Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications, Third Edition

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Catheter Ablation of Cardiac Arrhythmias Basic Concepts and Clinical Applications

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Catheter Ablation of Cardiac Arrhythmias Basic Concepts and Clinical Applications Third Edition Edited by

David J. Wilber, MD Douglas L. Packer, MD William G. Stevenson, MD

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© 1995 by Futura Publishing Company Inc., New York © 2008 by Blackwell Publishing Blackwell Futura is an imprint of Blackwell Publishing Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia All rights reserved. No part of this publication may be reproduced in any form or by any electronic or mechanical means, including information storage and retrieval systems, without permission in writing from the publisher, except by a reviewer who may quote brief passages in a review. First published 1995 Second edition 2000 Third edition 2008 1

2008

ISBN: 978-1-4051-3117-9 Library of Congress Cataloging-in-Publication Data Catheter ablation of cardiac arrhythmias : basic concepts and clinical applications / edited by David J. Wilber, Douglas L. Packer, and William G. Stevenson. – 3rd ed. p.; cm. Rev. ed. of: Radiofrequency catheter ablation of cardiac arrhythmias / edited by Shoei K. Stephen Huang and David J. Wilber. 2nd ed. c2000. Includes bibliographical references and index. ISBN-13: 978-1-4051-3117-9 (alk. paper) ISBN-10: 1-4051-3117-9 (alk. paper) 1. Catheter ablation. 2. Arrhythmia–Interventional radiology. I. Wilber, David J. II. Packer, Douglas. III. Stevenson, William G., MD. IV. Radiofrequency catheter ablation of cardiac arrhythmias. [DNLM: 1. Tachycardia, Supraventricular–therapy. 2. Atrial Fibrillation–therapy. 3. Catheter Ablation–methods. 4. Tachycardia, Ventricular–therapy. WG 330 C3637 2008] RD598.35.C39R33 2008 617.4′12059–dc22 2007034695 A catalogue record for this title is available from the British Library Commissioning Editors: Steve Korn and Gina Almond Development Editor: Beckie Brand Editorial Assistant: Victoria Pittman Production Controller: Debbie Wyer Set in 9.5/12 Palatino by Graphicraft Limited, Hong Kong Printed and bound in Singapore by COS Printers Pte Ltd For further information on Blackwell Publishing, visit our website: www.blackwellcardiology.com The publisher’s policy is to use permanent paper from mills that operate a sustainable forestry policy, and which has been manufactured from pulp processed using acid-free and elementary chlorine-free practices. Furthermore, the publisher ensures that the text paper and cover board used have met acceptable environmental accreditation standards. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The Publisher is not associated with any product or vendor mentioned in this book. The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.

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Contents

List of Contributors, vii Foreword, x Preface, xi

I Fundamentals 1 Overview of cardiac anatomy relevant to catheter ablation, 3 Siew Yen Ho 2 Biophysics and pathophysiology of lesion formation by transcatheter radiofrequency ablation, 20 David E. Haines 3 Alternative energy sources for catheter ablation, 35 Saman Nazarian and Hugh Calkins

9 Catheter ablation of atrioventricular nodal reentrant tachycardia, 120 Warren M. Jackman, Deborah Lockwood, Hiroshi Nakagawa, Sunny S. Po, Karen J. Beckman, Richard Wu, Zulu Wang, Benjamin J. Scherlag, Anton Becker, and Ralph Lazzara 10 Catheter ablation of accessory pathways, 149 Aman Chugh, Frank Bogun, and Fred Morady 11 Diagnosis and ablation of typical and reverse typical (type 1) atrial flutter, 173 Gregory K. Feld, Ulrika Birgersdotter-Green, and Sanjiv Narayan 12 Catheter ablation of macroreentrant right and left atrial tachycardias, 193 Hiroshi Nakagawa, Warren M. Jackman, Katsuaki Yokoyama, Richard Wu, Karen J. Beckman, Sunny S. Po, Deborah Lockwood, Sameer Oza, Himanshu Shukla, Lisa Herring, and Ralph Lazzara

4 Mapping for localization of target sites, 49 William G. Stevenson 5 Three-dimensional mapping technology and techniques: applications in atrial fibrillation, 60 Douglas L. Packer 6 Utility of intracardiac echocardiography in cardiac electrophysiology, 72 Douglas L. Packer 7 Catheter ablation in young patients: special considerations, 91 Edward P. Walsh

II Supraventricular tachycardia 8 Focal atrial tachycardias, 105 Satoshi Higa, Ching-Tai Tai, and Shih-Ann Chen

III Atrial fibrillation 13 Circumferential ablation of the pulmonary veins, 221 Carlo Pappone and Vincenzo Santinelli 14 Long linear lesions in the treatment of atrial fibrillation, 237 Li-Fern Hsu, Prashanthan Sanders, Mélèze Hocini, Michel Haïssaguerre, and Pierre Jaïs 15 Mapping the electrophysiologic substrate to guide atrial fibrillation ablation, 250 Koonlawee Nademanee, Mark Schwab, Joshua Porath, and Aharon Abbo 16 Ablation for rate control of atrial fibrillation, 261 Harish Doppalapudi and G. Neal Kay v

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Contents

IV Ventricular tachycardia 17 Ablation of idiopathic right ventricular tachycardia, 279 David J. Wilber and Sandeep Joshi 18 Idiopathic left ventricular tachycardias, 298 Akihiko Nogami and Hiroshi Tada 19 Catheter ablation of stable ventricular tachycardia after myocardial infarction, 314 William G. Stevenson

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20 Substrate-based ablation of postinfarction ventricular tachycardia, 326 David J. Wilber 21 Ablation of ventricular tachycardia associated with nonischemic structural heart disease, 342 Jason T. Jacobson, David Lin, Ralph J. Verdino, Joshua Cooper, and Francis E. Marchlinski Index, 364

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Contributors

Editors

Frank Bogun, MD

David J. Wilber, MD

Division of Cardiology University of Michigan Ann Arbor, MI, USA

Cardiovascular Institute Loyola University Medical Center Maywood, IL, USA

Douglas L. Packer, MD Division of Cardiac Electrophysiology/Cardiology Department of Internal Medicine Mayo Clinic and Foundation Rochester, MN, USA

William G. Stevenson, MD Director, Clinical Cardiac Electrophysiology Program Brigham and Women’s Hospital Associate Professor of Medicine Harvard Medical School Boston, MA, USA

Contributors Aharon Abbo, MD Clinical Development Biosense Webster (Israel) Tirat Carmel, Israel

Hugh Calkins, MD Division of Cardiology The Johns Hopkins Hospital Baltimore, MD, USA

Shih-Ann Chen, MD Division of Cardiology, Department of Medicine National Yang-Ming University, School of Medicine and Taipei Veterans General Hospital Taipei, Taiwan

Aman Chugh, MD Division of Cardiology University of Michigan Ann Arbor, MI, USA

Joshua Cooper, MD Assistant Professor of Medicine Hospital of the University of Pennsylvania Philadelphia, PA, USA

Harish Doppalapudi, MD Anton Becker, MD Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Division of Cardiovascular Disease University of Alabama at Birmingham Birmingham, AL, USA

Gregory K. Feld, MD Karen J. Beckman, MD Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Cardiac Electrophysiology Program Division of Cardiology, Department of Medicine University of California, San Diego School of Medicine San Diego, CA, USA

Ulrika Birgersdotter-Green, MD

David E. Haines, MD

Cardiac Electrophysiology Program Division of Cardiology, Department of Medicine University of California, San Diego School of Medicine San Diego, CA, USA

Heart Rhythm Center Cardiology Division William Beaumont Hospital Royal Oak, MI, USA

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Contributors

Michel Haïssaguerre, MD

David Lin, MD

Hôpital Cardiologique du Haut-Lévêque Bordeaux, France

Assistant Professor of Medicine Department of Cardiology Hospital of the University of Pennsylvania Philadelphia, PA, USA

Lisa Herring, RN Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Satoshi Higa, MD Second Department of Internal Medicine Faculty of Medicine University of the Ryukyu Okinawa, Japan

Siew Yen Ho, PhD, FRCPath, FESC Reader and Honorary Consultant Cardiac Morphology National Heart & Lung Institute and Royal Brompton Hospital London, UK

Mélèze Hocini, MD Hôpital Cardiologique du Haut-Lévêque Bordeaux, France

Li-Fern Hsu, MBBS Hôpital Cardiologique du Haut-Lévêque, Bordeaux, France

Warren M. Jackman, MD Professor of Medicine Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Jason T. Jacobson, MD Division of Cardiovascular Medicine Hospital of the University of Pennsylvania Philadelphia, PA, USA

Pierre Jaïs, MD Hôpital Cardiologique du Haut-Lévêque Bordeaux, France

Deborah Lockwood, MA, BM, BCh Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Francis E. Marchlinski, MD Professor of Medicine Hospital of the University of Pennsylvania Philadelphia, PA, USA

Fred Morady, MD Division of Cardiology University of Michigan Ann Arbor, MI, USA

Koonlawee Nademanee, MD Director of Electrophysiology Pacific Rim Electrophysiology Research Institute Inglewood, CA, USA

Hiroshi Nakagawa, MD, PhD Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Sanjiv Narayan, MD Cardiac Electrophysiology Program Division of Cardiology, Department of Medicine University of California, San Diego School of Medicine San Diego, CA, USA

Saman Nazarian, MD Cardiology Fellow Division of Cardiology The Johns Hopkins Hospital Baltimore, MD, USA

Akihiko Nogami, MD Sandeep Joshi, MD Cardiovascular Institute Loyola University Medical Center Maywood, IL, USA

Division of Cardiology Yokohama Rosai Hospital Yokohama, Japan

Sameer Oza, MD G. Neal Kay, MD Division of Cardiovascular Disease University of Alabama at Birmingham Birmingham, AL, USA

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Carlo Pappone, MD, PhD Ralph Lazzara, MD Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

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Department of Cardiology, Electrophysiology and Cardiac Pacing Unit San Raffaele University Hospital Milan, Italy

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Contributors

Sunny S. Po, MD, PhD

Ching-Tai Tai, MD

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Division of Cardiology, Department of Medicine National Yang-Ming University, School of Medicine and Taipei Veterans General Hospital Taipei, Taiwan

Joshua Porath, MSc, MBA Director of Business Development Biosense Webster (Israel) Tirat Carmel, Israel

Ralph J. Verdino, MD Assistant Professor of Medicine Hospital of the University of Pennsylvania Philadelphia, PA, USA

Prashanthan Sanders, MBBS, PhD Hôpital Cardiologique du Haut-Lévêque Bordeaux, France

Vincenzo Santinelli, MD Department of Cardiology, Electrophysiology and Cardiac Pacing Unit San Raffaele University Hospital Milan, Italy

Edward P. Walsh, MD Chief, Electrophysiology Division Department of Cardiology Boston Children’s Hospital Associate Professor of Pediatrics Harvard Medical School Boston, MA, USA

Zulu Wang, MD Benjamin J. Scherlag, PhD Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Richard Wu, MD Mark Schwab, MD Valley Isle Cardiology Wailuku, HI, USA

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Himanshu Shukla, MD

Katsuaki Yokoyama, MD, PhD

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Cardiac Arrhythmia Research Institute and Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City, OK, USA

Hiroshi Tada, MD Division of Cardiology, Gunma Prefectural Cardiovascular Center Maebashi, Japan

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Foreword

It is now more than 20 years ago that catheter ablation was introduced as a new tool in the management of cardiac arrhythmias. Since then, catheter ablation developed into one of the few curative therapies that we have at our disposal. Most of the current treatment modalities in cardiology will relieve symptoms and may prolong life, but do not result in a real cure, as is the case in coronary heart disease and heart failure. However, interruption of a re-entrant pathway or elimination of an arrhythmic focus can result in a permanent cure. After 20 years, catheter ablation is still in flux. New developments continue to occur as in our approaches to the different types of atrial fibrillation and ischemic ventricular tachycardia. The value of new energy sources such as cryo, laser, ultrasound, and microwave is now being evaluated. Catheter technology and catheter

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handling are changing, an example of which is magnetic catheter navigation. Also hybrid imaging, combining different imaging techniques, has been introduced to facilitate ablation of complex arrhythmias. Obviously, there is great need to be informed about those developments. Therefore, there is every reason to welcome the third edition of a book which, over the years, has become required reading for anyone involved in catheter ablation. It is of great help in selecting optimal mapping and ablation techniques for specific arrhythmias and clinical circumstances at minimal risk to the patient. The editors and authors are to be congratulated for their comprehensive, didactic, in-depth contributions. Hein J. Wellens, MD, PhD, FESC, FACC

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Preface

In the 20 years since radiofrequency energy was introduced to ablate tissue critical to the maintenance of cardiac arrhythmias, there has been a dramatic evolution in both the science and practice of catheter ablation. In the late 1980s, a few hundred procedures were performed annually in a limited number of referral centers; estimates from industry and healthcare databases suggest that up to 500,000 ablation procedures will be performed in 2007 worldwide. Approximately 10% of these procedures are for attempted cure of atrial fibrillation, an indication that did not exist 20 years ago. Since publication of the previous edition of this book in 2000, substantial changes have occurred in clinical concepts, tools and techniques. New arrhythmia syndromes have been identified, and their anatomic and pathophysiologic basis defined. Improved understanding of the substrates underlying common clinical entities such as atrial fibrillation and ventricular tachycardia in the setting of structural heart disease has led to fundamental shifts in how these arrhythmias are targeted for ablation. The 3-D integration of cardiac imaging with electrophysiological data has become increasingly sophisticated and moves closer to real time. New energy sources, catheter designs, and remote navigation systems are changing the landscape in which ablation is performed. The pace of new developments is attested to by the publication of more than 500 peer reviewed manuscripts annually on arrhythmia ablation since 2000, along with scores of monographs and texts. Reflecting these developments, the third edition of Catheter Ablation of Cardiac Arrhythmias has been completely revised. In order to provide more integrated and succinct presentations, the chapter format has been consolidated

and streamlined. A small number of contributors were selected on the basis of their clinical expertise and significant independent contributions to the field in the areas covered by their individual chapters. The book is divided into several sections. Part I is devoted to fundamental aspects of catheter ablation, including cardiac anatomy, the biophysics of various energy sources, the pathophysiology and pathology of lesion formation, and the contribution of mapping and imaging technologies. Parts II-IV cover current physiologic concepts and techniques for the ablation of specific arrhythmias and/or anatomic substrates, including several chapters devoted specifically to atrial fibrillation. Each chapter ends with the author’s personal view of optimal approaches and potential pitfalls. As in previous editions, our goal is to provide a contemporary summary of the technical and clinical aspects of catheter ablation in a single volume. It is our hope that it will remain a valued resource for reference, teaching and daily decision-making. The primary audience for this book is trainees and established practitioners in clinical electrophysiology. However, it should prove useful for general cardiologists, nurses, technicians, and all who care for patients with cardiac arrhythmias. This edition is published at a time of remarkable advances and future opportunities to provide curative therapy and long-term relief for patients suffering with cardiac arrhythmias. They remain our ultimate teachers, and the focus of our collective efforts. David Wilber MD Douglas Packer MD William Stevenson MD

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I

Fundamentals

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1

Overview of cardiac anatomy relevant to catheter ablation Siew Yen Ho

Every new diagnostic technique and every new surgical or interventional procedure in the heart leads to a review of the organ’s anatomy relevant to that particular technique or procedure. Although the anatomy of the heart has remained unchanged, the perspectives from which clinicians can approach the heart have evolved through the ages. Catheter ablation for cardiac arrhythmias is the relatively “new boy on the block” that has led to a new perception of cardiac anatomy in the normally structured as well as the congenitally malformed heart. In this chapter, I hope to provide an overview of the fundamentals in anatomy of the normally structured heart, with emphasis on features relevant to catheter ablation. Necessarily, much of the information is basic, although crucial to knowing where the ablation catheter isaparticularly for beginners who may be literally in the dark in the catheter laboratory.

The heart within the body The concept of viewing the heart in situ in the body is crucial to understanding the relationships between its chambers and structures, as well as the relationships between the heart and other anatomical structures. According to Walmsley [1], descriptions of cardiac anatomy disregard the cardinal principle of using terms in relation to anatomic position. He noted that many textual descriptions and innumerable figures throughout the medical literature view the heart as if it could be held in the hand, with the atria above the ventricles and the left and right hearts lying alongside each other in a sagittal planeabasic and false concepts that have caused untold confusion in the past. Standing the heart on its apex, it is easy to see how the anterior and posterior descending coronary arteries acquired their names. Yet, these same arteries have correct appellationsathe superior and inferior interventricular arteries, respectivelyain some of the older literature. In his elegant atlas, McAlpine [2] also emphasized the importance of describing the heart in its anatomical location

for appropriate clinical correlations. He termed the orientation of the heart, seen in its living condition, as “attitudinal.” Since electrophysiologists “view” the patient with the heart in situ, it is essential that the attitudinal approach [3] should be adopted when describing the spatial relationships of chambers and structures. The names of the chambers remain unaltered, although right heart chambers are not strictly to the right nor left heart chambers strictly to the left. The heart lies in the mediastinum of the thoracic cavity, between the left and right lungs. When viewed from the front, the heart has a trapezoidal silhouette. Two-thirds of its bulk lies to the left of the midline of the chest, with its apex directed to the left and inferiorly. The fibrous pericardium enclosing the heart has as its inner lining a thin membrane, the serous pericardium, which also lines the outer surface of the heart as the epicardium. The pericardial cavity is the space between the parietal lining and the epicardium (Fig. 1.1, upper panel). These layers are continuous at two cuffs, one around the aorta and pulmonary trunk and the other around the veins. Two recesses are found within this pericardial cavity. One, termed the transverse sinus, lies between the posterior aspect of the arterial trunks and the anterior aspect of the atrial chambers. The other, the oblique sinus, is behind the left atrium and limited by the right pulmonary veins and the caval veins to the right side and the left pulmonary veins to the left side (Fig. 1.1). For the ablationist, it is important to note that the right phrenic nerve descends along the lateral aspect of the superior caval vein to pass in front of the hilum of the right lung and then along the fibrous pericardium lateral to the right atrium to reach the diaphragm (Fig. 1.1, lower panel). Its course in front of the hilum can be as little as 1 or 2 mm from the right upper pulmonary vein, although it is frequently 0.5–1 cm or more distant [4]. The left phrenic nerve usually descends along the pericardium over the left atrial appendage, the obtuse cardiac margin and the left obtuse marginal vein and artery, or over the anterior descending artery and great cardiac vein [4]. 3

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PART I

Fundamentals

Figure 1.1 The diagram (top) shows the components of the pericardium and the pericardial sinuses. The specimen (bottom), viewed from the right, shows the cut edge of the pericardium (arrows) and the course of the right phrenic nerve (open circles). Ao, aorta; ICV, inferior caval vein; LA, left atrium; LV, left ventricle; RA, right atrium; RI, inferior right pulmonary vein; RS, superior right pulmonary vein; SCV, superior caval vein.

Relationships of cardiac chambers The relative positions of the cardiac chambers and great vessels are readily displayed with an endocast (Fig. 1.2). The so-called right heart chambers are anterior and to the right (Fig. 1.2A). From the frontal aspect, the right border of the cardiac silhouette is formed exclusively by the right atrium, with the superior and inferior caval veins joining at its upper and lower margins (Fig. 1.2B). The inferior border of the silhouette is marked by the right ventricle. The left border is made up of the left ventricle, but it merges with the pulmonary trunk near the upper border. Apart from the tip of its appendage curling around the edge of the pulmonary trunk, the left atrium is not visible from the frontal aspect (Fig. 1.2B, C). Being the most posterior of the cardiac chambers, the left atrium lies directly in front of the esophagus (Fig. 1.2D–F). While the esophagus is a useful portal for the echocardiographer monitoring procedures, potential risk of damage to the esophagus and 4

vagus nerves of the esophageal plexus must be a consideration when ablating from within the left atrium (Fig. 1.2F). A view from the posterior aspect shows the relationships between the great veins (Fig. 1.2D). The left and right pulmonary veins enter the “corners” of the left atrium, and there is considerable variability in the number and orientation of the veins. The right superior pulmonary vein passes behind the right superior caval vein, and the lower pulmonary vein courses behind the intercaval area of the right atrium. Viewing the endocast from the right aspect shows the location of the right atrium posterior and to the right of the right ventricle (Fig. 1.2A). The plane of the right atrioventricular junction, containing the annular insertion of the tricuspid valve, is orientated nearly vertically. In contrast, the plane of the pulmonary valve is nearly horizontal and located well cephalad, making the pulmonary valve the most superiorly situated of the cardiac valves. On the epicardial side, the root of the aorta is embraced by the musculature separating the inlet and outlet valves of the right ventricle (Fig. 1.2A). Thus, the right ventricle sweeps from posterior to anterior and passes cephalad, such that its outflow tract lies superior to that of the left ventricle (Fig. 1.2A, C, E). From the left aspect, the left ventricle can be seen projecting forward and leftward with the apex, directed inferiorly (Fig. 1.2C). The finger-like left atrial appendage points toward the pulmonary trunk. Unlike the right atrial appendage, the left appendage has a narrow neck, and its entrance (os) is related to the upper left pulmonary vein. As it passes cephalad, the right ventricular outflow tract wraps over the left ventricular outlet. The latter projects rightward and cephalad into the aortic arch, which in turn is directed leftward. Thus, the left and right ventricular outlets have a spiral spatial relationship. The aortic root is located centrally in the heart, with the aortic valve immediately adjacent to the mitral valve. Like the tricuspid valve, the plane of the annular insertion of the mitral valve, marking the atrioventricular junction, is more nearly vertical than horizontal. The great cardiac vein and its continuation into the coronary sinus pass along the epicardial side of the inferior wall of the left atrium (Fig. 1.2C–F). Although related to the posteroinferior and inferior quadrants of the mitral “annulus,” this venous structure does not run directly epicardial to the annulus, but is usually a centimeter or so away (Fig. 1.2F).

The atrial chambers Both the right and left atrial chambers lie to the right of the ventricular chambers that they open into. Each atrium has three componentsathe appendage, the venous part, and the vestibule. They share a septum that separates their

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CHAPTER 1

Overview of cardiac anatomy relevant to catheter ablation

Figure 1.2 A–E. The endocast, viewed from different perspectives, shows the spatial relationships between the right (colored blue) and left (colored red) cardiac chambers. F. The section through a specimen is in the same orientation as the endocast viewed from the left. It shows the course of the esophagus, running directly behind the left atrium. Note the distance between the hinge of the mitral leaflet (black arrow) and the great cardiac vein/coronary sinus (white arrow). Ao, aorta; E, esophagus; ICV, inferior caval vein; LA, left atrium; LB, left bronchus; LI, left inferior pulmonary vein; LS, left superior pulmonary vein; LV, left ventricle; PT, pulmonary trunk; RA, right atrium; RI, right inferior pulmonary vein; RS, right superior pulmonary vein; RV, right ventricle; SCV, superior caval vein.

cavities. Each atrium has morphologically distinct features, primarily based on the extent of pectinate muscles on the endocardial surface, the presence or absence of the terminal crest, and the shape of the appendage [5].

The right atrium Characteristically, the appendage of the right atrium is triangular in shape, with a broad base that meets with the venous component (Fig. 1.3A). In contrast to the smooth endocardial surface of the venous component and the septum, the atrial appendage contains a vast array of interleaving fronds of pectinate muscles that are separated by thin, almost membranous, atrial wall (Fig. 1.3A, B). The pectinate muscles can be traced as offshoots from one side of the terminal crest. On the epicardial aspect, a fat-filled groove corresponding to the terminal crest is a landmark for the location of the sinus node (Fig. 1.3C). The crest is a raised muscular ridge that springs medially from the septal aspect, curves around the anterior quadrant of the entrance of the superior caval vein, and then descends along the posterolateral wall of the atrium toward the entrance of the inferior caval vein (Fig. 1.3D). Its most distal part branches into narrower bundles that blend into the pectinate muscles. The array of pectinate muscles does not reach the hinge line (annular insertion) of the tricuspid valve, but is separated from it by the smooth wall of the vestibule (Fig. 1.3D, E). The area of the atrial wall between the orifice of the inferior caval vein and the hinge line or

annular insertion of the tricuspid valve is dubbed the “flutter isthmus” (or inferior isthmus). Morphologically, it has three zones. The posterior zone, closest to the inferior caval vein, is often fibrous, while the anterior zone is the vestibule (Fig. 1.3E). The middle zone contains the distal branches of the terminal crest and pectinate muscles, with fibrous tissue in between. Frequently, the middle zone is pouch-like, and the depression is known as the sinus of Keith or subeustachian sinus [6,7]. Anatomically, this appears to be the best isthmus to target for ablation, since it is shorter than a more laterally located isthmus and is further from the compact atrioventricular node than the so-called septal isthmus, which is located more medially (Fig. 1.3E). The triangle of Koch is a landmark on the endocardial aspect of the right atrium for locating the atrioventricular node and penetrating the atrioventricular bundle of His. These important structures lie within the superior apex of the triangle in the attitudinally oriented heart (Fig. 1.3F). The anterior border of the triangle is the hinge line of the septal leaflet, while the tendon of Todaro, buried in the musculature of the eustachian ridge, marks the posterior border [8]. At the superior apex of the triangle, the tendon inserts into the central fibrous body, whereas inferiorly the tendon continues into the free margin of the eustachian valve that guards the entrance of the inferior caval vein [8,9]. The ridge is prominent in some hearts, but flat in others. The orifice of the coronary sinus marks the inferior border of the triangle. The vestibule directly anterior 5

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PART I

Fundamentals

Figure 1.3 A. View of the right atrium from the right, with the location of the sinus node (dotted line) marked in the terminal groove. B. The endocast shows the impressions made by the pectinate muscles in comparison with the smooth surface of the vestibule, just proximal to the tricuspid valve (dotted line). C. The distal margin (blue dotted line) of the myocardial sleeve on the wall of the superior caval vein extends beyond 1 cm (red line) in this heart. The sinus node (red dotted line) is at the venoatrial junction. D. The right atrium is displayed to show the terminal crest separating the pectinate muscles from the smooth venous component (open arrows) between the orifices of the caval veins. The intercaval area, aortic mound, eustachian ridge, and vicinity of the coronary sinus orifice (blue arrow), together with the oval fossa, give the erroneous impression of an extensive septal aspect. E. The area between the orifice of the inferior caval vein (green broken line) and the hinge of the tricuspid valve is the region of the flutter isthmus. The anterior zone (a) is the vestibule of the tricuspid valve; the middle zone (m) is a fibromuscular area; and the posterior zone (p) is usually fibrous, with

scanty muscle fibers. The shortest distance (blue dotted line) is the so-called septal isthmus, while the longest distance (line with blue dashes and dots) is more laterally situated. The inferior isthmus (blue broken line) lies in between. F. The triangle of Koch is delineated anteriorly by the hinge line of the septal leaflet of the tricuspid valve (broken line) and posteriorly by the tendon of Todaro (row of circles), glistening in the musculature of the eustachian ridge. Transillumination shows the membranous septum at the apex of the nodal triangle. The atrioventricular node and bundle are superimposed. The putative slow pathway (blue arrow) approaches from inferior, and the fast pathway (double arrows) approaches from anterior and superior. G. An extensive valve, with small perforations, guards the orifice of the coronary sinus (arrow). AM, aortic mound; CS, coronary sinus; ER, eustachian ridge; ICV, inferior caval vein; OF, oval fossa; RA, right atrium; RI, right inferior pulmonary vein; RS, right superior pulmonary vein; SCV, superior caval vein; TC, terminal crest; TV, tricuspid valve; V, vestibule.

to the orifice is the area commonly known as the septal isthmus, which is ablated to eliminate the so-called slow pathway in atrioventricular nodal reentrant tachycardia (Fig. 1.3F) [10,11]. The so-called fast pathway, on the other hand, putatively sweeps from the anterior and superior

part of the atrium to approach the apex of the triangle of Koch [12,13]. Owing to its proximity, the atrioventricular node is at risk of damage, accounting for the higher incidence of postprocedural heart block in patients undergoing fast-pathway ablation [14].

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CHAPTER 1

The orifice of the coronary sinus marking the posterior part of the base of the nodal triangle is usually guarded by a flimsy crescent-shaped valve, the thebesian valve. This valve is attached posteroinferiorly and has variable morphologies, ranging from fibrous bands to a filigree network (Fig. 1.3G) [15]. Hellerstein and Orbison [16] reported large flap-like valves that may present as obstacles to intubation in 25% of hearts. Posterior and inferior to the coronary sinus is the orifice of the inferior caval vein. This venous opening is guarded by the eustachian valve, which attaches to its anterolateral borders. This valve is usually thin and membrane-like, but is muscular in some hearts. Occasionally, it is a Chiari network that may extend to cover the orifice of the coronary sinus. The entrance of the superior caval vein into the roof of the right atrium is not guarded by a valve. Instead, the terminal crest passes around its anterior and lateral borders. While the wall of the inferior caval vein is seldom covered by muscle on the outside, the superior cavoatrial junction is usually invested in a muscular sleeve that extends from the atrial wall to various lengths along the superior caval vein (Fig. 1.3C). This is clearly shown in an illustration in the paper by Keith and Flack [17] on their discovery of the sinus node. On the endocardial surface, the terminal crest demarcates the pectinated portion of the right atrium from the smooth-walled intercaval area, the venous component (Fig. 1.3D). The crest is the thickest part of the parietal wall [18]. The sinus node is located in the terminal crest in the anterolateral part of the junction [19,20]. In approximately 10% of hearts, however, the sinus node is horseshoeshaped and located in the anterior quadrant [21]. The septal aspect of the right atrium appears to be rather extensive at first sight. Walmsley and Watson [22] emphasized the importance of distinguishing between the “medial wall of the right atrium” and the “interatrial septum.” The anterior part of the “medial wall” is termed the aortic mound, on account of its close relationship to the right coronary aortic sinus (Fig. 1.3D, G). Perforation of the atrial wall in this region leads to the transverse pericardial sinus and the aortic root. The true extent of the atrial septum is discussed below.

The left atrium This chamber has an appendage that is characteristically narrow in humans and shaped like a crooked finger [5]. The appendage has a crenellated appearance externally and can give the appearance of lobes (Fig. 1.4A). The tip of the appendage can be directed anterosuperiorly, superiorly, inferiorly, or even curling over the body of the appendage (Fig. 1.4B) [23]. The appendage overlies the left atrioventricular groove containing the circumflex artery.

Overview of cardiac anatomy relevant to catheter ablation

In the majority of cases, it also overlies the left main stem or proximal portion of the anterior descending coronary artery and the left wall of the pulmonary trunk. The junction of the appendage with the rest of the atrial chamber athe os of the appendageais not marked by a muscle band equivalent to the terminal crest. The endocardial surface of the appendage is irregular, with an array or whorls of muscle bundles that occasionally extend beyond the os into the adjacent atrial wall. In between the muscle bundles, the wall of the appendage is thin, almost membranous. The os of the appendage is anterior to the orifice of the left superior pulmonary vein. The isthmus, the socalled left atrial ridge, between the pulmonary vein and the os varies from approximately 0.5 to 2.5 cm in the adult heart (Fig. 1.4C, D). The remainder of the left atrial wall has a fairly smooth endocardial surface that belies the complexity of its myocardial structure [24–26]. Since there are no pectinate muscles to provide the contrast in topography, the vestibular portion can only be described as that part of the atrial wall immediately proximal to the insertion of the mitral valve. This includes the so-called mitral isthmus, which is the atrial wall between the orifice of the left inferior pulmonary vein and the mitral valve (Fig. 1.4C, D). When ablating the left atrium for atrial fibrillation, many operators now add an ablation line in this isthmus in the posteroinferior wall of the left atrium. It is relevant to note that the circumflex artery and the great cardiac vein, in continuity with the coronary sinus, run along the epicardial side (Fig. 1.4C). Furthermore, small pits and crevices are found occasionally in this otherwise smooth isthmic region. These crevices are in thin areas in the atrial wall, resembling the thin walls that are between pectinate muscles. Since the mitral orifice is kidney-shaped rather than circular, the vestibule is similarly shaped. The gentle inner curvature accommodates the root of the aorta on the epicardial aspect. The venous component is the largest part of the left atrium. The superior wall of the left atrium is related to the bifurcation of the pulmonary arteries (Fig. 1.2D). The posterior atrial wall lies between the orifices of the pulmonary veins (Fig. 1.2D). While there are usually four veins, each inserting into a corner of the venous component, there is also considerable variation [27,28]. Where there are fewer than four orifices, this is due to two or more veins on the same side coming to a confluence before entering the atrium [29]. The orientation and configuration of the venous insertions also vary, and five types have been described [30]. The venoatrial junctions often are not discrete, especially when the veins widen as they approach the atrium. However, with respect to ablating the atrial wall in order to isolate the pulmonary veins, it is pertinent to note that the distance between left and right veins is wider than that between superior and inferior veins when there is the usual arrangement of four venous orifices. 7

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Fundamentals

Figure 1.4 A. The left atrial appendage, viewed from the left, shows the narrow neck (between the triangles) and the course of the oblique left atrial vein or ligament of Marshall (broken line). B. Endocasts of atrial appendages, showing the different shapes and angles relative to the os. C. The left atrial isthmus (blue arrows) lies between the orifice of the left inferior pulmonary vein, and the mitral valve is of variable thickness. On the epicardial side run the great cardiac vein (v) and the coronary artery (a). Note in this heart that the os of the appendage is adjacent to the orifice of the left superior pulmonary vein. D. This heart, sectioned in the same orientation as the previous one, shows a wide separation between the os and the left superior pulmonary vein. The left atrial isthmus (dashed and dotted line) passes through several small pits (arrow). A thin part of the atrial wall (pale color) is indicated by the asterisk. Note the transverse sinus (triangle) between the aortic root and the anterior left atrial wall. E, F. The right and left superior pulmonary veins, respectively, have been dissected from the outer surface to show the myocardial sleeves that extend beyond the venoatrial junction (broken line). The distal margin of the sleeves ends abruptly (small arrows) or fades out gradually (dotted line). Ao, aorta; LI, left inferior pulmonary vein; LS, left superior pulmonary vein; MV, mitral valve; PT, pulmonary trunk.

Moreover, muscular sleeves that continue from the atrial wall to the outer side of the venous wall are longer and occupy more of the circumference in the upper pulmonary veins than the lower veins (Fig. 1.4E, F) [25,28,31,32]. The sleeves are thickest at the venoatrial junctions and become thinner distally, where they terminate in a discrete margin or else taper and fade away (Fig. 1.4E, F). The posterior wall of the left atrium is adjacent to the esophagus (Fig. 1.2F), separated only by the fibrous pericardium and periesophageal tissues of esophageal arteries, fibrofatty tissues, nerve plexus, and lymph nodes. The minimal distance between the endocardial surface and the esophageal wall is approximately 3.5 mm, as measured in cadavers in a recent study [33].

The atrial septum Partitioning the atrial chambers, the atrial septum is not as extensive as is usually perceived [5]. The true septum, 8

which can be crossed without exiting the heart or traversing through epicardial tissues, is limited to the flap valve of the oval fossa and the immediate muscular rim that surrounds it on the right atrial aspect (Fig. 1.5A, B). The normal configuration of the septum can be likened to a door drawn tightly against and overlapping the door frame. The frame is an infolding of the right atrial wall, forming the rim (or limbus), while the door is the flap valve (Fig. 1.5C). While most hearts have a well-defined muscular rim on the right atrial aspect, allowing the operator to “feel” the “jump” from firm muscular rim to tenting of the thin valve with the catheter for safe transseptal puncture, some hearts have little change in topography and the valve is thicker (Fig. 1.5A, B). Using transesophageal echocardiography, Schwinger and colleagues [34] found an abrupt change from thick rim to thin valve in 82% of patients and gradual thinning in 18%. They also found that the valve had a mean thickness of 1.8 ± 0.7 mm on

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Overview of cardiac anatomy relevant to catheter ablation

Figure 1.5 A. This view into the right atrium shows a small oval fossa (between the arrows) without distinct margins. The eustachian valve is a Chiari network. B. The atrial chambers, sectioned through the oval fossa (open arrow) to show the fold (broken arrows) of the superior rim and the epicardial fat in the inferior rim (*). Note the proximity of the right pulmonary veins to the plane of the septum. C. This right atrial view shows a large oval fossa with a well-defined muscular rim. The aortic mound lies anteriorly. The open arrow indicates the site of probe patency in the fossa. D. The same heart, sectioned to show the left atrial aspect of the septum, shows the location of the crescentic opening (open arrow), corresponding to the probe patency. Note the thin atrial wall (red arrow) immediately opposite the crescentic opening and the proximity of the aortic root. The blue circles correspond to the muscular rim in the right atrium. AM, aortic mound; Ao, aorta; CS, coronary sinus; I, orifice of the inferior caval vein; ICV, inferior caval vein; MV, mitral valve; RI, right inferior pulmonary vein; RS, right superior pulmonary vein; S, orifice of the superior caval vein; SCV, superior caval vein; TC, terminal crest; TV, tricuspid valve.

echocardiographic assessment, whereas Shirani et al. [35] reported a mean thickness of 1.9 ± 0.99 mm in hearts from postmortems. Using intracardiac echocardiography to guide transseptal puncture in 19 patients, Hanaoka and colleagues [36] found that the needle entered the middle of the valve in only two cases. They commented that due to angulation of the sheath, the needle drifted cranially to be trapped in the upper edge of the fossa in the majority of patients. The anterior margin of the upper edge is where a probe-patent foramen ovale is sited, a regular finding in 27% of individuals at postmortem (Fig. 1.5B) [37]. This nonadherent margin of the valve has a C-shape (Fig. 1.5D). A catheter lodged in this crevice will have its tip directed toward the anterior wall of the left atrium. This part of the wall, just inferior to Bachmann’s bundle, can be very thin (Fig. 1.5D; see below).

The atrioventricular junctions The atrioventricular junctions are guarded by the tricuspid and mitral valves. The walls of the atria and ventricles are contiguous and without myocardial continuity, except for one pointai.e., at the site of the penetrating bundle of the atrioventricular conduction tissues. Importantly, it is at the atrioventricular junction that anomalous mus-

cular atrioventricular connections are found, which produce the Wolff–Parkinson–White variant of ventricular preexcitation [38]. In describing the location of the accessory bundles, attitudinal terminology is desirable [3]. Furthermore, the true septal component is limited to the area of the central fibrous body. The so-called “anterior septum” is contiguous with part of the supraventricular crest of the right ventricle, while the “posterior septum” is formed by the muscular floor of the coronary sinus overlying the diverging posterior walls of the ventricular mass, and the vestibule of the right atrium overlapping ventricular myocardium. Thus, anatomically, the atrioventricular junction can be described as comprising extensive right and left parietal junctions that meet with a small septal component (Fig. 1.6A, B). The right parietal junction is relatively circular and occupies a near-vertical plane in the heart, marked by the course of the right coronary artery in the atrioventricular groove. On the endocardial surface, the tricuspid vestibule overlies the ventricular wall (Fig. 1.6C). The superior and most medial part of the junction abuts directly on the membranous septum. The left parietal junction surrounds the orifice of the mitral valve, and part of it is the area of fibrous continuity between mitral and aortic valves (Fig. 1.6A). The potential for accessory atrioventricular connections is mainly limited to the junction supporting the hinge line of the mural leaflet of the mitral valve. This runs from 9

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Fundamentals

Figure 1.6 A. This view of the base of the heart shows the relative locations of the four cardiac valves. The left (L) and right (R) coronary arteries arise from the facing aortic sinuses. The orifices of the tricuspid and mitral valves are marked by the broken lines. The row of circles marks the span of fibrous continuity between the aortic and mitral valves. The filled shape indicates the membranous and muscular septal areas at the atrioventricular junction. The atrioventricular conduction bundle of His penetrates through this area. B. This heart, sectioned through the sagittal plane of the body and displayed in attitudinal fashion, has the right and left atrioventricular junctions superimposed to show that the greater parts of the junction are parietal. In this orientation, the tricuspid junction occupies the anterior, superior, and inferior parts parietally, while the mitral junction occupies the superior, posterior, and inferior parts. The red and black arrows indicate the

locations of the “anterior” and “posterior” descending interventricular coronary arteries. C. This section through the tricuspid vestibule (blue arrows) shows a gap between its underside and the ventricular wall. This inferior pyramidal space contains fatty tissues of the epicardium and the coronary artery (a). The eustachian ridge is prominent in this heart. D. This section through the left atrioventricular junction shows the mitral vestibule (blue arrows), overlying the inferior pyramidal space. Note the relationship of the middle cardiac vein (mcv) entering the coronary sinus (cs) and the coronary artery (a). Ao, aorta; CS, coronary sinus; ER, Eustachian ridge; ICV, inferior caval vein; L, left coronary artery; LAA, left atrial appendage; LI, left inferior pulmonary vein; LS, left superior pulmonary vein; MV, mitral valve; OF, oval fossa; PT, pulmonary trunk; R, right coronary artery; SC, supraventricular crest; TV, tricuspid valve.

posterosuperior to posterior and inferior when the heart is viewed in a left anterior oblique projection (Fig. 1.6B). The inferior area harbors the coronary sinus and its tributary, the great cardiac vein (Fig. 1.6D). The inferior paraseptal region, called the “posterior septum,” is the inferior pyramidal space, which contains epicardial fibrofatty tissues together with the artery supplying the atrioventricular node (Fig. 1.6C, D) [39,40].

valve, and the apical trabecular component. In the normal adult heart at autopsy, the parietal wall of the right ventricle is 3–5 mm thick, excluding trabeculations, and that of the left ventricle is 12–15 mm thick. Conventionally, these wall measurements are taken at 2 cm proximal to the pulmonary valve and 2 cm distal to the mitral valve. The ventricular septum curves as it is traced from the inlet toward the outlet portions, allowing the right ventricle to “wrap” over the left ventricle (Fig. 1.2E).

The ventricles Like the atrial chambers, each ventricle is best described as having three components: the inlet containing the atrioventricular valve, the outlet leading to the arterial 10

The right ventricle The inlet portion of the right ventricle extends from the hinge line of the tricuspid valve to the papillary muscles that anchor the leaflets, via the tendinous cords, to the

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ventricular wall. The leaflets can be distinguished as septal, anterosuperior, and inferior or mural. The septal leaflet, with its cords inserting directly into the ventricular septum, is characteristic of the tricuspid valve. The medial papillary muscle, a small out-budding from the septum, supports the zone of apposition (or commissure) between the septal and anterosuperior leaflets (Fig. 1.7A). A larger papillary muscle, the anterior papillary muscle, supports

Overview of cardiac anatomy relevant to catheter ablation

the extensive anterosuperior leaflet and its zone of apposition with the inferior leaflet. The zone of apposition between the anterosuperior and inferior leaflets is supported by a group of small papillary muscles, the inferior papillary muscles. Coarse muscular trabeculations criss-cross the apical portion. One of them, the moderator band, is characteristic of the right ventricle (Fig. 1.7A). This arises from the

Figure 1.7 A. The right ventricle, displayed to show its component parts. The supraventricular crest (SC) is clasped between the limbs (broken arrows) of the septomarginal trabeculation (SMT). The moderator band (MB) arises from the SMT, and the anterior papillary muscle (a) inserts into it. The stars mark the course of the atrioventricular conduction bundle in the myocardium behind the tricuspid valve, and the dark circles trace the course of the right bundle branch after it emerges at the base of the medial (m) papillary muscle. B. This section shows the relationship between the pulmonary infundibulum (blue arrows) and the left ventricular outlet, with the heart viewed from the front. The infundibulum adjacent to the aortic outlet is not septal (green arrows). C. The leaflets of the pulmonary valve have been removed to show the small semilunar areas of myocardium (*) enclosed within the sinuses, as distinct from the paler color of the arterial wall. D. This dissection of the atrioventricular junctions, with removal of two sinuses of the aortic valve, shows the relationship between the membranous septum (green dots) and the left ventricular outflow tract (LVOT). The mural leaflet of the mitral valve is extensive (broken arrows). The fibrous continuity between the aortic or anterior leaflet (AL) and the aortic valve lies between the left (l) and right (r) fibrous trigones (triangles). E. This view of the left ventricular outflow tract shows the membranous septum transilluminated and the span of valvar fibrous continuity (arrow). The atrioventricular conduction bundle penetrates the right margin of fibrous continuity, and the left bundle branch descends in the subendocardium. F. A false tendon (open arrows) crosses from the septum to the medial papillary muscle. AL, anterior leaflet; Ao, aorta; L, left coronary leaflet; LC, left coronary orifice; LV, left ventricle; LVOT, left ventricular outflow tract; MB, moderator band; MV, mitral valve; N, noncoronary leaflet; PT, pulmonary trunk; R, right coronary leaflet; SC, supraventricular crest; Sep, septum; SMT, septomarginal trabeculation; TV, tricuspid valve.

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Fundamentals

body of the septomarginal trabeculation to span the ventricular cavity and inserts into the parietal wall. The moderator band carries within its musculature a major fascicle of the right bundle branch. The anterior papillary muscle arises from the moderator band. The septomarginal trabeculation itself is a Y-shaped strap of muscular band that is adherent to the septal surface. It clasps between its limbs the infolding of the heart wall forming the ventricular roof, an area also known as the supraventricular crest (Fig. 1.7A). This crest separates the two right heart valves and is an integral part of the outlet, blending into the freestanding subpulmonary muscular infundibulum, which is a tube-like structure supporting the pulmonary valve (Fig. 1.7B). Although ablationists refer to septal and free wall portions of the right ventricular outflow tract, it should be noted that the infundibulum does not have a septal componentaa fact well known to cardiac surgeons, who harvest the pulmonary valve for the Ross procedure [41]. The septal component is only in its most proximal part, at the branch point of the septomarginal trabeculation. Furthermore, the right ventricular outlet curves to pass anterior and cephalad to the left ventricular outlet (Fig. 1.2C). Any perforation in the “septal” part is more likely to go outside the heart than into the left ventricle (Fig. 1.7B). From the anterior surface of the septomarginal trabeculation run further muscular bands called the septoparietal trabeculations, which insert into the parietal wall. The infundibulum immediately proximal to the pulmonary valve has a smoother wall. Since the crescentic hinge lines of the pulmonary leaflets cross the anatomic junction between the ventricular musculature and the arterial wall, they enclose within the sinuses small semilunar areas of myocardium (Fig. 1.7C) [42]. Two of the pulmonary sinuses are adjacent to two aortic sinuses, although the planes of the aortic and pulmonary valves are at an angle to one another (Fig. 1.6A). The adjacent or “facing” aortic sinuses are those giving origin to the coronary arteries. The third pulmonary sinus is unrelated to the aorta.

The left ventricle The left ventricle has an approximately conical shape and is located posteriorly within the ventricular mass. Viewed from the frontal aspect, its outlet overlaps its inlet. The hinge of the mitral leaflets at the entrance to the inlet has a very limited attachment to septal structures. Compared with that of the tricuspid valve, its septal attachment is further from the apex. The larger portion of the valve is hinged to the parietal atrioventricular junction, and one-third is the span of fibrous continuity with the aortic valve (Fig. 1.7D, E). The latter is attached to the septum at the right fibrous trigone and to the parietal musculature at the left fibrous trigone (Fig. 1.7D). The right trigone, in 12

continuity with the membranous septum, forms the central fibrous body. The two leaflets of the mitral valve are disproportionate in size. The “anterior” leaflet, in continuity with the aortic valve, is deep, whereas the mural (or “posterior”) leaflet is shallow (Fig. 1.7D). The latter leaflet frequently has a scalloped appearance. Unlike the tricuspid valve, the tension apparatus of both mitral leaflets inserts exclusively into two groups of papillary muscles. The apical component of the left ventricle extends out from the level of the origins of the papillary muscles to the ventricular apex. At the apex, the muscular wall tapers to only 1–2 mm thick. The trabeculations are finer than those found in the right ventricle. Occasionally, fine muscular strands or so-called false tendons extend between the septum and the papillary muscles or the parietal wall (Fig. 1.7F) [43,44]. These strands often carry the distal ramifications of the left bundle branch. Writing in Quain’s Anatomy in 1929, Walmsley [45] commented, “Tawara, however, gave them a new significance by stating that they [false tendons] were anomalies in the distribution of the atrioventricular bundle tissues.” In recent years, they have been implicated in idiopathic left ventricular tachycardia [46]. The left ventricular outlet is bordered by the muscular ventricular septum anterosuperiorly and the aortic (“anterior”) leaflet of the mitral valve posteroinferiorly. The upper part of the ventricular septum leading to the aortic valve is smooth. The common atrioventricular conduction bundle emerges from the central fibrous body to pass between the membranous septum and the crest of the muscular ventricular septum (Fig. 1.7E). From here, the left bundle branch descends in the subendocardium and usually branches into three main fascicles, which interconnect and further divide into finer and finer branches as the Purkinje network (see below). In the outlet, the landmark for the site of the atrioventricular conduction bundle is the fibrous body that adjoins the crescentic hinge lines of the right and noncoronary leaflets of the aortic valve (Fig. 1.7). Two leaflets of the aortic valve have muscular support, these being the ones adjacent to, or facing, the pulmonary valve. As discussed above, these two aortic sinuses give rise to the right and left coronary arteries. Like the pulmonary valves, these two sinuses contain small segments of ventricular myocardium within [47]. The third sinus, the noncoronary sinus, does not have muscular support. The musculature in the aortic sinuses may be a source of repetitive monomorphic ventricular tachycardia. Owing to the spatial relationship of the subpulmonary infundibulum and the left ventricular outlet (Fig. 1.7B), the foci may be ablated from within the part of the right ventricular outlet that overlies the adjacent aortic sinuses [48]. Since the main coronary arteries arise from the arterial part of the sinuses, they are not in the immediate field. Ablations

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within the sinuses without trauma to the coronary arteries have also been reported [49,50].

The coronary arteries As described above, the two major coronary arteries arise from the aortic sinuses (the Valsalva sinuses). The course and distribution of these two arteries allow designation of the sinuses as right and left coronary, with the third sinus being noncoronary (Fig. 1.6A). Only the right coronary sinus is situated anteriorly [51]. The arterial orifices are usually located eccentrically in the sinuses, close to the sinotubular junction [52]. Origin just above the junction is not unusual. Having emerged from the right coronary aortic sinus, the right coronary artery is directly related to the supraventricular crest, the muscular structure forming the roof of the right ventricle. In this region, it gives rise to a prominent infundibular branch and, in 55–60% of individuals, also a branch that supplies the sinus node [19,53]. Passing within the fatty tissues of the right atrioventricular groove, the right coronary artery gives off the acute marginal branch before turning posteriorly to the cardiac crux to give rise to the posterior descending coronary artery, which runs in the inferior interventricular groove. The right coronary can also be traced into the left atrioventricular groove to supply the inferior wall of the left ventricle. This coronary arrangement, known as right coronary arterial dominance, is found in 90% of individuals. In this arrangement, the right coronary also gives origin to the artery supplying the atrioventricular node in the majority of cases, but variations in origins have been described [39,40]. The left coronary artery, having emerged from its aortic sinus, enters the space between the left atrial appendage and the pulmonary trunk. Within 1 cm of its origin in most cases, the main stem usually divides into the anterior descending and the circumflex arteries. It is worth noting that the terms “anterior descending” and “posterior descending” reflect the previous anatomical practice of standing the heart on its apex and having the “anterior” interventricular groove in the midline. With the heart in situ, the “anterior” artery runs in the superior interventricular groove and the “posterior” artery runs in the inferior groove (Fig. 1.6B) [54]. McAlpine preferred to describe the two main branches of the left coronary artery as anterior and posterior divisions, to clarify their course and relations [55]. Be that as it may, the major branches of the “anterior” interventricular artery are the diagonal, septal perforating, and infundibular branches. The diagonal branches supply the anterior wall of the left ventricle, while the infundibular branches pass to the right ventricular outlet. The septal perforators pass perpendicularly into the ventricular septum. The circumflex artery

Overview of cardiac anatomy relevant to catheter ablation

supplies a branch to the sinus node in 45% of individuals. Its extent around the left atrioventricular junction is limited to supplying the obtuse margin of the left ventricle. Only in about 10% of individuals does it reach the cardiac crux to give rise to the “posterior” interventricular artery and a branch to the atrioventricular node at this juncture.

The coronary veins The venous return from the heart muscle is either channeled via small thebesian veins that open directly into the cardiac chambers or, more significantly, is collected by the greater coronary venous system, which drains 85% of the venous flow [56,57]. The main coronary veins in the greater system are the great, middle, and small cardiac veins. The great and middle veins run alongside the “anterior” interventricular and “posterior” interventricular, respectively, and drain into the coronary sinus. As the great cardiac vein turns into the left atrioventricular groove, it passes close to the first division of the left coronary artery and under the cover of the left atrial appendage. Approaching the coronary sinus, the great vein is joined by tributaries from the left ventricular obtuse margin and the inferior wall, as well as veins from the left atrium. The left ventricular veins may be utilized for ablating ventricular tachycardia from a source close to the epicardium [58]. However, although coronary veins are usually superficial to arteries, cross-overs are not uncommon [15]. Furthermore, care should be taken when catheters or wires are being deployed in superficial veins, since the venous wall is thin and “unprotected” by muscle on the epicardial side. The entrance of the vein of Marshall, or oblique left atrial vein, marks the venous end of the tube-shaped coronary sinus. When persistent, this is the left superior caval vein, which courses epicardially between the left atrial appendage and the superior pulmonary vein. In most individuals, the vein is a fibrous ligament, or if a lumen is present it is narrow, rarely exceeding 2 cm in length, before tapering to a blind end. If accessible, this channel may be entered for ablating the left atrial wall. In the absence of the vein of Marshall or its remnant, Vieussens’ valve is taken as the anatomic landmark for the junction between the coronary sinus and the great cardiac vein. This very flimsy valve has one to three leaflets, which can provide some resistance to the catheter. Another marker for the junction is the end of the muscular sleeve around the coronary sinus. However, in a proportion of cases, the sleeve may extend to 1 cm or more beyond the junction [59]. Bundles from the sleeve sometimes run into the left atrial wall and also cover the outer walls of adjacent coronary arteries [59,60]. Close to its right atrial orifice, the coronary sinus receives the middle cardiac vein. The middle vein passes 13

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Fundamentals

just superficial to the right coronary artery at the cardiac crux. It is a useful portal for ablating accessory atrioventricular pathways located in the inferior pyramidal space [61]. Very rarely, the entrance of the middle vein is dilated and surrounded by a cuff of muscle, giving the potential for accessory atrioventricular connections [62]. The small vein receives tributaries from the right atrium and the inferior wall of the right ventricle before coursing in the right atrioventricular junction to open to the right margin of the coronary sinus orifice, or into the middle cardiac vein. When joined by the acute marginal vein, or vein of Galen, the small vein becomes larger in size. Several other veins, from the anterior surface of the right ventricle and from the acute margin, drain directly into the right atrium. In some hearts, the anterior veins merge into a venous lake in the right atrial wall.

The cardiac conduction system Although the cardiac conduction system has been mentioned in the previous sections, it is appropriate to summarize the key features and put them in the context of the overall anatomy of the heart. Much has been written about “specialized internodal tracts” connecting the sinus node to the atrioventricular node. However, their existence in the form as originally defined by early anatomists has never been demonstrated [63 – 65]. The myocardium between the nodes bears no histological characteristic of specialization or cable-like arrangement that in any way resembles the ventricular bundle branches [66,67]. Instead, the internodal myocardium is arranged in broad bands that surround the orifices of the large veins, the tricuspid valve, and the oval fossa. Bands like the rim of the oval fossa and the terminal crest are raised ridges on the endocardial aspect and tend to have an orderly alignment in the myocardial fibers. The major interatrial band is Bachmann’s bundle, located anterosuperiorly in the subepicardium. Again, this bundle is not insulated by a fibrous sheath, nor does it have well-defined margins (Fig. 1.8A). There are further smaller muscular bundles that cross the interatrial groove to connect the right and left atrial walls anteriorly, superiorly, posteriorly, and inferiorly, the right atrium to the right pulmonary veins, the wall of the coronary sinus to the left atrium, and so on (Fig. 1.8B, C) [24 –26]. Fine bridges connecting the remnant of the vein of Marshall to the left atrial myocardium have also been demonstrated [68].

Figure 1.8 A. This dissection shows Bachmann’s bundle crossing the interatrial groove (open arrows). Usually, it is a broad band of aligned myofibers that blends into the right and left atrial myocardium. It is not encased in a fibrous sheath. The area of the left atrial wall immediately inferior to the bundle can be very thin in some hearts (pale area marked by **). B. This view from above shows Bachmann’s bundle crossing the interatrial groove (arrow). C. The superior caval vein, pulled forward, reveals smaller interatrial bridges from the left atrium (green arrow) and from the right superior pulmonary vein (red arrow). Ao, aorta; BB, Bachmann’s bundle; LS, left superior pulmonary vein; RS, right superior pulmonary vein; SCV, superior caval vein.

portion situated cephalad and close to the superior margin of the terminal groove. In most cases, the head is subepicardial, while the tail penetrates inferiorly into the myocardium of the terminal crest to lie closer to the subendocardium. The node is richly supplied with nerves from both the sympathetic chains and the vagus nerve. Nodal tissues are usually penetrated by a prominent nodal artery [70]. Although the specialized myocytes of the nodal cells are set in a fibrous matrix, the node is not encased in a fibrous sheath. The borders of the node are irregular, with frequent interdigitations between nodal and ordinary atrial myocytes, facilitating communication between node and right atrium [20,71].

The sinus node

The atrioventricular conduction system

The sinus node is crescent-like in shape, with a mean length of 13.5 mm in the adult heart [69]. It is usually described as having a head, body, and tail, with the head

In the normal situation, the atrioventricular conduction system provides the only pathway of muscular continuity between atrial and ventricular myocardium (Fig. 1.9A, B)

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Figure 1.9 A. This diagram from Walter Koch’s monograph [72, plate 13] depicts in exquisite detail the cardiac conduction system, but with the heart standing on its apex. B. The triangle of Koch and the proximal parts of the atrioventricular conduction system in this diagram are orientated more attitudinally. The arrows (a–d) indicate the corresponding levels of the histological sections (Ba–Bd), in which the conduction tissues are delineated with dotted lines. C. This diagram from Tawara’s monograph [73, plate 1] depicts the left bundle branch and its interconnecting ramifications. D. The Purkinje fiber network is displayed in the right parietal wall of a sheep heart. Ao, aorta; AV, atrioventricular; CS, coronary sinus; LBB, left bundle branch; LV, left ventricle; MB, moderator band; RBB, right bundle branch; RV, right ventricle.

[72]. Thus, there is an interface of transitional cells between ordinary atrial myocardium and the histologically specialized cells that make up the atrioventricular node. These cells are arranged to provide anterior, inferior, and deep inputs to the compact atrioventricular node. The anterior input sweeps from the anterior margin of the oval

fossa deep to the ordinary myocardium of the tricuspid vestibule. The inferior input approaches the compact node from the musculature in the floor of the coronary sinus and from the Eustachian ridge. The deep input bridges the compact node with the left atrial vestibule and inferior rim of the oval fossa. 15

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Located at the apex of Koch’s triangle is the atrioventricular node, described as the “Knoten” by Tawara [73] in his extensive monograph published in German in 1906 (Fig. 1.9B). The compact part of the node in the adult is approximately 5 mm long and wide [39]. In the majority of hearts, inferior extensions from the node pass to the right and left sides of the artery, which penetrates the compact node [74]. The right extension courses parallel and adjacent to the hinge of the tricuspid valve, while the left extension projects toward the mitral vestibule. The distance of the right inferior extension to the endocardial surface is approximately 1–5 mm. Put in the context of the right atrial landmarks of the triangle of Koch, right inferior extensions extend to the mid-level of the triangle, but may even extend to the vicinity of the coronary sinus in cases with a small triangle [39]. Ueng and colleagues [75] cautioned that ablation of slow pathways will only be successful in the “mid-septal” area in patients with larger nodal triangles. Superiorly, at the apex of Koch’s triangle, the penetrating atrioventricular conduction bundle of His passes through the central fibrous body to be sandwiched between the interventricular component of the membranous septum and the crest of the muscular ventricular septum, encased in a fibrous sheath (Fig. 1.9B). This short bundle of specialized myocardium is a direct extension of the compact atrioventricular node, enabling atrial activity to be conveyed to the ventricles. As discussed previously, the emergence of the bundle in the ventricles is directly related to the membranous septum and the aortic outflow tract. After a short distance, the bundle bifurcates into the left and right bundle branches (Fig. 1.9B). The left bundle branch fans out as it descends in the subepicardium of the septal surface of the left ventricle (Fig. 1.9C). In contrast, the right bundle branch is cord-like and descends the musculature of the ventricular septum to emerge in the subendocardium at the base of the medial papillary muscle, to run in the septomarginal trabeculation (Fig. 1.7A). Along the way, a prominent branch crosses to the parietal wall within the moderator band. Both bundle branches are insulated as they descend toward the apical parts of the ventricles. The branches then ramify as the Purkinje fibers, which run in the subendocardium and into the myocardium like a network. These have been shown in the diagrams drawn by Tawara [73] (Fig. 1.9C) and can be demonstrated in animal hearts by injections (Fig. 1.9D). In the subendocardium of the ventricular walls, they can be traced crossing the ventricular cavities in “false tendons” (Fig. 1.7F) and up the outflow tracts. Recently, triggers of ventricular fibrillation have been mapped to the Purkinje system in the right ventricular outflow tract and successfully ablated [76]. In some hearts, the atrioventricular bundle itself continues beyond the bifurcation as a third bundle. Termed 16

the dead-end tract, this runs on the crest of the septum and has not yet had any function ascribed to it [77].

Fat pads and innervation Extracardiac nerves from the mediastinum reach the heart through the areas bounded by the serous pericardium. These sites around the great veins at the cardiac base and around the pulmonary trunk and aorta are referred to as the hilum of the heart [78]. Nerves from the venous part of the hilum extend mainly to the atria, while those from the arterial pole predominantly reach the ventricles, but there are also multiple connections. Several branches of mediastinal nerves between the aorta and the pulmonary trunk connect with the aortic root and the superior region of the left atrium [79]. Six to ten collections of gangliaaganglionated subplexuses of the epicardiac neural plexusahave been described in the human heart [79,80]. Half of the subplexuses are located on the atria and the other half on the ventricles. Occasional ganglia are located in other atrial and ventricular regions of the epicardium [79]. The ganglionated subplexuses are generally associated with islands of adipose tissue, referred to as fat pads, that serve as visual landmarks for cardiac surgeons [81]. The locations described by Armour and colleagues [79] are depicted in Fig. 1.10. Pauza and colleagues [80] found up to 50% of all cardiac ganglia on the posterior and posterolateral surfaces of the left atrium, whereas Singh and colleagues [81] reported that the largest populations of ganglia are adjacent to the sinus and atrioventricular nodes. However, the studies are not comparable, since Pauza and colleagues [80] rejected counts from regions covered by abundant fat. The ganglia within each subplexus are interconnected by thin nerves, while ganglia of adjacent subplexuses are also interconnected, forming the meshwork of the epicardiac neural plexus. Further nerves penetrate into the myocardium, becoming thinner and thinner and devoid of ganglia [80]. Recent experimental and clinical studies will help clarify the functional nature of the different epicardial ganglionated subplexuses [82 – 84].

Conclusions Whilst the structure of the heart has remained unchanged over the ages, understanding of its anatomy has evolved over time, particularly with the development of new imaging methods and therapeutic strategies, each of which has required a review of the anatomy. The development of catheter ablation techniques has in many ways outpaced the understanding of relevant anatomy. Attitudinal orientation, as originally promoted by McAlpine [2], is crucial in understanding living anatomy. This chapter has

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Acknowledgment Dr. Ho and her unit receive funding support from the Royal Brompton and Harefield Hospital Charitable Fund and the Royal Brompton and Harefield Hospital National Health Service Trust.

References

Figure 1.10 The dots depict the areas of fat pads containing ganglionated plexuses of the epicardiac neural plexus. The nomenclature follows Armour et al. [79]. A. A sealant-filled heart specimen, viewed from the back. B. The frontal aspect. The posteromedial left atrial plexus and the posterior right atrial plexus invaginate into the interatrial groove, fusing to form the interatrial septal plexus. Ao, aorta; ICV, inferior caval vein; LA, left atrium; LC, left coronary orifice; PT, pulmonary trunk; RA, right atrium; RI, right inferior pulmonary vein; RS, right superior pulmonary vein; SCV, superior caval vein.

reviewed only hearts with normal connections and relations in the cardiac chambers. Postoperative arrhythmias are an increasing problem in adults with congenital heart disease. The complexities of the malformations can be daunting for ablationists, and the anatomy of the lesions will also need to be addressed. For advances in this field to be achieved, synergy and collaboration between anatomists and practitioners of catheter ablation are essential. In this chapter, I have drawn freely from many such collaborations and I acknowledge the help of all who have contributed, and are continuing to contribute, to our understanding of the heart.

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50 Hachiya H, Aonuma K, Yamauchi Y, Igawa M, Nogami A, Iesaka Y. How to diagnose, locate, and ablate coronary cusp ventricular tachycardia. J Cardiovasc Electrophysiol 2002;13:551–6. 51 Walmsley R, Watson H. The outflow tract of the left ventricle. Br Heart J 1966;28:435–47. 52 Muriago M, Sheppard MN, Ho SY, Anderson RH. Location of the coronary arterial orifices in the normal heart. Clin Anat 1997;10:297–302. 53 Busquet J, Fontan F, Anderson RH, Ho SY, Davies MJ. The surgical significance of the atrial branches of the coronary arteries. Int J Cardiol 1984;6:223–34. 54 Ho SY, Anderson RH. Commentary on Biosense left ventricular electromechanical mapping. Asian Cardiovasc Thorac Ann 1999;7:349–52. 55 McAlpine WA. Heart and Coronary Arteries. Berlin: Springer, 1975: 163–78. 56 Lüdinghausen VM, Schott C. Microanatomy of the human coronary sinus and its major tributaries. In: Meerbaum S, ed. Myocardial Perfusion, Reperfusion, Coronary Venous Retroperfusion. Darmstadt: Steinkopff, 1990: 93–122. 57 Gensini G, Giorgi SD, Coskun O, Palacio A, Kelly AE. Anatomy of the coronary circulation in living man. Circulation 1965;31:778–84. 58 Stellbrink C, Dien B, Schauerte P, et al. Transcoronary venous radiofrequency catheter ablation of ventricular tachycardia. J Cardiovasc Electrophysiol 1997;8:916–21. 59 Lüdinghausen VM, Ohmachi N, Boot C. Myocardial coverage of the coronary sinus and related veins. Clin Anat 1992;5:1–15. 60 Chauvin M, Shah DC, Haïssaguerre M, Marcellin L, Brechenmacher C. The anatomic basis of connections between the coronary sinus musculature and the left atrium in humans. Circulation 2000;101:647–52. 61 Kozlowski D, Kozluk E, Piatkowska A, et al. The middle cardiac vein as a key for “posteroseptal” space: a morphological point of view. Folia Morph 2001;60:293–6. 62 Omran H, Pfeiffer D, Tebbenjohanns J, et al. Echocardiographic imaging of coronary sinus diverticula and middle cardiac veins in patients with preexcitation syndrome: impact on radiofrequency catheter ablation of posteroseptal accessory pathways. Pacing Clin Electrophysiol 1995;18:1236 – 43. 63 Mönckeberg JG. Beiträge zur normalen und pathologischen Anatomie des Herzens. Verh Dtsch Pathol Ges 1910;14:64 –71. 64 Aschoff L. Referat über die Herzstörungen in ihren Beziehungen zu den specifischen Muskelsystemen des Herzens. Verh Dtsch Pathol Ges 1910;14:3–35. 65 Janse MJ, Anderson RH. Internodal atrial specialised pathways: fact or fiction? Eur J Cardiol 1974;2:117–37. 66 Anderson RH, Ho SY, Smith A, Becker AE. The internodal atrial myocardium. Anat Rec 1981;201:75–82. 67 Anderson RH, Ho SY, Becker AE. Anatomy of the human atrioventricular junctions revisited. Anat Rec 2000;260:81– 91.

