ventricle is flattened in diastole and moves paradoxically toward the right ventricle in systole. Specific quantification of shunt volume by echo-Doppler techniques has been attempted by several methods, all of which remain semiquantitative in clinical use. Pulsed Doppler determination of cardiac output has been validated with a high degree of accuracy in the experimental setting.[77] The ratio of pulsed Doppler cardiac output across the pulmonary and aortic valves gives an estimate of the pulmonary-to-systemic flow ratio (Qp /Qs ). This technique is not accurate if the flow across either valve is influenced by something other than the intracardiac shunt, such as valvular stenosis, subvalvular obstruction, or significant valvular regurgitation. Application of this method to the clinical arena has been less successful, partly because of the difficulty of obtaining accurate dimensions of the pulmonary annulus in adults. When color flow mapping became a part of the echocardiographic diagnostic armamentarium, there was initial enthusiasm for its quantitative potential. Planimetry of the area of the flow stream within the right atrium has been compared with shunt volumes but with poor correlations.[78] Better correlation has been shown when the diameter of the color flow stream at the atrial defect is compared with shunt ratios,[79] but this remains semiquantitative with considerable overlap between patients with small, moderate, and large shunts. This result might be expected because the color flow diameter simply reflects the anatomic dimension of the atrial defect, and although it bears a gross relationship to the size of the shunt, factors such as right ventricular compliance and pulmonary artery pressures cause variation in the volume of shunt for a given atrial septal defect size. The development of new intravenous contrast agents that pass through the pulmonary bed to the left-sided circulation has led to the possibility of an echocardiographic indicator dilution technique for quantifying shunts.[80] With videodensitometry, the concentration of sonicated albumin can be determined serially in the right ventricle during the initial appearance of contrast and then during the recirculation phase. An indicator dilution curve then can be constructed and the shunt ratio calculated in a manner similar to that used for radionuclide shunt calculation. This method requires that the

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sonicated albumin remain stable during the period of observation. Because the rate of disappearance of sonicated contrast has been shown to be pressure sensitive, shunt ratios in patients with higher pulmonary artery pressures might be underestimated.[81] Estimation of pulmonary artery pressure is an important part of the echocardiographic assessment of atrial shunts. The pulmonary artery pressure is easily and reliably determined by applying the simplified Bernoulli equation to the peak velocity of the tricuspid regurgitation jet to obtain the pressure gradient between right ventricle and right atrium.[82] Adding an assumed or actual right atrial pressure to the pressure gradient yields an estimated right ventricular systolic pressure (RVSP): RVSP = 4(TR jet velocity)2 + RA pressure where TR is tricuspid regurgitation and RA is right atrial. Right ventricular systolic pressure equals pulmonary artery pressure in the absence of pulmonary stenosis. If the patient does not have tricuspid insufficiency, other subjective signs of pulmonary hypertension may be present. For example, the interventricular septum is flattened in systole if right ventricular systolic pressure is greater than half the systemic pressure. Systolic notching on the pulmonic valve M-mode or the pulmonary artery Doppler flow profile also indicates significant elevation of pulmonary artery pressure. Applying the modified Bernoulli equation to the enddiastolic velocity of the pulmonary insufficiency jet provides quantitative information about pulmonary artery diastolic pressure as well. Associated abnormalities should be sought as part of the complete transthoracic examination. Mitral valve prolapse occurs with large right ventricular volume overload, usually from geometric distortion of the left ventricle but occasionally from a myxomatous mitral valve. A cleft in the anterior mitral leaflet is usually present with ostium primum atrial septal defects. Significant mitral regurgitation occurs with increasing age.[83] Valvular pulmonic stenosis is present in a small number of patients, and when it is significant it can promote right-to-left shunting across the atrial septal defect with resultant cyanosis. The drainage of all four pulmonary veins should be established if possible in any patient with an atrial septal defect. Anomalous return of the right upper and middle lobe veins is found in the majority of patients with superior sinus venosus atrial septal defects and in a small percentage of

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patients with ostium secundum atrial septal defects. The right veins drain to the superior vena cava either at the junction with the right atrium or more distally along the course of the superior vena cava. Echo-Doppler detection of this anomaly is difficult in adults, but it can be attempted with long- and short-axis right parasternal views of the superior vena cava and occasionally can be appreciated in subcostal views of the superior vena cava. A turbulent flow stream entering the superior vena cava laterally and posteriorly represents the pulmonary vein inflow. Anomalous drainage of the right lower vein to the inferior vena cava occurs with the "scimitar syndrome." Right parasternal views that focus on the inferior vena caval entry to the right atrium are most useful to search for the anomalous pulmonary venous inflow. Transesophageal echocardiography has proved to be superior to transthoracic study in adult patients for detecting patency of the foramen ovale, small secundum atrial septal defects, sinus venosus defects, and anomalous pulmonary venous return.[84] [85] [86] Although the presence of an interatrial shunt and an estimate of its hemodynamic 882

Figure 40-12 Transesophageal echocardiographic images of the interatrial septum in a patient with a secundum atrial septal defect undergoing transcatheter device closure with a Sideris device. A (color plate), The shunt across the defect is apparent by color flow Doppler. B, Measurement of defect size in the vertical plane image. C, Balloon sizing is performed by measuring the diameter of an inflated balloon (arrowheads) as it is pulled across the defect. D, The occluder of the Sideris device is demonstrated (arrowheads) being deployed along the left atrial surface. E, The counteroccluder (arrowheads) is positioned parallel to the right atrial septal surface. F, After removal of the guiding catheter and wire, the device (arrowheads) lies snugly against the interatrial septum. LA, left atrium; RA, right atrium.

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significance can be determined adequately by transthoracic echocardiography, defect sizing and specific anatomic detail are much more accurately obtained from the transesophageal window (Fig. 40-12) . The interatrial septum is easily imaged with the probe in the midesophageal position. In the transverse plane, the crux of the heart is well seen, and

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ostium primum or secundum atrial defects are most apparent. From the longitudinal plane, the superior vena caval entry to the right atrium is clearly defined and superior sinus venosus defects with anomalous pulmonary venous entry can be detected. The flaplike opening of the patent foramen ovale also can be appreciated in this view. Color flow mapping confirms the presence of shunting, and saline contrast injection may be useful if proof of right-to-left shunting is needed. Atrial septal defects vary in shape, making measurements of the defect in two orthogonal views important. The pulmonary veins can be identified from both the transverse and the longitudinal planes. Management

Patients with an isolated atrial septal defect with a significant left-to-right shunt should have elective closure of the defect because of the possibility of progressive pulmonary hypertension and the late development of right ventricular failure and atrial arrhythmias. Closure may be appropriate even for patients with smaller shunts because of the tendency for shunt size to increase with age, because of alterations in left ventricular compliance and the ever-present risk of paradoxical embolization. Surgical mortality for this lesion is quite low, and long-term follow-up shows improvement in symptoms, decrease or stabilization of pulmonary hypertension, and nearnormal long-term survival rates in patients repaired before the age of 25 years.[87] [88] [89] Patients with elevation of pulmonary arteriolar resistance greater than 15 U/m2 are not good surgical candidates and are better managed medically.[90] There is some divergence of opinion regarding closure of atrial defects in the older adult. One natural history study[91] found no difference in survival or symptoms and no difference in the incidence of new arrhythmias, stroke, emboli, cardiac failure, or progressive pulmonary hypertension between medically and surgically managed patients over the age of 25 years. A subsequent large series of adults over the age of 40 years, however, demonstrated a significant reduction in mortality and dramatic improvement in functional class after atrial septal defect closure compared with a similar group managed medically. The risk of atrial arrhythmias and attendant embolic complications was not altered by atrial septal defect closure.[92] Thus, with low surgical morbidity and mortality and with the availability of transcatheter closure devices, closure of atrial septal defects with a significant shunt without severe pulmonary hypertension is recommended regardless of age.

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At the present time, patients with an incidentally detected patent foramen ovale do not require intervention. The occurrence of an embolic stroke or peripheral embolus in the patient with a patent foramen ovale and no other obvious embolic source can be considered justification for surgical or device closure, particularly in the younger adult. Controlled studies are needed to determine if anticoagulation alone is an equally effective alternative to patent foramen ovale closure after an embolic event (see Chapter 37) . [93] For patients with contraindications to surgery or complex lesions requiring multiple surgical procedures, a non-surgical method of closing an atrial communication is particularly desirable. Several different transcatheter closure devices have been designed for this purpose, but most are currently still in the investigative stage in the United States.[93] [94] [95] The basic device is a flexible wire framework covered with fabric or foam that folds inside a catheter delivery system. One portion of the device is extruded on the left atrial side of the atrial septal defect, the sheath is withdrawn across the defect, and the other portion of the device is deployed along the right atrial side. Newer generation devices have a thicker central core that allows the device to be self-centering within the defect (Fig. 40-13) . This characteristic permits closure of larger atrial defects because less overlap is required to ensure that the device remains well-seated. For any of the current devices, the best results are achieved when the atrial defect is relatively centrally located in the interatrial septum because the extension of the device beyond the edges of the defect may impinge on the atrioventricular valves or extend into the superior vena cava, right upper pulmonary vein, or coronary sinus. Thus, most sinus venosus and ostium primum atrial septal defects would be excluded from consideration for device closure. Echocardiography plays an essential role in the selection of patients most suitable for device closure. Assessment of the defect size, the overall length of the interatrial septum, the amount of septal rim around the defect, and the degree of mobility or aneurysm of the septum primum are all important in evaluating a patient for device closure.[96] Although transthoracic echocardiography can provide some of this information, transesophageal echocardiography generally is more accurate in adults.[84] [85] [86] Because some traction is applied to the atrial septum in the process of placing the occluding device, the balloon-stretched diameter is the measurement that is most reliable in selecting a device that will not slip through the atrial septal defect. Thus, in clinical practice, transthoracic echocardiography is used to

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diagnose the shunt at the atrial level, categorize the location of the atrial defect and its approximate size, determine the shunt size, and detect any associated defects. If device closure is considered, transesophageal echocardiography before or during catheterization can further define the anatomy, and the balloon-stretched diameter can be measured. Transesophageal guidance in the catheterization laboratory has greatly facilitated the optimal placement of the closure device parallel to the plane of the interatrial septum and centered across the defect. Additionally, deployment in the atrial appendage or within the mitral valve orifice can be avoided under direct observation by transesophageal echocardiography. The fully deployed device can then be observed for a period of time before the procedure is completed to ensure that it remains in a good position. Color flow Doppler and contrast echocardiography determine residual 884

Figure 40-13 Current generation transcatheter closure devices for septal defects. A, The Das self-centering device. The edges of the left atrial disc are retracted to show the central collar, which promotes centering of this device within the septal defect. B, The Amplatzer septal occluder is a doubledisc device with a nitinol wire frame and a broad waist that centers the device. C, The Gore Helex device, which is extruded as a single helical disc with a narrow waist. D, The STARFlex version of the CardioSEAL septal occluder. Hinges midway along each leg promote retroflexion of the legs back toward the septum. Microsprings assist in centering the device in the defect. E, The Sideris button device modified with centering wires attached to the occluder (OCC), which is introduced with a pushing catheter (PUSH). (A, From Das GS, Voss G, Jarvis G, et al: Circulation 1993;88(part I):1756; B, From Sharafuddin MJ, Gu X, Titus JL, et al: Circulation 1997;95:2162. Reproduced with permission. Copyright American Heart Association. C, Courtesy of N. Wilson, MD; D, From Hausdorf G, Kaulitz R, Paul T, et al: Am J Cardiol 1999;84:1113. Reproduced with permission. Copyright Elsevier, Ltd.; E, From Sideris EB, Sideris SE, Fowlkes JP, et al: Circulation 1990;81:314.)

patency immediately after deployment (see Fig. 40-12) . Follow-up studies of device closure of atrial septal defects have shown a high rate of successful placement. Residual patency rates are moderate but trivial in degree, with a continued decrease in shunting over time. A small incidence of device embolization or unacceptable deployment is reported with all of the devices. Endothelialization of the device is thought to occur within 6 months when properly aligned flush with the native septum.[94] [95] [97] [98] [99]

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Ventricular Septal Defects Ventricular septal defects are the most common congenital anomaly recognized at birth, but they account for only about 10% of cases of congenital heart disease in the adult. This decrement in prevalence is due in part to a high rate of spontaneous closure during the first few years of life. In addition, moderate and large lesions generally cause symptoms of congestive heart failure, dyspnea, and failure to thrive in childhood, requiring medical and surgical intervention long before adulthood. The ventricular septal defects that persist in adult years are either small defects, larger defects that have diminished in size by one of several natural processes, or very large defects with irreversible pulmonary vascular disease. Spontaneous closure does occur in later years but is uncommon. The incidence of infectious endocarditis for patients with ventricular septal defects is low in the current antibiotic era; however, the risk is higher for adults than children, and it is higher for patients with associated aortic insufficiency.[8] The most common location for adult ventricular septal defects is the membranous ventricular septum. Shunt flow passes from the left ventricular outflow tract to the right ventricle just beneath the septal leaflet of the tricuspid valve. Membranous septal aneurysm formation may occur by fibrous tissue proliferation and incorporation of the septal tricuspid valve leaflet. The aneurysm limits shunt flow and occasionally closes the defect entirely. Aneurysms may become quite large and have been noted to cause turbulence and obstruction in the right ventricular outflow tract (Fig. 40-14) . Distortion of the septal leaflet from incorporation into the septal aneurysm may create a communication from the left ventricular outflow tract into the right atrium, a Gerbode defect. Over time, this defect leads to a right ventricular volume overload, right atrial enlargement, and atrial arrhythmias. In some membranous ventricular septal defects, the support of the right aortic cusp is undermined, leading to prolapse of this cusp into the defect (see Fig. 40-7) . Progressive aortic insufficiency often becomes a more important hemodynamic issue than the ventricular shunt. Subaortic membranes also may develop in association with membranous ventricular septal defects during adolescence or early adulthood.

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Figure 40-14 Apical four-chamber echocardiographic image from a

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patient with a perimembranous ventricular septal defect (closed arrowheads) and a large membranous septal aneurysm (open arrowheads). The aneurysm protrudes into the right ventricle (RV) and has incorporated tricuspid septal leaflet tissue. LV, left ventricle; RA, right atrium.

Muscular ventricular septal defects are the next most common. Because smaller defects of this type often close spontaneously, the ones that persist in adulthood are generally quite large, sometimes multiple, and associated with pulmonary vascular obstructive disease (Eisenmenger's syndrome). These patients may present with cyanosis from reversal of shunt flow. Pulmonary hypertension is avoided in a few individuals by the development of muscular hypertrophy of the right ventricular outflow tract, a sort of natural pulmonary banding referred to as the Gasul phenomenon. [100] Hypertrophy of the moderator band also can restrict shunt flow across sizable apical muscular defects, and when this occurs, the left ventricular and the right ventricular apex become one chamber, giving the cardiac apex an aneurysmal appearance. Defects of the supracristal or subpulmonary septum are found more commonly in patients of Asian background and are associated with a high incidence of aortic insufficiency.[101] Prolapse of the right or left coronary cusp into the ventricular septal defect actually may decrease the ventricular septal defect shunt while creating more severe aortic insufficiency. Occasionally the aortic sinus is extruded through the defect and ruptures, causing a fistula from the aorta to right ventricular outflow tract. Defects in the inlet septum are usually the result of a defect in the formation of the atrioventricular septum. Because the formation of this portion of the septum is intimately associated with the development of the atrioventricular valves and the crux of the heart, associated atrioventricular valve anomalies and a primum atrial septal defect are common (Fig. 4015) . Clefts in either the mitral or tricuspid valves or a common atrioventricular valve may occur. The tricuspid valve occasionally straddles the inlet ventricular septal defect, with chordal insertions that cross the defect into the left ventricle. When the ventricular septal defect is small, dense chordal tissue crossing the defect may effectively obstruct flow, limiting the shunt size. Fibrous aneurysms also occur with atrioventricular septal defects, decreasing or closing the ventricular septal communication. In most cases, however, an inlet ventricular septal defect is large and rarely closes spontaneously. Adults with this lesion develop pulmonary vascular obstructive disease early in life. Atrioventricular septal defects are frequently seen in adults with Down's syndrome, in whom surgery may

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have been avoided because of the patient's neurologic and functional limitations. Echocardiographic Evaluation

The interventricular septum is a complex fibrous and muscular structure requiring careful interrogation of all aspects by two-dimensional imaging and color Doppler to detect ventricular septal defects (Fig. 40-16) (Figure Not Available) . Membranous ventricular septal defects are best seen in the parasternal long- and short-axis views as echo dropout beneath the aortic valve and near the attachment of the septal leaflet of the tricuspid valve. Apical or subcostal five-chamber views also demonstrate the position of the defect in relation to the left ventricular outflow tract and tricuspid valve. Associated abnormalities of the right aortic cusp, subaortic region, and septal aneurysm formation should be delineated. The supracristal ventricular septal defect can be appreciated in the parasternal long-axis view of the right ventricular outflow tract or the parasternal short-axis view at the base of the heart, located immediately proximal to the pulmonic valve. If the right aortic cusp has become distorted and prolapses into the ventricular Figure 40-15 Apical four-chamber echocardiographic image of a type C complete atrioventricular canal defect. The large-inlet ventricular septal defect (arrowhead) and primum atrial septal defect (arrow) are crossed by a central bridging leaflet that has no chordal attachments to the crest of the interventricular septum. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 40-16 (Figure Not Available) (color plate.) Standard two-dimensional echocardiographic views with color coding of the location of the common types of ventricular septal defects. The membranous septum is coded in red, the supracristal or infundibular septum in orange, the inlet septum in green, and the muscular septum in blue. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; PV, pulmonary valve; RA, right atrium; RV, right ventricle; RVOT, right ventricular outflow tract. (From Levine RA, et al: Echocardiography: Principles and clinical application. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1554. Copyright 1989, Little, Brown, and Company.)

septal defect, the defect itself may not be detectable without color or pulsed

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Doppler. Muscular septal defects may be located anywhere within the trabecular septum. Careful scrutiny of parasternal short-axis sweeps as well as apical, off-axis apical, and subcostal views is required to detect muscular defects. Inlet ventricular septal defects are most apparent in apical or subcostal four-chamber views directed posteriorly toward the crux of the heart. Associated abnormalities of the atrial septum and the atrioventricular valves also can be appreciated from this vantage point. Assessment of left atrial and left ventricular chamber size and left ventricular function is important. Long-standing volume overload is associated with enlargement of left heart structures and may cause left ventricular failure in the older adult. In the clinical setting of endocarditis, vegetations can be detected on the aortic valve, the membranous septal aneurysm, or the tricuspid septal leaflet. Endarteritis at the site of the jet lesion within the right ventricle or right ventricular outflow tract is usually not detectable by two-dimensional imaging unless vegetations are extensive. Color flow mapping greatly enhances the sensitivity of detection of all forms of ventricular septal defects. Left-to-right shunts are readily detected as turbulent jets crossing the septum into the right ventricle when the pulmonary pressures are normal. Ambiguity may occur when there is little difference between left and right heart pressures, because shunt flow is low in velocity and difficult to distinguish from other low-velocity flow within the right heart.[102] [103] Pulsed and continuous wave Doppler studies are helpful to confirm the timing and velocity of shunt flow. With small membranous and supracristal ventricular septal defects, low-velocity diastolic shunt flow may precede the high-velocity systolic jet, presumably owing to slight differences in late diastolic pressures between left and right ventricles (Fig. 40-17) . This diastolic flow is sometimes mistaken clinically for aortic insufficiency or another aortic runoff lesion such as a sinus of Valsalva fistula or coronary artery fistula. Continuous wave Doppler measurement of the ventricular septal defect peak jet velocity allows estimation of right ventricular systolic pressures, and consequently pulmonary artery systolic pressures. By applying the modified Bernoulli equation, one can calculate the pressure gradient between the left and the right ventricle from the ventricular septal defect peak velocity. Subtracting this gradient from the cuff systolic blood pressure yields the right ventricular systolic pressure (Fig. 40-18) . Alignment as parallel as possible to the direction of the ventricular septal

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defect jet prevents underestimation of the gradient between the ventricles. Sampling from multiple windows or off-axis views may be required to achieve the best alignment. Shunt quantification by pulsed Doppler is performed in the same way as with atrial septal defects. Measurement of cardiac output across pulmonic and aortic valves is made, and the pulmonic-to-systemic flow ratio (Qp /Qs ) is computed. The turbulence created in the pulmonary artery by shunt flow from nearby membranous and supracristal defects may make measurement of the pulmonary flow velocity integral inaccurate. An alternative method for deriving shunt ratios involves calculating the volumetric shunt flow across the ventricular septal defect (VSD) and adding it to the systemic cardiac output to get pulmonary flow: Qp = Qs + VSD shunt The ventricular septal defect shunt volume is the product of the crosssectional area of the color flow jet at the Figure 40-17 Pulsed Doppler spectral tracing from the right ventricular aspect of the ventricular septum in a patient with a small perimembranous ventricular septal defect. A low-velocity left-to-right shunt is present in mid-diastole and late diastole (arrowheads) preceding the high-velocity shunt flow in systole.

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Figure 40-18 (color plate.) A, Shunt flow through a small perimembranous ventricular septal defect (VSD). d is the diameter of the flowstream at the septal surface. B, Continuous wave Doppler spectral tracing of the VSD shunt flow. The peak systolic velocity is 3.5 m per second. Dotted lines trace the flow velocity integral of the shunt flow. Estimation of right ventricular systolic pressure (RVSP) can be made by the formula on the lower left, using four times the square of the peak velocity. Calculation of the VSD shunt is possible using the formula on the lower right, including the diameter of the VSD and the flow velocity integral of the continuous wave Doppler tracing. Ao, aorta; LA, left atrium; LV, left ventricle; P, pressure; SBP, systolic blood pressure; VTI, velocity time integral.

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defect and the flow velocity integral of the continuous wave Doppler systolic flow signal (see Fig. 40-18) . In one study, this method had better correlation with shunt ratios determined by the Fick method than the standard pulsed Doppler calculation of Qp /Qs . [104] It may prove particularly useful in patients with pulmonary stenosis or in whom the pulmonary annulus or pulmonary flow profile is difficult to measure. Management

Surgical intervention for the adult with a small ventricular septal defect and normal pulmonary artery pressures is not necessary. Periodic follow-up is important to reinforce endocarditis prophylaxis, to reassess ventricular size and function, and to follow pulmonary artery pressures. Closure of a small ventricular septal defect may be indicated when intervention is needed for associated abnormalities such as significant aortic insufficiency or right ventricular outflow tract obstruction. Patients with large ventricular septal defects and irreversible pulmonary hypertension should be managed medically. Device closure of ventricular septal defects has been accomplished in selected cases when surgery was contraindicated, and it is now approved by the Food and Drug Administration for clinical application.[105] Appropriate placement requires a sufficient distance from the aortic valve or the atrioventricular valves to avoid damaging these structures. The eventual fate of devices in the actively contracting ventricle is unknown; however, with further development and modifications of transcatheter devices, this procedure may have wider application in the future. Patent Ductus Arteriosus The patent ductus arteriosus is a fetal necessity to allow diversion of flow from the nonfunctioning pulmonary circuit into the aorta and back to the placenta. The ductal channel arises from the pulmonary artery bifurcation near the origin of the left pulmonary artery and passes to the lesser curvature of the aorta just opposite the left subclavian artery. Ductal shape is quite variable, sometimes being a long, tortuous channel or a conical connection or even a very short window-like communication (Fig. 40-19) . The ductus arteriosus normally closes spontaneously within the first 24 to 48 hours of life. Persistence Figure 40-19 The various shapes of a patent ductus arteriosus as seen

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angiographically. The ductus is shown arising from the lesser curvature of the aortic arch. Its configuration varies from a window-like communication to a long tortuous channel (A to E). Knowledge of the ductal shape is important in choosing the best method of transcatheter closure. (Modified from Krichenko A, et al: Am J Cardiol 1989;63:878. Reprinted by permission of the publisher. Copyright 1989 by Excerpta Medica Inc.)

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beyond the neonatal period is abnormal, and spontaneous closure after the first year of life is distinctly uncommon. This lesion is found in only about 2% of adults with congenital heart disease. It is usually an isolated anomaly, but it can occur in association with complex lesions, ventricular septal defect, or coarctation. After 30 years of age, the ductal tissue becomes calcified and more friable. Aneurysms of the ductus arteriosus or the closed ductal diverticulum also occur and may rupture. Infectious endocarditis is more common in the second and third decades of life, affecting the pulmonary end of the ductal channel. The clinical presentation of an adult with a patent ductus arteriosus depends on the size of the shunt. Trivial shunts may be clinically silent, detected by an echo-Doppler study that was requested for an unrelated lesion. Small ductal shunts produce a continuous murmur at the upper left sternal border, which can be confused with the murmur of a coronary artery fistula, combined aortic stenosis and insufficiency, or a ventricular septal defect plus aortic regurgitation. Patients with moderate or large shunts develop congestive heart failure and atrial arrhythmias from the long-standing left ventricular volume overload. With the onset of pulmonary hypertension and reversal of the shunt, the murmur decreases in intensity or disappears and differential cyanosis of the lower extremities may be noticed. Echocardiographic Evaluation

Two-dimensional imaging of the ductus arteriosus is accomplished with ease in the neonate and young child, but it becomes progressively more difficult in adolescents and adults. The direct view of the ductal channel is best obtained in a high left parasternal window at the pulmonary artery bifurcation where the left pulmonary artery crosses the descending thoracic aorta. The main pulmonary artery appears to "trifurcate," with the third channel being the ductus. Visualization is possible also in suprasternal notch views of the aorta focused on the lesser curvature opposite the left subclavian artery. Diagnosis of a patent ductus arteriosus in the adult

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usually is made with color flow Doppler imaging rather than direct twodimensional imaging. The left-to-right flow stream appears as a red jet in diastole entering the main pulmonary artery near the left pulmonary artery origin (Fig. 40-20) . Although patent ductus arteriosus shunt flow is continuous, the systolic component is usually washed along with systolic flow in the main pulmonary artery. If flow can be visualized within the ductus itself, however, a continuous Doppler signal is present. As the pulmonary artery pressures rise, the velocity of the patent ductus arteriosus shunt decreases and it becomes more difficult to distinguish a discrete patent ductus arteriosus jet from other low-velocity flows within the dilated pulmonary vessel. Adults with a dilated main pulmonary artery often have a low-velocity retrograde flow in late systole from swirling of flow within the enlarged vessel. Pulsed Doppler can distinguish this from ductal flow by the difference in timing. Continuous flow into the pulmonary artery also is seen with coronary artery fistulas and with an aortopulmonary Figure 40-20 (color plate.) Parasternal short-axis echocardiographic view of the heart at the base, demonstrating a small patent ductus arteriosus. The stream of left-to-right shunt flow is shown in color as it passes from the descending thoracic aorta (DAo) to the pulmonary artery (PA). Ao, aorta.

window. Demonstration of the color Doppler flow stream emanating from the bifurcation and originating within the descending thoracic aorta should confirm that the shunt comes from a patent ductus arteriosus. Continuous wave Doppler sampling of ductal shunt flow is important for estimation of pulmonary artery pressure. When the ultrasound beam is aligned from the high left parasternal window directly into the mouth of the patent ductus arteriosus, systolic and diastolic flow velocity can be recorded. Applying the modified Bernoulli equation, the peak systolic velocity of the patent ductus arteriosus jet can be used to calculate the systolic gradient between the aorta and pulmonary artery. Subtracting this gradient from the cuff systolic aortic blood pressure yields the pulmonary artery systolic pressure. Shunt quantitation for a patent ductus arteriosus is performed in the same way as for atrial and ventricular shunts, measuring cardiac output across aortic and pulmonary valves. In the case of a patent ductus arteriosus, however, the shunt occurs after the flow crosses the pulmonary valve. Hence, the transpulmonary flow represents systemic flow, whereas the transaortic flow includes the shunt. The shunt ratio is computed by putting transaortic flow in the numerator and transpulmonary

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flow in the denominator.[106] Management

Closure of a patent ductus arteriosus is recommended for all but the clinically silent or the severely hypertensive ductus. Angiographic or magnetic resonance imaging delineation of the ductal shape is still necessary for surgical planning and for decisions regarding device closure in the 889

adult. Surgical mortality in repairing this lesion is low, but calcification of the ductus or a short, wide ductal shape complicates the procedure. Transcatheter closure of the ductus arteriosus is becoming the treatment of choice for children and adults. Several types of devices are currently in use, including a pluglike occluder within the ductus, umbrella devices that occlude the orifices at each end of the ductus, and coils that are extruded within the ductus and thrombose the channel. [107] [108] [109] Transesophageal echocardiographic guidance of device placement has not played as critical a role for the ductus arteriosus as for atrial septal defects. The difficulty in imaging the anatomic details of the ductus arteriosus by transesophageal echocardiography limits the usefulness of the modality, and fluoroscopic monitoring alone is sufficient for accurate placement. Transthoracic echo-Doppler assessment after device closure is quite helpful to ensure appropriate device position and assess residual shunting. [110] The highly reflective device can be appreciated by two-dimensional imaging at the pulmonary bifurcation and along the lesser curvature of the aorta. Malpositioning of the umbrella devices results in protrusion of a portion of the occluder into the aortic lumen or into the main pulmonary artery (Fig. 40-21) .[111] Residual shunt flow can be expected in about half of patients 24 hours after umbrella device placement, but this diminishes significantly over time. In one long-term follow-up study, 38% had detectable shunting at 1 year, and at late follow-up (3 to 4 years) about 10% of patients still manifested a small residual shunt by Doppler study.[110] Long-term results after coil occlusion are limited, but 1-year follow-up indicates that about one third have Doppler evidence of small clinically silent residual shunts. [109]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Coronary Fistulas A coronary fistula is an abnormal communication of a coronary artery with a cardiac chamber, great vessel, or Figure 40-21 Echocardiographic images from a patient after patent ductus arteriosus closure with a Sideris device. Left, In the parasternal short-axis view the counteroccluder (arrow) is seen near the origin of the left pulmonary artery (PA). Right, The occluder protrudes into the aortic lumen (double arrows) in the suprasternal notch view. Ao, aorta.

other vascular structure without passing through the myocardial capillary bed. Most coronary fistulas are congenital, resulting either from persistence of embryonic channels between the cardiac chambers and the developing coronary circulation or from aberrant connection of some of the coalescing coronary channels to the pulmonary artery. Coronary fistulas have been reported in 0.2% of coronary angiograms, usually as incidental findings.[112] The clinical presentation depends on the site of termination of the fistula and the degree of shunting. Over 90% of fistulas terminate in the right heart—right ventricle, right atrium, pulmonary artery, coronary sinus, or superior vena cava. A continuous murmur is caused by shunting from the aorta to the right heart. When the fistula communicates with the left ventricle, the murmur is audible only in diastole. Shunting is usually modest (Qp /Qs of 1.5:1), but it may progress over time by gradual enlargement of the fistulous tract or from the development of systemic hypertension. Signs of right ventricular volume overload and congestive heart failure may appear later in life from the long-standing left-to-right shunt. The shunt is rarely large enough to cause severe pulmonary hypertension. Angina, and rarely myocardial infarction, occurs in a small percentage of patients from "coronary steal" as the fistula diverts flow from the normal coronary circulation.[113] Echocardiographic Evaluation

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Echo-Doppler diagnosis of coronary artery fistulas begins with the detection of enlargement of the proximal coronary artery involved in the abnormal communication. The affected coronary vessel is diffusely enlarged (>0.6 cm) and can often be traced to the site of termination with knowledge of the expected coronary course and the usual sites of fistulous communication. Aneurysmal lakes may develop near the communication with the receiving chamber or vessel, appearing as large sonolucent regions (Fig. 40-22) . Enlargement of the right or left heart chambers 890

Figure 40-22 Echocardiographic images from a patient with a coronary artery fistula from right coronary artery (RCA) to right atrium (RA). A, In the parasternal short-axis view the RCA is markedly dilated and tortuous, feeding a large venous lake adjacent to the interatrial septum (arrowheads). B, Apical fourchamber view demonstrates the venous lake along the right atrial septal surface (arrowheads). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

gives an indication of the significance of left-to-right shunting. Color flow Doppler demonstrates continuous flow within the involved coronary artery and helps to localize the exit site.[114] [115] When a small fistula from the left coronary artery to the pulmonary artery is present, a tiny stream of continuous flow may be found incidentally in the proximal main pulmonary artery. Larger fistulas are diagnosed by scanning the right atrium, right ventricle, and left ventricle for a continuous turbulent flow signal (Fig. 40-23) . Transesophageal echocardiography also can detect coronary enlargement and visualize the enlarged and aneurysmal channels of the fistula. It is particularly helpful intraoperatively to assess residual fistulous flow and segmental wall motion after ligation of the feeding coronary vessel.[115] Figure 40-23 (color plate.) Apical echocardiographic images from a patient with a coronary artery fistula terminating in the right ventricular apex. A, A small venous lake (arrowheads) is apparent along the right septal surface. B, Entry of flow into the right ventricle from the fistula is clearly demonstrated by color flow Doppler. LV, left ventricle; RV, right ventricle.