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68 Kim DT, Lai AC, Hwang C, et al. The ligament of Marshall: a structural analysis in human hearts with implications for atrial arrhythmias. J Am Coll Cardiol 2000;36:1324 –7. 69 Sanchez-Quintana D, Cabrera JA, Farre J, Climent V, Anderson RH, Ho SY. Sinus node revisited in the era of electroanatomical mapping and catheter ablation. Heart 2005;91:189 –94. 70 Ryback R, Mizeres NJ. The sinus node artery in man. Anat Rec 1965;153:23 –30. 71 Chuaqui B. Lupenpräparatorische Darstellung der Ausbreitungszüge des Sinusknotens. Virchows Arch Abt A Path Anat 1972;356:141– 53. 72 Koch W. Der funktionelle Bau des menschlichen Herzens. Berlin: Urban & Schwarzenberg, 1922. 73 Tawara S. Das Reizleitungssystem des Säugetierherzens. Eine anatomisch-histologische Studie über das Atrioventrikularbündel und die purkinjeschen Fäden. Jena: Fischer, 1906. 74 Inoue S, Becker AE. Posterior extensions of the human compact atrioventricular node: a neglected anatomic feature of potential clinical significance. Circulation 1998;87:188 – 93. 75 Ueng KC, Chen SA, Chiang CE, et al. Dimensions and related anatomical distance of Koch’s triangle in patients with atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol 1996;7:1017–23. 76 Haïssaguerre M, Shah DC, Jaïs P, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lancet 2002;359:677–8. 77 Kurosawa H, Becker AE. Dead-end tract of the conduction axis. Int J Cardiol 1985;7:13 –20. 78 Pauza DH, Pauziene N, Tamasauskas KA, Stropus R. Hilum of the heart. Anat Rec 1997;248:322– 4. 79 Armour JA, Murphy DA, Yuan BX, MacDonald S, Hopkins DA. Gross and microscopic anatomy of the human intrinsic cardiac nervous system. Anat Rec 1997;247:289 – 98. 80 Pauza DH, Skripka V, Pauzine N, Stropus R. Morphology, distributions, and variability of the epicardiac neural ganglionated subplexuses in the human heart. Anat Rec 2000;259:353 – 82. 81 Singh S, Johnson PI, Lee RE, et al. Topography of cardiac ganglia in the adult human heart. J Thorac Cardiovasc Surg 1996;112:943 –53. 82 Nakajima K, Furukawa Y, Kurogouchi F, Tsuboi M, Chiba S. Autonomic control of the location and rate of the cardiac pacemaker in the sinoatrial fat pad of parasympathetically denervated dog hearts. J Cardiovasc Electrophysiol 2002;13: 896 –901. 83 Quan KJ, Lee JH, Van Hare GF, Biblo LA, Mackall JA, Carlson MD. Identification and characterization of atrioventricular parasympathetic innervation in humans. J Cardiovasc Electrophysiol 2002;13:735 – 9. 84 Cummings JA, Gill I, Akhrass R, Dery MA, Biblo LA, Quan KJ. Preservation of the anterior fat pad paradoxically decreases the incidence of postoperative atrial fibrillation in humans. J Am Coll Cardiol 2004;43:994 –1000.

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2

Biophysics and pathophysiology of lesion formation by transcatheter radiofrequency ablation David E. Haines

Radiofrequency catheter ablation has become established as the primary modality of transcatheter therapy for the treatment of symptomatic arrhythmias. Although it was initially selected as an ablation modality based on empirical observations in the animal laboratory, it was soon widely accepted as the ablation modality of choice because of a favorable profile of efficacy, safety, cost, and ease of use. Although new catheter technologies and ablation energy sources are in varying stages of development and implementation, it is unlikely that radiofrequency (RF) catheter ablation will ever lose its mainstay role in interventional electrophysiology. Despite the wide use of radiofrequency ablation and familiarity with this technology by all operators, an understanding of the mechanism of ablation and lesion formation can improve the clinician’s effectiveness in ablation procedures. The purpose of this chapter is firstly to review the biophysics of RF lesion formation. These data outline the theoretical basis for tissue heating with RF energy, and reconcile the theoretical construct with clinical observations. The second section reviews the biological basis of tissue injury caused by radiofrequency energy or other hyperthermic sources. Anatomical and pathophysiological observations allowing better prediction of the behavior of RF lesion formation in the myocardium are presented.

Biophysics of RF lesion formation Electrical characteristics of RF energy during catheter ablation When electrical current passes through a resistive medium such as myocardial tissue, some of the electrical energy is converted into thermal energy. Like any electrical circuit, there is a voltage drop across the resistive element. Radiofrequency energy is a form of alternating electric 20

current, with a typical frequency of 500 –1000 kHz. Any frequency of electrical energy results in resistive heating of tissue, including direct current. However, low-frequency electricity causes muscle and nerve stimulation, resulting in arrhythmia induction and pain if applied in the heart. Frequencies above 200–300 kHz avoid these problems in most cases. This has allowed RF catheter ablation to be carried out in all four cardiac chambers in patients who are under conscious sedation and with a minimal risk of proarrhythmia. Higher electrical frequencies can be used, but as frequencies enter the shortwave bands and approach microwave frequencies, energy transfer to tissue becomes less predictable. More energy is dissipated in the transmission line, and the mode of tissue heating shifts from electrical (resistive) heating to dielectric heating. The standard RF energy frequency used for clinical catheter ablation is therefore 500 kHz. RF current is typically delivered in a unipolar fashion between the tip of the ablation catheter and an indifferent ground electrode with a large surface area (100 –250 cm2) applied to the skin. Since it is alternating current, there is neither anode nor cathode. The magnitude of joule heating of tissue is proportional to the power density, which in turn is proportional to the square of the current density. The RF current has the highest density in close proximity to the ablation electrode and decreases in proportion to the square of the distance from the electrode. As a consequence, myocardial heating decreases in proportion to the fourth power of the distance from the electrode (Fig. 2.1) [1]. The RF current density is relatively uniform close to a typical 4-mm tip RF electrode, so that RF ablation tends to be relatively omnidirectional. However, larger asymmetrical electrodes have nonuniform field lines and current densities, due to a phenomenon known as the edge effect. At points of geometric transition, the current density increases and there are areas of increased heating. Thus, with long electrodes, maximum heating may occur at the

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Biophysics and pathophysiology of lesion formation by transcatheter radiofrequency ablation

tip and at the base of the active ablation electrode (Fig. 2.2) [2]. The RF energy that passes through the catheter is dissipated as heat through all segments of the electrical conduction circuit in proportion to the impedance of those segments. RF energy may be administered in a bipolar fashion, but this offers little advantage over unipolar delivery. The exception may be attempted linear atrial ablation, using a multiple electrode catheter oriented tangentially to the tissue. If excellent electrode–tissue contact is maintained with all electrodes, then bipolar energy

delivery between alternate electrodes will result in heating along all electrodes. In addition, if the phase of the RF energy is offset between contiguous electrodes, then current will flow in both a bipolar and unipolar fashion, leading to more uniform tissue heating [3]. The limitation of this technology (and all technologies that depend on tangential orientation of the electrodes) is the difficulty of maintaining close electrode–tissue contact. The dominant regions of higher impedance, voltage drop, and energy dissipation are at the catheter–tissue interface and at the interface between the skin and the dispersive electrode. In patients with high resistance at the dispersive electrode contact surface (due to dry skin or patch electrode placement), a relatively greater proportion of the total RF electrical energy may be dissipated at the skin, and a lesser proportion dissipated at the electrode–tissue interface. The result may be less myocardial heating and less effective lesion formation. One can address this issue by increasing the amplitude of power delivery so that, despite a lower fraction of the total power being converted to heat at the catheter tip, the absolute magnitude of the RF power density and tissue heating at the catheter tip is sufficient to accomplish the ablation. However, if there is a limited magnitude of power available for the ablation, then smaller ablation lesions will be the result (Fig. 2.3) [4]. This limitation may be reduced to some extent by more abrasive skin preparation or by the use of additional dispersive electrodes or dispersive

Figure 2.2 A finite-element analysis of the steady-state temperature distribution from radiofrequency ablation with a coil electrode 12 mm long. The legend of temperatures is shown at the right of the graph and ranges from the physiological normal (violet = 37 °C) to the maximum tissue temperature (red = 161 °C) located below the electrode edges.

In this analysis, the electrode temperature at the center of the electrode was maintained at 71 °C. There is a significant gradient of heating between the peak temperatures at the electrode edges and the center of the electrode. UV, ultraviolet. (Reproduced with permission from [2].)

Figure 2.1 The amplitude of current density and the magnitude of direct tissue heating versus distance from a radiofrequency electrical source. The current density falls with the square of the distance from the source. Since volume heating is proportional to the square of the current density, this diminishes with distance to the fourth power.

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Figure 2.3 The radial tissue temperature gradients in three conditions. The point at which the tissue temperature reaches the 50 °C temperature boundary defines the border of the radiofrequency (RF) lesion (vertical arrows). During low-power ablation without tip cooling, the surface temperature only slightly underestimates the peak tissue temperature. The lesion depth is small. During ablation with tip cooling, the surface temperature is maintained at a low level, thus allowing high-power delivery. The peak tissue temperature is measured > 2 mm below the endocardial surface. The resulting lesion is large. However, if the magnitude of convective cooling is too great, then a greater proportion of the RF energy will be dissipated by convection, and the tissue will absorb less power. The resulting lesion may be smaller than that created with standard, noncooled ablation. With tip cooling, high power should therefore be employed and an effort should be made to optimize the electrode–tissue contact.

electrodes with a larger surface area [5]. The location of the dispersive electrode does not appear to have a practical effect on the ablation results, although lesion sizes are a little larger experimentally if the dispersive electrode is placed directly contiguous to the heart on the chest wall [6]. Still, if a single electrode patch is employed, the ablation efficiency is somewhat enhanced if it is placed on the trunk, rather than on an extremity. Care should be taken to ensure complete and uniform skin contact with the entire surface of the electrode gel. Cases of severe skin burns have been reported during RF catheter ablation due to poorly placed dispersive electrodes, resulting in a high current density and skin heating at the contact points [7].

Thermodynamics of RF catheter ablation The mechanism of ablation from RF sources is tissue heating. Electrical current passing through a resistive medium such as myocardium generates heat in the region in close proximity to the source where current density is the highest. This is referred to as the region of volume heating, but does not represent the boundary of the lesion. The heat that is generated in this region of volume heating conducts outward to deeper tissue layers. Thermal conductive heating accounts for the bulk of lesion formation [1]. Factors that promote tissue heating are higher temperatures at the ablation source, a larger area of volume 22

heating, and a longer duration of tissue heating. The main factor that counteracts tissue heating is convective cooling from the circulating blood pool. Myocardial ablation from RF catheter ablation follows all of the biophysical rules that any thermodynamic process must follow. The mechanism and magnitude of influence of these factors can thereby be modeled, and the behavior of lesion formation from catheter ablation can be predicted [1,8,9]. Heat transfer in biological tissue has been modeled extensively using the bioheat transfer equation. This complex formula includes terms for metabolic heat production of the tissue and convective cooling from microvascular tissue perfusion. Because the rate of tissue heating is fast, the temperatures achieved are high, and the duration of heating is relatively brief with catheter ablation, the bioheat transfer equation can be greatly simplified. The simplified relationship implies that at a steady state, the lesion size will be directly proportional to the source temperature (Fig. 2.4) [1]. Although temperature is routinely monitored at the electrode–tissue interface with thermistors or thermocouples, the temperature recorded at the tissue surface usually underestimates the peak tissue temperature located 1–4 mm below the surface. Because of this limitation, measurement of the temperature at the electrode–tissue interface may be unreliable for assessing size of lesion formation. If the actual tissue temperature is recorded with a penetrating temperature sensor that extends beyond the endocardial surface, then the convective cooling at the endocardial surface that makes surface temperature monitoring unreliable is no longer an important factor. Once again, temperature correlates with lesion size [10]. Unfortunately, protruding needle temperature sensors are not practical for clinical application, due to the risk of perforation. Another correlate of lesion size is the steady-state power amplitude [11]. High power generally results in larger lesions. However, the efficiency of energy coupling to tissue is extremely variable, based on the amount of energy lost to the circulating blood pool by convective cooling. Thus, a high level of power delivery might result in a very large lesion, but might also result in a small lesion or no lesion at all if the electrode–tissue contact is very poor. The relationship between temperature, power, and lesion size is sometimes paradoxical [12,13]. In cases in which RF delivery is power-limited, the lesion size will be proportional to the temperature achieved. However, the delivered power becomes the dominant predictor of lesion size when the electrode–tissue interface temperature is held constant and the magnitude of convective cooling varies. A greater degree of convective cooling matched by a higher level of delivered power will yield larger lesions, as described below [14]. This observation led to the development of cooled-tip ablation systems. It is often desirable to create small, controlled ablative lesionsafor example, during the ablation of accessory

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Figure 2.4 Comparison of the depths of radiofrequency ablation lesions created in vitro with (A) the electrode–tissue interface temperature, (B) current, (C) power, and (D) energy. In this controlled setting with minimal convective cooling, the best indicator of lesion formation was the measured temperature. (Reproduced with permission from [1].)

pathways. Smaller lesions limit the likelihood of collateral damage and enhance the safety of the procedure. If the lesion is too small, however, there may be insufficient tissue injury to incorporate all of the arrhythmogenic components and eliminate the arrhythmia. In particular, ablation of some types of arrhythmia, such as atrial flutter and ventricular tachycardia, depends on successful ablation of wide and deep areas of myocardium. Thus, the goal of many ablation systems has been to increase the depth and volume of RF lesions, but to do so in a controlled fashion. Since high source temperatures and high power amplitudes should result in large lesions, one might conclude that in order to maximize the lesion size, maximum power should always be applied during catheter ablation. However, there is an upper limit to the magnitude of RF power that can be safely and effectively applied. As long as tissue temperatures do not exceed 100 °C, ablation proceeds unimpeded. If the electrode–tissue interface temperature reaches this threshold, however, blood at the surface begins to boil. This produces an adherent collection of denatured blood proteins that is referred to as coagulum. The coagulum accumulates on the electrode surface, resulting in less electrode surface area being available for conduction, and the local power density increases. Increasing power density results in more heating, more coagulum, and progressively less available conducting electrode surface area. Within a second, most of the electrode is covered with coagulum, and a sudden rapid rise

Figure 2.5 An example of simultaneous measurements of electrode tip temperature and impedance during radiofrequency catheter ablation in vivo. As the temperature approaches and then exceeds 100 °C, a sudden rise in electrical impedance is observed.

in electrical impedance ensues, preventing effective RF delivery from that point forward (Fig. 2.5) [15]. It is then necessary to remove the electrode from the patient and scrape the coagulum from the electrode before resuming ablation. In the worst case, coagulum can embolize from the catheter tip, leading to adverse consequences if 23

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ablation is being carried out in the left atrium or ventricle. Denatured protein can accumulate at the catheter tip at temperatures below 100 °C in areas of low flow [16], but this “soft thrombus” probably does not add to the thromboembolic risk. Monitoring the tip temperature has proved to be useful in preventing sudden rises in electrical impedance. Although the tip temperature can significantly underestimate the peak electrode–tissue interface temperature, maintaining a target temperature of 70 °C or less during ablation usually provides an adequate safety margin. Various cooled-tip ablation technologies have been implemented to increase the lesion size (see below). If the surface of the tissue is cooled but peak tissue temperatures below the endocardial surface exceed 100 °C, then a steam bubble may form and rupture through the endocardial or epicardial surface in order to vent [17]. A balance therefore has to be maintained to deliver a sufficient RF power amplitude to create a large lesion, while limiting the power in order to avoid steam pops and sudden rises in electrical impedance. The thermodynamic model of catheter ablation predicts that the lesion radius will be directly proportional to the radius of the heat source. Therefore, as the electrode size increases, the lesion depth and diameter should increase accordingly. This observation accounted for the early emergence of 4-mm tip ablation catheters. The increase in electrode size beyond the conventional 2-mm tip mapping catheters probably accounted for the early success of RF catheter ablation [18]. On the basis of this principle, catheters with tips of 8 and 10 mm are now routinely available. Because the larger electrode surface area results in a lower power density for any given power amplitude, the large-tip ablation catheters are most successful when they are coupled with RF generators with a higher peak power. The clinical value of RF catheter ablation with large-tip catheters has been confirmed, particularly with arrhythmic substrates such as the tricuspid–inferior vena cava isthmus in atrial flutter, which require longer and deeper lesions for the procedure to be successful [19,20]. Despite the improved success rate observed with ablation through large-tip catheters, there are some trade-offs that have to be accepted. As described above, the edge effect results in nonuniform power density and nonuniform heating around the electrode [2]. There is therefore still a risk of coagulum forming at the base of the catheter even if the temperature at the electrode tip does not exceed 60– 70 °C. The bipolar mapping resolution is optimized with small, closely spaced electrodes. Large-tip catheters therefore have a limited capacity for mapping localized electrophysiological signals. Finally, the excellent safety profile of catheter ablation has, in part, been due to the limited capacity of RF energy to create large and deep lesions. The use of large-tip ablation catheters may improve procedural efficacy, but may ultimately be associated with a 24

higher complication rate and more extracardiac collateral damage [21]. One method of creating a larger heat source and a larger lesion is to cool the electrode at the tissue interface. This can be accomplished actively by perfusing the electrode tip with saline in either an open or closed system. Significant cooling may occur passively as well, due to positioning of the catheter in areas of high blood flow, or due to sliding catheter contact. When the electrode–tissue interface is cooled, power can be increased without concern about the temperature exceeding 100 °C and coagulum forming, with a sudden rise in impedance. With higher power, the depth of volume heating is increased. Thus, the radius of the heat source (the rim of resistive tissue heating in contact with the catheter) is greater, and the lesion size increases proportionally [22]. When an open perfused catheter is employed, the ablation source not only includes the RF electrode, but also the interposed layer of heated saline. The difference between the temperatures measured at the electrode tip and the maximum tissue temperatures can be 40 °C or greater [9]. It should be noted that tip cooling does not uniformly result in increased lesion depth and size. Convective cooling of the electrode tip results in energy dissipation into the circulating blood pool (or the return line of the perfusate in closed systems). If the energy loss is not matched by increased energy delivery from the RF generator, then less net energy is transmitted into the tissue, and the lesion size will be smaller. If the electrode–tissue contact is poor, then energy coupling to the tissue will be poor and the lesions will be small, even if high RF power amplitude is employed [23]. Cooled-tip ablation has been successfully used clinically in arrhythmic substrates requiring deep and large lesion sizes, including atrial flutter and ventricular tachycardia [24–26]. The efficacy is similar to that achieved with large-tip ablation catheters, but because the electrode tip is only 4 mm, the mapping resolution may be better. The optimal duration of RF energy delivery depends on the type of ablation electrode used and the ablation site. Since a temperature of about 50 °C needs to be reached for permanent tissue ablation, lesion growth over time may be directly represented by the growth of the 50 °C isotherm boundary. Superficial heating occurs rapidly. Target temperatures are usually reached within seconds if the electrode has good contact with the tissue and there is little convective cooling. Temperature rises more slowly in deeper tissue planes. The lesion depth grows with a monoexponential function, with a half-time of 8 –10 s for ablation from a small RF source [27], or 20 –30 s from a source that produces significant volume heating [28]. The maximum lesion size can usually be achieved in 40–50 s for standard ablations, but longer application is required for ablations with large tips or cooled tips. In an experiment

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on pulmonary vein ablation with significant convective cooling, increasing the duration of RF power delivery from 60 s to 120 s significantly increased the lesion depth [29]. Of course, if the ablation target is superficial, then the duration of RF delivery can be much shorter, since 50% of the lesion depth is created in the first 10–30 s of RF delivery. This has led to a common practice of repositioning the catheter every 15 –20 s during linear ablation for atrial fibrillation. After the termination of radiofrequency energy delivery, the surface temperature decreases rapidly. However, the temperature changes at greater depth in the tissue are a balance of heat conduction from warmer to cooler tissue layers. Deeper tissue layers may actually become warmer after the termination of energy delivery as the heat from more superficial layers dissipates. This can result in a continued and progressive ablation effect, despite the fact that no energy is being applied [30]. It is important to recognize the thermal latency phenomenon, as ablation of unintended targets (such as the atrioventricular node) can occur despite timely interruption of radiofrequency energy delivery.

Pathophysiology of RF lesion formation The primary mechanism of tissue injury by RF ablation is likely to be thermally mediated [1,15,31,32]. The accelerated beats frequently observed at the onset of RF delivery may be caused by thermally induced cellular automaticity or triggered activity [32]. Irreversible loss of electrophysiological function can be usually be demonstrated immediately after a successful RF ablation; however, this finding may be delayed for up to several hours after the procedure. There may also be late recovery of electrophysiological function after an initially successful ablation. The underlying pathophysiological mechanisms that account for these early and late electrophysiological effects of RF ablation are discussed here.

Plasma membrane The plasma membrane is composed of a phospholipid bilayer and integral proteins that float within this bilayer. The hydrophobic, nonpolar hydrocarbon chains of the phospholipids face each other in the middle of the membrane, and the polar heads of the phospholipids are oriented to the aqueous phase inside and outside the cell. The degree of molecular motion of the hydrocarbon chains, which is primarily determined by the degree of saturation of the carbon–carbon bonds in the hydrocarbon chain, affects the fluidity of the membrane. Unsaturated hydrocarbon side chains allow more molecular motion, and hence make the membrane more fluid. Pure phospholipid bilayers are thought to undergo phase transitions at

different temperatures, resulting in different molecular orders. Below these transition temperatures, the phospholipids are in a solid-like state, while at temperatures above the phase transitions, the phospholipid bilayer becomes more fluid-like. Studies using cultured mammalian cells that have been heated to various temperatures have indicated two phase transitions. One transition was at 8 °C, and the other was between 23 °C and 36 °C [33]. No phase transition changes have been noted between 37 °C and 45 °C [34]; however, possible transition changes at temperatures above 45 °C have not been investigated. Membrane proteins serve as intracellular and extracellular receptors, transmembrane transporters, ion-specific channels, and ion-specific pumps. Hyperthermia is thought to cause protein conformational changes that result in protein inactivation. Studies using cultured mammalian cells have demonstrated that exposure of cells to temperatures of 39–46 °C results in inhibition of plasma membrane transport functions [35]. Intracellular ionic changes have also been observed after hyperthermic exposure. These changes depend on the cultured cell line used, as well as the magnitude and duration of the temperature change. Exposure of cultured Chinese hamster ovary cells to 42 °C for 15 min resulted in an increase in intracellular K+ uptake, which was inhibited by ouabain [36], suggesting that this was due to an increased activity of the Na+, K+–adenosine triphosphatase (ATPase) pump. Other studies have reported a decrease in intracellular K+ content when cultured mammalian cells were exposed to temperatures of 41–43 °C for 30–60 min, possibly because of increased permeability of the plasma membrane to K+ and consequent K+ efflux from the cell [37]. Potassium efflux has not been a universal finding, since other studies have shown no change in intracellular K+, Na+, Cl– or Mg2+ content after heating cultured cells to 42.0 – 45.5 °C for 30–40 min [38–40].

Cytoskeleton Mammalian cells are composed of a cytoskeletal filamentous network consisting of three types of filaments: microfilaments, microtubules, and intermediate filaments. In cultured cells, microfilaments, which are primarily composed of actin, form cytoplasmic bundles known as stress filaments. Stress filaments have also been shown to contain myosin, α-actinin, and tropomyosin in addition to actin. Stress filaments provide structural support to the plasma membrane and are responsible for maintaining cellular shape and morphology. Exposure of cultured Chinese hamster ovary cells to a temperature of 45 °C was demonstrated to result in a rapid disruption of the stress filaments [41]. Heat-induced damage to the stress filaments may be caused by depolymerization of the actin-containing microfilaments, dissociation of the 25

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Figure 2.6 Alternate frames (50 frames/s) of a human erythrocyte heated at a rate of 1 °C/s. Erythrocyte fragmentation occurs at a temperature of 50 °C. (Reproduced with permission from [43].)

microfilament bundles, or a combination of the two. Fragmentation of human erythrocytes has been shown to occur within 1 s at 50 °C [42] and may be the result of heatinduced denaturation of the major erythrocyte cytoskeletal protein spectrin (Fig. 2.6) [43]. In cultured mammalian cells, hyperthermia causes blebbing of the plasma membrane, which has been correlated with the loss of cellular viability [44]. Blebbing of the plasma membrane also occurs after exposure of cultured cells to trypsin, local anesthetics, actinomycin D, and cytochalasin [42]. These agents are known to affect the cellular cytoskeleton. Thus, heat-induced blebbing of the plasma membrane and cell death observed in cultured cells may be caused by disruption of the cytoskeletal network.

Nucleus Hyperthermia causes a disruption of both nuclear structure and function. Morphological studies have shown vesiculation of the nuclear membrane, decreased heterochromatin content, and a prominent condensation of cytoplasmic material into the perinuclear region following thermal exposure [45,46]. The nucleolus appears to be

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a very heat-sensitive organelle in cultured mammalian cells. Changes in nucleolar structure and inhibition of nucleolar function have been observed at temperatures ranging from 41 °C to 45 °C [47]. Heating of cultured mammalian cells to 42–45 °C results in inhibition of DNA synthesis, as measured by reduced incorporation of tritiated thymidine into cellular DNA. Heat-induced inhibition of DNA synthesis appears to be caused by both a reduced initiation of DNA synthesis and depression of DNA chain elongation [48]. Whether heat directly causes DNA damage is controversial [49]. Most studies indicate that hyperthermia alone does not cause DNA strand breaks. In some reports, DNA strand breaks have been observed, but this usually developed after the period of heating and was dependent on both the duration and temperature of the hyperthermic exposure [48]. The post-hyperthermic development of DNA strand breaks has been suggested to result primarily from cellular necrosis [50]. A reproducible experimental finding is that hyperthermia results in an increase in nuclear protein content that appears to correlate with heat-induced cell killing (Fig. 2.7) [51–53]. Several studies have suggested that a significant

40 80 120 160 HEAT EXPOSURE MINUTES

.001 1.00 1.30 1.60 1.90 2.20 2.50 2.80 RELATIVE NUCLEAR PROTEIN CONTENT

Figure 2.7 Left: The effects of heating at various temperatures on the nuclear protein content of HeLa cells. Left: Cellular survival as a function of protein content in HeLa cells immediately after heating to 45 °C. (Reproduced with permission from [53].)

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portion of the heat-induced excess nuclear protein is associated with the nuclear matrix [46]. One such protein is a heat shock protein known as Hsp70 [54]. This protein translocates from the cytoplasm into the nucleus during cellular heat exposure and exerts a protective effect on the cell. The exact mechanism of cellular protection against stress by Hsp70 is not known, but it is thought to function as a “molecular chaperone,” guiding the folding and refolding of proteins as they are synthesized and conveyed between cellular organelles [55]. An alternative hypothesis for the increase in nuclear protein content is that hyperthermia causes disruption of the cell’s cytoskeletal network, which leads to collapse of this structure toward the nucleus and absorption of cytoskeletal protein into the nuclear matrix [56]. The presence of this protein then results in disruption of nuclear function [53].

Cellular metabolism Hyperthermia has been reported to cause alterations in cellular metabolism. Morphological changes, including swelling, prominent cristae, and enlargement of the intracisternal spaces are observed in the mitochondria of cultured mammalian cells exposed to 42 °C for several hours [57]. In addition, metabolic studies have revealed inhibition of both respiration and glycolysis (aerobic and anaerobic) in tumor tissue and cultured tumor cells exposed to temperatures of 42– 43 °C [58]. The exact mechanisms involved in heat-induced inhibition of cellular energy metabolism and the association with structural changes of the mitochondria remain to be determined. Few data are available describing hyperthermic changes in myocardial cellular metabolism. It has been demonstrated that myocardial creatine kinase activity is reduced in heart muscle subjected to RF ablation [59]. Thermal inactivation of creatine kinase and other metabolic proteins may ultimately contribute to hyperthermic cellular injury.

The myocardial cellular electrophysiological effects of hyperthermia have been described in an in vitro model of isolated guinea pig right ventricular papillary muscle [32]. Hyperthermia was found to cause significant changes in myocardial cellular electrophysiological properties, which included: • A marked depolarization of the resting membrane potential at temperatures ≥ 45 °C. • Changes in the action potential, characterized by a temperature-dependent increase in the maximal rate of rise of the action potential and a temperature-dependent decrease in action potential amplitude and duration. • Reversible loss of cellular excitability at a median temperature of 48.0 °C (range 42.7–51.3 °C). • Irreversible tissue injury only at temperatures ≥ 50 °C • The development of abnormal automaticity at temperatures > 45 °C (Fig. 2.8). These experimental observations have provided some insight into the temperatures required to produce reversible and irreversible myocardial injury during RF ablation. In addition, the finding of thermally induced automaticity may explain the accelerated junctional beats frequently noted during RF ablation of the atrioventricular node or the “slow” atrioventricular nodal pathway. Another in vitro study investigated the effects of hyperthermia on myocardial conduction velocity in a model of superfused canine myocardium. Conduction was recorded from a multielectrode plaque during pacing at 600 ms. At temperatures between 38.5 °C and 45.4 °C, conduction velocity was supernormal. In the intermediate hyperthermic range (45–50 °C), conduction was slowed. Transient conduction block and automaticity were observed with

Cellular electrophysiology Hyperthermia exerts significant effects on many components of the sarcolemmal membrane and intracellular structures such as the sarcoplasmic reticulum and mitochondria. It is anticipated that perturbation of these structures by hyperthermic exposure would result in impairment of cellular excitability and excitation–contraction coupling. Ge et al. [60] tested the effects of RF catheter ablation on local action potentials in a model of superfused canine epicardial strips. They observed a loss of resting membrane potential, a decrease in dV/dt, and shortening of the action potential duration up to 6–8 mm from the lesion edge. However, severe abnormalities were only recorded within 2 mm of the pathological lesion.

Figure 2.8 The effect of hyperthermia on the development of automaticity in isolated guinea pig papillary muscle (data are presented as medians and interquartile ranges). The median temperature at which automaticity was observed was 50.1 °C, compared with 44.1 °C in preparations without spontaneous automaticity. (Reproduced with permission from [32].)

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temperatures of 49.5 –51.5 °C, and permanent block with temperatures ranging from 51.7 °C to 54.4 °C. Thus, the effects of brief hyperthermic exposure altered myocardial electrophysiology in vitro in a fashion similar to that seen in the clinical setting [61]. The mechanism of thermally induced myocardial injury is not completely defined. Isolated guinea pig right ventricular papillary muscles have been exposed experimentally to hyperthermic pulses. Cytosolic free calcium was measured using Fluo-3 AM dye, and papillary muscle tension was used as a surrogate marker for intracellular free calcium. Temperatures above 45 °C and below 50 °C resulted in reversible increases in papillary resting muscle tension. With temperature exposures ≥ 50 °C, irreversible contracture of the myocardium was observed. The Fluo-3 dye experiments confirmed an increase in cytosolic calcium proportional to the changes in muscle tension. Blocking sarcolemmal calcium channels with cadmium or verapamil did not attenuate these findings, whereas blocking sarcoplasmic reticulum reuptake of calcium with thapsigargin accentuated these effects. Based on these observations, it is hypothesized that hyperthermia results in a channel-independent sarcolemmal entry of calcium [62]. Other studies using cultured mammalian cells, such as HT-29 human colon cancer cells and HA-1 Chinese hamster ovary fibroblasts, have reported increases in cytosolic calcium concentration during exposure to 44 °C and 45 °C, respectively. In addition, an increase in calcium permeability of the plasma membrane at least partly mediated the heat-induced rise in cytosolic calcium concentration and was not prevented by calcium channel blockers [63]. The likely cause of hyperthermia-induced myocardial injury consistent with these observations is that nonspecific injury to the sarcolemmal membrane occurs with temperatures ≥ 45 °C. Extracellular sodium and calcium may then enter into the cell through the damaged plasma membrane, resulting in depolarization and an increase in resting tension of the myocardium, respectively. The extracellular calcium influx into the cell may initially be buffered by calcium uptake into the sarcoplasmic reticulum and mitochondria, which may yield reversible myocardial injury at temperatures between 45 °C and 50 °C. However, in isolated sarcoplasmic vesicles from rabbit skeletal muscle, the calcium accumulation rapidly declines at temperatures ≥ 50 °C [64]. Additionally, sarcoplasmic reticulum ATPase activity is also inhibited at temperatures ≥ 50 °C [65]. It is therefore hypothesized that irreversible injury to the myocardium occurring at temperatures ≥ 50 °C is mediated by cytosolic calcium overload due to calcium influx across the sarcolemmal membrane and inhibition of the intracellular calcium buffering systems. Simmers et al. [65] assessed the effects of radiofrequency energy and tissue heating on myocardial conduction in 28

vitro. In this experiment, they surgically created an isthmus in a preparation of canine ventricular myocardium superfused at 37 °C. They then heated this tissue with radiofrequency energy and measured the temperature at which conduction block through the isthmus was observed in response to pacing. Using this approach, transient conduction block was observed at 50.7 ± 3.0 °C, and irreversible conduction block was observed at 58.0 ± 3.4 °C. The dV/dt remained constant up to 45 °C, then began to fall between 45 °C and 50 °C. Above 49.5 – 51.5 °C, the tissue was inexcitable (Fig. 2.9). The threshold temperatures for conduction block were similar to those observed in response to heating from a pure thermal source [61]. The authors therefore concluded that the dominant effect of physiological injury from radiofrequency heating was thermal. Wood et al. examined the time course of electrophysiological abnormalities at the border zone of the ablative lesion. They observed that after acute lesions, the action potential duration and amplitude, as well as the conduction velocity, were all decreased 2.5 mm from the lesion border. However, 3 weeks after ablation, the border zone electrophysiological properties had normalized completely [66].

Figure 2.9 The dV/dt values in superfused canine myocardium recorded after 30 s of hyperthermic exposure (bottom), compared with control values (top). The bottom panel shows results from a single preparation. (Reproduced with permission from [65].)

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Tissue effects Hyperthermia and blood flow Erythrocyte velocity and vessel luminal diameter have been measured within the microvasculature of rabbit granulation tissue exposed to temperatures of 40–52 °C for 60 min [67]. In this study, microvascular blood flow increased with temperatures up to a critical value of 45.7 °C, but then rapidly declined at temperatures above this value. Histological studies using rat skeletal muscle exposed to temperatures of 43 – 45 °C for 20 min have demonstrated microvascular endothelial cell swelling and disruption, intravascular thrombosis, and neutrophil adherence to venular endothelium within 5 min of hyperthermic exposure. This was followed by an inflammatory cell infiltrate consisting of neutrophils and mononuclear macrophages that was most evident between 6 and 48 h after the hyperthermic insult (Fig. 2.10) [68,69].

Myocardial contrast echocardiography has been used to study the effects of RF ablation on myocardial microvascular blood flow in vivo using an open-chest canine model [70]. This study reported a marked reduction in microvascular blood flow within the acute pathological RF lesion. A significant reduction in microvascular blood flow extending beyond the edge of the acute pathological lesion was also demonstrated and was characterized by findings consistent with microvascular endothelial injury. The study concluded that the region of acute tissue injury produced by RF ablation was more extensive than the area of acute pathological injury, as demonstrated by histochemical staining. The microvascular ultrastructure is dramatically altered in response to hyperthermia. Exposure of pial microvessels to 43 °C resulted in platelet activation evidenced by degranulation, aggregation, and discoid platelets. The endothelial cells showed focal lucency, denudation vacuole formation, and membrane rupture [71]. Ultrastructural examination of the border zone region beyond the edge of an acute RF lesion in ventricular myocardium demonstrated marked endothelial changes. These included basement membrane disruption, plasma membrane dissolution, and erythrocyte stasis. These changes could be observed as far as 6 mm from the edge of the acute lesion. Thus, progression or resolution of the RF-induced tissue injury outside the acute pathological lesion may explain the late electrophysiological effects of RF ablation [70]. A clinical observation that has contributed to the wide acceptance of radiofrequency catheter ablation is the relative absence of coronary arterial complications, despite frequent application of radiofrequency energy in close contiguity to epicardial coronary arteries. Because arterial blood flow velocity is high, arteries create a formidable heat sink due to convective cooling. While this offers a protective effect against arterial injury, it may also prevent successful ablation of a targeted substrate if it is located contiguous to an artery. An in vitro study of radiofrequency catheter ablation demonstrated that a flow rate as low as 1 mL/min through an intramural artery could prevent uniform and transmural lesion formation. Highenergy ablation was needed to overcome the cooling effect with higher arterial flow rates [72].

Inflammatory response

Figure 2.10 Diagrammatic representation of some of the changes that may occur within the microcirculation during hyperthermia. (Adapted with permission from [68].)

Acute and chronic histological studies of RF lesions in dogs after catheter ablation of the atrioventricular junction have been reported [31,73]. Light-microscopic examination of RF lesions 4–5 days after the ablation have revealed well-circumscribed areas of coagulation necrosis surrounded by a peripheral zone of hemorrhage and inflammatory cells (consisting of mononuclear cells and neutrophils) [31]. Chronic RF lesions examined 2 months 29

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Figure 2.11 Electron micrographs (magnification 33 000 x) from three different regions outside of the edge of the acute pathological lesion created by radiofrequency ablation of ventricular myocardium. (Reproduced with permission from [74].) A. A sample from the near border zone (within 3 mm of the lesion border). There is a complete absence of a normal ultrastructure. Note the prominent inclusions (arrowheads) in the remnants of mitochondria, thickened Z-lines, loss of myofilaments, and absent plasma and basement membranes. B. A sample from the far border zone (3–6 mm form the lesion border). Variation in sarcomere length among adjacent myocytes and disruption of the plasma and basement membranes is observed. C. From a region remote from the ablation site, showing a normal ultrastructural architecture in the myocytes. BM, basement membrane; ID, intercalated disk; M, mitochondrion; PM, plasma membrane; SM, sarcomere; SR, sarcoplasmic reticulum; Z, Z-line.

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after the ablation have shown fibrosis, granulation tissue, fat cell deposition, cartilage formation, and chronic inflammatory cell infiltration [73]. The contribution of the inflammatory response in the lesion border zone to lesion growth in the first 48 h has not been determined.

Ultrastructure Profound ultrastructural changes have been observed in ventricular myocytes in the border zone outside of the region of acute coagulation necrosis of RF lesions (Fig. 2.11). The general appearance of the near border zone (within 3 mm of the lesion edge) was markedly disrupted with absent or severely distorted plasma membranes, missing basement membranes and extravasation of erythrocytes. The mitochondria were swollen, with discontinuous cristae membranes, and the T-tubules and sarcoplasmic reticulum were either absent or severely distorted. The sarcomeres were severely contracted or were extended with loss of myofilament structure. The far border zone (3–6 mm from the lesion edge) showed similar but less severe ultrastructural changes. The plasma membranes were still severely damaged, but the mitochondria were less deranged, and the sarcomeres showed variability in their contractile state. Gap junctions were very distorted or absent in the near zone, but appeared normal in the far border zone. The intercalated disks showed only minimal structural distortion [74]. Immunochemical staining of the intercellular gap junction protein connexin 43 in a canine model of atrial fibrillation confirmed the observation that the density of gap junctions adjacent to regions of RF catheter ablation is markedly reduced [75]. These observations are consistent with the physiological changes observed in the ablation border zone acutely [76].

Clinical studies of thermal injury Studies using mammalian cell culture lines have shown that cellular survival during hyperthermia is both timedependent and temperature-dependent [77]. Higher temperatures lead both to more rapid cell death and to a greater degree of cell death. RF catheter ablation typically results in high temperatures (70–90 °C) for short durations (up to 60 s) at the electrode–tissue interface, but significantly lower temperatures at deeper tissue sites. This leads to rapid tissue injury within the immediate vicinity of the RF electrode but slightly delayed myocardial injury with increasing distance from the RF electrode. Irreversible myocardial injury, as demonstrated by histochemical staining, has been reported to occur at an isotherm of 52–55 °C in an in vitro model of RF ablation using superfused and perfused porcine right ventricular free wall [28]. In this model, RF power was adjusted to maintain an electrode–tissue interface temperature of 85 °C for 60 s.

Clinically, the mean electrode–tissue interface temperature (as measured by a thermistor-tipped ablation catheter) associated with permanent block of accessory pathway conduction was 62 ± 15 °C [78]. Another clinical study examined the relationship of temperature to physiological effect using a power ramping protocol in patients undergoing atrioventricular junctional ablation. The mean temperature measured at the electrode–tissue interface was 51 ± 4 °C during hyperthermia-induced junctional automaticity, 58 ± 6 °C during reversible complete heart block, and 60 ± 7 °C during ablations that resulted in permanent complete heart block [79]. However, the values recorded by the catheter-mounted sensors underestimate the critical temperature required for a physiological effect within the targeted arrhythmia substrate, because of their remote location from the RF electrode and the fall-off in tissue temperature with increasing distance from the electrode.

Conclusion A working knowledge of the biophysics and pathophysiology of radiofrequency lesion formation will improve the clinical management skills of interventional electrophysiologists. Based on modeling, in vitro, in vivo, and clinical studies, a working framework of the mechanism of radiofrequency ablation can be established (Table 2.1). Radiofrequency electrical current passes through myocardium and generates heat by resistive heating. Heat conduction to deeper tissue layers creates the deeper thermal lesion. Large electrode tips and tip cooling allows higher power to be employed and larger lesions to be created. Too much power delivery can lead to excessive tissue heating, with surface char and coagulum formation, or subendocardial steam pops. The mechanism of tissue injury appears to be thermally mediated. The initial, reversible loss of conduction observed immediately after the initiation of RF energy delivery may be caused by heat-induced cellular depolarization. The likely mechanisms of depolarization include transient formation of nonspecific ionic pores in the plasma membrane and/or heat-induced effects on ion-channel/ion pump structure and kinetics. Cellular depolarization can cause spontaneous automaticity and may be the electrophysiological mechanism underlying the accelerated beats observed at the onset of RF ablation. Irreversible loss of electrophysiological function immediately after a successful ablation is probably caused by thermal tissue injury, resulting in a focal region of coagulation necrosis. The extent of tissue injury produced by RF ablation in vivo is larger than the region of acute coagulation necrosis, which results in a border zone of acutely injured but viable myocardium. A secondary inflammatory response and/or ischemia as a consequence of microvascular damage may cause 31

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Cellular effects Plasma membrane Phospholipids Proteins Cytoskeleton Nucleus Cellular metabolism

Tissue effects Microvasculature Inflammatory response

Table 2.1 Possible biological effects of radiofrequency ablation. Possible changes in membrane fluidity [33] Inhibition of membrane transport proteins [35] Kinetic and/or structural changes to ion channels and ion pumps [36–40] Disruption of stress filaments, [41] loss of plasma membrane support and membrane blebbing [44] Loss of nuclear structure and function [45–51,54] Inhibition of cellular metabolism [58] Denaturation of metabolic proteins [59]

Damage to microvasculature and reduced microvascular blood flow [67–71] Secondary inflammatory response to initial thermal injury [31,68,73]

progression of tissue injury within the border zone. Progressive tissue injury may result in RF lesion extension over time and may be the pathophysiological mechanism for the late loss of electrophysiological function observed after RF ablation. Alternatively, resolution of the RFinduced tissue injury within the border zone may lead to late recovery of electrophysiological function, which has been reported to occur in approximately 5–10% of patients after an initially successful ablation.

8

9 10 11

References 12 1 Haines DE, Watson DD. Tissue heating during radiofrequency catheter ablation: A thermodynamic model and observations in isolated perfused and superfused canine right ventricular free wall. Pacing Clin Electrophysiol 1989;12: 962–76. 2 McRury ID, Mitchell MA, Panescu D, Haines DE. Nonuniform heating during radiofrequency ablation with long electrodes: monitoring the edge effect. Circulation 1997;96: 4057–64. 3 Zheng X, Walcott GP, Rollins DL, et al. Comparison of the temperature profile and pathological effect at unipolar, bipolar and phased radiofrequency current configurations. J Interv Card Electrophysiol 2001;5:401–10. 4 Nath S, DiMarco JP, Gallop RG, McRury ID, Haines DE. Effects of dispersive electrode position and surface area on electrical parameters and temperature during radiofrequency catheter ablation. Am J Cardiol 1996;77:765 –7. 5 Tungjitkusolmun S, Woo EJ, Cao H, Tsai JZ, Vorperian VR, Webster JG. Finite element analyses of uniform current density electrodes for radio-frequency cardiac ablation. IEEE Trans Biomed Eng 2000;47:32–40. 6 Jain MK, Wolf PD. Temperature-controlled and constantpower radiofrequency ablation: what affects lesion growth? Trans Biomed Eng 1999;46:1405–12. 7 Goette A, Reek S, Klein HU, Geller JC. Case report: severe skin burn at the site of the indifferent electrode after

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radiofrequency catheter ablation of typical atrial flutter. J Interv Card Electrophysiol 2001;5:337– 40. Haines DE, Watson DD, Verow AF. Electrode radius predicts lesion radius during radiofrequency energy heating: validation of a proposed thermodynamic model. Circ Res 1990;67: 124 – 9. Gopalakrishnan J. A mathematical model for irrigated epicardial radiofrequency ablation. Ann Biomed Eng 2002;30:884–93. Eick OJ, Bierbaum D. Tissue temperature-controlled radiofrequency ablation. Pacing Clin Electrophysiol 2003;26:725 –30. Wittkampf FH, Hauer RN, Robles de Medina EO. Control of radiofrequency lesion size by power regulation. Circulation 1989;80:962 – 8. Mukherjee R, Laohakunakorn P, Welzig MC, Cowart KS, Saul JP. Counterintuitive relations between in vivo RF lesion size, power, and tip temperature. J Interv Card Electrophysiol 2003;9:309 –15. Petersen HH, Chen X, Pietersen A, Svendsen JH, Haunso S. Lesion dimensions during temperature-controlled radiofrequency ablation of left ventricular porcine myocardium: ablation site and electrode size related to convective cooling. Circulation 1999;99:319–25. Petersen HH, Svendsen JH. Can lesion size during radiofrequency ablation be predicted by the temperature rise to a low power test pulse in vitro? Pacing Clin Electrophysiol 2003;26: 1653 – 9. Haines DE, Verow AF. Observations on electrode–tissue interface temperature and effect on electrical impedance during radiofrequency ablation of ventricular myocardium. Circulation 1990;82:1034 – 8. Demolin JM, Eick OJ, Munch K, Koullick E, Nakagawa H, Wittkampf FH. Soft thrombus formation in radiofrequency catheter ablation. Pacing Clin Electrophysiol 2002;25:1219 –22. Juneja R, O’Callaghan P, Rowland E. Tissue rupture and bubble formation during radiofrequency catheter ablation: “echoes of a pop.” Circulation 2001;103:1333 – 4. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of atrioventricular junction using radiofrequency current in 17 patients: comparison of standard and large-tip catheter electrodes. Circulation 1991;83:1562–76.

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Biophysics and pathophysiology of lesion formation by transcatheter radiofrequency ablation

19 Feld G, Wharton M, Plumb V, et al. Radiofrequency catheter ablation of type 1 atrial flutter using large-tip 8- or 10-mm electrode catheters and a high-output radiofrequency energy generator: results of a multicenter safety and efficacy study. J Am Coll Cardiol 2004;43:1466–72. 20 Ventura R, Willems S, Weiss C, et al. Large tip electrodes for successful elimination of atrial flutter resistant to conventional catheter ablation. J Interv Card Electrophysiol 2003;8: 149–54. 21 Gillinov AM, McCarthy PM, Pettersson G, Lytle BW, Rice TW. Esophageal perforation during left atrial radiofrequency ablation: is the risk too high? J Thorac Cardiovasc Surg 2003;126:1661–2. 22 Nakagawa H, Yamanashi WS, Pitha JV, et al. Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation. Circulation 1995;91:2264–73. 23 Simmers TA, de Bakker JM, Coronel R, et al. Effects of intracavitary blood flow and electrode–target distance on radiofrequency power required for transient conduction block in a Langendorff-perfused canine model. J Am Coll Cardiol 1998;31:231–5. 24 Soejima K, Delacretaz E, Suzuki M, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct-related ventricular tachycardias. Circulation 2001;103:1858 – 62. 25 Madrid AH, Rebollo JM, Del Rey JM, et al. Randomized comparison of efficacy of cooled tip catheter ablation of atrial flutter: anatomic versus electrophysiological complete isthmus block. Pacing Clin Electrophysiol 2001;24:1525 –33. 26 Atiga WL, Worley SJ, Hummel J, et al. Prospective randomized comparison of cooled radiofrequency versus standard radiofrequency energy for ablation of typical atrial flutter. Pacing Clin Electrophysiol 2002;25:1172–8. 27 Haines DE. Determinants of lesion size during radiofrequency catheter ablation: the role of electrode–tissue contact pressure and duration of energy delivery. J Cardiovasc Electrophysiol 1991;2:509–15. 28 Whayne JG, Nath S, Haines DE. Microwave catheter ablation of myocardium in vitro: assessment of the characteristics of tissue heating and injury. Circulation 1994;89:2390 –5. 29 Guy DJ, Boyd A, Thomas SP, Ross DL. Increasing power versus duration for radiofrequency ablation with a high superfusate flow: implications for pulmonary vein ablation? Pacing Clin Electrophysiol 2003;26:1379–85. 30 Wittkampf FH, Nakagawa H, Yamanashi WS, Imai S, Jackman WM. Thermal latency in radiofrequency ablation. Circulation 1996;93:1083–6. 31 Huang SK, Bharati S, Graham AR, Lev M, Marcus FI, Odell RC. Closed chest catheter desiccation of the atrioventricular junction using radiofrequency energy: a new method of catheter ablation. J Am Coll Cardiol 1987;9:349 – 58. 32 Nath S, Lynch C III, Whayne JG, Haines DE. Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle: implications for catheter ablation. Circulation 1993;88:1826–31. 33 Lepock JR. Involvement of membranes in cellular responses to hyperthermia. Radiat Res 1982;92:433–8.

34 Mehdi SQ, Recktenwald DJ, Smith LM, Li GC, Armour EP, Hahn GM. Effect of hyperthermia on murine cell surface histocompatibility antigens. Cancer Res 1984;44:3394 –7. 35 Slusser H, Hopwood LE, Kapiszewska M. Inhibition of membrane transport by hyperthermia. Natl Cancer Inst Monogr 1982;61:85 –7. 36 Stevenson AP, Galey WR, Tobey RA, Stevenson HG, Jett JH. Hyperthermia-induced increase in potassium transport in Chinese hamster cells. J Cell Physiol 1983;115:75 – 86. 37 Yi PN, Chang CS, Tallen M, Bayer W, Ball S. Hyperthermiainduced intracellular ionic level changes in tumor cells. Radiat Res 1983;93:534 – 44. 38 Vidair CA, Dewey WC. Evaluation of a role for intracellular Na+, K+, Ca2+, and Mg2+ in hyperthermic cell killing. Radiat Res 1986;105:187–200. 39 Boonstra J, Schamhart DH, de Laat SW, van Wijk R. Analysis of K+ and Na+ transport and intracellular contents during and after heat shock and their role in protein synthesis in rat hepatoma cells. Cancer Res 1984;44:955 – 60. 40 Borrelli MJ, Carlini WG, Ransom BR, Dewey WC. Ionsensitive microelectrode measurements of free intracellular chloride and potassium concentrations in hyperthermiatreated neuroblastoma cells. J Cell Physiol 1986;129:175 – 84. 41 Glass JR, DeWitt RG, Cress AE. Rapid loss of stress fibers in Chinese hamster ovary cells after hyperthermia. Cancer Res 1985;45:258 – 62. 42 Coakley WT. Hyperthermia effects on the cytoskeleton and on cell morphology. Symp Soc Exp Biol 1987;41:187–211. 43 Coakley WT, Deeley JO. Effects of ionic strength, serum protein and surface charge of membrane movements and vesicle production in heated erythrocytes. Biochim Biophys Acta 1980;602:355 –75. 44 Borrelli MJ, Wong RS, Dewey WC. A direct correlation between hyperthermia-induced membrane blebbing and survival in synchronous G1 CHO cells. J Cell Physiol 1986;126:181– 90. 45 Warters RL, Roti Roti JL. Hyperthermia and the cell nucleus. Radiat Res 1982;92:458 – 62. 46 Warters RL, Brizgys LM, Sharma R, Roti Roti JL. Heat shock (45 degrees C) results in an increase of nuclear matrix protein mass in HeLa cells. Int J Radiat Biol Relat Stud Phys Chem Med 1986;50:253 – 68. 47 Simard R, Bernhard W. A heat-sensitive cellular function located in the nucleolus. J Cell Biol 1967;34:61–76. 48 Wong RS, Borrelli MJ, Thompson LL, Dewey WC. Mechanism of killing Chinese hamster ovary cells heated in G1: effects on DNA synthesis and blocking in G2. Radiat Res 1989;118:295 –310. 49 Raaphorst GP, Feeley MM. Comparison of recovery from potentially lethal damage after exposure to hyperthermia and radiation. Radiat Res 1990;121:107–10. 50 Warters RL, Henle KJ. DNA degradation in chinese hamster ovary cells after exposure to hyperthermia. Cancer Res 1982;42:4427–32. 51 Roti Roti JL, Henle KJ, Winward RT. The kinetics of increase in chromatin protein content in heated cells: a possible role in cell killing. Radiat Res 1979;78:522 –31. 52 Roti Roti JL. Heat-induced cell death and radiosensitization: molecular mechanisms. Natl Cancer Inst Monogr 1982;61:3–10.

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53 Roti Roti JL, Laszlo A. The effects of hyperthermia on cellular macromolecules. Hyperth Oncol 1988;1:13 –56. 54 Welch WJ, Feramisco JR. Nuclear and nucleolar localization of the 72,000-dalton heat shock protein in heat-shocked mammalian cells. J Biol Chem 1984;259:4501–13. 55 Meng X, Harken AH. The interaction between Hsp70 and TNF-alpha expression: a novel mechanism for protection of the myocardium against post-injury depression. Shock 2002;17:345–53. 56 Wachsberger PR. Cross RA. Effects of hyperthermia on the cytoskeleton and cell survival in G1 and S phase Chinese hamster ovary cells. Int J Hypertherm 6:67– 85, 1990. 57 Welch WJ, Suhan JP. Morphological study of the mammalian stress response: characterization of changes in cytoplasmic organelles, cytoskeleton, and nucleoli, and appearance of intranuclear actin filaments in rat fibroblasts after heat-shock treatment. J Cell Biol 1985;101:1198–1211. 58 Dickson JA, Calderwood SK. Effects of hyperglycemia and hyperthermia on the pH, glycolysis, and respiration of the Yoshida sarcoma in vivo. J Natl Cancer Inst 1979;63:1371– 81. 59 Haines DE, Whayne JG, Walker J, Nath S, Bruns DE. The effect of radiofrequency catheter ablation on myocardial creatine kinase activity. J Cardiovasc Electrophysiol 1995;6:79 – 88. 60 Ge YZ, Shao PZ, Goldberger J, Kadish A. Cellular electrophysiological changes induced in vitro by radiofrequency current: comparison with electrical ablation. Pacing Clin Electrophysiol 1995;18:323–33. 61 Simmers TA, de Bakker JM, Wittkampf FH, Hauer RN. Effects of heating on impulse propagation in superfused canine myocardium. J Am Coll Cardiol 1995;25:1457– 64. 62 Everett TH, Nath S, Lynch C III, Beach JM, Whayne JG, Haines DE. Role of calcium in acute hyperthermic myocardial injury. J Cardiovasc Electrophysiol 2001;12:563 – 9. 63 Mikkelsen RB, Reinlib L, Donowitz M, Zahniser D. Hyperthermia effects on cytosolic [Ca2+]: analysis at the single cell level by digitized imaging microscopy and cell survival. Cancer Res 1991;51:359–64. 64 Inesi G, Millman M, Eletr S. Temperature-induced transitions of function and structure in sarcoplasmic reticulum membranes. J Mol Biol 1973;81:483–504. 65 Simmers TA, de Bakker JM, Wittkampf FH, Hauer RN. Effects of heating with radiofrequency power on myocardial impulse conduction: is radiofrequency ablation exclusively thermally mediated? J Cardiovasc Electrophysiol 1996;7: 243–7.

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66 Wood MA, Fuller IA. Acute and chronic electrophysiologic changes surrounding radiofrequency lesions. J Cardiovasc Electrophysiol 2002;13:56 – 61. 67 Dudar TE, Jain RK. Differential response of normal and tumor microcirculation to hyperthermia. Cancer Res 1984;44:605 –12. 68 Reinhold HS, van den Berg AP. Effects of hyperthermia on blood flow and metabolism. In: Field SB, Hand JW, eds. An introduction to the Practical Aspects to Clinical Hyperthermia. London, England: Taylor & Francis; 1990: 77–107. 69 Ferguson MK, Seifert FC, Replogle RL. Leukocyte adherence in venules of rat skeletal muscle following thermal injury. Microvasc Res 1982;24:34 – 41. 70 Nath S, Whayne JG, Kaul S, Goodman NC, Jayaweera AR, Haines DE. Effects of radiofrequency catheter ablation on regional myocardial blood flow: possible mechanism for late electrophysiological outcome. Circulation 1994;89:2667–72. 71 Fahim MA, el Sabban F. Hyperthermia induces ultrastructural changes in mouse pial microvessels. Anat Rec 1995;242: 77– 82. 72 Fuller IA, Wood MA. Intramural coronary vasculature prevents transmural radiofrequency lesion formation: implications for linear ablation. Circulation 2003;107:1797–803. 73 Huang SK, Bharati S, Lev M, Marcus FI. Electrophysiologic and histologic observations of chronic atrioventricular block induced by closed-chest catheter desiccation with radiofrequency energy. Pacing Clin Electrophysiol 1987;10:805 –16. 74 Nath S, Redick JA, Whayne JG, Haines DE. Ultrastructural observations in the myocardium beyond the region of acute coagulation necrosis following radiofrequency catheter ablation. J Cardiovasc Electrophysiol 1994;5:838 – 45. 75 Elvan A, Huang XD, Pressler ML, Zipes DP. Radiofrequency catheter ablation of the atria eliminates pacing-induced sustained atrial fibrillation and reduces connexin 43 in dogs. Circulation 1997;96:1675 – 85. 76 Fuller IA, Wood MA. Intramural coronary vasculature prevents transmural radiofrequency lesion formation: implications for linear ablation. Circulation 2003;107:1797– 803. 77 Bauer KD, Henle KJ. Arrhenius analysis of heat survival curves from normal and thermotolerant CHO cells. Radiat Res 1979;78:251– 63. 78 Langberg JJ, Calkins H, el Atassi R, et al. Temperature monitoring during radiofrequency catheter ablation of accessory pathways. Circulation 1992;86:1469 –74. 79 Nath S, DiMarco JP, Mounsey JP, Lobban JH, Haines DE. Correlation of temperature and pathophysiological effect during radiofrequency catheter ablation of the AV junction. Circulation 1995;92:1188 –92.

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3

Alternative energy sources for catheter ablation Saman Nazarian and Hugh Calkins

Radiofrequency catheter ablation is a highly effective energy source for catheter ablation of cardiac arrhythmias. For most cardiac arrhythmias, radiofrequency catheter ablation is safe and effective. As a result, radiofrequency energy is the standard energy source used for catheter ablation today. Despite the widespread use of radiofrequency energy, some potential limitations of this energy source remain. These limitations of radiofrequency energy include restricted lesion size and shape, the need for constant tissue– catheter contact, tissue inflammation and hemorrhage [1], the potential for endocardial disruption and perforation, the possibility of coagulum formation [2], the potential for the development of pulmonary vein stenosis when radiofrequency energy is delivered to the pulmonary veins, and a small risk of stroke [3]. Because of these limitations of radiofrequency energy, alternative energy sources are being explored for use during catheter ablation procedures. These energy sources are particularly relevant for catheter ablation of atrial fibrillation, as the safety and efficacy of catheter ablation of atrial fibrillation using radiofrequency energy remains inadequate. The purpose of this chapter is to review the current state of knowledge regarding alternative energy sources for catheter ablation.

(Fig. 3.1). There is controversy about whether tissue destruction is predominantly due to freezing or subsequent ischemia. Ultrastructural studies suggest that ice crystals are formed within the cells during cryoablation and that the resultant cell damage is osmotic rather than mechanical, leading to secondary microcirculatory changes [4]. Initial freezing of extracellular fluid results in a hyperosmotic extracellular environment that draws water from the cells, resulting in cellular hypertonic stress, thereby damaging the membrane and cellular constituents. Inward flow of water on rewarming results in cellular swelling and further damage, leading to disruption of the cellular membranes. Further cooling results in freezing of the cellular fluid and disruption of the intracellular organelles and membranes, resulting in complete cell death. Extracellular freezing begins to occur at approximately –20 °C. The extent of damage depends upon the temperature reached. Cellular changes at –20 °C to –40 °C may be fully reversible, whereas cooling to the range of –70 °C to –80 °C will irreversibly damage cellular tissue [5].

Cryoablation Mechanism of tissue injury Cryoablation is carried out by delivering a pressurized liquid refrigerant, such as nitrous oxide, to the catheter tip through a thin injection tube. An abrupt gradient in the lumen diameter leads to an expansion chamber at the tip. Rapid expansion of the refrigerant facilitates evaporation of the liquid refrigerant and absorption of heat from the surrounding catheter surface and myocardium, thereby freezing the extracellular fluid, followed by cellular tissue

Figure 3.1 The mechanism of cryoablation. A pressurized liquid refrigerant such as nitrous oxide is delivered to the catheter tip through a thin injection tube. An abrupt gradient in the lumen diameter leads to gas expansion and cooling at the tip, resulting in the absorption of heat from the surrounding catheter surface and myocardium.

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Preclinical studies Initial studies to determine the effects of partial nodal ablation for atrioventricular reentry tachycardia were performed using cryoablation. In 1986, Holman et al. described the effects of cryosurgical atrioventricular node modification on retrograde atrioventricular conduction and the ventricular echo phenomenon in a canine model. In comparison with the sham procedure, dogs that underwent cryosurgery had a significantly prolonged retrograde Wenckebach point, atrioventricular nodal conduction time, functional refractory period of the atrioventricular node, effective refractory period of the atrioventricular node, and ventricular echo reflection time. No significant change in ventriculoatrial conduction was noted in the chronic cryosurgery group, but the ventricular echo was eliminated in 95% of the animals in the cryosurgery arm [6]. As discussed previously, despite the presence of transient conduction block, tissue changes at temperatures of 0 to – 40 °C may be reversible in some tissues. This characteristic of cryoablation offers the possibility of “ice mapping” by identifying successful sites before irreversible ablation. It is important to realize, however, that due to variations in tissue thickness and vascularity, the temperature required for irreversible ablation may be different within adjacent sites in the myocardium. To determine the reversibility of atrioventricular nodal lesions, Dubuc et al. carried out partial nodal cryoablation in eight dogs. Highdegree atrioventricular block was reversible in seven animals at a mean temperature of –40 °C. The electrophysiological parameters of the atrioventricular node were unchanged at 20 and 60 min, and after 56 days. There was no significant pathological modification of the atrioventricular node in the reversible lesions [7]. Cryoablation offers a lower risk of pulmonary vein stenosis in comparison with radiofrequency lesions. The acute and chronic effects of pulmonary vein cryoablation were evaluated by freezing at a temperature of –65 °C for a mean of 8.6 min in the pulmonary veins of anesthetized dogs. The mean threshold for atrial capture by pacing in the pulmonary veins increased from 1.3 mA to 9.4 mA acutely and 2.5 mA chronically. There was no evidence of any significant change in the angiographic pulmonary vein diameter acutely or after 2 months of follow-up [8]. More recently, Avitall et al. used liquid nitrous oxide delivered through a cryoballoon to apply sequential 3min circular ablation lesions to the pulmonary vein ostia in dogs. Total elimination of recorded pulmonary vein electrograms was highest (53%) after four applications. No significant changes in pulmonary vein diameter were noted [9]. Cryoablated lesions appear to be less thrombogenic than lesions induced by radiofrequency energy. Khairy 36

et al. compared thrombus formation due to radiofrequency ablation and cryoablation in 22 dogs at right atrial, right ventricular, and left ventricular sites in the setting of heparin pretreatment. Different catheter sizes (7 Fr and 9 Fr), cooling rates (–1 °C/s, –5 °C/s, and –20 °C/s) and target temperatures (–55 °C and –75 °C) were tested. Histologically, the cryolesions were discrete, with dense areas of fibrotic and contraction band necrosis. Radiofrequency ablation (50 W for 60 s) resulted in lesions of greater area and volume. After 7 days, the incidence of thrombus formation with radiofrequency ablation was 75.8%, versus 30.1% with cryoablation (P < 0.001). The thrombus volumes with radiofrequency were significantly larger than those associated with cryothermy. Unlike radiofrequency lesions, cryolesion dimensions were not predictive of thrombus size [10]. Another advantage of cryoablation may be an improved safety margin for ablation near coronary arteries [11]. An advantage of this type is most suitable for epicardial ablation. Lustgarten et al. assessed the safety and efficacy of epicardial cryoablation in a closed-chest dog model. Four-minute applications at –90 °C achieved transmural atrial and nontransmural ventricular lesions. Cryoablation over the epicardial coronary arteries resulted in transient stenoses, followed by restoration of Thrombolysis in Myocardial Infarction (TIMI) III flow within 5 min. Chronic histological injury, including neointimal proliferation, was observed to occur only in vessels less than 0.7 mm in diameter [12]. The lower risk of ablation near the coronary arteries has also led to the study of cryoablation in the coronary sinus. Ablation in the distal coronary sinus resulted in transient ST segment depression in three of 12 dogs. Cessation of electrical activity in the coronary sinus and increased pacing thresholds were noted after ablation. There was no evidence of stenosis or thrombosis within the coronary sinus or circumflex artery [13].

Clinical studies Cryoablation has a long track record for effectiveness in the surgical literature. Cox et al. first performed cryoablation in eight patients with atrioventricular node reentrant tachycardia. Using normothermic cardiopulmonary bypass, nine separate 3-mm cryolesions (– 60 °C for 2 min) were placed around the triangle of Koch in the lower right atrial septum. Each patient had a single atrioventricular node conduction curve after the procedure, and no atrioventricular node reentry was observed during a 5-year follow-up period. The procedure had no effect on AH or HV intervals, nor on the paced atrioventricular node Wenckebach cycle length [14]. Manasse et al. studied the acute histological changes due to cryoablation in atrial biopsies of patients undergoing

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Figure 3.3 A gradual transition to normal myocardium was documented at the edges of the treated area (hematoxylin–eosin, original magnification ?? x). (Reproduced with permission from [15].)

Figure 3.2 Myocardial specimen after cryoablation. The diffuse nuclear changes (arrow), irregular bands of contraction (double arrow) and indistinct membranes (arrowhead) should be noted (hematoxylin–eosin, original magnification ?? x). (Reproduced with permission from [15].)

mitral valve surgery [15]. The specimen was divided into two, and one part underwent cryoablation at –60 °C for 2 min. Acute specimens revealed extensive myocellular damage involving the full thickness of the atrial wall. The cytoplasm of the cells was shrunken and degenerated, with increased distance between the myocytes due to interstitial edema throughout the wall. Sarcoplasmic vacuolization and cellular edema with indistinct membranes, in addition to contraction bands, were noted (Fig. 3.2). There were no signs of acute inflammation. Analysis of tissue 1 month after ablation in a patient who underwent an autopsy after having died of septicemia revealed a lack of viable myocytes in the ablated region. The boundary zones showed a gradual transition from fibrosis to normal myocardium (Fig. 3.3). Cryoablation has also been used for the surgical treatment of atrial fibrillation in patients undergoing concomitant cardiac procedures. Lesions were created with an argon-based cryoprobe by freezing for 1 min after reaching – 40 °C (to a minimum temperature of –160 °C). The set of lesions included rings around the left and right pulmonary veins, the left atrial appendage, and connecting lesions between the mitral annulus and the left

inferior, appendage and left superior, and left and right inferior pulmonary veins. After 12 months, 88.5% of the patients had atrial fibrillation. There were no strokes, but one patient with a history of lupus anticoagulant had a superior mesenteric artery embolus [16]. Catheters for percutaneous cryoablation have now been developed. In April 2003, a flexible single-use cryocatheter (Freezor, CryoCath Technologies Inc., Montreal, Canada) that can reach tip temperatures as low as – 80 °C received marketing approval from the U.S. Food and Drug Administration for ablation of atrioventricular node reentry tachycardia. To assess the safety and efficacy of this type of catheter (Fig. 3.4), 14 patients with atrioventricular reentrant tachycardia and 13 patients with accessory pathway–mediated tachycardia were enrolled in a cryoablation study by Lowe et al. The number of energy applications and the procedure times were similar to those for patients undergoing radiofrequency ablation. The procedure was successful in 76% of the patients with atrioventricular reentrant tachycardia and 77% of those

Figure 3.4 The Freezor Xtra, manufactured by CryoCath Technologies Inc. (Montreal, Canada) is 7 Fr in diameter and has a 6-mm ablation electrode in addition to four mapping electrodes with a 2–5–2 spacing. (Reproduced with permission from CryoCath Technologies, Inc.)

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with accessory pathway–mediated tachycardia. The overall procedural discomfort was significantly less in patients treated with cryoablation than in those treated with radiofrequency. Cryomapping, with cooling to –40 °C to confirm a safe location before cooling to –70 °C, was carried out in patients with anteroseptal accessory pathways. This procedure identified safe targets for successful ablation in all four patients with such pathways [17]. However, it is important to note that a later study found that applying cryoablation at sites deemed to be safe on the basis of cryomapping could result in transient complete heart block. This is probably because cryolesions created during cryoablation may expand relative to the sites tested during cryomapping [18]. A more recent study assessing the short-term and long-term efficacy of cryoablation for treatment of atrioventricular node reentry tachycardia reported a 92% acute success rate and 85% effectiveness after 1 year in a group of 26 patients [19]. The risks of heart block associated with proximity of the atrioventricular node and His bundle to the cavotricuspid isthmus make cryoablation a suitable alternative to radiofrequency for the treatment not only of atrioventricular reentry tachycardia but also of atrial flutter. Manusama et al. performed cryoablation of the cavotricuspid isthmus in 35 patients with atrial flutter. Point applications were used to create the ablation line. Bidirectional isthmus conduction block and noninducibility of atrial flutter were acutely achieved in 97% of patients with a median of 14 applications at 10 sites, reaching a mean temperature of – 80.0 ± 5.0 °C. Lesions were applied for 3–5 min. During the chronic follow-up, 89% of patients were found to be free of atrial flutter [20]. In a follow-up study comparing the effectiveness of cryoablation using single versus double 5-min applications at –80 °C, cavotricuspid isthmus block was acutely achieved using single applications. Atrial flutter had a recurrence rate of 5% at 1 year [21]. A later study to assess the effectiveness of a 9-Fr (8-mm thick) cryocatheter for achieving cavotricuspid isthmus block reported a 96% acute success rate after an 8-min freeze at –75 °C. However, a repeat electrophysiological study after 6 months revealed conduction recurrence in 30% of the patients [22]. Pulmonary vein isolation with cryoablation was attempted in a recent multicenter study of patients with paroxysmal atrial fibrillation. Double 5-min cryoablations were performed at all sites of ostial pulmonary vein potentials. Immediate success was achieved in 97% of the pulmonary veins. At 6 months, 82% of the patients were free of symptomatic atrial fibrillation. However, repeat ablation with radiofrequency energy was necessary in 25% of the patients, due to long-term recurrences. Pulmonary vein computed tomography 3 and 6 months after ablation revealed no evidence of pulmonary vein stenosis [23].