Contrast echocardiography has been used in conjunction with angiography to detect fistulous communication when there are multiple entry sites of a

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coronary fistula.[116] [117] If the fistula terminates in both the right and the left ventricles, angiographic contrast may stream preferentially to the lowerpressure chamber. Faint opacification of the left ventricle easily may be overlooked. With injection of agitated saline into the arterial catheter, however, even a trace appearance of contrast in the left ventricle is obvious echocardiographically. Management Small, clinically silent coronary fistulas do not require closure. Patients with fistulas that are large enough to cause coronary dilation should be followed clinically for 891

the development of symptoms or significant right or left ventricular volume overload. Coronary angiography is generally necessary to completely evaluate the coronary circulation for coexistent atherosclerotic disease as well as for complete anatomic delineation of the fistula. Closure of large fistulas may be approached surgically or with transcatheter coil occlusion, depending on the specific anatomy of the lesion.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Complex Congenital Heart Disease Adults who survive with complex congenital heart defects represent a very small but intriguing fraction of an adult cardiology practice. In the current surgical era, most patients with complex lesions have had the benefit of either palliative or corrective surgery during childhood (see Chapter 41) . The occasional patient reaches adulthood and seeks medical attention for symptoms more typical of acquired heart disease—congestive failure, angina, valvular disease, arrhythmia, endocarditis—only to be found to have complex congenital heart disease, once a echocardiographic study is performed. A brief consideration is given to some of the complex lesions that permit natural survival into adulthood. Tetralogy of Fallot The tetralogy originally described by Fallot in 1888 consisted of a large ventricular septal defect, an overriding aorta, pulmonary stenosis, and right ventricular hypertrophy. About 15% of patients have an atrial septal communication (pentalogy of Fallot), and 25% have a right aortic arch. Anomalous origin of the left anterior descending coronary artery from the right coronary artery or bilateral left anterior descending vessels occurs in 5% to 9% of patients, complicating patch repair of the right ventricular Figure 40-24 Echocardiographic images from a patient with tetralogy of Fallot. A, Parasternal long-axis view of the left ventricle (LV) illustrates a large malalignment ventricular septal defect with aortic overriding of the interventricular septum (arrowheads). B, Anterior deviation of the parietal band (arrow) is apparent in the parasternal short-axis image, creating obstruction in the right ventricular outflow tract. Ao, aorta; PA, pulmonary artery; RV, right ventricle.

outflow tract because the anomalous vessel passes over the right ventricular outflow tract.[118] [119]

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Physiologically, the clinical picture with tetralogy of Fallot is that of a ventricular septal defect with right ventricular outflow obstruction of variable severity. Most patients develop severe cyanosis either at birth or within the first year of life, requiring surgical palliation or correction. Only 3% to 5% of patients survive beyond 25 years of age without intervention. [120] With only a modest degree of pulmonary stenosis, patients can survive with few symptoms into adult years. Paradoxically, the other group of late survivors without surgery includes patients with complete obstruction to right ventricular outflow. This subgroup—having pulmonary atresia with ventricular septal defect—has multiple congenital aortic-to-pulmonary collaterals capable of supplying the pulmonary circulation so as to produce only modest clinical desaturation. Cerebrovascular accidents or brain abscess, bacterial endocarditis, acquired aortic valve disease, and arrhythmias account for much of the morbidity and mortality in the adult with uncorrected tetralogy of Fallot. Echocardiographic Evaluation

Echo-Doppler evaluation can accurately define the characteristic features of tetralogy of Fallot. The malalignment ventricular septal defect usually is large and lies immediately beneath the dilated overriding aortic root (Fig. 40-24) . In parasternal views of the left ventricle, the size of the ventricular septal defect can be appreciated. The direction and velocity of shunt flow across the defect are easily determined in these planes by color flow and pulsed Doppler imaging. Unless the ventricular septal defect has become restrictive over time, the shunt is very low velocity and predominantly right to left. Parasternal short-axis views of the right ventricular outflow tract and aorta demonstrate the typical anterior deviation of the conal septum, narrowing the right ventricular outflow 892

tract (see Fig. 40-24) . A small pulmonary annulus, valvular pulmonary stenosis, and hypoplasia of the main and branch pulmonary arteries also are visible in this view. The systolic gradient across the stenotic outflow tract should be measured by continuous wave Doppler imaging. In patients with native or acquired pulmonary atresia, the right ventricular outflow tract is filled with muscle and ends blindly with no visible pulmonary valve leaflets and no detectable flow by pulsed Doppler. When the parasternal views are not able to visualize the pulmonary artery because of chest wall or lung interference, scanning from the suprasternal notch or high left subclavicular

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area may provide the necessary access to the branch pulmonary arteries. The proximal right pulmonary artery is measurable in nearly all patients with confluent pulmonary arteries. Suprasternal or high parasternal views of the ascending aorta are most accurate for measuring the right pulmonary artery, which passes behind the aorta as a small cross-sectional lumen in the long-axis plane, or a small linear vessel in the short-axis plane. Aortopulmonary collaterals can be detected, but they are not fully delineated by either magnetic resonance imaging or two-dimensional echocardiography.[121] [122] Apical and subcostal five-chamber views depict the large subaortic ventricular septal defect and the overriding aorta. Acquired aortic valve stenosis and insufficiency also can be further evaluated at this point in the examination. Moving the scan plane even more anteriorly from the five-chamber view brings the right ventricular outflow tract into view. This approach may provide better alignment of the Doppler cursor for sampling the right ventricular outflow tract gradient. In the cross-sectional views of the aortic root at the base of the heart, attempts should be made to visualize the coronary arteries. Enlargement of the right coronary orifice hints at a larger blood supply through this vessel, perhaps caused by the anomalous origin of the left anterior descending coronary artery. Careful attention should be directed to cross-sectional lumina seen anterior to the right ventricular outflow tract in high parasternal views and to anteriorly coursing vessels arising from the proximal right coronary artery. Although some success has been reported with transthoracic study of the coronary arteries in adults with tetralogy of Fallot,[123] coronary arteriography is still needed as part of the preoperative assessment in the adult. Transesophageal imaging in tetralogy of Fallot can provide nearly all the important diagnostic information, particularly with multiplane imaging probes. Malalignment of the conal septum is apparent in midesophageal longitudinal views of the right ventricular outflow tract or from the transgastric approach. The pulmonary valve anatomy and the size of the main and right pulmonary artery can be determined from transverse views in the midesophagus or high esophagus. The left pulmonary artery is often more difficult to image. The ventricular septal defect and overriding aorta can be appreciated in transverse views from the midesophagus and from transgastric views. Management

The majority of adults with tetralogy of Fallot should be candidates for

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complete repair. Surgery for this lesion can be accomplished in the adult with a reasonably low mortality (<3%) and with gratifying relief of cyanosis and improvement in functional class (see Chapter 41) . [124] , [125] In the subgroup with pulmonary atresia, decisions regarding surgical correction are based on the confluence and size of the pulmonary arteries as well as the size and distribution of aortopulmonary collaterals. Congenitally Corrected Transposition Congenitally corrected transposition, l-transposition (or levotransposition), is a malformation in which the great arteries are transposed but the ventricles are inverted and discordant relative to the atria, resulting in a "double switch" that physiologically corrects the circulation. In the absence of associated lesions, corrected transposition may go clinically unnoticed and is entirely compatible with a normal lifespan.[126] Ventricular septal defect, pulmonary outflow obstruction, and an Ebstein-like malformation of the left-sided tricuspid valve, however, are frequently present (Fig. 40-25) (Figure Not Available) . Complete heart block is commonly seen because of the abnormal pathway of the conduction system. Figure 40-25 (Figure Not Available) Anatomic features of congenitally corrected transposition. The aorta (Ao) lies anterior and to the left of the pulmonary artery (PA). It arises from the morphologic right ventricle (RV), which is left-sided. The most commonly associated lesions include pulmonary stenosis, ventricular septal defect (arrow), and an Ebstein-like malformation of the left-sided tricuspid valve. LA, left atrium; LV, left ventricle; RA, right atrium. (From King ME: Complex congenital heart disease: A pathologic approach. In Weyman AE [ed]: Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 1038, with permission.)

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Even with associated lesions, corrected transposition is quite compatible with survival into adult years. The limiting feature in many patients is the function of the systemic right ventricle. The anatomic right ventricle may not be functionally suited to carry the long-term burden of systemic afterload, particularly with additional volume loading from ventricular shunts or atrioventricular valve regurgitation.[127] The anatomic features and echocardiographic diagnosis of this complex are extensively reviewed in Chapter 39. Clinical echo-Doppler follow-up in patients with congenitally corrected transposition is directed primarily toward monitoring systemic right ventricular function and systemic

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atrioventricular valve insufficiency. Ventricular shunting and pulmonary outflow obstruction also require serial assessment. Standard geometric models for assessing left ventricular volumes and ejection fraction do not accurately model the unusual shape of the systemic right ventricle; therefore, the Simpson's rule method using two orthogonal apical planes may be a more accurate echocardiographic method for calculating systemic ventricular volume and function in this group. As three-dimensional echocardiography becomes more clinically applicable, it may be the optimal method for determining ventricular volumes because it does not require geometric assumptions.[128] Radionuclide rest and exercise ejection fractions and magnetic resonance imaging also are useful for following systemic right ventricular function.[129] The asymptomatic patient with corrected transposition requires no intervention. Both patient and physician need to be aware of the propensity to develop complete heart block, and invasive cardiac procedures should be avoided unless they contribute to clinical management. Also, because of ventricular inversion, the electrocardiogram in corrected transposition shows deep Q waves in the right precordial leads that can be mistaken for an ischemic injury. Right ventricular failure frequently develops with increasing age and medical therapy with afterload reduction is indicated.[127] Patients with associated ventricular septal defect and pulmonic stenosis should be managed in similar fashion to those with normal ventricular connections. Endocarditis prophylaxis should be rigorously followed. If pulmonary outflow obstruction is severe enough to require operative correction, ventricular septal defect closure and a left ventricular to pulmonary artery conduit has been the Figure 40-26 (Figure Not Available) Subtypes of double-outlet right ventricle (RV) based on the position of the ventricular septal defect (VSD). The VSD may lie immediately beneath the pulmonary artery (PA) (far left), predominantly below the aorta (Ao) with or without pulmonary stenosis (left center), or beneath both great vessels (right center) or may be unrelated to either great artery. LV, left ventricle. (From King ME: Complex congenital heart disease: A pathologic approach. In Weyman AE [ed]: Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 1042, with permission.)

traditional reparative procedure. Significant regurgitation of the systemic tricuspid valve may require tricuspid valve repair or replacement. Double-Outlet Right Ventricle

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As its name implies, double-outlet right ventricle is a condition in which both great arteries arise entirely or mostly from the right ventricle. A ventricular septal defect is present to allow the left ventricle to eject into the right-sided aorta and pulmonary artery. The great arteries are separated from the ventricles by bilateral subarterial conus and arise in parallel from the heart, often lying side by side. The location of the ventricular septal defect relative to the aorta or pulmonary artery, and the presence or absence of pulmonary stenosis, determines the hemodynamic picture of the patient with double-outlet right ventricle (Fig. 40-26) (Figure Not Available) . If the ventricular septal defect is subpulmonary, the physiology is similar to that of complete transposition. A subaortic ventricular septal defect with pulmonary stenosis is physiologically indistinguishable from tetralogy of Fallot. Survival to adolescence and adulthood is possible when the ventricular septal shunt is restricted by pulmonary stenosis of moderate degree. The patient is obligatorily cyanotic, but the degree of cyanosis is influenced by streaming across the ventricular septal defect and by the severity of pulmonary obstruction. Echocardiographic diagnosis of double-outlet right ventricle is made by demonstrating the origin of both great arteries primarily from the right ventricle (Fig. 40-27) (Figure Not Available) . In many instances, the posterior great vessel overrides the interventricular septum similar to the anatomy of tetralogy of Fallot or complete transposition with ventricular septal defect. The key distinguishing feature of double-outlet right ventricle is the lack of fibrous continuity between the mitral valve and its nearest semilunar valve. In the parasternal long-axis plane, this feature is apparent as a muscular separation between the base of the anterior mitral leaflet and whichever semilunar valve is more posterior. Doming of the pulmonary valve and the presence of subpulmonary stenosis can also be demonstrated in this view (Fig. 40-28) (Figure Not Available) . In the parasternal short-axis planes, the relative position and size of the great vessels are apparent. Sweeps from the base to the ventricular level demonstrate the anterior 894

Figure 40-27 (Figure Not Available) Parasternal long-axis echocardiographic view from a patient with double-outlet right ventricle. The view has been oriented to display the parallel origin of the great arteries from the anterior ventricle. The uncommitted ventricular septal defect is not seen in this plane. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery. (From Liberthson RR: Congenital heart disease in

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the child, adolescent, and adult. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1243, with permission. Copyright 1989, Little, Brown and Company.

and rightward origin of the outflow vessels. The right ventricle is enlarged and hypertrophied because it supplies both the pulmonary and systemic circuits. Left ventricular pressure may be suprasystemic if the ventricular septal defect is restrictive. Pulsed and continuous wave Doppler sampling of the ventricular septal defect velocity in the parasternal long- or short-axis views determines the pressure gradient between left and right ventricles. In this case, the left ventricular pressure is estimated by adding the ventricular septal defect gradient to the cuff systolic blood pressure. Apical and subcostal views are well suited to demonstrate the ventriculoarterial relationship and to establish the position of the ventricular septal defect relative to the great arteries. Delineation of the degree of override of the posterior great vessel can be demonstrated from these planes; however, variations in angulation can create marked variations in the apparent origin of the vessel in question. The parasternal long-axis view is more accurate to assess the degree to which the posterior vessel arises from the right ventricle. Inspection of the ventricular septal defect for tricuspid valve chordal apparatus is important because the tricuspid valve may have chordal attachments to the crest of the septal defect or to the conal septum. This scenario would make intracardiac repair of the ventricular septal defect more difficult and thus influences surgical planning. Finally, Doppler assessment of the transpulmonary gradient should be made from the apical or subcostal approach. Adults with double-outlet right ventricle who have a protected pulmonary bed and preserved ventricular function should be considered for complete repair to remove the complications of cyanosis, to remove the risk of cerebral embolus or brain abscess, and to prevent eventual right ventricular failure. Surgical correction ideally attempts to connect the left ventricle to the aorta, close the ventricular septal defect, and relieve pulmonary stenosis. These goals are achieved in different ways depending on the size and location of the ventricular septal defect (see Chapter 41) .[130] Truncus Arteriosus Persistent truncus arteriosus is a rare malformation in which a single arterial trunk arising from the heart supplies the coronary, pulmonary, and systemic circulation. A large ventricular septal defect is invariably present.

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Embryologically, this anomaly has been attributed to improper septation of the primitive arterial trunk, although another hypothesis attributes this malformation to infundibular and pulmonary atresia with subsequent failure of truncal septation, making persistent truncus arteriosus a close relative of tetralogy of Fallot.[131] Survival beyond 1 year of age without surgical intervention is rare; however, adult survival is possible if branch pulmonary stenoses or severe truncal valve stenosis protects the pulmonary circulation. Some patients survive to early adulthood despite developing pulmonary vascular obstructive disease. Several types of truncus arteriosus that differ in the Figure 40-28 (Figure Not Available) Parasternal long-axis echocardiographic view of double-outlet right ventricle with infundibular and valvular pulmonary stenosis. The aorta (Ao) is enlarged and lies anteriorly. The pulmonary artery (PA) is small with subvalvular (double arrows) and valvular (single arrow) pulmonary stenosis. LA, left atrium. (From King ME: Complex congenital heart disease: A pathologic approach. In Weyman AE [ed]: Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 1043, with permission.)

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Figure 40-29 (Figure Not Available) Subtypes of persistent truncus arteriosus. Most commonly, the main pulmonary artery arises from the posterolateral border of the truncus (type I) or the branches arise independently from the proximal vessel (type II). Rarely, the right pulmonary artery arises from the truncus and the left lung is supplied by collaterals from the descending aorta (type III). Another unusual variant includes hypoplasia of the ascending trunk with interrupted aortic arch. The pulmonary arteries arise from the proximal portion of the truncus arteriosus, and a large patent ductus arteriosus supplies the descending aorta (type IV). (From King ME: Complex congenital heart disease: A pathologic approach. In Weyman AE [ed]: Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 1045, with permission.)

origin of the pulmonary arteries from the main trunk have been described pathologically (Fig. 40-29) (Figure Not Available) . Types I and II are seen most commonly. The semilunar valve of a persistent truncus is frequently abnormal. The valve leaflets are thickened and stenotic, regurgitant, or both. The valve may have two (8%), three (61%), four (31%), or more cusps.[132] Echocardiographically, this anomaly must be distinguished from tetralogy of Fallot with pulmonary atresia. Both demonstrate a large central arterial

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vessel overriding the septum above a large malalignment ventricular septal defect. The aortic valve in truncus arteriosus is commonly abnormal in structure and function, whereas that in tetralogy of Fallot is usually normal. There is no semblance of a right ventricular outflow tract with a persistent truncus arteriosus, whereas in tetralogy of Fallot the outflow tract occupies its usual position but is small and filled with muscle. In the types of truncus arteriosus encountered most frequently, the main pulmonary artery or its branches arise directly from the ascending trunk, whereas in tetralogy of Fallot, the small pulmonary artery or branches cannot be shown to have direct communication with the ascending aorta. Both of these malformations have a right aortic arch in about one third of cases. High right and left parasternal views are the most useful in detecting the origins of the pulmonary arteries. Evaluation of the truncal valve is made in the same way one would assess a native aortic valve, inspecting the number of cusps in the parasternal short-axis views and the degree of stenosis and insufficiency by Doppler from the apex. Concentric hypertrophy of both left and right ventricles would be expected in the adult with truncus arteriosus, and ventricular function may be impaired. Patients with a protected pulmonary vascular bed are amenable to surgical correction with closure of the ventricular septal defect and a conduit from the right ventricle to the pulmonary artery. If the pulmonary arteries arise separately, some form of arterioplasty may be required to unify the pulmonary arteries. Truncal valve replacement may also be needed. Tricuspid Atresia Tricuspid atresia constitutes 1% to 3% of all congenital heart defects, and less than 10% of patients survive beyond childhood without surgery. [133] In this malformation, the arterioventricular valve of the morphologic right ventricle is absent or imperforate. The right ventricle is variably underdeveloped and the left heart is compensatorily enlarged. An atrial septal communication is present to allow egress of blood from the blind right atrium, and a ventricular septal defect of variable size is usually present. The great vessels may be normally related (60% to 70%) or transposed, with or without obstruction to pulmonary blood flow. The physiology in the adult is that of a central mixing lesion creating cyanosis, with ventricular septal defect and pulmonic stenosis, or ventricular septal defect and pulmonary vascular disease. The adult with uncorrected tricuspid atresia is susceptible to the usual complications of this physiologic state, namely endocarditis, brain abscess, and right-to-left embolic events.

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Echocardiographic Evaluation

In the place of the tricuspid valve, a thick band of fibromuscular tissue is recognized by two-dimensional imaging (Fig. 40-30) . No evidence of flow can be demonstrated by color or pulsed Doppler. The right atrium is enlarged, often with a prominent eustachian valve. The size of the right ventricle is related to the size of the ventricular septal defect during fetal development. It may be vestigial and slitlike with a small ventricular septal defect or nearly normal in size with a large ventricular septal defect. Progressive restriction of the ventricular septal defect may occur.[134] When the great vessels are normally related, progressive ventricular septal defect closure creates further obstruction to pulmonary blood flow. In patients with transposed great arteries, the systemic blood flow is jeopardized. Thus, serial determination of the ventricular septal defect size by two-dimensional imaging and ventricular septal defect gradient by Doppler is an important part of echocardiographic evaluation. The left ventricle in this anomaly is enlarged, and systolic function may be impaired from long-standing volume overload. Quantitative assessment of ventricular function is performed by the usual echocardiographic methods and is an important factor in determining surgical options.

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Figure 40-30 Transesophageal echocardiographic view of a patient with tricuspid atresia. The atretic tricuspid valve is shown as a thick, fibrous ridge (arrowheads) at the base of the enlarged right atrium (RA). A ventricular septal defect is present (arrow) leading into a tiny right ventricular chamber. LA, left atrium; LV, left ventricle.

Echocardiographic study in the patient with tricuspid atresia also must focus on the presence, size, and origin of the aorta and pulmonary artery. The orientation and relative size of the great arteries and associated abnormalities of the valvular and subvalvular region all can be appreciated from parasternal windows. Apical and subcostal images are particularly useful in establishing ventriculoarterial relationships and measuring gradients across the semilunar valves and outflow tracts. The interatrial septum in the adult with uncorrected tricuspid atresia generally has a large, unrestricted atrial defect in the form of a stretched patent foramen ovale or secundum atrial septal defect. Apical, subcostal, or

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right parasternal windows optimally should delineate the atrial septum and demonstrate right-to-left shunt by pulsed and color Doppler. Management

Patients with tricuspid atresia and restricted pulmonary blood flow may be candidates for a Fontan procedure, which diverts systemic venous return directly to the pulmonary artery. The optimal candidate must have good left ventricular function, no significant mitral insufficiency, and normal branch pulmonary artery anatomy and pulmonary resistance. Natural survivors with tricuspid atresia and pulmonary vascular disease are not currently amenable to surgical correction. Univentricular Heart The basic element of the univentricular heart is communication of both atria or a common atrium with a single main ventricular chamber. Natural survival of adolescents and adults with this complex congenital anomaly depends on fortuitous streaming of oxygenated and unoxygenated blood and protection of the pulmonary circulation by an optimal degree of pulmonary stenosis. Ventricular failure develops with increasing age. The important aspects to ascertain echocardiographically in patients with this anomaly are (1) the presence and location of an accessory chamber; (2) the number and functional status of the atrioventricular valves; (3) the number and orientation of the great vessels and their relation to the main or accessory chamber; (4) the presence and severity of outflow obstruction; (5) the functional performance of the systemic ventricle; and (6) the nature and adequacy of venous return in the case of atresia of one of the atrioventricular valves. Detailed discussion of the anatomic and echocardiographic features of univentricular heart can be found in Chapter 39 . Management

Adults with a univentricular heart may be considered for operative correction employing one of the several modifications of the Fontan procedure.[135] [136] Patient eligibility requires adequate pulmonary artery size and confluence, low pulmonary artery resistance, competent systemic atrioventricular valves, good ventricular function with low ventricular enddiastolic pressure, and no obstruction to ventricular outflow.[137]

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Chapter 41 - Echocardiographic Evaluation of the Adult with Postoperative Congenital Heart Disease John S. Child MD

Due to advances in diagnostic techniques and in medical, catheter, and surgical treatment, adults with postoperative congenital heart disease constitute a growing cardiac population.[1] Some surgical corrective techniques used today did not exist in the mid-1980s, but they can be applied to adolescents and adults whose physiology and anatomic substrate allowed them to survive either without surgery or with the benefit of palliative shunts. Other operative procedures are rarely or never performed today, but the results can be seen in the adult survivors. Familiarity with previous and currently applied "corrective" procedures is needed because surgical techniques have evolved for decades and continue to do so, and they can affect long-term outcome. Although ligation of an uncomplicated patent ductus arteriosus and primary closure of a simple secundum atrial septal defect may be curative, all other surgically modified cardiac anomalies leave behind residua or cause sequelae or complications ranging from the trivial to the serious.[1] Adults who have undergone operation ultimately are evaluated in "adult" echocardiographic laboratories that are accustomed to evaluating standard

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adult acquired cardiac diseases and, occasionally, simple congenital heart diseases. [2] Complex palliative and corrective procedures are generally not well understood by medical cardiologists without special training in adult congenital heart disease. The evaluation and management of these individuals requires detailed knowledge of (1) the original anatomy and physiology; (2) the dynamic changes in the anatomy and physiology that occur with time; (3) the effects of adult diseases (e.g., systemic arterial hypertension, coronary artery disease) or conditions (e.g., pregnancy) on that physiology; (4) the types of operative repair (both past and present) for each complex of lesions; (5) the presence and extent of possible postoperative residua, sequelae, and complications; and (6) the proper selection, performance, and interpretation of modalities required for anatomic imaging and hemodynamic assessment.[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15]

Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) are crucial for the evaluation of congenital heart disease.[2] [3] [4] [10] [11] [12] [13] [14] [15] Image interpretation is best performed using the segmental approach. This approach involves identification of the atrial, ventricular, and arterial segments and determination of (1) atrial and ventricular situs, (2) the connections of the atria to the ventricles and of the ventricles to the great arteries, and (3) the relationships of the ventricles and great arteries. It is impractical to repetitively catheterize these individuals; combined two-dimensional, color flow and spectral Doppler echocardiography often are more useful than angiography in providing details of valvular anatomy and in visualizing patches and ventricular wall thickness. Echocardiography is nearly equivalent to angiography in displaying the connections of the pulmonary and systemic veins to the atria, intra-atrial anatomy, and the connections of the atria or ventricles to the great arteries. Comprehensive 902

echocardiographic study includes complete anatomic delineation of intraand extracardiac structures using combined two-dimensional and color flow imaging and assessment of chamber sizes and myocardial function. Pulsed and continuous wave Doppler and color flow imaging permit a search for and quantitation of valvular, subvalvular, or supravalvular stenosis and regurgitation; extra- and intracardiac conduit stenosis; pulmonary and systemic venous obstruction; trans-septal or patch shunts; and intracardiac hemodynamics. [2] Conduit course and obstruction, pulmonary artery

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branches, or aortopulmonary collaterals also may require angiography or magnetic resonance imaging for full delineation, but in such instances these techniques can be applied selectively.[5] [6] [7] [8] [9] TEE is necessary for the evaluation of regions of the cardiovascular system not readily seen by surface imaging (e.g., coarctation of the aorta, sinus venosus atrial septal defects, pulmonary venous connections), for more complete depiction of complex anatomy and for intraoperative use.[10] [11] [12] [13] [14] [15] TEE anatomic and hemodynamic imaging evaluation must be complete because unsuspected lesions may be found (e.g., atrial septal defects, anomalous pulmonary venous connections, muscular ventricular septal defects) that should not go unrepaired at the time of intracardiac repair (Fig. 41-1) . [12] [13] [14] [15] TEE allows good visualization of the origins of the coronary arteries, main pulmonary artery branches, and entire aorta. [12] [13] [14] [15]

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Intraoperative Transesophageal Echocardiography TEE is now the standard for intra- and postoperative evaluation of complex congenital heart disease surgery.[12] [13] [14] [15] Before Figure 41-1 Postoperative residua. Transesophageal echocardiography performed to evaluate aortic valve prosthesis function because of loud systolic murmur. Residual perimembranous ventricular septal defect (PM VSD) as well as discrete subaortic membrane causing mild subaortic stenosis (SAS) unrecognized at time of mechanical aortic valve replacement (AVR) for bicuspid aortic valve at another institution. The AVR was shown (in other views) to have normal function. The PM VSD is nearly closed by superimposition of an "aneurysm" caused by the septal tricuspid valve (SEPTAL TV) leaflet. LA, left atrium; LV, left ventricle; MV, mitral valve; RVOT, right ventricular outflow tract; VS, ventricular septum.

TABLE 41-1 -- General Postoperative Issues in Congenital Heart Disease Postoperative Issue Electric instability

Residual anatomic defects

Examples Atrial arrhythmias after intra-atrial baffle procedures Ventricular arrhythmias after ventriculotomy Bicuspid aortic valve in patient with aortic coarctation Residual mitral regurgitation after cleft leaflet repair Pulmonic regurgitation after tetralogy of Fallot repair Dilated aortic root Missed muscular ventricular septal defect

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Prosthetic materials

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Chronic volume overload due to valve regurgitation Anatomic right ventricle functioning as the systemic ventricle Single functioning ventricle Degeneration of septal patches, intra- and extracardiac conduits Prosthetic valve dysfunction (see Chapter 24) Thrombus formation Risk of infective endocarditis (see Chapter 21) Obstruction or leaking of conduits

cardiopulmonary bypass, TEE may refine anatomic diagnosis and detect previously unsuspected lesions (each of which may require modification of the operative approach). After discontinuation of cardiopulmonary bypass and resumption of normal cardiac activity, adequacy of repair is evaluated and additional repair directed when the initial result is unsatisfactory. Any residua and surgical sequelae are documented. TEE in the intensive care unit elucidates the reasons for such complications as hypotension (e.g., tamponade, ventricular dysfunction, hypovolemia) or complications of specific congenital heart operations such as the Fontan procedure (e.g., lateral tunnel thrombus). [12] [15]

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General Postoperative Congenital Heart Disease Issues (Table 41-1) Atrial and Ventricular Incisions Electric instability may occur after atrial or ventricular incisions with subsequent scars or aneurysms or after insertion of intracardiac patches or conduits with possible disruption of the conduction system.[1] [2] [16] Patients with intra-atrial baffles or conduits (e.g., those used in the Mustard and Fontan procedures) frequently suffer from atrial arrhythmias; superimposed pressure overload on a ventriculotomy site may cause ventricular electric instability.[2] [16] Anatomic and Valvular Residua/Sequelae Postoperative anatomic and valvular sequelae and residua must be sought ( Fig. 41-2 and Fig. 41-3 ; see also 903

Figure 41-2 Intraoperative presurgical transesophageal echocardiographic study showing ventricular septal defect (VSD) patch and right ventricular outflow tract (RVOT) scar in tetralogy of Fallot. There was severe residual pulmonary regurgitation (see Fig. 41-3) caused by a dilated RVOT with an incisional scar and dilated pulmonary valve annulus (PVA) with virtual absence of pulmonary valve tissue owing to resection ( see also Fig. 41-3 and Fig. 41-18 ). Patient then underwent pulmonary valve replacement and repair of right pulmonary artery stenosis owing to previous right Blalock-Taussig shunt. AV, aortic valve; LA, left atrium; MPA, main pulmonary artery; RA, right atrium; TV, tricuspid valve.

Fig. 41-1 ).[1] [2] Bicuspid aortic valves, common with aortic coarctation, continue to pose risks of progressive stenosis, regurgitation, and endocarditis despite coarctation repair. Variations on a parachute mitral

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valve, also associated with coarctation, and other stenoses in sequence on the left-sided Figure 41-3 (color plate.) Severe pulmonary regurgitation in tetralogy of Fallot (TOF) status post (S/P) valvotomy. Pulsed Doppler study during presurgical intraoperative transesophageal echocardiography at the level of pulmonary valve annulus of the patient in Figure 41-2 shows virtually laminar pulmonary regurgitant flow ending in the presystolic period (arrowheads), an indication of "restrictive right ventricular physiology."

circulation are detected by imaging a decreased interpapillary muscle distance and evaluating Doppler evidence of inflow obstruction. Repair of an ostium primum atrial septal defect with cleft mitral leaflet may leave residual mitral regurgitation; subaortic stenosis owing to anomalous chordal attachments should be sought. In repaired tetralogy of Fallot, pulmonary regurgitation is a sequela to valvulotomy or transannular incision and patch ( see Fig. 41-2 and Fig. 41-3 ). Mild or moderate lowpressure pulmonic regurgitation is common and well tolerated; severe pulmonic regurgitation may cause right ventricular dilation and tricuspid regurgitation, particularly if there is residual right ventricular outflow obstruction. Muscular ventricular septal defects may have been missed and should be sought by color flow imaging.[17] A dilated aortic root or trunk may occur in tetralogy of Fallot, transposition of the great arteries, or single ventricle in association with pulmonic stenosis, and postoperative aortic regurgitation is common in adults. Atrioventricular valve regurgitation, common preoperatively in patients who underwent a Fontan procedure, may progress post-operatively. Ventricular Function The aforementioned valvular lesions not only pose a continuing risk for endocarditis but, if severe, affect long-term ventricular performance (Fig. 41-4) .[1] [2] Operative myocardial preservation often was faulty in earlier decades.[1] In addition, the later in life the patient is operated Figure 41-4 Biventricular dysfunction and complete heart block in tetralogy of Fallot (TOF) late postoperative (postop) intracardiac repair (ICR). Four-chamber apical transthoracic view in young man with previous intracardiac repair with ventricular septal defect (VSD) closure and pulmonary valvotomy who then had a mechanical bileaflet

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pulmonary valve replacement for severe pulmonary regurgitation, presenting for the first time to UCLA with congestive heart failure and atrial flutter. A pacer wire is seen in the right ventricle (RV) and in the right atrium (RA); in addition, there is the unusual development of subaortic stenosis (SAS). In real time, systolic ejection fraction was 25% for both ventricles. LA, left atrium; LV, left ventricle; MV, mitral valve.

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on, the less the regression of ventricular dilation and hypertrophy.[18] Long term, a subaortic right ventricle operating at systemic pressures or a single functioning ventricle in a univentricular heart (even after the Fontan procedure) may have an irreversible decline in contractility.[18] Ventricular function may suffer if a prosthetic patch or conduit origin is large, if an incisional aneurysm acts as a "windkessel," or if valvular or conduit obstruction, regurgitation, or shunt overloads the heart. Conduits, Patches, and Prosthetic Materials Septal patches, mechanical or bioprosthetic valves, and intra- and extracardiac conduits may degenerate ( Fig. 41-5 , Fig. 41-6 , Fig. 41-7 ).[2] [3] [4] Mechanical valvular prostheses risk thrombus formation and infective endocarditis. Bioprosthetic valves suffer obstruction and regurgitation caused by premature degeneration and calcification, particularly in adolescents and young adults.[19] Conduits (valved or nonvalved) engender late postoperative concerns of patency and longevity of Dacron conduits with porcine or aortic homograft bioprostheses.[1] [2] [3] [4] [20] External conduits may kink, be compressed between the heart and sternum, or develop intimal ingrowth.[2] [3] [4] Obstruction can exist at the exit from the ventricle, at a bioprosthetic valve, or at the distal conduit insertion. Valved conduits can develop bioprosthetic valvular degeneration with stenosis and regurgitation (see Fig. 41-7) . An internal conduit may develop leaks, internal obstruction, or kinking or may partially obstruct the chamber within which it sits. Some conduits have unusual courses because of altered great artery relationships; therefore, multiple precordial and Figure 41-5 (color plate.) Ventricular septal defect (VSD) patch leak in a late postoperative (postop) tetralogy of Fallot (TOF). Short-axis parasternal transthoracic view in same patient as Figure 41-4 shows the VSD patch leak, which was hemodynamically small. There is a mildly aneurysmal right ventricular outflow tract (RVOT) at the site of a

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previous incisional aneurysm. The mechanical pulmonary valve reverberation echoes (arrowhead) mask the main pulmonary artery. LA, left atrium; RA, right atrium; TV, tricuspid valve. Figure 41-6 Truncus arteriosus after a Rastelli procedure. The right ventricle-to-pulmonary artery (RV-PA) conduit is shown in this transthoracic parasternal short-axis view. LA, left atrium; RPA, right pulmonary artery.

subcostal transducer positions or multiplane TEE may be required for an adequate anatomic-hemodynamic evaluation.[2] [3] [4] [12] [13] [14] [15] [20] Continuous wave Doppler is directed into the conduit (with assistance of color flow imaging) to find the high-velocity jet from multiple angles. Most conduits are a continuous curve, and the proper angle of incidence to achieve the true peak velocity may be difficult to obtain.[2] [4] [20] Quantitation of atrioventricular valve regurgitation Figure 41-7 (color plate.) Truncus arteriosus status after a Rastelli procedure. Continuous wave Doppler (CWD) through the right ventricle-to-pulmonary artery (RV-PA) conduit of the patient in Figure 41-6 reveals mild conduit pulmonary stenosis (PS) with pulmonary regurgitation (PR), severe by color flow imaging. Note that the PR ends at the P wave with subsequent forward atrial boost in the immediate presystolic phase consistent with "restrictive" RV physiology.

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by continuous wave Doppler allows determination of ventricular systolic pressure and thus allows evaluation of possible significant conduit stenosis. [2] [4] [20]

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Palliative Procedures (Table 41-2) Pulmonary Artery Banding Pulmonary artery banding may be used to decrease the volume and pressure effects of a large unrestricted shunt at the ventricular level, thereby preventing either heart failure or pulmonary hypertension.[4] Although banding is not usually initiated in adults, we encounter adolescents and adults with previous banding with no subsequent definitive procedure. The site of the band relative to the pulmonary valve and the bifurcation is evaluated by two-dimensional echocardiographic anatomic imaging, the best placement being the midportion of the pulmonary artery; a band that is too close to the valve may interfere with valve function, and a band that has slipped onto the bifurcation may cause branch artery stenosis. Inadequate banding results in pulmonary vascular disease and pulmonary hypertension. Band stenosis gradient is quantitated by aligning the continuous wave Doppler beam with the acceleration of color flow into the iatrogenic stenosis.[4] [21] Because most lesions that require banding have large ventricular septal defects, pulmonary artery systolic pressure can be estimated as systolic systemic blood pressure minus the peak pressure gradient across the band (provided that there is no left ventricular outflow tract obstruction). [4] Palliative Aortopulmonary Shunts Palliative systemic arterial to pulmonary arterial shunts are performed for malformations characterized by decreased pulmonary arterial flow (e.g., tetralogy of Fallot). The shunts from the high-pressure aorta to the lowpressure pulmonary artery can be evaluated for patency by continuous wave Doppler, which should reveal non-laminar flow in both systole and diastole toward the pulmonary artery in the absence of pulmonary hypertension.[2] [3] [4] [12] [13] [14] [15] [22] [23]

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TABLE 41-2 -- Palliative Procedures for Congenital Heart Disease Name of Procedure Pulmonary artery banding

Description Constriction of main pulmonary artery

Complications Inadequate band with consequent pulmonary vascular disease

Branch pulmonary artery stenosis Pulmonic valve dysfunction Waterston Ascending aorta to right Pulmonary hypertension due to shunt pulmonary artery too large a shunt Potts shunt Descending aorta to left Kinking of branch pulmonary pulmonary artery arteries BlalockSubclavian artery to Inadequate shunt to maintain Taussig shunt branch pulmonary artery pulmonary blood flow Modified Gore-Tex graft from Excessive shunt resulting in Blalocksubclavian artery to pulmonary hypertension Taussig shunt pulmonary artery Glenn shunt Superior vena cava to Postoperative cyanosis due to right pulmonary artery increased collaterals from with division of main superior to inferior vena cava or pulmonary artery pulmonary arteriovenous fistulas Bidirectional Superior vena cava to Postoperative cyanosis due to Glenn shunt both (undivided) increased collaterals from pulmonary arteries superior to inferior vena cava or pulmonary arteriovenous fistulas The Waterston (ascending aorta to right pulmonary artery) and Potts (descending aorta to left pulmonary artery) shunts are discrete side-to-side connections. Potts and Waterston anastomoses are now rarely performed because of problems with precise control of size (and possible pulmonary hypertension) and kinking of branch pulmonary arteries, which complicate future repairs. Imaging of these two types of anastomosis is difficult in adults and is best done by TEE.[12] [13] [14] [15] Proper spectral Doppler alignment with color flow imaging on TEE makes it possible to calculate the gradient by the Bernoulli equation.[4] [12] [13] [14] [15] Pulmonary artery systolic pressure is estimated by subtracting the peak systolic pressure gradient from the brachial artery systolic peak pressure.[2] [4] As pulmonary

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artery pressures rise, the diastolic flow decreases more than does systolic flow. A diminutive or absent diastolic flow signifies increased diastolic pulmonary pressure. A classic Blalock-Taussig shunt is a direct end-to-side anastomosis between a subclavian artery and a branch pulmonary artery, usually on the side opposite the aortic arch. A modified Blalock-Taussig shunt uses a 4- to 5-mm Gore-Tex tube (rarely, a vein graft) between the aorta or subclavian artery and the pulmonary artery; thus, the subclavian artery is not sacrificed. Imaging of a Blalock-Taussig shunt may be successful using suprasternal and supraclavicular views augmented by color flow imaging.[2] [3] [4] To reliably visualize these shunts, vertical plane orientations of bi- or multiplane TEE must be used.[12] [13] [14] [15] Estimation of pulmonary artery pressure by the method mentioned previously is less reliable because the Blalock-Taussig shunt is a long narrow conduit; a low gradient may be seen in the presence of adequate flow and normal pulmonary artery pressures. [4] The flow should be virtually continuous; as such, it must be distinguished from a patent ductus.[23] If the shunt is small or becomes nonpatent, flow further decreases or is lost. Doppler is helpful in the early postoperative period in a patient who continues to demonstrate cyanosis, in order to assess the adequacy of the shunt versus an alternative cause of postoperative cyanosis (e.g., atelectasis).[2] If the shunt is too large and results in pulmonary hypertension (fortunately, an uncommon circumstance), the diastolic flow is the first to diminish, followed later by decreased systolic flow as 906

pulmonary vascular resistance rises to equal systemic vascular resistance. Glenn Shunts The classic Glenn shunt, typically used for tricuspid atresia with good initial palliation, is an anastomosis of the end of the superior vena cava to the side of the right pulmonary artery, which is divided from the main pulmonary artery, with ligation of the superior vena cava below as it enters the right atrium. The "bidirectional" Glenn, in which superior vena caval flow is directed to both (undivided) pulmonary arteries, provides satisfactory improvement in systemic oxygen saturation without producing ventricular volume overload. This type of shunt has been quite useful either as a definitive palliation or as a staging procedure for subsequent Fontan

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procedures in complex congenital heart disease not amenable to biventricular repairs. Direct imaging of the connection can be made from right supraclavicular or suprasternal notch windows, with attention to the course of the superior vena cava and the size of the connection to the right pulmonary artery. [3] TEE imaging in a vertical plane alignment identifies first the right atrium and upper "stump" of the superior vena cava, then, with rotation of the probe rightward, the upper to middle superior vena cava anastomosis to the right pulmonary artery.[12] [24] Combined color flow imaging and pulsed Doppler reveal if the anastomosis is patent. Recurrent postoperative cyanosis may be caused by increasing collateral venous flow from the superior to the inferior vena cava or from right lower lobe pulmonary arteriovenous fistulas.[1] [2] Contrast echocardiography detects these extracardiac right-to-left shunts; after injection into an arm vein, late flow into the left atrium identifies pulmonary arteriovenous fistulas, whereas prompt appearance in the right atrium reveals azygousvenous collaterals to the inferior vena cava.[2] Fistulas and venous collaterals are amenable to catheter intervention and coil embolization.[1]

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Corrective Procedures for "Simple" Lesions (Table 41-3) Simple lesions may be isolated shunts, obstructive malformations, or regurgitant lesions. Complex malformations (discussed later) consist of two or more simple lesions, often with malpositions of veins, chambers, or great arteries and with associated cyanosis. Atrial Septal Defects Atrial septal defects are some of the most common unoperated and postoperative congenital heart defects.[24] [25] Adults with a previously unrecognized, clinically silent atrial septal defect are regularly encountered in echocardiography laboratories. The secundum atrial septal defect is the most common and is closed by either direct suture repair, patch, or device closure (Fig. 41-8) , but we at UCLA continue to encounter previously unsuspected primum atrial septal defects in adults (Fig. 41-9) . [25] [26] [27] [28] [29] [30] Echocardiographic follow-up after atrial septal defect closure entails evaluation for residual shunting, associated mitral valve abnormalities, degree of pulmonary hypertension (by using the tricuspid regurgitant jet velocity), and degree of resolution of right heart chamber enlargement.[2] [26] [27] [28] Patch leaks are infrequently seen, provided that severe pulmonary hypertension was not present at operation.[2] Patients with a previously sizable shunt have a decrease in, but not necessarily normalization of, right ventricular size.[26] [27] Transcatheter closure devices are not yet routinely available, but TEE plays an important role in the interventional catheterization laboratory for sizing the defect to determine maximal usable occluder device size, imaging the septal rims, observing the placement of the device and the effectiveness of occlusion, and detecting unusual arm positions or new-onset valvular regurgitation.[28] [29] [30] Sinus venosus atrial septal defects, usually suspected because of right ventricular enlargement seen on TTE, and often associated with anomalous pulmonary venous connections to the superior vena cava, usually require

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TEE for precise diagnosis.[12] [13] [14] [24] , [27] Repair requires patching of the defect with autologous pericardium to also baffle the anomalous pulmonary venous drainage to the left atrium via the atrial septal defect. TEE is mandatory in adults to evaluate the adequacy of patch closure of the defect, with attention to the presence or absence of superior vena caval and pulmonary venous narrowing or obstruction.[12] [13] [14] [15] Atrioventricular canal-type defects are considered later (see "Repair of 'Complex' Malformations"). A coronary sinus atrial septal defect is the rarest form and consists of partial or complete absence of the coronary sinus with connection of the left atrium to the right atrium via the usual location of the coronary sinus ostium, usually with a persistent left superior vena cava that joins the roof of the left atrium.[24] A coronary sinus atrial septal defect may be associated with complete atrioventricular septal defects or tricuspid atresia (and may first be detected after a Fontan repair). Ventricular Septal Defects Ventricular septal defects, common congenital lesions, alone or in combination with other anomalies, may occur anywhere in the ventricular septum. [2] [31] [32] [33] They may be classified as perimembranous, muscular, inlet, outlet, or malalignment.[33] Defects may be characterized as restrictive or nonrestrictive according to whether there is a pressure gradient from left to right ventricle. In adults, substantial left-to-right shunt owing to a nonrestrictive ventricular septal defect is rare because pulmonary vascular disease (Eisenmenger's syndrome) typically has developed, resulting in bidirectional shunting. Spontaneous closure of perimembranous defects occurs frequently, mainly by adherence of septal tricuspid leaflet tissue but occasionally by prolapse of an aortic cusp into the defect.[34] Tricuspid or aortic regurgitation may develop or increase.[31] [32] [34] [35] Aortic regurgitation (especially with 907

TABLE 41-3 -- Corrective Procedures for "Simple" Congenital Heart Lesions Lesion Corrective Procedure Atrial septal Suture repair, patch

Complications and Residual Abnormalities Residual shunting

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defect

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closure, or transcatheter closure

Associated mitral valve abnormalities Persistent pulmonary hypertension Right heart chamber enlargement Ventricular Surgical repair (via right Residual patch leak septal defect transatrial approach) Arrhythmias if ventricular incision needed Patent Surgical ligation or Residual shunting (more likely if ductus catheter device closure calcified) arteriosus Bicuspid Surgical or balloon Associated lesions (ventricular aortic valve valvuloplasty septal defect, coarctation) Pulmonic autograft Restenosis Valve replacement Prosthetic valve dysfunction Subaortic Excision of membrane Aortic regurgitation stenosis or fibromuscular ridge Iatrogenic ventricular septal defect Mitral valve injury Recurrent stenosis Coarctation Multiple repair Residual or recurrent coarctation of aorta procedures Left ventricular hypertrophy Associated lesions (e.g., bicuspid aortic valve, supramitral ring) Ebstein's Surgical repair Residual tricuspid regurgitation anomaly Associated lesions (patent foramen ovale, atrial septal defects, pulmonic stenosis, ventricular septal defects) Pulmonic Balloon dilation Residual stenosis

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stenosis Surgical repair

Coronary artery anomalies

Various repair procedures

Pulmonic regurgitation Dynamic right ventricular outflow obstruction (early postoperative) Left ventricular dysfunction

Mitral regurgitation outlet supracristal defects) may occur; operative closure of the ventricular septal defect usually prevents progression of regurgitation.[31] [32] [33] [34] [35] [36] Small defects pose a risk of infective endocarditis; once endocarditis occurs, it may be argued that closure of the ventricular septal defect will diminish subsequent risk. Nine of 296 patients who underwent closure of isolated ventricular septal defect developed endocarditis; three of the nine had no known residual shunt.[37] Figure 41-8 Transesophageal echocardiography follow-up of device closure of secundum atrial septal defect. The rims of the device are seated on the left atrial (LA) and right atrial (RA) rims of the defect (arrows). There was no residual shunt by color flow or echocontrast. IVC, inferior vena cava; SVC, superior vena cava.

Simple ventricular septal defects now are closed via a right transatrial approach to avoid ventricular incisions and their electrical and mechanical consequences. [2] [31] Multiple muscular defects may require left ventriculotomy for adequate visualization, with the attendant risks of missed or incompletely closed defects, ventricular arrhythmia, and left ventricular dysfunction.[31] Investigation of the septal patch for leaks is imperative; it is preferable to detect these in the operating room at the time of closure to allow rerepair at that time. Color flow imaging after closure of a large ventricular septal defect may reveal previously undetected smaller defects.[12] [13] [14] [15] , [35] Transcatheter device closure has been helpful for multiple muscular ventricular septal defects, for persistent postoperative ventricular septal defect in complex conotruncal malformations, and even for acquired postinfarction defects.[38] TEE during the procedure decreases fluoroscopy time, detects the sites of multiple ventricular septal defects, determines the device position relative to the defect and adjacent valves, detects residual shunting, and may reveal other previously unrecognized

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defects.[38] Patent Ductus Arteriosus Patent ductus arteriosus is ordinarily detected in childhood, but a couple of undiagnosed cases per year are still found at UCLA during routine echocardiography for other reasons. Operative closure of simple patent ductus arteriosus in the young leaves few residua; in older patients, calcification is common and can tear during ligation.[1] , [39] Intraoperative TEE is useful in verifying complete uncomplicated closure.[40] Catheter device closure of a ductus is effective in adults provided the size is less than 7 mm and previous endarteritis at the site has not occurred, 908

Figure 41-9 Primum atrial septal defect (ASD). A, Prerepair intraoperative transesophageal echocardiography (TEE). B, Postoperative intraoperative TEE. A patch is seen closing the primum ASD from the attachments of the tricuspid valve (TV) and mitral valve (MV) to the secundum portion of the interatrial septum (IAS). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

which could weaken the vessel wall.[41] [42] [43] Gray et al[44] reported that surgical closure was more effective and less costly, but technical improvements are evolving. Using color flow imaging to search for residual shunting is essential to confirm success or the need for further device closure and for advice on anti-infective endocarditis prophylaxis. Bicuspid Aortic Valve Bicuspid aortic valve disease, the most common congenital cardiac malformation, may initially be functionally normal or stenotic, but with time most develop significant stenosis and regurgitation.[1] Common associated lesions (e.g., perimembranous ventricular septal defect, coarctation of the aorta) should be sought (Fig. 41-10 ; see also Fig. 41-1 ). There is an associated tissue defect of the aortic wall with a tendency to ascending aortic dissection.[1] Surgical or balloon catheter valvuloplasty is often palliative in young adults, but it can induce significant aortic regurgitation.[1] Most patients ultimately require valve replacement.[1] Options include a mechanical or bioprosthetic valve (homograft or heterograft) or a Ross procedure. The

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Ross procedure (pulmonary autograft to the aortic position, heterograft or homograft to the pulmonary position, with or without reimplantation of the coronary arteries) appears to reduce the incidence of bioprosthetic degeneration in the aortic position, which in turn should decrease the number of reoperations, and it does not require anticoagulation. Bioprosthetic degeneration at the pulmonary valve position in an otherwise low-pressure right ventricle should be tolerated well though repeat operation is likely sometime. Replacement of a homograft in the pulmonary position is a relatively lowrisk procedure with excellent results in skilled hands. [1] The chief uncertainty regarding pulmonary root autografts in the aortic position is the potential for dilation of the wall of the pulmonary artery with continued exposure to systemic arterial pressure and the development of progressive "neoaortic" valvular regurgitation.[45] [46] [47] [48] Because the duration of myocardial ischemia is longer than that of a simple valve replacement, meticulous attention to myocardial preservation and to the method of coronary reimplantation is required. Precise measurement of the pulmonary and aortic annuli to ensure parity and demonstration of only mild or no pulmonary regurgitation are helpful in deciding on the Ross procedure. Intraoperative TEE can achieve these goals and verify valvular and myocardial function.[48] The coronary reimplantation sites should be evaluated for patency and normal flow.[1] Subaortic Stenosis Subaortic stenosis, most commonly owing to a discrete fibromuscular ridge, may be mild to severe ( see Fig. 41-1 and Fig. 41-4 ). It may complicate perimembranous ventricular septal defects before or after closure and, rarely, may appear in tetralogy of Fallot. Aortic valve regurgitation is more likely the closer the membrane is to the aortic valve. Excision of the membrane or fibromuscular ridge in association with focal septal myomectomy is the treatment of choice to reduce the likelihood of recurrence. If associated aortic regurgitation is moderate or less, surgical repair may avoid replacement. Intraoperative TEE verifies relief of obstruction, lack of mitral injury, absence of iatrogenic ventricular septal defect, and only mild or absent aortic regurgitation.[12] [13] [14] [15] Surveillance for recurrence with stenosis and development or progression of aortic regurgitation is mandatory. Coarctation of the Aorta

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There are many survivors of coarctation repair. Adults are still encountered in echocardiographic laboratories or found by those astute enough to perform the often 909

Figure 41-10 Intraoperative transesophageal echocardiography before (A) and after (B) aortic coarctation (COARCT) repair. In real time, the proximal portion was quite expansile with little systolic expansion of the distal segment until after repair by end-to-end anastomosis after primary resection. AO, aorta; DESC, descending; PROX, proximal.

overlooked examination for the brachial-to-femoral pulse delay in the presence of systemic arterial hypertension (see Fig. 41-10) . Repairs include resection of coarctation with end-to-end anastomosis (see Fig. 4110) , patch aortoplasty with a prosthetic patch, or subclavian flap aortoplasty. If the condition is symptomatic, repair is best performed in infancy; otherwise, timing is "elective" in the recognition that the later in life the repair is performed, the more likely there is to be persistent hypertension and accelerated coronary artery disease.[1] [49] Echocardiographic follow-up using suprasternal notch views for anatomic imaging of residual or recurrent coarctation narrowing or aneurysm formation is useful.[2] [50] Color flow imaging may show the zone of narrowing with proximal acceleration; pulsed wave Doppler can show the acceleration at the site of narrowing, but continuous wave Doppler is necessary to show the peak systolic gradient.[2] [49] [50] Continued diastolic forward flow through the zone of narrowing denotes significant obstruction (Fig. 41-11) .[2] [49] [50] [51] [52] [53] Exercise echo-Doppler studies are useful in the follow-up of repaired coarctation to evaluate for exercise-related hypertension and aortic gradients.[52] TEE is more effective than surface echocardiography in evaluating the extent and degree of coarctation. [12] [13] [14] Magnetic resonance imaging is superior to standard surface echocardiography for imaging the aortic isthmus after surgical repair.[53] [54] The Doppler peak systolic velocity in the descending aorta correlates better with residual narrowing of the aortic isthmus or distal aortic arch than does the systolic blood pressure gradient between the upper and lower limbs; peak velocities greater than 2.5 m per second effectively detect greater than 25% narrowing.[53] Prolongation of anterograde flow during diastole indicates a significant morphologic abnormality (e.g., restenosis or aneurysmal dilation).[53] Hirsch et al[6] compared single-plane and biplane TEE with magnetic resonance imaging in a variety of congenital

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malformations and showed that each was equally effective in their only two patients with aortic coarctation. Left ventricular hypertrophy and function should be quantified; associated left-sided obstructive lesions (e.g., bicuspid aortic valve, supramitral ring) must be sought.[2] [49] Postoperative endarteritis is rare but can result in a pseudoaneurysm. Balloon catheter dilation is often applied to recurrent or residual postoperative coarctation, but it is effective and safe in children with native coarctation.[54] Intravascular echocardiography or TEE during balloon dilation is useful to detect a dissection.[55] [56] Ebstein's Anomaly Ebstein's anomaly is characterized by apical displacement of the septal tricuspid leaflet with adherence of the Figure 41-11 (color plate.) Continuous wave Doppler through preoperative aortic coarctation (COARCT) on intraoperative transesophageal echocardiography in the patient in Figure 41-10 . The angle of incidence makes the systolic peak velocity ( 3 m per second) an underestimate of the true severity, but the continued diastolic run-off indicates significant aortic coarctation.