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Advantages and disadvantages Cryoablation offers several potential advantages in comparison with radiofrequency energy. Firstly, cryoablation does not appear to cause pulmonary vein stenosis. This is of clear relevance for catheter ablation of atrial fibrillation. Secondly, cryoablation may lower the risk of stroke during catheter ablation of atrial fibrillation. Thirdly, cryoablation may lower the risk of atrioventricular block in comparison with radiofrequency energy when delivered close to the atrioventricular node. And fourthly, cryoablation offers the potential for “ice mapping,” in which tissue can be cooled but not destroyed in order to determine whether it is a critical component in the arrhythmia [24]. Despite these potential advantages of cryoablation and the approval of a catheter-based cryoablation system (Freezor) for clinical use, acceptance of cryoablation as a clinically relevant energy source has not been achieved. This reflects the following limitations. Firstly, the creation of lesions with cryoablation requires 2–5 min, in comparison with 30 s for standard radiofrequency lesions. The increased time is particularly relevant for catheter ablation of atrial fibrillation, in which large numbers of lesions are required. Secondly, the lesions created with cryoablation are smaller than those created with radiofrequency energy. Thirdly, high recurrence rates have been reported after cryoablation. And fourthly, the clinical utility of “ice mapping” has not been demonstrated. Research is continuing to address these remaining limitations of cryoablation. In particular, new catheter designs are being developed in order to achieve larger and linear lesions, and cryoballoons for more efficient pulmonary vein isolation are also under development.

Microwave Mechanism of tissue injury Microwave energy refers to electromagnetic radiation at frequencies of 915–2450 MHz. The electromagnetic field radiated by a microwave antenna can be focused into the myocardium, resulting in the oscillation of dipoles within polar molecules such as water (Fig. 3.5). Molecular oscillation causes tissue heating and destruction. Unlike radiofrequency, the tissue permeation of microwave is not limited by changes in the tissues surrounding the electrode. Microwave energy thus offers the potential of deeper and more even tissue penetration, with less surface heating. Microwave antennas can be designed with various lengths, delivering energy in a pattern suitable for performing linear ablations.

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Figure 3.5 The mechanism of microwave ablation. Oscillation of dipoles induced by the electromagnetic field radiated by a microwave antenna results in tissue heating and destruction.

Preclinical studies Microwave- and radiofrequency-induced catheter ablation lesions were compared in a study of 11 swine by Jumrussirikul et al. The lesions were allowed to mature over 1 month before sacrifice. Atrial radiofrequency lesions were larger (70 °C × 50 s, 22 W, 8.2 × 5.3 × 4.1 mm) than those created via microwave (70 °C × 50 s, 12 W, 6.6 × 3.4 × 1.9 mm). Ventricular lesions created by microwave were longer (15.3 × 4.5 × 3.5 mm), but did not differ in width and depth in comparison with lesions created by radiofrequency energy (9.1 × 5.8 × 4.6 mm). The lesion depth produced by microwave energy was directly proportional to catheter stability, measured by the evenness of the temperature profile over time at the midpoint of the ablation antenna [25]. Microwave ablation is contact-forgiving and continues to deliver energy despite the presence of coagulum. In order to control the continued delivery of energy despite coagulum formation, close monitoring and feedback through temperature control may be beneficial. An ablation system using a feedback control system to maintain a fixed target temperature for creating microwave lesions was tested by VanderBrink et al. Power regulation through a feedback control mechanism maintained a target temperature of 75 °C for 60 s, applied three times at each site within the canine heart. Using a mean power of 9.3 W, the mean lesion depth was 8.8 mm and the mean lesion

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volume was 304 mm3. Forty-four percent of the lesions were transmural. There was no evidence of endocardial thrombus [26]. It has been suggested that different microwave antenna designs may be capable of altering the generation of the electromagnetic field and power deposition in tissue. The in vitro temperature–distance profiles of monopolar and helical-coil antennas resonating at 915 and 2450 MHz have been tested in perfused wedges of porcine right ventricular free wall. Intramyocardial probes were used to determine temperatures at the lesion border zone. Lesion sizes and temperature profiles were similar for monopolar and helical antennas resonating at 915 and 2450 MHz. In contrast to radiofrequency ablation, in which lesion expansion was minimal after 60 s, with microwave at 915 MHz the lesion depth increased exponentially, with a half-time of 170 s [27]. A 2.25-turn spiral antenna capable of producing lesions of greater size and depth, as well as lateralfiring antenna designs capable of producing deep lesions of variable length, are also under development [28,29]. Another potential advantage offered by microwave ablation is the ease of real-time visualization of lesion production by intracardiac echocardiography. Catheter– endocardial contact and lesion production was confirmed in 125 ablations of ovine left ventricles by Tardif et al. Gas formation was evident during all ablations. The sensitivity of intracardiac echocardiography for identifying lesions was 88%, with a specificity of 92%. However, correlation between the echocardiographic lesion dimensions and the pathological dimensions was poor [30].

Clinical studies The safety and efficacy of microwave ablation has been well documented in the surgical literature. Venturini et al. assessed the intraoperative use of microwave ablation to restore sinus rhythm in patients with atrial fibrillation. In this study, 41 patients with atrial fibrillation underwent microwave isolation of the pulmonary vein ostia during concomitant cardiac surgery. There were no acute complications, and after a mean follow-up period of 14 months, 83% of the patients were maintaining sinus rhythm. At the time of follow-up, there was no echocardiographic evidence of left atrial thrombosis [31]. Another surgical trial of 43 patients with permanent atrial fibrillation undergoing valve surgery randomly assigned patients either to microwave ablation (24 patients) or to no additional intervention (19 patients). Lesions were produced using a 25-mm microwave antenna at 40 W for 25 s, forming continuous lines encircling the pulmonary veins and connecting to the mitral annulus. A continuous ablation line was also produced around the oversewn left atrial appendage. Ninety-two percent of the patients who underwent

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Figure 3.6 A characteristic histology sample collected from microwave ablation tissue, demonstrating clear foci of coagulative necrosis (N), irregular or complete loss of membranous borders, and shrunken, hypereosinophilic cytoplasm in the myocardial cells (hematoxylin–eosin, original magnification ?? x). (Reproduced with permission from [33].)

microwave ablation converted to sinus rhythm intraoperatively, in comparison with 32% of those in the control group. After 1 year, the patients in the microwave ablation group had a higher likelihood of maintaining sinus rhythm (80% vs. 33.3%; P = 0.036) [32]. The histology of microwave myocardial lesions was assessed by Manasse et al. in 15 patients after microwave ablation of the right atrial appendage during valve procedures. Ablation energy was applied at 65 W for 90 s.

Figure 3.7 A. Two myocytes with no significant ultrastructural alterations (electron microscopy). B. Sample after microwave energy ablation. The myocyte shows architectural disarray and severe loss of contractile filaments (electron microscopy). C. Sample after microwave energy ablation. Swollen

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Power loss through the connecting coaxial cable between the generator and the microwave antenna was estimated at 40%. The remaining 39 W was distributed at 9.75 W/cm along the 4-cm flexible antenna. Immediately after epicardial ablation, a tissue specimen was excised from the lesion site (1 cm2, right appendage) and another was excised from an adjacent nonablated site. Examination of the ablated tissue revealed lesions ranging from 0.4 to 1.0 cm in size. Microscopy revealed loss of nuclei, foci of coagulative necrosis, and irregular loss of membranous borders, with shrunken hypereosinophilic cytoplasms (Fig. 3.6). Ablated cells also demonstrated ultrastructural architectural disarray and loss of contractile filaments, in addition to mitochondrial swelling and focal interruption of plasma membranes (Fig. 3.7). In most cases, the lesions were transmural, with loss of cellular viability throughout the depth of the tissue specimens. However, several samples contained viable cells within the ablated myocardium [33].

Advantages and disadvantages Microwave ablation offers the potential to produce deeper and more homogeneous lesions, with less endocardial damage. Limitations include the need for closer monitoring of lesions, due to continued heating despite coagulum formation and tissue changes. Different antenna designs are being developed and further testing is required to determine the feasibility and safety of percutaneous microwave ablation.

mitochondria (M) with rupture of the cristae and an interrupted plasma membrane (arrows) in a hypercontracted myocyte (electron microscopy). (Reproduced with permission from [33].)

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Figure 3.8 The mechanism of ultrasound ablation. A piezoelectric crystal transducer vibrates at a fixed frequency, resulting in propagation of a mechanical wave through the medium. Ultrasound can be collimated over distance or focused at variable tissue depths, causing selective tissue heating and destruction.

Ultrasound Mechanism of tissue injury Propagation of sound waves in the frequency range of 500 kHz to 20 MHz can transmit energy to myocardial tissue, resulting in a localized temperature rise. To produce waves at these frequencies, a transducer with a piezoelectric crystal vibrates when electrical energy is applied. This energy is then propagated as a mechanical wave by the motion of particles within the medium. Particle absorption of this motion results in heating. Ultrasound is especially attractive as an energy source for ablation, because it is contact-forgiving and the energy can be collimated over a distance or focused at variable tissue depths without injuring the intervening or neighboring tissues (Fig. 3.8). Ultrasound can also be combined with an imaging device to aid in targeting and collimation at appropriate depths. This technology has previously been used in neurosurgery, urology, and oncology.

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focused ultrasound to create lesions in ex vivo cardiac tissues, including human newborn atrial septum and the right atrial appendage, was later studied by Lee et al. Specimens were suspended in a water bath at room temperature, followed by application of ultrasound energy at an acoustic intensity of 1630 W/cm2 or 2547 W/cm2 through a 1-MHz phased-array transducer. The duration required to achieve a visible change in the tissue characteristics varied from 3 to 25 s. Focused lesions 3 – 4 mm in size were observed through gross and microscopic examination, without any observed damage to the surrounding tissues [35]. The feasibility of ablating the atrioventricular junction within the beating heart using high-intensity focused ultrasound was tested by Strickberger et al. After undergoing thoracotomy, the hearts of 10 dogs were covered with a polyvinyl chloride membrane. Perfusion with degassed water above the membrane was used as a coupling medium for ultrasound. A 1.4-MHz high-intensity spherically focused ultrasound device with a focal zone of 1.1 × 8.3 mm at 63.5 mm from the ablation transducer was used. The ablation transducer was coupled to a 7.0-MHz diagnostic ultrasound probe calibrated to localize the focal zone of the ablation transducer on the two-dimensional ultrasound image. After the identification of target sites with diagnostic ultrasound, 2.8 kW/cm2 was delivered to the atrioventricular junction for 30 s during electrical diastole. Complete atrioventricular block was achieved in all 10 dogs with an average ultrasound application time of 6.5 × 30 s. The mean lesion volume was 124 mm3 and the lesion depth was approximately 6.7 mm. As seen in Fig. 3.9, histopathology showed well-demarcated necrosis and early inflammation [36].

Preclinical studies Ultrasound ablation was initially tested in both in vitro and in vivo models of canine cardiac tissue. Using frequencies of approximately 10 MHz, the lesion depth increased with prolonged energy delivery from 15 to 60 s. There was also a linear relationship between increasing power and the depth of the lesions. The maximum in vivo lesion depth for both epicardial and endocardial approaches was approximately 9 mm [34]. The ability of high-intensity

Figure 3.9 A well-demarcated line of transition between necrosed and normal tissue 4 h after production of an atrioventricular block using high-intensity focused ultrasound. The lesion shows early necrotic changes, increased cytoplasmic eosinophilia, prominent contraction bands, and early leukocyte infiltration. (Reproduced with permission from [36].)

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Figure 3.10 A. Diagram of the doubleballoon focused ultrasound ablation catheter, composed of an inner water/contrast-filled balloon and an outer carbon dioxide–filled balloon. The ultrasound transducer is located in the inner balloon and emits radially directed energy. The liquid–gas interface between the two balloons creates an impedance mismatch, allowing reflection and focusing of the ultrasound energy. B. The focused ultrasound system after inflation. (Reproduced with permission from [37].)

Meininger et al. reported the results of focused ultrasound ablation delivered around the ostia of canine pulmonary veins. In this study, ablation was carried out with a forward-directed focused ultrasound energy system (Transurgical, Inc., Setauket, New York, USA; now ProRhythm Inc., Ronkonkoma, New York) (Fig. 3.10). The catheter uses a multiple-lumen shaft, with a central lumen for passage of a 0.035-in wire and a separate lumen for access to an inner and an outer balloon. The ultrasound transducer is located at the distal end of the catheter and emits nonfocused, radially directed, ultrasound energy. Surrounding the transducer is an inner balloon filled with a coolant water/contrast solution, and an outer balloon filled with carbon dioxide gas. The impedance mismatch created by the interface of liquid and gas yields focused ultrasound directed toward the atrial tissue. The parabolic shape of the inner balloon focuses the energy forward in a ring, creating a circular lesion 2.0 cm in diameter. Nine dogs underwent pulmonary vein isolation with this device. Application of 40 acoustic watts for 30 –120 s yielded nearcircumferential and transmural ablation lines in six of 14 pulmonary veins. Proper alignment of the ultrasound transducer along the pulmonary vein ostium was necessary for circumferential ablation [37].

an 8-MHz centrally located ultrasound transducer. This device was used to isolate the upper pulmonary veins in 15 patients with atrial fibrillation refractory to medication. The lower pulmonary veins were also isolated if sinus mapping revealed extension of atrial muscle into the veins. The median number of lesions to isolate each pulmonary vein was reduced and no pulmonary vein stenosis was noted during the follow-up. After 35 weeks, five patients had recurrence of atrial fibrillation, three responded to previously ineffective medications, and two remained in atrial fibrillation [38]. Despite the encouraging results of this early study, this ultrasound ablation system is no longer in clinical trials due to the detection of several problems. These include poor long-term efficacy, as well as a risk for the development of phrenic nerve paralysis. Furthermore, as the target for the ablation of atrial fibrillation moved from within the pulmonary veins to the atrial tissue outside of the pulmonary veins, the relevance of a “side-firing” ultrasound balloon, which delivered lesions circumferentially around a balloon placed in a pulmonary vein, disappeared. Currently, the forward-directing ultrasound system developed by Transurgical is being evaluated in a feasibility clinical trial in the United States and Europe.

Clinical studies

Advantages and disadvantages

Natale et al. used an anatomic approach to isolate the pulmonary veins with circular lesions produced by ultrasound energy. The catheter ablation system (Atrionix Inc., Palo Alto, California, USA; now Biosense Webster, Diamond Bar, California) consisted of a 0.035-inch diameter luminal catheter with a distal balloon housing

Ultrasound energy may prove to be of clinical value, particularly for isolation of pulmonary veins as part of an atrial fibrillation ablation procedure. Ultrasound energy can produce transmural circumferential lesions around the ostium of pulmonary veins, resulting in electrical isolation. The chief advantage of ultrasound ablation is that

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the endothelium is relatively spared and contact with the ablation energy source and tissue is not required. Furthermore, the risk of coagulum formation is small. The chief limitation of ultrasound balloon ablation systems is that they require the ablation balloon to be aligned along the axis of a pulmonary vein. This can be challenging, particularly for pulmonary veins with multiple early branches. Another limitation of this technology is that it is not applicable for common left pulmonary veins, due to the large balloon size needed to engage a common ostium.

Laser Mechanism of tissue injury Light amplification by stimulated emission of radiation (LASER) yields a monochromatic, highly focused beam of energy with a specific wavelength that can be delivered for a set duration and intensity. A high-intensity flash of polychromatic light or other energy trigger is used to excite electrons of a particular medium into a higher energy state. Since a specific wavelength is absorbed in each substance, that specific wavelength is emitted upon relaxation (Fig. 3.11). Different substances therefore produce

Alternative energy sources for catheter ablation

beams of different wavelengths: helium-neon 633 nm, argon 488 and 515 nm, holmium 2100 nm, CO2 10 600 nm, ruby 693 nm, and neodymium:yttrium-aluminum-garnet (Nd:YAG) 1064 nm. Laser energy is phase-coherent, meaning that the light waves are in phase with one another and so nearly parallel that the beam can be focused with high precision and with negligible spreading due to distance. Lasers can deliver energy continuously or in a pulsed mode. Absorption of laser energy by a medium results in heating, and scatter in the tissue results in lesion enlargement. The extent of absorption versus scatter is determined by wavelength, duration, energy density, and tissue properties. Carbon dioxide and argon lasers produce wavelengths that have high absorption by water and cellular tissue, respectively. These lasers therefore produce superficial lesions. High scattering occurs with laser sources such as Nd:YAG, resulting in redirection of photons before they are absorbed. The high scatter leads to lesions of greater depth. Percutaneous laser devices require efficient energy transfer through a fiberoptic cable. Laser sources such as Nd:YAG and argon yield the most efficient transmission. Due to high absorption of laser energy by blood, methods have been developed to minimize the intracavitary distance between the laser source and the myocardium. Other efforts have included saline-filled balloons or continuous saline flushes to clear the path of the laser beam [39]. In conventional lasers, electron energy transitions of populations of individual atoms or molecules lead to energy emission, producing energy levels that can vary significantly. Diode lasers use semiconductors as the stimulated medium, in which the flow of electrons within the crystalline solid occurs in a discrete manner much like one large extended molecule, leading to the production of a beam that varies little in energy. Diode lasers can therefore yield controlled low-energy ablation and offer a lower risk of endocardial disruption. Diode lasers can be delivered through a range of optical fiber configurations, including loops and balloons, to produce thin, continuous lesions [40].

Preclinical studies

Figure 3.11 The mechanism of laser ablation. Laser ablation operates through the use of a monochromatic, focused beam of energy to excite electrons of a particular medium into a higher energy state. Upon relaxation, phase-coherent light with a characteristic wavelength is emitted. Absorption of laser energy by tissue results in heating and destruction.

Initial studies of laser cardiac ablation used high-energy pulsed laser. The effects of in vitro direct pulsed laser, in vivo transcatheter laser, and electrical energy were compared in canine hearts. The dimensions of laser-induced lesions correlated with the total dose of energy, but the depth correlated more closely with the duration. In vivo lesions were significantly larger than lesions produced by the equivalent doses of electrical energy delivered in vitro. In vitro lesions had a central vaporized crater surrounded by a rim of necrotic tissue. Endocardial in vivo laser lesions at 40 and 80 J over 0.5–2.0 s (7.9 × 5.4 × 6.6 mm and 7.9 × 43

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5.1 × 7.5 mm) were comparable with regard to gross morphology and size to those produced by electrical shock at 100 and 200 J. Transcatheter electrode shock produced significantly more ventricular tachycardia and wall motion abnormalities. Transcatheter laser was found to create endocardial lesions with less energy than transcatheter electrode shock, but high-energy pulse in vivo lesions were difficult to titrate and were associated with a risk of endocardial disruption and crater formation [41]. Fried et al. conducted in vitro and in vivo studies using a 50-W Nd:YAG laser ablation system in canine right ventricles. The system used flexible optical fiber tips oriented parallel to the tissue surface to deliver energy to the myocardium. Peak tissue temperatures of 50–60 °C were measured without tissue charring or vaporization (Fig. 3.12). Lesions 6 mm deep and 10 × 22 mm in area were created in both in vivo and in vitro preparations [42]. An optical fiber equipped with a diffusing needle tip for direct intramural, volumetric laser heating has also been tested with both thoracotomy and percutaneous approaches in canine hearts. ST segment depression recorded from the tip predicted lesion induction. Using this technique, large lesions (10 mm) were produced by low-power (2.0–4.5 W) diode laser light (805 nm). There was no visible surface damage, mural thrombi, or transmural perforation. Depending on the laser intensity, mean lesion widths were 5.8 –9.1 mm and 5.2– 7.9 mm in the thoracotomy and percutaneous groups, respectively. Pathological examination (Fig. 3.13) revealed elliptical to spherical lesions characterized by extensive contraction-band necrosis abruptly bordering viable tissue [43]. Linear laser catheters capable of producing lesions without discontinuities and gaps have also been evaluated using a diode laser in a caprine model [44]. Postprocedural pace-mapping confirmed that bidirectional blocks had been produced across linear lesions using this system in the atrium. Fried et al. also tested a fiberoptic balloon catheter in canine hearts as an alternative to radiofrequency ablation for the creation of circumferential pulmonary lesions. This catheter delivered Nd:YAG laser radially through diffusing optical fiber tips enclosed in a balloon catheter. The pulmonary veins were electrically isolated using 30–50 W applied for 60– 90 s. A single application produced transmural, continuous, and circumferential lesions with no evidence of tissue vaporization or endothelial disruption [45]. A diode laser balloon ablation catheter has also been tested for pulmonary vein isolation in an openchest caprine model. A laser balloon catheter was placed through the left atrial appendage into the pulmonary vein ostia in 19 goats. Delivery of a single burst at 3.7–5.4 W/ cm for 90–150 s yielded electrical isolation of the pulmonary veins in 70% of cases. Pulmonary vein isolation did not correlate with the dose or duration of the applications. Adequate orientation and contact of the laser 44

balloon catheter with the myocardium assessed through reflectance spectroscopy achieved 100% electrical isolation at 3.5 W/cm for 120 s. Two ablations (one at 3.7 W/cm and the other at 5.4 W/cm) resulted in damage to the adjacent lung tissue, but there were no cases of perforation or pulmonary vein stenosis [46].

Clinical studies Saksena et al. assessed intraoperative argon laser ablation in 20 patients with refractory sustained ventricular tachycardia or fibrillation. Fifteen of the patients were undergoing concomitant coronary bypass grafting and one was undergoing mitral valve replacement. A 15-W argon ion gas laser was used to deliver pulsed laser energy through a fiberoptic catheter delivery system. Thirty-eight ventricular tachycardia morphologies were mapped and ablated with laser energy (82%), combined laser ablation and mechanical resection (13%), or mechanical resection alone (5%). The 30-day postoperative mortality was 5%, and one patient required postoperative antiarrhythmic drug therapy. The remaining 18 patients were free of arrhythmia at discharge. The one-year survival rate was 90% [47]. Surgical experience also includes Nd:YAG laser systems. Pfeiffer et al. carried out epicardial laser ablation in nine patients who had suffered myocardial infarction with spontaneous sustained ventricular tachycardia. Clinical ventricular tachycardia was intraoperatively inducible in seven patients. Nd:YAG laser energy at 50 – 80 W was applied for 12–42 s to early epicardial activation sites 2 × 3 cm in area. Seven of the nine patients remained free of ventricular tachycardia for a mean 17-month follow-up period [48].

Advantages and disadvantages The most attractive aspect of laser ablation is the ability to create large, precise lesions suitable for ablation of ventricular tachycardia. Limitations include the requirement for a nearly perpendicular delivery angle to the myocardium for efficient energy delivery. Systems with mechanical prongs or suction devices to stabilize the tip in a suitable position are under development. Another limitation is that there is a high risk of coagulum formation due to increased endocardial disruption and crater formation.

Infrared Mechanism of tissue injury Infrared is electromagnetic radiation in the wavelength range of 400–2700 nm, typically produced by tungsten–

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Figure 3.12 Right ventricular lesions produced by continuous-wave Nd:YAG during in vivo and in vitro studies. Trichrome staining reveals normal myocardium as pink and thermally damaged tissue as blue. In vivo studies did not achieve transmural lesions, possibly due to tissue cooling due to blood flow from the endocardial surface. A. In vitro, slow heating (power

halogen light bulbs. In contrast to laser, this form of energy is noncoherent and causes photocoagulation only at focal points within sight of the emitter (Fig. 3.14). The infrared coagulator was initially developed to control parenchymal bleeding in surgical use.

Alternative energy sources for catheter ablation

30 W, time 180 s, E = 5.4 kJ). B. In vivo, slow heating (power 30 W, time 180 s, E = 5.4 kJ). C. In vitro, fast heating (power 50 W, time 60 s, E = 3.0 kJ). D. In vivo, fast heating (power 50 W, time 60 s, E = 3.0 kJ). (Reproduced with permission from [42].)

Preclinical studies An infrared coagulator was used by Kubota et al. to create atrial epicardial lesions in canine myocardium. The device used a reflector to focus infrared light into a conducting 45

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Figure 3.13 Light micrographs of catheterdirected diffuse low-power diode laser lesions (Movat’s pentachrome stain). A. Well-defined border of contraction band necrosis adjacent to viable tissue. B. Interstitial edema and coagulation necrosis at the center of the lesion, with no evidence of vascular thrombi. C. The endocardial ablation site is free of platelet aggregation or thrombus. Scattered subendocardial necrotic myocytes are evident with contraction bands (arrows). (Reproduced with permission from [43].)

of the left atrium within the lesion encircling the pulmonary vein [50].

Advantages and disadvantages Infrared produces superficial lesions that might be useful for atrioventricular node modification. However, preclinical experience with this technique is still in the very initial stages.

Summary Figure 3.14 The mechanism of infrared ablation. Electromagnetic radiation is produced from a tungsten–halogen bulb and transmitted through an optical fiber. The infrared light is then directed to the tissue surface by a lens or reflector.

quartz rod, thereby producing energy at 35 W/cm2 (wavelength 400–1600 nm). Transmural lesions were achieved at 21 s (Fig. 3.15). Conduction block with persistence at 3 months was documented [49]. The same technique has also been used in four dogs to create continuous circular lesions around pulmonary veins from an epicardial approach. After infrared photocoagulation, the potentials of both atria were recorded during sinus rhythm and during overdrive pacing from outside and inside the encircling coagulation. This methodology yielded electrical isolation 46

Many promising new energy sources are being explored for use during catheter ablation procedures. Microwave ablation is available for intraoperative use, as is cryoablation. However, among the alternative energy sources, the only one currently available for catheter-based clinical use is cryoablation. Despite the availability of percutaneous cryoablation, the adoption of this energy source for routine clinical use has been slow. This reflects the excellent results currently being achieved with radiofrequency energy for most cardiac arrhythmias. By far the greatest potential clinical role for an alternative energy source is for catheter ablation of atrial fibrillation. The two energy sources currently in clinical trials for atrial fibrillation ablation are cryoablation and focused ultrasound ablation. It is likely that other clinical trials will also be initiated to evaluate the safety and efficacy of laser and microwave ablation.

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Figure 3.15 Infrared coagulation of myocardium, resulting in a well-demarcated transmural lesion after 21 s. (Reproduced with permission from [49].

References 1 Bartlett TG, Mitchell R, Friedman PL, Stevenson WG. Histologic evolution of radiofrequency lesions in an old human myocardial infarct causing ventricular tachycardia. J Cardiovasc Electrophysiol 1995;6:625–9. 2 McRury ID, Panescu D, Mitchell MA, Haines DE. Nonuniform heating during radiofrequency catheter ablation with long electrodes: monitoring the edge effect. Circulation 1997;96:4057–64. 3 Zhou L, Keane D, Reed G, Ruskin J. Thromboembolic complications of cardiac radiofrequency catheter ablation: a review of the reported incidence, pathogenesis and current research directions. J Cardiovasc Electrophysiol 1999;10:611–20. 4 Whittaker DK. Mechanisms of tissue destruction following cryosurgery. Ann R Coll Surg Engl 1984;66:313 – 8. 5 Skanes AC, Yee R, Krahn AD, Klein GJ. Cryoablation of atrial arrhythmias. Card Electrophysiol Rev 2002;6:383 – 8. 6 Holman WL, Ikeshita M, Lease JG, Smith PK, Lofland GK, Cox JL. Cryosurgical modification of retrograde atrioventricular conduction: implications for the surgical treatment of atrioventricular nodal reentry tachycardia. J Thorac Cardiovasc Surg 1986;91:826–34. 7 Dubuc M, Roy D, Thibault B, et al. Transvenous catheter ice mapping and cryoablation of the atrioventricular node in dogs. Pacing Clin Electrophysiol 1999;22:1488 – 98. 8 Feld GK, Yao B, Reu G, Kudaravalli R. Acute and chronic effects of cryoablation of the pulmonary veins in the dog as a potential treatment for focal atrial fibrillation. J Interv Card Electrophysiol 2003;8:135–40. 9 Avitall B, Lafontaine D, Rozmus G, et al. The safety and efficacy of multiple consecutive cryolesions in canine pulmonary veins: left atrial junction. Heart Rhythm 2004;1:203 – 9. 10 Khairy P, Chauvet P, Lehmann J, et al. Lower incidence of thrombus formation with cryoenergy versus radiofrequency catheter ablation. Circulation 2003;107:2045–50.

11 Stevenson WG. To freeze or burn the epicardium? Heart Rhythm 2005;2:91–2. 12 Lustgarten DL, Bell S, Hardin N, Calame J, Spector PS. Safety and efficacy of epicardial cryoablation in a canine model. Heart Rhythm 2005;2:82 – 90. 13 Avitall B, Lafontaine D, Rozmus G, et al. Ablation of atrial– ventricular junction tissues via the coronary sinus using cryoballoon technology. J Interv Card Electrophysiol 2005;12: 203 –11. 14 Cox JL, Holman WL, Cain ME. Cryosurgical treatment of atrioventricular node reentrant tachycardia. Circulation 1987; 76:1329 –36. 15 Manasse E, Colombo P, Roncalli M, Gallotti R. Myocardial acute and chronic histological modifications induced by cryoablation. Eur J Cardiothorac Surg 2000;17:339 – 40. 16 Mack CA, Milla F, Ko W, et al. Surgical treatment of atrial fibrillation using argon-based cryoablation during concomitant cardiac procedures. Circulation 2005;112(9 Suppl):I1– 6. 17 Lowe MD, Meara M, Mason J, Grace AA, Murgatroyd FD. Catheter cryoablation of supraventricular arrhythmias: a painless alternative to radiofrequency energy. Pacing Clin Electrophysiol 2003;26:500 – 3. 18 Fischbach PS, Saarel EV, Dick M 2nd. Transient atrioventricular conduction block with cryoablation following normal cryomapping. Heart Rhythm 2004;1:554 –7. 19 Messali A, Lavergne T, Sebag C, et al. [Long-term evaluation of endocavitary cryoablation of nodal reentry; in French.] Arch Mal Coeur Vaiss 2005;98:628 – 33. 20 Manusama R, Timmermans C, Limon F, Philippens S, Crijns HJ, Rodriguez LM. Catheter-based cryoablation permanently cures patients with common atrial flutter. Circulation 2004;109:1636 – 9. 21 Manusama R, Timmermans C, Philippens S, Crijns HJ, Ayers GM, Rodriguez LM. Single cryothermia applications of less than five minutes produce permanent cavotricuspid isthmus block in humans. Heart Rhythm 2004;1:594 – 9.

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22 Montenero AS, Bruno N, Zumbo F, et al. Cryothermal ablation treatment of atrial flutter: experience with a new 9 French 8 mm tip catheter. J Interv Card Electrophysiol 2005;12:45 – 54. 23 Hoyt RH, Wood M, Daoud E, et al. Transvenous catheter cryoablation for treatment of atrial fibrillation: results of a feasibility study. Pacing Clin Electrophysiol 2005;28(Suppl 1):S78–82. 24 Lustgarten DL, Keane D, Ruskin J. Cryothermal ablation: mechanism of tissue injury and current experience in the treatment of tachyarrhythmias. Prog Cardiovasc Dis 1999;41:481– 98. 25 Jumrussirikul P, Chen JT, Jenkins M, et al. Prospective comparison of temperature guided microwave and radiofrequency catheter ablation in the swine heart. Pacing Clin Electrophysiol 1998;21:1364–74. 26 VanderBrink BA, Gilbride C, Aronovitz MJ, et al. Safety and efficacy of a steerable temperature monitoring microwave catheter system for ventricular myocardial ablation. J Cardiovasc Electrophysiol 2000;11:305–10. 27 Whayne JG, Nath S, Haines DE. Microwave catheter ablation of myocardium in vitro: assessment of the characteristics of tissue heating and injury. Circulation 1994;89:2390 –5. 28 Gu Z, Rappaport CM, Wang PJ, VanderBrink BA. A 2 1/4turn spiral antenna for catheter cardiac ablation. IEEE Trans Biomed Eng 1999;46:1480–2. 29 Liem LB, Mead RH, Shenasa M, Chun S, Hayase M, Kernoff R. Microwave catheter ablation using a clinical prototype system with a lateral firing antenna design. Pacing Clin Electrophysiol 1998;21:714–21. 30 Tardif JC, Groeneveld PW, Wang PJ, et al. Intracardiac echocardiographic guidance during microwave catheter ablation. J Am Soc Echocardiogr 1999;12:41–7. 31 Venturini A, Polesel E, Cutaia V, et al. Intraoperative microwave ablation in patients undergoing valvular surgery: midterm results. Heart Surg Forum 2003;6:409 –11. 32 Schuetz A, Schulze CJ, Sarvanakis KK, et al. Surgical treatment of permanent atrial fibrillation using microwave energy ablation: a prospective randomized clinical trial. Eur J Cardiothorac Surg 2003;24:475–80. 33 Manasse E, Colombo PG, Barbone A, et al. Clinical histopathology and ultrastructural analysis of myocardium following microwave energy ablation. Eur J Cardiothorac Surg 2003;23:573–7. 34 He DS, Zimmer JE, Hynynen K, et al. Application of ultrasound energy for intracardiac ablation of arrhythmias. Eur Heart J 1995;16:961–6. 35 Lee LA, Simon C, Bove EL, et al. High intensity focused ultrasound effect on cardiac tissues: potential for clinical application. Echocardiography 2000;17:563–6. 36 Strickberger SA, Tokano T, Kluiwstra JU, Morady F, Cain C. Extracardiac ablation of the canine atrioventricular junction by use of high-intensity focused ultrasound. Circulation 1999;100:203–8.

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37 Meininger GR, Calkins H, Lickfett L, et al. Initial experience with a novel focused ultrasound ablation system for ring ablation outside the pulmonary vein. J Interv Card Electrophysiol 2003;8:141– 8. 38 Natale A, Pisano E, Shewchik J, et al. First human experience with pulmonary vein isolation using a through-the-balloon circumferential ultrasound ablation system for recurrent atrial fibrillation. Circulation 2000;102:1879 – 82. 39 Wang PJ, Homoud MK, Link MS, Estes IN. Alternate energy sources for catheter ablation. Curr Cardiol Rep 1999;1:165 –71. 40 Keane D. New catheter ablation techniques for the treatment of cardiac arrhythmias. Card Electrophysiol Rev 2002;6:341– 8. 41 Lee BI, Gottdiener JS, Fletcher RD, Rodriguez ER, Ferrans VJ. Transcatheter ablation: comparison between laser photoablation and electrode shock ablation in the dog. Circulation 1985;71:579 – 86. 42 Fried NM, Lardo AC, Berger RD, Calkins H, Halperin HR. Linear lesions in myocardium created by Nd:YAG laser using diffusing optical fibers: in vitro and in vivo results. Lasers Surg Med 2000;27:295 –304. 43 Ware DL, Boor P, Yang C, Gowda A, Grady JJ, Motamedi M. Slow intramural heating with diffused laser light: a unique method for deep myocardial coagulation. Circulation 1999; 99:1630 – 6. 44 Keane D, Ruskin JN. Linear atrial ablation with a diode laser and fiberoptic catheter. Circulation 1999;100:e59 – 60. 45 Fried NM, Tsitlik A, Rent KC, et al. Laser ablation of the pulmonary veins by using a fiberoptic balloon catheter: implications for treatment of paroxysmal atrial fibrillation. Lasers Surg Med 2001;28:197–203. 46 Reddy VY, Houghtaling C, Fallon J, et al. Use of a diode laser balloon ablation catheter to generate circumferential pulmonary venous lesions in an open-thoracotomy caprine model. Pacing Clin Electrophysiol 2004;27:52–7. 47 Saksena S, Gielchinsky I, Tullo NG. Argon laser ablation of malignant ventricular tachycardia associated with coronary artery disease. Am J Cardiol 1989;64:1298 –304. 48 Pfeiffer D, Moosdorf R, Svenson RH, et al. Epicardial neodymium:YAG laser photocoagulation of ventricular tachycardia without ventriculotomy in patients after myocardial infarction. Circulation 1996;94:3221– 5. 49 Kubota H, Furuse A, Takeshita M, Kotsuka Y, Takamoto S. Atrial ablation with an IRK-151 infrared coagulator. Ann Thorac Surg 1998;66:95 –100. 50 Kubota H, Takamoto S, Takeshita M, Miyaji K, Kotsuka Y, Furuse A. Atrial ablation using an IRK-151 infrared coagulator in canine model. J Cardiovasc Surg (Torino) 2000;41:835 – 47.

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Mapping for localization of target sites William G. Stevenson

The mapping approach used to guide ablation depends on the type of arrhythmia being assessed. When the tachycardia has a focal origin from a small, discrete region, activation sequence mapping and pace-mapping are the major methods employed. Activation is seen to spread away from a central point, and pacing at that site produces a QRS or P wave similar to that of the tachycardia (Fig. 4.1). In contrast, large reentry circuits have continuous activation throughout the cardiac cycle (Fig. 4.2); activation maps and pace-mapping can be confusing,

Figure 4.1 Mapping data from ventricular ectopy with a focal origin at the anterior right ventricle. In the center, there is an activation sequence map, with earliest activation indicated as red and progressively later activation as orange, yellow, green, blue, and purple. Activation spreads out from a focus on the anterior free wall. Recordings from the earliest endocardial activation site (left panel) and an adjacent site (right panel) are also shown. From the top of each recording are surface electrocardiography leads and recordings from the mapping catheter (Map), showing a unipolar recording from the distal mapping catheter electrode (Map 1 Uni), with a

and entrainment mapping is often helpful to identify the reentry circuit.

Electrogram recording methods Activation sequence mapping relies on identifying the time of activation from the electrograms recordedaeither from electrodes in contact with the tissue, or mathematically reconstructed from multielectrode recording systems

high-pass filter set to 0.05 Hz (HP 0.05 Hz); a bipolar recording from the distal pair of electrodes (Map bipolar 1–2 HP); and unipolar recordings from the distal (Map 1) and proximal (Map 2) electrodes, with the high-pass filter at 30 Hz (HP 30 Hz). At the early site, the unipolar recordings show a QS configuration, and the first peak of the bipolar recording occurs with the initial down stroke of the unipolar recording. At the site remote from the tachycardia origin, the unipolar recordings have an rS configuration, and the first peak of the bipolar recording occurs after the onset of the unipolar recording.

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for the ventricular activation during antidromic conduction and for the atrial electrogram during retrograde conduction [2,3]. Unipolar “unfiltered” recordings have a large “field of view” that incorporates the activation of adjacent tissue as part of the “far-field” signal. A large far-field signal can obscure low-amplitude potentials of interest. High-pass filtering (e.g., at corner frequencies of 30 Hz and greater) removes much of the far-field signal, but also changes the morphology of the wavefront such that the morphology of the electrogram no longer indicates the direction of the propagating wavefront. Recordings obtained from two electrodes that are in contact with the tissue, or in close proximity to it, are referred to as bipolar. With closely spaced electrodes, the timing of the far-field signal is similar at both and is therefore subtracted out, making small local potentials easier to recognize. Local activation is generally taken as the first rapid peak of the bipolar signal. However, whether a potential of interest is beneath the distal recording electrode, the proximal electrode, or both electrodes cannot be determined from inspection of the bipolar recording alone. Tissue producing a target signal beneath a proximal electrode may not be ablated with energy applied to the distal electrode.

Figure 4.2 An activation sequence map of macroreentrant counterclockwise atrial flutter. The right atrium is viewed from a left anterior oblique projection. Activation times proceed from –120 ms (red) to yellow, green, blue, and then purple (140 ms). The defined activation sequence encompasses the entire tachycardia cycle length of 260 ms. With the fiducial point and window of interest selected for mapping, earliest meets latest activation (red adjacent to purple) in the inferoseptal region.

Activation sequence mapping

and projected onto an anatomic framework with “noncontact” mapping systems. Although all electrogram recordings are differential recordings between two electrodes, and hence bipolar, recordings obtained with only one of the two electrodesausually connected to the anodal (positive) input to the amplifieraare referred to as unipolar. The cathodal (negative) amplifier input is either the Wilson central terminal, or a remote electrode in the inferior vena cava. With “unfiltered” input or a relatively low corner frequency for the high-pass filter of 0.5 Hz or less, the shape of the unipolar recording provides some indication of the direction of wavefront propagation relative to the recording site. At sites remote from the focus, an initial R wave is inscribed as the wavefront propagates toward the electrode, followed by an S wave as the wavefront propagates past the recording electrode and propagates away (Fig. 4.1, adjacent site). The rapid downstroke of the unipolar recording coincides with local activation at the recording site in uniform, normal tissue. At the point of origin of a focal arrhythmia, a QS complex is recorded, as the wavefronts propagate away in all directions from the recording electrode [1]. Similarly, at the insertion site of an accessory pathway, a QS complex is usually identified

For tachycardias with a focal origin, such as ectopic atrial tachycardia and idiopathic right ventricular (RV) outflow tract tachycardia, the P wave or QRS is inscribed as the excitation wavefront propagates away from the focus to depolarize the remainder of the cardiac chamber (Fig. 4.1). Using the P wave or QRS onset as a fiducial point for timing, activation preceding the fiducial point will typically be identified in a small region, with progressively later activation at sites remote from that region (Fig. 4.1). At the area of earliest activation, a QS complex is present in the unipolar recording, with the onset of the S wave coincident with the first bipolar peak of the simultaneous bipolar recording (Fig. 4.1, left). For any mapping site, the relation between the activation time and the distance from the focus is related to the tissue conduction velocity. For example, in normal myocardium, in which the conduction velocity may be 0.4 m/s in the direction parallel to fiber orientation, every 10-ms increase in activation time translates into a 4-mm increase in distance from the focus. In contrast, if conduction is slowed to 0.1 m/s, a 10-ms increase in activation indicates only a 1-mm increase in distance from the focus. Anisotropic conduction also influences activation sequence maps, such that isochronal maps show the region of early activation as an oval with

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the long axis parallel to the direction of rapid conduction (e.g., parallel to the likely fiber orientation). For arrhythmias that are due to reentry, some portion of the circuit is depolarized by the circulating wavefront at every moment of the cardiac cycle. Within the circuit, there is no “earliest” and “latest” region. If the entire circuit is sampled by a mapping catheter, the activation sequence map shows continuous activity. Macroreentrant atrial flutter and scar-related ventricular tachycardias are usually due to large reentry circuits, such that continuous electrical activity is rarely recorded at one site [4–6]. In these activation sequence maps, the point designated as “early” is determined by selection of the fiducial point. A complete map of the circuit will show that the area identified as initial activation is next to the area marked as latest activation, in an “early meets late” configuration (Fig. 4.2). The difference in time between “earliest” and “latest” activation will equal the tachycardia cycle length. If the earliest and latest activation do not span the entire tachycardia cycle length, then a portion of the reentry circuit has not been identified or the arrhythmia is not due to reentry. Scar-related reentry circuits are often difficult to recognize and locate from activation sequence maps alone. The electrograms recorded from regions of abnormal tissue may be low-amplitude and fractionated, with multiple rapid peaks, so that identification of the local activation time may be difficult (see the discussion of far-field electrograms below). Multiple paths for propagation through areas of scar or infarction give rise to bystander regions in which activation can appear to be related to the reentry pathway. Some portions of the circuit may be intramural or epicardial and not identified with endocardial recordings.

Entrainment mapping Entrainment mapping circumvents many of the limitations of activation sequence mapping (Table 4.1) [7]. Entrainment is the continuous resetting of a reentry circuit (Fig. 4.3) [8 –11]. Reentry circuits that can be entrained have an excitable gap at each point in the circuit, defined by the time between recovery from the last depolarization and the arrival of the next excitation wavefront. During pacing from a site outside the reentry circuit, an appropriately timed stimulus produces a wave of excitation that propagates to the reentry circuit and depolarizes part of the circuit during this excitable gap. The wave then begins propagating in two directions in the circuit. The antidromic wave propagates in the reverse direction in comparison with the reentry circuit wavefronts and is extinguished when it collides with a previous orthodromic wavefront. The stimulated orthodromic wave follows the

Mapping for localization of target sites

Table 4.1 Uses of entrainment mapping. Determine if the pacing site is in the reentry circuit Post-pacing interval S-QRS n + 1 Entrainment with concealed fusion + S-QRS = EG-QRS Distinguish local potentials from far-field potentials Identify narrow isthmuses in reentry circuits Entrainment with concealed fusion Identification of specific arrhythmias Left versus right atrial macroreentry Bundle-branch reentry VT Atypical AV nodal reentry versus AV reentry using a paraseptal accessory pathway AV, atrioventricular; EG-QRS, electrogram QRS; VT, ventricular tachycardia.

path of the previous reentry circuit waves and resets the reentry circuit, continuing the tachycardia. This response to a single stimulus is referred to as resetting. Continuous resetting by each stimulus of a train is entrainment. To use entrainment mapping, it is important to distinguish reentrant arrhythmias from those due to automaticity. Although the majority of arrhythmias associated with scar in the atrium or ventricle are due to reentry, initiation and termination by programmed stimulation do not exclude triggered automaticity as the mechanism. When the mechanism is in doubt, demonstrating any of the entrainment criteria described by Waldo and colleagues establishes reentry as the tachycardia mechanism (Table 4.2) [8,9,11]. The easiest method of confirming entrainment is to demonstrate that constant fusion is present. For ventricular tachycardia (VT), fusion indicates that a portion of the ventricle is depolarized by a wavefront that has traveled orthodromically through the reentry circuit, and a portion of the ventricle is activated by wavefronts from the pacing site that are propagating in a different direction, such as the antidromic wavefronts in the circuit (Fig. 4.3). The antidromic and orthodromic wavefronts collide, and after a few beats of fixed rate pacing, the lines of collision are the same from beat to beat, producing constant fusion. Fusion is evident in the electrocardiogram (ECG) when the QRS complex during pacing has a morphology that is intermediate between that of VT and that produced by pacing in the absence of VT (Fig. 4.4). Constant fusion, with the identical morphology from beat to beat, is proof of entrainment. A change in QRS morphology during pacing does not by itself establish the presence of entrainment. If VT is due to an automatic focus, the focus may be overdriven during pacing, and the QRS then reflects only the activation sequence produced by wavefronts from the pacing site.

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Figure 4.3 Entrainment of a simple reentry circuit. A–C. The gray regions are areas of block that define part of the border of the reentry path. A narrow isthmus or channel is present between two regions of block. The circuit has an exit from which waves from the circuit (dotted arrows) propagate across the more distant myocardium, producing the QRS or P wave. The solid arrow indicates the propagating wavefront in the circuit. The tissue between the front of the arrow and the tail of the arrow has recovered excitability after the previous depolarization, creating an excitable gap at that region at the point in time shown. B. A stimulus at a site remote from the circuit (S) captures and produces a wavefront of activation that propagates to the circuit (dashed lines). RVA and RVS indicate recording sites, to illustrate the findings in D. The antidromic wavefront travels in the opposite direction to that of the tachycardia waves, and collides with an orthodromic wavefront (black arrow) and is extinguished. The stimulated wavefront that continues orthodromically through the isthmus in the circuit (black arrow) resets the tachycardia. C. The genesis of the post-pacing interval (PPI). The last stimulus produces a wavefront that propagates orthodromically through the circuit and then back to the pacing site.

The PPI is the sum of the conduction time from the pacing site, to the circuit, through the circuit and back to the pacing site. D. Entrainment of VT. VT has a cycle length of 400 ms. The last three stimuli at a cycle length of 380 ms are shown. All electrograms are accelerated to the paced cycle length. Pacing changes the QRS morphology compared to that during VT. The conduction time from the stimulus site to the RVS (RV septum) recording site is relatively short (arrows), and the site is depolarized antidromically during pacing, as indicated by the change in electrogram morphology. The RVA site is depolarized orthodromically by a wavefront that has propagated through the reentry circuit—as indicated by the long conduction time from the pacing site to the recording site (arrows from stimulus to electrogram accelerated to the pacing rate) and by the fact that the electrogram has the same morphology during pacing and during tachycardia. Thus, during pacing, both orthodromic and antidromic capture of portions of the ventricle are present, defining fusion. The PPI at the stimulation site is 520 ms (arrow), 120 ms longer than the tachycardia cycle length—indicating that the pacing site is remote from the tachycardia circuit.

This possibility is unlikely if the QRS during entrainment is clearly different than that produced by pacing in the absence of VT. Pacing at two different rates can be helpful (Fig. 4.4). Pacing at a faster rate increases the area of the ventricles depolarized by antidromic wavefronts, and the QRS comes to resemble that produced by pacing in the

absence of tachycardia more closelyaa finding known as progressive fusion. Fusion can also be demonstrated from the analysis of electrograms (Fig. 4.3) [9,12]. Activation of sites during pacing is described as orthodromic when the electrogram morphology remains the same as that during VT, and

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Table 4.2 Requirements for entrainment mapping. The arrhythmia is due to reentry and can be entrained (Waldo criteria) [11] Constant fusion during pacing (assessed from electrograms or ECG) Progressive fusion as the pacing rate is increased Block of the orthodromic wavefront terminates tachycardia and changes activation sequence Stable activation sequence (monomorphic) of tachycardia Stable tachycardia cycle length

Mapping for localization of target sites

depolarize the os of the coronary sinus after a relatively short conduction time (arrow), producing a different electrogram morphology than that observed after pacing stops. The lateral wall of the right atrium is activated orthodromically after a longer conduction time from the last stimulus. On one atrial beat, there is therefore antidromic and orthodromic activation, and this activation is constant during pacingaestablishing the existence of entrainment and therefore reentry.

Pacing captures Pacing does not change or terminate the arrhythmia (either activation sequence or cycle length) ECG, electrocardiography.

antidromic when the electrogram morphology changes during pacing. Fusion can be confirmed by finding sites that are activated orthodromically after a conduction delay consistent with propagation of the stimulated wavefront through the reentry circuit, and sites that are depolarized simultaneously antidromically (Fig. 4.3D). Fusion is often difficult to assess from P waves; the sequence and morphology of electrograms is more useful for assessing fusion. Figure 4.5A shows entrainment of common counterclockwise atrial flutter by pacing from the coronary sinus. Stimulated antidromic wavefronts

Post-pacing interval The post-pacing interval (PPI) is an indication of the proximity of the pacing site to the reentry circuit [7]. The PPI is measured from the last stimulus that entrains or resets the tachycardia to the next activation at the pacing site (Fig. 4.3). The last stimulated wave propagates to the circuit, then through the circuit, and back to the pacing site. Thus, the PPI is the sum of the conduction times from the pacing site to the circuit, the revolution time through the circuit, and from the circuit back to the pacing site. At pacing sites in the reentry circuit (Fig. 4.6), the PPI approximates the tachycardia cycle length. At pacing sites progressively further from the reentry circuit, the PPI exceeds the tachycardia cycle length by an increasingly greater interval (Fig. 4.3). A PPI–tachycardia cycle length difference

Figure 4.4 Progressive fusion during entrainment. VT with a cycle length (CL) of 335 ms is present in both figures. A. The last two stimuli (S) of a train with a cycle length of 310 ms. All electrograms and QRS complexes are accelerated to the pacing rate, and the QRS is altered in comparison with that of VT. From this tracing alone, entrainment cannot be distinguished from overdrive suppression of an automatic focus. B. Comparison of A with the findings in this panel during pacing at a faster rate (cycle length 280 ms) indicates that QRS fusion is present in A. At the faster-paced rate, the antidromic wavefronts propagate further (as indicated in the schematics below each tracing), producing greater changes in the QRS morphology (with development of R waves in leads II, III, and V6).

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Figure 4.5 Entrainment of common counterclockwise atrial flutter from a site in the distal coronary sinus (CS) outside the reentry circuit (A) and from a site in the circuit at the anterior (rightward) portion of the flutter isthmus between the tricuspid annulus and inferior vena cava (B). A. The flutter cycle length here is 215. The last three stimuli of pacing at a cycle length of 180 ms are shown. All electrograms are accelerated to the pacing rate. Arrows indicate electrograms accelerated to the paced cycle length. During pacing, CSp is activated antidromically (change in electrogram morphology) after a relatively short conduction time (arrows); the lateral right atrium (RAp) and isthmus are activated orthodromically after a longer conduction time. Simultaneous antidromic and orthodromic electrograms indicate that fusion is present. The post-pacing interval (PPI) measured at the pacing site in the distal CS is 300 ms, 85 ms longer than the tachycardia cycle length—indicating that this site is remote from the flutter circuit. B. Pacing at 205 ms from the common right atrial flutter isthmus accelerates all electrograms to the pacing rate, without altering their morphology or relative timing, with no evidence of fusion (concealed fusion). The PPI is equal to the tachycardia cycle length of 220 ms, consistent with a pacing site in the flutter circuit.

of 30 ms or less often indicates sufficient proximity for successful ablation of reentrant VTs (provided other markers of isthmus sites are present, as discussed below). The PPI–tachycardia cycle length difference is usually within 20 ms in atrial flutter circuits. The PPI does not indicate whether the pacing site is in a narrow isthmus in the circuit in comparison with a broad loop, in which ablation may be difficult. There are several important caveats. If conduction slows in the reentry circuit during pacing, the PPI will 54

increase. This may occur in patients who are receiving antiarrhythmic medications or after ablation has partially damaged the reentry circuit. The PPI may then falsely suggest that the pacing site is remote from the circuit. Oscillation of the tachycardia cycle length after pacing is an indication of conduction slowing in the reentry circuit, which may increase the PPI. The PPI will also increase if pacing extends lines of functional block that thereby extend the reentry circuit path, increasing the revolution time through the circuit [13]. Rapid pacing increases the

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Figure 4.6 Entrainment of VT at an outer loop site in the reentry circuit. A. The VT cycle length is 550 ms. The last three stimuli of a pacing train at a cycle length of 520 ms accelerate all electrograms and QRS complexes to the pacing rate. The PPI is equal to the tachycardia cycle length, consistent with pacing from within the circuit. The S-QRS is essentially 0, consistent with rapid propagation of stimulated wavefronts away from the pacing site. QRS fusion is subtle, but present; the R wave in lead I is narrower and sharper during pacing in comparison with that during VT, and there are

subtle changes in QRS morphology in other leads as well. Pacing at a faster rate, and examination of the 12-lead electrocardiogram, would likely make the presence of fusion more evident. B, C. The mechanism of these findings is shown schematically here. In B, stimulated antidromic wavefronts are dashed and orthodromic wavefronts are solid arrows. The stimulated orthodromic wavefront from the last stimulated beat returns to the pacing site after one revolution through the circuit, producing a post-pacing interval (PPI) equal to the tachycardia cycle length.

likelihood of conduction slowing and block. Therefore, pacing at a cycle length only 20 –30 ms faster than that of the tachycardia is favored for assessing the PPI.

the delay from the stimulus to depolarization at the remote recording site activation; TD is determined during tachycardia as the interval between activation at the mapping site and activation at the remote recording site; PPIr is the return cycle at the remote recording site measured from the last electrogram, accelerated to the pacing rate to the subsequent activation; TCL is the tachycardia cycle length. It should be noted that when the pacing site and remote recording site are the same, PD – TD = 0 and ER = PPI – TCL, as discussed above. When the remote recording site is activated orthodromically during entrainment (which is the most common situation), the PPIr equals the TCL, resulting in: PPIr – TCL = 0, such that ER = PD – TD. In regions of scar or infarction, the local potential is often a low-amplitude signal. Adjacent bands of myocytes and larger masses of myocardium some distance from the pacing site may also produce electrograms that are recorded from the electrodes at the pacing site. These far-field signals complicate measurement of the PPI [18]. In many cases, far-field signals can be recognized from inspection of electrograms during pacing (Fig. 4.7A) [19]. An electrogram that is present preceding the stimulus artifact is not directly depolarized by the pacing stimulus, and therefore is likely to originate some distance from the pacing site, provided that the pacing stimuli are capturing and accelerating all electrograms to the pacing rate. The PPI should be measured to a potential that is obscured

Far-field versus local potentials The PPI is measured to the electrogram that indicates depolarization at the pacing site and should be measured in the recordings from electrodes that are as close as possible to the pacing site (Figs. 4.3, 4.5 – 4.7) [14,15]. If the recordings from the pacing site are obscured by amplifier saturation during pacing, analysis of the electrograms from the proximal electrodes on the mapping catheter may be used (Figs. 4.6 and 4.7). The electrogram selected should be evident, with the same timing, on the distal electrode pair (e.g., recordings from “Abl 1–2” and “Abl 2–3” in Fig. 4.6A), and errors can occur when adjacent to regions of conduction block. The PPI can also be assessed by comparing the relative timing of the electrograms at the pacing site with a stable reference site, such as the QRS complex for VT, or a remote electrogram [16]. Recently, Hammer et al. [17] have shown that the PPI–tachycardia cycle length difference (which they defined as the entrainment response, ER) can be calculated from recordings at the pacing site and a remote recording site from the following formula: ER = (PD – TD) + (PPIr – TCL), where PD is determined during pacing as

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Figure 4.7 Entrainment from within a reentry circuit isthmus. A. VT with a cycle length of 350 ms. The last three stimuli of a train at a cycle length of 330 are shown. All electrograms and QRS complexes are accelerated to the pacing rate. The QRS morphology during pacing is identical to that during VT. The post-pacing interval (PPI) is equal to the tachycardia cycle length of 350 ms (arrow), consistent with a reentry circuit site. The S-QRS interval of 160 ms is 48% of the tachycardia cycle length, consistent with a central site in the reentry circuit. The S-QRS interval is equal to the electrogram to QRS interval measured during VT, also consistent with pacing at a reentry circuit site. B. The mechanism of entrainment with concealed fusion during pacing at this site is shown here schematically. The stimulated antidromic wave is

shown as the dashed gray arrow. The stimulated orthodromic wavefronts are solid black arrows. The S-QRS indicates the conduction time from the pacing site (S) to the circuit exit. Note that multiple potentials are recorded from mapping catheter electrodes 2 and 3, close to the pacing site. The largest, somewhat more rounded, potential is present during pacing, preceding each stimulus. Therefore, this potential is produced by tissue that is not directly captured by the pacing stimuli, and is termed a far-field potential (FFP). The post-pacing interval (PPI) and electrogram to QRS (EG-QRS) are therefore measured to the other potential present in that recording, as indicated by the arrows. C. A schematic view of the genesis of far-field potentials.

by the stimulus artifact during pacing. At some sites, multiple potentials of this type are present and should be recognized as a possible source of error in assessing the PPI and activation sequence.

in or near the circuit by collision with the returning orthodromic wavefronts and regions of scar, valve annulus, or functional block that define the borders of the isthmus. The orthodromic wavefront propagates from the pacing site to the exit of the reentry circuit, then through the circuit loops to reset the tachycardia. Entrainment occurs, but fusion produced by the antidromic wavefronts is contained in or near the circuit and is not evident in recordings remote from the circuit or in the surface electrocardiogram. This is entrainment with concealed fusion, also referred to as a form of concealed entrainment [7,20]. During entrainment of VT with concealed fusion, the interval between the stimulus and QRS onset (S-QRS) indicates the conduction time between the pacing site and the reentry circuit exit. A short S-QRS (< 30 ms) indicates a likely reentry circuit isthmus site. Longer S-QRS sites indicate positions further from the reentry circuit exit. S-QRS intervals exceeding 70% of the tachycardia cycle length appear to indicate sites that are in loops where ablation is less likely to interrupt the circuit despite entrainment with concealed fusion. Although entrainment with concealed fusion usually indicates that the pacing site is in a reentry circuit isthmus, where ablation has a high likelihood of interrupting

Entrainment with concealed fusion When pacing is performed remote from the reentry circuit, the antidromic wavefronts depolarize sufficient tissue to produce a detectable change in the ECG appearance of the arrhythmia, indicating fusion [7]. At such sites, entrainment occurs with fusion, and the PPI exceeds the tachycardia cycle length. Some circuits contain loops, such as those often present in the border of an infarct for some VTs (Fig. 4.6). At these sites, pacing produces wavefronts that entrain the tachycardia and also propagate away from the pacing site, altering activation of the ventricle and producing a change in QRS complex evident as fusion. The PPI, however, indicates that the pacing site is in the reentry circuit. These outer loop sites are broad, so that focal ablation is unlikely to interrupt tachycardia. During pacing in narrow isthmuses in reentry circuits (Fig. 4.7), the stimulated antidromic wavefront is contained 56

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the circuit, it is occasionally observed at bystander sites adjacent to the reentry circuit [20]. These are identified by a PPI that exceeds the tachycardia cycle length. They can also be identified by comparing the S-QRS with the electrogram QRS (EG-QRS) observed at the pacing site during tachycardia [20,21]. At sites that are in the reentry circuit, both the S-QRS and EG-QRS indicate the conduction time from the site to the circuit exit, and are equal. At bystander sites, the S-QRS typically exceeds the EG-QRS. For VTs, the presence of QRS fusion should be assessed from the 12-lead ECG [22]. Subtle changes in QRS morphology, indicating that the site is an outer loop rather than a reentry circuit isthmus, can escape detection when only a few ECG leads are assessed (Fig. 4.6). Such errors are more likely near reentry circuit exits and in outer loops, where the S-QRS is short. Increasing the pacing rate increases the proportion of ventricular activation from the antidromic wavefront and makes QRS fusion more obvious. At reentry circuit sites in a proximal portion of an isthmus, however, pacing at a faster rate may produce QRS fusion if the antidromic wavefront reaches a reentry circuit entrance, falsely suggesting that the pacing site is not in an isthmus.

Mapping for localization of target sites

Limitations of entrainment mapping Entrainment mapping requires a stable reentry circuit. It is not useful, and complicates mapping attempts, if pacing repeatedly changes the tachycardia from one circuit to another or terminates tachycardia. Entrainment mapping is difficult to apply to tachycardias that are unstable due to hemodynamic collapse, although brief episodes of tachycardia that can be reliably terminated can be assessed in some patients.

Uses of entrainment mapping (Fig. 4.8) Pacing is initially performed at cycle lengths only 10 – 30 ms shorter than that of the tachycardia, to reduce the chance that pacing will alter the reentry circuit or terminate the tachycardia. Care must be taken to ensure that all electrograms are accelerated to the pacing cycle length and that tachycardia resumes at its previous cycle length after pacing. Faster pacing cycle lengths and longer pacing trains are used if capture is difficult to assess. We prefer

Figure 4.8 The entrainment mapping classification scheme. PPI, post-pacing interval; TCL, tachycardia cycle length.

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unipolar pacing from the tip electrode of the ablation catheter, to avoid the possibility of capture at the proximal ring electrode, where ablation will not be applied. Bipolar pacing is commonly and effectively used, however, and has not been directly compared with unipolar pacing. Electrograms are recorded from the distal, middle, and proximal bipolar pairs, although with many recording systems the distal electrograms will be obscured for a time after pacing. Comparison of the distal and proximal recordings is important, however, if the PPI is assessed from the proximal electrode recordings.

Ventricular tachycardia For stable or incessant VTs, entrainment mapping is useful in identifying isthmuses for ablation [10,23]. Quick assessment of the PPI in the right ventricle allows rapid exclusion of this chamber as the source of the tachycardia in most patients with VT after myocardial infarction, and occasionally reveals the possibility of an RV circuit, particularly in patients with cardiomyopathy without coronary artery disease [24 –26]. A PPI that approaches the tachycardia cycle length when tachycardia is entrained from the RV apex should prompt a careful assessment for the presence of bundlebranch reentry VT [27].

Atrial tachycardias Entrainment mapping can be particularly useful for macroreentrant atrial tachycardias [4,28–36]. Pacing at the right lateral and septal aspects of the common flutter isthmus demonstrates a PPI–tachycardia cycle length difference < 10 ms in most patients with common flutter (slightly longer in the presence of antiarrhythmic medications) [34]. A longer PPI in the common flutter isthmus should prompt careful mapping and assessment of the possibility of other types of atrial tachycardia. Assessing fusion is usually not possible from the surface ECG P waves; intracardiac electrograms can be effectively used for this purpose [30,31,37]. Entrainment can be useful in rapidly determining whether left atrial mapping is required. When tachycardia has a left atrial origin, pacing at the lateral right atrium typically produces a PPI that exceeds the tachycardia cycle length by more than 50 –100 ms. The PPI becomes progressively shorter as the pacing site approaches the superior aspect of the atrial septum (near Bachmann’s bundle) or the coronary sinus. Pacing from within the coronary sinus may demonstrate a short PPI–tachycardia cycle length difference if the anterior portion of the left atrium is involved in the circuit, but will be long if the tachycardia is confined to the roof or posterior aspect of the left atrium. 58

Atrioventricular reentry and atrioventricular nodal reentry tachycardias During atrioventricular (AV) reentry tachycardia, entrainment at sites that are in the reentry path produces a relatively short PPI–tachycardia cycle length difference, but slowing of conduction in the AV node during entrainment increases the PPI. Entrainment is useful for distinguishing AV reentry using paraseptal accessory pathways from AV nodal reentry [38]. During AV nodal reentry, pacing from the RV apex entrains tachycardia with a PPI–tachycardia cycle length difference > 100 ms, due to the long conduction time from pacing site to AV node, then through the reentry circuit and back to the RV apex [27,38]. In contrast, the PPI at the RV apex is less than 100 ms longer than the tachycardia cycle length for AV reentry using a paraseptal accessory pathway.

References 1 Delacretaz E, Soejima K, Gottipaty VK, Brunckhorst CB, Friedman PL, Stevenson WG. Single catheter determination of local electrogram prematurity using simultaneous unipolar and bipolar recordings to replace the surface ECG as a timing reference. Pacing Clin Electrophysiol 2001;24:441– 9. 2 Barlow MA, Klein GJ, Simpson CS, et al. Unipolar electrogram characteristics predictive of successful radiofrequency catheter ablation of accessory pathways. J Cardiovasc Electrophysiol 2000;11:146 – 54. 3 Haïssaguerre M, Dartigues JF, Warin JF, Le Metayer P, Montserrat P, Salamon R. Electrogram patterns predictive of successful catheter ablation of accessory pathways: value of unipolar recording mode. Circulation 1991;84:188 –202. 4 Triedman JK, Alexander ME, Berul CI, Bevilacqua LM, Walsh EP. Electroanatomic mapping of entrained and exit zones in patients with repaired congenital heart disease and intraatrial reentrant tachycardia. Circulation 2001;103:2060 –5. 5 De Chillou C, Lacroix D, Klug D, et al. Isthmus characteristics of reentrant ventricular tachycardia after myocardial infarction. Circulation 2002;105:726 –31. 6 De Bakker JM, van Capelle FJ, Janse MJ, et al. Macroreentry in the infarcted human heart: the mechanism of ventricular tachycardias with a “focal” activation pattern. J Am Coll Cardiol 1991;18:1005 –14. 7 Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 1993;88:1647–70. 8 Okumura K, Henthorn RW, Epstein AE, Plumb VJ, Waldo AL. Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit. Circulation 1985;72:1293 –307. 9 Henthorn RW, Okumura K, Olshansky B, Plumb VJ, Hess PG, Waldo AL. A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion. Circulation 1988;77:1003 –12.

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10 Stevenson WG, Friedman PL, Sager PT, et al. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol 1997;29:1180 –9. 11 Waldo AL, MacLean WA, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery. Circulation 1977;56:737–45. 12 Kay GN, Epstein AE, Plumb VJ. Resetting of ventricular tachycardia by single extrastimuli: relation to slow conduction within the reentrant circuit. Circulation 1990;81:1507 –19. 13 Waldecker B, Coromilas J, Saltman AE, Dillon SM, Wit AL. Overdrive stimulation of functional reentrant circuits causing ventricular tachycardia in the infarcted canine heart: resetting and entrainment. Circulation 1993;87:1286 –305. 14 Hadjis TA, Harada T, Stevenson WG, Friedman PL. Effect of recording site on postpacing interval measurement during catheter mapping and entrainment of postinfarction ventricular tachycardia. J Cardiovasc Electrophysiol 1997;8:398 – 404. 15 Khan HH, Stevenson WG. Activation times in and adjacent to reentry circuits during entrainment: implications for mapping ventricular tachycardia. Am Heart J 1994;127:833 – 42. 16 Soejima K, Stevenson WG, Maisel WH, et al. The N + 1 difference: a new measure for entrainment mapping. J Am Coll Cardiol 2001;37:1386–94. 17 Hammer PE, Brooks DH, Triedman JK. Estimation of entrainment response using electrograms from remote sites: validation in animal and computer models of reentrant tachycardia. J Cardiovasc Electrophysiol 2003;14:52–61. 18 Bogun F, Knight B, Goyal R, Strickberger SA, Hohnloser SH, Morady F. Clinical value of the postpacing interval for mapping of ventricular tachycardia in patients with prior myocardial infarction. J Cardiovasc Electrophysiol 1999;10:43– 51. 19 Tung S, Soejima K, Maisel WH, Suzuki M, Epstein L, Stevenson WG. Recognition of far-field electrograms during entrainment mapping of ventricular tachycardia. J Am Coll Cardiol 2003;42:110–5. 20 Bogun F, Bahu M, Knight BP, et al. Comparison of effective and ineffective target sites that demonstrate concealed entrainment in patients with coronary artery disease undergoing radiofrequency ablation of ventricular tachycardia. Circulation 1997;95:183–90. 21 Fontaine G, Evans S, Frank R, et al. Ventricular tachycardia overdrive and entrainment with and without fusion: its relevance to the catheter ablation of ventricular tachycardia. Clin Cardiol 1990;13:797–803. 22 Ormaetxe JM, Almendral J, Martinez-Alday JD, et al. Analysis of the degree of QRS fusion necessary for its visual detection: importance for the recognition of transient entrainment. Circulation 1997;96:3509–16. 23 El-Shalakany A, Hadjis T, Papageorgiou P, Monahan K, Epstein L, Josephson ME. Entrainment/mapping criteria for the prediction of termination of ventricular tachycardia by single radiofrequency lesion in patients with coronary artery disease. Circulation 1999;99:2283–9. 24 Reithmann C, Hahnefeld A, Remp T, et al. Electroanatomic mapping of endocardial right ventricular activation as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Pacing Clin Electrophysiol 2003;26: 1308–16.