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septal and posterior tricuspid leaflets to the underlying myocardium, resulting in downward displacement of the functional annulus and an "atrialized right ventricular chamber" in its inflow portion.[1] [2] [57] The anterior leaflet often is redundant and may have abnormal fenestrations. The true tricuspid annulus is dilated; tricuspid regurgitation is usual. Comprehensive echocardiographic definition of the tricuspid anatomy usually is adequate for diagnosis and prediction of suitability for repair and avoids the need for preoperative catheterization.[57] Associated anomalies include patent foramen ovale, atrial septal defects—most commonly secundum, but other types such as sinus venosus atrial septal defect and partial anomalous pulmonary venous connection also are seen—pulmonary valve stenosis or atresia, ventricular septal defects, and tetralogy of Fallot. Left ventricular function can be decreased.[58] Ebstein's anomaly must be differentiated from acquired tricuspid regurgitation (e.g., endocarditis, right ventricular infarction, traumatic rupture of the tricuspid valve), atrial septal defect with a large left-to-right shunt, and right ventricular dysplasia or

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Uhl's anomaly.[2] [57] , [59] Distinguishing Ebstein's anomaly from right ventricular dysplasia or Uhl's anomaly is important because there is a significant difference in prognosis and in response to surgical treatment.[57] Tricuspid valve repair and annuloplasty with right ventricular plication and right atrial reduction are preferable to valve replacement.[60] An anterior leaflet that is elongated, untethered, and freely mobile is necessary for the best repair; conversely, a significantly dysplastic, tethered, or fenestrated valve is undesirable.[1] , [57] Intraoperative TEE should verify satisfactory reduction in tricuspid regurgitation yet minimal or no stenosis, as well as acceptable repair of any associated defects and adequacy of myocardial preservation. Pulmonic Stenosis Pulmonic stenosis may be at the subvalvular, valvular, or supravalvular level. Management requires elucidation of the severity and level of stenosis, as well as any associated abnormalities such as ventricular or atrial septal defects. [61] For isolated simple valvular pulmonic stenosis, balloon catheter dilation for relief of stenosis is virtually the norm at this time, albeit sometimes at the expense of increased pulmonary regurgitation and right ventricular enlargement.[61] [62] Some adults and adolescents are still encountered with previous surgical valvuloplasty. Follow-up of residual stenosis and pulmonary regurgitation is required.[2] [61] [62] [63] [64] Immediately after valvuloplasty the severely hypertrophied right ventricular outflow tract may develop significant dynamic subpulmonic stenosis manifest by late-peaking high velocities, which typically regress over time with beta blockers.[2] [61] Double-chambered right ventricle, a variation of subpulmonic stenosis, owing to aberrant muscle bundles at the junction of the inlet and outlet portions of the right ventricle proximal to the infundibulum, is often associated with ventricular septal defects and occasionally subaortic stenosis.[2] [61] [64] , [65] Only the inlet right ventricle is under pressure from the "pulmonic stenosis" and, despite hypertrophy of that portion, the electrocardiogram shows remarkably low-voltage right ventricular forces. [61] Resection of the obstructing muscle bundles is indicated when there is more than mild stenosis.[61] [65] Anomalies of the Coronary Arteries Anomalies of the coronary arteries include abnormal origin of the right, left main, or left coronary artery branches from one coronary cusp or the other,

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associated abnormal courses of the anomalous artery, and abnormal connections to other vessels or chambers (e.g., coronary arteriovenous fistula, anomalous origin of the left coronary artery from the pulmonary artery).[66] Some of these abnormalities are basically benign; others may result in myocardial ischemia, ventricular dysfunction, arrhythmias, and even sudden death.[66] Abnormalities of the course of the coronary arteries are also occasionally seen in tetralogy of Fallot and are common in transposition complexes; they are mainly important in relation to the technique of surgical repair.[66] Echocardiography, particularly TEE, has had some success in identifying abnormalities of coronary arteries.[2] [66] [67] [68] [69]

Anomalous origin of the left coronary artery from the pulmonary artery is often associated with myocardial ischemia, congestive heart failure, mitral regurgitation, and arrhythmias.[66] Surgical approaches have included simple ligation of the left coronary artery at its attachment to the pulmonary trunk, saphenous vein or internal mammary artery bypass grafting, direct reimplantation of the coronary to the aorta, and (via a surgically created aortopulmonary window) fashioning of a tunnel that directs blood flow from the aorta to the left coronary ostium.[66] Postoperative imaging of this connection in the operating room is necessary. Long-term echocardiographic evaluation includes quantitation of global and regional left ventricular function and degree of mitral regurgitation.

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Repair of "Complex" Malformations (Table 41-4) Atrial Switch Surgery Atrial switch surgery is the reason most adolescents and young adults born with complete transposition of the great arteries are alive today ( Fig. 41-12 and Fig. 41-13 ). [70] [71] [72] A combination of atrial septal tissue, pericardium, or synthetic material is used to fashion a baffle that reroutes systemic venous return to the subpulmonary morphologic left ventricle and pulmonary venous return to the subaortic morphologic right ventricle. The atrial cavity is therefore divided into two portions: an anterior chamber receiving the systemic venous return and a posterior chamber receiving the pulmonary venous return. Sequelae and complications include rhythm and conduction disturbances (see Fig. 41-12) , baffle leaks or obstruction ( Fig. 41-14 ; see also Fig. 41-13 ), vena caval and pulmonary venous obstruction, tricuspid regurgitation, and right ventricular dysfunction.[18] [70] [71] [72] [73] [74] [75] [76] [77] [78] [79] Residual defects may include pulmonic stenosis, left ventricular outflow tract obstruction, ventricular septal defect patch leaks, and pulmonary 911

TABLE 41-4 -- Corrective Procedures for "Complex" Malformations Lesion Transposition of the great arteries (TGA)

Corrective Procedure Atrial switch surgery (Mustard procedure)

Complications and Residual Abnormalities Rhythm and conduction disturbances Baffle leaks and obstruction Vena caval and pulmonary

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TGA

Tricuspid atresia or double-inlet single ventricle Atrioventricular canal defects

Tetralogy of Fallot

TGA with ventricular septal defect (VSD) and pulmonic stenosis

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Arterial switch procedure

Fontan repair (right atrium to pulmonary artery or right ventricle) Patching of atrial and/or ventricular septal defects combined with valve repair

VDS patch and relief of infundibular pulmonic stenosis

Rastelli repair (conduit from right ventricle to pulmonary artery with VSD patch directing subaortic flow)

venous obstruction Tricuspid regurgitation Right ventricular dysfunction Supravalvular pulmonic stenosis Supravalvular aortic stenosis (less common) Regional wall motion abnormalities of the left ventricle Cavoatrial shunting, atrial septal shunting, thrombus, right atrial to pulmonary artery obstruction Residual mitral regurgitation

Iatrogenic mitral stenosis Subaortic stenosis Patch leaks Pulmonic regurgitation

Right ventricular aneurysms (with older repairs) Residual right ventricular outflow obstruction Ventricular septal patch leaks VSD patch leak, subaortic obstruction

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TGA with VSD Damus-Kaye-Stansel and subaortic procedure stenosis Congenitally Various repairs, corrected TGA depending on associated defects

Double-outlet right ventricle

Rastelli repair

Prosthetic valve dysfunction VSD patch leak

Pulmonic regurgitation Left-sided atrioventricular valve regurgitation Heart block Systemic (anatomic right) ventricular systolic dysfunction Obstruction of left ventricular to aortic baffle Residual VSDs Obstruction in right-sided conduit

hypertension in those who underwent palliative Mustard procedures.[70] [71] [72] The long-term function of the right ventricle is a concern.[19] [70] [71] [72] [73] Echo-Doppler TTE from multiple windows (suprasternal, parasternal, apical, and subxiphoid) routinely allows visualization of the intra-atrial pulmonary venous and systemic venous portions of the atrial switch (see Fig. 41-12) .[70] [74] [75] [76] [77] [78] Presystolic flow reversal with atrial contraction into the hepatic venous confluence and superior vena cava provides indirect evidence of caval anastomotic patency. If echo contrast injected into a peripheral arm vein promptly enters the systemic venous atrium, the superior vena caval anastomosis is patent. In the obstruction at the superior vena caval connection, azygous or other venous collaterals to the inferior vena cava cause the contrast to first enter the inferior vena cava and then the systemic venous atrium. TEE is often needed for accurate detection of the site of baffle leaks and of the entrance site of all four pulmonary veins and for imaging of the caval junctions, particularly at the level of the inferior systemic venous baffle limb.[12] [13] [14] [80] Peripheral venous contrast injections detect baffle leaks.[76] With TEE, obstructed caval baffle, midbaffle, or pulmonary venous baffle ( see Fig. 41-13 and Fig. 41-14 ) sites are diagnosed by an increased peak velocity of continuous systolic and diastolic flow in combination with documented turbulent flow. [80] Sinus node dysfunction and atrial arrhythmias are frequent late

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complications.[70] [71] [72] Tricuspid regurgitation may occur with or without diminished right ventricular function, but once present it may contribute to right ventricular dysfunction. The long-term performance of the systemic right ventricle is often abnormal, especially in the ventricular septal defect repair subgroup.[18] [70] [71] [72] [73] Arterial Switch Surgery Because of the problems following atrial switch surgery, arterial switch surgery is now quite popular. Documentation of experience with postoperative echocardiography in adults who have undergone previous arterial switch operations is unavailable to my knowledge, but cardiologists must be prepared to encounter these patients as young adults in the near future. Postoperative echocardiography plays an important role in evaluating the arterial anastomoses. Supravalvular pulmonary stenosis is the most frequent complication of arterial level repair, supravalvular aortic stenosis less so; false aneurysm formation and endarteritis have also been described.[81] [82] [83] [84] [85] The status of the neoaortic (anatomic pulmonary) root and valve is a long-term concern. [70] Neoaortic regurgitation, although usually trivial to mild, can be significant, and long-term evaluation is required.[86] [87] [88] [89] Hourihan et al[89] noted normal growth of the anastomosis and stable growth of the dilated neoaortic annulus but progressive dilation of the neoaortic root. Similarly, the long-term growth and patency of the reimplanted coronary arteries are crucial.[70] Preoperative echocardiographic evaluation of proximal coronary anatomy in infants with d-loop transposition has become quite precise.[90] [91] Patency of the proximal coronary arteries can be confirmed by intraoperative echocardiography. [92] Myocardial perfusion defects are relatively common after an arterial switch operation; however, these generally lessen with exercise and are of unknown significance because the children have normal exercise tolerance without symptoms or change in electrocardiographic pictures.[93] Echocardiographic regional wall motion 912

Figure 41-12 d-transposition of the great arteries and intra-atrial baffle procedure (Mustard operation). Transthoracic echocardiography fourchamber views aligned to demonstrate the pulmonary venous atrium (PVA) (A) and the systemic venous atrium (SVA)(B) in an adult woman with conduction defects and a pacemaker (PM) placed many years after the Mustard procedure. The baffles and venous connections were unobstructed. The right

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ventricle (RV) was dilated with mildly dilated RV ejection fraction (EF) (40%). DA, descending aorta; LV, left ventricle; LSPV, left superior pulmonary vein; MV, mitral valve; PVA, pulmonary venous atrium; SVA, systemic venous atrium; TV, tricuspid valve. "Recovery" indicates image obtained after stress echocardiography to evaluate for ventricular function (improved RVEF to 45%).

abnormalities have been seen after two-stage repairs and correlate with myocardial perfusion defects.[94] Total Anomalous Pulmonary Venous Connection Total anomalous pulmonary venous connection is due to lack of development of communication of the common pulmonary vein and the left atrium. Most adults arrive already diagnosed and corrected with connection of the common pulmonary vein to the left atrium and closure of the obligatory atrial septal defect. After repair of total anomalous venous connection, color flow and pulsed Doppler provide useful information regarding the presence of pulmonary venous obstruction.[95] [96] Fontan Atrial Surgery Fontan atrial surgery is used in cases in which biventricular connections are not usually possible (e.g., tricuspid atresia or double-inlet single ventricle or complex straddling of atrioventricular valves, often in association with crisscross relationships or superoinferior ventricles), whereby two functioning ventricles cannot be effectively Figure 41-13 Transesophageal echocardiography (TEE) in the cardiac catheterization laboratory in a young man with hemoptysis and pulmonary venous congestion caused by pulmonary venous baffle obstruction in a Mustard procedure for d-transposition of the great arteries. A, TEE view of the stenosed pulmonary venous connection to the right atrium (RA) and right ventricle. The aorta is anterior and rightward of the main pulmonary artery (MPA). B, Continuous wave Doppler through the stenosis shows continuous flow obstruction with accentuation during diastole.

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Figure 41-14 Catheter intervention transesophageal echocardiography of stent dilation of a Mustard pulmonary venous baffle obstruction in the patient in Figure 41-13 . PVA, pulmonary venous atrium; RA, right

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atrium.

established. The several variants of the Fontan repair all result in complete or near-complete (hemi-Fontan) separation of the pulmonary and systemic circulations in patients not eligible for biventricular repair.[1] [97] The right atrium is an integral part of the Fontan anatomy and can be anastomosed directly to the pulmonary artery or to the small right ventricle; a lateral tunnel or extracardiac conduit may use the lateral wall of the right atrium to bring the inferior vena cava to the main pulmonary artery or to the orifice of the superior vena cava, which has been attached to the (usually) right pulmonary artery to result in a total cavopulmonary connection.[1] In a double-inlet single ventricle a direct atriopulmonary connection with patch exclusion of the right atrioventricular valve was a common modification of the Fontan procedure. Patch exclusion may result in right atrioventricular valve regurgitation. Postoperative development of subaortic stenosis (Fig. 41-15) (at the bulboventricular foramen in single ventricle, at the subaortic conus in tricuspid atresia with transposed great arteries) must be sought.[98] The most common complications in the atrial portion of the Fontan circulation include cavoatrial shunting, atrial septal shunting, thrombus (Fig. 41-16) , and right atrium to pulmonary artery obstruction.[12] [13] [14] [98] [99] [100] Surgical sequelae purposely left behind in high-risk patients include atrial fenestrations and adjustable atrial septal defects.[12] [13] [14] [97] , [98] Right atrial to right ventricular conduits sometimes can be assessed with appropriate precordial examination, whereas right atrial to pulmonary anastomotic sites often are not completely visualized. In a series of 18 patients (mean age, 13 years) the success rate of visualization of various forms of Fontan anastomoses was 86% with single-plane TEE versus 48% with TTE.[99] TTE diagnosed only 31% of the complications detected by TEE.[99] Using biplane or multiplane TEE, we have consistently imaged the anatomy of the Fontan anastomosis, although not always with the necessary alignment to allow accurate spectral Doppler assessment of peak velocity profiles.[12] [13] [14] The classic right atrial to pulmonary arterial anastomosis is better seen with a vertical plane equivalent (Fig. 41-17) , whereas the old right atrial to right ventricular anastomosis is better seen with a horizontal plane equivalent. Lateral tunnel total cavopulmonary anastomoses require both planes for complete evaluation. In the Fontan patient, an important determinant of outcome is the function of the systemic ventricle and its atrioventricular valve, both of which are usually readily evaluated by echo-Doppler TTE studies.[2] [98] TEE is useful when directed at suspected complications or known residua of the Fontan

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atrial anatomy (baffle shunts, thrombi, stenotic connections). [12] [13] [14] Figure 41-15 Subaortic stenosis (SAS) in right atrial (RA)–pulmonary artery Fontan connection. A, Transthoracic parasternal view of SAS caused by significant subaortic hypertrophy from ventricle (VENT) to aortic valve (AV). B, Continuous wave Doppler through the SAS at 3.27 m per second (pressure gradient, 42.7 mm Hg) is at an extreme angle of incidence and thus is an underestimate of the true degree of SAS. LA, left atrium.

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Figure 41-16 Transesophageal echocardiography (TEE) detection of thrombus in right atrial (RA)–pulmonary artery Fontan connection in a univentricular heart with patch exclusion of the RA. This young woman with a univentricular heart had developed paroxysmal atrial flutter and ventricular systolic dysfunction. TEE was performed before cardioversion and possible radiofrequency ablation.

With no functioning subpulmonary right ventricle in most patients with the Fontan repair, pulmonary artery flow patterns resemble those with parchment right ventricle or Uhl's anomaly, that is, a biphasic flow pattern with diastolic velocities equal to or greater than systolic, with particular accentuation of diastolic velocity at the time of right atrial contraction.[59] [101] [102] [103] Inspiration augments pulmonary artery flow velocities, and pulmonary and systemic venous flow profiles remain relatively normal in patients with normal left (or single) ventricular function. Abnormal systemic ventricular performance is reflected in a reduced pulmonary arterial flow pattern velocity with decreased change on inspiration and a predominantly systolic profile. Intraoperative TEE is used to ensure patent connections (see Fig. 41-17) and to help size any surgical atrial septal defect, a common procedure in lateral tunnel total cavopulmonary anastomoses at UCLA.[24] [97] Postoperative TEE may be required in the intensive care unit in patients with Fontan repair to search for known complications (e.g., increasing pulmonary artery pressures with decreased cardiac output and "right heart failure" owing to lateral tunnel Fontan thrombus embolization).[12] [13] [14] [99] , [100] TEE also can be used in the interventional catheterization laboratory to guide postoperative closure of surgical atrial septal defects.[98]

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Atrioventricular Canal Defects Atrioventricular canal defects are a group of anomalies that share a defect at the site of the atrioventricular septum and abnormalities of the atrioventricular valves.[104] They are considered complex lesions because of the usual association of two or more abnormalities. These defects may be partial (partial endocardial cushion or primum atrial septal defects, cleft mitral leaflet, and/or inlet ventricular septal defect) or complete and usually were corrected in childhood or adolescence, although they may be first diagnosed de novo in adults. [2] [104] The usual form found in adults is a defect of the primum portion of the atrial septum (see Fig. 41-9) with an associated cleft of the anterior mitral leaflet, with abnormal attachments to the left ventricular outflow tract and variable degrees of mitral regurgitation. Repair requires patching of the primum atrial septal defect and repair of the mitral valve. Complete atrioventricular canal defects, rarely first diagnosed in adults, are seen in patients surviving to adulthood after repair in childhood. The complete defect is Figure 41-17 Intraoperative transesophageal echocardiography in right atrial–to–pulmonary artery (RA-PA) Fontan connection (A with conversion to an intracardiac lateral tunnel cavopulmonary connection (B). A young man with univentricular heart with double-inlet left ventricle had a RA-PA Fontan a decade earlier, now undergoing "conversion" to a lateral tunnel "Fontan" because of intractable atrial arrhythmias. IVC, inferior vena cava; LA, left atrium; MPA, main pulmonary artery; PA, pulmonary artery; RA, right atrium; RAA, right atrial appendage.

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characterized by a large septal defect with interatrial and interventricular components, and by a common atrioventricular valve that connects both atria and both ventricles. [104] Echocardiographic follow-up examines the adequacy of mitral repair, with attention to the degree and progression of mitral regurgitation, and assessment for the presence of iatrogenic mitral stenosis and subaortic stenosis.[2] [3] Subaortic stenosis result from a discrete fibromuscular narrowing or the usual abnormal left ventricular outflow tract attachments of anomalous chords and leaflet tissue, or it may develop postoperatively because of reduction of left ventricular outflow size as the cleft in the mitral leaflet is apposed.[105] [106] Because of combined preoperative right and left

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ventricular volume overload, the size and function of both ventricles must be quantified postoperatively. Occasionally, tricuspid regurgitation can be substantial and tricuspid valvular repair requires postoperative evaluation. In addition, in complete atrioventricular canal repairs, investigation of the ventricular septal defect patch is necessary. Some of these patients, especially those with Down's syndrome, may have significant pulmonary vascular disease, and pulmonary artery pressure should be quantified using the tricuspid and pulmonary regurgitant jets. To minimize significant residual defects (e.g., valvular regurgitation, patch leaks), intraoperative TEE should be used.[12] [13] [14] [15] [107] Biventricular Repairs Biventricular repairs result in two well-formed functional ventricles with a subpulmonic ventricle and a subaortic ventricle that are able to provide circulation in series without admixture of venous and systemic blood.[108] [109] Most complex congenital cardiac malformations amenable to biventricular repair are cyanotic and consist of a mixture of septal defects; obstructive and regurgitant valvular, subvalvular, or supravalvular lesions; and malpositions of the cardiac chambers and great arteries.[108] , [109] Anatomic substrates that are typical candidates include tetralogy of Fallot ( Fig. 41-18 ; see also Fig. 41-2 , Fig. 41-3 , Fig. 41-4 , Fig. 41-5 ), pulmonary atresia with ventricular septal defect, transposition complexes of the great arteries (Fig. 41-19) , and double-outlet ventricles. The basic theme includes patch closure of a ventricular septal defect and reconstitution of ventricular to pulmonary arterial blood flow. If pulmonic stenosis cannot be directly repaired for anatomic or conduction system reasons, the pulmonary artery must be ligated or the valve oversewn and a ventricular to pulmonary arterial conduit placed. Long-term postoperative survival is affected by age at operation, degree of relief of the loading conditions imposed on the ventricular myocardium, myocardial protection during operation, electrophysiologic sequelae, and the durability of prosthetic materials, especially valved or nonvalved conduits. [1] [108] , [109] Tetralogy of Fallot Tetralogy of Fallot, the prototype of complex congenital heart disease, is one of the most common complex Figure 41-18 Intraoperative transesophageal echocardiography (TEE) in tetralogy of Fallot after intracardiac repair before pulmonary valve

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replacement and right pulmonary artery stenosis repair in the patient from Figure 41-2 and Figure 41-3 . A, TEE four-chamber equivalent view shows the ventricular septal defect (VSD) patch and the overriding aortic valve (AV). LA, left atrium; LV, left ventricle; MV, mitral valve; RV, right ventricle. B, Stenosis of the right pulmonary artery (RPA) is a consequence of a previous right Blalock-Taussig shunt. SVC, superior vena cava.

congenital malformations occurring with cyanosis at birth in which patients live to adulthood because of the length of time that palliative and corrective procedures have been available.[1] [110] It is a complex caused by anterior deviation of the outlet septum with associated infundibular narrowing and a malaligned ventricular septal defect.[1] [2] [108] [109] [110] Echocardiography demonstrates aortic override of a malaligned ventricular septal defect in conjunction with a spectrum of obstructive lesions of the right ventricular outflow tract and pulmonary artery, varying from mild to complete pulmonary atresia.[2] [3] [4] [108] [109] [110] There are numerous associated defects, ranging from common to rare, that must be identified for proper surgical and postoperative management.[110] For example, there may be associated 916

Figure 41-19 d-transposition of the great arteries (D-TGA) late after a Rastelli procedure. A, Deep transgastric transesophageal echocardiography (TEE) shows a patent left ventricle (LV) intracardiac conduit connection and ventricular septal defect patch to the aorta and aortic valve (AV), which originally arose from the right ventricle (RV). B, TEE aligned through the RV–to–pulmonary artery (PA) conduit. TV, tricuspid valve; VS, ventricular septum.

atrial septal defects, endocardial cushion abnormalities, Ebstein's malformation of the tricuspid valve, additional muscular ventricular septal defects, an absent pulmonic valve, absent left pulmonary artery or abnormal origin of one pulmonary artery from the aorta, pulmonary atresia, systemic and pulmonary venous anomalies, discrete subaortic stenosis (see Fig. 41-4) , right-sided aortic arch, aortopulmonary window, aortopulmonary collaterals, and coronary artery anomalies.[110] [111] [112] [113] [114] [115] [116]

In general, repair of tetralogy of Fallot includes closure of the ventricular septal defect with a patch ( see Fig. 41-2 , Fig. 41-4 , Fig. 41-5 and Fig. 4118 ) and a right ventricular outflow tract incision (see Fig. 41-2) to relieve infundibular stenosis.[108] [109] [110] The right ventricular incision at times must extend through the pulmonary annulus, which may then receive a

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transannular patch. Pulmonary valve, trunk, or branch artery stenosis should be relieved (see Fig. 41-18) if there is extreme pulmonic stenosis or pulmonary atresia, or, as in truncus arteriosus, a conduit (usually valved) connects the right ventricle to the pulmonary artery ( see Fig. 41-6 and Fig. 41-7 ). After intracardiac repair of tetralogy of Fallot, the long-term postoperative concerns focus on the right ventricle and its outflow tract ( see Fig. 41-2 and Fig. 41-3 ), the pulmonic valve and pulmonary artery ( see Fig. 41-2 , Fig. 41-3 , and Fig. 41-18 ), the left ventricle (see Fig. 414) , the aortic valve, and electrophysiologic residua and sequelae (see Fig. 41-4) .[2] [108] [109] [110] When intracardiac repair is performed in the first 5 years of life, late postoperative right ventricular function remains normal in the absence of significant right ventricular outflow obstruction, provided that postoperative low-pressure pulmonic valve regurgitation is only mild to moderate.[1] [2] [18] Severe pulmonic regurgitation ( see Fig. 41-3 and Fig. 414 ) may cause right ventricular dilation and failure, and tricuspid regurgitation, particularly if there is any residual right ventricular outflow tract, pulmonary valve, or pulmonary artery (e.g., branch stenosis) obstruction (see Fig. 41-18B) . Postoperative right ventricular outflow tract scars and aneurysms, uncommon when current surgical techniques are employed for tetralogy of Fallot, may be present in patients operated on in the past (see Fig. 41-2A) . Two-dimensional echocardiographic and color flow imaging with continuous wave Doppler are used to examine the right ventricular outflow and pulmonary artery anatomy for obstruction; continuous wave Doppler tricuspid regurgitant jet velocities reflect right ventricular systolic pressure.[2] [108] Ventricular septal patch leaks, usually eccentric in location, may occur anywhere along the patch and require color flow imaging for accurate detection (see Fig. 41-5) .[2] [4] [108] If right ventricular outflow tract or pulmonary artery (main trunk, branches) obstruction is inadequately relieved by operation, particularly if there is a significant residual ventricular septal defect, the resultant right ventricular pressure overload superimposed on the ventriculotomy scar can cause ventricular arrhythmias or sudden death.[1] [2] [108] [109] [110] Isolated right ventricular restrictive physiology late after repair of tetralogy of Fallot or truncus arteriousus is common as detected by Doppler hemodynamics ( see Fig. 41-3 and Fig. 41-7 ). [116] The A wave contributes to forward pulmonary flow and shortens the duration of pulmonary regurgitation, resulting in less right ventricular enlargement and better exercise tolerance.[116] When severe pulmonary regurgitation results in impaired exercise performance (increasing right ventricular size with decreasing right ventricular systolic

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function and increasing tricuspid regurgitation), pulmonary valve replacement is necessary. Aerobic capacity has been shown to improve after pulmonary valve replacement for severe pulmonary regurgitation after previous repair of tetralogy of Fallot even if the right ventricular size and function does not.[117] Late postoperative left ventricular function (see Fig. 41-4) in tetralogy of Fallot is related to age at the time of intracardiac repair and to previous volume overload from palliative shunt procedures.[18] Patients with severe cyanotic tetralogy of Fallot have decreased left heart volumes and decreased left ventricular ejection fractions 917

related to the reduction in pulmonary arterial blood flow.[1] [18] Intraventricular repair undertaken in the first 2 years of life allows left ventricular mass and volume to normalize. If intracardiac repair is undertaken after 2 years of age, left heart volumes increase but left ventricular function remains subnormal.[18] In lesions associated with a dilated aortic root or trunk (e.g., tetralogy of Fallot, transposition of the great arteries, or single ventricle in association with pulmonic stenosis), aortic regurgitation is common and at times has resulted in biventricular failure.[2] [108] [109] [110] [117] Any combination of persistent ventricular septal defect patch leaks, ventricular to pulmonary outflow obstruction, and significant valvular regurgitation may cause serious ventricular overload. Inadequate operative myocardial preservation or the preexistence of volume overload (as with large palliative shunts before more complete hemodynamic repair) may cause ventricular failure over the long term. Common Transposition of the Great Arteries Transposition complexes may be generally categorized as having each great artery arising from the wrong ventricle (ventriculoarterial discordance). This definition is independent of the spatial relationships of the great arteries and the presence or absence of a subaortic infundibulum.[109] In common transposition of the great arteries, each atrium connects to its anatomically appropriate ventricle (atrioventricular concordance), but that ventricle gives rise to an anatomically inappropriate great artery (ventriculoarterial discordance).[70] [109] The aorta arises from the right ventricle (with aortic-mitral discontinuity) and usually sits right of and anterior to the pulmonary artery, which emerges from the left ventricle.

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This situation results in two separate and parallel circulations, and some communication between the two circulations must exist or be made iatrogenically after birth to sustain life. In transposition complexes, combined two-dimensional echocardiography and color flow imaging must define the course of each of the great arteries and (1) identify the size and location of a ventricular septal defect, (2) confirm the presence and severity of pulmonic stenosis, (3) detect other shunts, and (4) evaluate the presence and severity of valvular regurgitation. [2] [109] Dynamic subvalvular pulmonic stenosis can be due either to systolic anterior motion of the mitral leaflet into the outflow tract or to dynamic subpulmonic septal contraction with obstruction versus fixed subvalvular stenosis. The pulmonary valve also may be malformed, resulting in obstruction. The location of the obstruction affects surgical planning; if not addressed, residual pulmonary outflow obstruction contributes to postoperative morbidity and mortality. [70] [109] The long-term outcome of surgical intervention for common transposition of the great arteries, ventricular septal defect, and pulmonic stenosis depends on the technique of intracardiac repair.[1] [70] [109] In the past, most patients underwent intra-atrial baffle procedures (e.g., Mustard procedure [ see Fig. 41-12 , Fig. 41-13 , Fig. 41-14 ]), resulting in persistence of an anatomic right ventricle and tricuspid valve in the systemic circuit (see earlier). More recently, arterial switch surgery has been widely used with the potential advantage that the anatomic left ventricle becomes the systemic ventricle. The Rastelli repair, whether for transposition complexes or for doubleoutlet right ventricle with ventricular septal defect and pulmonary stenosis, consists of an external conduit from right ventricle to pulmonary artery and an intraventricular conduit to route the left ventricle to the aorta via the ventricular septal defect ( see Fig. 41-6 , Fig. 41-7 , Fig. 41-19 ). An internal intraventricular conduit may develop a patch leak or internal obstruction owing to kinking, or it may partially obstruct the chamber through which it transits. Long-term concerns include the durability of a bioprosthesis, the patency of conduits, ventricular septal defect patch leaks, and continuing postoperative electrophysiologic residua and sequelae.[70] [109] The Damus-Kaye-Stansel procedure is a form of biventricular repair when applied to common transposition with a ventricular septal defect without pulmonic stenosis but with subaortic stenosis.[70] [109] This technique, also used in single ventricle with subaortic stenosis owing to bulboventricular

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foramen obstruction, consists of an end-to-side anastomosis of the proximal pulmonary artery to the side of the aorta, with oversewing of the aortic valve or proximal aorta; the septal defect is patched. Imaging of the pulmonary arterial to aortic anastomosis establishes lack of obstruction. The right ventricle is connected to the distal main pulmonary artery, now separated from the proximal main pulmonary artery, by a valved conduit. Search is made for pulmonary regurgitation, and the septal patch is checked for leaks. Long-term follow-up is limited.[70] Congenitally Corrected Transposition of the Great Arteries Congenitally corrected transposition of the great arteries consists of both atrioventricular discordance (the right atrium enters the left ventricle via a mitral valve, the left atrium enters the right ventricle via a tricuspid valve) and ventriculoarterial discordance (the left ventricle gives rise to the pulmonary artery, the right ventricle gives rise to the aorta).[109] [118] Echocardiographic attention to the crux anatomy reveals the left atrioventricular valve to be more apically placed than the right atrioventricular valve, identifying them as tricuspid and mitral, respectively. Because the atrioventricular valves follow their ventricles, they identify the left-sided (systemic) ventricle as the anatomic right ventricle and vice versa. The aorta can be seen to exit the right ventricle leftward, anterior, and superior with the left ventricle connecting to a rightward, posterior, and inferior pulmonary trunk, particularly with good short-axis parasternal views or careful, angulated apical or subcostal views. [109] [118] Associated anomalies include (1) atrial septal defects; (2) an Ebstein-like malformation of the left-sided atrioventricular valve (anatomically tricuspid), with consequent left-sided atrioventricular valve (tricuspid) regurgitation that is physiologically equivalent to mitral regurgitation; (3) ventricular septal defects; (4) pulmonic stenosis at the subvalvular (fixed or dynamic), valvular, or supravalvular level; (5) subaortic obstruction; 918

(6) aortic stenosis or regurgitation; and (7) coarctation of the aorta.[109] [118] [119] Subaortic or aortic arch obstruction is particularly likely to be associated with an Ebstein malformation of the left atrioventricular valve with severe regurgitation.[118] [120] A large ventricular septal defect, with or without pulmonic stenosis or

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systemic atrioventricular valve regurgitation, prompts consideration of an intraventricular operation. A variant of the Rastelli procedure (see earlier) may be used in congenitally corrected transposition of the great arteries with a ventricular septal defect and subvalvular pulmonary stenosis. The left ventricle is connected to the pulmonary artery via a valved conduit, whereas the right ventricle supplies the aorta once the ventricular septal defect is patched.[109] [118] In such a case, the pulmonary valve or proximal pulmonary artery is ligated; the subpulmonary stenosis is often not resected because of the high incidence of complete heart block.[109] [118] Patients who survive may achieve good functional results, although the three major concerns that materially influence long-term postoperative survival are (1) development of left atrioventricular valve regurgitation, (2) a high incidence of heart block induced by operation, and (3) a progressive decrease in function of a morphologic right ventricle in the systemic location.[1] [109] [118] , [119] Atrioventricular valve regurgitation is common preoperatively, is difficult to repair (often requiring replacement instead), may progress postoperatively, poses a continuing risk of endocarditis, and may affect long-term ventricular performance.[1] , [109] Double-Outlet Right Ventricle Double-outlet right ventricle is a heterogeneous category of defects. The common feature is that both great arteries are committed to the right ventricle (or at least one is totally committed to the right ventricle and the other overrides a malaligned ventricular septal defect with greater than 50% commitment to the right ventricle).[121] The ventricular septal defect can be committed to the aorta (subaortic, infracristal), to the pulmonary artery (subpulmonic, supracristal), to both (doubly committed, subarterial), or to neither, which affects the streaming characteristics of blood, the degree of cyanosis, and the capacity for and type of repair. The presence or absence of pulmonary stenosis or increased pulmonary vascular resistance is a determinant of outcome. Double-outlet right ventricle with a subpulmonary ventricular septal defect and a right ventricular or biventricular pulmonary trunk (Taussig-Bing anomaly) may clinically resemble complete transposition of the great arteries with a nonrestrictive ventricular septal defect. Cyanosis is usually mild initially but progresses as pulmonary vascular resistance rises. Favorable regulation of pulmonary blood flow occasionally establishes adequate but not excessive flow, with consequent amelioration of left ventricular volume overload. Echocardiography for double-outlet right ventricle must address the spatial

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relationships between the great arteries, the outflow tract for each artery, the location and type of ventricular septal defect, and the relationship of that defect to the great arteries.[109] [122] Associated anomalies must be sought (e.g., abnormalities of situs, of the ventricles, and of the atrioventricular canal). The Rastelli repair for double-outlet right ventricle with subaortic ventricular septal defect and pulmonic stenosis consists of an external conduit from right ventricle to pulmonary artery and an intraventricular conduit to route the left ventricle to the aorta via the ventricular septal defect.[109] [121] The intraventricular course of the left ventricular to the aortic baffle can be quite long, and kinking or obstruction may occur; this is best evaluated intraoperatively with TEE.[12] [13] [14] [15] [122] A valved conduit from right ventricle to pulmonary artery may develop obstruction. In some patients with double-outlet right ventricle of a tetralogy of Fallot-type with normally related great arteries and a subaortic ventricular septal defect, the repair may use a septal patch and primary repair of the site of pulmonic stenosis without resort to a conduit.[13] [109] Residual defects in the ventricular septum or around the patch may be more frequent in repair of double-outlet right ventricle than in tetralogy of Fallot, presumably because the distance from the ventricular septal defect to the aorta is greater and more complex as a result of both the proximity of tricuspid valve tissue and anomalies of the ventricular septal musculature. "Intramural" residual interventricular defects seen after repair of conotruncal malformations, most commonly double-outlet right ventricle, are found around the anterior portion of the patch between the neosystemic outflow tract and right ventricle, and they require careful color flow imaging to detect.[123] In such cases, umbrella placement has reduced the shunt; successful surgical closure may necessitate removal and reattachment of the anterior portion of the patch.[123]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Since the 1940s, tremendous strides in surgical and medical management have allowed many patients with congenital heart disease to reach adulthood. Most echocardiographic laboratories that focus on adults in general are unprepared to examine the full range of adults with previously repaired congenital heart disease. To do so requires detailed knowledge of (1) the anatomic and hemodynamic faults of the original defect; (2) the types of operative repair (both past and present) available for each complex of lesions; (3) the potential residua, sequelae, and complications of the "old" and "new" repairs; and (4) the imaging and hemodynamic modalities most useful for elucidation of the operated heart. The patient with postoperative congenital heart disease requires comprehensive two-dimensional TTE and color flow imaging and spectral Doppler study. Goals include the evaluation of chamber sizes and myocardial function, detection and quantitation of stenosis (valvular, subvalvular, or supravalvular) and valvular regurgitation, and quantitation of intracardiac hemodynamics. The patency of external and internal conduits, residual shunts, atrial baffle function, and pulmonary and systemic venous obstruction must be determined. TTE must at times be supplemented by TEE and magnetic resonance imaging. Intraoperative echocardiography has become an integral 919

part of congenital heart disease surgery. It allows detection of previously unknown malformations, refinement of existing anatomy, detection of unsatisfactory surgical results to allow intraoperative revision, and immediate documentation of postoperative residua and sequelae.

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Section 9 - The Echocardiography Laboratory

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Chapter 42 - Education and Training of Physicians and Sonographers Edward F. Gibbons MD Carol Kraft RDCS

Education and training in echocardiography require more than just matriculation in the cognitive and technical skills of echocardiography. The student of echocardiography must also acquire an appreciation for the appropriate context of echocardiography in meeting cardiology service needs, meeting diagnostic and disease management challenges, and providing cost-effective medical care. The fully proficient echocardiography laboratory director must come to his or her position with additional skills, including a practical business sense, leadership talent in managing a diverse staff, and a practiced understanding of how and when to introduce new technology and methodology based on the results of emerging research. The curriculum of training in echocardiography that this chapter outlines assumes a broader professional scope than would be implied by the rote

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performance of a cardiac test. The consensus panels that have published the training recommendations outlined here have emphasized the professional components of the clinical practice of echocardiography. The trainee in echocardiography must also understand the basic elements of a working laboratory, the structure of which will facilitate both clinical care and clinical learning.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Structure of the Echocardiography Laboratory Personnel An echocardiography laboratory of any size (Fig. 42-1) needs a medical director function, a sonographer function, 924

Figure 42-1 Organizational components of an echocardiography laboratory.

a nursing function, a data collection and archiving function, a reportgenerating function, and a "public relations" function for interaction with patients, referring physicians, and local administration. In an academic setting, trainees at various levels are included in the work flow, and separate educational, supervisory, and testing functions must be provided. Acquisition of Clinical and Echocardiographic Data Over just 30 years, echocardiography has evolved from a technology with limited application to the most common cardiac test ordered after electrocardiogram. [1] [2] The echocardiography laboratory has functionally replaced the stethoscope for most subtleties of cardiac auscultation and has also replaced significant elements of the cardiac catheterization laboratory in the assessment of hemodynamics, valvular and congenital heart disease, ischemic coronary disease, cardiomyopathy, and pericardial disease.[3] [4] [5] The echocardiography laboratory in any moderate-size to large hospital or clinic performs at least 1000 echocardiographic studies per year and has

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become a significant conduit for the recognition of cardiac disease, a triage source for further cardiology consultation, and a readily usable technique for evaluation of subsequent medical and surgical treatments. As a result, the efficiency and quality of the echocardiographic laboratory play a central role in the efficiency and quality of cardiology services in general. The responsibilities that accompany such a central role, therefore, include (1) a clear understanding of the evidence-based clinical applications of echocardiography,[6] [7] [8] (2) a clear communication path to understanding what clinical question is being asked,[9] [10] [11] [12] [13] [14] [15] [16] [17] (3) the best echocardiographic approach to obtaining an answer to the clinical question posed, and if not echocardiography, what imaging technique, (4) a format of reporting that can provide a cogent, clinically relevant, and complete summary of echocardiographic findings to the referring clinician. Recently, regional and national regulatory agencies associated with the Health Care Finance Administration (HCFA) and Medicare have charged echocardiography laboratories with the responsibility of recognizing reimbursable cardiac diagnoses (ICD-9 codes) for echocardiography and for notifying the patient undergoing an echocardiographic study if the referring diagnosis is not covered by insurance.[18] [19] Yet the performance of an echocardiographic examination has as much to do with ensuring the quality of the examination performed as with defining the appropriate clinical context in which it is performed. In the United States and Canada, unlike the practice in many European countries, most echocardiographic studies are performed by skilled cardiac sonographers rather than by cardiologists themselves. The burden of complying with professional, institutional, and governmental guidelines and regulations, therefore, falls as much to cardiac sonographers as it does to cardiologist medical directors of echocardiography laboratories. Already, measures have been proposed in several state legislatures to require stricter laws governing payment for radiologic and echocardiographic studies, and to link payment to laboratory credentialing and accreditation.[20] Thus, the professional scope of the sonographer and the cardiologistechocardiographer will likely become more inextricably linked, not just by habit, but also by governmental fiat. To this end, it is important to review the current recommendations for the training and education of both physicians and sonographers: for the beginner to know the breadth of his or her task ahead, and for the advanced practitioner to update his or her portfolio or laboratory profile.

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Data Management The complexity of the echocardiographic examination has expanded to such a degree that most busy laboratories must have computer resources to manage patient demographic data and qualitative and quantitative data output regarding M-mode, cross-sectional, Doppler, and stress testing data. Moreover, echocardiography laboratories must have an efficient format for standard study protocols, sonographer-cardiologist preliminary communication via worksheet or direct personal collaboration, study final report and proofreading, and archiving of original data, images, and reports. The coordination and streamlining of this complex process via the digital echocardiography laboratory is now being realized (see Chapter 44) . Communication of Test Results

925

In practical terms, the value of the final report from an echocardiographic study is only as good as the communication that precedes it and the quality of the clinical inquiry that follows the study. In many clinical settings, the echocardiogram provides the basis for formal, and often informal "curbside," consultation. To the extent that an echocardiography laboratory is "open to visitors" for direct inspection of images and discussion of nuances of interpretation, and has the capacity for ready access to the primary image and calculation data, these consultations and the echocardiographic studies will be made valuable. Undoubtedly, the efficiency and potential for image transfer provided by the digital echocardiographic laboratory will enhance these functions.

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Structure of the Echocardiography Laboratory Personnel An echocardiography laboratory of any size (Fig. 42-1) needs a medical director function, a sonographer function, 924

Figure 42-1 Organizational components of an echocardiography laboratory.

a nursing function, a data collection and archiving function, a reportgenerating function, and a "public relations" function for interaction with patients, referring physicians, and local administration. In an academic setting, trainees at various levels are included in the work flow, and separate educational, supervisory, and testing functions must be provided. Acquisition of Clinical and Echocardiographic Data Over just 30 years, echocardiography has evolved from a technology with limited application to the most common cardiac test ordered after electrocardiogram. [1] [2] The echocardiography laboratory has functionally replaced the stethoscope for most subtleties of cardiac auscultation and has also replaced significant elements of the cardiac catheterization laboratory in the assessment of hemodynamics, valvular and congenital heart disease, ischemic coronary disease, cardiomyopathy, and pericardial disease.[3] [4] [5] The echocardiography laboratory in any moderate-size to large hospital or clinic performs at least 1000 echocardiographic studies per year and has

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become a significant conduit for the recognition of cardiac disease, a triage source for further cardiology consultation, and a readily usable technique for evaluation of subsequent medical and surgical treatments. As a result, the efficiency and quality of the echocardiographic laboratory play a central role in the efficiency and quality of cardiology services in general. The responsibilities that accompany such a central role, therefore, include (1) a clear understanding of the evidence-based clinical applications of echocardiography,[6] [7] [8] (2) a clear communication path to understanding what clinical question is being asked,[9] [10] [11] [12] [13] [14] [15] [16] [17] (3) the best echocardiographic approach to obtaining an answer to the clinical question posed, and if not echocardiography, what imaging technique, (4) a format of reporting that can provide a cogent, clinically relevant, and complete summary of echocardiographic findings to the referring clinician. Recently, regional and national regulatory agencies associated with the Health Care Finance Administration (HCFA) and Medicare have charged echocardiography laboratories with the responsibility of recognizing reimbursable cardiac diagnoses (ICD-9 codes) for echocardiography and for notifying the patient undergoing an echocardiographic study if the referring diagnosis is not covered by insurance.[18] [19] Yet the performance of an echocardiographic examination has as much to do with ensuring the quality of the examination performed as with defining the appropriate clinical context in which it is performed. In the United States and Canada, unlike the practice in many European countries, most echocardiographic studies are performed by skilled cardiac sonographers rather than by cardiologists themselves. The burden of complying with professional, institutional, and governmental guidelines and regulations, therefore, falls as much to cardiac sonographers as it does to cardiologist medical directors of echocardiography laboratories. Already, measures have been proposed in several state legislatures to require stricter laws governing payment for radiologic and echocardiographic studies, and to link payment to laboratory credentialing and accreditation.[20] Thus, the professional scope of the sonographer and the cardiologistechocardiographer will likely become more inextricably linked, not just by habit, but also by governmental fiat. To this end, it is important to review the current recommendations for the training and education of both physicians and sonographers: for the beginner to know the breadth of his or her task ahead, and for the advanced practitioner to update his or her portfolio or laboratory profile.

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Data Management The complexity of the echocardiographic examination has expanded to such a degree that most busy laboratories must have computer resources to manage patient demographic data and qualitative and quantitative data output regarding M-mode, cross-sectional, Doppler, and stress testing data. Moreover, echocardiography laboratories must have an efficient format for standard study protocols, sonographer-cardiologist preliminary communication via worksheet or direct personal collaboration, study final report and proofreading, and archiving of original data, images, and reports. The coordination and streamlining of this complex process via the digital echocardiography laboratory is now being realized (see Chapter 44) . Communication of Test Results

925

In practical terms, the value of the final report from an echocardiographic study is only as good as the communication that precedes it and the quality of the clinical inquiry that follows the study. In many clinical settings, the echocardiogram provides the basis for formal, and often informal "curbside," consultation. To the extent that an echocardiography laboratory is "open to visitors" for direct inspection of images and discussion of nuances of interpretation, and has the capacity for ready access to the primary image and calculation data, these consultations and the echocardiographic studies will be made valuable. Undoubtedly, the efficiency and potential for image transfer provided by the digital echocardiographic laboratory will enhance these functions.

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Definitions in Training and Credentialing Training refers to a curriculum of study provided by an educational institution, which optimally provides a theoretical and practical framework for understanding and learning a set of intellectual and technical skills. The training levels for echocardiography and its special applications are outlined in this chapter. Certification is a process of formal examination by which an agency tests and confirms a minimum level of proficiency in a defined skill to support its practice. Currently, certification is available for adult echocardiography and intraoperative echocardiography for physicians, and for adult echocardiography for diagnostic medical sonographers. Credentialing is a local hospital or clinic function by which professional criteria in the medical staff bylaws must be applied uniformly for all applicants who wish to obtain privileges to perform a certain function, such as interpretation of echocardiograms, transesophageal studies, or coronary angiograms. The credential is granted based on departmental criteria, which are set to include evidence of relevant training and experience and evidence of current competence. There is no current national standard for setting these criteria, and the Joint Commission for the Accreditation of Health Care Organizations allows local factors to govern their definition. Accreditation is a status of official recognition, endorsement, and approval given by an oversight organization to a program, laboratory, or institution that has been determined by the accrediting agency to be in "substantial compliance" with the standards and guidelines set forth by a defined professional organization. Thus echocardiography laboratories seek accreditation by the Intersocietal Commission for the Accreditation of Echocardiographic Laboratories (ICAEL) (see Chapter 43) . Quality assurance is a local institutional process involving quality planning, quality control, and quality improvement, the components of

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Definition of Clinical Competence in Echocardiography In response to both a local and a national need for guidelines in the definition of clinical competence for the grading of hospital staff privileges, The American College of Physicians, the American College of Cardiology, the American Heart Association, and the American Society of Echocardiography have collaborated to produce procedure-specific definitions for competence. The published guidelines are of various ages, however, and must necessarily be integrated into a comprehensive program of training or credentialing to make practical sense. Also, since the objective of training and credentialing is to ensure the provision of competent and complete clinical care, it is important to emphasize that echocardiography represents a family of procedures, each of which must be performed competently, as must be integration of the knowledge acquired in their serial performance. It is important to emphasize that both early[22] [23] [24] and later [25] [26] [27] [28] [29] guidelines for training in adult echocardiography have emphasized that the physician, not just the sonographer, be trained and competent to perform as well as interpret echocardiographic studies. Thus, competence in the performance of adult transthoracic echocardiographic studies involves a full technical as well as cognitive repertoire for physician training. Given that physicians vary in aptitude and dexterity in manipulation of the echocardiographic machine, the time involved in learning, and maintaining, such skills will vary. Cognitive Skills The cognitive skills required for the performance of adult echocardiography are listed in Table 42-1 . These presuppose a curriculum of thorough training in cardiovascular anatomy and physiology, and, optimally, extensive experience in the cardiac physical examination and the diagnostic process. In the process of learning echocardiography, it will be important

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for the trainee to develop a working knowledge of chest radiography, invasive and interventional cardiology, invasive hemodynamic monitoring, nuclear perfusion imaging, computed axial tomography, magnetic resonance imaging, and positron emission tomography. To the extent that the trainee is able to draw corroborative information from other imaging studies, he or she will develop a deeper understanding of the strengths and weaknesses of echocardiography and alternative measures of cardiac structure and function. These cognitive skills must be further developed to enhance the "public relations" function of the echocardiographer. Patient, referring physician, and fellow consultants each have different perspectives on the usefulness and potential for echocardiography to answer their questions. The written and verbal discussion of results should have the flexibility to address those needs. Technical Skills The technical skills required for competency in adult echocardiography are also listed in Table 42-1 . The exposition 926

TABLE 42-1 -- Skills Needed to Perform Adult Echocardiography Competently Cognitive Skills Knowledge of appropriate indications for echocardiography and its elements Knowledge of differential diagnostic problem in each case and echocardiographic techniques needed to investigate these possibilities Knowledge of alternatives to echocardiography Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Knowledge of normal cardiac anatomy Knowledge of pathologic changes in cardiac anatomy due to acquired and congenital heart disease Knowledge of fluid dynamics of normal blood flow

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Knowledge of pathologic changes in cardiac blood flow due to acquired and congenital heart disease Knowledge of cardiac auscultation and electrocardiography for correlation with results of the echocardiogram Ability to distinguish an adequate from an inadequate echocardiographic examination Ability to communicate results of examination to patient, medical record, and other physicians Technical Skills Technical proficiency with operation of ultrasonographic machine and all controls affecting the quality of the received signals Ability to position and direct ultrasound transducer to obtain desired tomographic images and Doppler flow velocity signals Ability to perform a complete standard examination including all locally available elements of echocardiographic study Ability to record and recognize the electrocardiogram for correlation with the echocardiographic data Ability to recognize abnormalities of anatomy and flow to modify standard examination to accommodate perceived diagnostic needs Ability to perform quantitative analysis of the echocardiographic study and to produce a written report From Popp RI, et al: Circulation 1990;81:2032–2035. of these skills assumes that the physician has a close working relationship with the sonographer and has the capacity to extend the echocardiographic study as necessary to answer an expected or unexpected clinical problem. This guideline further assumes that the physician is capable of both recognizing and circumventing image and Doppler signal artifact, acting alternately as mentor and assistant to the sonographer in this regard. The physician is also expected to develop the skills, with either online or offline analysis, to supplement the echocardiographic report with a comprehensive, directed quantitative analysis of echocardiographic information. This skill set should include the ability to calculate left ventricular ejection fraction, ventricular mass and volume, Doppler indices of diastolic dysfunction, valvular regurgitation and stenosis, and shunt evaluation. Finally, the trainee must master the ability to translate both descriptive and quantitative information into a clinically relevant and comprehensive summary report.

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Levels of Physician Training in Echocardiography Training in echocardiography for a cardiology fellow is an essential component for competence in clinical cardiology. Not all cardiologists who complete their training will have primary responsibility for echocardiography study interpretation or laboratory administration. The guideline for training, therefore, stratifies length and extent of echocardiography training according to the expected experience a trainee needs to acquire to practice optimally. Three levels of training in echocardiography have been defined (Table 422) and are based on expert consensus opinion and limited empirical data.[24] [27] [28] [30] , Level 1 training is required for all cardiology fellows and provides a basis for understanding the practice of and potential for echocardiography. Cardiology fellows who expect to provide independent interpretation and performance of echocardiograms are expected to complete an additional 3 months of level 2 training during their fellowship. This experience then provides the basis for further training in more specialized applications of echocardiography, including transesophageal echocardiography (TEE), perioperative echocardiography, stress echocardiography, and adult cardiologists' training in pediatric echocardiography. Level 3 training is recommended for cardiology fellows who wish to define their clinical career in echocardiography and have the potential to administrate an echocardiography laboratory. An additional 6 months is considered desirable to obtain the experience necessary for this role. During this extended period of training, the cardiology fellow would be expected to master the skills necessary to perform and interpret TEE, stress echocardiograms, perioperative echocardiograms, and contrast echocardiograms. Cardiologists who have completed their formal fellowship training and who

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wish to expand their involvement in echocardiography should ideally extend their training in collaboration with a training laboratory to achieve equivalency to levels 2 or 3, as their responsibilities demand. Finally, cardiologists in practice who have achieved level 2 training are urged to ally their activities to a level 3 laboratory for collaboration and specialized diagnostic testing.