Mapping for localization of target sites

25 Harada T, Aonuma K, Yamauchi Y, et al. Catheter ablation of ventricular tachycardia in patients with right ventricular dysplasia: identification of target sites by entrainment mapping techniques. Pacing Clin Electrophysiol 1998;21:2547–50. 26 Ellison KE, Friedman PL, Ganz LI, Stevenson WG. Entrainment mapping and radiofrequency catheter ablation of ventricular tachycardia in right ventricular dysplasia. J Am Coll Cardiol 1998;32:724 – 8. 27 Merino JL, Peinado R, Fernandez-Lozano I, et al. Bundlebranch reentry and the postpacing interval after entrainment by right ventricular apex stimulation: a new approach to elucidate the mechanism of wide-QRS-complex tachycardia with atrioventricular dissociation. Circulation 2001;103:1102 –8. 28 Delacretaz E, Ganz LI, Soejima K, et al. Multiatrial macro-reentry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping. J Am Coll Cardiol 2001;37:1665 –76. 29 Zrenner B, Dong J, Schreieck J, et al. Delineation of intra-atrial reentrant tachycardia circuits after mustard operation for transposition of the great arteries using biatrial electroanatomic mapping and entrainment mapping. J Cardiovasc Electrophysiol 2003;14:1302 –10. 30 Molenschot M, Ramanna H, Hoorntje T, et al. Catheter ablation of incisional atrial tachycardia using a novel mapping system: LocaLisa. Pacing Clin Electrophysiol 2001;24:1616 –22. 31 Della BP, Fraticelli A, Tondo C, Riva S, Fassini G, Carbucicchio C. Atypical atrial flutter: clinical features, electrophysiological characteristics and response to radiofrequency catheter ablation. Europace 2002;4:241– 53. 32 Akar JG, Kok LC, Haines DE, DiMarco JP, Mounsey JP. Coexistence of type I atrial flutter and intra-atrial re-entrant tachycardia in patients with surgically corrected congenital heart disease. J Am Coll Cardiol 2001;38:377– 84. 33 Kanter RJ, Papagiannis J, Carboni MP, Ungerleider RM, Sanders WE, Wharton JM. Radiofrequency catheter ablation of supraventricular tachycardia substrates after Mustard and Senning operations for d-transposition of the great arteries. J Am Coll Cardiol 2000;35:428 – 41. 34 Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation 1996;94:398 – 406. 35 Kalman JM, VanHare GF, Olgin JE, Saxon LA, Stark SI, Lesh MD. Ablation of “incisional” reentrant atrial tachycardia complicating surgery for congenital heart disease: use of entrainment to define a critical isthmus of conduction. Circulation 1996;93:502 –12. 36 Horlitz M, Schley P, Shin DI, et al. Identification and ablation of atypical atrial flutter: entrainment pacing combined with electroanatomic mapping. Z Kardiol 2004;93:463 –73. 37 Bogun F, Bender B, Li YG, Hohnloser SH. Ablation of atypical atrial flutter guided by the use of concealed entrainment in patients without prior cardiac surgery. J Cardiovasc Electrophysiol 2000;11:136 – 45. 38 Michaud GF, Tada H, Chough S, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing. J Am Coll Cardiol 2001;38:1163 –7. 59

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5

Three-dimensional mapping technology and techniques: applications in atrial fibrillation Douglas L. Packer

Introduction As electrogram recording technology has evolved over the past 50 years, single-channel electrophysiologic evaluations have given way to simultaneous, multichannel recording systems, resulting in more detailed temporal characterization of specific arrhythmias. In the process, it has become more difficult to keep track of an everincreasing number of channels of electrograms and analyze them within the context of their specific chamber of origin. Fortunately, the advent of microprocessors has since led to the development of computer-based mapping, which chronicles both the temporal and spatial characteristics of cardiac activation. This development has also been driven by the need for increasing accuracy in arrhythmia localization, as required for catheter ablation [1]. The ultimate test for these subsequent generations of mapping systems is in the application for deciphering the mechanisms of atrial fibrillation (AF). This arena provides substantial challenges, not only because of the complexity of impulse initiation and propagation in AF, but also because of the underlying structural abnormalities of the heart that are present in affected patients. Nevertheless, since the original elucidations of reentry around an area of functional block by Allessie et al. [2– 4], much progress has been made in the mapping of AF. This chapter will first review the characteristics of mapping systems required for “high-end” arrhythmia elucidation, with information presented that is adapted from a general review of mapping technology [5]. Without attempting to chronicle the history of AF mapping, recent progress in mapping will then be presented.

General requirements of cardiac mapping systems At a minimum, computer-based cardiac mapping systems 60

capable of assisting in unraveling the complexities of AF should: • Accurately replicate the cardiac anatomy underlying an arrhythmia, regardless of the complexity of that anatomy. • Provide a plausible representation of activation of that chamber, as linked to the specific anatomic site of data acquisition. • Readily capture and intelligibly display other details of physiology. • And catalogue the site of interventions. The first requirement provides the context for the arrhythmia. A mapping system should faithfully replicate the anatomy of a chamber under examination and those structures both entering and exiting that chamber. In short, the geometry needs to look like the chamber under study. The extent to which this is accomplished is a matter of “man vs. machine.” The resolution of the anatomy is a function of the number of points taken in the process of creating the surrogate geometry. The more points, the closer the image rendering comes to replicating the chamber under evaluation. This is an operator issue. Mapping of the left atrium (LA), if enlarged, will require more points to delineate the specifics of the chamber. The problem from the mapping system side comes from the algorithms used to graphically connect three or more points identified with, or sampled by, a roving catheter to create a surface segment and subsequent volume. While interpolation between points along an uncomplicated surface readily produces a clear image of that surface, the process is strained at the junction between chambers and sites of entering or exiting “veins and valves,” or at areas of complex structures, including within pulmonary veins (PVs). The system must easily preserve the complexities of anatomy at those points, along with intervening acute and oblique angles between structures, without losing requisite detail. Some systems are more prone to “interpolation obliteration” of those junctions, with smoothing over the angles defining the underlying structures.

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Figure 5.1 An electroanatomical map acquired in a patient undergoing ablation of atrial fibrillation. Each pulmonary vein was acquired as an individual structure, providing a more robust surrogate representation of the real underlying anatomy.

This is particularly problematic in anatomically mapping PVs. One way to minimize this is to treat PVs or neighboring structures as separate volumes or maps, which some systems readily allow (Fig. 5.1). The creation of separate geometries of PVs also serves to replicate those structures better than is possible with simply “pulling” a tube to represent the vessel. Another challenge of mapping systems is created by the inherent difficulty in displaying three-dimensional (3D) structures on a monitor screen in two-dimensional views. Here, the ability to show multiple views simultaneously is of paramount importance to give the 3D perspective. The addition of virtual endoscopic views from within a chamber is enormously helpful. Transparency features incorporated into the system can be useful, or may create confusion. Other features are as outlined in detail elsewhere [5]. These challenges of anatomic rendering and display are not a trivial matter, since under the best of circumstances these features allow the user to clearly understand and navigate the underlying geometry. Under the worst of circumstances, bad geometry may be dangerous. The accuracy of the surrogate geometries will become increasingly important, as interventions are guided by those very images. Remarkably, very few validation studies addressing these issues in any mapping system are available. Additional investigations will therefore be required in order to ensure that the surrogate mapping geometries accurately depict actual anatomy. A second function of a mapping system is to catalog local physiology as linked to the anatomic site of data

acquisition. The system should readily “arrange” sequential sampling site activation times and voltages within the context of the entire surface geometry to provide the global indication of the activation sequence. Furthermore, the resulting depictions of chamber activation must be consistent with the first principles of cardiac electrophysiology. A map of sinus rhythm or any arrhythmia must be “plausible,” whether the activation sequence is displayed in terms of progressive activation times, voltage transients, or any other physiologic parameter. While mapping systems should make a case easier, the user still has the obligation of knowing when it is serving up “jewels” or “junk,” without relegating this responsibility solely to an industry representative. Again, success in this process partly involves man and partly involves machine. While large circuits, such as macroreentry following AF ablation, can be dissected with relatively few mapping points, progressively more points at a sufficient density are required to resolve arrhythmia circuits of decreasing size or increasing complexity (Fig. 5.2), as is seen in the microreentry around scar lines of linear AF ablation [6]. A reasonable goal for the ideal system is ultimately to provide adequate resolution and mechanistic disclosure on the same order as found with optical mapping systems used in ex vivo studies. The use of advanced computational capabilities should simplify this process by cataloging all sites of data acquisition with the accompanying electrograms, without confusing interpolation across lines of block or other boundaries of the circuits. This should be extended to allow mapping of rapid tachycardias, nonsustained arrhythmias, or tachycardias with complex activation pathways involving several different chambers. Third, the system must lend itself readily to capturing and intelligibly displaying other details or the “physiologic quirks” contributing to an arrhythmia. This implies system versatility in extracting relevant features from electrograms or other sensors and providing real-time parametric displays. Most electrophysiologists are familiar with unipolar or bipolar voltage mapping to reflect underlying tissue integrity and pathophysiology in patients with a prior myocardial infarction. “Scar mapping” has been used, for example, to identify the site of possible circuits in patients with unstable ventricular tachycardias that defy activation sequence mapping [1,7]. An example of this approach is shown in Fig. 5.3. Some investigators have used a 0.5–1.0 mV cut-off point to reflect dense scar. It should be noted, however, that the presence of dense scar does not exclude the possibility of pathways within that scar that are incapable of generating a 1-mV signal. In atrial mapping of flutters in patients with congenital heart disease, or in patients with recurrent arrhythmia following AF ablation, for example, scar cut-offs of 0.1 or even 0.05 mV may better detect the underlying tissue 61

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Figure 5.2 Map of a microreentrant circuit along the interatrial septum in front of the right inferior pulmonary vein. The number of points taken to resolve the circuit should be noted.

A

MV

LVA

B

LVA

MV

Figure 5.3 An electroanatomical voltage map, generated during the evaluation of a patient with rapid unstable ventricular tachycardia. A. The voltage map, with manually adjusted voltage settings to identify the interface between normal tissue (purple) and low voltage scar (red) more specifically. The yellow through blue isovoltage lines occurred at the assumed boundary between normal and abnormal tissue. B. The creation

of an ablative line along the subendocardial border zone of the infarction, which was successful in eliminating the patient’s ventricular tachycardia. Linear ablation, maroon dots; also shown is the site of the 12-over-12 match between the underlying ventricular tachycardia and the QRS morphology during pacing (black arrow). MV (white arrow) indicates the position of the mitral annulus; LVA, left ventricular apex.

pathophysiology (Fig. 5.4) and reflect relevant active circuit components [1]. Any mapping system should also chronicle the voltage changes of repolarization, even if this would require alternative signal amplification and filtering. Mapping systems should also identify and catalog the presence and location of double potentials, fractionated

electrograms, or the switching sequences of activation around a line of a fixed or physiologic block, and archive and display these “quirks” in real-time, three-dimensional space (Fig. 5.4). Ideally, it should also be possible to exploit any characteristic of the electrogram at each site to better explain an arrhythmia. For example, it would be highly

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Figure 5.4 Voltage map of atrial flutter in a patient with congenital heart disease. Application of a voltage cut-off of 0.1 mV was required to tease out the central core of the flutter circuit. The black dot identifies the site of successful ablation. The areas of scar should also be noted (gray) and double potentials (teal dots), defining the boundaries of the circuit.

useful if signal amplitude, width, fractionation, or evidence of specific patterns of temporal activation, such as repetitive firing, could be translated into specific maps through straightforward signal processing. This would be of particular importance in “mapping” areas of high frequency or complex electrograms for guiding AF ablation. In theory, the ideal advanced mapping system should also display mechanical events, such as motion, wall stress or tension, or any other fourth- or fifth-dimensional contraction parameter and allow easy visualization, understanding, and metrics to assess those processes. Activation mapping of several chambers may thereby give a clearcut indication of inter- or intraventricular dyssynchrony, while voltage or other mapping over the course of a single cardiac cycle may disclose the possibility of intramural dyssynchrony. Finally, the ability to catalog the site of an intervention (either performed or planned), such as a specific ablation, or marking the site of cellular or other factor injections, is highly useful (Fig. 5.5). While this annotation might be done with a marking pen on an acetate film taped over a fluoroscopic monitor, such an approach has been eclipsed by the availability of central processing units with a high computational speed. These characteristics of the available systems are described elsewhere [5].

LAO Right Atrium

E

LI

E RS

Fibroblast Injections

AV node

CS Os

Figure 5.5 Map-guided delivery of autologous fibroblasts injected around the atrioventricular conduction system to modify atrioventricular conduction. (Reproduced from Bunch et al., Circulation 2006;113:2485 with permission from Lippincott, Williams and Wilkins).

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Characterization of the underlying anatomy The ultimate advantage for the cardiovascular surgeon is the ability to directly visualize the anatomy of the heart. In the course of inspection of each cardiac chamber during an operative intervention, characteristic structural features are identified and used to guide the intervention. While the vantage point of the interventional electrophysiologist is more limited, mapping technology does provide a surrogate anatomy to guide catheter laboratory-based procedures, as outlined above. Moreover, the successful ablation of AF is largely dependent on clear visualization and understanding of the anatomy. Multiple studies have documented the sentinel role of the PVs in the genesis of AF [8 –11]. In the case of ablation directed at the resident foci serving as triggers for AF, intervention directed at PV isolation is anatomically guided to a substantial degree, even though the assessment of the end point of ablation is based on changes in the physiology of impulse conduction along muscle fibers. While circular or “lasso” catheters have been used extensively in this process [9,10,12], the anatomic context provided by a fluoroscopically visualized catheter loop at the orifice of the vein may be of even greater utility in the ablative process. Relatively simple catheters are therefore tools of anatomic mapping of a PV. Linear ablation, targeting the underlying substrate responsible for more persistent or chronic AF, has also been largely anatomically directed [6,13–15]. The ultimate example of intervention based on LA anatomy is the surgical maze procedure. As an additional example, the ablation of the lateral LA isthmus is useful in interrupting potential flutter circuits, which may emerge over the course of ablation [16,17]. Ablation between the PVs and the mitral annulus, which effectively compartmentalizes the LA, is anatomy-guided. As is the case with more established chronic AF, extensive linear ablation is required to achieve the goal of AF elimination [6,18,19]. The widearea circumferential ablative approach to AF is likewise largely dependent on identification of the location and size of PVs. Both electroanatomical and impedance-based imaging systems have been used extensively in this process (Fig. 5.6). Even in the absence of the acquisition of actual activation maps, these mapping systems provide a three-dimensional construct for successful intervention. Creation of surrogate anatomy of each PV is useful in establishing the precise venoatrial junction, which is seen as the confluence between each vein (as “mapped” by Carto or NavX mapping) and the LA itself. In this process, ablative rings can be positioned well outside the venoatrial junction, both to decrease the risk of PV stenosis and to increase the efficacy by ablating peri-vein tissue responsible for microreentry, other foci, or mother or daughter rotors [20–22]. While 64

RI

E

LS

LI

E RM

RS CS

MV

Figure 5.6 NavX map of the left atrium and accompanying pulmonary veins (PVs) as established during ablative intervention for atrial fibrillation. The right and left superior PVs (RS and LS) are shown as teal-colored mapping spheres. The right middle PV (RM) is shown in green, and the right and left inferior veins (RI and LI) in blue. The position of the esophagus posterior to the left atrium (E) is shown by the white spheres. CS, coronary sinus catheter; MV, mitral valve annulus.

wide-area approaches can be undertaken without threedimensional mapping systems, advanced technology simplifies the chronicling of line placement. Using anatomic imaging presupposes that the geometry rendered by this mapping system is accurate. The validity of electroanatomical mapping for reflecting the actual dimensions of actual geometry has recently been examined in patients undergoing ablation for AF. Piorkowski and co-workers [23] demonstrated only modest deviation between the Carto-acquired and computed tomography– produced dimensions of the LA. For example, the distance between the left upper pulmonary vein (LUPV) ostium and the right upper pulmonary vein (RUPV) ostium measured by Carto was 43 ± 8 mm, compared with 49 ± 8 mm seen on computed tomography (CT) (P = 0.001). The difference between these two imaging modalities was also significant in assessing the RUPV ostium–esophagus distance (Carto 27 ± 9 mm, CT 31 ± mm; P = 0.001). Similarly, the distance between the superior RUPV ostium and the inferior right lower pulmonary vein ostium was slightly different (37 ± 6 mm vs. 44 ± 6 mm; P = 0.001). Of note, these differences, while statistically significant, are minor, especially considering the magnitude of variability that could occur because of differences in rhythm, inspiratory phase, and the exact portion of the cardiac cycle examined during the two data-set acquisitions [24]. With the advent of anatomically based balloon catheter procedures, careful examination or “mapping” of underlying PV anatomy is also of increasing importance. A

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variety of investigators have characterized the morphology of PVs in CT and magnetic resonance (MR) studies [25,26]. Most recently, Ahmed and co-workers [26] used MR data acquired in paroxysmal AF ablation patients to generate three-dimensional surface reconstructions of the PVs. A common left-sided ostium was identified in 94% of patients, which is a significantly higher rate than reported by others [25]. Branching of left PVs subsequently occurred at a depth of 0 –5 mm from the common left ostium in 43 patients, 5 –15 mm in 37 patients, and greater than 15 mm away from the common ostium in 14 patients. In patients with either distinct left PV ostia or a common os < 15 mm in size, the individual left superior/ left inferior PV ostial circumferences were 67 ± 12 mm and 58 ± 9 mm, respectively. Right-sided PV circumferences were 68 ± 11 and 66 ± 11 mm for the right superior and right inferior PVs, respectively. These anatomic data provide a more detailed notion of the minimal diameters of the balloons required to engage the respective PVs. These investigators proposed that the balloon size for the right superior PV should be 29 mm; for the right inferior, 28 mm; for the left superior, 29 mm; for the left inferior, 24 mm; and for the left common PV, 40 mm. While not classically considered as “mapping,” in fact such anatomic investigations may be of substantial importance in ablating with new devices.

Contributing left atrial structures Three-dimensional mapping has similarly elucidated structure–activity relationships contributing to AF occurrence. Markides et al. [27] provided a detailed noncontact map-generated characterization of LA activation considered within an anatomic context. They demonstrated that LA activation during sinus rhythm occurred in both medial to lateral and lateral to medial directions. The earliest LA endocardial activation during sinus rhythm occurred anterior to the right PV in seven patients and on the anterosuperior septum in two patients [27], likely reflecting activation of the LA from Bachmann’s bundle. Spread of activation proceeded laterally, with return activation of the LA near the coronary sinus in the opposite direction. This was facilitated by a posterior and superior area of conduction block, related to the anatomy and histology of the LA. A line of conduction block was seen along the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence recorded via a coronary sinus catheter in two-thirds of patients. This 3D mapping information provides additional relevant documentation of the structure–activity relationships created by the underlying left atrial anatomy, and explains the substrate for macroreentrant arrhythmias involving the LA [28].

Triggers and substrate of atrial fibrillation Recent 3D mapping studies have also elucidated the triggers of AF beyond what is possible with simple multipolar mapping catheters. Several investigators have examined local activation in the area of triggers using a pseudo-3D “flower” catheter [29]. This catheter employs 20 electrodes, oriented in high density along five radiating splines covering a local mapping area 3.5 cm in diameter. While this was a highly simplified three-dimensional approach, the resulting high-density mapping provided a snapshot view of the origin of atrial tachycardias, which mapped to a PV orifice in five patients, to the LA in 16, and to the right atrium in six of 16 patients studied. In addition to demonstrating a focal site of origin in 70% of atrial tachycardias, this array identified localized reentry in 30% of tachycardias (Fig. 5.7). Interestingly, 95 ± 5% of the entire tachycardia cycle length could be recorded within the 3.5-cm mapping field. Specific conduction properties of the microreentrant circuits were also disclosed. A companion study also documented the utility of this limited 3D mapping approach in identifying the site of origin of AF [30]. Spontaneous focal activity was observed at sites in the left atrium and along the anterior, roof, and posterior and inferior components of the LA, in episodes lasting only seconds. In more complicated studies, Saksena et al. [31] also applied three-dimensional noncontact mapping to identify the site of origin of atrial premature beats contributing to the onset of spontaneous AF. Thirty-one percent of patients with paroxysmal or persistent AF had both right and left atrial foci. Biatrial and noncontact mapping showed organized monomorphic atrial tachyarrhythmias arising in the right atrium in 38%, the interatrial septum in 38%, and in the left atrium in 47% of patients studied. The region of distribution of the identified triggers was more extensive in patients with structural heart disease and persistent AF in comparison with those without these contributing factors. This information demonstrates the utility of simultaneous biatrial and noncontact mapping to identify the origins of AF and provide support for the presence of a spectrum of biatrial triggers and tachycardias in the genesis of this arrhythmia. The understanding of the mechanisms underlying AF in the different populations should be highly useful in successful ablative interventions, although additional studies will be required to document the translation of such high-resolution mapping into enhanced ablation success. The pathophysiology of ganglion plexuses in the genesis of AF is emerging, in part from 3D mapping studies. Several studies provide a link between these mediators of parasympathetic and sympathetic nerve activity and specific anatomic locations [32–35]. These studies show the spatial distribution of pacing-invoked decrements in AV conduction during AF, bradycardia during normal 65

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Figure 5.7 Local activation mapping within the left atrium using a flower catheter. (Reproduced with permission from [29].)

sinus rhythm, and blood pressure drops, as manifestations of triggered vagal activity. These are located superiorly and laterally to the right superior PV, superiorly and medially to the left superior PV, inferiorly to and between the right and left inferior veins, and along the interatrial septum [33,34]. Although the direct activity from the parasympathetic nervous system is beyond the resolution of the 66

available mapping systems, the localization of these areas provides a better understanding of the pathophysiology underlying AF and a framework for successful intervention. Recent studies have also demonstrated the utility of advanced mapping in the ablation of complex fractionated electrograms or areas of high-frequency activity during AF [36]. Here again, most of the relevant target areas

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are closely linked to specific anatomy. Several investigators have localized the presence of fractionated and highfrequency electrograms to areas superior to and between the left and right PVs, along the interatrial septum in front of the right PVs, along the medial and inferior portion of the right inferior PV, and along the left side of the interatrial septum. Septal locations within the right atrium have also been documented. Indeed, there is substantial overlap with those areas of inducible vagal activity. Modified electroanatomical mapping software has been developed to display AF physiology in terms of the specific frequency content of the electrograms at each mapping site. Frequencies over a range of 50 –300 Hz are displayed in standard map format, with repetitive firing at cycle lengths of 50–100 ms considered to be “high-frequency.” These maps provide the specific visual information needed for frequency-targeted ablative intervention [36]. Advanced signal processing has also been used to extract the mechanistic physiology of triggering and sustaining drivers of AF and predict the outcome of ablation. Takahashi and co-workers [37], in examining the frequency spectra of fibrillatory electrograms, found differences in the complexity of activity perpetuating AF in patients with single PV-mediated arrhythmia compared with those with two or three PV-driven arrhythmias. The mean dominant frequency observed decreased by ≥ 0.25 Hz with isolation of a “driver” PV. Patients with a single driving PV also showed a significantly higher baseline organization index (the ratio of the area under the dominant frequency plot and its harmonics to the total power) than seen in patients with multiple driving PVs (0.45 ± 0.08 vs. 0.35 ± 0.07; P = 0.009). The baseline organization index was also significantly higher in patients who had termination of AF during mitral isthmus ablation than those patients who did not (0.50 ± 0.10 vs 0.38 ± 0.07; P < 0.008). Thus, a higher organization index of atrial electrograms was associated with termination of AF during limited ablation, which may lead to selection of more or less aggressive ablative intervention, depending on the physiology mapped at the time of the procedure.

Integrated, anatomy-based mapping The last five years have also seen the rapid development of integrated, anatomy-based mapping and ablation. This has been driven by a realization of both the critical dependence of arrhythmias on their underlying anatomy and the limitations of surrogate geometries of contemporary mapping systems in reflecting that anatomy. Over the same period, intracardiac ultrasound and rapid CT and MR systems have emerged as the mainstays of imaging in the electrophysiology laboratory [1]. Helical CT and MR studies with 16 – 64 rows provide a broad

RPA

LPA LS

RS

LI

RI

Figure 5.8 Segmented left atrium and pulmonary veins created from a multislice computed-tomography image set. The common left pulmonary vein antrum should be noted. (Reproduced with permission from [25].)

“gestalt” or “anatomy library” of an individual patient at one point in time (Fig. 5.8). Intracardiac ultrasound is highly useful for providing focused real-time images of the endocardial surfaces critical for positioning catheters, establishing catheter tip–tissue contact, and for monitoring energy delivery in the beating heart. Both changing tissue echogenicity and microbubbles reflect tissue heating, with the latter providing a signal for energy termination. In each of these tasks, ultrasound focuses on specific “books” and “shelves” within the “global library” established by prior CT on MR imaging. At present, segmented CT volumes can be downloaded onto Carto and NavX mapping platforms, with similar integration work under way for other systems. With each of these approaches, the chamber of interest is segmented out of the entire CT axial image setaalthough this requires substantial user effort to sculpt or segment out the chamber of interest. Both systems display the CT image volume along with the surrogate geometries rendered from sequential mapping for side-by-side comparison. While this is useful in correlating electrophysiology and CT anatomies, manipulating image files slows down the general map-processing time noticeably.

Validation of 3D image-based mapping Additional work is also under way to fully “register” the surrogate map onto the actual anatomy [1]. At this point, some systems do accommodate merging the CT segmented volume and accompanying 3D maps, through matching three to six specific anatomic locations seen on both anatomic renderings. Displaying the ablation 67

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Figure 5.9 Segmented computed tomography (CT) rendering of the left atrium and pulmonary veins (PVs) in a patient with atrial fibrillation. Each PV is shown in red, and the registration of the noncontact map obtained during the atrial premature contraction (APC) is fully registered to the underlying CT volume. Atrial activation spreads from the APC origin (light blue) out of the left superior PV toward the rest of the left atrium.

catheter and integrating its position onto the CT geometry is also possible. True registration of mapping details onto the exact surface of the CT or MR anatomy, however, is not yet clinically available. Nevertheless, Figure 5.9 is an example of the registration of an activation sequence generated by an atrial premature contraction onto the underlying left atrial anatomy, as established by multiplerow CT scanning. Integration of such three-dimensional volume images from CT or MR scanning or intracardiac ultrasound and 3D mapping technologies should provide the most robust guidance for intervention. Imaging provides more direct visualization, while mapping delineates the physiology of an arrhythmia. The successful application of such multimodality imaging, however, requires a test of the accuracy of merging different 3D data sets and displaying the resultant images within a common coordinate system. The utility of this combination is now being critically examined. To provide more detailed validation of the integration process, Tops and co-workers [38] recently assessed merging electroanatomical maps and LA and PV anatomy “segmented” or extracted from 64-slice CT images in patients with AF. The resulting segmented volume was imported into the Carto electroanatomical mapping workstation, and the 3D map and CT images were thereafter aligned within the same coordinate system. The fusion process was accomplished by picking specific left atrial landmarks within the left atrial appendage and other PV-related sites. Quantitative analysis of the hybrid images produced demonstrated the quality of match, manifested as the mean distance between the mapping 68

points and the paired CT surface points. This variability ranged between 2.8 ± 1.2 mm and 7.8 ± 1.8 mm (average 5.1 ± 0.2 mm). Nevertheless, the study demonstrates the feasibility of combining data sets to provide a more robust anatomically based image for guiding ablative interventions. Similar results have been reported, demonstrating a limited 3-mm variation in CT in comparison with electroanatomical geometric tag points [39 ,40]. It remains unclear, however, whether the application of this process will alter ablation times, increase efficacy, or improve the safety of the intervention. It has been argued that differences in these two data sets, related to differences in volume status, cardiac cycle, inspiratory phase, or rhythm present at the time of the image or map acquisition, may prove confounding to the registration process [24]. However, Kistler et al. [41] examined registration error in patients undergoing ablation for paroxysmal and persistent AF. They found that cardiac rhythm at the time of CT acquisition did not have a significant effect on the total or regional surface registration accuracy. In AF, the mean total registration error was 2.5 ± 0.3 mm, and 2.3 ± 0.5 during sinus rhythm (not significant). In addition, there was no variability in error dependent on the region of the LA registered. All registration errors were within 1.7 and 2.2 mm. This information provides initial validation of the registration process. Again, larger clinical studies will be required in order to establish the utility of this type of image integration for improving AF ablation.

Intracardiac ultrasound/CT fusion Image fusion, applied more widely in other medical disciplines, is now being introduced into the electrophysiology arena. Studies are under way to “fuse” intracardiac ultrasound images with CT or MR volume images. This provides the best of all possible imaging worlds: the combination of high-resolution (but offline) 3D tomographic images with real-time ultrasound. In this process, the radiographic images provide the context, and the ultrasound provides the real-time feedback for positioning catheters, establishing catheter tip–tissue contact, assessing the impact of energy delivery, and monitoring for beneficial and detrimental effects of ablation. We have recently reported the fusion of these two imaging modalities to produce the visual basis for guiding catheter ablation, without fluoroscopy [42]. Figure 5.10 shows a pre-acquired CT of the canine heart obtained offline before the interventional procedure. Using phased-array ultrasound, two-dimensional vector images were obtained and merged into the segmented CT volumes. This process was facilitated by an electroanatomical position sensor embedded into the ultrasound catheter tip to allow orientation of the acquired images into a common coordinate

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physiology in a specific patient. Already, the Stereotaxis system is available for controlled positioning of a catheter as guided by an individual mapping system. The Hansen catheter manipulation system is being developed as an alternative means of precise catheter manipulation within an established 3D geometric framework. Similar approaches using more traditional robotics systems will undoubtedly become commonplace. With fully integrated CT, ultrasound, and any other physiologic data set, it will be possible to plan an ablative session by marking the exact locations of the desired intervention on the surface anatomy (Fig. 5.11). The system will then semi-automatically drive ablation or other interventions according to these preset locations.

Figure 5.10 Fused image created from pre-acquired CT (in brown) and intracardiac ultrasound data sets. The right inferior pulmonary vein is seen extending to the left of the image.

system. Such fusion, if available on a real-time basis, could provide the advantages of both systems, as outlined above.

Image-guided intervention The next task will be the development of clear capabilities for intervening within the context of these multipleparameter images. Of substantial interest is the utility of mapping for guiding robotic navigation. The use of magnetic and direct sheath manipulation is dependent on an understanding of the anatomy and the underlying electro-

The future of cardiac mapping of atrial fibrillation Automatic segmentation and registration and the ability to fuse multimodality imaging technologies into a single coherent display will undoubtedly evolve over the next 3–5 years. It is highly likely that the ablative interventions within this time frame will be based on these kinds of multimodality image fusion. With the advent of ultrarapid CT and rotational angiographic imaging, multiple image sets over the course of a single cardiac cycle will also be available for integration into the overall mapping system. When synchronized in both the spatial and temporal domains, this approach will solve some of the vexing problems of image registration, and will also allow higher anatomic resolution down to the submillimeter level.

FI Fi ac an Fi th Fi ve sp bl th el th in Fi cu sit bo Fi m Fi fo PV th Fi Fi ve Fi an vo th Fi Th Fi ar ha do is

Fi 1. tr va ev

Figure 5.11 Electroanatomic map of the left atrium in a patient undergoing Stereotaxis guided ablation around the left pulmonary veins. The desired line for the left wide area circumferential ablation was created by hand through mouse clicks onto the Carto map as purple dots and accompanying lines (arrow). This was then downloaded onto the Stereotaxis system to semi-automatically guide ablation. The position of the esophagus is shown as black filled circles.

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Systems of the future will also display a wide variety of physiologic parameters beyond activation times and voltage. Future systems will be able to display any parametric process, including vectors, strains, contraction patterns, or will even be based on the characteristics of an electrogram. Mapping capabilities demonstrating fractionation of electrograms are already being developed to disclose dominant frequencies. Any other parametric display will be limited only by whether that parameter can be measured with a sampling system. In this regard, it may be that these approaches will also be the “great equalizer” for facilitating complicated studies that otherwise would require an insurmountably steep learning curve. Nevertheless, future generations of systems will have to be affordable within the context of prevailing reimbursement paradigms. This would be facilitated by multiple-use catheters, inexpensive higherresolution imaging and more automatic segmentation, and robust registration software, all designed to reduce procedure times and increase the number of procedures that can be safely performed in a day. Undoubtedly, this will lead to even better, expedited care for patients with substantial arrhythmia burdens.

References 1 Packer DL. Evolution of mapping and anatomic imaging of cardiac arrhythmias. J Cardiovasc Electrophysiol 2004;15:839–54. 2 Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. Circ Res 1973;33:54–62. 3 Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit atrial muscle as a mechanism of tachycardia, 2: the role of nonuniform recovery of excitability in the occurrence of unidirectional block as studied with multiple microelectrodes. Circ Res 1976;39:168–77. 4 Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit atrial muscle as a mechanism of tachycardia, 3: the “leading circle” concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977;41:9–18. 5 Packer DL. Three-dimensional mapping in interventional electrophysiology: techniques and technology. J Cardiovasc Electrophysiol 2005;16:1110–6. 6 Packer DL. Linear ablation for atrial fibrillation. In: Zipes DP, Haïssaguerre M, eds. Catheter Ablation of Arrhythmias. Armonk, NY: Futura, 2001: 107–29. 7 Marchlinski F, Callans D, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101:1288–96. 8 Jais P, Haïssaguerre M, Shah D, et al. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation 1997;95:572–6.

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9 Haïssaguerre M, Jais P, Shah D, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659 – 66. 10 Haïssaguerre M, Jais P, Shah D, et al. Electrophysiological endpoint for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation 2000;101:1409–17. 11 Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 1999;100:1879 – 86. 12 Packer DL, Asirvatham S, Munger TM. Progress in nonpharmacologic therapy of atrial fibrillation. J Cardiovasc Electrophysiol 2003;14(12 Suppl):S296–309. 13 Pappone C, Oreto G, Lamberti F, et al. Catheter ablation of paroxysmal atrial fibrillation using a 3D mapping system. Circulation 1999;100:1203 –8. 14 Oral H, Scharf C, Chugh A, et al. Catheter ablation for paroxysmal atrial fibrillation: segmental pulmonary vein ostial ablation versus left atrial ablation. Circulation 2003;108: 2355 – 60. 15 Swartz JF, Pellersels G, Silvers J, Patten L, Cervantez D. A catheter-based curative approach to atrial fibrillation in humans [abstract]. Circulation 1994;90(Suppl 1):I-335. 16 Jais P, Hocini M, Hsu L, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004;110:2996–3002. 17 Brady PA, Bedi AK, Lee SC, et al. Ablation of the lateral left atrial isthmus during wide area circumferential ablation for atrial fibrillation: feasibility and proof of isthmus block and impact on procedural success and arrhythmia recurrence. Heart Rhythm 2004;1(Suppl 1):S170. 18 Haïssaguerre M, Hocini M, Sanders P, et al. Catheter ablation of long-lasting persistent atrial fibrillation: clinical outcome and mechanisms of subsequent arrhythmias. J Cardiovasc Electrophysiol 2005;16:1138 – 47. 19 Haïssaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long-lasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophysiol 2005;16:1125 –37. 20 Packer DL, Bluhm CM, Monahan KH, et al. Outcome of AF ablation using a wide area circumferential ablative approach: a comparison with lasso-guided ablation. Heart Rhythm 2004;1(Suppl 1): S11. 21 Verma A, Marrouche N, Natale A. Pulmonary vein antrum isolation: intracardiac echocardiography-guided technique. J Cardiovasc Electrophys 2004;15:1335 – 40. 22 Pappone C, Rosanio S, Augello G, et al. Mortality, morbidity, and quality of life after circumferential pulmonary vein ablation for atrial fibrillation: outcomes from a controlled nonrandomized long-term study. J Am Coll Cardiol 2003;42:185 –97. 23 Piorkowski C, Hindricks G, Schreiber D, et al. Electroanatomic reconstruction of the left atrium, PVs, and esophagus compared with the “true anatomy” on multislice computed tomography in patients undergoing catheter ablation of AF. Heart Rhythm 2006;3:317–27. 24 Noseworthy PA, Malchano ZJ, Ahmed J, Holmvang G, Ruskin JN, Reddy VY. The impact of respiration on left atrial and pulmonary venous anatomy: implications for imageguided intervention. Heart Rhythm 2005;2:1173 –8.

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25 Packer DL, Asirvatham S, Seward JB, Breen JF, Robb RA. Imaging of cardiac and thoracic veins. In: Chen SA, Haïssaguerre M, Zipes DP, eds. Thoracic Vein Arrhythmias: Mechanisms and Treatment. Elmsford, NY: Blackwell Futura, 2004: 77–98. 26 Ahmed J, Sohal S, Malchano ZJ, Holmvang G, Ruskin JN, Reddy VY. Three-dimensional analysis of pulmonary venous ostial and antral anatomy: implications for balloon catheterbased PV isolation. J Cardiovasc Electrophysiol 2006;17:251–5. 27 Markides V, Schilling RJ, Ho SY, Chow AW, Davies DW, Peters NS. Characterization of left atrial activation in the intact human heart. Circulation 2003;107:733 –9. 28 Betts TR, Roberts PR, Morgan JM. High-density mapping of left atrial endocardial activation during sinus rhythm in coronary sinus pacing in patients with paroxysmal AF. J Cardiovasc Electrophysiol 2004;15:1111–7. 29 Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardias using high-density mapping. J Am Coll Cardiol 2005;46:2088–99. 30 Takahashi Y, Hocini M, O’Neill MD, et al. Sites of focal atrial activity characterized by endocardial mapping during AF. J Am Coll Cardiol 2006;47:205–12. 31 Saksena S, Skadsberg ND, Rao HB, Filipecki A. Biatrial and three-dimensional mapping of spontaneous atrial arrhythmias in patients with refractory AF. J Cardiovasc Electrophysiol 2005;16:1–11. 32 Scherlag BJ, Nakagawa H, Jackman WM, et al. Electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation. J Interv Card Electrophysiol 2005;13(Suppl 1): 37–42. 33 Nakagawa H, Scherlag B, Lockwood D, et al. Localization of left atrial autonomic ganglionated plexuses using endocardial and epicardial high frequency stimulation in patients with atrial fibrillation. Heart Rhythm 2005;2(Suppl 1): S10.

34 Armour C, Johnson P, Anticevich S, et al. Mediators on human airway smooth muscle. Clin Exp Pharmacol Physiol 1997;24:269 –72. 35 Lemery R, Birnie D, Tang AS, Green M, Gollob M. Feasibility study of endocardial mapping of ganglionated plexuses during catheter ablation of atrial fibrillation. Heart Rhythm 2006;3:387– 96. 36 Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044 –53. 37 Takahashi Y, Sanders P, Jais P, et al. Organization of frequency spectra of atrial fibrillation: relevance to radiofrequency catheter ablation. J Cardiovasc Electrophysiol 2006;17:382– 8. 38 Tops LF, Bax JJ, Zeppenfeld K, et al. Fusion of multislice computed tomography imaging with three-dimensional electroanatomic mapping to guide radiofrequency catheter ablation procedures. Heart Rhythm 2005;2:1076 – 81. 39 Dong J, Dickfeld T, Dalal D, et al. Initial experience in the use of integrated electroanatomic mapping with three-dimensional MR/CT images to guide catheter ablation of AF. J Cardiovasc Electrophysiol 2006;17:459 – 66. 40 Dong J, Dickfeld T, Lamiy SZ, Calkins H. Catheter ablation of AF guided by registered computed tomographic image of the atrium. Heart Rhythm 2005;2:1021–2. 41 Kistler PM, Earley MJ, Harris S, et al. Validation of threedimensional cardiac imaging integration: use of integrated CT image into electroanatomic mapping system to perform catheter ablation of AF. J Cardiovasc Electrophysiol 2006;17: 341– 8. 42 Packer DL, Bunch TJ, Johnson SB, Mahapatra S, Altmann AC, Govari A. Multimodality 3-D ultrasound and computedtomographic image fusion: a novel basis for catheter navigation and electroanatomic mapping. Circulation 2005;112: II-622.

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Utility of intracardiac echocardiography in cardiac electrophysiology Douglas L. Packer

Introduction Over the past three decades, the understanding of fundamental cardiac electrophysiology in the genesis and maintenance of cardiac arrhythmias has expanded substantially. Information obtained with surface electrocardiography (ECG) has now been supplemented with extensive data from multichannel intracardiac recordings and three-dimensional cardiac mapping systems. These technologies have helped clarify the factors critical to the occurrence of automatic, triggered, and reentrant atrial and ventricular arrhythmias. This basic physiological understanding has been coupled with increasingly detailed clinical data providing insight into the epidemiology, pathophysiology, manifestations, and outcomes of a wide variety of arrhythmias. The resulting insights have in turn contributed to improved pharmacological and nonpharmacological treatment strategies.

Linking fundamental physiology and anatomy A more complete understanding of arrhythmogenesis has been facilitated by improved insight into the specific anatomy underlying arrhythmias. For example, images generated by fluoroscopy in the electrophysiology laboratory provide the anatomic underpinnings for left-bundle, inferior axis ventricular tachycardias arising within the right ventricular outflow tract [1– 4]. This union of electrophysiology and anatomy allows more precise differentiation between septal and free-wall origins of outflow tract ventricular tachycardia (VT), as manifested by the specific QRS morphologies seen on individual ECG leads [1–4]. Right-bundle, left-axis deviation tachycardias have similarly been localized to a very specific anatomic region in the posterior interventricular septum. A variety of studies have mapped their point of origin to the posterior aspect 72

of the septum, typically two-thirds of the distance from the base to the apex [5–7]. Additional imaging using transesophageal echocardiography has suggested an additional relationship between this arrhythmia and a false tendon anchoring in the septum [8]. In more recent studies, specific characteristics of the QRS complex in left bundle-branch block tachycardias have also made it possible to localize other arrhythmias to a region in the aortic cusp (Fig. 6.1) or above the pulmonary valve [9,10]. Companion studies in patients with previous inferior wall infarction have clarified the role of the submitral valve isthmus of infarct-spared tissue in the genesis of mitral isthmus–dependent ventricular tachycardia [11]. The appearance of a left-bundle, left-axis or right-bundle, right-axis QRS morphology on the surface ECG in this setting now has a specific anatomic connotation for the site of origin of the VT. Similarly, correlation studies based on the QRS morphology during ventricular tachycardia have made it possible to provide a reasonable first estimate of the specific anatomic origin of the arrhythmia in the context of other infarct locations [12,13]. In parallel, the role of anatomy in the expression of atrial arrhythmias has been increasingly appreciated. Over the last 15 years, the role of the cavotricuspid isthmus in generating typical atrial flutter has been establishedaso much so that the arrhythmia is now referred to as “isthmusdependent” atrial flutter. This anatomic location is suggested by the negative P waves (classically saw-toothed) in ECG leads II, III, and aVF. In contrast, P waves that are negative in ECG lead aVL have been more typically localized to the left atrium [14]. Still other studies have localized the many atrial tachycardias to the crista terminalis region of the posterolateral right atrium (RA). Because of its contribution to arrhythmogenesis, this specialized anatomic region has been referred to as the “ring of fire” [15]. A more compelling coupling of physiology and anatomy has arisen from the observation that the triggers responsible for the initiation of atrial fibrillation arise

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Figure 6.1 Cross-sectional short-axis images of the left atrium and aortic root as imaged from below the tricuspid annulus with the catheter directed toward the outflow tract. In A, the three cusps of the aortic valve (arrows) are open, but they are closed in panel B. The anterior-to-posterior projection of the left atrium (LA) is evident, extending from the transverse sinus behind the aortic valve to the posterior wall of the left atrium. The appendage is

likewise seen, although, obscured by a midline ultrasound noise line. In B, the left atrium is more widely evident, as is the left superior pulmonary vein (arrow head), as is the left atrial appendage (LAA). There is no evident thrombus within this view of the left atrial appendage. The right ventricular outflow tract extension to the pulmonary valve (PV) and pulmonary artery (PA) is also shown (arrows).

within the pulmonary veins. The success of pulmonary vein isolation alone [16 –18] provides the ultimate proof required to establish this electroanatomical relationship. In many patients, this anatomically based trigger also has a prominent role in maintaining atrial fibrillation. Mapping of arrhythmias to the vein of Marshall, coronary sinus, or superior vena cava [19 –22] has also received renewed interest.

better understanding of the physiology of ablation had to await the development of alternative imaging approaches.

Anatomic imaging in electrophysiology Given each of these critical links, it is not surprising that there has been rapidly growing interest in visualizing the anatomy underlying arrhythmogenesis. During the first 20 years of the history of clinical cardiac electrophysiology, anatomic imaging was limited to what was possible with fluoroscopy. This approach provided reasonable visualization of the cardiac silhouette, but grasping the three-dimensional context of cardiac arrhythmias was only possible by comparing the two-dimensional images from single planes. While the external borders of the heart can be visualized, the location of specific internal cardiac structures, including the endocardial surface, can only be inferred from the available surface contours. Imaging of a specific catheter and its contact with the subendocardial surface, as well as imaging during therapeutic interventions, were simply not possible. For example, it was difficult with fluoroscopy to visualize the crista terminalis and identify the specific location of Bachmann’s bundle. A

Transesophageal echocardiography Echocardiography has developed into a valuable tool for clarifying the specific anatomic structures involved in arrhythmogenesis. The first foray into ultrasound imaging was in patients with atrial fibrillation. The value of transesophageal echocardiography (TEE) in chronicling the occurrence of atrial enlargement and thrombus formation in patients with this type of arrhythmia has been extensively documented. In addition, TEE images more clearly defined the relationship between successful ablation sites for accessory pathway–mediated arrhythmia and the mitral or tricuspid valve annulus [23–25] (Fig. 6.2). Early studies also showed a facilitating role for transesophageal echocardiography in the ablation of ventricular tachycardia [25,26]. These studies were nevertheless limited to the examination of relatively few patients. While the images generated in this way opened up a new vista for cardiac electrophysiologists, the use of prolonged esophageal intubation was problematic due to patient discomfort, the risk of aspiration pneumonia, and the requirement for a second operator skilled in the art of echocardiography. TEE-based contraction analysis was also used to identify the pathway of origin of arrhythmia in patients with Wolff–Parkinson–White syndrome. Kuecherer et al. [27,28] 73

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Figure 6.2 Long-axis view of the left ventricle (LV) as imaged from the right ventricular outflow tract. Shown are the LV posterior wall and the parietal pericardium (arrows). The posterior (PPM) and anterior (APM) papillary muscles are seen individually, along with the chordae support of the mitral valve. A candidate annular site for a left posterior accessory pathway underneath the mitral valve leaflets is shown by the bold arrow.

were able to localize accessory pathways using TEE, provided that sufficient preexcitation was present to shift mechanical activation from the more typical inward systolic endocardial motion seen with activation of the interventricular septum to an eccentric pathway location. In contrast, with adenosine administration and the resulting increase in preexcitation, these investigators documented a shift in the site of earliest activation to the pathway location. With the enhancement of preexcitation, this type of alteration in the mechanical activation sequence was seen in the form of paradoxical motion at the preexcited area, with accompanying changes in phase angles.

Figure 6.3 Single element cross sectional intracardiac ultrasound image of the left (LA) and right (RA) atria. This image is obtained at the level of the membranous fossa (arrow).

Intracardiac echocardiography

crista terminalis [31], the eustachian ridge [32,33], and the tricuspid annulus [32,33] in both humans [31–36] and animals [37–39]. However, this approach was limited by poor tissue penetration [40] and difficulty in visualizing far-field structures. In addition, due to the short axis and cross-sectional images generated, it is difficult to distinguish between several different catheters within a single cardiac chamber. The steering capability of these catheters was also inadequate for improving the imaging of specific targets.

Intracardiac mechanical single-element imaging

Phased-array imaging

The use of echocardiography in electrophysiology was substantially advanced by the development of mechanical, single-element ultrasound devices capable of being introduced via 6–10-French catheters. The earliest catheterbased approaches imaged at frequencies of 10–30 MHz during ultrarapid 360° element rotation using a single crystal embedded in the catheter tip. The resulting highfrequency 360° images have a high resolution, with excellent near-field visualization of the right atrium and other vascular structures. Context is provided for the images by the visualization of other components of a given chamber around the catheter tip (Fig. 6.3). Early studies also demonstrated the usefulness of this imaging format for visualizing the fossa ovalis [29,30], the

Miniaturization of the imaging stacks to a diameter of 10 French made it possible to apply phased-array systems via catheters positioned within the heart. With this approach, 64–128 elements are used to produce a forward-viewing, 60–90° sector of echocardiographic visualization, in a plane longitudinal to both the catheters and the cardiac chambers. Although ultrasound frequencies of 2–5 MHz have been commonly used for transthoracic and transesophageal imaging, frequencies of 5.5 –10.0 MHz are more often used in intracardiac imaging systems [41]. Images of 7.5–8.5 MHz are optimal for acquiring far-field images (Fig. 6.4), including images of the left atrium, pulmonary veins, and left ventricle from the right atrium [41]. The pericardium, mitral and aortic valves, the coronary

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Figure 6.4 2-D phased-array image of the right heart with catheter tip positioned in the right atrium (RA). The tricuspid valve (TV) is seen with coapted leaflets and minor degree of concentric regurgitation (arrow). The cavotricuspid isthmus (Is) is seen posteriorly (along with the Eustachian ridge EuR) before falling off into the IVC. Also seen is tribeculation within the apex of the right ventricle (RV). The outflow tract (RVO) is clearly seen wrapping around the aortic root (Ao).

sinus, and to a lesser degree the proximal epicardial coronary arteries are also well seen. This technology has also allowed spectral Doppler-based imaging, including color flow, pulsed-wave and continuous-wave Doppler, and tissue velocity and acceleration imaging. With phased-array imaging, context is provided for the image within the heart by visualization of the surrounding structures in the forward-viewing image and of those to the left or right of targeted structures, obtained with minimal clockwise or counterclockwise rotation of the catheter.

Intracardiac imaging venues During electrophysiology studies, the most convenient imaging venue is from within the right atrium. Directing the catheter anteriorly, with or without flexion of the imaging tip, from a position immediately above the junction of the inferior vena cava (IVC) and right atrium allows excellent imaging of the tricuspid valve (Fig. 6.4), the pectinate muscles entering the cavotricuspid isthmus, and the coronary sinus. The support apparatus of the tricuspid valve within the right ventricle is also best viewed from this angle. This is also a useful image plane during intrapericardial access for mapping purposes [42,43]. Further advancement of the catheter into the right atrium allows clear visualization of the junction between the superior vena cava (SVC) and right atrium, the region of the anterior crista terminalis or precaval bundle, the crista terminalis proper, and the pectinate muscles that arise from it (Fig. 6.5) [41].

Figure 6.5 Intra-right atrial (RA) view of the anterior cristal (AC) band, giving rise to well-delineated pectinate muscles (arrows) with alternating ridges and valleys.

The left atrial structures are usually visible with the catheter positioned approximately one-third of the distance between the IVC/RA and SVC/RA junctions. This circumvents the need for transseptal catheterization solely for imaging purposes. Beginning with the image vector directed anteriorly, the right ventricle and tricuspid valve are seen. With progressive clockwise rotation, the aortic valve comes into view, followed by the mitral annulus and associated valve support apparatus. Further clockwise rotation from a right femoral vein insertion site allows visualization of the left atrial appendage. It should be noted, however, that this imaging view is inadequate for detecting thrombus. A better view of the left atrial appendage can be obtained from a region immediately below the tricuspid annulus, with the catheter advanced toward the right ventricular outflow tract. Further rotation of the catheter within the RA allows imaging of the left superior and subsequently the left inferior pulmonary veins (Fig. 6.6) [41]. Occasionally, the head of the imaging catheter has to be tilted to one side or the other, or flexed or extended to match the image plane with that of the veins and to see around the transseptal sheaths. The right inferior pulmonary vein emerges with further clockwise rotation. Occasionally, the catheter has to be advanced further into the right atrium and tipped backward (or anteriorly) to see this vessel in a long-axis view (Fig. 6.7). More consistently, further rotation shows the “owl’s eyes” (Fig. 6.8) of the right superior and right inferior pulmonary veins as viewed en face to the orifice [41]. It should be noted that with imaging of both the left-sided and right-sided veins, it is important to visualize the carina between the inferior margin of the superior veins and the superior margin of the inferior veins. This establishes 75

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Figure 6.6 An ultrasound image of the left atrium (LA) and the left superior (LS) and inferior (LI) pulmonary veins obtained from within the right atrium at the mid-region between SVC and IVC. The circumference of the left atrium is clearly delineated. The left superior and the left inferior pulmonary vein join to form a very short-neck antrum (double arrowheads) before joining with the left atrium proper. [4]

Figure 6.8 Imaging from within the right atrium across the interatrial septum to display the right superior (RS) and inferior (RI) pulmonary vein orifices en face showing the “owl’s eyes.” The right pulmonary artery (RPA) is seen immediately adjacent to the RS pulmonary vein. This image was obtained with the ICE catheter tip positioned low in the right atrium, from which the long-axis view of the right veins is more difficult to obtain. [41]

Figure 6.7 Ultrasound image of the medial left atrium (LA) and a longaxis view of the right inferior (RI) pulmonary vein. This image was obtained within the LA, hence the absence of the interatrial septum at the top of the imaging. Also seen is the left atrial tissue running down into the RI pulmonary vein. The vein orifice at that site (plus signs) measured 18.9 mm.

Figure 6.9 Long-axis, superior-to-inferior view of the left atrium (LA) and esophagus with an ultrasound beam originating in the right atrium. The smooth posterior wall of the LA (arrows) is noted. Of greater interest, however, is the visualization of the esophagus (dark stripe) with an internal temperature probe (light stripe) running right to left immediately posterior to the LA. The descending aorta (DAo) is also seen behind the LA.

at least one point on the plane of the vessel orifice that is useful in the ablative approach to atrial fibrillation (AF). Further rotation provides a long-axis view of the right superior pulmonary vein, along with its branches. With this imaging scan from the left to the right pulmonary veins, the esophagus can also be visualized as it runs along the posterior wall of the left atrium [44] (Fig. 6.9). Further advancement of the catheter immediately across the tricuspid valve toward the right ventricular 76

outflow tract, which can be done without fluoroscopy, is useful for alternative high-resolution imaging of left-heart structures. The position of the catheter in this process is very similar to that of a His bundle catheter positioned to record electrograms from the atrioventricular (AV) conduction system. Advancement of the catheter tip further into the outflow tract provides a better image of the

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left superior pulmonary vein and the left atrial appendage, along with the “Q-tip” ridge between these two structures, is easily imaged. This is also a more reliable view for examination of the left atrial appendage than from the RA. Further rotation provides the best view of the aortic root and right and left coronary valve cusps, along with the left main coronary artery (Fig. 6.13). Usually, the point of bifurcation between the left anterior descending and circumflex arteries can be visualized with imaging from this venue. Color flow and pulsed-wave Doppler imaging is possible anywhere along these rotational planes, showing detailed pulmonary vein physiology (Fig. 6.14).

Figure 6.10 View of the right ventricular outflow tract (RVO). The pulmonary leaflets (arrows) are present as shown. Color flow imaging shows the presence of minor pulmonary insufficiency (orange jet) back into the outflow tract.

pulmonary valve and right ventricular outflow tract, as the vector stack is rotated superiorly (Fig. 6.10). Further rotation from an anterior location in a clockwise direction first brings the interventricular septum into view, with clear visualization of the fiber orientation along the septum. Subsequent rotation visualizes the posterior aspect of the left ventricle, the papillary muscles, and subsequently the mitral valve (Fig. 6.11). Additional rotation from that point provides an anteroposterior view of the left atrium and the aortic root (Fig. 6.12) [41]. The

Figure 6.11 Long-axis view of the left ventricle (LV) obtained from within the right ventricle by directing the catheter underneath the tricuspid valve and toward the right ventricular outflow tract. Seen are the papillary muscles (PM), the chordae support apparatus and the anterior and posterior cusps of the mitral valve. A small region of concentric regurgitation is noted (arrow), as is the posterior pericardial effusion (PE) immediately below the posterior papillary muscle. [41]

Figure 6.12 Short-axis view of the aortic root (Ao) and left atrium (LA) obtained from beneath the tricuspid valve. Also shown is the left atrial appendage (LAA) separated from the left superior (LS) pulmonary vein by the “Q-tip” ridge or crest (arrow).

Figure 6.13 An additional short-axis image of the aortic root (Ao) and cusps in a closed position. The left main coronary artery is also seen in this image (arrow). With rotation of the ICE catheter, the bifurcation of the left main to form the circumflex and anterior descending coronary arteries is usually seen.

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Figure 6.14 Left pulmonary veins under color flow examination. Turbulent flow is arising from the left superior (LS) pulmonary vein with normal blood flow in the left inferior (LI) vein. The descending aorta (DAo) is seen immediately adjacent to the orifice of the left inferior pulmonary vein.

Figure 6.15 Ultrasound-guided transseptal catheterization. This image obtained from the right atrium (RA) shows the left atrium (LA) and the interatrial septum (arrows). A Brockenbrough needle (arrowheads) is advanced through a dilator and produces marked tenting of the membranous fossa. [48]

Image-guided catheter manipulation More importantly, intracardiac ultrasound is useful in positioning specific catheters for use during mapping and ablation [45 – 48]. One such application is for transseptal catheterization for accessing left atrial ablation sites [48]. During imaging from a right atrial venue, the specific point of contact of the transseptal dilator tip with cardiac structures can be followed from the SVC/RA junction across the superior limbic ridge, to the membranous fossa target, which appears in a superior-to-inferior projection. When it is appropriately positioned, tenting of the fossa membrane is observed. The introduction of the Brockenbrough needle across the septum is manifested by the abrupt appearance of turbulent, high-pressure saline flow from the needle tip within the left atrium, and by the release of the tenting of the fossa membrane produced by tip contact (Fig. 6.15) [41]. With experience, this approach can also be used safely before or after the administration of heparin. The role of transseptal catheterization under ultrasound guidance has been documented by a number of investigators [29,30,48–51]. Intracardiac ultrasound imaging further establishes the relationship between the specific catheter tip and underlying tissue. Both contact and orientation at any target can be monitored in real time (Fig. 6.16). Intracardiac echocardiography (ICE)-guided catheter positioning of this type is also highly accurate as judged by validation studies performed in vivo. Ultrasound also accurately demonstrates catheter tip–tissue contact, which is not clearly detected with fluoroscopy [52]. A comparison of ICE and fluoroscopic guidance of catheter placement by Hanaoka et al. [53] demonstrated better radiofrequency ablative lesion 78

Figure 6.16 Imaging of the mitral valve annulus during radiofrequency ablation. The image is obtained from within the right atrium (RA) across the septum into the left atrium (LA). The catheter tip (white arrows) is positioned against the mitral valve annulus. Acoustical shadowing from the tip (black arrows) is also present. This image shows an oblique catheter tip/tissue orientation.

formation in ICE-guided ablations, as manifested by the postablation tissue pathology. This guidance method led to a higher percentage of successful applications and a higher mean temperature. Chan et al. [54] also used ICE to target specific sites, which were marked by the creation of ablative lesions. At evaluation on pathology, 28 of 38 lesions fell within 0.2 mm of the target center and 33 of 38 within 2 mm of the target.

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Imaging to guide energy titration This imaging modality has been proposed as an alternative means of assessing the effect of energy delivery. Classically, energy delivery has been guided by cathetertip thermometry. This may be inaccurate, however, with ablation using large-tipped or irrigation-tip catheters [55,56]. Echocardiographic tissue changes and microbubble formation may be observed with energy delivery, although the extent of the tissue change varies. However, discrete lesions with sharply demarcated borders are seen in fewer energy deliveries [38,48,54,57]. Excellent correlation between echocardiographic and histological lesion depths has also been documented [38,54,57,58]. There is a poorer correlation between echocardiography and histology in relation to the width of lesions. This is not surprising, since accurate width assessment has to be made echocardiographically from the same plane as that used in tissue analysis. This requires some practice and tenacity. However, using an in vitro model of ablation, Kalman et al. [38] demonstrated improved correlation with additional experience in judging the borders of the lesion. The exact determinants of such discrete lesion appearances have not been established, although the tissue location, power level, and occurrence of an impedance rise are likely contributors.

Figure 6.17 Dense microbubble formation during radiofrequency energy application. Reproduced from [63] with permission.

ICE microbubble imaging An unexpected finding in early transesophageal echocardiographic imaging during ablation of accessory pathways was the occurrence of showers of microbubbles and tissue disruption [22,59]. While the more aggressive appearance of dense microbubbles was subsequently identified as an echocardiographic manifestation of catheter tip–tissue interface superheating (Fig. 6.17) [48], the occurrence of more gentle microbubbles was seen as an indication of underlying tissue heating. Chu et al. [35] noted microbubble formation in up to 61% of energy deliveries. In an in vitro study, Saxon et al. noted the occurrence of microbubble formation beginning with tip temperatures > 65 °Cafindings remarkably similar to those observed by Haines [61] in an in vitro preparation. Asirvatham and co-workers [62] first suggested that microbubbles might be a better indicator of tissue heating and resulting lesion formation than catheter-tip temperature monitoring. In the early studies, atrial tissue lesion depth, volume, and overall tissue penetration were better predicted by microbubble formation and tissue changes than was possible with thermography (Fig. 6.18). Subsequently, others have used microbubbles as a means of titrating energy delivery [63 – 65]. Clinical studies have shown better results with this intracardiac echocardiographic approach for guiding ablation than were possible with classic empirical methods [63,64,66–68].

Figure 6.18 Comparison of ultrasound versus temperature feedback to guide radiofrequency ablation of the atrium. Shown are the percentage of complete trans-mural lesions, lesion volumes, and occurrence of catheter tip coagulum formation with 31 temperature guided and 111 ICE guided energy deliveries.

Nevertheless, microbubble generation is not a sensitive finding of ablation. Bruce et al. [56] established a relationship between microbubble occurrence and actual tissue heating during ablation at the pulmonary vein orifice, using a closed-loop irrigation catheter. With increasing power, catheter-tip temperatures plateaued at 36 –39 °C, while tissue temperature increased to a mean of 75 ± 3 °C at 45 W and a maximum temperature of > 100 °C. Of 72 energy deliveries carried out during power titration, 45 (63%) were accompanied by type I microbubbles (gentle), 79

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while type II microbubbles (vigorous) occurred in 19 of the ablations (26%). Type I and II microbubble formation occurred at similar powers, while catheter-tip and tissue temperatures were discrepant during energy delivery, with lower temperatures seen at the occurrence of type I than of type II microbubbles. Of relevance to the issue of the sensitivity of these phenomena, no microbubbles were seen in 19 of the ablations (26%), despite powers of up to 26 ± 9 W and tissue temperatures up to 81 ± 17 °C. Therefore, neither the absence of microbubbles nor the presence of type I microbubble formation ensures that there is no excessive tissue heating. These data suggest that the appearance of microbubbles should be viewed as a sign of excessive tissue heating, prompting a reduction and/or discontinuation of energy delivery.

Ablative lesion assessment Real-time intracardiac ultrasound detection and monitoring of the creation of radiofrequency (RF) lesions may also be useful in guiding ablation, although the sensitivity, specificity, and positive predictive value (PPV) of this method for assessing lesion formation and transmural depth have been incompletely studied. Up to 70–80% of lesions created in the ventricular myocardium may be visible. The yield in atrial tissue is poorer, ranging between 30% and 50%. This has prompted the use of alternative imaging approaches to highlight the lesions (Fig. 6.19). To characterize these techniques statistically, RomanGonzales et al. [69] analyzed lesion generation and development using standard two-dimensional gray-scale imaging, Doppler tissue velocity (DTV) imaging, Doppler

Figure 6.19 Left ventricular lesion formation with absent uptake of echo contrast. Significant microvascular destruction is observed in the left panel where there is a negative contrast view (arrow) without echo contrast uptake. This matches nearly completely the gross pathology seen on sectioning of the left ventricle.

80

tissue acceleration (DTA) imaging, and Doppler tissue energy (DTE) imaging. The predictive value for lesion formation and transmural depth was assessed using each modality. Fifty-nine lesions (95%) seen at autopsy were 14.4 ± 5.7 mm long, 10.9 ± 3.1 mm wide, and 10.3 ± 3.1 mm deep, with a volume of 985 ± 865 mm3. Harmonic imaging was most sensitive for detecting an ablative lesion (80%), which was followed by DTE (77%) and gray-scale examination (76%). The highest specificity values were also seen with harmonic imaging (100%) and echo contrast (100%) imaging, followed by gray-scale visualization (50%). All of the above modalities had positive predictive values of 96–100% and negative predictive values of 0 –20%. For prediction of transmural depth, the following imaging modalities had the highest sensitivity: gray scale (50%), harmonic (50%), and DTE (37%), with specificities of 91%, 94%, and 92%, respectively. A reduction of the intracardiac electrogram by > 80% had a sensitivity of 10% and a specificity of 100% for the prediction of lesion formation. The same modalities had a sensitivity of 25% and a specificity of 92% for the prediction of transmural depth. ICE imaging was therefore more sensitive and equally specific for predicting lesion formation and transmural depth than local changes in the electrogram. This superiority of ICE over the conventional approach should be of value for accurate energy delivery and monitoring of RF lesions. This is particularly important with linear ablation.

Ablation of atrial arrhythmias The first use of intracardiac ultrasound in cardiac electrophysiology was for facilitating the ablation of atrial arrhythmias. In the process, additional mechanisms underlying the arrhythmias emerged. Olgin et al. [32] used singlecrystal mechanical ultrasound to clarify the role of the anatomy underlying atrial flutter. The authors definitively demonstrated the specific role of the cavotricuspid isthmus as a mandatory component of the reentrant circuit. Furthermore, using anatomic sites chosen by ultrasound examination, they demonstrated an extended line of function block in the posterolateral wall of the right atrium, corresponding to the crista terminalis. In a companion article, Kalman et al. [33] further clarified the role of these additional structures. The value of intracardiac ultrasound for guiding ablation of the sinus node has likewise been demonstrated in several studies. This has been predicated on histological studies showing that the sinus node is at the upper end of the crista terminalis, with extension along the anterior cristal band at the SVC/RA junction. Kalman et al. guided sinus-node elimination through ICE-guided ablation [70]. A 31% decrease in the intrinsic heart rate was achieved in animal models by initially targeting the superior aspect

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Table 6.1 Pulmonary vein ostial dimensions in patients with paroxysmal atrial fibrillation. First author (ref.)

Technique

Patients (n)

RSPV

RIPV

LSPV

LIPV

RMPV

LCA

Packer [103] Tsao [104] Scharf [105] Kato [106] Schwartzman [75] Wittkampf [107] Martin [64]

CT MRI CT MRI CT MRI ICE

40 24 58 28 70 42 16

20 ± 9 18.0 ± 4.4 19 ± 4 18.0 ± 2.8 22 ± 5 18.8 ± 2.7 15.6 ± 2.0

25 ± 12 12.7 ± 2.5 16 ± 4 18.5 ± 3.0 20 ± 4 17.9 ± 2.9 15.0 ± 2.8

23 ± 9 15.6 ± 2.9 19.5 ± 3.0 18.5 ± 2.7 20 ± 4 18.7 ± 2.9 14.0 ± 2.1

22 ± 7 10.8 ± 3.1 17 ± 3 18.0 ± 2.4 18 ± 3 15.9 ± 3.1 16.2 ± 0.8

– –

– – 32.5 ± 0.59 – 30 ± 3 27.3 ± 6.2 25.0 ± 2.9

9.9 ± 1.9 – 10 ± 3 7.6 ± 3.1 –

CT, computed tomography; ICE, intracardiac echocardiography; LCA, left common antrum; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MRI, magnetic resonance imaging; RIPV, right inferior pulmonary vein; RMPV, right middle pulmonary vein; RSPV, right superior pulmonary vein. (From imaging of cardiac and thoracic veins) [74].

of the crista terminalis, with additional energy delivery further inferior along this structure. Lee et al. reported similar results in patients with inappropriate sinus tachycardia [71]. Again, the superior aspect of the crista terminalis was targeted during isoproterenol infusion. It should be noted, however, that ablation of the anterior cristal ridge as well as up to 4 – 5 cm of the crista terminalis was required in order to eliminate the sinus arrhythmia [40]. We have used intracardiac ultrasound to identify this cristal ridge as a target for the ablation of sinus tachycardia in conjunction with noncontact mapping. Using ICE, other groups have documented the importance of additional right atrial structures in contributing to arrhythmias. Friedman and co-workers [72] identified a line of double potentials in the posteromedial aspect of the right atrium, also serving as a turn-around site in the reentry of classical atrial flutter. This site was 1–2 cm away from the crista terminalis, as established by intracardiac ultrasound examination. These findings were consistent with a second crista or interdigitating right and left atrial fibers [73]. The maximum short-axis diameter may also be important in the occurrence of transverse conduction block during classical atrial flutter. The role of the crista terminalis as a site of origin of atrial tachycardias has also been established [31].