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Training Site Structure The cardiology fellowship or post-fellowship training site should be large enough to accommodate training in all three levels of expertise. Since specific components of the curriculum are not outlined in the guidelines, a broad clinical and academic base is essential. Thus, an active cardiac surgery program, inpatient and outpatient TEE and stress echocardiography and invasive cardiology programs are necessary to provide the broad experience for most practices. In addition, the patient population must be varied enough to provide a wide clinical experience, especially in specialized echocardiographic procedures.[31] Dedicated reading sessions with a senior mentor, direct observation of procedure performance, and evaluation of study reports are all integral to a comprehensive training program. The trainee in echocardiography should be encouraged to keep a personal log of echocardiographic study experience to document his or her development and to supplement that experience as deficiencies become clear. An adequate exposure to case mix, and the development 927

TABLE 42-2 -- Training Requirements for Echocardiography Number of Objectives Duration Cases/Level Physicians in a Cardiology Training Program Level Introductory 3 months 150 two1 Experience dimensional/M-mode and Doppler examinations

Total Number of Cases 150

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6 months, including level 1

150 twodimensional/M-mode and Doppler examinations

300

450 two12 months, 750 including dimensional/M-mode levels 1 and 2 and Doppler examinations and special procedures Physicians in Post-Cardiology Training Responsibility for Variable level 250–300 300 performance and of comprehensive twointerpretation of achievement dimensional/M-mode echocardiograms equivalent to and Doppler level 2 above examinations Direct Variable level 450 comprehensive 750 echocardiography of expertise two-dimensional/Mlaboratory in equivalent to mode and Doppler hospital or large level 3 above examinations group practice Modified from Pearlman AS, Gardin JM, Martin RP, et al: Am J Cardiol 1988;60:158–163; and Stewart WJ, Aurigemma GP, Bierman FZ, et al: J Am Coll Cardiol 1995;25:16–19.

of technical expertise will vary across the population of trainees. While the guidelines list specific numbers for achieving training competence at each level of training, these have been listed as optimal, rather than minimum requirements, to be inclusive of most training programs. Finally, trainees who expect to achieve level 3 experience should be encouraged to design and complete a research project in echocardiography. Even though this is not listed as a requirement by the consensus panel, most training programs consider training in research to be essential to the intellectual development of the trainee, and the ability to integrate new knowledge into the laboratory. Similarly, the postgraduate cardiologist can accomplish this component of level 3 training through, for example, a database review, quality assurance project, or prospective clinical study.

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Specialized Applications for Echocardiography Transesophageal Echocardiography In TEE, the clinician has combined invasive imaging with a traditionally noninvasive tool. The technical requirements are incrementally more challenging than for transthoracic echocardiography, and the clinical questions that are best answered by TEE require additional insight and training to answer. Thus, level 2 training is felt to be a necessary foundation for training in TEE. The structure of training in TEE has been outlined for general[32] [33] and specific[34] [35] [36] [37] [38] [39] applications. Again, the consensus guideline for training in TEE has defined additional cognitive and technical requirements for competence (Table 42-3) . The cognitive requirements that should be emphasized in training in TEE include a comprehensive review of cardiovascular anatomy and the tomographic anatomy of the great vessels and mediastinum, as well as the intracardiac and extracardiac conduits of inborn and post-surgical adult congenital heart disease. The technical skills required for competence in TEE involve not only the safe intubation of the esophagus and comprehensive physician imaging of the heart and great vessels but also the ability to manage the conscious sedation and respiratory status of the instrumented patient. Perioperative transesophageal echocardiography has additional skill requirements beyond routine TEE examination. Because of the unique collaborative relationships that have developed among cardiologist, anesthesiologist, and surgeon, this topic is discussed later under "perioperative echocardiography." It is also essential for the physician and sonographer to collaborate in providing a complete study based on the clinical question asked. Both physician and sonographer must recognize when additional transthoracic imaging is necessary to supplement TEE imaging, such as for left

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ventricular apical imaging or evaluation of pericardial fluid or peak Doppler velocity signals. The optimal quantity and setting for TEE training is summarized in Table 42-4 . In this guideline, the number of recommended studies to be performed by the trainee is relatively small (50 studies) and is preceded by training in esophageal intubation, either with a gastroenterologist performing upper gastrointestinal endoscopy, or at the beginning of a TEE examination (25 studies). Perhaps more important is the setting in which TEE training takes place: the training laboratory should be large, performing more than 2000 total echocardiographic studies per year, and diverse, performing TEE in the surgical, inpatient, critical care, and ambulatory settings. Since most large laboratories perform TEE as 5% to 8% of yearly volume, the trainee in level 3 would be exposed to at least 150 TEE procedures in the year of training and should perform at least one third of these. It is recommended that 928

TABLE 42-3 -- Skills Needed to Perform Transesophageal Echocardiography (TEE) Competently Cognitive Skills

Knowledge of appropriate indications, contraindications, and risks of TEE Understanding of differential diagnostic considerations in each clinical case Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Familiarity with the operation of the ultrasonographic instrument,

Knowledge of other cardiovascular diagnostic methods for correlation with TEE findings Ability to communicate examination results to patient, other health professionals, and medical record Technical Skills

Proficiency in performing a complete standard echocardiographic examination, using all echocardiographic modalities relevant to the case Proficiency in safely passing the TEE transducer into the esophagus

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including the function of all controls and stomach and in adjusting probe affecting the quality of the data position to obtain the necessary displayed tomographic images and Doppler data Knowledge of normal Proficiency in operating correctly cardiovascular anatomy, as visualized the ultrasonographic instrument, tomographically including all controls affecting the quality of the data displayed Knowledge of alterations in Proficiency in recognizing cardiovascular anatomy resulting abnormalities of cardiac structure from acquired and congenital heart and function as detected from the disease transesophageal and transgastric windows, in distinguishing normal from abnormal findings, and in recognizing artifacts Knowledge of normal cardiac hemodynamics and fluid dynamics Knowledge of alterations in Proficiency in performing cardiovascular hemodynamics and qualitative and quantitative analysis blood flow resulting from acquired of the echocardiographic data and congenital heart diseases Understanding of component Proficiency in producing a cogent techniques for general written report of the echocardiography and TEE, echocardiographic findings and including when to use these methods their clinical implications to investigate specific clinical questions Ability to distinguish adequate from inadequate echocardiography data and to distinguish an adequate from an inadequate TEE examination From Pearlman AS, et al: J Am Soc Echocardiogr 1992;5:187–194. the practicing echocardiographer maintain these skills by continuing to perform at least 50 to 75 TEE procedures per year. Exercise and Pharmacologic Stress Echocardiography A separate set of guidelines for the performance and interpretation of stress

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and pharmacologic echocardiography arose from experienced echocardiographers' impression that left ventricular wall motion analysis is one of the most difficult and challenging of our clinical tasks.[40] [41] [42] [43] The training guideline is summarized in Table 42-5 . As with TEE, stress echocardiography is held to be an advanced skill requiring a foundation of level 2 training. Based on both consensus opinion and empirical proof,[44] the volume of stress echocardiographic studies recommended TABLE 42-4 -- Training Requirements for Performance and Interpretation of Adult Transesophageal Echocardiography

Fellows in Training Qualifications Level 2 training in for Training echocardiography

Laboratory performing >2000 echocardiographic studies per year under a level 3 director with recognized expertise in TEE. TEE studies are to include intraoperative, critical care, and ambulatory settings. Type of Cases Esophageal Recommended intubation to learn TEE probe insertion. Supervised TEE examinations and interpretations. Maintenance Annual TEE studies

Conditions of Training

Postfellowship Training Level 2 training or equivalent to 6 months of echocardiographic training Laboratory performing >2000 echocardiographic studies per year under a level 3 director with recognized expertise in TEE. TEE studies are to include intraoperative, critical care and ambulatory settings. Esophageal intubation to learn TEE probe insertion. Supervised TEE examinations and interpretations. Annual TEE studies

Number of Studies to Complete 300 complete transthoracic studies

Not applicable

25

50

50–75

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of Skills Modified from Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. for competence in training includes active participation and performance with image acquisition in at least 50 studies, with interpretation of at least 100 studies. Careful attention to refinements in test performance as well as review of digital images and videotape should be part of the training curriculum.[45] [46] [47] [48] Ongoing maintenance of skill in interpretation should be sought with at least 15 studies per month after training. The clinical setting of training in stress echocardiography also deserves emphasis. The training stress echocardiography laboratory should perform more than 40 studies per month and be led by a level 3–trained cardiologist with experience in more than 200 stress echocardiographic studies. Given the ample availability of corroborative testing in ischemic coronary disease with nuclear perfusion imaging and coronary angiography, these data should be sought out by the trainee in stress echocardiography to gain further insight into his or her interpretive 929

TABLE 42-5 -- Training Requirements for Performance and Interpretation of Stress Echocardiography Fellows in Training Qualifications Level 2 training for Training and ability to interpret resting wall motion Conditions of Laboratory Training performing ≥40 stress echocardiographic studies per month Supervisor with level 3 training, and experience

Postfellowship Training Level 2 training or equivalent current active practice of echocardiography Laboratory performing ≥40 stress echocardiographic studies per month Supervisor with level 3 training, and experience

Maintenance of Skills Not applicable

Not applicable

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with >200 stress with >200 stress echocardiographic echocardiographic studies studies Number of Participation and Participation and Interpretation of Cases performance of at performance of at at least 15 stress echocardiographic least 50 exercise Recommended least 50 exercise echocardiographic echocardiographic studies per month and/or and/or pharmacologic pharmacologic stress stress echocardiographic echocardiographic studies. studies. Interpretation of at Interpretation of at least 100 stress least 100 stress echocardiographic echocardiographic studies with studies with supervision as supervision as above. above. Modified from Popp R, Agatson A, Armstrong W, et al: J Am Soc Echocardiogr 1998;11:95–96. ability. Also, given the small but measurable serious complication rates of stress and pharmacologic echocardiography, the trainee should also master the skills necessary to detect the beginnings of such complications early in their development.[49] [50] [51] [52] [53] Pediatric and Fetal Echocardiography In most clinical practices and academic centers, the discipline of pediatric echocardiography is a separate service performed by pediatric cardiologists, and the discipline of fetal echocardiography is a service provided by a highrisk pregnancy team of pediatricians, radiologists, and pediatric cardiologists. In smaller medical centers and in rural communities, these functions may fall to a general adult echocardiographer. With limited experience, an adult echocardiographer may only be able to function in a triage capacity, referring to more specialized care centers once cardiac pathology is discovered.[54] [55] [56] [57] [58] To define the levels of expertise needed for a practitioner to be competent in these areas, the consensus guidelines for pediatric echocardiography,

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pediatric TEE, and fetal echocardiography have been published or supplemented[59] [60] [61] [62] [63] and are summarized in Table 42-6 . Parallel to adult echocardiography, these guidelines emphasize both the setting of training and the case mix number recommended for achieving competence. Furthermore, pediatric cardiologists who have achieved level 2 training are strongly urged, as are adult cardiologists, to ally themselves with a level 3 laboratory once in practice to ensure the availability of collaboration and more specialized diagnostic capacity. Emerging Technologies It appears certain that new echocardiography technologies will develop that will require new credentials. The skill required for some of these techniques may be mastered "on the job," after a review course or workshop, as for contrast echocardiography.[64] [65] [66] More complex or invasive emerging technologies, such as three-dimensional and intravascular echocardiography await both a repertoire of clinical applications and a set of guidelines to foster their application. The principles of technical and cognitive competence already outlined should serve as a template for future guidelines.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography Training for Noncardiologist Physicians Perioperative Echocardiography The consensus guidelines for training in intraoperative and perioperative echocardiography have necessarily been a product of interdisciplinary collaboration (Table 42-7) (Table Not Available) . Inpatient and ambulatory TEE requires considerable training, but perioperative echocardiography requires on-the-spot diagnosis and decision making and collaboration with surgical management and implications for surgical outcome and, in general, a lack of opportunity to repeat the study or obtain leisurely consultation with a colleague in complex decision making. To the extent that the guideline[38] has been a collaboration of members of the Society of Cardiovascular Anesthesiologists, American College of Cardiology, and the American Society of Echocardiography, each discipline can learn from that collaboration. The cognitive and technical skills required for perioperative echocardiography are at once similar to those for TEE in general and specific to the operative setting. Cardiologists should note well that the basic skills of equipment handling, infection control, electrical safety recommendations, and recognition of hemodynamic manifestations of general anesthesia, air embolism, and anaphylaxis are listed as requirements, as these are not skills commonly taught in TEE training. The development of the guidelines has been contentious in some areas, because of the apparent "short-track" to basic skills in echocardiography outlined for anesthesiologists. Those of us who trained ourselves in TEE and stress echocardiography can both sympathize with the anesthesiologists' desire to apply a very useful 930

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TABLE 42-6 -- Training Guidelines for Performance of Pediatric and Feta Echocardiography Duration and Objectives Conditions Physicians in a Cardiology Training Program Level 1 Introductory 3 months experience

Level 2

Sufficient experience to take independent responsibility for echocardiographic studies

Level 3

Sufficient expertise to direct a pediatric echocardiography laboratory

Special Pediatric general Procedures and intraoperative TEE

Number of Cases/Level

Total Numb of Cas

150 200 twodimensional/Mmode and Doppler exams; one half done on patients younger than 1 year 400 6 months 200 twoincluding level 1 dimensional/Mmode and Doppler exams; one half done on patients younger than 1 year 350 two12 months 750 including levels 1 dimensional/Mand 2 mode and Doppler examinations and special procedures Level 2 or 25–30 equivalent transesophageal intubations, most in patients younger than 2 years 30–50 supervised complete pediatric TEE studies

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TEE continued competence Fetal Level 2 or echocardiography equivalent 3 months in formal fetal echocardiography laboratory Independent 6 months interpretation and direction of fetal echocardiographic program

50 complete studies per year 50 supervised complete fetal echocardiographic studies, including high-risk pregnancies 100 general fetal echocardiographic studies

100 fetal studies of high-risk patients, with serial study Fetal Continued echocardiography membership in continued fetal-maternal competence management team Adapted from Meyer RA, et al: J Am Soc Echocardiogr 1988;1:285–286; Fyfe DA, et al: J Am Soc Echocardiogr 1992;5:640–644; and Meyer RA, et al: J Am Soc Echocardiogr 1990;3:1–3. technology and also agree that rigorous application of credentialing be applied within the medical community. The practitioners at the Cleveland Clinic[36] have outlined a comprehensive, year-long perioperative echocardiographic training curriculum available to cardiologists, anesthesiologists, and surgeons. Additional skills in epicardial echocardiography and valve repair assessment are included and constitute a level of even more advanced training. More specifically, optimal goals of examinations done are listed in the curriculum and are in the range of experience dictated by a cardiology fellow's level 2 training, in-training TEE experience, plus an additional 75 perioperative TEE or epicardial echocardiographic procedures. As in general echocardiography, the principle of an experience hierarchy is implied in these guidelines. That is, anesthesiologists who have mastered

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the basic skills (level 1) are encouraged in training either to master advanced skills (level 2) or to ally themselves with an advanced practitioner in the postgraduate setting (level 3, including valve repair assessment). There is substantial merit to having TEE be an anesthesiologist skill, but there is also justification for adhering to training guidelines to provide the best clinical outcomes.[35] [67] [68] [69] [70] [71] [72] [73] [74] Given the multiple tasks an anesthesiologist must pursue, it seems desirable that TEE collaboration with fellow anesthesiologists and cardiologists should take place. The training pathway chosen by a given practitioner may be as limited or as demanding as his or her practice and research interests dictate (Fig. 42-2) . A comprehensive echocardiography laboratory is defined especially by the level of training of its physicians and sonographers, and only in a subordinate sense by its technologic armamentarium. Thus, a level 3 echocardiography laboratory is defined by its leadership experience, not by how many new machines it has. A deeply experienced level 3 echocardiography laboratory is competent in all pathways of training illustrated. Emergency Department It is a further testament to the broad usefulness of echocardiography that emergency room physicians have begun performing "limited" echocardiographic studies to answer "focused" questions in critically ill patients presenting to the emergency department.[75] The proposed training standard for physicians performing echocardiography in the emergency department[76] recommends a minimum of 25 to 50 echocardiograms. The American Society of Echocardiography has issued a Position Statement on the use of echocardiography in the Emergency Department, [77] expressing the conviction that the proposed number of cardiac echograms for emergency department physicians' training is inadequate to assess the multitude of causes of "acute hemodynamic instability." The authors of the statement further argue that the emergency department "community has posed an eminently testable hypothesis: that [emergency department physicians] after a very modest amount of training, can use ultrasound to correctly diagnose acute and life-threatening conditions, in a time frame too short for a cardiologist or an echocardiography lab extender to arrive."[78] Thus far, this hypothesis 931

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TABLE 42-7 -- Skills Needed to Perform Intraoperative Transesophageal Echocardiography (TEE) (Not Available) Adapted from Savage RM, et al: Anesth Analg 1995;81:399–403; and Thys DM, et al: Anesthesiology 1996;84:986–1006.

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Figure 42-2 Pathways of training in echocardiography. Proficiency in multiple pathways requires additional training. A, Anesthesiologist training pathway; C, cardiologist training pathways; P, pediatric cardiologist training pathway.

has not been tested, and emergency department physician credentialing in echocardiography remains unvalidated, although the potential for echocardiography services in the emergency department remains significant.[79] , [80] Rural Medicine Geographic as well as temporal separation from a level 2 or 3 echocardiography laboratory poses similar restrictions on the availability of echocardiography services in rural areas. General internists and radiologists not uncommonly provide echocardiography interpretation in these settings. Formal alliance with a level 3 echocardiography laboratory is to be encouraged for technical support to rural echocardiography. Soon, ready access to telemedicine consultation via the Internet or broadband transmission of digital echocardiographic studies will make near real-time consultation with a level 3 laboratory a reality and sustain the local imaging prerogative. [58] Integrated Echocardiography Services Comprehensive echocardiography services involve multiple service lines in a medical center and must extend to noncardiology and remote sites. A fully integrated tertiary referral echocardiography laboratory (Fig. 42-3) should function centrally for level 3 training and level 2 and level 1 support, with ongoing training, learning, and mutual benefits present at

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluating and Maintaining Competence The American Board of Internal Medicine has, since 1983, required that medical residents be assessed in procedural skills as a requirement for board certification. This assessment has been of such skills as thoracentesis, cardiopulmonary resuscitation, lumbar puncture, and sigmoidoscopy. The evaluation and documentation of competence in these procedures has been left to individual training program directors. Despite the level of sophistication and potential risk of cardiac procedures, no such standard exists for cardiology fellows. Individual training programs are left to define and have reported success in Figure 42-3 Oversight responsibilities of a comprehensive tertiary care referral echocardiography laboratory.

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measuring competence,[81] achieved through programmatic goals (procedures done) and the in-house training examination. Formal fellowship training provides multiple opportunities for senior observation and mentorship of cardiology fellows in diagnostic and technical skills. The Echocardiography Specialized Examinations The cardiology fellow should ideally be measured by a national competence standard, both as an affirmation of training adequacy and to ensure that a national professional standard is being maintained. For these reasons, the Examination of Special Competence in Adult Echocardiography was developed and is now administered by the National Board of Examiners. The person who has successfully taken this examination has a credential in echocardiography that parallels other

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cardiac subspecialties such as electrophysiology and interventional cardiology. In addition, a separate Certification Examination in Perioperative Transesophageal Echocardiography is offered by the NBE to credential special competency in this discipline. These examinations are open to cardiologists, sonographers, anesthesiologists, surgeons, and internists who have an interest in testing their skills in a written examination. Although technical skill is not directly measured in these examinations, it appears optimal that a passing grade be associated with at least level 2 training in adult echocardiography or advanced training in perioperative echocardiography. Successful passage of these examinations seems to be a prudent goal for those individuals who wish to practice echocardiography. Additional means for measuring and maintaining competence include workshops, national and regional meetings, continuing medical education (CME) accredited videotapes, CD-ROM courses, and specialty textbooks. Accreditation under the Intersocietal Commission for Accreditation of Echocardiography Laboratories (ICAEL) includes the recommendation that physicians maintain at least 30 category 1 CME credit hours in echocardiography every 3 years.[82] Governmental Regulation and the Echocardiography Laboratory Thus far, there is no national governmental policy requiring specific credentialing, certification, or accreditation of echocardiography laboratories or their personnel. However, state legislatures, under whose jurisdiction such prerogatives lie, have begun to make such demands. Four states—New York, Ohio, Wisconsin, and Louisiana—have enacted laws requiring that, in part or whole, laboratory functions and personnel be ICAEL accredited or be associated with an ICAEL-accredited lab.[83] This trend is expected to spread to other states. The implications for laboratories include the need to document personnel training and to meet the essentials and standards of ICAEL (see Chapter 43) . If enforced, these regulations will have an immediate impact on regional HCFA reimbursement for echocardiography services.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Sonographer Training in Echocardiography The complexity of echocardiography has been magnified many-fold from the days of simple imaging and M-mode measurements to routine quantitative measurements of left ventricular systolic performance, diastolic relaxation, and complex Doppler evaluation of valvular and congenital heart disease. The demands of exercise and pharmacologic stress studies, transesophageal echocardiography, and intravenous contrast examinations have also been introduced to the field in the past 20 years (Table 42-8) . Training The cardiac sonographer can no longer be adequately trained in an "on the job" fashion, as was once acceptable. It is clear that the sonographer must possess extensive cognitive ability to adequately perform diagnostic examinations on increasingly more sophisticated equipment. As outlined previously in Table 42-1 , the cognitive and technical skills needed to obtain a diagnostic echocardiogram are demanding and apply to both physician and sonographer. It would be a disservice to the profession of cardiac sonography to underestimate the responsibilities that have been assigned to and accepted by this sophisticated group of practitioners. Echocardiography is a very "operator-dependent" modality, relying heavily on the skills and knowledge of the individual acquiring the diagnostic images. In most cases, it is the cardiac sonographer, not the physician, who makes basic decisions as to which images, Doppler patterns, and manifestations of pathology are recorded to represent the diagnostic examination.[84] [85] [86] The cardiac sonographer often has the responsibility for the decision to use an echocardiographic contrast agent, for left ventricular opacification, or agitated saline to evaluate intracardiac shunts. It is imperative TABLE 42-8 -- Developments in the Field of Echocardiography

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Echocardiography in 1980 M-mode tracings and measurements Two-dimensional imaging with limited two-dimensional measurements available Limited pulsed and continuous wave Doppler capabilities Intravenous agitated saline contrast Echocardiography in 2000 M-mode tracings and measurements Two-dimensional imaging with advanced two-dimensional measurement capabilities including volumes, ejection fraction, and cardiac output Pulsed and continuous wave Doppler with advanced calculation measurements of valve area, peak gradients, mean gradients, stroke volume/cardiac output, shunt ratios, regurgitant fractions, diastolic relaxation, and compliance Color Doppler echocardiography Exercise stress echocardiography Pharmacologic stress echocardiography Transesophageal echocardiography Intraoperative echocardiography Contrast echocardiography

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that the cardiac sonographer have the ability to analyze data continually during a procedure and integrate these data with information obtained from other diagnostic testing to provide an accurate impression of the cardiac status for the interpreting physician. It is only through rigorous education and training that one acquires these skills. The American Society of Echocardiographers has revised the recommended educational curriculum for cardiac sonographers and sonography students.[87] [88] The guideline addresses many concerns involved not only in training new sonographers but also in defining the skills needed by practicing adult sonographers to obtain stress echocardiograms and transesophageal echocardiograms. The didactic courses that must be

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included during clinical training are quite specific (Table 42-9) . The recommendations include curriculum in cardiac anatomy, physiology and pathophysiology, medical ethics, and pharmacology. Important ancillary patient care skills in the recommendations include cardiopulmonary resuscitation, sterile technique, and universal precautions. One of the most important recommendations is that of a clinical internship of supervised full-time instruction for at least 6 months. During this internship, the student intern should be involved with at least four echocardiographic TABLE 42-9 -- 12-Month Didactic Curriculum for Cardiac Ultrasonography A Course include: Anatomy and physiology Pathophysiology Algebra and trigonometry Basic sciences (e.g., biology, chemistry, and physics) ASE Recommended Educational Curriculum for Cardiac Sonographers Cardiac anatomy and physiology Physical principles of ultrasound Cardiac pathology and pathophysiology Medical ethics and legal issues Professionalism, health care delivery Pharmacology Special Procedures Cardiopulmonary resuscitation Isolation techniques Universal precaution technique Sterile technique Basic history-taking and cardiac physical examination Electrocardiography interpretation Echocardiography modalities: techniques and applications Echocardiography quantitative methods

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Determinants of echocardiographic image quality Basic interpretation and understanding of other cardiac diagnostic methods Understanding of cardiovascular therapeutic techniques and intervention: echocardiographic evaluation Research techniques and statistical analysis 6-Month Clinical Internship Full-time supervised instruction should include: Hands-on scanning incorporating two-dimensional, M-mode, spectral, and colorflow Doppler with measurement and preliminary impressions on 40 patients per month (2 per day) Additional 240 echocardiograms observed and reviewed (2 per day) Perform hands-on imaging on 10 stress echocardiograms (recommended that these be performed on patients undergoing stress electrocardiography procedure only) Adapted from Ehler D, Carney DK, Dempsey AL et al: J Am Soc Echocardiogr 2001;14:77–84. Assumes college-level prerequisites have been met.

graphic procedures per day with the expectation of making all measurements and calculations and giving preliminary impressions with at least half of those. The recommendations of the new guideline comprise the repertoire for entry-level competence in cardiac sonography. There are many pathways by which a sonographer can obtain proficiency in the field of echocardiography. There are certificate programs only months in length that are unlikely to meet all of the recommendations of the ASE. Two-year programs offer the participant an associate's degree in ultrasonography or cardiovascular technology with an emphasis on either pathway. Four-year programs offer a baccalaureate degree in medical ultrasonography. Not all of these programs are accredited. Credentialing The two certifying bodies that currently offer testing in echocardiography are the American Registry of Diagnostic Medical Sonographers and

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Cardiovascular Credentialing International. They both require minimum standards of education and experience to sit for examination, typically met by matriculants of accredited educational programs. The accreditation process for training programs is rigorous, and it is recommended that students attend programs that are accredited by the Joint Review Committee for Diagnostic Medical Sonography (JRC-DMS), the Commission on Accreditation of Allied Health Programs (CAAHEP), or the Joint Review Committee for Cardiovascular Technology (JRC-CVT). These credentialing organizations, as well as ICAEL, require a minimum of 30 hours of echocardiography-related continuing medical education over a 3-year period. It should be the joint responsibility of the individual sonographer and his or her clinical institution to meet or exceed continuing education goals. Career Promotion Sonographer skill level continues to be defined in a somewhat simplistic fashion as either entry-level or experienced. Little heed is paid to the duration or breadth of education the sonographer has achieved in assigning job classification. The scope of practice for sonographers has lately received more intense scrutiny[89] the Society of Diagnostic Medical Sonography will soon publish its summary recommendations for scope of practice. Hospital and state legislatures have, until only recently, required demonstration of basic skills to grant a credential or a license to practice cardiac sonography. Now, the formalization of accreditation of echocardiography services through ICAEL has directed attention back to defining credentialing through involvement of the profession[84] [89] [90] rather than through mere state licensing. This trend should allow the experienced sonographer to be recognized for professional achievement and acquisition of new skills and to open pathways toward advanced practice in ultrasonography.[91] [92] Sonographers, through their professional organizations, are beginning to define 935

career pathways for echocardiography practice as "physician assistants" or "echocardiography practitioners" working more independently but in association with a level 3 laboratory. Such forward-thinking approaches to providing service have been successful in electrophysiology and invasive

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cardiology. It may be possible to meet echocardiography needs in rural medicine, emergency departments, and noncardiology areas through such programs.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions The guidelines outlined in this chapter have been put forth by our professional organizations as optimal levels of training. Individuals and training programs should apply these guidelines to develop specific curricula of study and develop tools to measure competence.[93] [94] [95] [96] Certainly, not all physicians who interpret echocardiograms independently or perform TEE have achieved level 2 competence[97] and, in particular, may not have developed or maintained the technical skill to perform complete examinations independently. Their sonographers are the most immediate resource available to redevelop these skills, along with a level 3 laboratory alliance. Training of noncardiology professionals in echocardiography remains a formidable challenge, one likely to be met at a local institution level with strong central echocardiography laboratory leadership. Optimal practice may be difficult to achieve, but it appears that regional government has recognized laboratory accreditation as a measure of competence and will at some level link the definition of professional achievement with reimbursement.