Ablation of atrial fibrillation Intracardiac ultrasound has been used most extensively for guiding the ablation of atrial fibrillation. The original studies by Haïssaguerre et al. [17] and others [18,19] demonstrating the preeminence of the pulmonary veins as a site of triggers for atrial fibrillation provides the context for anatomy-guided interventions. A number of studies have established the number and location of the pulmonary veins and confirmed the presence of an antrum formed by the left superior and inferior pulmonary veins in 15 –30% of patients [74]. This region has

been identified as a consistent source of arrhythmogenic atrial ectopy in many AF patients [75]. In contrast, the occurrence of a separate right middle pulmonary vein, with an orifice independent of either the right superior or right inferior pulmonary vein, is significantly less common and of less arrhythmogenic importance. Ultrasound imaging also provides quantitative information about the pulmonary veins. Table 6.1 shows the diameters of each pulmonary vein seen with ICE examination and similar information with computed tomography (CT) and magnetic resonance imaging (MRI) [74]. Monahan and co-workers [76] demonstrated a good correlation between intracardiac ultrasound and CT pulmonary vein diameters, a finding also confirmed by Wood et al. [77]. It should be noted, however, that since ultrasound generates a two-dimensional image, any correlation between intracardiac ultrasound and CT or MRI examinations has to be considered in the context of the imaging planes used and the portion of the pulmonary veins imaged. For example, an ultrasound examination of the left superior pulmonary vein from beneath the tricuspid valve yields an anterior-to-posterior projection. The coronal and sagittal images in CT studies provide a superior-to-inferior dimension, as seen with the ICE catheter positioned in the RA. Misaligned imaging would be expected to provide discrepant information. The size of the pulmonary veins also undoubtedly changes throughout the respiratory phase and the atrial cycle. Pulmonary veins in patients with chronic atrial fibrillation may also be larger in diameter than in patients without any arrhythmia abnormality [78], while there may be no clear difference in pulmonary vein size between patients with and without paroxysmal atrial fibrillation. Similar findings have been demonstrated on CT evaluation (Table 6.1), although these findings have been less consistent. There is also a good correlation between the constituent layers of the pulmonary vein wall seen on ultrasound 81

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imaging and those seen on direct examination of the underlying anatomic structures. Cabrera et al. [79] examined 32 pulmonary veins from eight patients who had died of noncardiac causes. Mechanical ultrasound (3.2 Fr, 30 MHz) was used to create images of the venous architecture. An inner echogenic layer seen on ultrasound was found to correlate with both the endothelium and the connective tissue of the media. The maximum thickness was 1.4 ± 0.3 mm. A middle hypoechoic region corresponded with the sleeves of left atrial myocardium surrounding the external aspect of the venous media. This layer was found to be the thickest at 2.6 ± 0.8 mm. An outer echo-dense layer with a mean thickness of 2.2 ± 0.4 mm corresponded to fibrofatty adventitial tissue. Most importantly, ultrasound has provided a straightforward means of locating the precise venoatrial junction. Because of the shape of the veins, establishing the precise orifice of the left and right inferior pulmonary veins is a straightforward process. The assessment of the superior veins, which are more conical at their orifice, is more challenging. Establishing the orifice of these veins, however, is facilitated by visualizing the carina between the superior and inferior veins. This tethering point clearly demarcates one side of the true orifice, while the opposite side of the orifice can be located with additional catheter angulation. This approach is significantly more accurate than is possible with contrast venography [77,79]. Arruda et al. [80] demonstrated that the true orifice of the vein was 5– 10 mm away from the apparent orifice suggested by venography. This allows better positioning of the guidance and ablation catheters used in the ablation process. Lasso catheters, used to mark the anatomic perimeter of pulmonary veins during isolation, have a tendency to drift into the pulmonary vein [81], creating a false indication of the true orifice of the vessel on fluoroscopy (Fig. 6.20). The resulting ablation based on this erroneous information may be too far into the vein and may increase the risk of pulmonary vein stenosis and reduce the efficacy of AF ablation [11]. Intracardiac ultrasound guidance may be even more useful in the positioning of balloon catheters for isolation of pulmonary veins. Several groups have demonstrated improved efficacy of ablation with such guidance. Asirvatham [82] showed that leaks around the pulmonary vein balloon correlated with acute isolation failure in vivo. Similarly, Sarabanda et al. [83] showed improved acute pulmonary vein isolation rates with cryoballoon ablation at the orifice of the pulmonary vein, as guided by intracardiac ultrasound. A success rate of 82% for creating an entrance block was seen in cases in which pulmonary vein flow had been completely occluded by the cryoballoon, but in only 10% of those in which a persistent blood flow lead was seen [83]. Other studies have identified specific ICE targets for other atrial structures, such as the vein of Marshall, relev82

Figure 6.20 Left inferior pulmonary vein (LI) with branches extending both superiorly (lingular) and inferiorly (inferior lobe). A lasso catheter (asterisks) can be seen at the bifurcation of that vein. An ablation catheter (arrows) has also been positioned down to the lasso. Ablation here, within the LI, could result in a higher risk of pulmonary vein stenosis and lower AF ablation success.

ant in the ablation of atrial fibrillation. Asirvatham et al. [47] demonstrated a consistent relationship between the “Q-tip” ridge (Fig. 6.12) between the LA appendage and the left superior pulmonary vein seen on ICE and the vein or ligament of Marshall. On pathology studies, this relationship was seen in over 95% of cases. We have used this as a specific vein of Marshall target for energy delivery from an endocardial approach, making ablation of this structure within the coronary sinus system unnecessary in many cases. Again, this image is best seen with the ultrasound catheter advanced beneath the tricuspid valve in a direction pointing toward the RV outflow tract. Since the catheter tip in the optimal imaging position is quite close to the tricuspid annulus, the imaging venue can be lost if the catheter flips back across the tricuspid valve into the right atrium. Recent data have identified a role for ICE guidance of linear ablation [39,64,84,85]. In this case, ultrasound in the clinical arena helps identify irregularities in the surface across the length of an ablation, beginning with the mitral valve annulus and continuing across the lateral LA isthmus to the pulmonary vein orifice. Roithinger et al. [85] showed that long linear lesions could be safely and effectively created in the canine left atrium using a deflectable-tip multipolar-electrode catheter. Intracardiac echocardiography was superior to fluoroscopy with respect to the actual number of lesion-generating coil electrodes visualized, as well as lesion continuity. This imaging modality was 85% sensitive and 54% specific in predicting lesions created by individual multipolar electrode coils.

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Each of these factors translates into an increase in the efficacy of AF ablation [66,68 –70]. This overall benefit comes in part from the appropriate positioning of guide catheters, as well as ensuring that ablation is well outside the venoatrial junction. The observation of appropriate tissue contact with the catheter may also be useful. Similar findings were reported by Olgin et al. [39], who used ICE guidance to position a multiple-coil array catheter and create linear lesionsafirstly, from the crista terminalis to the tricuspid annulus; secondly, from the fossa ovalis to the crista terminalis; and thirdly, from the inferior vena cava to the tricuspid annulus, with tissue heating up to 65 ± 4 °C at a power of 21 ± 10 W. Epicardial mapping 2 weeks later demonstrated complete conduction block in all animals, with split potentials and disparate activation times of up to 64 ± 16 ms across the lesions. The lesions were within 0.3 ± 0.5 mm of their targeted anatomic locations. Spectral Doppler imaging may also be useful in predicting the recurrence of atrial fibrillation after pulmonary vein isolation. Verma et al. [86] compared Doppler surrogates of LA function immediately after pulmonary vein isolation in patients with or without an AF recurrence. Patients with AF recurrences at 6 months had a significantly lower left atrial appendage peak emptying velocity (19 ± 10 cm/s versus 29 ± 11 cm/s) and lower peak pulmonary vein systolic wave velocities (36 ± 17 cm/s versus 46 ± 22 cm/s) than patients without recurrences. This analysis of atrial function is undoubtedly related to the underlying tissue integrity, but may provide a useful means of identifying patients requiring ongoing drug therapy or closer surveillance after ablation.

Ultrasound imaging in ventricular tachycardia patients Idiopathic VT ablation Intracardiac ultrasound has been less commonly applied in the ablative approach to patients with ventricular tachycardia. VTs occurring in patients with no underlying heart disease most commonly arise from the posterior interventricular septum [5 –7], the right ventricular outflow tract [1– 4], or from the aortic root and cusps [9,10]. In each of these cases, intracardiac ultrasound provides excellent images of the underlying coupled anatomy, and clearly delineates surrounding structures at risk for collateral damage. In the case of right bundle-branch block, left-axis deviation idiopathic LV ventricular tachycardias, earlier studies using transesophageal echocardiography demonstrated the presence of a false tendon at the site of earliest ventricular activation during VT [8]. This finding has

been proposed as a guide to ablation of this type of VT. However, limitations of the report have been suggested by other data describing an incomplete correlation between the anatomy and physiology [87]. In either event, ultrasound demonstrates nicely the interventricular septum, as well as the adjacent posterior wall. Lesions created during ablation are typically apparent in this setting, providing images obtained from beneath the tricuspid valve. In the case of right ventricular outflow tract VT, ultrasound images, again obtained from below the tricuspid valve, show the anterior aspect of the outflow tract, the septal boundary, and the posterior wall relevant to the establishment of catheter tip–tissue contact during ablation. As shown in Fig. 6.13, the aortic root is also visualized from either a right atrial imaging venue or from beneath the tricuspid valve. The images from the right atrium typically show a more long-axis view and demonstrate the position of the catheter tip from the cusps further into the aortic root. Images from beneath the tricuspid valve first show the aortic valve in cross-section (Fig. 6.12). With further clockwise rotation of the catheter from a site further into the outflow tract, a long-axis view of the aortic root is also obtained. The left main coronary artery is seen in virtually all cases, establishing a clear-cut reference for this site to be avoided.

Ablation of scar-dependent VT Similarly, the ultrasound delineation of various tissue types is useful in dealing with postinfarction, scar-dependent ventricular tachycardia. A variety of studies during the past 20 years have shown that infarct-related ventricular tachycardia typically arises along the infarct borders, as either microreentrant or macroreentrant circuits. In the early 1980s, the nonpharmacological treatment of choice was surgical subendocardial resection at the scar margin to interrupt these circuits. Surgery was directed by endocardial mapping or strictly by surgical inspection of the scar boundary. Success rates of 80–95% were possible in patients with anterior or lateral infarctions, while surgical treatment of posterior or inferior wall VTs were more difficult, due to epicardial origins in up to one-third of patients. This visual advantage is also possible with intracardiac ultrasound, in which normal or abnormal tissue is delineated by the hinge points between normal myocardium and regions of dense scar. This has been studied extensively in animal infarcts. Callans et al. [88] demonstrated a good correlation between dense scar seen on ICE imaging and electroanatomical mapping, using a lower voltage cut-off point of 1.0 mV. Preliminary clinical studies have also suggested that ultrasound can be useful for identifying motion abnormalities in the regional wall, including those related to dense scarring, along with hinge-point boundaries between 83

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pathological and normal tissue. Razavi et al. [89] used this approach in eight patients with ventricular tachycardia related to underlying structural abnormalities who were undergoing standard electrophysiological evaluation under intracardiac ultrasound guidance. In each patient, an attempt was made to map the underlying VT with a conventional electroanatomical or noncontact mapping approach. However, these approaches were unsatisfactory due to an inability to localize a specific origin of tachycardia, the presence of extensive scarring throughout a large region of the myocardium, limiting localization, or an inability to deliver sufficient energy empirically to ablate a VT focus. In these patients, ultrasound was used to identify the location of the scar and guide ablative energy delivery. In each case, a linear lesion was created from within the scar to an anatomic obstacle such as the mitral valve annulus, or was positioned along a margin of an anatomic defect or region of scar. Seven of eight patients were rendered noninducible at the time of the post-ablation electrophysiological testing, while six of the eight were free of VT during a 15-month follow-up period. These data support the use of intracardiac ultrasound images in a fashion similar to electroanatomical mapping. Regions of scarring, identified by 0.5-mV electroanatomical mapping in these patients, correlate best with dense scarring on ICE examination [89]. However, further research will be needed before this can be more widely applied.

Monitoring for ablation-related complications Several investigators have reported the early detection or avoidance of catheter-related complications using ICE imaging. Several investigators have used this approach in monitoring for thrombus related to transseptal sheaths and accompanying catheters [90,91]. Bruce et al. [90] demonstrated that 21 of 270 patients (8%) undergoing AF ablation had evidence of catheter-related intracardiac thrombus. In each case, it was possible to remove the thrombi with suction generated by high negative pressure via the catheter sheath before thrombus enlargement, without evidence of peripheral thromboembolic events. Ren et al. [91] have similarly shown the value of intracardiac ultrasound for the early detection and removal of thrombi of this type. This information has also been used to recommend the maintenance of higher preventative anticoagulation levels during AF ablation [92]. Emerging pericardial effusions (Fig. 6.21) have been detected earlier in their course. Bunch et al. [93] reviewed the value of an ICE approach in 632 AF ablation procedures conducted during a 5-year period. Fifteen procedures (2.4%) were complicated by perforation, requiring 84

Figure 6.21 Long-axis view of the left ventricle (LV) as obtained from the right ventricular outflow tract. Both anterior (APM) and posterior (PPM) papillary muscles are noted, as are chordae and their connective sites with the mitral valve leaflets. A small clear space behind the left ventricle (black arrows) is due to a pericardial effusion.

pericardiocentesis. The perforation site was in the LA in nine patients (60.0%), in the right atrium (RA) in one (6.7%), and in the right ventricle (RV) in five (33.3%). Intracardiac echocardiography was used for monitoring in 13 patients (86.7%) and revealed an effusion in 11 (73%) before overt instability developed. Despite an LA site of perforation, surgical intervention was required only once. This was due in part to early detection and patient stabilization using more conservative ultrasound-guided therapeutic interventions [93]. Developing pericardial effusions during ablation are typically first seen in the region posterior to the left AV groove. This tends to be a more dependent position within the pericardium. Effusions of increasing size are subsequently seen around the right AV groove, as well as the right ventricular apex. The use of intracardiac ultrasound to identify specifically the best location for pericardiocentesis has also been reported, and it has been reported that imaging of a saline contrast injection through an intrapericardial catheter is useful for confirming the appropriate intrapericardial position of the catheter [93]. It should be noted, however, that with certain ablative procedures, minor pericardial effusion can occur without progression to tamponade physiology. These cases can be distinguished from progressive effusions by their stability. Pulmonary vein stenosis is yet another potential complication of AF ablation that may be mitigated by the application of ICE techniques [94]. Spectral Doppler imaging can also contribute to the surveillance process. Pulsedwave Doppler imaging, available with phased-array intracardiac echocardiography, may demonstrate changes in pulmonary vein blood flow velocities heralding the

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Figure 6.22 Color flow and pulsed wave Doppler of the right inferior (RI) pulmonary vein. The left atrium (LA) is also seen from the right atrial imaging venue. Both systolic and diastolic components of blood flow are evident on the pulsed Doppler tracing. These are used to determine the appearance of pulmonary vein stenosis. [41]

emergence of significant stenosis [95,96] (Fig. 6.22). Blood flow velocities in the pulmonary veins of 1.0 m/s or less do not predict progression to significant stenosis [95], while flow velocities in excess of 1.6 m/s have been observed in patients who subsequently developed significant pulmonary vein narrowing [95]. It should be noted, however, that Doppler flow velocities can be highly influenced by the presence of atrial fibrillation, which decreases pulmonary vein blood flow velocities, and isoproterenol infusions, which increase the velocities [96]. The occurrence of an atrio-esophageal fistula has emerged as the most vexing problem of AF ablation [44,97,98]. In affected patients, energy delivery via the esophagus results in an inflammatory response that leads to a connection between the structures, accompanied by acute endocarditis and air embolus. Several ways of avoiding this have been suggested. Initially, temperature monitoring from within the esophagus was considered protective, provided that energy delivery was discontinued at the first sign of any temperature increase. However, subsequent studies have shown that external esophageal temperatures may rise appreciably even in the absence of demonstrable increments in the internal temperature. Temperature monitoring from within the esophagus is therefore insufficient as a means of providing protection against this complication. An additional approach has been to avoid energy delivery over the esophagus by visualizing and avoiding the structure during the ablation. The use of barium paste can mark the location of the esophagus and also demonstrate its motility and general movement during the course of the procedure. The posi-

tion of a temperature probe on biplanar fluoroscopy can also be used to locate the esophagus and avoid direct energy delivery over the esophagus. A more straightforward approach is provided by intracardiac echocardiographic monitoring. Imaging along the posterior aspect of the left atrial wall provides clear-cut images of the esophagus from the superior to the inferior portion of the atrial–esophageal contact area. ICE imaging is also useful in monitoring for microbubble formation. A recent study by Cummings et al. [44] showed that the internal esophageal temperatures were significantly higher in the presence of microbubble formation. This was found to be a better predictor of the esophageal heating power. While microbubble formation provides a clear indication that energy delivery should be discontinued, it may be insufficiently sensitive, as significant heating of collateral structures can occur even in the absence of microbubble formation [55,56]. Nevertheless, the esophageal monitoring approach is clearly better than power monitoring, which does not correlate with the development of microbubbles or increases in internal temperature [44].

Limitations of intracardiac ultrasound imaging Several limitations of intracardiac echocardiography should be considered. One potential disadvantage of the routine application of this technology is its cost. The first expense is the catheter cost itself. The cost of phased-array catheters is higher than that of single-element mechanical devices. This is offset by the full spectrum of imaging capabilities afforded by phased-array imaging, such as spectral Doppler and improved tissue penetration and far-field imaging. A second cost comes from the need for a dedicated ultrasound imaging platform in high-volume electrophysiology laboratories. On the other hand, intracardiac ultrasound imaging can be carried out easily by the interventionalist without the need for an additional echocardiographer. Other advantages over transesophageal echocardiographic imaging relate to patient comfort and safety. An additional consideration is the learning curve required to become familiar with and acquire expertise in the imaging venues unique to ICE imaging. The period of the learning curve is strongly dependent on the user’s previous experience with ultrasound and the available expertise in the electrophysiology laboratory.

The future of ICE imaging The pericardial space is emerging as an additional imaging venue for cardiac ultrasound examination. Rodrigues 85

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et al. [99] studied a relatively less invasive method of introducing an ultrasound catheter into the pericardial space via a subxiphoid approach in animals. In all cases, longitudinal and short-axis views of the right-sided and leftsided chambers and valves equivalent to those obtained in transesophageal echocardiography were obtained. In each case, the atrial appendage, pulmonary veins, coronary arteries, and coronary sinus were visible in the majority of cases. No untoward arrhythmias were induced with catheter manipulation in pericardial space. Roman-Gonzalez et al. [42,43] have also demonstrated the value of ultrasound imaging from within the RA and RV for the positioning of intrapericardial catheters. In an in vivo study, multipolar microcatheters were introduced via a catheter sheath into the pericardial space. These were then positioned immediately along the medial border of the right pulmonary veins, the lateral border of the left pulmonary veins, and in the oblique sinus between the pulmonary veins. Seventy-five percent of the electrodes used for ablation were well visualized, despite the nature of the pericardial reflection around the pulmonary veins. Lesions created during energy delivery were also evident. Additional experience is needed with this approach to provide support for more routine use of the method.

Three-dimensional imaging A substantial amount of work is now under way to merge the electrophysiology-based maps obtained with various computer-based mapping systems and the underlying anatomy as imaged using CT and MRI. Several industry groups have developed the software tools to superimpose activation or voltage maps onto segmented volume images of the LA. It should be noted that this is limited to the display of overlapping images, rather than true

registration in which each and every voxel of the threedimensional map is assigned or registered to the surface of the LA image. The present author [100] has demonstrated that this type of “registration” of map information onto the surface of rendered CT volumes provides a more complete and integrated view of an underlying arrhythmia. Similarly, Sra and co-workers [101] have shown that the premature contractions initiating atrial fibrillation can be registered to the surface of a rendered CT volume, with mapping from noncontact arrays. Reddy and co-workers [102] were successful in registering ablative lesions onto the surface of an accompanying CT data set. The authors found that the best match between electroanatomical and CT data was obtained with radiographic images from the end-expiratory period. At other times, significant distortion or mismatch was present. These limitations provide the incentive for the use of ICE imaging in the registration process. Intracardiac ultrasonography provides a real-time image that demonstrates the target tissue, visualizes interventional catheters, establishes the specific point of catheter tip–tissue contact, and monitors changes in the tissue echo density or the occurrence of microbubbles. An ideal interventional scenario would be to register the activation or voltage images from three-dimensional electroanatomical images to real-time three-dimensional ultrasound geometries, using real-time catheter positions seen simultaneously with both anatomic and mapped images. Early data have shown that the addition of an electroanatomical sensor to the ultrasound catheter facilitates the collection of this type of linked electrophysiological and anatomic data. This can provide complete three-dimensional volumes from ultrasound imaging (Fig. 6.23), offering a better real-time context for cataloguing the actual heart contours during ablation, serving as a scaffold for registering accompanying electroanatomical maps, and chronicling the specific positions of ablative interventions on the surfaces.

Figure 6.23 Three-dimensional ICE image creation. The first panel shows a 2D planar image of the left ventricular (LVO) and right ventricular (RVO) outflow tracts. In the second panel, the endocardial edge contours of two components of the LV outflow tract are carefully marked. Additional detected edges from other ventricular locations imaged with subsequent catheter rotation tracked by Carto sensor in the ICE catheter tip provide contours of both the left and right ventricles. These individual endocardial rings are used in an interpolation algorithm, based on their acquisition angle, to create a complete, nearly real-time volume image of each ventricle (third panel).

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Even more impressively, several three-dimensional ultrasound systems have been created that provide specific procedure-guiding images on a nearly real-time basis. These may make it possible to use a simple threedimensional ICE view to guide ablative intervention around pulmonary veins or other structures, without the potential flaws associated with CT data sets collected outside the electrophysiology laboratory at a different time, in a different rhythm, or in different volume conditions. The application of such images in electrophysiology offers an important new avenue of investigative and clinical work. Future research will focus on the actual logistics for creating combined and fused images, as well as identifying specific areas in which this type of imaging can improve the overall outcome.

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M, Zipes DP, eds. Thoracic Vein Arrhythmias: Mechanisms and Treatment. Malden, MA: Blackwell Futura, 2004: 77–98. Schwartzman D, Bazaz R, Nosbisch R. Common left pulmonary vein: a consistent source of arrhythmogenic atrial ectopy. J Cardiovasc Electrophysiol 2004;15:560 – 6. Monahan K, Peterson L, Asirvatham S, Breen J, Packer D. Comparison of intracardiac echocardiographic and spiral CT pulmonary vein dimensions in patients undergoing ablation for paroxysmal atrial fibrillation [abstract]. Pacing Clin Electrophysiol 2002;25:679. Wood M, Wittkamp M, Henry D, et al. A comparison of pulmonary vein ostial anatomy by computerized tomography, echocardiography, and venography in patients with atrial fibrillation having radiofrequency catheter ablation. Am J Cardiol 2004;93:49 – 53. Packer D, Stevens C, Munger T, Bergman D. Characterization of pulmonary vein anatomy and physiology in patients with and without atrial fibrillation. J Am Coll Cardiol 2000;35: 131A. Cabrera J, Sanchez-Quintana D, Farre J, et al. Ultrasonic characterization of the pulmonary veinous wall: echographic and histological correlation. Circulation 2002;106: 968 –73. Arruda M, Wang Z, Patel A, et al. Intracardiac echocardiography identifies pulmonary vein ostia more accurately than conventional angiography. J Am Coll Cardiol 2000;35:110A. Packer D, Darbar D, Bluhm C, et al. Utility of phased array intracardiac ultrasound for guiding the positioning of the lasso mapping catheter in pulmonary veins undergoing AF ablation [abstract]. Circulation 2001;104:620. Asirvatham S. Utility of intracardiac ultrasound (ICUS) Doppler hemodynamics with tandem balloon catheter pulmonary venous ablation [abstract]. J Am Soc Echocardiogr 1999; 12:410. Sarabanda AV, Bunch TJ, Johnson SB, et al. Efficacy and safety of circumferential pulmonary vein isolation using a novel cryothermal balloon ablation system. J Am Coll Cardiol 2005;46:1902 –12. Epstein L, Mitchell M, Smith T, Haines D. Comparative study of fluoroscopy and intracardiac echocardiographic guidance for the creation of linear atrial lesions. Circulation 1998;98:1796 – 801. Roithinger F, Steiner P, Godeki Y, et al. Low-power radiofrequency application and intracardiac echocardiography for creation of continuous left atrial linear lesions. J Cardiovasc Electrophysiol 1999;10:680 – 91. Verma A, Marrouche N, Yamada H, et al. Usefulness of intracardiac Doppler assessment of left atrial function immediately post-pulmonary vein antrum isolation to predict short-term recurrence of atrial fibrillation. Am J Cardiol 2004;94:951– 4. Saxon LA, Stevenson WG, Fonarow GF, Middlekauff HR, et al. Transesophageal echocardiography to guide energy delivery and catheter position during radiofrequency catheter ablation of ventricular tachycardia. Am J Cardiol 1993;72: 658 –661. Callans D, Ren J, Michele J, Marchlinski F, Dillon S. Electroanatomic left ventricular mapping in the porcine model of healed anterior myocardial infarction: correlation 89

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with intracardiac echocardiography and pathological analysis. Circulation 1999;100:1744–50. Razavi M, Munger T, Shen W, Packer D. Intracardiac ultrasound validation of dense scar delineation by electroanatomic voltage mapping [abstract]. Pacing Clin Electrophysiol 2003; 26:930. Bruce C, Friedman P, Asirvatham S, et al. Frequency of left atrial thrombus occurrence in patients with atrial fibrillation during pulmonary vein isolation despite anticoagulation. Circulation 2003;108:IV-321. Ren J, Marchlinski F, Callans S. Left atrial thrombus associated with ablation for atrial fibrillation: identification with intracardiac echocardiography. J Am Coll Cardiol 2004;43: 1861–7. Wazni O, Rossillo A, Marrouche N, et al. Embolic events and char formation during pulmonary vein isolation in patients with atrial fibrillation: impact of different anticoagulation regimens and importance of intracardiac echo imaging. J Cardiovasc Electrophysiol 2005;16:576–81. Bunch TJ, Asirvatham SJ, Friedman PA, et al. Outcomes after cardiac perforation during radiofrequency ablation of the atrium. J Cardiovasc Electrophysiol 2005;16:1172 – 9. Packer D, Keelan P, Munger T, et al. Clinical presentation, investigation, and management of pulmonary vein stenosis complicating ablation for atrial fibrillation. Circulation 2004;111:546–54. Saad E, Cole C, Marrouche N, et al. Use of intracardiac echocardiography for prediction of chronic pulmonary vein stenosis after ablation of atrial fibrillation. J Cardiovasc Electrophysiol 2002;13:986–9. Ren J, Marchlinski F, Callans D. Effect of heart rate and isoproterenol on pulmonary vein flow velocity following radiofrequency ablation: a Doppler color flow imaging study. J Interv Card Electrophysiol 2004;10:265 – 9. Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 2004;109:2724 – 6.

98 Sosa E, Scanavacca M. Left atrial–esophageal fistula complicating radiofrequency catheter ablation of atrial fibrillation. J Cardiovasc Electrophysiol 2005;16:249 – 40. 99 Rodrigues A, d’Avila A, Houghtaling C, Ruskin J, Picard M, Reddy VY. Intrapericardial echocardiography: a novel catheter-based approach to cardiac imaging. J Am Soc Echocardiogr 2004;17:269 –74. 100 Packer D. Evolution of mapping and anatomic imaging of cardiac arrhythmias. J Cardiovasc Electrophysiol 2004;15:839 – 54. 101 Sra J, Krum D, Hare J, et al. Feasibility and validation of registration of three-dimensional left atrial models derived from computed tomography with a noncontact cardiac mapping system. Heart Rhythm 2005;2:55 – 63. 102 Reddy V, Malchano Z, Holmvang G, et al. Integration of cardiac magnetic resonance imaging with three-dimensional electroanatomic mapping to guide left ventricular catheter manipulation: feasibility in a porcine model of healed myocardial infarction. J Am Coll Cardiol 2004;44:2202 –13. 103 Packer DL, Asirvatham S, Friedman PA, et al. Three Dimensional Pulmonary Vein Analysis in Patients Undergoing Focal AF ablation. Circulation 102;526,2000. 104 Tsao HM, Yu WC, Cheng HC, Wu MH, et al. Pulmonary vein dilation I patients with atrial fibrillation: Detection by magnetic resonance imaging. J Cardiovasc Electrophysiol 2001;12: 809. 105 Scharf C, Sneider M, Case I, Chugh A, et al. Anatomy of the pulmonary veins in patients with atrial fibrillation and effects of segmental ostial ablation analyzed by computed tomography. J Cardiovasc Electrophysiol 2003;14:150 –55. 106 Kato R, Lickfett L, Meininger G, Dickfield T, et al. Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation. Lessons learned by use of magnetic resonance imaging. Circulation 2003;107:2004–2010. 107 Wittkampf FHM, Vonken EJ, Derksen R, Loh P, et al. Pulmonary vein ostium geometry. Analysis by magnetic resonance imaging. Circulation 2003;107:21–23.

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7

Catheter ablation in young patients: special considerations Edward P. Walsh

Table 7.1 Unique features of radiofrequency ablation in pediatric patients.

Introduction Transcatheter ablation has become the treatment of choice for a wide variety of tachyarrhythmias in patients of all agesabut for the young patient in particular, this mode of treatment is especially appealing, for several reasons. Firstly, it can obviate the need for prolonged exposure to antiarrhythmic medications with their uncertain efficacy and potential side effects for an individual who may require treatment over the course of many decades. Secondly, ideal ablation targets such as accessory pathways (APs) are congenital disorders that often produce their most debilitating symptoms early in life, and thus may require definitive treatment before the patient reaches adulthood. Furthermore, there is a rapidly growing population of young patients following surgical repair of congenital heart disease (CHD) who develop scar-related postoperative atrial and ventricular reentrant arrhythmias that are notoriously resistant to control by pharmacologic means, but may be amenable to catheter therapy. It is not at all surprising that catheter ablation was adopted early as the cornerstone of tachycardia treatment for the young population [1–4]. While the fundamental principles of mapping and intracardiac lesion creation are similar across age groups, there are a number of unique considerations that have a substantial impact on the techniques and indications for ablation in the pediatric patient (Table 7.1). It is the purpose of this chapter to highlight such features, and to provide a general overview of ablation results for children, as well as young adults, with congenital heart disease.

Technical considerations Sedation The proper sedation strategy for pediatric ablation procedures will vary according to the patient’s age, the tachy-

Technical Sedation Vascular access Catheter size Anatomy in congenital heart disease Conduction system in congenital heart disease Electrophysiologic Natural history considerations Incessant tachycardia and cardiomyopathy Congenital heart disease Preoperative tachycardias Postoperative tachycardias Biophysical/developmental Radiofrequency lesion extension? Coronary artery injury? Small size of Koch’s triangle Outcome data Pediatric Electrophysiology Society studies Indications

cardia mechanism, and the availability of experienced anesthesia staff. In general, fairly deep levels of sedation are utilized when procedures are performed for common tachycardia substrates such as APs or atrioventricular (AV) nodal reentry. In many pediatric laboratories, this is accomplished with a general anesthetic involving intubation and mechanical ventilation. Besides providing reliable analgesia and amnesia, a general anesthetic eliminates any potential for unpredictable patient movement during ablation energy delivery and other critical catheter manipulations such as transseptal puncture. It also simplifies access to the internal jugular or subclavian vein in young patients, who are usually quite sensitive to instrumentation near the facial area. In addition, the ventilator cycle for an intubated subject can be manipulated in a held-inspiratory or held-expiratory phase during ablation 91

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energy applications, which can improve catheter stability by preventing tip movement in response to diaphragmatic excursion. Both isoflurane and propofol have been tested carefully as anesthetic agents during electrophysiologic procedures in children [5,6], and apart from one report of refractory period prolongation in accessory pathways with isoflurane [7], all other data indicate a lack of significant interference with conduction measurements or the ability to induce common forms of reentrant tachycardia. Lighter levels of sedation with intravenous agents such as midazolam or narcotic are certainly an acceptable alternative in cooperative youngsters, provided that backup measures for deeper anesthesia and appropriate airway support are readily available if the child does not respond adequately. General anesthesia is now used in nearly 75% of children undergoing ablation at our own institution, but deep levels of sedation are purposely avoided in the subgroup of patients with catecholamine-sensitive tachycardias, such as ectopic atrial tachycardia (EAT) and focal ventricular tachycardia (VT). Automatic arrhythmias of this sort may become quiescent under heavy sedation, making mapping and ablation difficult, if not impossible [8,9]. Ablation for automatic tachycardia is probably best accomplished under light levels of conscious sedation whenever feasible.

Vascular access and catheter manipulation The femoral vein of a teenager or young adult can easily and safely accommodate up to three standard electrode catheters, but this luxury is absent in smaller patients with reduced venous caliber. Children in the weight range of 10–35 kg can usually accept two standard catheters per femoral vein, and infants weighing less than 10 kg are generally instrumented with a single catheter per vein [10]. These vascular access limitations can be overcome with simple maneuvers that reduce catheter requirements, including the use of a single multipolar catheter for combined His bundle recording and right ventricular pacing, or the use of the proximal electrodes on the coronary sinus recording catheter for atrial pacing [11]. Deflectable catheters with up to 10 electrodes are commercially available in the sizes of 4 Fr and 5 Fr, which will serve these combined functions extremely well in small patients. Placement of an esophageal electrode for left atrial stimulation and recording can further economize on vascular access requirements. With these modifications, it is possible to perform even the most complex ablation procedure with only one or two intravascular catheters in a very young child when necessary (Fig. 7.1). Alternatively, the recent introduction of ultrathin diagnostic catheters in sizes of 2 Fr or less permits deployment of up to three electrodes through a single venous sheath [12]. We have not 92

Esophageal lead

5 Fr ablation catheter

Figure 7.1 Frontal projection of the cardiac silhouette and catheter position during ablation of a posterior-septal accessory pathway in a 1.8-kg infant with intractable tachycardia. A single 5-Fr ablation catheter with a 3-mm tip was used for mapping and successful ablation, with a bipolar esophageal lead for atrial pacing.

used ultrathin catheters in our own laboratory except for mapping in distal coronary venous branches and a few exceptional cases in which mapping was carried out in the right coronary artery. However, they are used on a more routine basis for conventional pacing and recording during ablation procedures at some pediatric centers. The femoral arterial caliber is also reduced in small children, which is one of several reasons why the transseptal technique is preferred over the retrograde approach to the left heart in many pediatric laboratories [13]. Straightforward entry to the left atrium through a patent foramen ovale is possible in a high percentage of young patients, so the septum should routinely be probed for patency with the ablation catheter tip before one resorts to the Brockenbrough puncture technique. The catheter can be coaxed through a patent foramen in as many as 50% of infants, and about 30% of older children [14]. When a Brockenbrough procedure is required in young patients, it is important to use the needle with the reduced radius of curvature along with the short sheath designed specifically for pediatric use. Catheter manipulation in small children requires a gentle touch, owing to thin cardiac walls and small chamber dimensions. Because the image of a young child’s heart projected by fluoroscopy is usually magnified to fill the screen dimensions better, relatively small hand motions by the operator will translate into large movements of the catheter tip. Considerable experience is needed to acquire the proper feel for well-controlled catheter movement in small hearts.

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Catheter ablation in young patients: special considerations

Issues related to congenital heart disease (CHD) Children and young adults with congenital heart disease present unique challenges during ablation procedures. The most obvious of these relates to distorted anatomy that invalidates the familiar fluoroscopic landmarks that are relied on for catheter manipulation in a normal heart. Details of the underlying cardiac anatomy and the specifics of all surgical interventions must be ascertained well in advance of the case in order to anticipate chamber malpositions, surgical patches, or redirected vasculature that could confound catheter positioning or otherwise hinder access to an ablation target site. This is particularly true for patients with complicated intra-atrial baffles of the type used for the Mustard, Senning, and Fontan operations. The capacity for biplanar fluoroscopy can be exceptionally helpful while navigating through complex CHD, and angiography will often prove useful to define chamber orientation (Fig. 7.2) and locate the true level of the atrioventricular (AV) groove (Fig. 7.3). Not surprisingly, distorted anatomy in CHD is frequently associated with anomalies of the specialized conduction tissues. The position of the normal AV node can be displaced far outside Koch’s triangle in some cardiac

PA

Ao

MV

RV

Atrium

LV

Figure 7.2 Frontal projection of a ventricular angiogram serving as a roadmap during ablation in a child with complex congenital heart disease (situs inversus, dextrocardia, superior–inferior ventricular arrangement, double-outlet right ventricle). The ablation catheter tip (dark arrow) is located along the superior rim (dashed line) of the displaced mitral valve. Angiography was exceedingly helpful in clarifying the chamber orientation and identifying the AV groove. Ao, ascending aorta; LV, left ventricle; MV, mitral valve annulus; PA, pulmonary artery; RV, right ventricle.

Figure 7.3 Frontal projection of a selective right coronary angiogram in a teenager with severe Ebstein’s disease who was undergoing ablation for a right-sided accessory pathway. It should be noted that the true level of the tricuspid ring, indicated by the overlying right coronary artery, is displaced dramatically far to the left (relative to the spine), due to severe right atrial enlargement.

malformations, especially among patients with AV discordance (e.g., “corrected” transposition) and those with AV canal defects [15]. In order to minimize the chance of inadvertent damage to the AV node or His bundle, it is essential to have a good working knowledge of conduction system embryology and anatomy in CHD before attempting ablation in these patients, and to spend time carefully locating a high-quality His potential. Some forms of CHD are also prone to a high incidence of accessory atrioventricular connections. As many as 50% of patients who have Ebstein’s malformation of the tricuspid valve are found to have APs or Mahaim (atriofascicular) fibers, and in many of these cases, multiple APs are present [16]. Even more exotic is a subset of patients with heterotaxy syndrome and single ventricle who may actually have “twin AV nodes,” involving a duplicated conduction system with two discrete nodes and two His bundles, often with a connecting “sling” of conduction tissue between them that can serve as a perfect substrate for reentry [17]. The embryologic accidents of CHD can result in some rather fascinating conduction pathology, and the clinician must be prepared for surprises. Knowledge of anatomic and surgical detail is also important as a guide to the location of potential circuits for postoperative macroreentrant tachycardias within atrial or ventricular muscle. As will be discussed later in this 93

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chapter, macroreentry circuits often develop late after surgery for CHD as a consequence of conduction block or delayed propagation near suture lines and intracardiac patches [18]. Understanding the precise location of all such conduction barriers will assist greatly in the mapping process whenever ablation is undertaken. Because many forms of congenital heart disease allow right-to-left shunting, anticoagulation with heparin is used during all procedures, even when there are no plans to enter the left heart directly. Furthermore, it is important to consider in-hospital intravenous hydration on the evening before ablation for all patients who have polycythemia from cyanotic heart disease. Some of these children can become dehydrated while fasting before the procedure, and even mild degrees of volume depletion can result in further hemoconcentration that may raise the risk of clot formation. At our institution, any patient with a hematocrit above 50% is admitted to the hospital on the evening before ablation for maintenance intravenous fluids.

Electrophysiologic considerations Natural history of accessory pathways Accessory pathways (APs) are the most common mechanism underlying supraventricular tachycardia in the fetus, infant, and young child [19]. However, it has long been appreciated that an AP may become nonfunctional in a significant number of these young patients sometime during the first year or so of life. The exact percentage who have complete and permanent regression of their AP may be difficult to determine, since in many cases the pathway could simply lose its ability to conduct in the anterograde direction, but still endure as a concealed AP with the capacity for orthodromic reentry. In this situation, a patient with Wolff–Parkinson–White syndrome who had frequent supraventricular tachycardia (SVT) as an infant may acquire a normal electrocardiogram and be arrhythmia-free for many years in the absence of triggering atrial or ventricular premature beats, only to present again with tachycardia as a teenager or young adult [20]. The incidence of true AP regression may be overestimated in natural history studies involving children if very close follow-up is not extended over several decades or some form of electrophysiologic testing is not performed. Currently, the best approximation of complete AP resolution in children appears to be the data published by Benson et al., who carried out transesophageal atrial stimulation studies in a group of 35 patients with a mean age of 1 year in whom AP-mediated tachycardia had been documented in early infancy. The authors found entirely negative studies in 11 of the 35 patients [21]. Granted, retrograde conduction was not tested directly with the 94

transesophageal technique, but intracardiac testing would have been hard to justify. Similar estimates of complete AP resolution during the first year of life have been confirmed by others [22]. This potential for spontaneous “cure” of AP-mediated tachycardia in one-third of infants will influence any decision regarding ablation, and strongly encourages a policy of medical therapy when possible during the first 12 months of life.

Incessant tachycardias with secondary cardiomyopathy Certain forms of SVT can be incessant in nature, eventually leading to advanced degrees of cardiomyopathy if the ventricular rate is consistently elevated. Ectopic atrial tachycardia (EAT) and the permanent form of junctional reciprocating tachycardia (PJRT) are the two most notorious mechanisms for this scenario, and both disorders typically have their initial presentation during childhood. The ability to eradicate SVT and restore normal ventricular function with a single catheter procedure [23] has been one of the most dramatic benefits of ablation for the pediatric patient. Ectopic atrial tachycardia is caused by a single focus of abnormal atrial automaticity arising from a site outside the sinus node. Successful drug suppression is possible in some cases, but often this disorder proves refractory to all pharmacologic efforts. Ablation has now become the preferred treatment whenever the response to drug therapy is unsatisfactory or ventricular dysfunction is present. The ectopic focus in children may occur anywhere in the right or left atrium, but is generally found near the pulmonary veins or the appendages, or along the crista terminalis [24]. Mapping is accomplished by identifying the site of earliest atrial electrical activity, which typically has a local activation time that precedes the onset of the surface P wave by 20–50 ms. Termination of EAT in response to a properly positioned ablation catheter is usually quite rapid, suggesting that these abnormal foci are quite small in size. The results for ablation of this disorder in children have been very encouraging, with acute success in more than 90% of cases, and a low rate of recurrence [25]. Importantly, these patients will benefit from prompt resolution of ventricular dysfunction, which usually has reversed within 6 months of a successful procedure [23]. The permanent form of junctional reciprocating tachycardia is due to a slowly conducting AP with unidirectional retrograde properties, located in the posterior septal region near the mouth of the coronary sinus in most cases. As in EAT, pharmacologic therapy for PJRT may be difficult, typically requiring the use of agents such as flecainide or amiodarone. Ablation is clearly the treatment of choice for young patients with ventricular dysfunction at presentation, but even for those who still have well-

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preserved function, ablation is often preferred over the chronic use of potentially toxic medications. Mapping for PJRT is similar to the technique used for conventional accessory pathways, involving a search for the site of earliest retrograde atrial activation during sustained tachycardia, as well as identification of a discrete AP potential [26]. The acute success rate for PJRT ablation exceeds 90%, and as in EAT, rapid resolution of ventricular dysfunction can be expected within a few weeks or months after the procedure [27].

Preoperative and postoperative arrhythmias in congenital heart disease As mentioned, there is a strong association between certain congenital cardiac defects and the presence of accessory pathways. While Ebstein’s malformation is recognized as the most important condition in this regard, APs can occur in a variety of other malformations as well. It is generally agreed that attempts should be made to ablate such pathways in advance of surgical correction, since catheter access to an area of interest may become difficult following repair. Equally important, recurrent SVT may become quite problematic in the postoperative setting when catecholamine levels are elevated, and it is clearly desirable to eliminate this source of morbidity preoperatively. However, it must be understood that accessory pathway ablation in CHD is difficult [28]. Even with careful angiography and echocardiography to define anatomy, this is a demanding exercise. Overall, the outcome for AP ablation in CHD still falls short of the more optimistic results seen with ablation in patients with normal hearts [16,28]. Lower acute success rates in the order of 80 – 85% are reported, and the recurrence risk may be as high as 15–20%. But, even in the event of failure or recurrence, preoperative mapping data are still valuable, since consideration can be given to intraoperative pathway interruption by the surgeon under direct vision as a backup intervention at the time of the hemodynamic repair. Among older children and young adults who have undergone prior surgical repair of CHD, a large and growing number of cases are being encountered with late-onset postoperative tachyarrhythmias that may be suitable targets for catheter ablation therapy. The largest group includes those with intra-atrial reentrant tachycardia (IART), which continues to be a source of high morbidity and mortality following the Mustard or Senning operation for transposition, and the Fontan operation for single ventricle. Because pharmacologic therapy for this condition has proved so ineffectual [29], aggressive clinical efforts are under way at select centers to develop catheter ablation as a more definitive treatment option. Unlike common type 1 atrial flutter in normal hearts (which follows a fairly predictable circuit around the tricuspid ring), IART

Catheter ablation in young patients: special considerations

circuits in CHD patients are highly variable and usually involve macroreentry related to suture lines and surgical patches. Armed with knowledge of the precise surgical anatomy, clear and accurate maps of IART circuits can now be generated in almost all cases using modern threedimensional mapping techniques (Fig. 7.4) in conjunction with entrainment pacing maneuvers and traditional electrogram analysis [30,31]. Experience with IART mapping has now accrued to the point that IART circuit locations can be predicted with reasonable accuracy according to the specific type of CHD and the specific surgical intervention [32]. While it would appear that the major mapping challenges have been overcome, creating effective transmural lesions across wide conduction corridors in thick-walled atria is still far from perfected. Thus, although acute success rates may approach 90%, the recurrence risk for IART after acutely successful ablation performed with conventional 4-mm tipped catheters and a 50-W radiofrequency generator remains disappointingly high, particularly among Fontan patients, 40% or

Figure 7.4 Electroanatomical mapping of intra-atrial reentrant tachycardia (IART) in a 14-year-old, 8 years after a Fontan operation for tricuspid atresia. The lateral wall of the right atrium is shown. The colors reflect activation times, proceeding from red (early) to yellow, blue, and purple (late). There is a narrow corridor for conduction (bounded by the arrowheads) just anterior to a scar zone (gray area). Ablation in this area terminated the IART. Ant, anterior; IVC, inferior vena cava; Post, posterior; SVC, superior vena cava.

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more of whom will experience at least one recurrence of IART within 2 years of the procedure [33]. Fortunately, more recent data demonstrate improvement in both the acute and long-term outcomes [34] with modifications in catheter design that enhance lesion size, such as irrigatedtip electrodes or 6–8-mm electrodes coupled with a highoutput RF generator. Late postoperative VT can occur in a subset of patients who require a ventriculotomy or ventricular patch as part of their CHD surgery. This is of most concern following tetralogy of Fallot repair, especially among patients who had their surgery later in life [35]. The macroreentrant circuit in this setting typically arises in the right ventricular outflow tract, and commonly utilizes a path near the margin of the subpulmonary patch and upper rim of the ventricular septal defect (Fig. 7.5). A large number of isolated case reports have now described successful mapping and acute ablation for this arrhythmia [36–38], but data remain scarce with regard to the long-term recurrence risk. Only two series have ever been assembled on this topic with sizable patient numbers, and unanticipated VT recurrences were noted in both study groups [39,40]. Because VT can result in sudden death for CHD patients [41], and because the chance of permanent cure with catheter ablation is less than certain at the present time, we

RVOT

TV RVA

Figure 7.5 Electroanatomical mapping of ventricular tachycardia that developed in a young woman many years after surgical repair for tetralogy of Fallot. There is a large area of scar (gray region) in the right ventricular outflow area. The macroreentrant circuit appears to propagate in a counterclockwise fashion around this scar. RVA, right ventricular apex; RVOT, right ventricular outflow tract; TV, tricuspid valve annulus.

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hesitate to rely on ablation as the sole therapy for this condition at our center. An implantable defibrillator (ICD) is currently our preferred therapy for VT in CHD patients [42], but ablation still retains an important role as a tool for minimizing the number of appropriate ICD discharges for select patients who experience frequent VT episodes.

Biophysics and safety considerations Unique features of immature myocardium Animal experiments in the 1980s evaluating radiofrequency (RF) ablation in cardiac tissue revealed wellcircumscribed lesions with relatively uniform coagulation necrosis. This type of injury appeared far superior to the irregular and potentially arrhythmogenic lesions produced with the older technique of direct-current ablation [43], and follow-up of many thousands of adults and children who subsequently underwent RF ablation procedures during the 1990s attest to the general safety of the technique. However, careful analysis of RF lesions created in young experimental animals indicates some potentially important differences between mature and immature myocardium. In a study of infant lambs [44], histological examination of healed RF lesions revealed a less distinct boundary along the scar margin, with irregular extension of fibrotic tissue into the surrounding myocardium. Furthermore, it appeared that scars in immature atrial or ventricle muscle could grow or expand with time. More recently, experiments involving a piglet model have raised additional concerns related to long-term coronary artery status when RF applications are made along the relatively thin wall of the right AV groove [45]. This observation might be particularly noteworthy in the light of a few anecdotal case reports describing acute coronary injury during RF ablation in infants, as well as in some children with Ebstein’s anomaly, in whom the AV groove is exceptionally thin [46,47]. Thus far, there have been no published data describing comparable experiments in young animals using cryoablation, and it remains unknown whether late lesion expansion or coronary damage can be eliminated entirely in very young patients with this alternative energy source. Data on this issue are eagerly anticipated. The significance of these animal findings for a human child are uncertain, but the potential for unanticipated long-term consequences with RF ablation should encourage a policy of strictly limiting ablation lesions to the smallest effective volume in young children. While RF technology does not permit precise titration of tissue damage, certain practical measures can be taken to achieve a gross reduction in lesion size, such as the use of a 5-Fr catheter with a 3-mm tip electrode to reduce the ablation

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Table 7.2 Maneuvers for improving safety during radiofrequency ablation near normal conduction tissues in children [49–52]. • • • • • • •

Low-temperature 50° radiofrequency “test” applications 5-Fr catheter with a 3-mm or 4-mm tip electrode Long vascular sheaths to improve catheter tip stability Held respiration during radiofrequency delivery to reduce tip motion Jugular vein approach for anteroseptal accessory pathways Angiography of the coronary sinus to clarify landmarks Radiofrequency delivery during sinus rhythm to monitor for accelerated junctional rhythm or subtle changes in atrioventricular conduction

surface area, limiting the duration of RF applications to 15 –30 s, and reducing the settings for maximum tip temperature to the range of 55 – 60 °C. In addition, nonproductive RF damage can be minimized by compulsory mapping and prompt termination of any application that does not achieve the desired effect within a few seconds.

Catheter ablation in young patients: special considerations

ABLATI0N TARGET MECHANISMS Children’s Hospital Boston 2002–2004

VT 5%

Other 2%

EAT 5% IART 20%

AP’s 46%

AVNRT 22%

Figure 7.6 Distribution of tachycardia mechanisms encountered during ablation procedures in a recent 2-year period (2002–2004) at Boston Children’s Hospital. AP, accessory pathway; AVNRT, atrioventricular nodal reentry; EAT, ectopic atrial tachycardia; IART, intra-atrial reentrant tachycardia; VT, ventricular tachycardia.

Minimizing the risk of AV node injury The small dimensions of Koch’s triangle in young children [48] leave less room for error during ablation in the vicinity of the normal conduction tissues. While the recent availability of cryoablation has certainly lessened this concern for older children, commercial cryocatheters are still limited to a size of 7 Fr, with large curves intended for a typical adult heart, and may be inappropriate for some young patients. Until a wider selection of cryocatheters becomes available, RF current may still be the only recourse for septal region ablation in special cases. When using RF energy near the AV node or His bundle, a variety of precautions [13,49 – 52] are routinely taken in our laboratory (Table 7.2) that appear to minimize the risk of inadvertent AV block for small children. Equally importantly, the clinician must always interpret mapping data in the light of the patient’s clinical symptoms and decide whether it is indeed wise to proceed with ablation. It may sometimes be the better part of valor to postpone ablation and return to medical therapy when mapping reveals a target in close proximity to the normal conduction tissues in small children, anticipating that the risks could be lower when the patient is older [52].

Outcomes and indications for ablation Patient characteristics The case mix for various arrhythmia mechanisms encountered during a recent 2-year experience with ablation at Boston Children’s Hospital is shown in Fig. 7.6. Tachycardia due to some form of AP was by far the most common indication for ablation. It is noteworthy that AV node

reentry, while accounting for nearly 50% of SVT ablations in the adult age group, was a less common mechanism in this predominantly pediatric experience. Also of interest, 28% of this group had CHD, and 5% had some degree of tachycardia-induced myopathy, so that the indication for ablation in roughly one-third of our patients extended beyond simple tachycardia control alone. The age distribution (Fig. 7.7) shows that the majority of procedures were carried out in patients in early adolescence at a mean age of 11 years, but there was also a sizable number of young adults with CHD treated for postoperative IART or VT. Ablation in the infant age group (< 1 year) was relatively rare, and was reserved only for cases in which there was no suitable treatment alternative.

Outcome data Since the inception of RF ablation, extensive data regarding the success and risk for young patients have been gathered by members of the Pediatric Electrophysiology Societyainitially through the Pediatric RF Ablation Registry, managed by Dr. John Kugler between 1991 and 1999, and more recently through the ongoing National Institutes of Health–supported Prospective Assessment after Pediatric Cardiac Ablation (PAPCA) trial managed by Dr. George Van Hare. These two databases now contain information on more than 8000 ablation procedures conducted in patients aged less than 21 years. The initial publication from the Registry in 1994 detailed acute and follow-up data for the first 725 procedures from 24 centers, with a mean patient age of 12 years [53]. A definite learning curve was observed in this series [54], but the overall success rate at the high-volume pediatric centers 97

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Ablation age distribution Children’s Hospital Boston 2002–2004 % of total n = 416 30 25 20 % 15 10 5 0 0–1 y

1–5 y

6–10 y

11–15 y 16–20 y 21–25 y 26–30 y Age

was still quite respectable, in the order of 93%. Not surprisingly, it was clear from this early experience that acute success was lower for very small patients and those with CHD, regardless of institutional experience. The incidence of serious complications related to ablation was 1.5% (second-degree or third-degree AV block in five cases, perforation in one, valve damage in one, acute death in one, and late death in three), and it appeared that patient weight less than 15 kg was an independent risk factor for such complications. Three of the four deaths involved young children less than 4 years old, and all four had cardiac comorbidity in the form of either complex CHD or dilated cardiomyopathy. The Registry project, while incredibly useful, was not structured for recording long-term outcomes and thus could not adequately address the issue of tachycardia recurrence. The multicenter Prospective Assessment after Pediatric Cardiac Ablation (PAPCA) trial was organized in 1999 with more detailed follow-up in mind, and represents procedures performed closer to the plateau of the RF learning curve using more modern technology. As might be expected, the acute success rate improved to 96%, but it was nonetheless remarkable to observe that recurrence rates as high as 10% overall were encountered following ablation for common SVT substrates after 1 year of followup [55]. Recurrence was clearly highest after ablation of right-septal APs (over 20%), and lowest after left-sided AP ablation and slow pathway modification (both < 5%). How these recurrence data would compare to procedures done in an older populations is actually uncertain, since no comparable multicenter prospective analysis has been completed for adult patients. The PAPCA trial may be unique in the scope and intensity of its follow-up. 98

> 30 y

Figure 7.7 Age distribution for catheter ablation procedures in a recent 2-year period (2002–2004) at Boston Children’s Hospital.

Indications for ablation As technology advances and new clinical outcome data become available, indications for catheter ablation in young patients will continue to develop. The recent introduction of cryoablation, for instance, will almost certainly result in more liberal indications for ablation of septal APs and AV nodal slow-pathway modification in children. Still, as highlighted at multiple points throughout this chapter, the technical challenges and potential risks associated with ablation in very small children and the CHD population must always be taken into account. Final decisions will ultimately require case-by-case analysis, based on a combination of the patient’s age, weight, symptom status, arrhythmia mechanism, response to prior drug trials, the presence of CHD, the presence of tachycardiainduced myopathy, the patient’s emotional maturity, the attitude of the parents and referring physician, and finally, the experience of the institution and the electrophysiologist performing the procedure. A sample patient selection scheme of the type in current use at Boston Children’s Hospital is shown in Table 7.3 in a simplified form as a guide for this discussion [56]. Patients are first divided according to age, and are then subcategorized according to the severity of their symptoms, as well the presence or absence of CHD or tachycardiainduced myopathy. The customary designations of class I (indicated), class II (possibly indicated), and class III (contraindicated) are used here. It should be noted that ablation is never viewed as an attractive option for the neonate and infant group in our center, given the limitations of vascular access, the potential increased risk of complications, and the distinct likelihood that many of

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Table 7.3 Indications for catheter ablation in children. < 1 year

1–4 years

4–12 years

> 12 years

Symptoms Mild Moderate Severe

III III II

III II I

II I I

I I I

CHD

II

I

I

I

Myopathy

II

I

I

I

Catheter ablation in young patients: special considerations

as well as aggressive sedation during the procedure. All these issues were recently addressed in detail by a consensus conference organized by the North American Society of Pacing and Electrophysiology. The publication by this group, which included clinical experts from both pediatrics and internal medicine, should be consulted for an expanded discussion of the indications for ablation in children [62].

Conclusion CHD, congenital heart disease. Myopathy: tachycardia-induced myopathy. I, class I (indicated); II, class II (possibly indicated); III, class III (contraindicated). See text for details.

those with APs could benefit from spontaneous resolution of their disorder. Exceptions are made only for rare infants with life-threatening symptoms or advanced cardiomyopathy when medical therapy has failed [57–59], or those infants with CHD scheduled for corrective surgery in whom the planned repair would effectively block future catheter access to an arrhythmia target site [60]. The 1–4year-old age group is also approached with some degree of caution. A weight of 15 kg is roughly the 50th percentile for a 4-year-old, and outcome data support the notion that complications may be more common below this weight [53]. Admittedly, the 15-kg figure may be a rather arbitrary line drawn in shifting sand, but it probably still serves as a reasonable reflection of the comfort level for most pediatric electrophysiologists in the current era. Indications are thus a bit more liberal for 1–4-year-olds in comparison with infants, but if the child has only mild symptoms and/or good rhythm control on relatively benign drug therapy, ablation is often deferred to allow growth. The 4–12-year-age group comprises children for whom the procedural risks appear to be no higher than in older populations, but technical challenges related to vascular access and the need for small catheters still exist. As long as the procedure is conducted by an experienced team with the proper equipment on hand to meet these challenges, ablation seems to be a reasonable undertaking for all but the mildly symptomatic patient. Beyond the age of 12, when patients approach a weight of 35 kg or more, vascular caliber has usually progressed to the point that a full complement of standard catheters can be deployed in most cases. There are few absolute contraindications to ablation in this group, and the decision to proceed is usually a matter of lifestyle choice by the patient and parents, revolving around such issues as sports participation, adolescent difficulties with medication compliance, anxiety, and driving restrictions. Perhaps the biggest challenge in these teenagers relates to their psychological adaptation to the hospital setting and medical procedures [61]. Many will need high levels of emotional support before ablation,

Catheter ablation has greatly improved the management of tachycardia in children, and has earned an excellent overall record for efficacy and safety when performed at high-volume pediatric institutions. Pharmacologic therapy still retains a role in tachycardia management for infants [63], as well as some older children with relatively mild symptoms, but this role is continuing to decline as new technologies such as cryoablation lessen the risks of the procedure. Ablation in the very young patient, or in a patient of any age with complex congenital heart disease, still presents many unique challenges that are best addressed by experienced teams at centers equipped with the proper catheters, mapping systems, imaging capabilities, and support staff needed to maximize safety and success.

References 1 Van Hare GF, Velvis H, Langberg JJ. Successful transcatheter ablation of congenital junctional ectopic tachycardia in a ten-month-old infant using radiofrequency energy. Pacing Clin Electrophysiol 1990;13:730 –5. 2 Dick M, O’Connor BK, Serwer GA, LeRoy S, Armstrong B. Use of radiofrequency current to ablate accessory connections in children. Circulation 1991;84:2318 –24. 3 Walsh EP, Saul JP. Transcatheter ablation for pediatric tachyarrhythmias using radiofrequency electrical energy. Pediatr Ann 1991;20:388 – 92. 4 Van Hare GF, Lesh MD, Scheinman M, Langberg JJ. Percutaneous radiofrequency catheter ablation for supraventricular arrhythmias in children. J Am Coll Cardiol 1991;17: 1613 –20. 5 Lavoie J, Walsh EP, Burrows FA, Laussen P, Lulu JA, Hansen DD. Effects of propofol or isoflurane anesthesia on cardiac conduction in a pediatric population. Anesthesiology 1995;82: 884 –7. 6 Erb TO, Kanter RJ, Hall JM, Gan TJ, Kern FH, Schulman SR. Comparison of electrophysiologic effects of propofol and isoflurane-based anesthetics in children undergoing radiofrequency catheter ablation for supraventricular tachycardia. Anesthesiology 2002;96:1386 –94. 7 Chang RK, Stevenson WG, Wetzel GT, Shannon K, Baum VC, Klitzner TS. Effects of isoflurane on electrophysiological

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measurements in children with the Wolff–Parkinson–White syndrome. Pacing Clin Electrophysiol 1996;19:1082 – 8. Walsh EP. Transcatheter ablation of ectopic atrial tachycardia using radiofrequency current. In: Huang SKS, ed. Radiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications. Mount Kisco, NY: Futura, 1994: 421–43. Walsh EP. Intracardiac electrophysiologic studies. In: Lock JE, Keane JF, Perry SB, eds. Diagnostic and Interventional Catheterization in Congenital Heart Disease, 2nd ed. Boston: Kluwer Academic, 1999: 325–55. Pass RH, Walsh EP. Intracardiac electrophysiologic testing in pediatric patients. In: Walsh EP, Saul JP, Triedman JK, eds. Cardiac Arrhythmias in Children and Young Adults with Congenital Heart Disease. Philadelphia: Lippincott Williams & Wilkins, 2001: 57–94. Dick M 2nd, Law IH, Dorostkar PC, Armstrong B, Reppert C. Use of the His/RVA electrode catheter in children. J Electrocardiol 1996;29:227–33. Stabile G, De Simone A, Turco P, et al. Feasibility and safety of two French electrode catheters in the performance of electrophysiological studies. Pacing Clin Electrophysiol 1998;21: 2506–9. Saul JP, Hulse JE, De W, Lock JE, Walsh EP. Catheter ablation of accessory atrioventricular pathways in young patients: use of long vascular sheaths, the transseptal approach, and a retrograde left posterior parallel approach. J Am Coll Cardiol 1993;21:571–83. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20. Mullen MP, VanPraagh R, Walsh EP. Development and anatomy of the cardiac conduction system. In: Walsh EP, Saul JP, Triedman JK, eds. Cardiac Arrhythmias in Children and Young Adults with Congenital Heart Disease. Philadelphia: Lippincott Williams & Wilkins, 2001: 3–22. Reich JD, Auld D, Hulse E, Sullivan K, Campbell R. The Pediatric Radiofrequency Ablation Registry’s experience with Ebstein’s anomaly. J Cardiovasc Electrophysiol 1998;9: 1370–7. Epstein MR, Saul JP, Weindling SN, Triedman JK, Walsh EP. Atrioventricular reciprocating tachycardia involving twin atrioventricular nodes in patients with complex congenital heart disease. J Cardiovasc Electrophysiol 2001;12:671– 9. Triedman JK, Saul JP, Weindling SN, Walsh EP. Radiofrequency ablation of intraatrial reentrant tachycardia following surgical palliation of congenital heart disease. Circulation 1995; 91:707–14. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992;69:1028–32. Perry JC, Garson A Jr. Supraventricular tachycardia due to Wolff–Parkinson–White syndrome in children: early disappearance and late recurrence. J Am Coll Cardiol 1990;16: 1215–20. Benson DW, Dunnigan A, Benditt DG. Follow-up evaluation of infant paroxysmal atrial tachycardia: transesophageal study. Circulation 1987;75:542–9.

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22 Rhodes LA, Walsh EP, Saul JP. Programmed atrial stimulation via the esophagus for management of supraventricular tachycardias in infants and children. Am J Cardiol 1994;74: 353 – 6. 23 Fishberger SB, Colan SD, Saul JP, Mayer JE, Walsh EP. Myocardial mechanics before and after ablation of chronic tachycardia. Pacing Clin Electrophysiol 1995;19:42 –9. 24 Walsh EP, Saul JP, Hulse JE, et al. Transcatheter ablation of ectopic atrial tachycardia in young patients using radiofrequency current. Circulation 1992;86:1138 – 46. 25 Walsh EP. Ablation of ectopic atrial tachycardia in young patients. In: Huang SKS & Wilber DJ, eds. Radiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications, 2nd ed. Armonk, NY: Futura, 2000: 115 –38. 26 Ticho BS, Saul JP, Hulse JE, De W, Lulu J, Walsh EP. Variable location of accessory pathway causing the permanent form of junctional reciprocating tachycardia and confirmation with radiofrequency ablation. Am J Cardiol 1992;70:1559 – 64. 27 Ticho BS, Saul JP, Walsh EP. Radiofrequency catheter ablation for the permanent form of junctional reciprocating tachycardia. In: Huang SKS, ed. Radiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications. Mount Kisco, NY: Futura, 1994: 397–409. 28 Chetaille P, Walsh EP, Triedman JK. Outcomes of radiofrequency catheter ablation of atrioventricular reciprocating tachycardia in patients with congenital heart disease. Heart Rhythm 2004;1:168 –73. 29 Garson A Jr, Bink-Boelkens M, Hesslein PS, et al. Atrial flutter in the young: a collaborative study of 380 cases. J Am Coll Cardiol 1985;6:871– 8. 30 Triedman JK, Alexander ME, Berul CI, Bevilacqua LM, Walsh EP. Electroanatomic mapping of entrained and exit zones in patients with repaired congenital heart disease and intraatrial reentrant tachycardia. Circulation 2001;103:2060 –5. 31 Delacretaz E, Ganz LI, Friedman PL, et al. Multiple atrial macroreentry circuits in adults with repaired congenital heart disease: entrainment mapping combined with threedimensional electroanatomic mapping. J Am Coll Cardiol 2001;37:1665 –76. 32 Collins KK, Love BA, Walsh EP, Saul JP, Epstein MR, Triedman JK. Location of acutely successful radiofrequency catheter ablation of intraatrial reentrant tachycardia in patients with congenital heart disease. Am J Cardiol 2000;86:969 –74. 33 Triedman JK, Bergau DM, Saul JP, Epstein MR, Walsh EP. Efficacy of radiofrequency ablation for control of intraatrial reentrant tachycardia in patients with congenital heart disease. J Am Coll Cardiol 1997;30:1032–38. 34 Triedman JK, Alexander MA, Love BA, et al. Influence of patient factors and ablative technologies on outcomes of radiofrequency ablation of intra-atrial tachycardia in patients with congenital heart disease. J Am Coll Cardiol 2002;39: 1827–35. 35 Walsh EP, Rockenmacher S, Keane JF, Hougen TJ, Lock JE, Castaneda AR. Late results in patients with tetralogy of Fallot repaired during infancy. Circulation 1988;77:1062 –7. 36 Biblo LA, Carlson MD. Transcatheter radiofrequency ablation of ventricular tachycardia following surgical correction of tetralogy of Fallot. Pacing Clin Electrophysiol 1994;17:1556– 60.

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37 Goldner BG, Cooper R, Blau W, Cohen TJ. Radiofrequency catheter ablation as a primary therapy for treatment of ventricular tachycardia in a patient after repair of tetralogy of Fallot. Pacing Clin Electrophysiol 1994;17:1441– 6. 38 Burton ME, Leon AR. Radiofrequency catheter ablation of right ventricular outflow tract tachycardia late after complete repair of tetralogy of Fallot using the pace mapping technique. Pacing Clin Electrophysiol 1993;16:2319–25. 39 Gonska BD, Cao K, Raab J, Eigster G, Kreuzer H. Radiofrequency catheter ablation of right ventricular tachycardia late after repair of congenital heart defects. Circulation 1996; 94:1902–8. 40 Morwood JG, Triedman JK, Berul CI, et al. Radiofrequency catheter ablation of ventricular tachycardia in children and young adults with congenital heart disease. Heart Rhythm 2004;1:301–8. 41 Alexander ME, Walsh EP, Saul JP, Epstein MR, Triedman JK. Value of programmed ventricular stimulation in patients with congenital heart disease. J Cardiovasc Electrophysiol 1999; 10:1033–44. 42 Alexander ME, Cecchin F, Walsh EP, Triedman JK, Bevilacqua LM, Berul CI. Implications of implantable defibrillator therapy in congenital heart disease and pediatrics. J Cardiovasc Electrophysiol 2004;15:72–6. 43 Nath S, DiMarco JP, Haines DE. Basic aspects of radiofrequency catheter ablation. J Cardiovasc Electrophysiol 1994;5: 863–76. 44 Saul JP, Hulse JE, Walsh EP. Late enlargement of radiofrequency lesions in infant lambs: implications for ablation procedures in small children. Circulation 1994;90:492 – 9. 45 Bokenkamp R, Wibbelt G, Sturm M, et al. Effects of intracardiac radiofrequency current application on coronary artery vessels in young pigs. J Cardiovasc Electrophysiol 2000;11:565–71. 46 Paul T, Kakavand B, Blaufox AD, Saul JP. Complete occlusion of the left circumflex coronary artery after radiofrequency catheter ablation in an infant. J Cardiovasc Electrophysiol 2003;14:1004–6. 47 Bertram H, Bokenkamp R, Peuster M, Hausdorf G, Paul T. Coronary artery stenosis after radiofrequency catheter ablation of accessory atrioventricular pathways in children with Ebstein’s malformation. Circulation 2001;103:538 – 43. 48 Goldberg CS, Caplan MJ, Heidelberger KP, Dick M. The dimensions of the triangle of Koch in children. Am J Cardiol 1999;83:117–20. 49 Walsh EP. Radiofrequency catheter ablation for cardiac arrhythmias in children. Cardiol Rev 1996;4:200 –7. 50 Cote JM, Epstein MR, Triedman JK, Walsh EP, Saul JP. Low-temperature mapping predicts site of successful abla-

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Catheter ablation in young patients: special considerations tion while minimizing myocardial damage. Circulation 1996; 94:253 –7. Rhodes LA, Wieand TS, Vetter VL. Low temperature and low energy radiofrequency modification of atrioventricular nodal slow pathways in pediatric patients. Pacing Clin Electrophysiol 1999;22:1071– 8. Mandapati R, Berul CI, Triedman JK, Alexander ME, Walsh EP. Radiofrequency catheter ablation of septal accessory pathways in the pediatric age group. Am J Cardiol 2003;92: 947– 50. Kugler JD, Danford DA, Deal B, et al. Radiofrequency catheter ablation in children and adolescents. N Engl J Med 1994;330: 1481–7. Danford DA, Kugler JD, Deal B, et al. The learning curve for radiofrequency ablation of tachyarrhythmias in pediatric patients. Am J Cardiol 1995;75:587– 90. Van Hare GF, Javitz H, Carmelli D, et al. Prospective assessment after pediatric cardiac ablation: recurrence at 1 year after initially successful ablation of supraventricular tachycardia. Heart Rhythm 2004;1:188 – 96. Walsh EP. Ablation therapy. In: Deal B, Wolff G, Gelband H, eds. Current Concepts in Diagnosis and Management of Arrhythmias in Infants and Children. Armonk, NY: Futura, 1998: 329 – 67. Erickson CC, Walsh EP, Triedman JK, Saul JP. Efficacy and safety of radiofrequency ablation in infants and children less than 18 months of age. Am J Cardiol 1994;74:944 –7. Case CL, Gillette PC, Oslizlok PC, Knick BJ, Blair HL. Radiofrequency catheter ablation of incessant, medically resistant supraventricular tachycardia in infants and small children. J Am Coll Cardiol 1992;20:1405 –10. Carmichael TB, Walsh EP, Roth SJ. Anticipatory use of venoarterial extracorporeal membrane oxygenation for a high-risk cardiac procedure. Respir Care 2002;47:1002 – 6. Levine J, Walsh EP, Saul JP. Catheter ablation of accessory pathways in patients with congenital heart disease including heterotaxy syndrome. Am J Cardiol 1993;72:689 – 94. DiMaso DR, Spratt EG, Vaughan BL, D’Angelo EJ, VanDerFeen JR, Walsh EP. Psychological functioning in children and adolescents undergoing radiofrequency catheter ablation. Psychosomatics 2000;41:134 – 9. Friedman RA, Walsh EP, Silka MJ, et al. NASPE expert consensus conference: radiofrequency catheter ablation in children with and without congenital heart disease. Pacing Clin Electrophysiol 2002;25:1000 –17. Weindling SN, Saul JP, Walsh EP. Risks and efficacy of medical therapy for supraventricular tachycardia in neonates and infants. Am Heart J 1996;131:66 –72.

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8

Focal atrial tachycardias Satoshi Higa, Ching-Tai Tai, and Shih-Ann Chen

Introduction Focal atrial tachycardia (AT) is defined as supraventricular tachycardia originating from a discrete focus from which activation spreads to both atria [1]. Ablation of the focus eliminates this tachycardia. This chapter reviews the current state of the mapping techniques, strategies, safety, and efficacy associated with catheter ablation of focal AT.

Clinical characteristics Focal AT is a relatively infrequent form of supraventricular tachycardia. The prevalence of this type of tachycardia has been reported as 0.34% in asymptomatic individuals and 0.46% in symptomatic patients [2]. According to the classic definition of focal AT, the atrial rate is less than 250 beats/min, and discrete P waves are present, separated by isoelectric intervals. It is now recognized that focal AT can be substantially faster. It may be either paroxysmal or persistent and incessant. Focal AT can occur in children or adults without structural heart disease, but in the elderly it is often associated with structural heart disease [3 –16]. The persistent or incessant type of focal AT can cause tachycardia-induced cardiomyopathy, which is more common in children than adults [17–19]. Catheter ablation has an important role in the management of drugrefractory focal AT, and is now considered to be a first-line therapy in the guidelines published by the American College of Cardiology, American Heart Association, and European Society of Cardiology [20].

Electrophysiological characteristics Mechanisms Focal ATs can be caused by any of three potential mechan-

isms: abnormal automaticity, triggered activity, or microreentry [12,21–28]. Automatic AT is suggested by the following characteristics: • The onset of AT is followed by a gradual acceleration or “warm-up,” and termination follows slowing or “cool-down.” • AT is initiated spontaneously or with the administration of isoproterenol. • AT cannot be initiated, entrained, or terminated by programmed electrical stimulation. • AT can be transiently suppressed with overdrive atrial pacing, but subsequently resumes, with a gradual increase in the atrial rate [12,23]. Triggered activity is suggested by the following characteristics [12,24–26]: • AT is initiated or terminated by programmed electrical stimulation, and its initiation is cycle length–dependent. • Pacing does not entrain tachycardia, but can produce suppression or termination. A reentry mechanism is suggested by the following characteristics: • AT is reproducibly initiated and terminated by programmed electrical stimulation. • AT can be entrained by pacing. The distinction between triggered activity and reentry is often difficult. Further study is needed to assess whether the likely arrhythmia mechanism is related to clinical behavior of the arrhythmia and its response to treatment.

Pharmacological responses The response of AT to pharmacologic interventions probably depends on the AT mechanism. Most focal ATs can be terminated by adenosine, verapamil, and propranolol, suggesting triggered activity as the mechanism [12,27–30]. Recently, Chiale et al. reported a lidocaine-sensitive form of AT; the mechanism is unknown [31]. Termination of AT by adenosine suggests a focal AT. When adenosine fails to terminate AT, it usually produces an AV block that 105

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facilitates identification of P waves; this is also diagnostically useful, because it excludes AV reentry using an accessory pathway and makes AV nodal reentry unlikely as tachycardia mechanisms. In adults, failure of adenosine to terminate atrial tachycardia often suggests atrial macroreentry as the tachycardia mechanism [27].

Diagnostic criteria During the electrophysiologic (EP) study, AT can be diagnosed if the following criteria are present: • The atrial activation sequence during the tachycardia is different from that during sinus rhythm and from that produced by V–A conduction during ventricular pacing. • Atrioventricular nodal block occurs without affecting the tachycardia. • Changes in the PR and RP intervals follow changes in the atrial rate [12,32,33]. The AT origin can be adjacent to a valve annulus or the AV node, in which case pacing maneuvers are often helpful to distinguish AT with 1 : 1 AV conduction from atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia using a concealed accessory pathway [12,32,33]. Our first step is to carry out ventricular stimulation during tachycardia (Fig. 8.1). AT can be excluded if a ventricular premature beat that does not conduct to the atrium terminates the tachycardia. If a premature ventricular beat advances atrial activation when

the bundle of His is refractory, the presence of an atrioventricular pathway is confirmed, although this does not prove that the pathway is causing the tachycardia. Trains of ventricular stimuli at a cycle length just shorter than the tachycardia cycle length are also useful. If the ventricles are dissociated from the tachycardia, AV reentry using an accessory pathway is excluded. If ventricular pacing produces V–A conduction and a different atrial activation sequence from that of the tachycardia, AT is likely. If ventricular pacing produces VA conduction without interrupting tachycardia, the pattern of resumption of tachycardia distinguishes atrial tachycardia from AV or AV nodal reentry [33]. If the last atrial electrogram (A) that is advanced by the ventricular stimulus is followed by a ventricular (V) or His deflection (A–V response), AV nodal reentry or AV reentry is the mechanism. When the last stimulated A is followed by another A that continues tachycardia (A–A–V response) (Fig. 8.1), AT is the diagnosis [32]. A third useful maneuver is atrial pacing faster than the tachycardia. The faster rate typically induces some AV nodal delay, which resolves when pacing is terminated and the rate slows back to the tachycardia rate. After pacing, a fixed VA interval (variation less than 10 ms) as the tachycardia cycle length varies indicates that AV nodal reentry or AV reentry using an accessory pathway is likely. In contrast, a variable VA interval suggests AT (Fig. 8.2) [33]. Finally, AV block when pacing the atrium at the tachycardia cycle length immediately after tachycardia termination suggests that AV nodal conduction is required for tachycardia and that AT is unlikely.

Common sites of origin of focal atrial tachycardia

Figure 8.1 The intracardiac recordings show three ventricular stimuli with coupling intervals of 340 and 300 ms during atrial tachycardia. The last stimulus advanced atrial activation to an A–A interval of 380 ms. The tachycardia continued after a subsequent atrial electrogram (A–A–V response), consistent with atrial tachycardia. CS, coronary sinus; HIS, bundle of His; HRA, high right atrium; O/P/M/D, ostium, proximal, middle, distal. (Reproduced from [89].) (Hsieh and Chen et al. Figure 1 on page 188. 2nd Edition of Catheter Ablation of Arrhythmias. 2002: 185–203. With permission from Futura Publishing).

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Focal ATs tend to originate in characteristic locations associated with anatomic structures (Figs. 8.2– 8.5). Common right atrial origins are the crista terminalis, the right side of the interatrial septum, including the vicinity of the AV node, the tricuspid annulus, the coronary sinus ostium, the right atrial appendage, and the superior vena cava (SVC) [11,29,34–43]. In the left atrium, the majority of AT foci are found at the ostial portion of the pulmonary veins, the base of the left atrial appendage, the left side of the interatrial septum, the distal portion of the coronary sinus, the mitral annulus, or the ligament of Marshall or a leftsided superior vena cava (when present) [44 –52]. There are two types of AT involving the sinus node. Firstly, sinus nodal reentrant tachycardia is defined as a tachycardia originating from the sinus nodal complex that can be induced and terminated with programmed atrial stimulation [53,54]. The P wave morphology of the 12-lead surface ECG and the endocardial activation sequence during the tachycardia are identical or similar to those

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Figure 8.2 Anteroseptal atrial tachycardia (AT). A. Spontaneous termination of AT on the 12-lead electrocardiograph. The arrows indicate the last P wave of AT, which is biphasic in lead V1 and positive in leads II, III, and aVF. B. Right atrial pacing (S1) inducing AT. Earliest atrial activation is recorded from the area of the bundle of His. The VA interval after atrial pacing is variable—longer immediately after pacing, suggesting atrial

tachycardia rather than AV nodal reentry. CS, coronary sinus; HIS, bundle of His; HRA, high right atrium; RVA, right ventricular apex; O/P/M/D, ostium, proximal, middle, distal. (Reproduced from [36].) (Chen et al. Figure 1 on page 746. J Cariovasc Electrophysiol. 2001; 11: 744–749, with permission from Blackwell Publishing.

Figure 8.3 Midseptal atrial tachycardia (AT). A. AT on 12-lead electrocardiography. B. A premature stimulus (S) terminating the AT, followed by a sinus beat with biphasic P waves (positive–negative) in V1. Comparison of the last AT beat (arrow) and the sinus beat shows that this mid-septal AT exhibits a biphasic P wave (negative–positive) in lead V1 and a

negative P wave in lead II. CS, coronary sinus; HIS, bundle of His; HRA, high right atrium; O/P, ostium, proximal. (Reproduced from [36].) (Chen et al. Figure 1 on page 746. J Cariovasc Electrophysiol. 2001; 11: 744–749, with permission from Blackwell Publishing.)

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Figure 8.4 Posteroseptal atrial tachycardia (AT). A. The 12-lead electrocardiogram of the AT. Two premature ventricular stimuli were delivered during AT to expose the P wave. The P wave of AT is positive in lead V1 and negative in leads II, III, and aVF. B. Simultaneous intracardiac recordings. Earliest activation during AT is at the CS os. CSO, coronary

sinus orifice; CSD, distal portion of the coronary sinus; His-P, His-M, His-D, proximal, middle, and distal parts of the bundle of His recording; HRA, high right atrium; RVA, right ventricular apex. (Reproduced from [36].) (Chen et al. Figure 1 on page 746. J Cariovasc Electrophysiol. 2001, 11: 744–749, with permission from Blackwell Publishing.)

during sinus rhythm. Whether this AT truly originates from the sinus node or adjacent tissue is unclear [55,56]. Secondly, inappropriate sinus tachycardia (IST) also originates from the sinus node region along the crista terminalis. It is characterized by an increased heart rate (more than 100 beats/min) at rest or with minimal exertion [57–59]. Diagnosis requires exclusion of secondary causes of the sinus tachycardia, such as hyperthyroidism, and exclusion of other ATs arising from the upper portion of the crista terminalis or superior vena cava. The underlying mechanism of this type of tachycardia is not clear; abnormal autonomic nervous system function and a primary abnormality of the sinus node itself have been suggested [60]. The site of the earliest activation may shift along the crista terminalis as the autonomic tone changes. It is often difficult to distinguish between inappropriate sinus tachycardia and focal AT originating from the upper portion of the crista terminalis (Fig. 8.6). The relation of AT origins to specific anatomic structures has been cited as evidence for a possible role of

anisotropy, poor intercellular coupling, and embryologically derived conduction tissue as the arrhythmogenic substrates of these tachycardias [11,38].

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Mapping methods Noninvasive mapping techniques Twelve-lead surface ECG. The configuration of the 12-lead ECG P wave can be used to obtain an approximate estimate of the location of the AT (Figs. 8.2–8.5, 8.7). In general, focal AT is characterized by discrete P waves separated by isoelectric intervals in all leads. However, a continuous undulating P wave without an isoelectric baseline, or a chaotic and irregular baseline without discernible P waves, is seen in some focal ATs [61– 65]. Additionally, merging of P and preceding T waves often obscures the morphological details of the P waves. In such cases, delivery of premature ventricular stimuli to advance the

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Figure 8.5 Atrial tachycardia originating from the tricuspid annulus. A. The 12-lead electrocardiogram, showing two premature ventricular stimuli during AT, allowing definition of the P wave morphology (arrows). The P waves are negative in the precordial leads and inferior leads, and positive in lead I and AVL. The P wave polarity favors an origin of the AT from the tricuspid annulus. B. The ablation site electrogram during sinus rhythm shows a small A wave and a large V wave, indicating an origin near the tricuspid

annulus. The earliest atrial activation time before the onset of the surface P wave is 43 ms. C. AT terminates during radiofrequency (RF) ablation. LRA, low right atrium; CSD, distal portion of the coronary sinus; CSM, middle portion of the coronary sinus; CSO, coronary sinus ostium; HIS, bundle of His area; ABL, ablation catheter; TA, tricuspid annulus. (Reproduced from [89].) (Hsieh and Chen. Figure 5 on page 192. 2nd Edition of Catheter Ablation of Arrhythmias. 2002: 185–203, with permission from Futura Publishing.)

QRS (Figs. 8.4, 8.5) or creation of transient AV block with carotid sinus massage or adenosine is helpful to obtain a clear view of the P waves during the tachycardia. Leads aVL and V1 are helpful for distinguishing right atrial from left atrial foci [66]. A negative or isoelectric P wave in lead aVL and a positive P wave in lead V1 suggest a left atrial origin. In contrast, a positive or biphasic P wave in lead aVL and a negative or biphasic P wave in lead V1 favor a right atrial origin. In addition, positive P waves in the inferior leads suggest a superior or anterior origin, and biphasic or negative P waves in the inferior leads indicate a posterior or inferior origin. Other proposed P wave morphologies that suggest the relation of a tachycardia focus to specific anatomic structures are as follows: • A negative P wave in lead aVR usually indicates a crista terminalis origin [67]. • A negative P wave in the anterior precordial and inferior leads suggests AT from the inferoanterior portion of the tricuspid annulus [38]. • The combination of a negative P wave in V6, a positive P wave in V1, and negative P waves in all three inferior

leads suggests a posteroseptal AT around or below the coronary sinus ostium [36]. • A monophasic positive P wave in lead V1, observed with ATs originating from the vicinity of the AV node, favors a left-sided interatrial septal origin [37]. • An almost identical P wave morphology during the tachycardia to sinus rhythm indicates an origin at the upper portion of the crista terminalis or sinus tachycardia [11,53,54,57–59]. Endocardial electrograms usually reveal an electrically silent period, with absence of atrial electrograms and an isoelectric baseline between each P wave on the surface ECG. Unusual patterns are observed, however, when the tachycardia cycle length is short and there is intra-atrial conduction delay such that the atrial activation time during the tachycardia can occupy a large proportion of the tachycardia cycle length. The P wave morphology may then demonstrate an atrial flutter–like pattern, with continuous undulation without an isoelectric baseline in the ECG [61–63]. Rapid AT can be the cause of atrial fibrillation and serve as a focal source of the atrial fibrillation. 109

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Figure 8.6 Catheter modification of the sinus node in a patient with inappropriate sinus tachycardia. Intracardiac echocardiography (ECG) was used to position the ablation catheter along the crista terminalis. A. Intracardiac electrograms from the superior vena cava (SVC) and along the crista terminalis (CT). The electrogram from the ablation site (ABL) at the crista terminalis is 16 ms earlier than the ECG P wave. B. Radiofrequency ablation produces a sudden decrease in the heart rate. C. Intracardiac echocardiography demonstrates the anatomic site of the ablation catheter tip (ABL) along the crista terminalis (CT). The superior vena cava (SVC) and right atrium (RA) are indicated. (Reproduced from [89].) (Hsieh and Chen. Figure 6 on page 194. 2nd Edition of Catheter Ablation of Arrhythmias. 2002: 185–203, with permission from Futura Publishing.)

A very fast focal discharge with variable exit block from the focus, or nonuniform centrifugal conduction away from the focus with a fibrillatory conduction pattern in the atria, can give rise to an electrocardiographic pattern of atrial fibrillation [64,65]. Body surface mapping. It has been suggested that body sur110

face mapping can identify the region of the AT focus and may be useful prior to intracardiac mapping, particularly if AT is not inducible in the electrophysiology laboratory or if only single atrial beats are available for mapping [68]. Initial systems had limited resolution and predictive accuracy and did not come into widespread use. It is hoped that more sophisticated analysis of surface recordings and

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Figure 8.7 The algorithm shows a scheme for assessing the likely origin of atrial tachycardia, based on the P wave morphology in the 12-lead electrocardiogram. A negative or isoelectric P wave in lead I or aVL suggests a left atrial focus. Positive P waves in inferior leads indicate superior (cranial) origins. (Reproduced from [89].) (Hsieh and Chen. Figure 6 on page 194. 2nd Edition of Catheter Ablation of Arrhythmias. 2002: 185–203, with permission from Futura Publishing.)

use of a multielectrode vest to record 224 body-surface electrograms may improve the value of noninvasive recordings [69].

Invasive mapping techniques Endocardial activation mapping using electrode catheters. Traditionally, endocardial activation mapping begins with assessment of atrial activation from catheters positioned at routine sites in the high right atrium, coronary sinus, and bundle of His region. Further detailed mapping is achieved by an ablation catheter positioned within the region of interest to identify the earliest activation time relative to the onset of the P wave or a fixed atrial electrogram reference recorded from the coronary sinus ostium or high right atrium. The earliest activation time at the successful ablation site is usually at least 30 ms before the onset of the P wave, but may vary greatly among patients [3–16]. Conventional endocardial mapping has limitations aparticularly the limited number of recording sites for sampling brief arrhythmias. An expandable multielectrode basket catheter (Constellation; Boston Scientific, Natick, Massachusetts, USA) has been deployed for global atrial endocardial mapping to identify the AT origin more rapidly and allows the ablation catheter to be navigated inside the basket catheter (Astronomer System; Boston Scientific) [13,70]. Limitations are incomplete endocardial coverage of the atrium, especially in the appendage and isthmus, and a risk of systemic thromboembolism during mapping in the left atrium. The “two-catheter technique” is another useful method to shorten the mapping time.

Focal atrial tachycardias

Two roving ablation catheters are alternately moved to progressively earlier sites to identify early atrial activation. Then one is left in place as a reference and the other catheter is moved around the reference catheter to find an even earlier site of activation. Atrial anatomy is complex, and adjacent structures can create misleading signals that complicate mapping. The right superior pulmonary vein is in close proximity to the right atrium, such that signals from both structures can be recorded simultaneously. Furthermore, AT from either site can have a similar P wave morphology. Thus, when the AT apparently originates from the upper portion of the crista terminalis or sinoatrial junction, the possibility of a right upper pulmonary vein tachycardia should be considered [11,71,72]. Identification of far-field pulmonary vein potentials from the high posteromedial right atrial recording indicates a right pulmonary vein tachycardia [72]. AT with an apparent high right atrial origin can originate from within the superior vena cava, requiring careful mapping for identification [73 –75]. Identification of septal ATs can be challenging (Figs. 8.2–8.4). Focal AT may originate from either side of the interatrial septum in the vicinity of the AV node [37]. RF ablation in this area carries a substantial risk of AV block. Confirmation that tachycardia is not left atrial in origin is warranted before applying ablation lesions in this region, particularly if earliest right atrial activation is ≤ 15 ms preceding the P wave onset or when AT has a monophasic positive P wave in lead V1 [37,48]. Earliest right atrial activation near the putative Bachmann’s bundle region can also occur with a left atrial origin. ATs can also originate from epicardial structures such as the ligament of Marshall, which can be electrically connected to the pulmonary veins, left atrial musculature, or the distal coronary sinus [76,77]. If the earliest endocardial site is in close proximity to the posterolateral mitral annulus or at the left superior or inferior pulmonary veins, a potential epicardial tachycardia focus should be considered. Pacing from the distal coronary sinus advances potentials from the ligament of Marshall relative to the coronary sinus ostium or left atrium, helping to distinguish them from pulmonary vein potentials (Fig. 8.8) [76,77]. After the earliest activation region is identified, additional features of the local electrogram can be used to fine-tune localization of the targeted site. At the region of earliest activation, the unipolar electrogram (unfiltered or high-pass–filtered at a low corner frequency such as 0.5 Hz) should display a QS complex with an initial rapid intrinsic deflection downstroke (Fig. 8.9) [8]. Fractionated or spiked potentials are often present at the successful ablation site (Fig. 8.9), but may also be seen at other sites nonspecific and not sensitive [11]. ATs that originate from the mitral or tricuspid valve annulus have large V and smaller A deflections recorded at their origin (Fig. 8.5). 111

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Figure 8.8 A. Recordings of epicardial left atrial tract potentials (arrows) from a catheter inside the left superior pulmonary vein (LSPV; around 6–18 mm from distal to ostium) during sinus rhythm. Note that the left atrial tract potentials (arrows) occur later than the fused deflections of left atrium (asterisks) and pulmonary vein (arrowhead) musculature potentials, and are simultaneous with the His bundle deflection (H). LSPV-O, ostium of the left superior pulmonary vein; LSPV-D, distal left superior pulmonary vein; LAPW, left atrial posterior wall; HIS, bundle of His area; CSM, middle portion of the coronary sinus; CSO, coronary sinus ostium. B. During pacing from the distal coronary sinus (S1S1 = 500 ms), the left atrial tract potentials fuse with the left atrium–pulmonary vein musculature potentials, suggesting simultaneous activation. C. Intracardiac recordings of sinus beat followed by an ectopic beat originating from the distal portion of the LSPV. With the ectopic beat, it should be noted that the pulmonary vein musculature potential (arrowheads) precedes the left atrial potential (asterisk) and the left atrial tract potential (arrow) to form triple potentials around the pulmonary vein ostium area. Activation time (40 ms) from the middle portion of the coronary sinus (CSM) to the left atrial tract (LAT) is the same during the sinus beat and the ectopic beat, suggesting insertion of the LAT into the musculature of the CSM and nearby left atrium. D, E. A posterior view of the right and left atria, showing the bipolar recording sites (asterisks), the stimulating site (black dot) and the location

of ligament of Marshall (LOM). During sinus rhythm (SR), the electrical impulse originating from the sinus node spreads anteriorly around the superior vena cava (SVC), proceeding from right to left across Bachmann’s bundle to reach the base of the left atrial appendage (LAA; solid lines). The wavefront traversing the posterior right atrial appendage (RAA) propagates between the vena cava onto the posterior left atrium beneath the right pulmonary veins (PV; solid lines). The LAT within the LOM is activated following activation of the coronary sinus (CS) ostium, because the LOM is insulated from the left atrial wall (broken line). During distal CS pacing, the activation wavefronts spread simultaneously along the proximal CS and the LOM (broken lines), through the CS ostium, and propagate onto the posterior right and left atria (solid lines). IVC: inferior vena cava; SAN, sinoatrial node. F. Intracardiac recordings of an ectopic beat originating from the left atrial tract (LAT) within the ligament of Marshall (LOM). It should be noted that the LAT potential (arrow) precedes the left atrial potential (asterisk) and the pulmonary vein musculature potential (arrowheads). LAT-D, distal portion of the left atrial tract; LAT-P, proximal portion of the left atrial tract; HRA, high right atrium; LRA = low right atrium; CSO = coronary sinus ostium; CSM = middle coronary sinus. (Modified from figures in [76].) (Tai et al. Figure 1, 3–6 on page 1495, 1497–1500, Pacing Clin Electrophysiology. 2000; 23: 1493–1501, with permission from Blackwell Publishing.)

Paced activation sequence mapping can also be used to help localize an AT focus [5,10,12,14]. Atrial pacing is performed from the roving ablation catheter that is positioned at or near the site of earliest activation. Comparison

of the paced P wave morphology and endocardial atrial activation sequence with that of AT beats can suggest whether the pacing site is close to the AT origin or needs to be moved in one direction or another. The spatial resolution

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Figure 8.9 Unipolar and bipolar recordings from the successful ablation site during atrial tachycardia (the first three beats from the left side of the figure) and sinus rhythm after spontaneous termination of atrial tachycardia (last beat). The arrows indicate the onset of the atrial electrograms recorded from the ablation site. Bipolar recordings from the ablation catheter show fractionated electrograms during tachycardia and discrete electrograms during sinus rhythm. The unipolar recording shows a QS pattern during tachycardia, consistent with wavefronts moving away from the recording site, and an rS pattern during sinus rhythm. HRA, high right atrium; HIS, bundle of His area; CSO, coronary sinus ostium. (Reproduced from [89].) (Hsieh and Chen. Figure 7 on page 196. 2nd Edition of Catheter Ablation of Arrhythmias. 2002: 185–203, with permission from Futura Publishing.)

of this technique is limited, being at most ± 1.7 cm; it is usually employed only as an approximate guide when AT is difficult to induce or nonsustained [78]. Electromagnetic mapping system (Carto). This electroanatomical mapping system (Carto, Biosense Webster, Diamond Bar, California, USA) relies on a sequential mapping method that allows reconstruction of the chamber geometry and activation sequence during point-by-point sampling from a roving catheter [15,79 – 82]. Repeated sampling from closely adjacent points can create high-resolution maps in the region of the earliest activation to identify tachycardia foci. The major limitation of this system is the requirement for point-by-point sampling, which makes mapping of nonsustained ATs difficult and impairs the creation of complete, detailed maps of some AT foci. Noncontact mapping system (EnSite). A noncontact mapping system (EnSite; Endocardial Solutions/St. Jude Medical, Inc., St. Paul, Minnesota, USA) has been shown to facilitate identification of ectopic foci and catheter navigation to the target sites. It allows precise reconstruction of atrial geometry [83,84]. Its major advantage over sequential mapping techniques is the simultaneous acquisition of electrical signals from across the atrium during a single beat, facilitating mapping of nonsustained AT. Recently, this technology has shown that preferential routes for rapid conduction in the atrium influence atrial activation during right atrial tachycardias, complicating identification of AT foci [83]. The spread of activation can be nonuniform rather than radial. Activation from AT in the crista terminalis may spread superiorly and inferiorly more quickly than laterally, due to prominent anisotropic conduction in

this structure. A focus between the crista terminalis and the tricuspid annulus may appear to display early activation some distance from the focus, due to preferential conduction through portions of the atrium (Fig. 8.10).

Intracardiac echocardiography Intracardiac echocardiography has been used in conjunction with conventional catheter mapping to assess the relation of mapping sites to endocardial structures and assess catheter stability for ablation. Intracardiac echocardiography is useful for guiding the mapping or ablation catheter along the crista terminalis. It is also useful for assessing the proximity of a mapping site to the superior vena cava, upper portion of the crista terminalis, and right superior pulmonary vein [71], facilitating precise mapping and the interpretation of far-field potentials from neighboring structures [11,58].

Ablation techniques Once the AT focus is identified, radiofrequency energy with power typically between 20 and 50 W is delivered for 30–60 s. Acceleration of AT followed by termination is an excellent indication that the lesion will be effective. Heating presumably induces automaticity, followed by quiescence with permanent injury. Rapid termination of AT within 10 s of initiating radiofrequency energy is also a good predictor of success. Ablation of the origin and/or tissue along the proximal area of preferential conduction has been effective in eliminating focal AT. Ablation that produces exit block from a 113

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Figure 8.10 Noncontact mapping showing the origin and preferential conduction path for a focal atrial tachycardia from the right atrium. The right atrium is shown in a lateral caudal view. The color scale for the isochronal map has been set so that white indicates earliest activation and purple indicates the latest activation time. Focal activation originates from the anterior portion of the junction between the right atrium and inferior vena cava (IVC) and then propagates up to the middle portion before spreading out to the rest of the atrium. The contact and noncontact unipolar electrograms show a QS pattern at the origin and an rS pattern at

the breakout site. The electrograms at the origin and region of preferential conduction reveal multiple components. The noncontact unipolar electrograms recorded at the origin, preferential conduction region, and breakout site were nearly identical to electrograms obtained with simultaneous contact mapping from these areas. O, origin of AT; P, preferential conduction; BO, breakout site of AT; IVC, inferior vena cava. (Reproduced from [83].) (Higa et al. Figure 5 on page 89, Circulation. 2004; 109: 84–91, with permission from Lippincott Williams & Wilkins.)

focus can be effective. For example, electrical disconnection of the superior vena cava can prevent ATs originating from the muscle sleeve around the SVC, despite continued focal activity in the sleeve [42,73]. For ATs that originate within a pulmonary vein, ablation that targets the focus is highly successful. However, there is a risk of pulmonary vein stenosis; isolation of the arrhythmogenic PV at the atria–PV junction may be preferable in some patients to avoid PV stenosis [44]. Some ATs that have early activation in the area between the left superior PV ostium and atrioventricular groove originate from the ligament of Marshall. A discrete potential is present that can be distinguished from atrial and pulmonary vein potentials by pacing maneuvers, so that inappropriate RF lesions can be avoided (Fig. 8.8) [76]. Mechanical interruption of AT by catheter manipulation at the presumed AT origin may also be a good predictor of a potentially successful ablation site [10]. Mechanical trauma may, however, suppress AT for several hours, impairing the ability to assess the effectiveness of ablation lesions.

marized in Tables 8.1–8.5. In pooled data from a total of 622 patients with focal AT from 19 relevant publications, the average acute success rate of RF ablation was 89%, and the recurrence rate was 8% (Table 8.1). Left-sided ATs accounted for 19% of cases, and 7% of patients had multiple foci. Success rates were lower for left-sided ATs than for right-sided ATs. Patients with multiple AT foci had a higher recurrence rate than those with a single focus. Patient age is an independent predictor of the existence of multiple ATs and recurrence of AT after an initial successful ablation [85]. Older age is associated with atrial fibrosis that is likely to increase vulnerability to arrhythmias. Significant complications were observed in 1% of patients, including cardiac perforation, phrenic nerve palsy, and sinus node dysfunction.

Ablation outcomes The efficacy of catheter ablation of focal AT and modifications of IST described by many investigators are sum114

Avoiding common pitfalls and complications ATs from the anterior atrial septum or Koch’s triangle, where there is a risk of ablation-induced AV block, are not uncommon. These tachycardias can mimic slow–fast or fast–intermediate AVNRT or AVRT using a concealed septal accessory pathway [29,34,35]. Appropriate maneuvers to confirm the diagnosis, discussed above, are important before mapping and ablation. Once the diagnosis of

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Focal atrial tachycardias

Table 8.1 Radiofrequency catheter ablation of focal atrial tachycardias. First author (ref.)

Year

Mapping tool

Patients (n)

Total ablated AT foci (R/L)

Multiple foci

Success

Complications

Recurrence

Follow-up (months)

Walsh [3] Goldberger [4] Tracy [5] Kay [6] Lesh [7] Wang [9] Poty [8] Pappone [10] Kalman [11] Chen [85] Weiss [14] Natale [15] Schmitt [13] Weiss [80] Anguera [16] Schmitt [84] Wetzel [82] Hoffmann [81] Higa [83]

1992 1993 1993 1993 1994 1995 1996 1996 1998 1998 1998 1998 1999 2000 2001 2001 2002 2002 2004

C C C C C C C C C / ICE C C Carto Basket Carto C EnSite Carto C / Carto EnSite

12 15 10 15 17 13 36 45 27 112 48 24 31/16* 15 105 10/8* 32/30* 42/37† 13

12 (5/7) 15 (15/0) 10 (8/2) 15 (14/1) 22 (17/5) 15 (10/5) 36 (33/3) 45 (36/9) 31 (27/4) 105 (95/10) 52 (40/12) 29 (16/13) 31 (21/10) 15 (14/1) 105 (91/14) 8 (8/0) 34 (22/12) 38 (27/11) 14 (14/0)

0 (0%) 2 (13%) 2 (20%) 1 (7%) NA 1 (8%) 3 (8%) NA NA 17 (15%) NA 1 (4%) 3 (10%) 0 (0%) 7 (7%) 0 (0%) 3 (10%) 3 (8%) 1 (8%)

11 (92%) 12 (80%) 7 (70%) 15 (100%) 16 (94%) 9 (69%) 31 (86%) 42 (93%) 25 (93%) 100 (98%) 44 (92%) 24 (100%) 15 (94%) 15 (100%) 80 (76%) 7 (88%) 33 (97%)‡ 32 (86%) 12 (92%)

1 (8%) 0 (0%) 0 (0%) 1 (7%) 0 (0%) 1 (8%) 0 (0%) 3 (7%) 0 (0%) 0 (0%) 0 (0%) NA NA 0 (0%) 2 (2%) 0 (0%) 0 (0%) 0 (0%) 0 (0%)

1 (9%) 2 (17%) 2 (29%) 3 (20%) 2 (13%) 1 (8%) 4 (13%) 3 (7%) 4 (16%) 3 (3%) 5 (11%) 1 (4%) NA 2 (13%) 8 (10%) 0 (0%) 1 (3%) 4 (13%) 1 (8%)

13 (range 3–21) 19 ± 7 7±4 9±4 10 ± 1 17 ± 14 18 ± 15 22 ± 12 10 ± 6 NA range 4–58 NA NA 9±6 33 ± 15 6±2 16 ± 9 7±6 8±5

622/598

632 (513/119)

44 (7%)

530 (89%)

8 (1%)

47 (8%)

Total

AT, atrial tachycardia; Basket, basket catheter–guided; C, conventional mapping; Carto, Carto electromagnetic mapping system; EnSite, EnSite noncontact mapping system; ICE, intracardiac echocardiography; R/L, right-sided/left-sided (atrial tachycardia); NA, data not available. * The number indicates patients who received ablation of AT. † Only 37 patients completed the electroanatomical mapping and 38 of 45 AT patients received ablation. ‡ Numbers indicate number of AT foci; 33 out of 34 AT foci were eliminated in this study.

Table 8.2 Radiofrequency catheter ablation of septal atrial tachycardias.

First author (ref.)

Year

Mapping tool

Patients (n)

Location of AT origin

Total ablated AT foci (R/L)

Multiple foci

Success

Complications

Recurrence

Follow-up (months)

Connors [35] Frey [37] Marrouche [48]

2000 2001 2002

C C C / Carto

8 16 5

Koch triangle Septum Septum

8 (8/0) 16 (10/6) 5 (2/3)

0 (0%) 0 (0%) 0 (0%)

8 (100%) 16 (100%) 5 (100%)

1 (13%) 0 (0%) 0 (0%)

1 (13%) 2 (13%) 0 (0%)

NA 8 (1–68) 14 ± 8

AT, atrial tachycardia; C, conventional mapping; Carto, Carto electromagnetic mapping system; NA, data not available; R/L, right-sided/left-sided AT.

Table 8.3 Radiofrequency catheter ablation of annular atrial tachycardia.

First author (ref.)

Year

Mapping tool

Patients (n)

Location of AT origin

Total ablated AT foci (R/L)

Multiple foci

Success

Complications

Recurrence

Follow-up (months)

Morton [38] Matsuoka [40] Kistler [52]

2001 2002 2003

C C C

9 5 7

TA TA / MA MA

9 (9/0) 6 (4/2) 7 (0/7)

0 (0%) 1 (20%) 0 (0%)

9 (100%) 5 (100%) 7 (100%)

0 (0%) 0 (0%) 0 (0%)

1 (11%) 0 (0%) 1 (14%)

9±6 32 ± 11 17 ± 10

AT, atrial tachycardia; C, conventional mapping; MA, mitral annulus; R/L, right-sided/left-sided AT; TA, tricuspid annulus.

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Table 8.4 Radiofrequency catheter ablation of atrial tachycardias from thoracic veins (pulmonary vein, coronary sinus, superior vena cava, ligament of Marshall).

First author (ref.)

Year

Mapping tool

Patients (n)

Location of AT origin

Total ablated AT foci (R/L)

Multiple foci

Success

Complications

Recurrence

Follow-up (months)

Kistler [44] Volkmer [49] Navarrete [50] Ino [42] Dong [43] Polymeropoulos [51]

2003 2002 2003 2000 2002 2002

C Carto Carto C Carto Carto

27 1 1 1 1 1

PV CS CS SVC SVC LOM

28 (0/28)* 1(0/1) 1(0/1) 1(1/0) 1(1/0) 1(0/1)

1 (4%) 0 (0%) 0 (0%) 0 (0%) 0 (0%) 0 (0%)

28 (100%) 1 (100%) 1 (100%) 1 (100%) 1 (100%) 1 (100%)

0 (0%) 0 (0%) 0 (0%) 1 (100%)† 0 (0%) NA

4 (14%) 0 (0%) 0 (0%) 0 (0%) 0 (0%) 0 (0%)

25 ± 22 5 6 15 3 3

AT, atrial tachycardia; C, conventional mapping; Carto, Carto electromagnetic mapping system; CS, coronary sinus; LOM, ligament of Marshall, PV, pulmonary vein; R/L, right-sided/left-sided AT; SVC, superior vena cava. * 25 ATs received focal ablation and three ATs received isolation of the arrhythmogenic pulmonary vein. † Transient phrenic nerve palsy. Table 8.5 Radiofrequency catheter ablation and modification of sinus tachycardias. Patients (n)

End points

Success

Complications

Recurrence

Sinus node reentrant tachycardia Sanders [54] 1994 C

10

–

10 (100%)

0 (0%)

0 (0%)

9±6

Inappropriate sinus tachycardia Lee [57] 1995 Callans [58] 1999 Man [59] 2000

16 10 29

Total abl /25% HR* 30 beats/min† < 90 beats/min‡

16 (100%) 8 (80%) 19 (66%)

2 (13%) 0 (0%) 2 (7%)

2 (17%) NA 6 (27%)

7±2 NA 32 ± 12

First author (ref.)

Year

Mapping tool

C / ICE C / ICE C

Follow-up (months)

Abl, ablation; AT, atrial tachycardia; C, conventional mapping; HR, heart rate; ICE, intracardiac echocardiography; NA, data not available. * Total ablation of sinus node and more than 20% reduction in the baseline sinus rate. † Abrupt decrease (more than 30 beats/min) in the baseline sinus rate. ‡ Reduction of the baseline sinus rate to < 90 beats/min and a 20% or greater reduction in sinus rate during isoproterenol infusion.

AT is confirmed, the presence of a presumed AV nodal potential or bundle of His potential at the ablation site is not a contraindication for an energy application. Titrated energy applications (5 –10 W increments, starting from 10 W to a maximum output of 40 W) during continuous monitoring of AV conduction can be considered in order to minimize the risk of AV block. Wong et al. reported the use of cryomapping (–30 °C) to identify foci near the AV node and assess the impact of cooling on AV conduction before applying a permanent cryoablation lesion (less than –70 °C) if the site was deemed to be safe [86]. If ablation is carried out in a venous structure such as a pulmonary vein, limiting the temperature (less than 50 –55 °C) can reduce the risk of thrombus formation, catheter adhesion to the venous wall, and venous stenosis. If an epicardial focus is suspected, use of a large-tip (8 mm) electrode catheter or saline-irrigated catheter may allow ablation of the epicardial focus from within the atrium, rather than from within an epicardial vein. However, fatal atrio-esophageal fistulas can occur with this type of aggressive radiofrequency ablation at the posterior aspect of the left atrium [87]. It is very important 116

to evaluate the anatomical relation between the esophagus and left atrium before ablation in this region and to limit RF power when the target site is located along the esophagus. Catheter ablation of the sinus node for inappropriate sinus tachycardia often requires extensive ablation. RF applications should start from the most superior aspect of the crista terminalis, with subsequent lesions moving downward to the inferior aspect of the crista in order to achieve approximately a 25–30% decrease in the maximal heart rate during the infusion of isoproterenol and/or atropine. A number of complications can result from aggressive ablation in this region (Fig. 8.6) [57–59]. Permanent sinus node dysfunction requiring a pacemaker implantation can occur. Stenosis of the superior vena cava–right atrial junction, with acute or late superior vena cava syndrome, has been reported. Injury to the adjacent right phrenic nerve can occur. Proximity to the phrenic nerve can be evaluated by pacing at high output and assessing phrenic nerve capture prior to ablation. Some ATs originate from within the muscular coat surrounding the coronary sinus [88]. Sanders et al. reported

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ablation to electrically disconnect the CS to isolate an AT trigger causing atrial fibrillation [88]. Electrical disconnection of the CS musculature may be an alternative approach when the focus-oriented approach fails in eliminating CS tachycardia, but AV block and coronary injury are potential risks.

Conclusions Focal AT can be readily diagnosed in electrophysiological studies and localized by conventional endocardial mapping and/or advanced three-dimensional mapping systems. Knowledge of anatomic–electrophysiological relationships is often helpful in guiding mapping and ablation. Most focal ATs can be eliminated with a high success rate and low recurrence and complication rates when appropriate precautions are taken.

References 1 Saoudi N, Cosio F, Waldo A, et al. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the working group of arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2001;12:852–66. 2 Poutiainen AM, Koistinen MJ, Airaksinen KE, et al. Prevalence and natural course of ectopic atrial tachycardia. Eur Heart J 1999;20:694–700. 3 Walsh EP, Saul JP, Hulse JE, et al. Transcatheter ablation of ectopic atrial tachycardia in young patients using radiofrequency current. Circulation 1992;86:1138–46. 4 Goldberger J, Kall J, Ehlert F, et al. Effectiveness of radiofrequency catheter ablation for treatment of atrial tachycardia. Am J Cardiol 1993;72:787–93. 5 Tracy CM, Swartz JF, Fletcher RD, et al. Radiofrequency catheter ablation of ectopic atrial tachycardia using paced activation sequence mapping. J Am Coll Cardiol 1993;21:910–7. 6 Kay GN, Chong F, Epstein AE, Dailey SM, Plumb VJ. Radiofrequency ablation for treatment of primary atrial tachycardias. J Am Coll Cardiol 1993;21:901–9. 7 Lesh MD, Van Hare GF, Epstein LM, et al. Radiofrequency catheter ablation of atrial arrhythmias: results and mechanisms. Circulation 1994;89:1074–89. 8 Poty H, Saoudi N, Haïssaguerre M, Daou A, Clementy J, Letac B. Radiofrequency catheter ablation of atrial tachycardias. Am Heart J 1996;131:481–9. 9 Wang L, Weerasooriya HR, Davis MJ. Radiofrequency catheter ablation of atrial tachycardia. Aust N Z J Med 1995;25:127–32. 10 Pappone C, Stabile G, De Simone A, et al. Role of catheterinduced mechanical trauma in localization of target sites of radiofrequency ablation in automatic atrial tachycardia. J Am Coll Cardiol 1996;27:1090–7.

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11 Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998;31:451–9. 12 Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adults: electrophysiologic characteristics, pharmacologic responses, possible mechanisms, and results of radiofrequency ablation. Circulation 1994;90:1262–78. 13 Schmitt C, Zremmer B, Schneider M, et al. Clinical experience with a novel multielectrode basket catheter in right atrial tachycardia. Circulation 1999;99:2414 –22. 14 Weiss C, Willems S, Cappato R, Kuck KH, Meinertz T. High frequency current ablation of ectopic atrial tachycardia: different mapping strategies for localization of right- and leftsided origin. Herz 1998;23:269 –79. 15 Natale A, Breeding L, Tomassoni G, et al. Ablation of right and left atrial tachycardias using a three-dimensional nonfluoroscopic mapping system. Am J Cardiol 1998;82:989 –92. 16 Anguera I, Brugada J, Roba M, et al. Outcomes after radiofrequency catheter ablation of atrial tachycardia. Am J Cardiol 2001;87:886 –90. 17 Sanchez C, Benito F, Moreno F. Reversibility of tachycardiainduced cardiomyopathy after radiofrequency ablation of incessant supraventricular tachycardia in infants. Br Heart J 1995;74:332–3. 18 Chiladakis JA, Vassilikos VP, Maounis TN, Cokkinos DV, Manolis AS. Successful radiofrequency catheter ablation of automatic atrial tachycardia with regression of the cardiomyopathy picture. Pacing Clin Electrophysiol 1997;20:953 –9. 19 Wu MH, Lin JL, Lai LP, et al. Radiofrequency catheter ablation of tachycardia in children with and without congenital heart disease: indications and limitations. Int J Cardiol 2000; 72:221–7. 20 Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmiasaexecutive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation 2003;108:1871–909. 21 Scheinman MM, Basu D, Hollenberg M. Electrophysiologic studies in patients with persistent atrial tachycardia. Circulation 1974;50:266 –73. 22 Haines DE, DiMarco JP. Sustained intraatrial reentrant tachycardia: clinical, electrocardiographic and electrophysiologic characteristics and long-term follow-up. J Am Coll Cardiol 1990;15:1345 –54. 23 Gillette PC, Garson A Jr. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia. Circulation 1977;56:571–5. 24 Rosen MR, Reder RF. Does triggered activity have a role in the genesis of cardiac arrhythmias? Ann Intern Med 1981;94: 794 – 801. 25 Johnson NJ, Rosen MR. The distinction between triggered activity and other cardiac arrhythmias. In: Brugada P, Wellens HJJ, eds. Cardiac Arrhythmias: Where to Go from Here? Mount Kisco, NY: Futura, 1987: 129–45. 117

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26 Aronson RS, Hariman RJ, Gough WB. Delayed afterdepolarization and pathologic states. In: Rosen MR, Janse MJ, Wit AL, eds. Cardiac Electrophysiology: a Textbook. Mount Kisco, NY: Futura, 1990: 303–32. 27 Iwai S, Markowitz SM, Stein KM, et al. Response to adenosine differentiates focal from macroreentrant atrial tachycardia: validation using three-dimensional electroanatomic mapping. Circulation 2002;106:2793–9. 28 Engelstein ED, Lippman N, Stein KM, Lerman BB. Mechanism-specific effects of adenosine on atrial tachycardia. Circulation 1994;89:2645–54. 29 Iesaka Y, Takahashi A, Goya M, et al. Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular node transitional area. J Cardiovasc Electrophysiol 1997;8: 854–64. 30 Markowitz SM, Stein KM, Mittal S, Slotwiner DJ, Lerman BB. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol 1999;10:489 – 502. 31 Chiale PA, Franco DA, Selva HO, Militello CA, Elizari MV. Lidocaine-sensitive atrial tachycardia: lidocaine-sensitive, raterelated, repetitive atrial tachycardia: a new arrhythmogenic syndrome. J Am Coll Cardiol 2000;36:1637– 45. 32 Knight BP, Zivin A, Souza J, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol 1999;33:775–81. 33 Knight BP, Ebinger M, Oral H, et al. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol 2000;36:574 – 82. 34 Lai LP, Lin JL, Chen TF, Ko WC, Lien WP. Clinical, electrophysiological characteristics, and radiofrequency catheter ablation of atrial tachycardia near the apex of Koch’s triangle. Pacing Clin Electrophysiol 1998;21:367–74. 35 Connors SP, Vora A, Green MS, Tang AS. Radiofrequency ablation of atrial tachycardia originating from the triangle of Koch. Can J Cardiol 2000;16:39–43. 36 Chen CC, Tai CT, Chiang CE, et al. Atrial tachycardias originating from the atrial septum: electrophysiologic characteristics and radiofrequency ablation. J Cardiovasc Electrophysiol 2000;11:744–9. 37 Frey B, Kreiner G, Gwechenberger M, Gossinger HD. Ablation of atrial tachycardia originating from the vicinity of the atrioventricular node: significance of mapping both sides of the interatrial septum. J Am Coll Cardiol 2001;38:394– 400. 38 Morton JB, Sanders P, Das A, Vohra JK, Sparks PB, Kalman JM. Focal atrial tachycardia arising from the tricuspid annulus: electrophysiologic and electrocardiographic characteristics. J Cardiovasc Electrophysiol 2001:12:653 –9. 39 Nogami A, Sugut M, Tomita T, et al. Novel form of atrial tachycardia originating at the atrioventricular annulus. Pacing Clin Electrophysiol 1998;21:2691–4. 40 Matsuoka K, Kasai A, Fujii E, et al. Electrophysiological features of atrial tachycardia arising from the atrioventricular annulus. Pacing Clin Electrophysiol 2002:25:440 –5. 41 Mizui S, Mori K, Kuroda Y. Ectopic atrial tachycardia due to aneurysm of the right atrial appendage. Cardiol Young 2001;11:229–32.

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42 Ino T, Miyamoto S, Ohno T, Tadera T. Exit block of focal repetitive activity in the superior vena cava masquerading as a high right atrial tachycardia. J Cardiovasc Electrophysiol 2000;11:480–3. 43 Dong J, Schreieck J, Ndrepepa G, Schmitt C. Ectopic tachycardia originating from the superior vena cava. J Cardiovasc Electrophysiol 2002;13:620 – 4. 44 Kistler PM, Sanders P, Fynn SP, et al. Electrophysiological and electrocardiographic characteristics of focal atrial tachycardia originating from the pulmonary veins: acute and long-term outcomes of radiofrequency ablation. Circulation 2003;108:1968 –75. 45 Hatala R, Weiss C, Koschyk DH, Siebels J, Cappato R, Kuck KH. Radiofrequency catheter ablation of left atrial tachycardia originating within the pulmonary vein in a patient with dextrocardia. Pacing Clin Electrophysiol 1996;19:999 –1002. 46 Wagshal AB, Applebaum A, Crystal P, et al. Atrial tachycardia as the presenting sign of a left atrial appendage aneurysm. Pacing Clin Electrophysiol 2000;23:283 –5. 47 Mallavarapu C, Schwartzman D, Callans DJ, Gottlieb C, Marchlinski FE. Radiofrequency catheter ablation of atrial tachycardia with unusual left atrial sites of origin: report of two cases. Pacing Clin Electrophysiol 1996;19:988 –92. 48 Marrouche NF, SippensGroenewegen A, Yang Y, Dibs S, Scheinman MM. Clinical and electrophysiologic characteristics of left septal atrial tachycardia. J Am Coll Cardiol 2002; 40:1133–9. 49 Volkmer M, Antz M, Hebe J, Kuck KH. Focal atrial tachycardia originating from the musculature of the coronary sinus. J Cardiovasc Electrophysiol 2002;13:68 –71. 50 Navarrete AJ, Arora R, Hubbard JE, Miller JM. Magnetic electroanatomic mapping of an atrial tachycardia requiring ablation within the coronary sinus. J Cardiovasc Electrophysiol 2003;14:1361–4. 51 Polymeropoulos KP, Rodriguez LM, Timmermans C, Wellens HJ. Images in cardiovascular medicine: radiofrequency ablation of a focal atrial tachycardia originating from the Marshall ligament as a trigger for atrial fibrillation. Circulation 2002;105:2112–3. 52 Kistler PM, Sanders P, Hussin A, et al. Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol 2003;41: 2212–9. 53 Gomes JA, Hariman RJ, Kang PS, Chowdry IH. Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents. J Am Coll Cardiol 1985;5: 45 –57. 54 Sanders WE Jr, Sorrentino RA, Greenfield RA, Shenasa H, Hamer ME, Wharton JM. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol 1994;23:926 –34. 55 Boineau JP, Canavan TE, Schuessler RB, Cain ME, Corr PB, Cox JL. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation 1988;77:1221–37. 56 Allessie MA, Bonke FI. Direct demonstration of sinus node reentry in the rabbit heart. Circ Res 1979;44:557– 68. 57 Lee RJ, Kalman JM, Fitzpatrick AP, et al. Radiofrequency catheter modification of the sinus node for “inappropriate” sinus tachycardia. Circulation 1995;92:2919 –28.

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58 Callans DJ, Ren JF, Schwartzman D, Gottlieb CD, Chaudhry FA, Marchlinski FE. Narrowing of the superior vena cava–right atrium junction during radiofrequency catheter ablation for inappropriate sinus tachycardia: analysis with intracardiac echocardiography. J Am Coll Cardiol 1999;33:1667–70. 59 Man KC, Knight B, Tse HF, et al. Radiofrequency catheter ablation of inappropriate sinus tachycardia guided by activation mapping. J Am Coll Cardiol 2000;35:451–7. 60 Morillo CA, Klein GJ, Thakur RK, Li H, Zardini M, Yee R. Mechanism of “inappropriate” sinus tachycardia: role of sympathovagal balance. Circulation 1994;90:873 –7. 61 Sehra R, Coppess MA, Altemose GT, Militello CA, Miller JM. Atrial tachycardia masquerading as atrial flutter following ablation of the subeustachian isthmus. J Cardiovasc Electrophysiol 2000;11:582–6. 62 Goya M, Takahashi A, Nuruki N, et al. A peculiar form of focal atrial tachycardia mimicking atypical atrial flutter. Jpn Circ J 2000;64:886–9. 63 Ouali S, Anselme F, Savoure A, Cribier A. An atypical atrial flutter of focal origin: a study using a noncontact mapping system. Pacing Clin Electrophysiol 2003;26:1410 –2. 64 Jaïs P, Haïssaguerre M, Shah DC, et al. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation 1997;95:572–6. 65 Mecca AL, Guo H, Telfer A, Olshansky B. Atrial tachycardia originating from a single site with exit block mimicking atrial fibrillation eliminated with radiofrequency applications. J Cardiovasc Electrophysiol 1998;9:1100–8. 66 Tang CW, Scheinman MM, Van Hare GF, et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardial 1995;26:1315–24. 67 Tada H, Nogami A, Naito S, et al. Simple electrocardiographic criteria for identifying the site of origin of focal right atrial tachycardia. Pacing Clin Electrophysiol 1998;21:2431–9. 68 SippensGroenewegen A, Roithinger FX, Peeters HA, et al. Body surface mapping of atrial arrhythmias: atlas of paced P wave integral maps to localize the focal origin of right atrial tachycardia. J Electrocardiol 1998;31(Suppl):85–91. 69 Ramanathan C, Ghanem RN, Jia P, Ryu K, Rudy Y. Noninvasive electrocardiographic imaging for cardiac electrophysiology and arrhythmia. Nat Med 2004;10:422–8. 70 Arentz T, von Rosenthal J, Blum T, et al. Feasibility and safety of pulmonary vein isolation using a new mapping and navigation system in patients with refractory atrial fibrillation. Circulation 2003;108:2484–90. 71 Belhassen B, Viskin S. Atrial tachycardia and “kissing catheters.” J Cardiovasc Electrophysiol 2000;11:233. 72 Soejima K, Stevenson WG, Delacretaz E, Brunckhorst CB, Maisel WH, Friedman PL. Identification of left atrial origin of ectopic tachycardia during right atrial mapping: analysis of double potentials at the posteromedial right atrium. J Cardiovasc Electrophysiol 2000;11:975–80. 73 Tsai CF, Tai CT, Hsieh MH, et al. Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation. Circulation 2000;102:67–74. 74 Lee SH, Tai CT, Lin WS, et al. Predicting the arrhythmogenic foci of atrial fibrillation before atrial transseptal procedure:

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implication for catheter ablation. J Cardiovasc Electrophysiol 2000;11:750 –7. Kuo JY, Tai CT, Tsao HM, et al. P wave polarities of an arrhythmogenic focus in patients with paroxysmal atrial fibrillation originating from superior vena cava or right superior pulmonary vein. J Cardiovasc Electrophysiol 2003;14:350 –7. Tai CT, Hsieh MH, Tsai CF, et al. Differentiating the ligament of Marshall from the pulmonary vein musculature potentials in patients with paroxysmal atrial fibrillation: electrophysiological characteristics and results of radiofrequency ablation. Pacing Clin Electrophysiol 2000;23:1493 –501. Katritsis D, Giazitzoglou E, Korovesis S, Paxinos G, Anagnostopoulos CE, Camm AJ. Epicardial foci of atrial arrhythmias apparently originating in the left pulmonary veins. J Cardiovasc Electrophysiol 2002;13:319 –23. Man KC, Chan KK, Kovack P, et al. Spatial resolution of atrial pace mapping as determined by unipolar atrial pacing at adjacent sites. Circulation 1996;94:1357–63. Kottkamp H, Hindricks G, Breithardt G, Borggrefe M. Threedimensional electromagnetic catheter technology: electroanatomical mapping of the right atrium and ablation of ectopic atrial tachycardia. J Cardiovasc Electrophysiol 1997;8:1332–7. Weiss C, Willems S, Rueppel R, Hoffmann M, Meinertz T. Electroanatomical mapping (CARTO) of ectopic atrial tachycardia: impact of bipolar and unipolar local electrogram annotation for localization the focal origin. J Interv Card Electrophysiol 2001;5:101–7. Hoffmann E, Reithmann C, Nimmermann P, et al. Clinical experience with electroanatomic mapping of ectopic atrial tachycardia. Pacing Clin Electrophysiol 2002;25:49 –56. Wetzel U, Hindricks G, Schirdewahn P, et al. A stepwise mapping approach for localization and ablation of ectopic right, left, and septal atrial foci using electroanatomic mapping. Eur Heart J 2002;23:1387–93. Higa S, Tai CT, Lin YJ, et al. Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation. Circulation 2004;109:84 –91. Schmitt H, Weber S, Schwab JO, et al. Diagnosis and ablation of focal right atrial tachycardia using a new high-resolution, non-contact mapping system. Am J Cardiol 2001;87:1017–21. Chen SA, Tai CT, Chiang CE, Ding YA, Chang MS. Focal atrial tachycardia: reanalysis of clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol 1998;9:355 – 65. Wong T, Markides V, Peters NS, Davies DW. Clinical usefulness of cryomapping for ablation of tachycardias involving perinodal tissue. J Interv Card Electrophysiol 2004;10:153 –8. Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 2004;109:2724 –6. Sanders P, Jaïs P, Hocini M, Haïssaguerre M. Electrical disconnection of the coronary sinus by radiofrequency catheter ablation to isolate a trigger of atrial fibrillation. J Cardiovasc Electrophysiol 2004;15:364– 8. Hsieh MH and Chen SA. Catheter ablation of focal atrial tachycard. From Zipes DP, Haissaguerre M: 2nd Edition of Catheter Ablation of Arrhythmias. Futura Publishing Co., Inc. Armonk, NY, 2002: 185–203.

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Catheter ablation of atrioventricular nodal reentrant tachycardia Warren M. Jackman, Deborah Lockwood, Hiroshi Nakagawa, Sunny S. Po, Karen J. Beckman, Richard Wu, Zulu Wang, Benjamin J. Scherlag, Anton Becker, and Ralph Lazzara

Introduction Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia referred for treatment by catheter ablation [1]. AVNRT frequently occurs in patients without structural heart disease [1]. Women are more commonly affected (78% in our experience) [2]. Children are also commonly affected. Children aged < 5 years, < 10 years, and < 16 years represent 1.8%, 3%, and 13%, respectively, of patients undergoing catheter ablation of AVNRT at our center [2]. The diagnosis of AVNRT covers a group of tachycardias in which the reentrant circuit is thought to incorporate two atrial inputs to the atrioventricular (AV) node. While it is generally accepted that the circuits include tissue within the triangle of Koch, recent data suggest that most of the circuits include segments of the interatrial septum, left atrium, and/or coronary sinus (CS) myocardium [3– 5]. There is an anatomically distinct atrial input forming the fast pathway (short conduction time) and there are at least two slow AV nodal pathways which can be identified at electrophysiologic study [5 – 8], and these two may be formed by the rightward and leftward inferior extensions of the AV node (Fig. 9.1) [9]. The target for ablation is the atrial input to the AV node, forming the slow AV nodal pathway participating in the reentrant circuit. The approach to ablation differs somewhat between centers, as well as between the types of AVNRT. This chapter describes a classification schema that we use to differentiate the types of AVNRT and our approach to ablation of this group of tachycardias. The circuits for the various forms of AVNRT are still incompletely understood. Observations thus far allow classification into at least five forms of AVNRT on the basis of the site of earliest atrial activation, the site of ablation of a slow pathway being used for anterograde

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Rightward Inferior Extension Figure 9.1 The location of the compact part of the atrioventricular (AV) node and the rightward and leftward inferior extensions of the AV node are superimposed on the right-sided view of the AV septal junction in the same human heart. (Adapted from [9] with permission from Lippincott, Williams and Wilkins.)

or retrograde conduction, and the relationship between the A–H and H–A intervals during tachycardia. We refer to these five forms of AVNRT as: 1 Typical (“rightward inferior extension”) slow/fast AVNRT. 2 “Leftward inferior extension” slow/fast AVNRT. 3 Left atrial slow/fast AVNRT. 4 Slow/slow AVNRT. 5 Fast/slow AVNRT. Like the three forms of slow/fast AVNRT, slow/slow AVNRT often has a short R–P interval (H–A interval ≤ 120 ms) [10]. We distinguish between slow/fast and slow/slow AVNRT with a short H–A interval on the basis of the site of earliest retrograde atrial activation during the tachycardia (Fig. 9.2) [11]. The site of earliest activation is identified by mapping the right atrium and coronary sinus during the tachycardia, using closely spaced electrodes.

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Figure 9.2 Schematic representation of the interatrial septum, triangle of Koch (bounded by the tendon of Todaro, tricuspid annulus, and coronary sinus), and coronary sinus (CS) in the right anterior oblique (RAO) projection (left) and the left anterior oblique (LAO) projection (right). For atrioventricular nodal reentrant tachycardia (AVNRT) with a long A–H interval and a short H–A interval (< 120 ms), the authors differentiate between slow/fast AVNRT and slow/slow AVNRT on the basis of the site of earliest retrograde atrial activation during tachycardia. The short H–A interval AVNRT with the earliest retrograde atrial activation recorded posterior to the tendon of Todaro on the interatrial septum (red area) is defined as slow/fast AVNRT. The short H–A interval AVNRT with the earliest retrograde atrial activation recorded within the inferior aspect of the triangle of Koch or within the coronary sinus (blue area) is defined as slow/slow AVNRT. Post, posterior; Ant, anterior; HB, His bundle; Retro FP, retrograde fast pathway; Retro SP, retrograde slow pathway.

Catheter ablation of atrioventricular nodal reentrant tachycardia

Definition of AVNRT with Short R-P (H-A < 120 ms) Based on Site of Earliest Atrial Activation Posterior to Tendon of Todaro — Slow/Fast (S/F) AVNRT Inferior Triangle of Koch or CS — Slow/Slow (S/S) AVNRT Superior Post

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We define retrograde conduction over the “fast AV nodal pathway,” and the tachycardia as slow/fast AVNRT when the earliest retrograde atrial activation is recorded posterior to the tendon of Todaro, outside of the triangle of Koch (Fig. 9.2). Earliest activation is usually recorded 5–15 mm inferior and posterior to the site recording the earliest (most proximal) anterograde His bundle potential, and usually precedes atrial activation at the site recording the proximal His bundle potential by approximately 10 ms (Fig. 9.3) [12]. In early studies employing widely spaced bipolar catheter electrodes (5–10 mm interelectrode spacing), the earliest atrial activation during slow/fast AVNRT was recorded in the same bipolar electrogram that recorded the His bundle potential [1]. This suggested that earliest atrial activation was recorded within the triangle of Koch. However, the wide bipolar electrodes probably recorded activation over a wide region spanning from the interatrial septum (posterior to the triangle of Koch) to the proximal right bundle branch. We define retrograde conduction as occurring over a “slow AV nodal pathway” and the tachycardia as slow/ slow AVNRT when the H–A interval is relatively short and earliest retrograde atrial activation is recorded within the inferior region of the triangle of Koch (between the tricuspid annulus and coronary sinus ostium) or within the coronary sinus (Fig. 9.2) [11]. In our experience of 650 consecutive patients with AVNRT exhibiting a short H–A interval, earliest retrograde atrial activation was recorded

Mitral Annulus

LAO Projection

posterior to the tendon of Todaro (slow/fast AVNRT) in 543 (83%) patients and within the triangle of Koch or CS (slow/slow AVNRT) in 109 (17%) patients [2]. The technique we use to determine whether the mapping catheter is located anterior or posterior to the tendon of Todaro (inside or outside of the triangle of Koch, respectively) is to set the angle of the fluoroscope in the left anterior oblique (LAO) projection such that the catheter recording the distal His bundle or proximal right bundle branch potential is perpendicular to the plane of the radiographic image (Fig. 9.3A, B). Gentle clockwise torque on the His bundle catheter places it against the septum, constrained by the tricuspid annulus and tendon of Todaro (i.e., across the apex of the triangle of Koch). Orientation of the mapping catheter leftward of the His bundle catheter in the LAO projection indicates that the mapping catheter is not constrained by the apex of the triangle of Koch, but instead is located posterior to the tendon of Todaro on the interatrial septum (fast pathway area, Fig. 9.3A, B). Manipulation of the catheter along the posterior edge of the tendon of Todaro should be performed gently to avoid catheter trauma to the transitional cell fibers crossing the tendon, which can produce transient block in fast AV nodal pathway conduction. Recovery of catheter-induced block of fast pathway conduction may be delayed, limiting the use of certain mapping techniques (such as resetting) and preventing the use of noninducibility of AVNRT as an end point for ablation.

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Figure 9.3 The site of the earliest retrograde atrial activation during slow/ fast AVNRT. Radiograph (A) and schematic representation (B) in the left anterior oblique projection, showing the His bundle catheter (HB) positioned perpendicular to the plane of the page. The HB catheter is recording proximal His bundle activation. The mapping catheter (RA Septum), positioned at the site of earliest retrograde atrial activation (Earliest Retro A), is oriented leftward of the HB catheter and approximately 15 mm inferior and posterior of the tip of the HB catheter. The leftward deviation of the mapping catheter indicates a position posterior to the tendon of Todaro on

the right side of the interatrial septum (RA Septum). C. Electrograms during slow/fast AVNRT. Of the His bundle electrograms (HBp – HBd), only the distal bipolar electrogram (HBd) records a His bundle potential (H), suggesting that the tip of the catheter is near the proximal His bundle region. Atrial activation recorded on the distal bipolar electrogram from the mapping catheter (RA Septdist) preceded atrial activation in the HBd electrogram by 10 ms. RAA, right atrial appendage; RV, right ventricle; TA, tricuspid annulus; MA, mitral annulus; CSp – CSd, proximal to distal CS electrograms; A, atrial potential. (Adapted from [2] with permission from Elsevier.)

Figure 9.4 Recordings of earliest retrograde atrial activation on the right and left sides of the interatrial septum simultaneously during slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). A. Radiograph in the left anterior oblique (LAO) projection, showing the two catheters positioned to record the earliest retrograde atrial activation from the right and left sides of the interatrial septum. It should be noted that the His bundle catheter (HB) is positioned perpendicular to the plane of the page. The catheter recording the earliest right atrial activation (RA Sept) was positioned on the right atrial septum, leftward of the His bundle (HB)

catheter (indicating a location posterior to the tendon of Todaro). Left atrial mapping was performed via a patent foramen ovale. The earliest left atrial activation was recorded on the septum (LA Sept), directly opposite the right atrial mapping catheter. B. Electrograms recorded from the right atrial septum (RA Sept) and left atrial septum (LA Sept) during slow/fast AVNRT show nearly simultaneous onset of the downstroke of the bipolar atrial potentials (arrows, RA and LA). These potentials precede atrial activation in the His bundle electrogram by more than 10 ms. V, ventricular potential.