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Chapter 43 - Maintaining Quality in the Echocardiography Laboratory Benjamin F. Byrd III MD

Echocardiography is the most rapidly proliferating, frequently performed major diagnostic test in the United States. Well over 10 million echocardiograms were performed in 2000, at an average cost of $500 per study. Doppler echocardiographic studies are the most operator-dependent of noninvasive cardiac studies. Thorough training of the operator in image acquisition is essential to both reliable demonstration of cardiac structures and interrogation of intracardiac blood flow. An understanding of cardiac pathophysiology is necessary to determine which imaging and flow information is critical to diagnosis in a given patient. Even assuming a high-quality work environment (adequate space, few disturbances, and excellent instrumentation), performance of high-quality studies demands sonographers who are not only well trained but also continually educated, who perform an adequate volume of studies annually, and who are stimulated to excellence by their peers and physicians in the laboratory. Interpretation of echocardiographic studies is for the most part subjective (with the exception of a few M-mode and Doppler measurements) and extremely dependent on the proficiency level of the interpreting physician. The American College of Cardiology (ACC) and the American Society of Echocardiography (ASE) have established training guidelines for cardiologists in surface, transesophageal, and stress echocardiography, [1] [2]

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[3]

but there are no true board examinations as in electrophysiology. In a parallel fashion, there are sonographer organizations that provide voluntary testing and registration (e.g., the American Registry of Diagnostic Medical Sonographers), but competing organizations exist, and there is no unanimity on training requirements. Until recently, therefore, recommendations for the initial training, continuing education, and annual procedure volumes of sonographers and physicians were provided,[4] as were guidelines for the clinical use of echocardiography,[5] but no laboratory accreditation organization existed to confirm that established, across-the-board standards of quality were being met by an echocardiography laboratory. Establishment of quality standards for all aspects of laboratory performance (Fig. 43-1) is actually highly useful to the patients, workers, and payers whose paths cross in the echocardiography laboratory. Patients are assured a high-quality study and interpretation, with reports generated in a timely fashion. Sonographers are assured adequate instrumentation, education, and time to perform optimal studies. Physicians in the laboratory are assured that the best quality study that can be performed will be performed on each patient, and the Medical Director is provided with a vehicle for assuring consistent performance and commitment to excellence from all physicians working in the laboratory. Finally, payers are assured that study performance and interpretation are up to a nationwide standard. In the next few years, digital image storage and transfer under the DICOM standard will facilitate the electronic transfer of echocardiographic studies when patients move between hospitals. The need to repeat studies could fall dramatically, with great cost savings, but only if a consistent level of performance is assured by widespread laboratory accreditation. The Intersocietal Commission for the Accreditation of Echocardiography Laboratories (ICAEL) was established by collaboration between the ACC, the ASE, and several other interested organizations, including the Society of Pediatric Echocardiography. ICAEL has established standards for the practice of echocardiography based on the guidelines of these professional organizations.[6] It accredits laboratories based on these standards in all three major areas of echocardiography: transthoracic, stress, and transesophageal. In addition to documentation of adequate facilities and instrumentation, adequate initial and continuing education, adequate procedure volumes for sonographers and physicians, and a quality assurance (QA) process in the laboratory, videotapes of studies from each laboratory are reviewed by ICAEL sonographer and physician volunteers.

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To date, more than 500 laboratories have been accredited by ICAEL. The major stimulus to applying for ICAEL accreditation has previously been a simple commitment to excellence on the part of each laboratory's sonographers, physicians, and administrators. However, an external stimulus is now being applied, as Medicare carriers in several states Figure 43-1 Elements of echocardiography laboratory accreditation.

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now stipulate that billing echocardiography laboratories be ICAELaccredited. As previously occurred with vascular ultrasonography, Medicare carriers nationwide will likely soon require accreditation of echocardiography laboratories for reimbursement. Thus, the ICAEL guidelines for maintaining quality in the adult echocardiography laboratory, summarized in Table 43-1 Table 43-2 Table 43-3 , assume ever-increasing importance. TABLE 43-1 -- Adult Laboratory Organization Category Description Personnel and Supervision Medical Director training and Completion of a 12-month formal training program. experience or Completion of a 6-month formal training program with at least 600 echocardiogram interpretations. or Three years of echocardiography practice experience with at least 1800 echocardiogram interpretations. responsibilities Responsible for all clinical services provided and for the determination of the quality and appropriateness of care provided.

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CME

Technical Director training and experience

responsibilities

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May supervise or delegate the entire operation of the laboratory. Responsible for ensuring the medical and technical staffs' adherence to the standards and the supervision of their work. Thirty hours of category I CME credits continuing education in echocardiography over a period of 3 years. At least 20 of the continuing education hours must be category I AMA. An appropriate credential in echocardiography. or Successful completion of an ultrasonography or cardiovascular technology program that includes verified didactic and supervised clinical experience in echocardiography. or Completion of 12 months full-time (35 hours/week) clinical echocardiography experience performing echocardiograms plus one of the following: completion of a formal 2-year program in another allied health profession completion of an unrelated bachelors degree possession of an MD or DO degree or equivalent or Three years of echocardiography practice experience with the performance of at least 1800 echocardiogram/Doppler examinations. All laboratory duties delegated by the Medical Director. General supervision of the technical and ancillary staff. The delegation, when warranted, of specific responsibilities to the technical staff and/or the

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CME Medical staff experience and training

responsibilities CME

Technical staff experience and training

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ancillary staff. Daily technical operation of the laboratory (e.g., staff scheduling, patient scheduling, laboratory record keeping). Operation and maintenance of laboratory equipment. Ensuring the technical and ancillary staffs' adherence to the standards. Working with the Medical Director, medical staff, and technical staff to ensure quality patient care. Technical training. At least 30 hours of echocardiography-related continuing education over a period of 3 years. Completion of a 6-month training program in echocardiography that includes interpretation of at least 300 echocardiographic examinations. or Three years of echocardiography practice experience with interpretation of at least 900 echocardiographic examinations. To perform and/or interpret clinical studies. Fifteen hours of AMA category I CME credits continuing education in echocardiography over a period of 3 years. An appropriate credential in echocardiography. or Successful completion of an ultrasonography or cardiovascular technology program that includes verified didactic and supervised clinical experience in echocardiography. or Completion of 12 months full-time (35 hours/week)

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clinical echocardiography experience performing echocardiograms plus one of the following: completion of a formal 2-year program in another allied health profession completion of an unrelated bachelors degree possession of an MD or DO degree or equivalent or Twelve months of echocardiography practice experience with the performance of at least 600 echocardiogram/Doppler examinations. responsibilities Responsible for the performance of clinical examinations and other tasks as assigned. CME At least 15 hours of echocardiography-related continuing education over a period of 3 years. Trainees Training, if conducted, does not compromise patient care and benefits the trainee. Ancillary personnel Ancillary personnel (e.g., clerical, nursing, transport) necessary for safe and efficient patient care should be provided. Physical Facilities Examination areas Examinations shall be performed in a setting providing reasonable patient comfort and privacy. Interpretation and Adequate designated space shall be provided for the storage space interpretation of the echocardiogram and the preparation of reports. Examination Data Archiving, Examination Interpretation, Examination Reports, and Laboratory Records Echocardiographic A system for recording and archiving examination data echocardiographic data (images, measurements, and final reports) obtained for diagnostic purposes must be in place. A permanent record of the images and interpretation must be made and retained in accordance with applicable state or federal guidelines for medical records, generally for 5 to 7 years.

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Echocardiographic data should be readily retrievable for comparison with new studies. Recorded data should consist of real-time (or its digital equivalent) systolic and diastolic images of all cardiac valves, chambers, and great vessels, plus pertinent images that document the presence of pathology. Archiving media include, but are not limited to, videotape, paper strip chart recordings, and digital storage. A log documenting all echocardiographic procedures performed and interpreted by each member of the medical and technical staff should be maintained on an ongoing basis. The log should contain patient, sonographer, and physician identification information sufficient to allow for the review of staff procedure volumes and for the retrieval of previous studies on the same patient. Examinations are interpreted and reported by the Medical Director or a member of the medical staff of the laboratory. Echocardiography reporting must be standardized in the laboratory. All physicians interpreting echocardiograms in the laboratory should agree on uniform diagnostic criteria and a standardized report format. The report should accurately reflect the content and results of the study. The report should include, but not be limited to, a report header, a table of twodimensional and M-mode numeric data, which includes the measurements performed in the course of the examination and/or interpretation, Doppler evaluation and hemodynamic data, and report text that includes an overview of the results of the examination, including any pertinent positive and negative findings. Reports must be typewritten, include a physician signature line (including the name of the interpreting physician), and be signed by the interpreting

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physician. Quality Assurance Instrument maintenance

Echocardiography conferences

Case review

Instrumentation Cardiac ultrasonographic systems

Instrumentation is maintained in good operating condition; this includes recording of method and frequency of maintenance, policy for routine safety inspections and electrical safety and routine instrument cleaning. Four quality assurance conferences per year to review results of comparative studies and address discrepancies, difficult cases, and lab issues. Twice-monthly echocardiographic departmental conferences are recommended. Peer review of performance and interpretation of selected studies to determine quality, accuracy, and appropriateness of the examination. M-mode imaging.

Two-dimensional imaging. Spectral display for pulsed wave and continuous wave Doppler studies. Color flow imaging. Video screen or other display method of suitable size and quality for observation and interpretation of all modalities. Where data are derived from a given line of interrogation (e.g., M-mode or pulsed wave Doppler), a reference line should be available on the screen within a frozen two-dimensional image, except for nonimaging continuous wave Doppler. Range or depth markers should be available on all displays. Capabilities to measure the distance between two points, an area on a two-dimensional image, blood flow velocities, time intervals, and peak and mean

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gradients from spectral Doppler studies. At least two imaging transducers, one of low frequency (2–2.5 MHz) and one of high frequency (3.5 MHz or higher), or a multifrequency transducer that includes these frequencies, plus a transducer dedicated to the performance of continuous wave Doppler studies should be available for each study. Indications, Ordering Process, and Scheduling Indications Echocardiographic testing is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process Echocardiography testing is appropriately ordered and scheduled. Definition of Complete imaging study: examines all of the cardiac procedure types and chambers and valves and the great vessels from protocols multiple views, then uses the available information to completely define any recognized abnormalities. Complete Doppler study: examines every cardiac valve and the atrial and ventricular septi for antegrade and/or retrograde flow. In addition, a complete Doppler study provides functional hemodynamic data. Limited study: generally performed only when the patient has undergone a complete recent examination and there is no clinical reason to suspect any changes outside the specific area of interest. A limited study generally examines a single area of the heart or answers a single clinical question. Scheduling Sufficient time is allotted for each study according to the procedure type. The performance time of an uncomplicated complete (imaging and Doppler) transthoracic examination is 45 to 60 minutes (from patient encounter to departure). An additional 15 to 30 minutes may be required for complicated studies. Elements and Components of Examination Performance Examination performance should include proper technique.

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Elements of study performance

Elements of study quality

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Proper patient positioning. Transducer selection and placement. Optimization of equipment gain and display settings. Performance of a two-dimensional/M-mode/Doppler examination according to the laboratory-specific and appropriate protocol. Utilization of appropriate Doppler technique (including proper Doppler alignment) and measurements. Definition of endocardium. Display of standard (on-axis) imaging planes (e.g., avoidance of foreshortening). Delineation of the details of valvular anatomy. Measurements of left ventricular dimensions from standard orthogonal imaging planes. Optimal recording and evaluation of Doppler flows (which should include alignment of the Doppler beam parallel to flow). Accurate spectral Doppler recording and recording of abnormal Doppler flow signals in multiple views. Adherence to the laboratory-specific and appropriate protocol. A protocol must be in place that defines the components of the standard examination.

Components of the transthoracic echocardiogram Complete M-mode Standard views from multiple planes including and two-dimensional views of all cardiac structures and selected examination extracardiac structures. These include, but are not limited to left ventricle right ventricle left atrium right atrium

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aortic valve pulmonic valve mitral valve and tricuspid valve proximal ascending aorta yransverse aorta proximal descending aorta main pulmonary artery and proximal branches inferior vena cava hepatic vein pericardium Complete Doppler Includes spectral Doppler and/or color flow study interrogation of all normal and abnormal flows within the heart, including the valves, the great vessels, and the atrial and ventricular septa. Limited examination A limited study is generally performed only when the patient has undergone a recent complete examination and there is no clinical reason to suspect any changes outside the specific area of interest. A limited study generally examines a single area of the heart or answers a single clinical question. Standard twoParasternal long-axis view. dimensional views Parasternal short-axis views (basal, mitral valve, left ventricle at the mid-papillary muscle level, left ventricular apex). Right ventricular inflow view. Parasternal long-axis view of the pulmonary artery. Apical four-chamber view. Apical two-chamber view. Apical five-chamber view. Apical long-axis view. Subcostal four-chamber view.

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Subcostal short-axis view (when indicated). Subcostal IVC/hepatic vein view. Suprasternal notch view (when indicated). Two-dimensional or The left ventricular internal dimension at endM-mode diastole. measurements of The left ventricular internal dimension at endthe left heart systole. The left ventricular posterobasal free wall thickness at end-diastole. The ventricular septal thickness at end-diastole. The left atrial dimension at end-systole. The aortic root dimension at end-diastole. The four cardiac valves—forward flow spectra for Doppler flow evaluations each valve, and any regurgitation, shown in at least two imaging planes with color Doppler. For aortic stenosis, the highest systolic velocity must be evaluated from multiple transducer positions (e.g., apical, suprasternal, and right parasternal). The tricuspid regurgitation spectrum should always be sought for estimation of systolic right ventricular pressure. Atrial and ventricular septa—color Doppler screening for defects. Left ventricular outflow tract velocity. Use of nonimaging transducer in appropriate views such as apical, right parasternal, and suprasternal notch to assess valvular abnormalities (such as AS, MS, or TR) is strongly encouraged. Velocity-time integrals and hepatic and pulmonary vein flow spectra are optional. Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 600

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proficiency

echocardiograms annually. Each member of the medical staff should interpret a minimum of 300 studies annually. Each member of the technical staff should perform a minimum of 300 studies annually. The total volume of studies interpreted and performed by each staff member may be combined from sources other than the applicant laboratory.

Results Comparison and confirmation of results

Results of transthoracic echocardiography laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, MRI/CT, nuclear studies and PET scans. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

TABLE 43-2 -- Adult Transesophageal Echocardiography Category Instrumentation Cardiac ultrasonography systems

Description M-mode imaging.

Two-dimensional imaging. Spectral display for pulsed wave and continuous wave. Doppler studies. Color flow imaging. Video screen or other display method of suitable size and quality for observation and interpretation of all modalities. Where data are derived from a given line

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of interrogation (e.g., M-mode or pulsed wave Doppler), a reference line should be available on the screen within a frozen two-dimensional image, except for non-imaging continuous wave Doppler. Range or depth markers should be available on all displays. Capabilities to measure the distance between two points, an area on a two-dimensional image, blood flow velocities, time intervals, and peak and mean gradients from spectral Doppler studies. Transesophageal Transesophageal ultrasound transducers should be ultrasonography those manufactured for the ultrasonography system transducer of the laboratory. Transesophageal ultrasound transducers should incorporate biplane or multiplane imaging capabilities. Indications, Ordering Process, and Scheduling Indications Transesophageal echocardiographic testing is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process The TEE order and/or requisition should clearly indicate the type of study to be performed, reason(s) for the study, and the clinical question(s) to be answered. Definition of In general, TEE should be performed to answer procedure types and clinical questions that cannot be answered by protocols transthoracic imaging. A TEE study is one that examines all of the cardiac chambers, valves, and great vessels from multiple imaging planes, then uses the information to completely define any recognized abnormalities. The study should include appropriate Doppler interrogation of all cardiac valves and structures (e.g., pulmonary veins and atrial appendage) and provide any hemodynamic data felt to be of importance for patient care.

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Scheduling

Sufficient time should be allotted for each study according to the procedure type. The performance time for an uncomplicated complete study (outside of the operating room) is estimated to be 45 to 60 minutes (from patient encounter to departure), with an additional 15 to 30 minutes for complicated studies. Sufficient time must be included in the scheduling process for the adequate post-procedure monitoring of the patient, especially if conscious anesthesia is utilized. Elements and Components of Examination Performance Examination performance should include proper technique. Training Transesophageal echocardiography is a semi-invasive test that, if performed incorrectly, can lead to serious harm to patients and therefore should be performed by appropriately trained personnel. Elements of study Include, but not limited to performance transducer insertion optimization of equipment gain and display settings utilization of appropriate Doppler technique and measurements optimization of image orientation to enhance Doppler display performance of a two-dimensional/Doppler transesophageal examination according to the laboratory-specific and appropriate protocol Elements of study Demonstration of cardiac structure and function. quality Evaluation of atrial-septal integrity. Evaluation of left and right atria and appendices. Delineation of the details of valvular anatomy. Optimal recording and evaluation of Doppler flows.

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Adherence to the laboratory-specific and appropriate protocol. Technical personnel Due to the complexity of the TEE study, appropriate technical personnel should be available to assist the performing physician. These personnel may include a sonographer and a nurse. The duties of these individuals include, but are not limited to, preparing the patient for the test, assisting the physician with the ultrasonographic equipment, monitoring the patient during and after the examination, and administering anesthetic medication as allowed by law. Preparation of the To perform TEE studies safely, appropriate safety patient guidelines must be in place. Patients should have a functioning intravenous access in place. Cardiac monitoring with standard telemetry leads should be utilized. Instrumentation to monitor the oxygen saturation of the patient before, during, and after the examination should be available, as well as oxygen with appropriate delivery devices, if needed. All procedures must be explained to the patient and/or the parents or guardians of those unable to give informed consent. Consent should be obtained in a manner consistent with the rules and regulations required by the hospital or facility. Monitoring of the During the procedure, the vital signs and medical patient stability of the patient should be periodically evaluated and recorded by the performing physician or the technical assistant. The development of instability in either the vital signs or comfort of the patient should be addressed by the performing physician. Laboratory guidelines for the monitoring of patients who receive intravenous anesthesic agents are

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required. A list of periprocedural complications should be maintained. Recovery of the Prior to discharge from the TEE laboratory, the patient patient should be monitored for a sufficient amount of time to ensure that no complications have arisen either from the procedure or the medication administered. The patient and/or the family should be instructed on any postprocedure care that the physician feels is necessary. Information should be given to outpatients that will allow them to contact the performing physician should complications arise after patient discharge. A list of post-procedural complications should be maintained. Components of the A protocol must be in place that defines the standard examination components of the TEE examination. A complete TEE and TEE-Doppler examination includes standard views from multiple planes, including views of all cardiac structures and selected extracardiac structures. Standard views in Gastric short-axis and long-axis views. complete examination Standard two- and four-chamber views. Short- and long-axis views of the aortic valve with appropriate Doppler. Multiple imaging planes of the mitral valve with appropriate Doppler. Multiple imaging planes of the tricuspid valve with appropriate Doppler. Longitudinal view of the pulmonic valve with appropriate Doppler. Multiple imaging planes of the left and right atria and appendices with appropriate Doppler.

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Cleansing of the TEE transducer

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In cases of suspected cardiac source of emboli, appropriate use of contrast methods to evaluate for the presence of intracardiac shunting. Multiple imaging planes of the atrial septum and foramen ovale with appropriate Doppler. Imaging of the pulmonary veins with appropriate Doppler. Short- and long-axis views of the ascending, descending, and transverse arches of the aorta. Short- and long-axis views of the main pulmonary artery and proximal portions of the right and left pulmonary arteries. Images of the proximal inferior and superior vena cava. Imaging of the pericardial space and pericardium. Evaluation of extracardiac structures visualized by TEE ultrasonography. Published guidelines exist for the appropriate care and cleansing of the TEE transducer. These guidelines should be followed, except in circumstances in which the recommendations of the manufacturer differ but are equivalent.

Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 50 TEEs proficiency annually. It is recommended that each member of the medical staff who performs or interprets TEEs should perform a minimum of 50 studies annually. The total volume of studies interpreted and performed by each medical staff member may be combined from sources other than the applicant laboratory. Results

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Comparison and confirmation of results

Results of TEE laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, and MRI/CT. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

TABLE 43-3 -- Adult Stress Echocardiography Category Instrumentation Cardiac ultrasonography systems

Digital acquisition systems

Description Hardware and software to perform two-dimensional imaging. Image display device (monitor) that identifies the parent institution, the name of the patient, the date and time of the study, the ECG, and range or depth markers. Measuring capabilities including the ability to measure the distance between two points and an area on a two-dimensional image. A minimum of two imaging transducers, one of low frequency and one of high frequency, or a multifrequency transducer. Image recording device, videotape recorder, and digital recording device. Digital acquisition of the echocardiographic image must be available and utilized for the performance and interpretation of stress echocardiography. The digital acquisition system may be either integrated (part of the ultrasonography system) or nonintegrated (a separate digitizing unit that is connected to the ultrasonography system). This system should allow for accurate "triggered"

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acquisition of images and side-by-side image display. The digitizing system should have adequate memory to allow performance of multistage stress echocardiographic studies and should have a digital recording device capable of recording the resultant side-by-side images. Indications, Ordering Process, and Scheduling Indications Stress echocardiography is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process Echocardiography testing is appropriately ordered and scheduled. Definition of Two phase examines and compares left ventricular procedure types wall segments before stress and after stress and is usually accomplished using treadmill exercise (and is sometimes accomplished using pacing methods). Three phase examines and compares left ventricular wall segments before, during, and after stress and is usually accomplished using bicycle exercise ergometry (and is sometimes accomplished using pacing methods). Four phase examines and compares left ventricular wall segments before, during, and/or after stress and is usually accomplished using pharmacologic stress agents or supine bicycle ergometry (and is sometimes accomplished using pacing methods). Doppler compares antegrade and retrograde flow (if present) before, during, and/or after stress. Doppler stress echocardiography may be performed alone or in conjunction with a two-phase, three-phase, or fourphase stress echocardiography examination (and is sometimes accomplished using pacing methods). Contrast examines and compares left ventricular wall segments before stress and after stress following the injection of a contrast agent that is used to enhance endocardial border definition. Contrast may also be

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used to enhance the Doppler signal when performing Doppler stress echocardiography. Contrast stress echocardiography may be used in conjunction with two-phase, three-phase, four-phase, and Doppler stress echocardiography. Scheduling Sufficient time is allotted for each study according to the procedure type. The performance time for a two-phase or three-phase stress echocardiogram is 45 to 60 minutes from patient encounter to departure. An additional 15 to 30 minutes per study may be needed for the performance of a pharmacologic stress echocardiogram, since these procedures require that intravenous access be obtained. Additional time will also be required when adding Doppler to any standard stress echocardiography. Elements and Components of Examination Performance Examination performance should include proper technique. Training Stress echocardiography is a diagnostic test that, if performed and/or interpreted incorrectly, can lead to serious consequences for the patient. Accurate performance of stress echocardiography requires that the performing sonographer and interpreting physician be adequately trained and experienced to perform and interpret stress echocardiograms. Elements of study Proper patient positioning during image acquisition. performance Appropriate transducer selection and placement. Achievement of optimal heart rate. Optimization of the ultrasonographic equipment gain and display settings. Appropriate and consistent scan depth selection for each phase of image acquisition. Rapid post-stress image acquisition (ideally, all post-

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Elements of study quality

Stress echocardiography laboratory arrangement

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stress images should be obtained within 60 seconds of stress cessation). Optimization of digitized images for side-by-side comparison. Utilization of artifact-free ECG for digital triggering purposes. Appropriate ECG lead placement. Utilization of appropriate Doppler technique (including proper alignment) and measurements. Performance of a stress echocardiogram according to the laboratory-specific and appropriate protocol. Definition of endocardium. Display of standard, on-axis imaging planes (e.g., avoidance of foreshortening). Measurements of left ventricular dimensions (when performed) obtained from standard orthogonal imaging planes. Accurate digital triggering (from ECG R wave). Appropriate side-by-side image display. Adherence to the laboratory-specific and appropriate protocol. Stress echocardiograms should be performed in a laboratory designed to ensure patient safety and to facilitate rapid acquisition of post-stress images. Elements of the stress echocardiography laboratory arrangement include Proper placement of the examination table next to the treadmill. Proper placement of the ultrasonographic equipment next to the examination table. Proper placement of the examination table to allow access to both sides of the table. Proper placement of emergency equipment (crash

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Stress echocardiography standard components

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cart and oxygen) such that they are easily accessible. A protocol must be in place that defines the components of the various types of stress echocardiograms. Indications for the performance of a pharmacologic stress echocardiogram and/or a standard exercise stress echocardiogram should be included. Alternative views may be obtained if contrast is used. A two-phase stress echocardiogram includes the following views, obtained both before and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. Timers are recommended and should be activated when exercise stops. It is also recommended that post-stress images be obtained within 60 seconds. A three-phase stress echocardiogram includes the following views, obtained before, during, and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. A four-phase stress echocardiogram includes the following views, obtained before, during, and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. Additional images obtained during a four-phase stress echocardiogram may include low-level stress images, mid-level stress images, and/or peak-level stress images, depending on the clinical question that is being answered with the stress echocardiogram. A Doppler stress echocardiogram includes interrogations of flow velocities (from the same site) before, during, and/or immediately following stress.

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Doppler stress echocardiography may be used to document gradient changes that occur with stress or to evaluate diastolic filling pattern changes that occur with stress. Patient preparation To adequately perform stress echocardiographic studies, appropriate safety guidelines must be in place. All stress echocardiographic procedures must be explained to the patient and/or the guardian of those unable to give informed consent. Consent should be obtained in a manner consistent with the rules and regulations outlined by the hospital or facility. Patients undergoing pharmacologic or contrast echocardiography must have a functioning intravenous access in place. Emergency equipment (standard crash cart) with additional medications utilized for reversing the effect of the pharmacologic stress agent(s) must be readily available at all times. Adequate personnel (a minimum of two individuals) should be present during all stress echocardiographic procedures. Personnel should be certified in Basic Cardiac Life Support (BCLS). Patient monitoring During the image acquisition phase and during the recovery phase of the examination, the vital signs of the patient should be periodically evaluated in accordance with the stress testing protocol. Cardiac monitoring with standard stress testing leads should be used. A list of procedural complications should be maintained. Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 100

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proficiency

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stress echocardiographic examinations annually. Each member of the medical staff who interprets stress echocardiograms should interpret a minimum of 100 stress echocardiograms annually. Each member of the technical staff who performs stress echocardiograms should perform a minimum of 100 stress echocardiograms annually. The total volume of studies interpreted and performed by each member may be combined from sources other than the applicant laboratory.

Results Comparison and confirmation of results

Results of transthoracic echocardiography laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, and MRI/CT. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

References 1. Stewart WJ, Aurigemma GP, Bierman FZ, et al: Guidelines for training in adult

cardiovascular medicine. Core Cardiology Training Symposium (COCATS). Task Force IV: Training in echocardiography. J Am Coll Cardiol 1995;25:16–19. 2. Pearlman AS, Gardin JM, Martin RP, et al: Guidelines for physician training in

transesophageal echocardiography: Recommendations of the American Society of Echocardiography Committee for Physician Training in Echocardiography. J Am Soc Echocardiogr 1992;5:187–194. 3. Popp R, Agatston A, Armstrong W, et al: Recommendations for training and

performance and interpretation of stress echocardiography. J Am Soc Echocardiogr 1998;11:95–96. 4. Kisslo J, Byrd BF III, Geiser EA, et al: Recommendations for continuous quality

improvement in echocardiography. J Am Soc Echocardiogr 1995;8:S1–S28.

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5. Cheitlin MD, Alpert JS, Armstrong WF, et al: ACC/AHA guidelines for the clinical

application of echocardiography. Circulation 1997;95:1686–1744. 6. ICAEL Essentials and Standards for Adult Transthoracic Echocardiography Testing,

Parts I–IV. Intersocietal Commission for Accreditation of Echocardiography Laboratories, 8840 Stanford Boulevard, Suite 4900, Columbia, Maryland 21045.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26082022/1031/363.html/top

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947

Chapter 44 - The Digital Echocardiography Laboratory Douglas S. Segar MD

Although not new, the concept of the digital echocardiography laboratory is rapidly expanding and evolving. Some laboratories have embraced the digital echocardiography laboratory in part or in total for more than a decade.[1] [2] [3] It is only within the past few years, however, that a digital echocardiography laboratory has become a practical and embraceable reality for the majority of laboratories. The concept encompasses a single echocardiography used as a reading station to a far-reaching network with potentially worldwide accessibility. The major impetus for the digital echocardiography laboratory was the advent of stress echocardiography. It was under that modality that the first images were digitized and the advantages of a digital approach realized. The pioneer of digital echocardiography, Dr. Harvey Feigenbaum, has been quoted as saying that it was only digital echocardiographic systems that allowed stress echocardiography to become a clinical and not just a research tool.[4] [5] [6] [7] Understanding the digital echocardiography laboratory requires a basic understanding of computer networking vocabulary and principles. A glossary of terms is provided for assistance (Table 44-1) . The basic

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premise of a digital echocardiography laboratory is that the information is acquired, processed, interpreted, and stored in a digital modality. All echocardiographs convert the ultrasound information into a digital format at some point in the imaging chain. Traditionally, the output has been converted into an analog signal for display and storage (videotape). A digital approach avoids at least part of the analog step by recording and storing the image in a digital file format. Newer instrumentation allows for recording of the actual digital image rather than the older method of digitizing (through a frame grabber) the analog video output. The advantages of digital versus digitized output have been described. For research purposes, a true digital output may have significant utility for the analysis of color Doppler signals[8] [9] [10] and multicenter trials.[11]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Setting Up the Digital Echocardiography Laboratory One of the most difficult problems in establishing a digital echocardiography laboratory is the initial design and implementation of the digital echocardiography networking and hardware components. It is important early on in the process that the various personnel (equipment manufacturer, computer support, hardware engineer, software applications, and information systems) involved be included in the design process so that areas of overlap can be avoided and communication enhanced.[12] [13] [14] [15] Of paramount importance early on in the process is determining who is responsible for the various components of the laboratory. This requires that the network, echocardiography, and information system directors determine who is going to service and be responsible for questions on each component on the digital echocardiography laboratory. One of the primary determinants of the scope of the digital laboratory is the volume of studies being performed and the number of echocardiographs and users that will be involved. Determining a digital laboratory solution requires knowing how many machines will be involved, the type of machine, the digital output of each machine, and how the digital output will be interfaced with the computer interpretation and recording systems. One must determine whether the users will be all within one network system or whether there will be both internal and external users. Obviously, the complexity of stringing fiberoptic cable or Ethernet line is quite different if one is dealing with one machine and one computer on one floor versus trying to interface numerous points of service on different floors, different buildings, or even different cities. The location of the echocardiographs and the location of reading stations for sonographers as well as for interpreting physicians will need to be determined at the outset. It 948

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TABLE 44-1 -- Terms Used in Digital Echocardiography Term access

access time

analog

A/D Converter

ATM

bandwidth

baud (rate)

bit

Definition To send or retrieve data from a disc drive or from another computer. Usually refers to discs and network entry. The amount of time that elapses between a request and a response. An example is the time between when one requests data from a disc drive and when it appears on the monitor's display. Continuous signals; data presented or collected in continuous form. These data are shown on an instrument that can change constantly. For example, speedometers or thermometers are analog devices. Analog signals can represent many different realworld things, such as video, audio (voice, music), and physiologic waveforms (electrocardiogram, heartsounds, respiration). A device that converts an analog signal into a digital signal. Complex waveforms are converted into simple strings of numbers. Acronym for "Asynchronous Transfer Mode," an emerging technology for high-speed networking, with transmission capacity ranging from 1.544 Mbps (T1) to 2 Gbps (SONET OC 48), but typically in the 150 Mbps range (OC-3c). 1. The difference in Hertz (Hz) between the highest and lowest frequencies of a transmission channel. 2. The amount of data that can be sent through a given communications circuit per second, usually expressed in Kbps or Mbps. A unit of data transmission equal to the number of discrete conditions per second. In a system of binary states, represents the number of bits per second. The unit of information; the amount of information obtained by asking a yes-or-no question; a computational quantity that can take on one of two

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broadband

bridge

byte (B)

CD-R

CD-ROM

client/server

clinical data compression

compression

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values, such as true and false or 0 and 1; the smallest unit of storage sufficient to hold 1 bit. Loosely defined physical medium specification for analog signals for multiple data channels (video, audio). A device and software that links similar-to-similar network environments (e.g., Ethernet and Token Ring). LAN bridges are used to create a single logical LAN from multiple physical ones, including remote LANs. A bridge typically separates at the upper half of the data link layer. One of the bridge standards is IEEE 802.1 A component in the machine; now most often 8 bits. A byte typically holds one character or for the Primer discussions, one pixel. Acronym for "Compact Disc-Recordable." This form of CD media allows user-defined data to be recorded onto the disc. It is different from audio CDs and other forms of CD-ROMs, which are typically massproduced from a master disc. Acronym for "Compact Disc-Read Only Memory." The digital information on the disc is created by mass production pressing techniques. A client sends requests to a server, according to some protocol, asking for information or action, and the server responds. There may be either one centralized server or several distributed ones. This model allows clients and servers to be placed independently on nodes in a network, possibly on different hardware and operating systems appropriate to their function. All data with clinical content; includes images, waveforms, measurements, findings, and reports. A general description for a family of mathematical techniques that can reduce the amount of data and therefore improve digital storage efficiency and retrieval rates. A description for the amount of reduction in the

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factor/compression amount of data from the original, expressed as a ratio. ratio Conformance A document provided by manufacturers of DICOMStatement compatible equipment that identifies the subset(s) of the DICOM standards that individual products actually support. database A collection of related information about a subject, arranged in a useful manner. The information in a database provides a base for understanding information, drawing conclusions, and making decisions. DICOM Acronym for "Digital Imaging and Communications in Medicine." A communications standard for the exchange of medical information developed by the National Electrical Manufacturers Association and the American College of Radiology. DICOMDIR A file reserved to store DICOM file information stored on the same media where the file resides. digital image An image that has been discretized both in the spatial coordinates and in brightness. dpi Acronym for "Dots Per Inch." A measure of resolution for printers, scanners, and displays. DVD Acronym for "Digital Video Disc." Ethernet The term used to refer to several different physical types of computer networks. Different types of wire and speeds are available under the term Ethernet. Refer to the IEEE 802.3/ISO8802.3 standards. file set A collection of files that share a common naming spacing, where File ID(s) are unique within the file set. DICOM File sets must contain a single file with the File ID of DICOMDIR. DICOMDIR contains information on the other files contained in the DICOM file set. File Set Creator A system that can produce DICOM media under a (FSC) specific Application Profile as described in the system's Conformance Statement.

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File Set Reader (FSR) File Set Updater (FSU) Gbps

GByte gray scale resolution HIS HL7

hub

Hz icon interchange

internet IP

ISO

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A system that can read DICOM media under a specific Application Profile as described in the system's Conformance Statement. A system that can add information to a DICOM media under a specific Application Profile as described in the system's Conformance Statement. Abbreviation for "Gigabits per Second." A measurement of the data transfer capacity of a system. Gigabit stands for 1 billion bits. Abbreviation for "GigaByte." Gigabyte stands for 1 billion bytes. Sometimes called gray scale. The resolution of image brightness expressed by the number of bits used to represent the light intensity of a pixel. Acronym for "Hospital Information System." Acronym for "Health Level 7," a common protocol for communicating with hospital and radiologic information systems. A device that connects several nodes to a network. Hubs are used in conjunction with routers to produce subnetworks. Abbreviation for "Hertz," a unit of frequency equal to one occurrence per second. A small picture intended to represent something (a file, directory, or action) in a graphic user interface. Generally refers to the exchange of diagnostic imaging studies between institutions. Sometimes it is also used in the context of exchange within an institution. Any set of networks interconnected with routers. The Internet is the biggest example of an internet. Acronym for "Internet Protocol." The network layer for the TCP/IP protocol suite widely used on Ethernet networks. A prefix for "International Organization for Standardization."

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ISDN

Acronym for "Integrated Services Digital Network," a twin 64 Kbps digital phone line for high speed data communication at a lower cost than a T1 line. Widely available in Europe and gaining popularity in the United States. JPEG Acronym for "Joint Photographic Experts Group." JPEG-DCT Acronym for "Joint Photographic Experts Group – Discrete Cosine Transform." It is the lossy compression algorithm used to store echocardiograms in DICOM. jukebox A storage device that contains an automatic media changer. When a computer asks for data not stored on the loaded media, the jukebox automatically loads the correct media. Kbps Abbreviation for "Kilobits per Second." A measurement of the data transfer capacity of a system. Kilobit stands for 1000 bits. LAN Acronym for "Local Area Network." lossless A category of digital image compression types that compression possess the following characteristics: (1) The original digital images can be exactly (bit for bit) reproduced as originally acquired. (2) It does not affect postdecompression digital image processing. (3) It can achieve only relatively low levels of data reduction. lossy compression A category of digital image compression types that possess the following characteristics: (1) The original digital images cannot be exactly reproduced as originally acquired, but the changes may not be visually apparent. (2) The compression algorithms can introduce artifacts into the images and affect postdecompression digital image processing. (3) The prevalence of artifacts increases as the amount of compression increases or as the image detail content increases. (4) Much higher degrees of compression are possible than with lossless compression. MB Abbreviation for "MegaByte." MegaByte stands for 1 million bytes of information.

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Mbytes/sec

Media

network

node

optical disc pixel POTS RAID

repeater

router

spatial resolution

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Abbreviation for "Megabits per Second." A measurement of the data transfer capacity of a system. Megabit stands for 1 million bits. Abbreviation for "MegaBytes per Second." A measurement of the data transfer capacity of a system. MegaByte stands for 1 million bytes. Used in DICOM to describe any one of the physical data storage devices approved in the DICOM standard in part 12. The currently approved media are 120 mm CD-R, 90 mm magneto-optical disc, 130 mm 650 MB magneto-optical disc, 130 mm 1.2 GB magneto-optical disc, 1.44 MB discette. Application profiles define which specific media is required for interchange. The connection between two or more computers to create a communications and data exchange system. See LAN and WAN. A connection for a device to be attached to the network. Nodes could also refer to the number of computer systems on the network. A group of media products that use a magneto-optical media for storage of information. The elements of a digital image array. The smallest element a monitor can display. Acronym for "Plain Old Telephone System." Acronym for "Redundant Array of Inexpensive Discs," any of six arrangements of conventional disc drives to increase speed and/or reliability. A device that repeats the signal or bit by bit from one physical segment to the next. Used to effectively extend the distance covered by the LAN. Links multiple networks. It selects the best path for data between networks based on link speed and number of hops (from one network into the next one). Sometimes called resolution. The resolution of image in the horizontal and vertical directions, expressed by the number of pixels used to make up the image.

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TCP

The most common transport layer protocol used on Ethernet and the Internet. It was developed by U.S. Department of Defense. TCP is built on top of Internet Protocol (IP) and is nearly always seen in the combination TCP/IP (TCP over IP). TCP/IP Acronym for "Transmission Control Protocol over Internet Protocol." The de facto standard Ethernet protocols. TCP/IP was developed by US Department of Defense for internetworking, encompassing both network layer and transport layer protocols. While TCP and IP specify two protocols at specific layers, TCP/IP is often used to refer to the entire protocol suite. temporal The resolution of images in time, expressed by the resolution number of images per second. T-1 A specialized digital phone line with a maximum speed of 1.544 Mbps. ThickNet Ethernet see 10Base5 ThinNet Ethernet see 10Base2 UID Acronym for "Unique Identifier." Used throughout DICOM to identify information uniquely throughout the world. It uses the structure defined by ISO 8824 for OSI Object Identifiers. WAN Acronym for "Wide Area Network." 10Base5 A term referring to Ethernet using a thick coaxial cable ("yellow cable"), maximum length 500 m, maximum 100 nodes per segment. The "10" means 10 Mbps, "base" means "baseband" as opposed to RF and "5" means a maximum single cable length of 500 m. Also called ThickNet Ethernet. 10Base2 A term referring to Ethernet using RG-58 cable or similar, maximum length 185 m, maximum 30 nodes per segment. If BNC connectors are used, T-connector must be on interface card. The "10" means 10 Mbps, "base" means "baseband" as opposed to RF, and "2" means a maximum single cable length of 200 m. Also called ThinNet Ethernet.

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10BaseT

A term referring to Ethernet using twisted-pair cable, maximum length 100 m; hubs are required to connect nodes. Also called Twisted-Pair Ethernet. Modified from Leong D, Adams DB. In Kennedy TE, Nissen SE, Simon R, et al (eds): Digital Cardiac Imaging in the 21st Century: A Primer. Bethesda, MD, American College of Cardiology, 1997, pp 224–231.

is important to keep in mind the anticipated growth of an echocardiography service so that one leaves room for expansion. In some cases, it may be more cost-effective to place network ports into potential echocardiography examination rooms initially, rather than adding on in the future. Careful consultation with contractors is necessary to determine whether existing wiring can be used or new wiring will need to be strung. If one is using existing wiring, it is extremely important that the added traffic required for a digital echocardiography system will not exceed the available bandwidth in existing cabling. In some circumstances, it may be worth the extra cost to string dedicated lines serving only the echocardiography computer network to avoid sharing bandwidth with hospital or office systems. In all aspects of the decision making process, one must trade off concerns of capital with concerns of speed and accessibility. As briefly mentioned earlier, one also needs to determine who will be responsible for the maintenance of all the systems, including wiring, routers, nodes, servers, storage devices, computers, and software. When determining the structure of the network system, leaving room for expansion is clearly important. Keep in mind that computer systems typically outdate themselves within a relatively short period of time and when one is buying a network one is buying essentially only a few years worth of service. Additional options to consider would be remote interpretation of echocardiographic studies via Internet access, modem, cable modem, or even satellite transmission. Block diagrams representing two different digital laboratory solutions are displayed in Figure 44-1 and Figure 44-2 . The first figure demonstrates a digital laboratory solution in an office practice between two different floors. This system has the advantage of using the same echograph and digital output in all systems. In this example, all wiring, servers, switches,

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and nodes are dedicated to the echocardiographic system, requiring no sharing of resources. The advantages of this solution are an increase in speed, a decrease in access time, and the avoidance of traffic-related issues. Relatively speaking, this type of solution is perhaps more expensive to implement, with the trade-off being the advantages just listed. The system represented in Figure 44-2 is a more extensive approach using existing connections between multiple hospitals and points of service. In this particular system, network access is shared by existing lines, although there are dedicated servers and reading stations for the echocardiography laboratory. Stringing fiberoptic cable between different hospitals solely for the purpose of an echocardiography laboratory is in most circumstances cost-prohibitive. This particular system is a hybrid. Although bandwidth is shared, access time is kept to a minimum by the use of dedicated servers, storage devices, and reading stations for echocardiography. Another potential advantage of this system is that the computer and network access can be used for nonechocardiography laboratory applications, improving multitasking of each computer unit. Numerous other set-ups and variations are possible. One is limited only by the scope of the problem and the resources and finances available.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

DICOM DICOM (Digital Imaging and Communications in Medicine) is a formatting standard constructed by the National Electrical Manufacturers Association (NEMA). [16] [17] [18] The most recent version (3.0) incorporates a wide variety of image types, including ultrasonograms. The DICOM document encompasses 12 parts, each of which can be updated without updating the entire document. DICOM specifies a hierarchical organization standard that should allow for communication between different systems. When utilizing an echograph that can export a study in a DICOMcompatible format, a digital echocardiogram reader should be able to view the demographic information, individual images, and loops and have access to regional and pixel calibrations. A manufacturer may elect to adhere to all or part of the DICOM standard. This is documented in the DICOM conformance statement. When evaluating a digital echocardiography laboratory system as well as echograph, it is important that the degree of adherence to the DICOM standard be defined. For example, an echograph manufacturer may elect not to put all of the calibration information into the digital download, making it impossible to read calibrations.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Acquisition of Signal Output Digital versus Digitized One of the earliest steps in the digital laboratory process is acquiring the signal output from the echograph. The majority of contemporary machines have the option 951

Figure 44-1 Depiction of the layout for a digital echocardiography laboratory using a separate series of network connections—an intranet. Abbreviations and terms are given in Table 44-1 . The intranet is wired between two separate floors within one building. A centralized server and optical jukebox is used, with switches on each floor. There is highspeed connectivity between switches and server. The physician reading stations are served by 400 megabit lines. The inset box in the upper left is a separate office that operates in a similar fashion but is not linked to the other floors.

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Figure 44-2 Depiction of the layout for a digital echocardiography laboratory network between four different institutions that are physically separate by several blocks. The systems do not use one vendor (as shown in Figure 44-1 ) but allow for the connectivity of several different types of echographs and computer workstations. The systems use a fiberoptic backbone provided by the University; therefore, bandwidth is shared with other applications. The connections between each local institution and the backbone involve a dedicated 10 Mbps switch. All images are stored on one 200 GB RAID array. This arrangement is a hybrid, with components of dedicated and shared resources.

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of a true digital output via a network card, Ethernet card, or some other modality. Older machines will have only an analog signal output, which then must be digitized via a frame grabber system. Once the image has been placed in a digital format, either digital or digitized, the remainder of the process remains essentially the same. The advantages of a true digital signal have been reported. With time, it is anticipated that the echographs requiring digitizing will be phased out, allowing implementation of a true digital signal and all the benefits inherent to it. For systems that do require digitization, several additional steps must be considered. The entire analog signal cannot be concisely digitized, so compromises must be made. These compromises include the length of time that is digitized, the interval between each digitized segment or frame, and the length of time encoded. The playback speed of the digitized signal must be determined. In the early days of echocardiography, it was customary to use an eightframe loop, which was formed by creating frames in increments of 50 to 67 msec. This interval was shown to be reasonable for two-dimensional recordings. When diastolic features needed to be emphasized, it was necessary to either increase the digital interval to 83 to 100 msec or to add a built-in start delay of 30 to 50 msec after the initial R wave before the digital triggering process was begun. It was customary to trigger on the R wave, as it was an easily recognizable signal from the echograph. The original eight-frame loop was chosen mostly out of necessity because of limited memory. As the field progressed, memory became less of an issue and cycle lengths of any dimension could be included. With the advent of a true digital output, it became apparent that one was limited more by memory available in the system than by any other determinant. Typically, 953

one can elect to acquire a digital image stream beginning at the R wave from the electrocardiographic signal, or one can determine to acquire a signal based solely on a length of time one wishes to review. The advantage of triggering from the R wave is that the cardiac cycle has an easily recognized start point and end point. One may elect to trigger off the R wave and acquire one, three, five, or even 10 continuous cycles for review. In practice, this tends to be a more effective solution than simply grabbing

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a preset length of time with cardiac cycles. With use of the latter scheme, the image may begin somewhere in systole or diastole and tends to be disorienting, unless the image can be trimmed to a recognizable start point. The latter approach has the advantage in cases with significant arrhythmias or artifactual electrocardiographic signals that may cause problems in R wave triggering. Loop versus Streaming One of the advantages of a digital system is the ability to determine whether one is going to replay a loop of cardiac cycles in an endless fashion or whether one wants to instead try to do a form of digital streaming. The advantage of a loop is that it allows endless access to the same view, providing for meticulous attention and interpretation. Digital streaming is more of a real-time interpretation modality. It is beyond the resources of most systems to allow a typical 20-minute examination to be entirely encoded in a digital format and stored without using immense amounts of memory. One of the goals of a digital echocardiography system is not to simply replace videotape with digital and have the examiner try to fast-forward through a digital file as one would fast-forward through a videotape. Streaming may have more applicability to teleconferencing or remote telemedicine than it does for a routine application in a digital echocardiography laboratory. Exceptions are obviously possible. One may elect to stream a limited subset of information into an acquisition and storage system. Intertwined into all discussions of acquisition, display, storage, and transmission of images is the complexity of computer memory. Increasing image resolution, shades of color, and rate of digitization all increase the size of a file and the memory required to store that file. The more memory that is required, the more difficult it is to store and transmit the image. Therefore, a compromise must always be inherent in any digital echocardiography laboratory between the amount of information that one wishes to acquire and the ability of one to deal with that information in an effective fashion. Although a 512 × 512 pixel display may be a "standard," a 256 × 256 display essentially carries the same information with very little, if any, loss in resolution. The actual resolution of the signal exiting the echograph has a typical resolution of 256 × 256; thus, there is little to be gained by increasing the display resolution or the exported signal resolution in most circumstances. The advantages of some existing systems are in the

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Sonographer Training A digital acquisition approach is believed to place more of a burden on the sonographer. The sonographer must decide whether to digitally acquire an image and if the acquired image is representative and of diagnostic quality. Rather than taping 10 to 20 minutes of a study, the study is represented by a series of 10 to 30 loops or frames of images. This requires that the sonographer actively review each image and determine whether to save or delete it from the image set. The mechanics of digital acquisition are quickly learned. This process may be facilitated by visiting an established laboratory or by training with an applications specialist. Initially, this process will lengthen the echocardiography examination until the sonographer becomes comfortable with the process. Once the initial training is completed, sonographers will find that the digital approach improves the quality of the study by ensuring that the information needed is displayed. Arguments have been made that if the sonographer does not recognize an abnormality, he or she will not acquire the proper view. The same argument could be made of videotape (the sonographer would not have pushed the record button). Guidelines are being formulated by the American Society of Echocardiography that will suggest a set of "standard" views that should be obtained on all patients. The purpose of the guidelines is to avoid the problem that could potentially arise from not acquiring enough information during a digital examination. During the implementation of a digital examination, close collaboration between the sonographer and echocardiographer is essential. One of the advantages of the digital laboratory is the facility for careful review of selected images so that questions can be addressed. One can quickly review a study to determine whether additional images or Doppler is needed.

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Storage Devices The field of computer memory storage is always in evolution. In the early days of digital echocardiography, studies were stored on 5¼-inch floppy discs. Within a few years, 3½-inch discs became standard, with a small increase in memory. More recently, the field has evolved to include optical discs, compact discs, digital tape, and a RAID array. The newer devices all share common features of being able to store massive amounts of digital data in a format that allows for relatively fast accessibility and retrieval. Intertwined with the access time of the storage devices are the ever-present issues of networking traffic, server traffic, and available bandwidth. When one is choosing a long-term storage device, all of these factors must be kept in mind and discussed with an information system specialist. Currently, the most common options include a CD jukebox, RAID array, DVD jukebox, or MOD system. Long-term Data Archiving and Back-up Keeping medical records for 7 years appears to be the norm at most institutions. Obviously, a massive disc failure, 954

fire, or other natural disaster could potentially destroy thousands if not hundreds of thousands of patients' data quickly. It is recommended that all information be backed up and stored at a separate site. A back-up system need not have the rapid accessibility, flexibility, or portability of the primary system. Storage of back-up information should be in a separate site, fireproof safe, or similar location. One of the advantages of the digital echocardiography laboratory is that information can be copied, and each copy remains the exact duplicate of the primary source. This clearly separates the digital modality from videotape,

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Display Many options exist for the monitor display of the digital echocardiographic image. The majority of current systems use a series of thumbnail images, which may be either static or dynamic (Fig. 44-3) . By placing the mouse cursor over the thumbnail image and clicking, the examiner can get an enlarged view, which allows for interpretation (Fig. 44-4) . The number of views arranged on the screen is usually a user-definable option. For example, when comparing serial studies, one may elect to compare two or four views at once. In other cases, one may choose the same screen size for only one view, allowing for increased image size. Offline measurements would typically be performed on a full-screen image to maximize accuracy. Other examples of multiple views playing simultaneously would be for stress echocardiography, in which case such a display is essential. How the information is displayed is a software-definable option within the parameters of the monitor hardware. As such, the user should have the choice in determining which set-up is most effective.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Interpretation of the Digital Echocardiographic Image One of the key questions in the interpretation of a digital echocardiographic image is whether such interpretation is comparable to interpretation that would be made from the same images recorded on videotape. This question has been addressed and answered in several studies. Several authors have reported their results comparing videotape to digital interpretation of echocardiograms using a variety of different digital techniques. The majority of the digital techniques have compared different forms of compression algorithm (JPEG, MPEG) or lossless compression. Digital interpretation of images was supported by Segar et al,[19] in whose study 110 echocardiographic examinations were recorded simultaneously on videotape and with a commercially available digitized frame grabber. Studies were stored using a lossless compression algorithm. In this study, exact agreement of interpretation between the videotape and digital image was found for 83% of patients. A major discrepancy in the interpretation was found in only 2% and a minor discrepancy in 15%. Most discrepancies occurred in the setting of valvular heart disease. When compared with a consensus interpretation, there were an equal number of errors between the digital and the videotape interpretation. Interestingly, in this study, it was shown that there were findings noted in the digital interpretation that were not found in the videotape. When reviewed, the videotape revealed in each case that the finding was present but had been overlooked in the initial interpretation. This was believed to reflect the thought that during interpretation of a videotape one may be subjected to information overload. The cine loop format of a digital recording allows for repeated visual exposure to an image. This potentially allows for increased recognition of abnormalities. Similar results were reported by Mobarek et al.[20] Among 1156 parameters or measurements assessed, there was a 99% concordance rate for normal versus abnormal. Karson et al[21] [22] reported that JPEG compression of up to 20:1 is possible

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without any interpretation errors being introduced by the compression algorithm. Although JPEG does result in some loss of information, image quality is not adversely affected unless very high ratios are used. JPEG ratios of 20:1 are similar to s-VHS images. Ratios of 40:1 have been used for M-mode or spectral Doppler, and 65:1 for color images.[10] [21] [22] MPEG compression has also been used. It was designed for moving images and clearly is necessary for any live transmission or telemedicine type applications. It currently is not supported by the DICOM 3.0 standards.[23] [24] [25] Spencer et al[25] reported that compression ratios of up to 200:1 demonstrated no degradation in endocardial visualization quality or diagnostic content. Compression to this degree can markedly decrease the size of image files. The advantages of compression algorithms have been well documented. By allowing compression, one is able to allow the digital echocardiographic information to be condensed into a format that allows for easier storage, transmission, and access. Essentially one is allowing for the information to be stored in a fraction of the space that would be needed had it not been compressed. Advantages of a digital approach include access to old studies, not just to the old reports. In the past, it was commonplace to compare a current study to an old report. The virtue of the digital approach is that it allows the actual old images to be compared to the new images in a side-by-side fashion. Measurements can be repeated and the interpretation can be checked and rechecked. The digital approach also allows for easy review by clinicians, house staff, medical students, and echocardiographers. It is no longer necessary for a videotape to be pulled out of an echograph, rewound to the correct study, and then shown. Such accessibility increases the utility of echocardiography for patient care. Interpretation of digital echocardiograms from a physician's standpoint appears to be rather straightforward. One new feature of a digital echocardiographic study is that the physician has the option and in fact the requirement to check and remeasure the images and Doppler information. This capability has been difficult to implement in the past with a videotape system. It not only 955

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Figure 44-3 Still frame image from a commercially available software program used for digital echocardiography. Depicted at the bottom is a series of thumbnail images representing a series of quad-screen loops and still frame Doppler images. The demographic information for the patient is shown on the left, and the upper portion contains the toolbar commands.

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Figure 44-4 Depiction of how thumbnail images can be clicked on with a mouse cursor, bringing up a quad-screen display. The thumbnail images of the remaining views are displayed to the left.

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requires that the physician be able to perform the measurements but also allows for an excellent method of feedback to the sonographer. It enhances communication between the physician and sonographer. DICOM allows for image calibration information to be stored in an appropriate file format, which can be read by a majority of DICOM readers. This allows for measurement packages to incorporate the calibration information so that accurate measurements can be made. Other advantages of a digital approach include the ability to perform stat interpretations for echocardiograms obtained in the operating, intensive care unit, emergency room, clinic, or outreach center. The ability to interpret these images may exist at home if there is a connection between the echocardiography network and the physician's home computer. With the advent of satellite and cable modem capabilities, these connections should be more prevalent. Not all digital echocardiography laboratories rely solely on the digital image. For stress echocardiography, arguments exist that a digital interpretation may not be as good as a combined digital and videotape review.[26] Other investigators have reported the reproducibility in interpretation with digital stress echocardiographs to be quite good.[27]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Reporting of Information Once a digital echocardiographic study is interpreted, the digital report can be placed on the hospital information system platform, printed out, faxed, or even e-mailed to physicians' offices. As in any computer-based information system, adequate security and passwording is essential. Different encryption algorithms have been developed to protect patient confidentiality and the security of the medical information. Systems exist for Internet browser access to patient reports. In the future, it is anticipated that both reports and image clips will be readily available on the Web.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Changes in Practice Patterns One of the common limitations of the traditional videotape-driven echocardiography laboratory was the problem of the videotape always residing within the echocardiographic instrument. This commonly resulted in a number of current studies on one tape, which could not be interpreted until late in the day after all the patients were seen. For the physician, this meant that results were not available on the same day that the study was performed. For the echocardiographer, this meant late nights in the echocardiography laboratory interpreting studies. Clinicians, surgeons, and other medical personnel would not have easy access to the echocardiographic images, resulting in clinical decision making from dictated reports or, all too commonly, from sonographer interpretations. The ability of an echocardiographer to almost instantly interpret a digital study allows the patient to leave the echocardiography laboratory with a completed and final report. Not only can patients know the result of their study, their treating physician can have a timely, completed report in hand. The physician may also have unlimited access to the echocardiographic study through any reading station. Reading stations may be located not only in the echocardiography laboratory, but also in the cardiac catheterization laboratory, the critical care unit, the intensive care unit, the operating room, and outpatient offices. With a digital echocardiography laboratory, rapid interpretation of echocardiograms is limited only by the availability of the echocardiographer, not by the logistical limitations of the laboratory. In large practices with dedicated echocardiographers, it may be reasonable to assign an echocardiographer to the laboratory throughout the day so that studies can be interpreted as they are completed. This would also allow the echocardiographer to review every study, ensuring that all necessary information and views are obtained before the patient leaves the laboratory.

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Remote interpretation of echocardiograms from sites physically removed from the echocardiography laboratory may become routine. Use of a digital approach in the operating room has been described and compared to more traditional formats.[28] Telemedicine applications have been reported for pediatrics[29] and for interpretation of echocardiograms[30] [31] and dobutamine stress echocardiograms from the emergency room.[32] For example, at Indiana University it is routine for a physician to be asked to interpret a study from the VA hospital or Krannert Institute of Cardiology on an urgent basis. This can be easily accomplished from one's office computer, since all echocardiograms performed on campus are accessible from one network. As the field of telemedicine grows, it is anticipated that remote interpretation of studies from different states or outer space will become common.[33] The digital echocardiography laboratory is no longer a concept, it is a reality. There is sufficient experience to justify the implementation of a digital echocardiography laboratory in every functioning laboratory today.

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