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(ASP potential, Fig. 9.5) proximal coronary sinus. An even later potential is occasionally recorded higher in the triangle of Koch, slightly inferior to the site recording the most proximal His bundle potential. This can result in the recording of two atrial potentials from the proximal electrodes on the His bundle catheter when the catheter is positioned to record the most proximal His bundle potential from the distal pair of electrodes (Fig. 9.6). The first potential is the recording of activation posterior to the tendon of Todaro (retrograde fast pathway activation). The second potential is the recording of activation within the triangle of Koch (Fig. 9.7) [13]. Occasionally, only the second potential is recorded from the His bundle catheter. Since the timing of this potential is later than the timing of activation in the proximal coronary sinus, the tachycardia may be incorrectly identified as slow/slow AVNRT (Fig. 9.8). Retrograde fast pathway conduction can be correctly identified by mapping the region of the right atrial

Slow/fast AVNRT The reentrant circuit in typical slow/fast AVNRT has not been fully elucidated. However, a number of observations, some of which are described below, suggest that the left atrium and CS myocardium participate in the circuit.

Retrograde conduction over the fast AV nodal pathway During retrograde fast pathway conduction, earliest atrial activation is recorded simultaneously on the right and left sides of the interatrial septum, posterior to the tendon of Todaro (Fig. 9.4). In contrast, the timing of atrial activation at the inferior aspect of the triangle of Koch (between the tricuspid annulus and the coronary sinus ostium) is late, even later than the timing of activation in the roof of the A

RAO Projection

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B

RAA

RAA

RV

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HB HB Figure 9.5 Late timing of activation at the inferior aspect (base) of the triangle of Koch during typical slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). A, B. Radiographs in the right anterior oblique (RAO) and left anterior oblique (LAO) projections show the mapping catheter (Inf Sept) positioned at the base of the triangle of Koch, between the inferoseptal tricuspid annulus and the coronary sinus ostium. The coronary sinus catheter (CS) was inserted via the right subclavian vein and is positioned along the CS floor. CS4, CS7, and CS10 identify the fourth, seventh, and tenth bipolar pairs of electrodes from the tip of the CS catheter. C. The electrogram recorded during slow/fast AVNRT from the base of the triangle of Koch (Inf Sept dist) shows a small, rounded far-field atrial potential (Afar) followed by a sharp atrial potential (ASP). The ASP potential begins 55 ms after the onset of the earliest far-field atrial potential recorded in the His bundle electrograms (first vertical line). It should be noted that the ASP potential is later than activation along the floor of the proximal coronary sinus (CS7 – CS10 and second dotted line).

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First Potential Outside Triangle of Koch (Aout) Second Potential Inside Triangle of Koch (Ain)

A I II V1

B

A

RAA HB4 HB3 HB2 HBd

AOut

CS 8 CS 7 CS 6 CS 5 CS 4 CS 3 CS 2 CS d

H

V

H

H

V

100 ms

Two Potentials Recorded in His Bundle Region During Retrograde Fast Pathway Conduction Site of First Potential

Eustachian Ridge

Tendon of Todaro HB

Site of Second Potential

Superior

CS

Post

Ant Inferior

Tricuspid Annulus RAO Projection Figure 9.7 Schematic representation of the right atrial septum and triangle of Koch in the right anterior oblique (RAO) projection, showing the postulated sites generating the two sets of atrial potentials recorded in the proximal His bundle electrograms during retrograde conduction over the fast atrioventricular nodal pathway (shown in Fig. 9.6). The first set of potentials is generated posterior to the tendon of Todaro and inferior to the site recording the proximal His bundle potential (red area). The second set of potentials is postulated to be generated in the apex (superior aspect) of the triangle of Koch (blue area). The arrows show the direction of propagation of the first and second sets of potentials.

124

AIn

AOut

AIn

42

A

Figure 9.6 Two distinct sets of atrial potentials recorded in the proximal His bundle electrograms during slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). A. The His bundle catheter was positioned to record the proximal His bundle potential from the distal pair of electrodes (HBd electrogram). Two distinct sets of atrial potentials were recorded in the HB2 and HB3 electrograms. The first set of potentials originate posterior to the tendon of Todaro, outside the triangle of Koch (AOut). The authors postulate that the second set are generated close to the tricuspid annulus, inside the triangle of Koch (AIn). B. The His bundle catheter was withdrawn proximally, so that only a tiny, far-field His bundle potential was recorded in the first complex (H). AV block occurred during the second complex, allowing clear identification of the two sets of atrial potentials in the absence of the ventricular potential. The first set of potentials (AOut) was activated in the distal-to-proximal direction (left arrows in HBd and HB2 electrograms). The second set of potentials (AIn) propagated in the proximal-to-distal direction (right arrows in HB3 to HBd). The time between the first and second potentials in HBd was 42 ms.

septum, posterior to the tendon of Todaro (fast pathway area). Recording activation posterior to the tendon of Todaro before activation within the CS and triangle of Koch establishes the diagnosis of slow/fast AVNRT (Fig. 9.8). During retrograde fast pathway conduction, the observation that activation within the triangle of Koch follows activation at the roof of the proximal coronary sinus suggests that the tissue within the triangle of Koch may be activated by the coronary sinus myocardium. The CS myocardium is richly connected to the adjacent left atrial myocardium (Fig. 9.9), and forms an electrical connection between the left atrial myocardium and the atrial myocardium within the triangle of Koch [14,15]. From these observations, we postulate that the following sequence of atrial activation is produced by retrograde conduction over the fast AV nodal pathway (Fig. 9.10) [2]. Transitional cell fibers carry the impulse across the tendon of Todaro to activate the right and left sides of the interatrial septum (1 in Fig. 9.10). In our hypothesis, activation from the right atrial septum is unable to penetrate the triangle of Koch due to block at the Eustachian ridge (2 in Fig. 9.10). Activation from the left atrial septum propagates around the mitral annulus in the counterclockwise direction (as viewed in the LAO projection). The left atrium activates the coronary sinus myocardial coat. The coronary sinus myocardium propagates the impulse to the CS ostium, activating the atrial myocardium in the inferior

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CHAPTER 9

RAO Projection

A

Catheter ablation of atrioventricular nodal reentrant tachycardia

LAO Projection

B

RAA

RAA

HBp

HB3

HBd

RV

HBd RA Septum

RV RA Septum CS

Slow/Fast AVNRT

C I II V1

A

RAA HBp HB3 HB2 HBd RA Septum

CSp

CS

A

A-A 320

A

310

A

300

2nd Potential

H

H-H 320

H

H2

310

V

290

V2

V3

H3

60

1st Potential

CSd RV

S2

S3

100 ms

Figure 9.8 Slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) simulating slow/slow AVNRT. A, B. Radiographs in the right anterior oblique (RAO) and left anterior oblique (LAO) projections show the location of the His bundle catheter positioned to record the proximal His bundle potential (H) from the distal pair of electrodes (HBd) and the location of the mapping catheter on the right atrial septum (RA Septum) positioned to record earliest retrograde atrial activation during AVNRT. In the LAO projection, the mapping catheter is deviated leftward in relation to the His bundle catheter, indicating a position posterior to the tendon of Todaro. The tip of the mapping catheter is located approximately 1 cm inferior, 1 cm posterior, and 0.8 cm leftward of the tip of the His bundle catheter (the “fast pathway area”). C. Electrograms during slow/fast AVNRT. Two ventricular extrastimuli (S2 and S3) were delivered to advance the ventricular

potential (V2 and V3) in the His bundle and coronary sinus electrograms to clearly visualize the timing of the atrial potentials. Earliest atrial activation (1st potential) is recorded on the right atrial septum electrogram (RA Septum), posterior to the tendon of Todaro, indicating retrograde conduction over the fast AV nodal pathway. This potential is not recorded in the His bundle electrogram. Only the second potential (2nd potential), 60 ms later, is recorded on the proximal His bundle electrograms (HBp and HB3). Therefore, the atrial potentials recorded on the His bundle electrograms are later than the timing of activation in the proximal coronary sinus (long vertical line), simulating retrograde conduction over a slow AV nodal pathway (i.e., simulating slow/slow AVNRT). Only by mapping the right atrial septum posterior to the tendon of Todaro (outside the triangle of Koch) can this tachycardia be correctly identified as slow/fast AVNRT.

aspect of the triangle of Koch (4 in Fig. 9.10). Activation of the myocardium between the coronary sinus ostium and the tricuspid annulus produces a single late high-frequency potential (ASP potential, Fig. 9.5) [16]. The impulse con-

tinues to propagate superiorly within the triangle of Koch to produce the second of the two potentials, which is occasionally recorded from the proximal electrodes on the His bundle catheter (5 in Fig. 9.10). 125

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CS Myocardial Coat Conducts Activation From LA to Triangle of Koch Great Cardiac Vein

Posterior Coronary Vein

LA

Figure 9.9 Photograph (inferior view) of a human heart, showing the myocardial coat of the coronary sinus. The epicardium and fat have been removed. The translucent appearance of the great cardiac vein and posterior coronary vein should be noted. In contrast, the coronary sinus is covered by a myocardial coat, which is connected to the epicardial surface of the left atrium (LA) and the triangle of Koch via the coronary sinus ostium. The coronary sinus myocardium forms an electrical connection between the left atrial myocardium and the triangle of Koch. LV, left ventricle; IVC, inferior vena cava. (Photograph courtesy of Anton Becker.)

IVC

LV LV

CS Myocardial Coat

Middle Cardiac Vein

Postulated Atrial Activation Sequence Following Retrograde Fast Pathway Conduction RAO Projection

Fast Pathway

Tendon of Todaro

1

LAO Projection

Superior Post

Ant Inferior

HB

Tendon of Todaro

Fast Pathway

2

Fast Pathway

HB 1

1

Mitral Annulus

2 RA Activation

ASP

5

6

CS Os Eustachian Ridge

Potential Tricuspid Annulus

Figure 9.10 Schematic representation of the atrial activation sequence following retrograde conduction over the fast AV nodal pathway, as postulated by the authors. Retrograde conduction over the fast pathway activates the right and left sides of the interatrial septum, posterior to the tendon of Todaro at a level slightly inferior to the level of the His bundle (1, red arrows). Right atrial activation (2, green lines) fails to reenter the triangle of Koch, presumably due to conduction block at the Eustachian ridge (short perpendicular green lines in the right anterior oblique projection). Left atrial

Slow AV nodal pathway conduction At least two slow AV nodal pathways can be identified during retrograde conduction by the presence of two distinct sites of earliest retrograde atrial activation and H–A interval (Fig. 9.11). Retrograde conduction over both of the slow pathways can be demonstrated in a small number of patients (Fig. 9.12) [6]. In one, earliest 126

3

Eustachian Ridge

LA Activation

4

IVC

CS Tricuspid Annulus

Activation of CS Myocardium

activation propagates from the septum and around the mitral annulus in the counterclockwise direction, as viewed in the left anterior oblique projection (3, green arrows). The left atrium activates the CS myocardium (4, brown arrows). Activation propagates septally along the CS myocardium to the CS ostium (brown arrows) and activates the inferior region of the triangle of Koch between the CS ostium and tricuspid annulus (5, brown arrows) to generate the Asp potential (6, blue arrows). Each anatomical structure will be colored the same on all schematic figures throughout this chapter.

atrial retrograde activation is recorded from the roof of the proximal coronary sinus, 2–4 cm from the coronary sinus ostium (Fig. 9.12C, first complex). This slow pathway usually has the shorter retrograde conduction time (H–A interval). During retrograde conduction over the second slow pathway, usually with a longer H–A interval (Fig. 9.12C, second complex), earliest activation is recorded in the region between the inferoseptal tricuspid annulus

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Postulated Sites of Earliest Activation for Retrograde Conduction Over the Rightward and Leftward Inferior Extensions of the AV Node RAO Projection HB

Tendon of Todaro

Eustachian Ridge

LAO Projection

Tendon of Todaro Tricuspid Annulus

Tricuspid Annulus

CS

HB

Mitral Annulus

Eustachian Ridge

CS

IVC

Figure 9.11 Schematic representation of the sites of earliest atrial activation postulated by the authors following retrograde conduction over the rightward inferior extension (area 1 followed by activation of area 2) and leftward inferior extension (area 3) of the atrioventricular node.

Area #1 Retro Right Inferior Extn

Area #2 Retro Right Inferior Extn (slightly later than Area #1)

A

(slightly later than Area #1)

B

RAO Projection

LAO Projection RAA

RAA Figure 9.12 Two distinct retrograde atrial activation sequences following retrograde conduction over two different slow atrioventricular nodal pathways. A, B. Radiographs in the right anterior oblique and left anterior oblique projections show the catheter positions. There are two catheters in the coronary sinus: one inserted via the right subclavian vein and positioned along the floor of the coronary sinus (CS Floor); and one inserted via the right femoral vein and positioned along the roof of the CS (CS Roof). The mapping catheter (RA Septum) is positioned on the right atrial septum, posterior to the tendon of Todaro in the “fast pathway area.” C. Electrograms recorded following two paced ventricular complexes. Retrograde atrial activation following the first ventricular complex has an H–A interval of 100 ms, measured from the end of the retrograde His bundle potential to earliest atrial activation, which was recorded on the roof of the CS, approximately 3 cm from the CS ostium (left arrow). It should be noted that activation on the right atrial septum (RA Sept) in the fast pathway area (FP Area) is later, excluding retrograde conduction over the fast pathway. This pattern of activation may represent retrograde conduction over the leftward inferior extension of the AV node. Atrial activation following the second ventricular complex has a longer H–A interval (440 ms) and different retrograde atrial activation sequence. Earliest CS activation is recorded at the floor of the CS ostium (second arrow). This pattern may represent retrograde conduction over the rightward posterior extension of the AV node. S, pacing stimulus.

Area #3 Retro Left Inferior Extn

Area #2 Retro Right Inferior Extn

RV

HB RA Sept

RV

HB

CS Roof

RA Sept CS Roof

CS Floor

CS Floor

2 Retrograde Slow Pathways

C II

A

RAA HBp

100

HBd

H

A

A

440

A FP Area

H

A

RA Sept Prox

CS Roof Dist Prox

CS Floor Dist

RV

A

A S

S

100 msec

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100 msec

Figure 9.13 The postulated pattern for retrograde slow pathway conduction over the rightward inferior extension of the AV node. A, B. Radiographs in the right anterior oblique and left anterior oblique projections show the catheter positions. The mapping catheter (Inf Sept) is positioned between the tricuspid annulus and coronary sinus (CS) ostium (at the level of the middle of the CS ostium). The arrows represent the postulated sequence of activation in the triangle of Koch (blue arrow, septal activation), CS myocardium (brown arrows), left atrium (green arrows), and right atrium (green arrows). C. Electrograms during fast/slow atrioventricular nodal reentrant tachycardia show the earliest activation (blue arrow, ASP) recorded between the tricuspid annulus and CS ostium (Inf Sep dist electrogram), followed by activation of the CS myocardium (CS Myo, brown arrow) and left atrium (LA, green arrows) as recorded from electrodes positioned along the floor of the CS. It should be noted that only a single potential is recorded from the coronary sinus distal to CS5 (CS4 to CSd)—presumably the result of simultaneous activation of CS myocardium and left atrial myocardium close to the CS. The first of the two potentials recorded in the proximal CS electrograms (CS7 and CS6) probably represents activation of the CS myocardium. The second potential probably represents left atrial activation, which is delayed as a result of reversing the direction of left atrial activation towards the septum. The late atrial potential in the Inf Sep prox electrogram is probably generated by the right atrium located posterior to the Eustachian ridge (green arrow in A), after the atrial septum is activated by the left atrium. Similarly, the late atrial potential in the His bundle electrograms is probably generated from the right atrium posterior to the tendon of Todaro.

and the coronary sinus ostium (retrograde ASP potential, Figs. 9.13 and 9.14). Activation appears to propagate further inferiorly and enter the coronary sinus at the floor of the coronary sinus ostium (Figs. 9.12–9.14). The impulse is propagated leftward through the coronary sinus myocardium, activating the inferobasal left atrium. Left atrial activation then propagates laterally and septally along the mitral annulus. The timing of activation propagating laterally is similar in the coronary sinus myocardium and in the left atrium, producing what appears to be a single potential at sites located lateral to the site of earliest left atrial activation. However, for left atrial activation to propagate towards the septum, the impulse must reverse direction. This produces a significant conduction

delay, which is often recorded as a second potential in the proximal coronary sinus electrograms (Fig. 9.13). Our interpretation of the second retrograde slow pathway activation pattern is shown schematically in Fig. 9.15. The evidence for exit block from the triangle of Koch to the right atrium (across the tendon of Todaro and Eustachian ridge) is demonstrated in one patient by the effects of catheter trauma (Fig. 9.16). During fast/slow AVNRT in this patient, the retrograde ASP potential was recorded first at the midseptal region and second at the inferoseptal region of the triangle of Koch (Fig. 9.16A). Catheter trauma to the inferoseptal region eliminated the ASP inferiorly, but not at the midseptal region (Fig. 9.16B). Elimination of the retrograde ASP potential before reaching the floor of

A

B

RAO

LAO RAA

RAA RV

RA Activation

HB Septal Activation

CS

Inf Sept (ASP)

RV HB

LA Activation

Inf Sept (ASP)

CSd CS6

CS Myocardial Activation

C

CS Myocardial Activation

Fast/slow AVNRT

I II V1

A

RAA HB3 HB2 HBd

A

Inf prox A SP Sep dist 7 6 5 CS 4 3 2 d

CS

A H

H ASP

LA CS Myo

LA

RV

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A

Catheter ablation of atrioventricular nodal reentrant tachycardia

B

Fast/slow AVNRT

I II V1

Sinus rhythm

A

RAA

A

p

HB m d

p

A

45

H

A

Roof CS

9 7

Afar

A 65 H

Afar

Inf Sept

d

H

ASP

ASP

LA

LA

CSM

5 3 d 8 7

CSM

LA

CSM

LA

LA

Floor CS 5 3

d

100 ms Figure 9.14 Electrograms recorded from the region between the tricuspid annulus and coronary sinus (CS) ostium (Inf Sept), the roof of the proximal CS (Roof CS), and the floor of the proximal CS (Floor CS) during fast/slow atrioventricular nodal reentrant tachycardia (AVNRT) and sinus rhythm. A. During fast/slow AVNRT, the earliest retrograde atrial activation (ASP) is recorded at the Inf Sept region, followed by activation of the floor of the coronary sinus (CS) ostium (CSM in Floor CS 8 electrogram), activation laterally along the CS (Floor CS7 to Floor CSd), and activation of the left atrium by the CS myocardium (Roof CS 6 electrogram), consistent with

retrograde conduction over the rightward inferior extension of the AV node. The late far-field potential (Afar) following the ASP potential in the Inf Sept electrograms is probably the recording of activation of right atrium posterior to the Eustachian ridge. The similar timing of the Afar potential and atrial activation recorded in the His bundle electrograms (A) should be noted. The A–H interval is shorter during fast/slow AVNRT (45 ms) than sinus rhythm (65 ms). B. During sinus rhythm, atrial activation in the inferoseptal region (ASP potential, arrow) is later than atrial activation in the His bundle electrograms and the proximal coronary sinus (vertical line).

the CS ostium prevented activation of the CS myocardium, the left atrium, and the right atrium, and terminated the tachycardia (Fig. 9.16B). The failure to activate the right atrium without first activating the left atrium provides evidence for the absence of direct conduction between the triangle of Koch and right atrial septum during retrograde slow pathway conduction. These two activation patterns for retrograde slow pathway conductionashorter H–A interval with earliest activation in the roof of the coronary sinus, and longer H–A interval with earliest activation between the tricuspid annulus and coronary sinus ostium, followed by activation in the floor of the coronary sinus ostiumaappear to correlate with the leftward and rightward inferior extensions of the AV node, respectively, described by Inoue and Becker (Fig. 9.1) [9]. Retrograde activation over the longer rightward inferior extension is the pattern that is present most often in patients exhibiting only one pattern

of retrograde slow pathway conduction. In addition, the response to ablation suggests that the rightward inferior extension forms the slow pathway in the AVNRT reentrant circuit in most patients.

Reentrant circuit in typical slow/fast AVNRT We define typical slow/fast AVNRT as using the long rightward inferior extension of the AV node for anterograde slow pathway conduction and the fibers crossing the tendon of Todaro for retrograde fast pathway conduction. The atrial activation sequence we propose is the same as described above for retrograde fast pathway activation, with simultaneous earliest activation at the right and left atrial septum (recorded posterior to the tendon of Todaro, 5–15 mm posterior and inferior to the site recording proximal His bundle activation), followed sequentially by activation of the inferoseptal left atrium, proximal CS, CS 129

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Postulated Atrial Activation Sequence Following Retrograde Slow Pathway Conduction (Rightward Inferior Extension) RAO Projection

LAO Projection

Tendon of Todaro

RA Activation

HB 1 7

CS

2

Slow Pathway

RA Activation

Tendon of Todaro

6

7

Tricuspid Annulus

ASP

Potential Eustachian Ridge

Slow Pathway

HB

Mitral Annulus

5

LA Activation 4

IVC

3 Tricuspid Annulus

Eustachian Ridge

Activation of CS Myocardium

Figure 9.15 Schematic representation of the atrial activation sequence following retrograde conduction over the slow atrioventricular nodal pathway (rightward inferior extension), as postulated by the authors. Retrograde conduction over the rightward inferior extension (1, upper blue arrow) activates the myocardium between the inferoseptal tricuspid annulus and the coronary sinus ostium to produce the retrograde ASP potential (2, lower blue arrow) and then activates the coronary sinus at the floor of the ostium (brown arrows). Activation in the triangle of Koch does not cross the Eustachian ridge to the right atrium (green line), but proceeds leftward along the coronary sinus myocardium (3, brown arrows in the left anterior

oblique projection) to activate the left atrium. Left atrial activation propagates rapidly in the leftward or clockwise direction (4, solid green arrow in the left anterior oblique projection), but must first reverse direction to propagate in the septal or counterclockwise direction (5, dotted green line). The reversal produces late left atrial activation at the inferoseptal region and a second potential in proximal CS electrograms. This counterclockwise left atrial wave front activates the interatrial septum (6, dotted green line), which is followed by activation of the right atrium posterior to the tendon of Todaro and Eustachian ridge (7, green arrows in right and left anterior oblique projections).

ostium, base of the triangle of Koch (generating the ASP potential), and finally with activation propagating superiorly in the triangle of Koch (Fig. 9.17). Participation of the proximal CS myocardium and the region between the tricuspid annulus and CS ostium in the slow pathway component of the reentrant circuit has been verified using the “resetting” response [17]. During slow/fast AVNRT, a late atrial extrastimulus (after the onset of retrograde atrial activation) delivered to either of these two sites advances the next His bundle potential and resets the tachycardia (the following H–H interval is the same as the tachycardia cycle length). Since the late atrial extrastimulus could not have penetrated the fast pathway (the extrastimulus was delivered after fast pathway activation), an advance in the timing of the His bundle potential represents an advance in conduction over the slow pathway, and indicates that these pacing sites are close to (or within) the slow pathway. The lower common pathway (LCP) in AVNRT represents the tissue between the His bundle and the junction at the end of the anterograde conducting pathway and beginning of the retrograde conducting pathway. The conduction time over the LCP (as a reflection of its length) differs between the various forms of AVNRT. AVNRT with a long LCP (slow/slow and fast/slow AVNRT) may be incorrectly identified as atrial tachycardia, because second-degree AV block proximal to the His bundle

potential (block within the LCP) may occur without terminating the tachycardia (Fig. 9.16B) and ventricular extrastimuli that advance the His bundle potential by up to 60 ms may not advance the next atrial potential and reset the tachycardia. These observations, showing disassociation of the His bundle potential from the tachycardia, do not exclude AVNRT with a long LCP. One technique for estimating the conduction time over the lower common pathway is to compare the H–A interval during tachycardia to the H–A interval during ventricular pacing at the same cycle length as the tachycardia [10,18]. The H–A intervals should be compared at the same autonomic tone by initiating ventricular pacing immediately after terminating the tachycardia [18]. The greater the difference between the H–A interval during pacing and the H–A interval during tachycardia, the greater the conduction time over the LCP. The H–A interval should be measured from the most proximal His bundle potential. Therefore, during tachycardia, the H–A is measured from the onset of the most proximal His bundle potential; while during ventricular pacing, the H–A interval should be measured from the end of the most proximal retrograde His bundle potential. Right ventricular pacing is best performed at the superior basal right ventricular septum close to, but not capturing, the His bundle or proximal right bundle branch (“para-Hisian” pacing site) to visualize the

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A II V1

A

RAA Figure 9.16 Evidence during fast/slow atrioventricular nodal reentrant tachycardia (AVNRT) that retrograde slow pathway activation must reach the coronary sinus in order for the atria to become activated. A. During fast/slow AVNRT, the electrogram recorded from the inferoseptal region between the inferoseptal tricuspid annulus and the coronary sinus ostium (ISd) exhibits a large, sharp retrograde ASP potential (arrow, ASP) preceding activation in the coronary sinus. The midseptal tricuspid annulus electrogram (MSd) recorded between the level of the His bundle and coronary sinus (superior to the IS electrograms) shows a retrograde ASP potential (top arrow, ASP), 9 ms before the ASP potential recorded in the ISd electrogram. The order of the retrograde ASP potentials suggests conduction in the triangle of Koch in the superior-to-inferior direction. B. Continuation of the episode of fast/slow AVNRT with 2 : 1 atrioventricular block. The ASP potential is unchanged in the midseptal electrogram (MSd). However, the ASP potential in the inferoseptal electrogram (ISd) becomes smaller in amplitude, delayed, and then absent (unfilled arrow, No ASP), indicating block inferior to the MS region and superior to the IS region. Loss of the ASP potential in the ISd electrogram is associated with loss of activation in the coronary sinus, left atrium, and right atrium, and termination of the tachycardia. This suggests that activation within the triangle of Koch may not be able to activate the right atrium directly, due to block across the Eustachian ridge.

AFar

MSp MSd

ASP

ISp ISd

ASP

CSp CSd RV V

100 ms

B

II V1

A

RAA MSp MSd ISp ISd CSp

ASP

ASP

ASP

ASP*

ASP

No ASP

CSd RV

end of the most proximal retrograde His bundle potential [19]. Pacing at this site allows the ventricular wave front to propagate away from the His bundle recording site before entering the Purkinje system to generate the retrograde His bundle potential. Another technique for estimating the LCP uses ventricular extrastimuli during AVNRT [20]. The greater the advance in His bundle activation (shortening of the H1–H2 interval) that is required to advance the next atrial activation (A2), the longer the lower common pathway conduction time. The H1–H2 interval is measured from the onset of the His bundle potential during tachycardia (H1) to the end of the paced retrograde His bundle potential (H2). It is important to measure H1 and H2 from the most proximal

V

200 ms

site at which His bundle activation can be recorded. Measuring distal to that site will artificially decrease the H1–H2 interval, suggesting that a greater advance in His bundle activation is required to advance atrial activation, simulating a longer conduction time over the LCP. Recording the end of the most proximal H2 requires the ventricular extrastimulus to be delivered at the superior basal right ventricular (RV) septum (para-Hisian site) [21]. In typical slow/fast AVNRT, ventricular extrastimuli begin to advance the timing of the next atrial potential (and reset the tachycardia) as soon as the end of the paced His bundle potential (H2) is advanced by only 5 ms [22]. When comparing the H–A intervals, the H–A interval during tachycardia is slightly longer (by 9 ± 8 ms) than the 131

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Supraventricular tachycardia

Postulated Circuit and Ablation Site for Typical Slow/Fast AVNRT (SP is Rightward Inferior Extension) RAO Projection Fast Pathway

LAO Projection

Tendon of Todaro HB

Slow Pathway RA Activation

ASP

Potential

CS Eustachian Ridge

Fast Pathway

ToT

Slow Pathway

LA Activation

Eustachian Ridge IVC

SP Ablation Region (Rightward Inferior Extension)

CS Myocardium

Ablation Sites

H–A interval during ventricular pacing at the same cycle length, and the H–A interval during ventricular pacing is usually < 70 ms [10,18]. These observations suggest a very short LCP in typical slow/fast AVNRT [10,18,20]. The greater H–A interval during tachycardia might be explained by the requirement for the reentrant impulse to reverse direction when the slow pathway activates the fast pathway. The change in direction may be less when the fast pathway is activated retrogradely during ventricular pacing. In addition, the amount of current activating the fast pathway retrogradely may be greater following retrograde activation of the His bundle (ventricular pacing) than when activated by the slow AV nodal pathway. The short lower common pathway in slow/fast AVNRT may explain the relatively constant H–A interval during different episodes of tachycardia throughout an electrophysiologic study.

Catheter ablation of typical slow/fast AVNRT Prior to ablation, we attempt to induce sustained AVNRT for mapping the right atrium and CS to differentiate between slow/fast and slow/slow AVNRT based on the site of earliest retrograde atrial activation. Most of our procedures are performed under general anesthesia, which may depress retrograde conduction over the fast pathway, preventing the induction of sustained AVNRT. A lowdose isoproterenol infusion (0.25–0.5 µg/min) frequently enhances retrograde fast pathway conduction enough to allow the induction of sustained AVNRT without excessive hypercontractility, such that catheter positions remain stable. When sustained AVNRT cannot be achieved, mapping is performed during RV pacing (para-Hisian site), after confirming that the retrograde atrial activation sequ132

Fast Pathway

HB

Figure 9.17 Schematic representation of the circuit and ablation sites for typical slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) (using the rightward inferior extension of the AV node for the anterograde slow pathway), as postulated by the authors. The activation pattern is the same as that shown in Fig. 9.10, and then followed by anterograde conduction over the rightward inferior extension (squiggly blue arrow, slow pathway). The ASP potential identifies activation over the region of the rightward inferior extension located between the floor of the coronary sinus ostium and the area of slow conduction superiorly. Ablation between the inferoseptal tricuspid annulus and the anterior (apical) margin of the coronary sinus ostium (black crosshatched area and black dots) interrupts anterograde conduction over the rightward inferior extension and eliminates typical slow/fast AVNRT.

ence during ventricular pacing is the same in the CS, His bundle, and right atrial appendage electrograms as during nonsustained AVNRT or atrial echo complexes. The target for ablation of typical slow/fast AVNRT is the atrial end of the rightward inferior extension of the AV node (hatched area in Fig. 9.17). Our approach is to interrupt the rightward inferior extension by creating a short linear lesion between the tricuspid annulus (at the level of the middle of the CS ostium) and the anterior (apical) edge of CS ostium (black dots in Fig. 9.17). We attempt to limit radiofrequency (RF) applications to sites inferior to the level of the superior margin of the CS ostium. This reduces the risk of permanent AV block to less than 0.5% [21]. Early in the development of slow pathway ablation, we targeted the earliest potential during retrograde conduction over the slow AV nodal pathway when retrograde slow pathway conduction could be elicited (ASP potential, Figs. 9.13C and 9.14A) [13]. We soon found that the same high-frequency potential was recorded during sinus rhythm at the same region between the tricuspid annulus and the CS ostium (ASP potential in Fig. 9.14B). The ASP potential can be recognized by its timing and morphology [13]. The electrogram at this site has an initial small farfield atrial potential (generated by activation of the right atrium posterior to the Eustachian ridge), which is followed by the sharp ASP potential and a large, sharp ventricular potential. The large ventricular potential is generated by the ventricular septal myocardium underneath the atrial myocardium in the muscular AV septum. The ASP potential during sinus rhythm is recorded after activation in the roof (and often the floor) of the proximal CS (Figs. 9.14B and 9.18). The late timing of the ASP potential during sinus rhythm may be explained by conduction block at the

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CHAPTER 9

A

Catheter ablation of atrioventricular nodal reentrant tachycardia

B

RAO

LAO RAA

RAA RV

HB

HB RV

LA

CS Myocard

CS IS ASP Potential

CS ASP Potential

CS Myocardium

IS

C

I II V1 RAA HBp HBd ISp ISd CS10 CS9

A

A

A

A

H

H

ASP

ASP A CS Myocardium

A

CS Myocardium

CS5 CSd RV Figure 9.18 Origin and timing of the ASP potential during sinus rhythm. A, B. Radiographs in the right anterior oblique and left anterior oblique projections show the position of the electrode catheters, including the catheters in the coronary sinus (CS) and the inferoseptal region between the inferoseptal tricuspid annulus and coronary sinus ostium (IS). The arrows represent the activation pattern described below. C. Electrograms during sinus rhythm showing atrial activation in the coronary sinus electrograms proceeding from proximal (CS10) to distal (CSd). The authors propose that the left atrium (green arrow) activates the coronary sinus myocardium

(brown arrows) between electrograms CS9 and CS8.. CS activation propagates laterally in parallel with the left atrial myocardium (lower brown arrow in panel C), producing a single potential. CS activation reverses direction to proceed septally between CS8 and CS10 (upper brown arrow in panel C). The ASP potential is recorded after the timing of CS myocardial activation in the roof of the proximal coronary sinus (CS10), suggesting the ASP represents activation of the inferior aspect of the triangle of Koch by the CS myocardium (blue arrow).

Eustachian ridge, with the sinus impulse entering the triangle of Koch either from the inferior right atrium (extension of activation from the inferior crista terminalis, Fig. 9.19A) or from the CS due to rapid activation of the

left atrium over Bachmann’s bundle, followed by activation of the CS myocardium (Figs. 9.18 and 9.19B). Delivering RF current with good catheter contact at sites recording an ASP potential usually produces accelerated 133

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Supraventricular tachycardia Activation of the triangle of Koch during sinus rhythm A Postulate #1 LAO projection

RAO projection

Bachmann’s Bundle Fast pathway

HB

HB RA ac tiv

FO ASP

Eustachian ridge IVC

LA activation

RA activation potential

IVC

TA

CS

Mitral annul us

Eustachian ridge

TA Activation of CS Myocardium

B Postulate #2 Christa terminalis

Fast pathway

HB

HB RA ac tiv Eustachian ridge IVC

RA activation

FO ASP

CS

LA activation Mitral annul us

Eustachian ridge

potential

IVC

TA TA

CS

Figure 9.19 Schematic representation of two possible patterns of activation in the triangle of Koch during sinus rhythm that may explain the late ASP potential. A. In postulate 1, right atrial activation does not penetrate the triangle of Koch, due to conduction block across the Eustachian ridge (green arrows). The left atrium is activated rapidly over Bachmann’s bundle (green arrow in the left anterior oblique projection). Left atrial activation proceeds inferiorly and laterally (counterclockwise direction, green arrows in the left anterior oblique projection), activating the coronary sinus (CS) myocardium (brown arrows). Activation propagates in the septal direction along the CS myocardium to the CS ostium (brown arrows) and activates the inferior region of the triangle of Koch between the CS ostium and tricuspid annulus (brown arrows), to generate the late

Asp potential (blue arrows). B. In postulate 2, septal right atrial activation does not cross the Eustachian ridge to activate the triangle of Koch (similar to postulate 1). Activation inferiorly along the crista terminalis (and lateral to the crista terminalis) activates the region between the tricuspid annulus and Eustachian ridge (subeustachian isthmus) in the counterclockwise direction (long green arrow in the left anterior oblique projection). Continued right atrial activation in the counterclockwise direction (short squiggly green arrow in the left anterior oblique projection) activates the inferior region of the CS ostium (brown arrows) and the inferior region of the triangle of Koch to generate the late Asp potential (blue arrows). This postulate does not easily explain the usual finding that the Asp potential is later than CS activation during sinus rhythm.

junctional rhythm with retrograde conduction over the fast AV nodal pathway (Fig. 9.20). Junctional extrasystoles or an accelerated junctional rhythm were present during the RF application that eliminated slow/fast AVNRT in 95 of 100 consecutive patients [2]. The absence of atrial activation before His bundle activation during the junctional rhythm indicates heat-induced automaticity of tissue directly connected to the AV node (i.e., rightward inferior extension of the AV node). Retrograde conduction over the fast AV nodal pathway following His bundle activation during the accelerated junctional rhythm indicates the absence of injury to the fast pathway during the RF application [22]. The occurrence of very rapid junctional rhythm during RF application has been reported by some groups to

identify a high risk of AV block [23]. However, rapid junctional rhythm does not imply a high risk of AV block when RF energy is delivered inferior to the level of the superior margin of the CS ostium (usually > 2 cm from the site recording the proximal His bundle potential). The loss of 1 : 1 retrograde fast pathway conduction during junctional rhythm can indicate injury to the AV node or fast pathway [24,25]. However, the loss of 1 : 1 retrograde fast pathway conduction can occur without indicating injury to the AV node or fast pathway when the rate of the junctional rhythm exceeds the retrograde conduction capability of the fast pathway. We use decremental ventricular pacing immediately prior to the RF applications to identify the cycle length at which V–A block occurs. Junctional rhythm at shorter cycle lengths will produce V–A block without

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Junctional Automaticity During RF Application at ASP Site II V1

ARetro

A

ARetro

RAA HBp HBm Figure 9.20 Accelerated junctional rhythm beginning within 2 seconds of the onset of an application of radiofrequency current (RF On) at 30 W delivered to the inferoseptal region at a site recording an Asp potential. Each His bundle potential of the accelerated junctional rhythm (HJunct) was followed by retrograde conduction over the fast AV nodal pathway (ARetro), consistent with heating-induced automaticity of the slow pathway.

HBd

H

V

HJunct

HJunct

HJunct

30 Watts Power RF On

necessarily indicating injury to the fast pathway. During RF applications, atrial extrasystoles or atrial tachycardia with the same atrial activation sequence as during retrograde fast pathway conduction, which precede His bundle activation (especially without 1 : 1 A–H conduction), could indicate heating (and injury) to the fast pathway. Our present approach is to perform a continuous pullback during the RF application, beginning just on the ventricular side of the tricuspid annulus. This starting point is recognized by the absence of an ASP potential on the unipolar electrogram recorded from the ablation tip electrode, while recording an ASP potential on the unipolar electrogram from the second electrode (Fig. 9.21A). RF energy is delivered at each site during the pull-back until the atrial potential on the tip unipolar electrogram is markedly diminished. An accelerated junctional rhythm usually begins during the pull-back when the distal unipolar electrogram records the Asp potential (Fig. 9.21B). The RF application is maintained at each site producing junctional extrasystoles or accelerated junctional rhythm until 15–20 s after cessation or marked slowing of the accelerated junctional rhythm (Fig. 9.22). The RF pull-back is continued until the ablation electrode reaches the apical edge of the CS ostium. Before reaching the CS ostium, we use an RF power of 30–45 W (electrode temperature < 60 °C). This high power is relatively safe, since a steam pop is unlikely to produce perforation due to the presence of ventricular myocardium underlying the muscular AV septum. However, a steam pop can produce transient AV block proximal to the His bundle potential. AV nodal conduction usually recovers within 1–2 min. On approaching the margin of the CS ostium during the pull-back, we reduce RF power to 20–25 W. The ablation tip electrode is

then positioned within the apical edge of the CS ostium. We avoid delivering RF energy near the floor of the CS ostium, to prevent injury to the coronary artery [26,27]. When the ablation line is complete, an ASP potential may be recorded inferior to the line. However, delivering RF energy there usually will not produce an accelerated junctional rhythm, since the ablation line above this site should have interrupted the rightward inferior extension. An ASP potential may not be recorded superior to the ablation line, but an RF application there will produce accelerated junctional rhythm, even after the elimination of AVNRT. Our end points for ablation of typical slow/fast AVNRT, determined by programmed atrial and ventricular stimulation in the baseline state and during isoproterenol administration (1–4 µg/min), are: firstly, elimination of inducibility of AVNRT (single slow/fast atrial echo complexes are allowed); and secondly, elimination of 1 : 1 anterograde conduction over the slow AV nodal pathway during decremental atrial pacing. In our experience, this end point is achieved and associated with a long-term success (absence of recurrence of AVNRT) in 99.4% patients with typical slow/fast AVNRT [21]. Many investigators have reported similarly high success [28–31]. Cryoablation has been tested as a potentially safer energy source [32,33]. AV nodal block occurring during a cryoapplication often reverses if the cryoapplication is terminated immediately [32,33]. However, the recurrence of AVNRT is higher following cryoablation, with a longterm success rate of only 86% [34]. Improvement in results may occur with newer, larger cryoelectrodes. The most common reason for failure to achieve an accelerated junctional rhythm during RF ablation at sites 135

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SP ablation during sinus rhythm Pull-back starting point

A I II V1

A

RAA

A

HBp HBd

ASP

Bip 1-2

ASP

Afar

Inf Sep Uni 2 Uni 1

CSp

LA CS

CSd RV 100 ms

B

RF #1 – Catheter pull-back

I II V1 RAA CSp

CSd Start pull-back

Junctional rhythm

RF power RF on

RF application - Junctional automaticity during pull-back

II

A

RAA HBp HBm HBd CSp CSm CSd

H

Acceleration

Deceleration

Figure 9.21 Onset of a linear radiofrequency (RF) application delivered between the inferoseptal tricuspid annulus and the apical (anterior) margin of the coronary sinus (CS) ostium for ablation of the slow atrioventricular (AV) nodal pathway used in typical slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) (rightward inferior extension of the AV node). A. Recordings from the ablation catheter (Inf Sep electrograms) at the starting point, showing a sharp ASP potential on the bipolar electrogram (ASP on Bip 1–2 electrogram), the unipolar electrogram recorded from the second electrode (ASP on Uni 2 electrogram), but not on the unipolar electrogram recorded from the ablation tip electrode (ASP on Uni1 electrogram), indicating that the bipolar ASP potential was generated from the second electrode. The absence of an atrial or ASP potential on the unipolar tip electrogram (Uni1) indicates the tip electrode is located on the ventricular side of the tricuspid annulus. B. Recordings during the beginning of the linear RF application (RF On). There are no junctional extrasystoles or junctional rhythm at the ablation starting point located on the ventricular side of the inferoseptal tricuspid annulus. An accelerated junctional rhythm (arrow, junctional rhythm) begins soon after the catheter is withdrawn 2–3 mm onto the atrial side of the inferoseptal tricuspid annulus (arrow, start pull-back).

Figure 9.22 The pattern of the accelerated junctional rhythm during pull-back of the ablation catheter from the inferoseptal tricuspid annulus to the apical margin of the coronary sinus (CS) ostium while maintaining radiofrequency (RF) delivery throughout. As the catheter is withdrawn to a new site, there is abrupt shortening of the junctional rhythm cycle length (arrow, acceleration) with 1 : 1 retrograde fast pathway conduction, indicating heating of transitional tissue connected to the slow pathway (rightward inferior extension). The junctional rhythm then slows (arrow, deceleration), even though the catheter remains in the same location.

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Ablation catheter deflected away from the ablation site by the eustachian ridge RAO Figure 9.23 Radiographs in the right anterior oblique (RAO) and left anterior oblique projections, showing displacement of the ablation catheter tip from the inferoseptal region by the Eustachian ridge. The RAO projection suggests that the catheter tip was in contact with the inferoseptal region (arrow, IS). This was supported by sharp ASP and ventricular potentials recorded from the distal bipolar and unipolar electrograms (not shown). However, the RAO projection shows the catheter tip pointing laterally, away from the septum (arrow, IS). Because the Eustachian ridge acts like a fulcrum, increasing clockwise torque on the ablation catheter pushes the tip further away from the septum. RVPH, right ventricular catheter positioned for para-Hisian pacing.

RAA RAA RVPH

HB

IS

CS

RVPH

HB

IS

CS

movement of the catheter tip in systole and leftward movement in diastole. The sharp ASP potential, falsely suggesting stable contact, is recorded briefly during diastole. A long sheath can be used to position the catheter around the Eustachian ridge to the septum. We frequently use an SL-3 sheath (St. Jude Medical) after manually straightening the most proximal curve (Fig. 9.25).

Eust ridge Eust valve TA

CS

LAO

TV Septal Leaflet

Linear ablation site

Figure 9.24 The opened right side of a human heart, showing a prominent Eustachian valve (Eust Valve) and ridge (Eust Ridge), which could easily explain pushing of the ablation catheter tip away from the linear ablation site (outlined in red). TV Septal Leaflet, septal leaflet of the tricuspid valve. (Adapted from [9] with permission from Lippincott, Williams and Wilkins.)

recording a sharp ASP potential is poor electrode–tissue contact. This is usually due to a prominent Eustachian ridge pushing the catheter away from the septum during systole (Figs. 9.23 and 9.24). This problem is recognized fluoroscopically in the LAO projection as a rightward

Catheter ablation of “leftward inferior extension” slow/fast AVNRT In approximately 5% of patients with slow/fast AVNRT, ablation between the tricuspid annulus and the anterior edge of the CS ostium (at sites recording an ASP potential) produces brisk accelerated junctional rhythm (indicating injury to the rightward inferior extension) but fails to eliminate AVNRT. In this form of slow/fast AVNRT, the leftward inferior extension of the AV node may form the anterograde slow pathway in the reentrant circuit (Figs. 9.1 and 9.26). One approach to ablate this tachycardia is to deliver RF energy at progressively higher sites in the triangle of Koch. Since this approach may increase the risk of AV block, it may be preferable to try to target the atrial end of the leftward inferior extension (anterograde slow pathway). The location of the atrial end is unknown, but it may be near the roof of the proximal CS, based on the site of atrial activation during retrograde conduction (first beat in Fig. 9.12). We empirically target the roof of the proximal CS. We begin the ablation 2–4 cm from the CS ostium and continue proximally to the superior– anterior edge of the CS ostium (Figs. 9.26 and 9.27). When in the proximal CS, close to the CS ostium, we try to avoid 137

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Use of Long Sheath to Stabilize Ablation Catheter at Inferoseptal Region RAO Projection

LAO Projection RAA

RAA HB

RAA

RV

RV

RV

HB CS

HB

CS

IS

CS

IS

IS

Diastole Figure 9.25 A long sheath is used to bring the ablation catheter around a prominent Eustachian ridge to position the tip electrode against the inferoseptal tricuspid annulus (IS), the pull-back ablation starting site. The tip electrode is in firm contact throughout the cardiac cycle (diastole and systole in the left anterior oblique projection). The coronary sinus (CS)

Systole

catheter is located along the CS roof. It should be noted that the ablation tip electrode (arrow) is located at the level of the middle of the CS ostium. The pull-back ablation at this level produced junctional automaticity and eliminated typical slow/fast atrioventricular nodal reentrant tachycardia.

Postulated Circuit and Ablation Site for “Leftward Inferior Extension” Slow/Fast AVNRT RAO Projection Fast Pathway

RA Activation

LAO Projection

Tendon of Todaro

CS

HB

Fast Pathway

Slow Pathway

Slow Pathway

ASP

Potential

ToT

HB

Fast Pathway

LA Activation

Eustachian Ridge IVC

Eustachian Ridge

Activation of CS Myocardium Figure 9.26 Schematic representation of the circuit and ablation sites postulated by the authors for “leftward inferior extension” slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). Retrograde conduction over the fast pathway activates the right and left sides of the interatrial septum, posterior to the tendon of Todaro at a level slightly inferior to the level of the His bundle (red arrows). Just as in typical slow/fast AVNRT, right atrial activation (green lines) fails to reenter the triangle of Koch, presumably due to conduction block at the Eustachian ridge (short perpendicular green lines). Left atrial activation propagates from the septum, around the mitral annulus in the counterclockwise direction (green arrows in the LAO projection). The left atrium activates the coronary

138

SP Ablation Site

sinus (CS) myocardium (brown arrows) and the atrial end of the leftward inferior extension of the AV node (short dotted purple lines). Activation propagates along the leftward inferior extension of the AV node in the anterograde direction towards the compact AV node (squiggly purple arrows), forming the slow pathway and completing the reentrant circuit. For ablation of the atrial end of the leftward inferior extension of the atrioventricular node (anterograde slow pathway), we empirically target the roof of the proximal CS, beginning the ablation 2–4 cm from the CS ostium and continuing proximally towards the superior–anterior edge of the CS ostium (black cross-hatched area).

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RF #7 – Roof of proximal CS B RAO LAO

A

RAA

RAA

RV HB

RV HB

CS Roof

CS Roof CS Floor

After RF 7

C II V1

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RAA HB

CS Floor

A

H

145

360

S

S

A

A H

A

Block

65

100

H

S A

125

H

A

Block

CS d RV No SP conduction

200 ms

Figure 9.27 Catheter ablation of “leftward inferior extension” slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) by radiofrequency (RF) ablation on the roof of the proximal coronary sinus (CS). The first three RF applications were delivered between the inferoseptal tricuspid annulus and CS ostium at the level of the middle of the CS os. They produced vigorous accelerated junctional rhythm, but sustained slow/fast AVNRT remained inducible by programmed atrial stimulation. Two RF applications were then delivered between the tricuspid annulus (at the level of the superior margin of the CS os) and the anterior–superior CS ostium. These RF applications again produced an accelerated junctional rhythm, but sustained slow/fast AVNRT remained inducible. Two RF applications were then delivered along the roof of the proximal coronary sinus. Radiographs in the right anterior oblique projection (A) and left anterior oblique projection (B) show the

position of the ablation catheter (CS Roof) for the second of these two RF applications (RF 7), which eliminated all residual anterograde slow pathway conduction and eliminated the inducibility of AVNRT. C. Recordings during decremental pacing of the right atrial appendage (S, pacing stimuli in the RAA electrogram) following RF 7 delivered along the roof of the proximal coronary sinus. A decrease in atrial pacing cycle length to 360 ms was associated with Wenckebach block in fast pathway conduction, with a longest A–H interval of only 145 ms, suggesting complete absence of anterograde conduction over any slow pathway. It is likely that ablation between the inferoseptal tricuspid annulus and the CS os eliminated conduction over the rightward inferior extension and ablation at the roof of the proximal CS eliminated conduction over the leftward inferior extension of the atrioventricular node, eliminating all slow pathway conduction.

positioning the catheter straight upward (perpendicular to the CS roof) with force, since ablation at this site may injure the fast pathway.

ablation between the tricuspid annulus and the CS ostium, along the roof of the proximal CS and the anterior– superior edge of the CS ostium, fails to eliminate the tachycardia. In some of these patients, a component of the slow pathway used in the circuit is located in the left atrium close to the inferolateral mitral annulus [2,35–37]. This is identified by delivering a late atrial extrastimulus (after the onset of retrograde atrial activation) in the

Catheter ablation of “left atrial” slow/fast AVNRT In less than 1% of the patients with slow/fast AVNRT,

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A

B

RAO

LAO

RAA RV

RV

RAA

MAIL

HB

HB

MAIL CS

CS

Resetting slow/fast AVNRT at the inferolateral mitral annulus

C

II V1

A

RAA

A

HBp HBd

A

305 305

H

305

H

295

305

H

H

MAd S

RV

100 ms

Slow pathway ablation at the inferolateral mitral annulus

D II V1

ARetro

ARetro

A

RAA HBp HBd

H

CSp

HJunct

HJunct

HJunct

CSd Power 1 sec

RF On

Immediate junctional automaticity with retrograde fast pathway conduction 140

Figure 9.28 Testing for resetting followed by catheter ablation of “left atrial” slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) close to the inferolateral mitral annulus. A, B. Radiographs in the right anterior oblique and left anterior oblique projections show the catheter positions, including the transeptal mapping catheter in the left atrium close to the inferolateral mitral annulus (MAIL). C. During slow/fast AVNRT with the cycle length constant at 305 ms, an atrial extrastimulus was delivered to the mapping catheter at the inferolateral mitral annulus (arrow, S in MAd electrogram) after retrograde atrial activation had occurred (A–A = 305 ms in the HBp electrogram). The atrial extrastimulus advanced the next His bundle potential by 10 ms (H–H = 295 ms in the HBd electrogram). The advanced His bundle potential was followed by an H–H interval equal to the tachycardia cycle length (resetting response). The resetting of the tachycardia suggests that the site to which the left atrial extrastimulus was delivered was located close to an atrial connection of the anterograde slow pathway in the reentrant circuit. D. An application of radiofrequency current at the same site in the left atrium (RF On in the power tracing) produced an immediate accelerated junctional rhythm. Each His bundle potential of the accelerated junctional rhythm (HJunct) was followed by retrograde conduction over the fast atrioventricular nodal pathway (ARetro), consistent with heating-induced automaticity of the slow pathway.

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left atrium, close to the inferolateral mitral annulus. An advance in the next His bundle potential by ≥ 10 ms, followed by an H–H interval equal to the tachycardia cycle length (resetting of the tachycardia), indicates that the left atrial extrastimulus site is located close to an atrial connection of the anterograde slow pathway of the reentrant circuit (Fig. 9.28A–C). Ablation at this site frequently produces accelerated junctional rhythm with retrograde fast pathway conduction, indicating slow pathway automaticity, and eliminates the tachycardia (Fig. 9.28D) [2,35,36]. Ablation is usually not successful if a late atrial extrastimulus fails to advance the next His bundle potential and reset the tachycardia. Some patients with “left atrial” slow/fast AVNRT have unusual electrophysiologic features, such as a short H–A interval during the tachycardia (< 20 ms) or, during programmed atrial stimulation, two His bundle potentials following a single atrial extrastimulus (the “two-for-one response”).

val, the tachycardia is classified as fast/slow AVNRT. Slow/slow AVNRT most often (but not exclusively) uses the long rightward inferior extension for the anterograde limb of the reentrant circuit and the leftward inferior extension for the retrograde limb [38] (“counterclockwise reentry,” as viewed in the RAO projection, Fig. 9.29A). Fast/slow AVNRT most often uses the leftward inferior extension for the anterograde limb and the rightward inferior extension for the retrograde limb (“clockwise reentry,” as viewed in the RAO projection, Fig. 9.29B). Both forms have a long lower common pathway, which can result in great variability in the A–H and H–A intervals, even within the same episode of tachycardia. In addition, when ventricular extrastimuli are being used to verify the diagnosis of AVNRT, the extrastimuli must retrogradely advance the His bundle potential by 30–90 ms before advancing the next atrial activation. If ventricular extrastimuli advance the His bundle potential by 30–40 ms without advancing the next activation, fast/slow or slow/slow AVNRT may be incorrectly diagnosed as atrial tachycardia.

Slow/slow and fast/slow AVNRT Fast/slow AVNRT has been labeled as such because of the relatively short A–H interval, with the presumption that the anterograde limb of the reentrant circuit is the fast AV nodal pathway and the retrograde limb is the slow AV nodal pathway. However, we propose an alternative hypothesisa that slow/slow AVNRT and fast/slow AVNRT result from reentry between the rightward and leftward inferior extensions of the AV node [38]. The tachycardia is classified as slow/slow AVNRT when earliest atrial activation is recorded in the inferior triangle of Koch or CS and the A–H interval is significantly longer than the H–A interval. When earliest atrial activation is recorded in the triangle of Koch or CS with a longer H–A interval than A–H inter-

A

In general, the A–H interval during slow/slow AVNRT is long (> 200 ms), but the H–A interval ranges widely from very short (< 20 ms) to very long (up to 315 ms, mean 96 ± 65 ms) [39]. The H–A interval can vary in the same patient (and same episode) and occasionally becomes negative (Fig. 9.30B). This variability in the H–A interval, and the frequent finding of a short H–A interval during tachycardia (Fig. 9.30), can both be explained by a long lower common pathway (Fig. 9.31). Another manifestation of the long lower common pathway is a much longer H–A interval during ventricular pacing than during tachycardia (Fig. 9.30) [10,18].

Slow/slow AVNRT

Hypothesis B

Compact AV Node

Leftward Inferior Extension

Figure 9.29 The authors’ hypothesis that slow/slow atrioventricular nodal reentrant tachycardia (AVNRT) and fast/slow AVNRT result from reentry between the rightward (blue arrows) and leftward (purple arrows) inferior extensions of the atrioventricular node in the counterclockwise (A) and clockwise (B) directions, respectively, as viewed in the right anterior oblique projection.

Slow/slow AVNRT

Rightward Inferior Extension

FO

Fast/slow AVNRT Compact AV Node

Leftward Inferior Extension

Rightward Inferior Extension

FO CS

CS

Counterclockwise Reentry

Clockwise Reentry

RAO View 141

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A

Ventricular pacing

B Slow/slow AVNRT

II V1 490

RAA HBp HBd ISp ISd

A

A H

H

H

A

A 180

55 95

Afar

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CSd RV

A

15

105

ASP

ASP

Afar

ASP

390 S

S

Retro FP

C

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Slow/slow AVNRT

Slow/fast AVNRT

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A

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35

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H

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H

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520

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CSd RV 100 ms

Slow/slow AVNRT with a short H–A interval mimics slow/fast AVNRT, but can be differentiated from slow/ fast AVNRT by the site of earliest retrograde atrial activation [11,39,40]. A late ventricular extrastimulus is often helpful to visualize the atrial potentials, by separating the ventricular and atrial potentials (Fig. 9.32A). Earliest atrial activation during slow/slow AVNRT is recorded along 142

Figure 9.30 Recordings from a patient with slow/slow atrioventricular nodal reentrant tachycardia (AVNRT) and slow/fast AVNRT. A. Decremental ventricular pacing. There was a shift from retrograde fast pathway conduction to retrograde slow pathway conduction when the ventricular pacing cycle length reached 390 ms. During retrograde fast pathway conduction (first complex, Retro FP), the ASP potential was recorded after the timing of atrial activation in the His bundle and coronary sinus (CS) electrograms. The far-field atrial potential (Afar) in the inferoseptal electrograms (ISp and ISd) probably represents activation of the right atrium posterior to the Eustachian ridge. Retrograde block in the fast pathway with retrograde conduction over the slow pathway (second complex, Retro SP) was associated with an increase in the H–A interval (measured from the end of the retrograde His bundle potential) in the His bundle electrograms, from 55 ms to 180 ms. The H–ASP interval increased from 95 ms to 105 ms, and the ASP potential preceded activation in the CS and all atrial sites. B. During slow/slow AVNRT, the retrograde ASP potential preceded His bundle activation by 15 ms. This negative H–A interval (–15 ms) is a manifestation of a long lower common pathway. The short H–A interval in the His bundle electrograms simulates slow/fast AVNRT. The markedly shorter H–ASP interval during slow/slow AVNRT (–15 ms) than during ventricular pacing (180 ms, second complex in panel A) should be noted. C. Shift from slow/slow AVNRT (first two complexes) to slow/fast AVNRT (last two complexes) due to retrograde block in slow pathway conduction, manifested by the shift in timing of the ASP potential from earliest to late. The continuation of slow/fast AVNRT suggests that both tachycardias utilized the same slow pathway for anterograde conduction. The same H–A interval in the His bundle electrograms (35 ms) during the two tachycardias suggests that the fast pathway was entrained in the retrograde direction during slow/slow AVNRT.

the roof of the proximal CS in approximately 62% of patients (Fig. 9.32), and between the inferoseptal tricuspid annulus and CS ostium in 38% (Fig. 9.30) [38]. Half of the patients with slow/slow AVNRT have retrograde conduction over both the fast and slow AV nodal pathways (Fig. 9.30), while the other half have retrograde conduction only over the slow pathway.

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Slow/slow AVNRT (Counterclockwise reentry) RAO projection Tendon of Todaro

Retro SP

LAO projection

HB

HB

LCP

LCP

(Lt Inf Ext)

Ante SP

ASP

Eustachian ridge

potential Eustachian ridge

(Lt Inf Ext)

(Rt Inf Ext)

(Rt Inf Ext) CS

Retro SP

Ante SP

IVC

TA

CS Myocardium

Ante SP Ablation Site Figure 9.31 Schematic representation of reentry between the rightward inferior and leftward inferior extensions of the AV node, postulated by the authors to be the reentrant circuit in slow/slow atrioventricular nodal reentrant tachycardia (AVNRT). Activation propagates in the anterograde direction along the rightward inferior extension of the AV node (Rt Inf Ext, blue arrows) to activate the lower common pathway in the anterograde direction (LCP, squiggly black arrows) and the leftward inferior extension in the retrograde direction (Lt Inf Ext, purple arrows). The leftward inferior extension activates the coronary sinus myocardium, which propagates the impulse to the floor of the coronary sinus ostium (brown arrows) to activate

A.

the rightward inferior extension in the anterograde direction (blue arrows), completing the circuit. The fast pathway does not participate in the circuit, even though the H–A interval is often short. Prolongation of the conduction time over the lower common pathway delays His bundle activation, shortening the H–A interval during tachycardia mimicking slow/fast AVNRT. Our approach to ablation is to target the atrial end of the retrograde limb of the circuit (usually the leftward inferior extension of the AV node, Retro SP ablation site), followed by ablation of the atrial end of the anterograde limb (usually the rightward inferior extension of the AV node, Ante SP ablation site).

CS prox Roof dist

A

A

RAA HBp HBd

B. RV pacing

Slow/slow AVNRT

II V1

Figure 9.32 A. Recordings during slow/slow atrioventricular nodal reentrant tachycardia (AVNRT) show a short V–A interval with overlapping atrial and ventricular potentials, suggesting slow/fast AVNRT. A late ventricular extrastimulus (S) was used to advance the ventricular potentials and unmask the atrial activation sequence. The earliest activation was recorded in the roof of the proximal coronary sinus (arrows), confirming slow/slow AVNRT. B. During ventricular pacing, retrograde conduction occurred only over the retrograde slow pathway used during tachycardia (possibly the leftward inferior extension of the AV node). Retrograde conduction over the fast pathway was absent.

Retro SP Ablation Site

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Catheter ablation of slow/slow AVNRT Early in our experience, our approach to the ablation of slow/slow AVNRT was to target the slow pathway being used for retrograde conduction during the tachycardia.

V

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This was achieved by delivering radiofrequency current to the site of earliest retrograde atrial activation. Acute success, defined as elimination of retrograde slow pathway conduction and the inducibility of tachycardia, was achieved in all patients with slow/slow AVNRT. However, 143

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the recurrence rate was higher than in patients with slow/ fast AVNRT (8% vs. 0.4%). In addition, the recurrent tachycardia was usually fast/slow AVNRT or slow/fast AVNRT (not slow/slow AVNRT), with a different site of earliest retrograde atrial activation. These results led to our current practice in ablation of slow/slow AVNRT, which is to initially target retrograde slow pathway conduction, followed by ablation of anterograde slow pathway conduction. RF energy is delivered to the site of earliest retrograde atrial activation, which is usually located in the roof of the proximal CS (Figs. 9.32 and 9.33) and less commonly between the inferoseptal tricuspid annulus and CS ostium. We prefer to ablate retrograde slow pathway conduction during ventricular pacing, rather than during tachycardia. When ablation is performed during tachycardia, retrograde block in the slow pathway terminates the tachycardia, producing a post-pause increase in contractility and change in anatomical relationships, which may dislodge the catheter. If 1 : 1 anterograde conduction over a slow pathway is present following ablation of retrograde slow pathway conduction, we target anterograde slow pathway conduction. This usually involves ablation of the rightward inferior extension between the tricuspid annulus and CS ostium, as in ablation of typical slow/fast AVNRT (site similar to Fig. 9.18A, B). We prefer to ablate anterograde slow pathway conduction during sinus rhythm to observe accelerated junctional rhythm as evidence of slow pathway injury. Since retrograde fast pathway conduction is either absent or poor in most patients with slow/slow AVNRT, accelerated junctional rhythm is frequently associated with V–A block (Fig. 9.34). As previously mentioned,

RAA

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LAO Projection Figure 9.33 Radiograph in the left anterior oblique projection, showing the usual target site for ablation of the retrograde limb in slow/slow atrioventricular nodal reentrant tachycardia (AVNRT) (usually the leftward inferior extension of the AV node). Two catheters with multiple closely spaced bipolar electrodes are positioned along the roof (CS Roof) and floor (CS Floor) of the coronary sinus. During slow/slow AVNRT, the earliest atrial activation was recorded from the fourth bipolar electrogram on the coronary sinus roof catheter (Earliest Activ). The ablation catheter tip electrode was maneuvered to the same site (Ablation CS Roof).

Ablation of Slow/Slow AVNRT I II V1

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Targeting Anterograde Slow Pathway Conduction

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Figure 9.34 Recordings during a radiofrequency application (30 W) at the inferoseptal region targeting anterograde slow pathway conduction in a patient with slow/slow atrioventricular nodal reentrant tachycardia (AVNRT). Heating of the anterograde slow pathway by radiofrequency current produces a rapid junctional rhythm (HJunct) with 2 : 1 retrograde slow pathway conduction (the arrow marks the V–A block). The complete absence of retrograde fast pathway conduction during the accelerated junctional rhythm does not indicate injury to the anterograde fast pathway in this patient. Ventricular pacing prior to ablation showed no retrograde conduction over the fast pathway.

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it is helpful to perform decremental ventricular pacing before ablation to determine the cycle length at which retrograde fast pathway conduction will block. The occurrence of V–A block during accelerated junctional rhythm does not necessarily indicate injury to anterograde fast pathway conduction, as long as the ablation catheter is positioned inferior to the level of the superior margin of the CS ostium and the junctional rhythm cycle length is shorter than the cycle length of retrograde block in fast pathway conduction during ventricular pacing. Alternatively, anterograde fast pathway conduction can be monitored during ablation by atrial pacing at a rate faster than the accelerated junctional rhythm.

ior extension of the AV node in the anterograde direction (Fig. 9.35). Left atrial activation propagates rapidly to the atrial septum to activate the fast pathway (producing the short A–H interval), while anterograde conduction is occurring over the leftward inferior extension and the lower common pathway. In this hypothesis, the fast pathway serves as a bystander (Fig. 9.35). Another possible manifestation of the long lower common pathway is the occurrence, in some patients, of V–A block during ventricular pacing at cycle lengths longer than the tachycardia. Presumably, retrograde block occurs in the lower common pathway, preventing activation of the retrograde slow pathway. The second, and less likely, hypothesis does not consider the His bundle to be activated by the fast pathway in fast/slow AVNRT. Rather, the His bundle is activated by anterograde conduction over the leftward inferior extension (anterograde slow pathway) and the lower common pathway. This hypothesis attributes the short A–H interval to simultaneous conduction anterogradely over the lower common pathway (LCP) and retrogradely over the rightward inferior extension, arriving at the atrial end of the rightward inferior extension (the Asp site) and activating the coronary sinus, left atrium and right atrium shortly before arriving at the proximal His bundle. This hypothesis requires a relatively long LCP. Reentry between the two slow AV nodal pathways may be facilitated by

Fast/slow AVNRT During fast/slow AVNRT, the H–A interval ranges widely from 165 ms to 365 ms (mean 266 ± 66 ms) [40]. The A–H is shorter than during slow/slow AVNRT, in the range of 80–220 ms (mean 127 ± 62 ms) and may be even shorter than during sinus rhythm (Figs. 9.13 and 9.14). The short A–H interval does not necessarily indicate that the fast pathway is part of the reentrant circuit. We consider two hypotheses for the short A–H interval. In the first hypothesis, retrograde conduction over the rightward inferior extension activates the CS myocardium (which activates the left atrium) and activates the leftward infer-

Fast/Slow AVNRT

(Clockwise Reentry) RAO Projection RA Activation

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Potential Eustachian Ridge

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Retro SP Ablation Site Figure 9.35 Schematic representation of reentry between the leftward inferior and rightward inferior extensions of the AV node, postulated by the authors to be the reentrant circuit in fast/slow atrioventricular nodal reentrant tachycardia (AVNRT). Activation propagates in the anterograde direction along the leftward inferior extension of the AV node (Lt Inf Ext, purple arrows) to activate the lower common pathway in the anterograde direction (LCP, squiggly black arrows) and the rightward inferior extension in the retrograde direction (Rt Inf Ext, blue arrows). The rightward inferior extension activates the floor of the coronary sinus ostium. The coronary

CS Myocardium

LA Activation

sinus myocardium propagates the impulse laterally (brown lines) to activate the left atrium (green arrows) and the leftward inferior extension in the anterograde direction (purple arrows), completing the circuit. Left atrial activation propagates rapidly to the atrial septum (green arrows in the left anterior oblique projection) to activate the fast pathway (red arrows), producing a short A–H interval. The fast pathway serves as a bystander. Ablation is targeted to the atrial end of the retrograde slow pathway in the inferoseptal region at a site recording a sharp retrograde ASP potential (Retro SP ablation site).

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conduction block across the Eustachian ridge common pathway (tissue between the proximal junction of the inferior extensions of the AV node and the atrium). Retrograde conduction over the rightward inferior extension of the AV node activates the leftward inferior extension in the anterograde direction and the upper common pathway in the retrograde direction. Retrograde conduction over the upper common pathway activates and tendon of Todaro [14,41], rendering the region around the inferior extensions of the node relatively protected.

Catheter ablation of fast/slow AVNRT The initial target in ablation of fast/slow AVNRT is the retrograde slow pathway in the tachycardia circuit, followed by ablation of anterograde slow pathway conduction, if present. RF energy is delivered to the site of earliest retrograde atrial activation, which in fast/slow AVNRT is usually the site recording the retrograde ASP potential in the region between the inferoseptal tricuspid annulus and CS ostium (Figs. 9.13 and 9.14). In some patients, the retrograde ASP potential is not initially apparent, and earliest activation appears to be located along the floor of the proximal CS. However, the finding of earliest activation in the floor of the CS, close to the ostium, should strongly suggest retrograde conduction over the rightward inferior extension of the AV node. Further mapping outside the CS will usually identify a retrograde ASP potential that is earlier than the timing of activation in the CS. Ablation outside the CS at the site recording the retrograde ASP potential has the greatest likelihood of eliminating retrograde slow pathway conduction and fast/slow AVNRT. In addition, we prefer to avoid ablation along the floor of the proximal CS, since the distal branch of the right or left coronary artery is frequently close by. If a coronary artery is within a few millimeters of the ablation electrode on the floor of the CS, delivering RF energy may injure the artery [42]. When a retrograde ASP potential is identified, fast/slow AVNRT is perhaps the easiest form of AVNRT to ablate. Acute ablation success is achieved in essentially all patients. The recurrence rate for fast/slow AVNRT in our experience is 1.2%, intermediate between slow/fast and slow/slow AVNRT.

Summary In AVNRT with a short R–P interval, our first step is to identify the site of earliest retrograde atrial activation. An earliest atrial activation recorded posterior to the tendon of Todaro is considered to represent retrograde conduction over the fast AV nodal pathway, and the tachycardia

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is labeled slow/fast AVNRT. We initially assume that anterograde conduction is occurring over the rightward inferior extension of the AV nodeai.e., typical slow/fast AVNRT. Ablation is targeted to the proximal end of the rightward inferior extension of the AV node during sinus rhythm, either directly to the site recording the ASP potential or by creating a linear lesion between the inferoseptal tricuspid annulus and the anterior margin of the coronary sinus ostium. In either approach, the ablation is usually performed at the level of the middle of the coronary sinus ostium. Radiofrequency applications in this region usually: 1 Produce junctional extrasystoles or accelerated junctional rhythm. 2 Eliminate 1 : 1 anterograde conduction over the slow AV nodal pathway during decremental atrial pacing. 3 Eliminate the inducibility of typical slow/fast AVNRT. A failure to produce junctional extrasystoles and eliminate AVNRT is usually the result of poor contact between the ablation electrode and the inferoseptal region (most often due to the presence of a prominent Eustachian ridge). If slow/fast AVNRT is not eliminated by inferoseptal ablation despite good catheter contact and brisk junctional automaticity, we consider the possibility that the anterograde slow pathway in the reentrant circuit is formed by the leftward inferior extension of the AV node (i.e., “leftward inferior extension” slow/fast AVNRT). We attempt to induce retrograde conduction over a slow pathway to target the site of earliest activation, in the hope that this would be the same slow pathway forming the anterograde limb of the reentrant circuit. In the absence of retrograde slow pathway conduction, we empirically target the leftward inferior extension by ablation along the roof of the proximal coronary sinus (1– 4 cm from the ostium) and at the superior and apical (anterior) margin of the coronary sinus ostium. Care should be taken not to position the tip of the catheter in a straight superior orientation within the proximal coronary sinus close to the ostium, since radiofrequency energy delivered in this manner has the potential to injure the fast pathway on the left atrial septum. If slow/fast AVNRT is not eliminated by ablation either at the inferoseptal region or the roof of the proximal CS, we next consider a left atrial slow pathway (“left atrial” slow/fast AVNRT). These slow pathways are often located close to the inferolateral mitral annulus, and can be identified by delivering a late atrial extrastimulus to that site (without effecting retrograde conduction over the fast pathway) and noting an advance in the timing of the next His bundle potential (usually 10 ms) and resetting of the tachycardia. Ablation at the site of successful resetting usually eliminates the AVNRT (90%) by elimin-

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ating conduction over the anterograde slow pathway in the reentrant circuit. Ablation at sites without successful resetting usually fails to affect the AVNRT. The resetting technique can also be used earlier in the ablation selection process to verify that tissue in the inferoseptal region (rightward inferior extension of the AV node) or roof of the proximal CS (leftward inferior extension) is participating in the reentrant circuit. AVNRT with a short R–P interval and earliest activation at the inferoseptal region or CS is classified as slow/slow AVNRT. When earliest activation is recorded within the roof of the proximal coronary sinus, we assume that the leftward inferior extension forms the retrograde slow pathway and that the rightward inferior extension forms the anterograde slow pathway. When the earliest retrograde atrial activation is recorded at the inferoseptal region or at the floor of the CS ostium, we assume that the rightward inferior extension of the AV node forms the retrograde slow pathway and that the leftward inferior extension forms the anterograde slow pathway. In either case, we initially target the retrograde slow pathway and then follow with ablation of the anterograde slow pathway. Both limbs are targeted to reduce the recurrence of AVNRT as slow/fast or fast/slow AVNRT. In fast/slow AVNRT, the retrograde limb is almost always formed by the rightward inferior extension of the AV node, resulting in a retrograde ASP potential in the inferoseptal region, followed by activation in the floor of the coronary sinus ostium and then laterally along the CS and left atrium. The most effective approach is to target the retrograde ASP potential during ventricular pacing or fast/slow AVNRT. If a retrograde ASP potential is not evident, but earliest activation appears to be recorded at the floor of the coronary sinus ostium, this strongly suggests retrograde conduction over the rightward inferior extension, and further exploration of the inferoseptal region will usually identify the retrograde ASP potential for ablation. We avoid ablation at the floor of the coronary sinus ostium and along the floor of the proximal coronary sinus, due to the potential risk of injuring the distal right or left coronary artery.

3 Tondo C, Beckman KJ, McClelland JH, et al. Response to radiofrequency catheter ablation suggests that the coronary sinus forms part of the reentrant circuit in some patients with atrioventricular nodal reentrant tachycardia [abstract]. Circulation 1996;94:I-380. 4 Otomo K, Beckman KJ, McClelland JH, et al. Resetting response suggests the absence of an upper common pathway in slow/fast and presence in slow/slow atrioventricular nodal reentrant tachycardia [abstract]. Pacing Clin Electrophysiol 1996;19:730. 5 McGuire MA, Lau KC, Johnson DC, et al. Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia: evidence that a common pathway of nodal tissue is not present above the reentrant circuit. Circulation 1991;83: 1232 – 46. 6 Foresti S, Lockwood DJ, Po SS, et al. Two distinct retrograde slow pathways are consistent with rightward and leftward posterior extensions of the AV node [abstract]. Heart Rhythm 2004;1:S45. 7 Yeh SJ, Wang CC, Wen MS, et al. Radiofrequency ablation therapy in atypical or multiple atrioventricular node reentry tachycardias. Am Heart J 1994;128:742– 58. 8 Kuck KH, Kuch B, Bleifeld W. Multiple anterograde and retrograde AV nodal pathways: demonstration by multiple discontinuities in the AV nodal conduction curves and echo time intervals. Pacing Clin Electrophysiol 1994;7:656 – 62. 9 Inoue S, Becker AE. Posterior extensions of the human compact atrioventricular node: a neglected anatomic feature of potential clinical significance. Circulation 1998;97:188 – 93. 10 Heidbüchel H, Beckman K, McClelland J, et al. Presence or absence of a lower common pathway differentiates slow/ slow from slow/fast AV nodal reentrant tachycardia [abstract]. Pacing Clin Electrophysiol 1994;17:759. 11 Baerman J, Wang X, Jackman WM. Atrioventricular nodal reentry with an antegrade slow pathway and retrograde slow pathway: clinical and electrophysiologic properties [abstract]. J Am Coll Cardiol 1991;17:338A. 12 Otomo K, Antz M, Beckman KJ, et al. Left atrial activation precedes right atrial activation in slow/fast atrioventricular nodal reentrant tachycardia [abstract]. Circulation 1996;94:I-683. 13 Jackman WM, Lockwood DJ, Foresti S, et al. Double atrial potentials in the His bundle electrograms during slow/fast AV nodal reentrant tachycardia suggest block at tendon of Todaro [abstract]. Heart Rhythm 2004;1:S47. 14 Von Lüdinghausen M, Ohmachi N, Boot C. Myocardial coverage of the coronary sinus and related veins. Clin Anat 1992;5:1–15. 15 Antz M, Otomo K, Arruda M, et al. Electrical conduction between the right atrium and the left atrium via the musculature of the coronary sinus. Circulation 1998;98:1790–5. 16 Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry, by radiofrequency catheter ablation of slow pathway conduction. N Engl J Med 1992;327:313 – 8. 17 Jackman WM, Beckman KJ, McClelland JH, et al. Participation of atrial myocardium (posterior septum) in AV nodal reentrant tachycardia: evidence from resetting by atrial extrastimuli [abstract]. Pacing Clin Electrophysiol 1991;14:646.

References 1 Wu D, Denes P, Amat-y-Leon F, et al. Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol 1978; 41:1045–51. 2 Lockwood D, Otomo K, Wang X, et al. Electrophysiological characteristics of atrioventricular nodal reentrant tachycardia: implications for the reentrant circuits. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: from Cell to Bedside, 4th ed. Philadelphia: Saunders, 2004: 537–57.

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18 Heidbüchel H, Ector H, De Were FV. Prospective evaluation of the length of the lower common pathway in the different diagnosis of various forms of AV nodal reentrant tachycardia. Pacing Clin Electrophysiol 1998;21:209 –16. 19 Hirao K, Otomo K, Wang X, et al. Para Hisian pacing: a new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node. Circulation 1996;94:1027–35. 20 Thibault B, Beckman K, McClelland J, et al. Use of ventricular stimuli to examine lower common pathway in S/F AVNRT [abstract]. Circulation 1994;90:I-214. 21 Antz M, McClelland J, Gonzalez M, et al. Ablation along a line between the tricuspid annulus and the coronary sinus and within the coronary sinus ostium results in a low recurrence of atrioventricular nodal reentrant tachycardia despite residual slow pathway conduction [abstract]. Circulation 1996;94:I-683. 22 Wang X, McClelland JH, Beckman KJ, et al. Accelerated junctional rhythm during slow pathway ablation [abstract]. Circulation 1991;84:II-582. 23 Lipscomb KJ, Zaidi AM, Fitzpatrick AP. Slow pathway modification for atrioventricular node re-entrant tachycardia: fast junctional tachycardia predicts adverse prognosis. Heart 2001;85:44–7. 24 Thakur RK, Klein GJ, Yee R, et al. Junctional tachycardia: a useful marker during radiofrequency ablation for atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1993;22:1706 – 10. 25 Jentzer JH, Goyal R, Williamson BD, et al. Analysis of junctional ectopy during radiofrequency ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia. Circulation 1994;90:2820–6. 26 Nakagawa H, Chandrasekaran K, Pitha J, et al. Early detection of coronary artery injury produced by radiofrequency ablation with the coronary sinus using intravascular ultrasound imaging [abstract]. Circulation 1995;92:I-610. 27 Arruda M, Nakagawa H, Chandrasekharan K, et al. RF ablation in the coronary venous system is associated with risk of coronary artery injury which may be prevented by use of intravascular ultrasound [abstract]. J Am Coll Cardiol 1996; 27:160A. 28 Kay GN, Epstein AE, Daily SM, et al. Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia. Circulation 1992;85:1675–88. 29 Haïssaguerre M, Gaita F, Fischer B, et al. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy. Circulation 1992;85;2162–75.

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30 Jazayeri MR, Hempe SL, Sra JS, et al. Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia. Circulation 1992;85:1318 –28. 31 Chen SA, Chiang CE, Tsang WP, et al. Selective radiofrequency catheter ablation of fast and slow pathways in 100 patients with atrioventricular nodal reentrant tachycardia. Am Heart J 1993;125:1–10. 32 Friedman P, Dubuc M, Green M, et al. Cryomapping and cryoablation of A-V nodal reentrant supraventricular tachycardia: results of the “Frosty” trial [abstract]. Pacing Clin Electrophysiol 2003;26:979. 33 Skanes AC, Dubuc M, Klein G, et al. Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia. Circulation 2000;102:2856 – 60. 34 Greiss I, Novak PG, Khairy P, et al. Slow pathway ablation for AVNRT: a comparison between cryoablation and radiofrequency energy in a 5-year experience [abstract]. Heart Rhythm 2005;2:S270. 35 Tondo C, Otomo K, McClelland J, et al. Atrioventricular nodal reentrant tachycardia: is the reentrant circuit always confined in the right atrium? [abstract] J Am Coll Cardiol 1996;27:159A. 36 Po SS, Beckman KJ, Lockwood D, et al. AV nodal reentrant tachycardia requiring ablation from mitral annulus: selection of effective ablation site [abstract]. Pacing Clin Electrophysiol 2003;26:979. 37 Chen SA, Tai CT, Lee SH, Chang MA. AV nodal reentrant tachycardia with unusual characteristics: lessons from radiofrequency catheter ablation. J Cardiovasc Electrophysiol 1998;9: 321–3. 38 Wang Z, Otomo K, Shah N, et al. Slow/slow and fast/slow atrioventricular nodal reentrant tachycardia use anatomically separate retrograde slow pathways [abstract] Circulation 1999;100:I-65. 39 Heidbuchel H, Jackman WM. Catheter ablation of atypical atrioventricular nodal reentrant tachycardia. In: Zipes DP, Haïssaguerre M, eds. Catheter Ablation of Cardiac Arrhythmias, 2nd ed. Armonk, NY: Futura, 2002: 321–43. 40 Heidbuchel H, Jackman WM. Characterization of subforms of AV nodal reentrant tachycardia. Europace 2004;6:316 –29. 41 Ashar M, Otomo K, Wang Z, et al. Late activation in the triangle of Koch suggests block at the tendon of Todaro in slow/ fast AVNRT [abstract]. Pacing Clin Electrophysiol 2002;25: 542. 42 Sun Y, Po S, Arruda M, Beckman K, et al. Risk of coronary artery stenosis with venous ablation for epicardial accessory pathways [abstract]. Pacing Clin Electrophysiol 2001;24:266.

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10

Catheter ablation of accessory pathways Aman Chugh, Frank Bogun, and Fred Morady

Introduction Accessory pathways are anomalous muscular tracts that connect the atria and ventricles. The vast majority of accessory pathways traverse the atrioventricular (AV) annuli and are referred to as AV pathways. Pathways that skirt the anterior, lateral, or posterior aspects of the AV valves are referred to as free-wall pathways. Accessory pathways that insert near the septal aspect of AV valves are called septal pathways. In general, left free-wall pathways (60%) are more prevalent than septal pathways (25%), which are in turn more common than right free-wall pathways (15%). One may also encounter unusual varieties of accessory pathways on the right side that include atriofascicular, nodofascicular, and nodoventricular pathways. The clinical presentation of a patient with an accessory pathway varies considerably, from an asymptomatic patient in whom preexcitation is diagnosed on a screening electrocardiogram (ECG) to a young patient presenting with aborted sudden death. Accessory pathways may participate in orthodromic reciprocating tachycardia (ORT) or antidromic reciprocating tachycardia (ART), or may act as bystanders during other arrhythmiasa e.g., atrial fibrillation (AF) or atrioventricular nodal reentrant tachycardia (AVNRT). In this chapter, the electrocardiographic localization, mapping, and catheter ablation of various accessory pathways will be discussed.

Preprocedure evaluation In general, patients with symptoms and documented tachycardia or preexcitation on the electrocardiogram are referred for electrophysiologic testing and ablation. The combination of tachycardia and evidence of preexcitation on the electrocardiogram (Wolff–Parkinson–White syndrome) is a class I indication for electrophysiologic evaluation [1]. Even in the absence of symptoms, patients with

high-risk occupationsae.g., pilots or bus driversamay be considered for catheter ablation as well. Electrophysiologic evaluation is usually not recommended in patients with preexcitation who are otherwise asymptomatic, as they are thought to be at low risk for adverse events [1]. However, more recent data indicate that an electrophysiologic assessment may be helpful in risk stratification in asymptomatic patients [2]. In addition, there are data suggesting that catheter ablation is helpful in reducing the risk of syncope and sudden death in patients with highrisk features [2].

Electrocardiographic characteristics and localization Accessory pathways may conduct in the anterograde direction, resulting in manifest preexcitation. Manifest or overt preexcitation is defined as a PR interval of < 120 ms and a QRS width of > 120 ms. Minimal preexcitation may present as slurring of the QRS upstroke with a QRS duration < 120 ms and a PR interval > 120 ms. When evaluating for minimal preexcitation on the electrocardiogram, it is helpful to note that normal activation of the interventricular septum proceeds from left to right, resulting in Q waves in the left precordial leads. Absence of a “septal” Q wave in lead V6 on the ECG is helpful in differentiating minimal preexcitation from normal ventricular activation (Fig. 10.1) [3]. Concealed accessory pathways, on the other hand, are not able to conduct anterogradely and therefore are not apparent on the ECG. Many accessory pathways conduct in both anterograde and retrograde directions. The electrocardiogram of a patient with preexcitation is helpful in localizing the accessory pathway prior to the electrophysiology procedure. Although several algorithms have been devised for reliable localization of accessory pathways [4–6], a few simple observations usually suffice. A positive delta wave in lead V1 and a negative delta wave in leads I and aVL are suggestive of a left-sided 149

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Figure 10.1 A. The QRS complex in surface lead V6 in a patient with minimal preexcitation prior to radiofrequency ablation of a left lateral accessory pathway. The dotted line indicates the onset of the delta wave. B. Surface lead V6 after radiofrequency ablation. The dotted line indicates the onset of the QRS complex. A septal Q wave has replaced the delta wave (arrow).

accessory pathway. A negative delta wave in lead V1 and a positive delta wave in leads I and aVL are consistent with a right-sided accessory pathway. The inferior leadsa i.e., leads III and aVFaare helpful in localizing the accessory pathway further on the mitral or tricuspid annulus. A positive delta wave in these leads is suggestive of anterior, anterolateral (Fig. 10.2), and anteroseptal pathways. Negative polarity of the delta wave in leads III and aVF is compatible with posterior, posterolateral (Fig. 10.3), or posteroseptal [7] accessory pathways. A steeply negative delta wave in lead II suggests an epicardial origin of a posteroseptal pathway (Fig. 10.4) [8]. Of course, these “rules” are only approximations that serve as a rough guide to the localization of accessory pathways. These generalizations may not be applicable in every case, especially in the absence of significant preexcitation on the electrocardiogram. For anteroseptal and midseptal accessory pathways, a few additional observations are needed for electrocar-

diographic localization. Typically, a negative delta wave is inscribed in lead V1 with manifest anteroseptal and midseptal accessory pathways (Fig. 10.5). Septal accessory pathways along the tricuspid annulus may be distinguished from right free-wall pathways if the QRS transition (negative to positive) occurs at or before lead V3 on the electrocardiogram [5]. If the transition occurs between V3 and V4, then the amplitude of the delta wave in lead II is useful in discriminating between a septal (≥ 1.0 mV) and a right free-wall (< 1.0 mV) pathway [5]. An R to S ratio of ≥ 1 in lead III is compatible with an anteroseptal pathway, whereas a ratio of < 1 is consistent with a midseptal accessory pathway [4]. Some investigators have also commented on a subset of anteroseptal accessory pathways, referred to as para-Hisian accessory pathways [8]. These pathways are defined by the presence of a His deflection of > 0.1 mV on the ablation catheter and the lack of separation of the tip electrodes of the ablation catheter and a catheter at the His position in any fluoroscopic view [8]. In the absence of preexcitation on the ECG, there may be clues during narrow complex tachycardia that may be helpful in ascertaining the mechanism. Development of a bundle branch block during tachycardia may be helpful not only in differentiating ORT from other forms of supraventricular tachycardia but also in localizing the accessory pathway. Slowing of the rate with development of a bundle branch block localizes the accessory pathway to the side ipsilateral to the blocked bundle branch. Electrocardiographic localization may also be helpful in informing the patient and family about the relative success and complication rates of the procedure. For example, a patient with relatively mild symptoms and an electrocardiogram suggestive of an anteroseptal or midseptal

Figure 10.2 Electrocardiogram in a patient with a right anterolateral accessory pathway. One should note the predominantly negative delta wave in V1, transition at V5, and a positive delta wave in the inferior leads—all consistent with a right anterolateral accessory pathway. The paper speed is 25 mm/s.

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Figure 10.3 Electrocardiogram in a patient with a manifest right posterolateral accessory pathway. One should note the negative delta wave in lead V1, with a late transition across the precordium and a negative delta wave in lead III. The paper speed is 25 mm/s.

Figure 10.4 Electrocardiogram in a patient with a manifest posteroseptal accessory pathway. One should note the steeply negative delta wave (asterisk) in lead II, which is suggestive of an epicardial location of the pathway.

accessory pathway may prefer medical therapy rather than face a small risk of AV block.

Anatomy The nomenclature of accessory pathways is derived from the surgical experience. A new classification scheme that is more anatomically correct has been proposed [9]; how-

ever, accessory pathways are generally referred to as in the surgical literature. Accessory pathways connect the atrial with the ventricular myocardium via the AV groove. They may have an oblique rather than a strictly perpendicular course. The insertion is the atrial myocardium and the basal ventricular myocardium. They may consist of a broad band or of multiple isolated or communicating branches that may make the ablation procedure particularly challenging. Rarely, their insertion occurs at a site distant from the annulus (see below), and these pathways are referred to as non-AV pathways. A predominantly epicardial course has been described for right-sided and left-sided accessory pathways. Pathways located in the posteroseptal area are divided into right-sided and left-sided posteroseptal pathways. Whereas right posteroseptal pathways insert along the tricuspid annulus in close proximity to the coronary sinus ostium, left-sided posteroseptal pathways may have a subepicardial course close to the proximal coronary sinus and the middle cardiac vein, or may be located subendocardially along the ventricular aspect of the posterior mitral annulus. The former are often associated with a diverticulum of the coronary sinus or within the middle cardiac vein [10]. Accessory pathways can be associated with different forms of congenital heart disease. L-transposition of the great arteries, hypertrophic cardiomyopathy, and Ebstein’s anomaly have been associated with the presence of accessory pathways. In Ebstein’s anomaly, there is ventricularization of the tricuspid leaflets. This congenital anomaly is often associated with multiple accessory pathways, which are mainly located on the right side [11]. 151

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Figure 10.5 Electrocardiogram in a patient with an anteroseptal accessory pathway. One should note the negative delta wave in lead V1 and transition by V3, consistent with an anteroseptal pathway. The paper speed is 25 mm/s.

Electrophysiologic evaluation During the diagnostic portion of an electrophysiology study, the anterograde and retrograde block cycle lengths and refractory periods of the accessory pathway and the AV node are determined. In patients with preexcitation, a 12-lead ECG should be obtained during atrial pacing at a cycle length 20 –30 ms longer than the accessory pathway block cycle length. Analysis of the maximally preexcited ECG permits a more precise determination of the delta wave vector than when there is fusion. Even in a patient with documented tachycardia and preexcitation on the electrocardiogram, it is helpful to induce tachycardia before catheter ablation. The patient may have tachycardia unrelated to the accessory pathwaya e.g., atrial tachycardia or AVNRTaor may have an additional pathway or pathways, the presence of which is only apparent during tachycardia. It is also helpful to evaluate retrograde conduction over the pathway prior to ablation. Sometimes anterograde conduction is eliminated but the pathway is still capable of retrograde conduction and participation in orthodromic tachycardia. Comparing the preablation and postablation retrograde atrial activation sequence may be critical in determining whether the retrograde limb has also been successfully ablated. In the absence of preexcitation, several observations and pacing maneuvers may be helpful in ascertaining the presence of an accessory pathway and its participation in a tachycardia. If atrial tachycardia has been ruled out, eccentric atrial activation is suggestive of ORT as the 152

mechanism. Orthodromic reciprocating tachycardia utilizing a concealed septal accessory pathway may be distinguished from atypical AVNRT by the post-pacing interval during right ventricular pacing. A post-pacing interval minus the tachycardia cycle length < 115 ms is consistent with ORT as the mechanism [12]. A very specific indicator of the presence and participation of a right or left free-wall accessory pathway during tachycardia is the observation of ventriculoatrial (VA) interval prolongation by ≥ 35 ms during right or left bundle branch block, respectively (Fig. 10.6) [13]. With anteroseptal and midseptal accessory pathways, the VA interval during right bundle branch block may lengthen by ≤ 30 ms or not change at all [14]. The presence of an accessory pathway is confirmed by advancement of the atrial electrogram by a ventricular extrastimulus introduced during tachycardia coincident with His bundle refractoriness (Fig. 10.7). If the tachycardia terminates during this maneuver without affecting the atrial electrogram, participation of the accessory pathway in tachycardia is confirmed. If ORT is nonsustained or noninducible in a patient with a concealed accessory pathway, the presence of an accessory pathway may also be apparent by eccentric atrial activation during ventricular pacing. This technique works best for free-wall accessory pathways and pathways without decremental conduction. However, atrial activation over septal and slowly conducting pathways may not be distinguishable from activation over the AV node. If retrograde conduction occurs over both the pathway and the AV node, the resultant fusion may also make it difficult to compare activation times. Thus, concealed

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Figure 10.6 The effect of a right bundle branch block (RBBB) on the ventriculoatrial (VA) interval during orthodromic reciprocating tachycardia (ORT) in a patient with a concealed accessory pathway. The VA interval, as measured on the high right atrial (HRA) catheter during RBBB, is 35 ms longer, consistent with a right free-wall accessory pathway. Shown are ECG leads I, II, and V1. Also shown are bipolar electrograms as recorded by catheters at the HRA, the tricuspid annulus (MAPd and MAPp), and the right ventricular apex (RV). The vertical lines represent the onset of ventricular activation.

Figure 10.7 The response to a ventricular extrastimulus coincident with His bundle refractoriness during tachycardia. The subsequent atrial electrogram is advanced by 20 ms, confirming the presence of an accessory pathway. Hisd, Hism, and Hisp refer to bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA, high right atrium; RV, right ventricular apex; Stim, stimulus channel.

septal and slowly conducting accessory pathways are optimally mapped during ORT. The technique of para-Hisian pacing is particularly helpful in diagnosing the presence of a concealed septal accessory pathway [15]. A minimum of two catheters are needed to perform this maneuveraone at the His position and a second catheter in the right atrium. High-output pacing with the catheter at the His position captures both the His bundle and the local ventricular myocardium,

resulting in a relatively narrow QRS complex. As the output is decreased, only the local ventricular myocardium is captured, resulting in a wider QRS complex. One then compares the stimulus–atrial (SA) interval with and without His bundle capture. If the SA intervals are the same and there is no change in atrial activation, the presence of a septal accessory pathway is confirmed (Fig. 10.8). If the SA interval during His bundle capture is shorter and there is no change in the His bundle–atrial interval or 153

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Figure 10.8 The response to pacing from a catheter placed at the His position. Pacing is performed at low output yielding capture of the local ventricular (V) myocardium only, and then increased to where both the ventricle and His bundle (V+H) are captured. The stimulus–atrial interval is the same regardless. This response is consistent with conduction over an accessory pathway. HBE d, HBE m, and HBE p refer to bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA d and p, distal and proximal high right atrium; RVA, right ventricular apex.

Figure 10.9 The response to pacing from a catheter placed at the His position. Pacing is performed at high output yielding capture of the local ventricular myocardium and the His (V+H) and then decreased to where only the ventricle is captured (V). The stimulus–atrial interval is longer with capture of the ventricle in comparison with capture of both the ventricle and His. This represents a nodal response that is consistent with retrograde conduction through the atrioventricular node. BP, blood pressure; Hisd, Hism, and Hisp refer to bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA, high right atrium; RV, right ventricular apex; Stim, stimulus channel.

atrial activation, retrograde activation is occurring over the AV node (Fig. 10.9). This maneuver should be performed before and after radiofrequency current application to document the complete elimination of a septal accessory pathway. The operator must be cognizant of the limitations of para-Hisian pacing. First, one must rule out concomitant atrial capture, which will lead to an inaccurate assessment of retrograde atrial activation. Also, para-Hisian pacing may yield a nodal response even in the presence of a 154

septal accessory pathway if the retrograde conduction over the pathway is slower than that of the AV node. Para-Hisian pacing may be least reliable in patients with pathways traversing the left free wall and those with decremental conducting properties [15]. Lastly, one may also observe a “mixed” response that results from activation over both the accessory pathway and the AV node. This is verified by noting a change in atrial activation with loss of His bundle capture. Other techniques to differentiate retrograde conduction over the accessory pathway

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and the AV node include the administration of adenosine [16,17] and comparing the SA times when pacing from apical and basal ventricular sites [18].

Catheter ablation of accessory pathways

Arterial access is obtained with an 8-Fr sheath in one of the femoral arteries. A standard 7-Fr deflectable quadripolar ablation catheter with a 4-mm distal tip is most commonly used. Prior to positioning the catheter in the arterial system, a bolus of 3000 –5000 units of heparin is given, followed by

a continuous infusion of 1000 units/h in order to keep the activated clotting time above 250 s as long as a catheter is within the arterial system. The catheter is then advanced under fluoroscopic guidance into the left ventricular cavity using a 30–40° left anterior oblique projection, and the catheter tip is manipulated into the AV groove underneath the mitral valve leaflets. The catheter tip should target the poles of the coronary sinus catheter with the shortest VA conduction time in the case of a concealed pathway. An indicator of a satisfactory position of the ablation catheter at the mitral valve annulus is the presence of a clear atrial component in the local electrogram obtained from the distal poles of the ablation catheter. Radiologically, a satisfactory position is achieved when the catheter is within close proximity to the coronary sinus catheter and moves in synchrony with the coronary sinus. An advantage of the retrograde approach is that the ablation catheter can be wedged under the mitral valve in a stable position. With the transseptal approach, it may be more challenging to achieve a stable catheter position (Fig. 10.10). It has been shown that most left-sided accessory pathways have an oblique course, and that the ventricular insertion can be located up to 30 mm from the atrial insertion [19,20]. The earliest VA interval obtained with the coronary sinus catheter indicates the location of the atrial insertion. Given the oblique course of accessory pathways, juxtaposition of the retrogradely introduced mapping catheter to the site of the shortest VA interval may not identify a successful ablation site, since the atrial insertion may not be encompassed by a lesion created at the ventricular aspect of the annulus. The ventricular insertion is best identified by the presence of an accessory pathway potential preceding ventricular activation during manifest preexcitation, or by the presence of an accessory pathway potential during ventricular pacing for concealed pathways. If retrograde AV nodal conduction interferes with mapping a concealed pathway during ventricular pacing, administration of verapamil may be helpful in better exposing retrograde accessory pathway conduction. Figure 10.11 illustrates how an oblique accessory pathway may affect mapping of the atrial and ventricular insertion sites.

Table 10.1 Comparison of the retrograde and transseptal approaches.

Retrograde approach

Transseptal approach

Longer vascular recovery Vascular/coronary artery injury Difficult Good Lower than transseptal if ICE used

No arterial access necessary Perforation/air embolus Easy May be difficult to achieve Higher if used with ICE

Left free-wall accessory pathways After the diagnostic portion of the electrophysiologic study has been completed, the ablation catheter is positioned in close proximity to the accessory pathway. This is accomplished by paying attention to the shortest VA interval in patients with concealed accessory pathways, preferably during orthodromic reciprocating, or during ventricular pacing. In patients with manifest preexcitation, the earliest ventricular activation time at the mitral annulus is sought.

Transseptal versus retrograde approach The presence of a patent foramen ovale should be sought in all patients with left-sided pathways, since this will permit rapid and safe access into the left atrium. In its absence, the approach to map and ablate left-sided accessory pathways via a retrograde versus a transseptal approach depends on the preference and experience of the operating electrophysiologist. In experienced hands, both approaches have a success rate of > 96% and a relatively low risk. Contraindications to a retrograde approach include: the presence of either a prosthetic aortic valve or severe aortic valvular disease, and severe peripheral vascular disease. A relative contraindication to a transseptal procedure is distortion of the intracardiac anatomy secondary to dilatation of the aortic root, for example. Table 10.1 outlines advantages and disadvantages of the two approaches.

Retrograde approach

Arterial access Risk Maneuverability Stability Cost

ICE, intracardiac echocardiography.

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Figure 10.10 The electrogram morphology recorded by the mapping catheter (Abl d and Abl p) after a transseptal procedure at the atrial side of the mitral annulus. In addition to the recordings from the ablation catheter, the surface leads I, II, V1, and V5, and the intracardiac tracings from a coronary sinus catheter (CS d, CS m, CS p) are displayed. One should note the changing morphology of the electrograms (arrows) recorded by the distal electrode pair of the mapping catheter (Abl d) due to catheter instability.

If a transseptal approach is used, no heparin should be given before the puncture. Various sheaths are available for the transseptal puncture. Some are preshaped to facilitate manipulation of the catheter towards the annulus. A detailed description of transseptal catheterization is available elsewhere [21]. Once the transseptal catheter

has been advanced across the septum, the patient should be heparinized with 5000 units of heparin, followed by a continuous heparin infusion of 1000 units/h in order to achieve a target activated clotting time (ACT) of > 250 s. After flushing the sheath with heparinized solution, the ablation catheter is advanced into the left atrium and mapping is performed to identify the atrial insertion of the accessory pathway. Since the mapping catheter is on the

A

B

Figure 10.11 The oblique course of a left-sided accessory pathway that was mapped with a transseptal procedure. A. During sinus rhythm, there is manifest preexcitation. The ablation catheter (Abl d and Abl p) is positioned at a site at the lateral mitral annulus, where a small, sharp spike precedes the ventricular electrogram. The ventricular activation is simultaneous with the onset of the delta wave. The dotted line indicates the onset of the delta

wave. B. During ventricular pacing, there is no obvious accessory pathway potential present. The ventriculoatrial time is 200 ms. Radiofrequency energy delivery at this site temporarily abolished accessory pathway conduction; when radiofrequency energy application was terminated, accessory pathway conduction resumed in the anterograde and retrograde directions.

Transseptal approach

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C

D

E

F

Figure 10.11 (continued) C. This schema illustrates the mapping catheter being juxtaposed to the ventricular insertion site while being located on the atrial side of the mitral valve annulus. The red arrow indicates conduction over the accessory pathway (AP) in the anterograde direction during sinus rhythm. The corresponding electrograms are shown in red. There is an accessory pathway potential preceding the ventricular electrogram. The black arrow indicates retrograde conduction over the accessory pathway during ventricular pacing. The corresponding electrograms are displayed in black. There is no accessory pathway potential present. D. The mapping catheter (Abl) is positioned at the lateral mitral annulus, where the ventricular activation occurs 10 ms after the onset of the delta wave. E. During ventricular pacing at this site, a possible accessory pathway

potential (AP) precedes the ventricular electrogram. The VA time here was 175 ms, which was the shortest VA time detected during the mapping procedure. Radiofrequency energy application at this site eliminated conduction via the accessory pathway. F. This schema illustrates an oblique accessory pathway (AP), with the tip of the mapping catheter at the atrial insertion site of the accessory pathway. The red arrow indicates conduction over the accessory pathway in an anterograde direction. This corresponds to the electrograms also displayed in red. The black arrow indicates conduction over the accessory pathway in a retrograde direction during ventricular pacing. The corresponding electrogram in black shows an accessory pathway (AP) potential that is present only during ventricular pacing.

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atrial side of the mitral valve, mapping should focus on the atrial insertion site.

Posteroseptal accessory pathways The posteroseptal space has been compared to a trihedral pyramid with the base representing the fibrous trigone and epicardium, the right side representing the septal right atrium, and the left side representing the left atrium. The third side of the pyramid consists of the muscular ventricular septum. The pyramidal space contains adipose tissue and the anterior portion of the coronary sinus. Accessory pathways that are within 1–2 cm of the ostium of the coronary sinus are considered posteroseptal in location, and those beyond 1–2 cm are considered to be left freewall pathways. The latter pathways are best approached with a left-sided endocardial approach. Electrocardiographic clues favoring a posteroseptal location include positive delta waves in I and aVL, negative delta waves in leads II, III, aVF, and an R : S ratio > 1 in V2 [22]. Electrocardiographic clues that indicate the need for a left-sided procedure include an R : S ratio > 1 in lead V1, a 10 –30-ms increase in the VA time during ORT with a left bundle branch block [23], and a delta VA of > 25 ms during ORT or during ventricular pacing when the VA interval at the His position is subtracted from the VA interval of the earliest atrial activation in the coronary sinus (Fig. 10.12) [24]. However, these mapping criteria are not necessarily predictive of where the effective ablation site is located. Dhala et al. showed that most posteroseptal accessory pathways can be successfully ablated from the right side or from within the first 1 cm of the coronary sinus os, regardless of the above-mentioned electrophysiologic criteria [25]. A positive or biphasic delta wave in lead V2 has been particularly helpful in predicting an effective right-sided ablation site for a posteroseptal pathway [4,25]. A left ventricular or left atrial approach should be considered if several right-sided lesions are ineffective or create only transient accessory pathway block. Some posteroseptal pathways cannot be ablated either from the left or right side of the septum and may be located epicardially. Epicardial posteroseptal pathways may be associated with a diverticulum or may be located in the coronary sinus or middle cardiac vein [25]. An electrocardiographic clue for the presence of an epicardial accessory pathway in the posteroseptal area is a steeply negative delta wave in lead II (Fig. 10.4), a steeply positive delta wave in aVR and a deep S in V6 [26]. A coronary sinus venogram is useful, especially if no suitable ablation sites can be identified in the posteroseptal region outside the coronary sinus. Figure 10.13 shows a diverticulum in the middle cardiac vein in a patient with preexcitation. Successful ablation was achieved in the neck of the coronary 158

Figure 10.12 Tracings from a patient with a posteroseptal accessory pathway that required a left-sided approach for ablation of the accessory pathway. Pacing is performed from the right ventricular apex. Shown are leads V1, intracardiac tracings from the His catheter (HBE), the mapping catheter (LV), and recordings from the coronary sinus catheter (proximal CS, mid-CS, and distal CS). For calculation of the delta VA interval, the shortest VA interval within the coronary sinus (here 190 ms) is subtracted from the VA interval recorded by the His catheter. A delta VA of more than 25 ms argues for a left-sided approach in the setting of a posteroseptal bypass tract. The delta VA is 90 ms. Accordingly, the shortest VA interval (180 ms) was recorded by the mapping catheter (LV) at the ventricular side of the posteroseptal mitral annulus. Radiofrequency energy delivery at this site resulted in successful ablation of the accessory pathway.

Figure 10.13 A venogram of the coronary sinus, demonstrating a large diverticulum (arrows) originating from the middle cardiac vein.

sinus diverticulum where a large accessory pathway potential was present (Fig. 10.14). At the University of Michigan, among 255 posteroseptal accessory pathways, 67% were right-sided, 28% were left-

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sided, and 5% were ablated within the coronary sinus or the middle cardiac vein. The overall success rate was 96%.

Permanent junctional reciprocating tachycardia

Figure 10.14 Pacing is carried out from a catheter placed at the high right atrium (HRA) in the same patient as in Fig. 10.13. The surface leads I, II, III, V1, and aVF as well as the recordings from the HRA and the mapping catheter within the diverticulum are displayed. The mapping catheter is located at the neck of the coronary sinus (CS) diverticulum. At this site, atrial and ventricular electrograms are fused. The ventricular electrogram is preceded by an accessory pathway potential (APP). Radiofrequency energy was delivered at this site, resulting in permanent elimination of accessory pathway conduction.

Permanent junctional reciprocating tachycardia (PJRT) is the incessant form of orthodromic reciprocation, using a slowly conducting accessory pathway that is usually posteroseptal. The electrocardiographic hallmark is a long RP tachycardia with inverted P waves in the inferior leads (Fig. 10.15). Due to its incessant nature, this type of tachycardia can result in tachycardia-mediated cardiomyopathy that is reversible with ablation of the accessory pathway. The optimal target site is the location with the earliest atrial activation during orthodromic reciprocating tachycardia (Fig. 10.16).

Right-sided accessory pathways Mapping the ventricular insertion Once a manifest accessory pathway has been targeted for ablation, mapping of the ventricular insertion may be

Figure 10.15 Incessant long RP tachycardia with a rate of 545 ms. P waves in the inferior leads are inverted. The electrophysiology study demonstrated a posteroseptal accessory pathway with decremental conduction properties.

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Figure 10.16 The intracardiac electrograms during an electrophysiology study in the same patient as in Fig. 10.15. Mapping in the posteroseptal area (Abl d, Abl m, Abl p) showed the earliest VA interval just inferior to the coronary sinus ostium (405 ms). Radiofrequency energy delivery at this site permanently eliminated accessory pathway conduction. The dotted line indicates the beginning of the QRS, which was used as a reference for measuring the VA interval. CL, cycle length; HRA, high right atrium; RVA, right ventricular apex.

performed during sinus rhythm or atrial pacing. When there is fusion, atrial pacing is helpful in identifying the onset of the delta wave. For free-wall accessory pathways, the operator maps the tricuspid annulus typically with assistance of a long vascular sheath for catheter stability. Unlike the mitral valve annulus, the location of which is approximated by the coronary sinus catheter, there is no analogous landmark on the right side. One may insert a small-caliber electrode into the right coronary artery to delineate the tricuspid valve annulus [27], but this is rarely necessary and may increase procedure times and risks of the ablation procedure. An optimal tricuspid annulus position is characterized by sharp, near-field atrial and ventricular electrograms. Catheter stability may be difficult at anterolateral and anterior (10-o’clock to 12-o’clock positions) tricuspid annulus sites. This limitation can be overcome by gently advancing the catheter and sheath as a unit from the 6-o’clock position “upward” in the left anterior oblique projection. One may also opt for specially designed sheaths that provide additional stability at these sites [28]. Alternatively, the operator may choose to access the lateral and anterior annulus sites using a superior vena caval approach. The ventricular insertion of the accessory pathway is characterized by earliest ventricular activationai.e., the interval from the steepest portion of the ventricular electrogram on the ablation catheter to the onset of the delta wave on the electrocardiogram (Fig. 10.17).

160

Figure 10.17 The successful ablation site in a patient with a manifest right posterior accessory pathway. It should be noted that the ventricular activation (VaQRS) precedes the delta wave by 10 ms. Abl d and p, distal and proximal ablation channel; HRA, high right atrium; RV, right ventricular apex.

Mapping the atrial insertion Frequently, the presence of an accessory pathway is only apparent during orthodromic tachycardia or ventricular pacing because of lack of preexcitation on the ECG. Obviously, in these instances, the operator must map the atrial aspect of the tricuspid annulus. The atrial insertion of an accessory pathway is characterized by the shortest VA time during ORT or the shortest stimulus to atrial electrogram interval on the ablation channel during ventricular pacing. When mapping during ventricular pacing, the operator must consider the possibility of atrial activation through the AV node as well as the accessory pathway.

Radiofrequency current application It is preferable to perform radiofrequency ablation during sinus rhythm for manifest pathways. Ablation during tachycardia may be hindered by poor catheter and electrogram stability. In cases of concealed accessory pathways, one may carry out ablation during tachycardia or ventricular pacing, barring retrograde conduction over the AV node. Right ventricular pacing at close to the cycle length of the tachycardia may enhance catheter stability particularly when the tachycardia abruptly terminates (Fig. 10.18). Typical generator settings for radiofrequency catheter ablation of accessory pathways are 30–50 W and 60 –70 °C for 30–60 s. The temperature at the tissue–catheter interface during radiofrequency energy delivery should be at least 55 °C to minimize recurrence [29]. Temperatures greater than 70 °C should be avoided to prevent coagulum formation, resulting in thromboembolic events. The target

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Figure 10.18 The effect of radiofrequency current application during orthodromic reciprocating tachycardia, using a concealed right free-wall accessory pathway. The ablation catheter is placed at the anterolateral aspect of the tricuspid annulus. Ventricular pacing was used to improve stability. One should note the fusion of the atrial and ventricular electrograms on the distal ablation channel (Abld). Conduction block across the accessory pathway occurred shortly after initiation of radiofrequency current application (arrow). HRA, high right atrium; RV, right ventricular apex; Stim, stimulus channel.

temperature may not be achieved during radiofrequency ablation of right free-wall accessory pathways, in comparison with left-sided pathways using the retrograde aortic approach [29,30]. Tissue temperature must therefore be higher than that achieved at the catheter tip in order to eliminate conduction across these pathways. The relatively lower temperature achieved during ablation of right-sided accessory pathways in comparison with left-sided pathways in part explains the lower success and higher recurrence rates reported in the earlier literature [27,31,32]. Several electrogram features have been shown to be associated with successful ablation of manifest accessory pathways. These include electrogram stability, presence of a probable or possible accessory pathway potential (Fig. 10.19), and ventricular activation preceding the delta wave [33]. Another clue for a potentially successful ablation site is the sudden loss of preexcitation due to mechanical trauma of the catheter tip. For concealed accessory pathways, electrogram stability is observed more frequently at successful versus unsuccessful sites [33]. Fusion of ventricular and atrial electrograms (Fig. 10.18), resulting in continuous electrical activity, may also be helpful in identifying an effective target site for ablation of a concealed accessory pathway [33]. If the aforementioned mapping criteria are fulfilled and the target temperature is reached, the delta wave usually disappears within seconds (Fig. 10.20). If radiofrequency energy is delivered during ORT or ventricular pacing, successful ablation is heralded by prompt termination of tachycardia in the retrograde limb or VA block during

Figure 10.19 The presence of a possible accessory pathway potential (arrows) in a patient with a right posterior accessory pathway. Radiofrequency current application abolished preexcitation. Abl d, distal ablation channel; HRA, high right atrium.

pacing (Fig. 10.18). If elimination of accessory pathway conduction is observed, radiofrequency energy is delivered for a total of 60 s and an additional 60-s lesion may be delivered at the successful site to minimize the possibility of recurrent accessory pathway conduction. If no effect is seen within 10 –15 s, radiofrequency energy delivery should be terminated and the catheter should be moved to a different site. Before the procedure is deemed successful, it is important to document the lack of accessory pathway conduction in the anterograde and retrograde directions. After successful ablation of anterograde conduction, retrograde accessory pathway conduction may still be present. During mapping of the retrograde limb, one must bear in mind the oblique course of many accessory pathways [20].

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Figure 10.20 The effect of a radiofrequency energy application in a patient with a manifest right anterolateral accessory pathway. Very shortly after the initiation of energy delivery (arrow), accessory pathway automaticity is observed (asterisk), followed by the disappearance of the delta wave. Abl d, m, and p, distal, mid, and proximal ablation channel; HRA, high right atrium; RV, right ventricular apex.

For epicardial accessory pathways that are ablated in the coronary sinus, animal experiments have documented that radiofrequency energy delivery is safe [34]. This has been also demonstrated in humans. In a study of nine patients with an epicardial posteroseptal pathway and a prominent accessory pathway potential recorded within the coronary sinus, ablation within the coronary sinus was performed without complications other than transient coronary sinus spasm [35]. In this study, the power setting was 5 –30 W and radiofrequency energy was delivered for 5 –30 s; small branches of the coronary sinus were avoided. Within the coronary venous system the initial target temperature is set to 45 °C. This is gradually titrated up until accessory pathway conduction is blocked. The application is then continued for 30 s. When radiofrequency energy is delivered in the coronary sinus, we prefer a 7-Fr catheter within the body of the coronary sinus and a 6-Fr ablation catheter when radiofrequency energy is delivered within a branch. If there is a high impedance (> 130 Ω) during ablation, radiofrequency energy may be delivered with an irrigated or cooled-tip electrode, or a cryoablation catheter can be used. Some authors advocate performing coronary angiography and choosing the energy form based on the distance of the right coronary artery or one of its branches from the ablation site.

Troubleshooting during ablation of accessory pathways Occasionally, no suitable ablation site can be identified despite extensive endocardial mapping on the atrial and ventricular sides of the mitral annulus for left-sided pathways. It should be kept in mind that a left-sided accessory 162

Figure 10.21 A. An accessory pathway potential in the distal coronary sinus. Endocardial ablation failed in this patient and ablation within the coronary sinus was successful. It should be noted that despite the epicardial location, the delta wave in lead II is upright and not steeply negative, as one would expect with an epicardial accessory pathway. B. This tracing was recorded after successful ablation of the accessory pathway (AP) from within the coronary sinus. The accessory pathway potential has disappeared, and there is no more preexcitation. CS, coronary sinus; RF, radiofrequency application.

pathway may be epicardial, and mapping in the coronary sinus may reveal a large accessory pathway potential that can be targeted from within the coronary sinus (Figs. 10.21– 10.23). Common reasons for failure of ablation of right-sided pathways consist of inaccurate mapping and catheter instability. Use of an ablation catheter with an 8-mm or 10-mm tip may be helpful in difficult cases. Also, catheter

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Figure 10.22 A. Intracardiac recordings during orthodromic reciprocating tachycardia in a patient with a left free-wall accessory pathway that was ablated within the coronary sinus. The tachycardia cycle length is 280 ms. The earliest endocardial VA was recorded at the posteroseptal mitral annulus (LV PS = 110 ms). The VA interval at the coronary sinus ostium (CS os = 105 ms) was even earlier. B. Recordings from the proximal CS near the middle cardiac vein (MCV) with an earlier VA interval (100 ms). A sharp accessory pathway (AP) potential precedes the atrial electrogram (A). Radiofrequency (RF) energy delivery was successful at this site, as indicated on the right side of the tracing. The orthodromic reentry tachycardia terminates and sinus rhythm resumes. RA, right atrium.

Figure 10.23 The position of the ablation catheter (arrow) at the successful ablation site in same patient as in Fig. 10.22. There was no coronary sinus diverticulum present.

adherence during cryoablation may optimize catheter stability. Catheter ablation of an accessory pathway in a patient with Ebstein’s anomaly may be challenging. Although the leaflets of the tricuspid valve are displaced apically in this condition, the annulus retains its normal anatomical position. The enlarged right atrium, fractionated, low-amplitude annular electrograms, and the presence of multiple accessory pathways may make successful ablation difficult. The acute success rate in patients with Ebstein’s anomaly

is somewhat lower than in patients without structural heart disease, but approaches 80–85% [36,37]. However, the recurrence rate in these patients has been reported to be as high as 25% [36,37]. Rarely, a right-sided accessory pathway may connect the right atrial appendage to the right ventricle [38,39], may be truly epicardial, or may occur after cardiac surgery at a suture line [40]. The possibility of these rare accessory pathways should be considered if there are no annular sites where local ventricular activation precedes the onset of the delta wave or if there is no site along the tricuspid annulus at which the VA time during ORT is not shorter than at adjacent sites. If an accessory pathway is thought to be epicardial, a percutaneous, transpericardial catheter mapping and ablation procedure is an option [41]. Three-dimensional electroanatomical mapping may be useful in unusual circumstances such as changing retrograde atrial activation during ORT suggestive of multiple accessory pathways. Three-dimensional mapping may be particularly helpful in the case of non-AV pathways that insert at unusual locations, such as the right ventricular free wall (see below).

Anteroseptal and midseptal accessory pathways While much of the preceding discussion also relates to anteroseptal and midseptal accessory pathways, their 163

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unique location has an important implication for mapping and radiofrequency ablation. These accessory pathways may be defined based on both anatomic and electrophysiologic characteristics. An anteroseptal accessory pathway is characterized by a more anterior and superior location than the His bundle recording site in the left anterior oblique view. A catheter overlying the ventricular aspect of a midseptal pathway is inferior and posterior to the His bundle recording site but superior to the coronary sinus ostium. Electrophysiologically, an anteroseptal pathway may be differentiated from a midseptal pathway by the simultaneous inscription of a His and accessory pathway potential in the former [42]. Mapping of anteroseptal and midseptal accessory pathways is similar to mapping of pathways at other locations, with a few notable exceptions. For concealed pathways in these locations, one is not able to make use of ventricular pacing since retrograde activation over the AV node and the accessory pathway may be difficult to distinguish. Thus, concealed septal accessory pathways are optimally mapped during ORT. Furthermore, the proximity of anteroseptal and midseptal accessory pathways to the conduction system increases the risk of AV block. Pooling the results of several studies, the risk of high-degree AV block caused by ablation is 2% and 4% for anteroseptal and midseptal pathways, respectively [43]. A few techniques may help minimize the risk of AV block with ablation of anteroseptal and midseptal pathways. Most importantly, the operator should seek a site without a His potential on the ablation catheter or a site with the smallest His deflection. Whether to initiate radiofrequency application on the ventricular or atrial side of the tricuspid annulus is a matter of debate. Some investigators recommend the former, arguing that the specialized conduction tissue is deeper and less vulnerable to the effects of radiofrequency energy at the ventricular aspect [44,45]. Others have noted excellent results with ablation from the atrial aspect of the tricuspid annulus [46,47]. It is prudent to start the delivery of a radiofrequency energy application at low powerae.g., 10 –20 Waand a temperature of 50 °C. The operator then observes for accelerated junctional ectopy, PR prolongation, AV block, or widening of the QRS complex consistent with increasing preexcitation. All these warning signs mandate the immediate termination of the energy application. Although one monitors for VA block during junctional ectopy during slow pathway ablation for AVNRT, this strategy is not feasible for ablation of septal pathways. During junctional ectopy, 1 : 1 VA conduction may occur over the accessory pathway. After junctional ectopy abates, one may be left with AV block. If junctional ectopy cannot be avoided during ablation of a concealed septal pathway,

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atrial pacing should be performed at a cycle length shorter than that of the junctional rhythm while radiofrequency energy is delivered. If the QRS complex becomes more preexcited during ablation, the energy application should be immediately turned off. If no effect on the accessory pathway is seen after about 5–10 s, radiofrequency current should be turned off and another site should be sought. Given the increased risk of AV block with radiofrequency ablation of septal accessory pathways, other energy modalities have been evaluated. The operator may opt for the use of cryoenergy. Cryothermic lesions are achieved by delivery of a refrigerant solution to the target site. Typically, the catheter tip is first cooled to –30 °C while the operator observes the effect. The initial cooling results in adhesion of the catheter to the target site, thereby enhancing catheter stability. If the desired effect is observedai.e., abolition of accessory pathway functionathen the catheter tip is further cooled to –70 °C (cryoablation). If cryomapping results in AV block, the catheter is then rewarmed, allowing resumption of conduction. The main advantage of cryoablation is that the lesion is reversible, allowing the operator to gauge the safety and efficacy of ablation at a particular site. Another advantage of cryotherapy is that it is less likely to result in destruction of tissue architecture and thrombus formation [48]. Cryoablation has been shown to be safe and effective in patients with septal accessory pathways [49]. In one series, the procedure was acutely successful in all 20 patients and there was no instance of AV block. However, four patients required a repeat procedure because of recurrence accessory pathway conduction. In a more recent report, cryoablation was successful in eliminating accessory pathway function in 69% of cases [50]; however, the number of patients with septal accessory pathways was not reported. Although the success rate in this series was relatively modest in comparison with conventional radiofrequency ablation, it is noteworthy that the incidence of AV block was zero. Cryoablation should be considered as an alternative to radiofrequency ablation when the accessory pathway is in close proximity to the specialized conduction system.

Multiple accessory pathways In patients with manifest preexcitation, a delta wave pattern that is not typical of any single location, as well as different delta wave morphologies during atrial fibrillation, are clues suggesting the presence of multiple pathways. In patients with concealed pathways, a variable pattern of retrograde atrial activation is strong evidence of multiple accessory pathways (Fig. 10.24).

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Figure 10.24 Multiple right-sided accessory pathways participating in retrograde conduction during orthodromic reciprocating tachycardia. Shown are surface leads I, II, V1, and V5 and the intracardiac tracings of the mapping catheter (Abl d, Abl p), as well as the recordings from a catheter located at the high right atrium (HRA) and the lateral tricuspid annulus (lat TA). One should note the change in the activation sequence, as indicated by the red arrows. RVA, right ventricular apex.

Outcomes of accessory pathway ablation Of a total of 6065 patients undergoing an ablation procedure for an accessory pathway at several institutions between 1997 and 2002, the long-term success rate was 98%, and 2.2% of the patients required a repeat procedure [51]. Serious complications, including tamponade, AV block, injury to a coronary artery, retroperitoneal hemorrhage or stroke, occurred in 0.6% of patients, and death occurred in one patient (0.02%) [51]. The annual risk of sudden death in patients with the Wolff–Parkinson–White syndrome is estimated to be 0.05–0.5% [52]. This compares favorably with the outcome of radiofrequency ablation procedures. The fact that the procedural risk is significantly lower than the cumulative risk associated with the Wolff–Parkinson–White syndrome argues for catheter ablation as first-line therapy in such patients. Although the overall success rate of catheter ablation of accessory pathways is very high, the success rate of ablation of right free-wall and septal pathways may be somewhat lower as compared with left free-wall pathways [53]. The slightly lower success rate of ablation of right-sided pathways observed during the earlier experience seems to have been largely overcome by the use of long vascular sheaths that help improve catheter stability around the tricuspid annulus.

Complications of accessory pathway ablation For left-sided pathways, use of the retrograde aortic

approach has been associated with complication rates of 1.9–7.4%, and complications have included arterial injury, coronary artery occlusion, thromboembolic events, and valvular damage [32,44,54,55]. The complication rate with the transseptal approach has varied from zero to 6.1%, with the complications including air embolism and left atrial perforation [47,56]. Complications of catheter ablation of right-sided accessory pathways are less likely than with left-sided pathways. This is primarily due to the fact that the diagnostic and ablation procedures are restricted to the venous circulation. Collateral damage to the coronary arterial system during ablation of right-sided accessory pathways, not including posteroseptal pathways, is unusual but has been reported [57]. The risk of AV block during ablation of anteroseptal and midseptal pathways has been discussed previously. For patients undergoing catheter ablation of posteroseptal accessory pathways, the risk of AV block is low. Specifically, among 255 patients with posteroseptal accessory pathway who underwent an ablation procedure at the University of Michigan, the prevalence of AV block was < 1%. Other complications of posteroseptal accessory pathway ablation within the coronary sinus include pericarditis and cardiac tamponade [44].

Non-AV accessory pathways The vast majority of accessory pathways connect to the atrial and ventricular myocardium at the atrioventricular annulus. Accessory pathways that do not connect at the annulus have unusual properties that require a very different approach to mapping and ablation. Atriofascicular pathways connect the right atrium to the right bundle.

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Other non-AV pathways include nodoventricular and nodofascicular pathways.

Electrocardiographic and electrophysiologic properties of atriofascicular pathways The electrocardiogram of a patient with an atriofascicular accessory pathway typically shows little or no preexcitation (Fig. 10.25). The ECG during preexcited tachycardia shows a typical left bundle branch block pattern and a precordial transition which may be delayed to beyond lead V4 (Fig. 10.26). Electrophysiologically, atriofascicular pathways differ from typical AV pathways in many ways. First, atriofascicular pathways typically only conduct in the anterograde direction. Therefore, these pathways can only participate in antidromic tachycardia or as bystanders during AVNRT or atrial fibrillation. Second, these pathways demonstrate decremental conduction (Fig. 10.27). These pathways are also vulnerable to AV block with the administration of adenosine. Because of their decremental

properties and their response to adenosine, atriofascicular pathways have been likened to “accessory AV nodes.” Some AV pathways may also demonstrate these properties, making the distinction somewhat blurry. The timing of the right ventricular apical electrogram may be helpful in distinguishing an atriofascicular pathway from a slowly conducting, right free-wall AV pathway. The right ventricular apical electrogram is relatively early in the former and late in the latter, compared to the delta wave on the electrocardiogram. The most common arrhythmia observed in patients with an atriofascicular pathway is antidromic reciprocating tachycardia, in which the anterograde limb is the accessory pathway and the retrograde limb is the AV node. The right bundle is activated before the His bundle since activation of the specialized conduction system occurs in a retrograde manner. The presence of an atriofascicular pathway is demonstrated by insertion of an atrial premature depolarization during tachycardia, when the septum is refractory (Fig. 10.28). If the subsequent ventricular electrogram is advanced, this is proof of an extranodal pathway. If the advanced ventricular electrogram then

Figure 10.25 A 12-lead electrocardiogram in a patient with a history of a wide complex tachycardia, the mechanism of which was shown to be antidromic reciprocating tachycardia over an atriofascicular accessory pathway. The lack of preexcitation should be noted. The paper speed is 25 mm/s.

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Figure 10.26 An electrocardiogram showing antidromic reciprocating tachycardia over an atriofascicular accessory pathway. The typical left bundle branch block pattern and the QRS transition at V4 should be noted.

Figure 10.27 The response to atrial pacing at a cycle length of 350 ms in a patient with an atriofascicular pathway. One should note the gradual increase in the stimulus–delta (S–δ) interval and in the degree of preexcitation. With progressive preexcitation, the His potential (arrows) merges with the ventricular electrogram on the His bundle recording. AH, atrial–His interval; Hisd, Hism, and Hisp, bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA, high right atrium; HV, His–ventricular interval; RV, right ventricular apex; Stim, stimulus channel.

resets the tachycardia, participation of the accessory pathway in ART is assured.

Mapping and ablation of atriofascicular pathways Due to the unique aspects of atriofascicular pathways, one is unable to apply the mapping strategies used for typical AV pathways. Activation mapping during antidromic

tachycardia or atrial pacing is inefficient, since the diameter of the distal insertion site may be up to 2 cm [58]. Although radiofrequency ablation at this site may be successful, it typically results in a subtle change in the pattern of preexcitation or right bundle branch block. Since atriofascicular pathways do not conduct retrogradely, ventricular pacing is unhelpful as well. The atrial insertion may be targeted by seeking the shortest stimulus-to-delta wave interval around the tricuspid annulus [59,60]. Alternatively, the atrial insertion may be sought by identifying an annular 167

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Figure 10.28 The response to the insertion of an atrial extrastimulus during antidromic reciprocating tachycardia in a patient with an atriofascicular pathway. The extrastimulus is delivered at the time of refractoriness of the atrial septum and advances the subsequent ventricular electrogram by 30 ms. The morphology of the advanced QRS complex is exactly the same as that during tachycardia, consistent with conduction over the accessory pathway. The arrow corresponds to a retrograde His deflection. Hisd, Hism, and Hisp, bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA, high right atrium; RV, right ventricular apex; Stim, stimulus channel.

site which affords the longest-coupled atrial extrastimulus that advances the subsequent ventricular electrogram during antidromic tachycardia [60,61]. The major limitation of these methods is that each pacing site must be equidistant from the tricuspid annulus in order to obtain a meaningful comparison of the intervals. Although these pathways do not insert at the tricuspid annulus, the fact that they must traverse the annulus facilitates the mapping procedure. Mapping typically is performed during sinus rhythm. The target site is characterized by a sharp potential between the atrial and ventricular electrograms on the ablation catheter (Fig. 10.29). The fluoroscopic position and the timing of the pathway

potential serve to distinguish it from a His potential. These potentials may be found over a wide area around the annulus, extending from the 6-o’clock to 12-o’clock positions on the tricuspid annulus in the left anterior oblique projection. Most atriofascicular pathways are successfully ablated at the posterolateral, lateral, or anterolateral tricuspid annulus. In a given patient, the pathway potential may be found only at a very discrete location at the tricuspid annulus, making for a challenging mapping procedure. Ablation at sites displaying a pathway potential is almost always successful. Once the target site has been identified, radiofrequency current may be delivered during sinus rhythm, atrial pacing, or preexcited

Figure 10.29 The electrogram recorded by the ablation catheter (Abld and Ablp) at the successful site in a patient with antidromic reciprocating tachycardia due to an atriofascicular pathway. The ablation catheter was positioned at the posterolateral aspect of the tricuspid annulus. The sharp deflection on the ablation catheter, which represents the accessory pathway potential, should be noted. HRA, high right atrium; RV, right ventricular apex.

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Figure 10.30 A. An example of antidromic reciprocating tachycardia in a patient with an atriofascicular accessory pathway. B. The effect of radiofrequency current application in the same patient at the posterolateral tricuspid annulus, at a site where the electrogram in Fig. 10.28 was recorded. Delivery of radiofrequency energy resulted in accessory pathway automaticity, with the same QRS morphology as during preexcited tachycardia, and eliminated preexcitation, and rendered the tachycardia noninducible. Abld and Ablp, distal and proximal ablation channels; Hisd, Hism, and Hisp, bipolar electrograms recorded by the distal, mid, and proximal electrodes of a catheter placed at the His position; HRA, high right atrium; RV, right ventricular apex.

tachycardia. During application of radiofrequency energy, one may observe accessory pathway automaticity, analogous to junctional ectopy during ablation of the slow AV nodal pathway (Fig. 10.30) [62]. In fact, a recent report showed that atriofascicular pathways are capable of spontaneous automaticity as well [63]. Atriofascicular pathways also seem to be quite vulnerable to catheter trauma, a characteristic that allows for another method of mapping these pathways [59]. This property may be attributable to the superficial endocardial course of atriofascicular tracts. The acute success rate of ablation of atriofascicular accessory pathways is approximately 95%, and the recurrence rate is low.

Nodoventricular and nodofascicular pathways Nodoventricular and nodofascicular accessory pathways connect the AV node to the ventricular myocardium or the right bundle branch, respectively. During sinus rhythm, the QRS complex may be normal or preexcited. At electro-

physiology study, atrial pacing results in a shortening of the HV interval and more pronounced preexcitation. During maximal preexcitation, the QRS has a typical left bundle branch block pattern. Although nodoventricular/ nodofascicular accessory pathways are thought to conduct only anterogradely, concealed pathways have been reported [45,64]. Often, definitive proof of retrograde conduction over these pathways is lacking and an alternative hypothesis may explain the observations. Theoretically, the presence of a concealed nodofascicular (nodoventricular) pathway in tachycardia with VA dissociation may be proven by advancement of the His (ventricular) electrogram during insertion of a ventricular extrastimulus simultaneous with His bundle refractoriness. Coexistence of AVNRT and nodoventricular pathways has also been reported [65,66]. Table 10.2 highlights the electrophysiologic distinctions between atriofascicular and nodoventricular accessory pathways. Preexcited tachycardia utilizing nodoventricular and nodofascicular accessory pathways may be associated with VA block (Fig. 10.31). This observation rules out ART utilizing an AV pathway or an atriofascicular pathway. Because

Table 10.2 Distinctions between atriofascicular and nodoventricular accessory pathways. VA block during tachycardia Premature junctional complex APD on septal atrial electrogram Accessory pathway potential at TA

Atriofascicular

Nodoventricular

No Not preexcited Advances ventricular electrogram Yes

Yes Preexcited No effect No

APD, atrial premature depolarization; TA, tricuspid annulus; VA, ventriculoatrial.

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Figure 10.31 The induction of preexcited tachycardia using a nodoventricular accessory pathway with double atrial extrastimuli. The VA block during tachycardia should be noted. AH, atrial–His interval; AV, atrioventricular interval; HBE, His bundle catheter; HRA, high right atrium; HV, His–ventricular interval; RVA, right ventricular apex.

of the rarity of these pathways, guidelines regarding mapping and ablation are lacking. As such, catheter ablation of these pathways may be quite challenging. The proximal insertion of nodoventricular and nodofascicular pathways may be found near the fast or slow AV nodal pathways [65,66]. Alternatively, one might attempt to map the distal insertion of these pathways by identifying the site of earliest ventricular activation. Reports from the operating room have documented successful elimination of nodoventricular pathways at the free wall of the right ventricle [67]. Electroanatomical mapping may be helpful in mapping and ablation of these unusual accessory pathways (Fig. 10.32).

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Figure 10.32 An activation map of the right ventricle (right anterior oblique view) from a patient with a nodoventricular accessory pathway. The map was created using an electroanatomical mapping system (Carto; (Biosense Webster, Inc., Diamond Bar, California, USA) during maximal preexcitation. The earliest site was at the mid–anterior wall, where radiofrequency current application (red tag) resulted in elimination of preexcitation.

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in Wolff–Parkinson–White syndrome. Circulation 1993;88: II437– 46. Calkins H, Yong P, Miller JM, et al. Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. The Atakr Multicenter Investigators Group. Circulation 1999;99:262–70. Schluter M, Geiger M, Siebels J, et al. Catheter ablation using radiofrequency current to cure symptomatic patients with tachyarrhythmias related to an accessory atrioventricular pathway. Circulation 1991;84:1644 – 61. Calkins H, el-Atassi R, Kalbfleisch SJ, et al. Effect of operator experience on outcome of radiofrequency catheter ablation of accessory pathways. Am J Cardiol 1993;71:1104 –5. Lesh M, van Hare G, Scheinman M, et al. Comparison of the retrograde and transseptal methods for ablation of left free wall accessory pathways. J Am Coll Cardiol 1993;22:542–9. Khanal S, Ribeiro PA, Platt M, et al. Right coronary artery occlusion as a complication of accessory pathway ablation in a 12-year-old treated with stenting. Catheter Cardiovasc Interv 1999;46:59 – 61. Haïssaguerre M, Cauchemez B, Marcus F, et al. Characteristics of the ventricular insertion sites of accessory pathways with anterograde decremental conduction properties. Circulation 1995;91:1077–85. Cappato R, Schluter M, Weiss C, et al. Catheter-induced mechanical conduction block of right-sided accessory fibers with Mahaim-type preexcitation to guide radiofrequency ablation. Circulation 1994;90:282–90. Klein LS, Hackett FK, Zipes DP, et al. Radiofrequency catheter ablation of Mahaim fibers at the tricuspid annulus. Circulation 1993;87:738 – 47. Tchou P, Lehmann MH, Jazayeri M, et al. Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit. Circulation 1988;77:837– 48. Braun E, Siebels J, Volkmer M, et al. Radiofrequency-induced preexcited automatic rhythm during ablation of accessory pathways with Mahaim-type preexcitation: does it predict clinical outcome? Pacing Clin Electrophysiol 1997;20:1124. Sternick EB, Sosa EA, Timmermans C, et al. Automaticity in Mahaim fibers. J Cardiovasc Electrophysiol 2004;15:738 – 44. Hluchy J, Schlegelmilch P, Schickel S, et al. Radiofrequency ablation of a concealed nodoventricular Mahaim fiber guided by a discrete potential. J Cardiovasc Electrophysiol 1999;10: 603 –10. Kottkamp H, Hindricks G, Shenasa H, et al. Variants of preexcitationaspecialized atriofascicular pathways, nodofascicular pathways, and fasciculoventricular pathways: electrophysiologic findings and target sites for radiofrequency catheter ablation. J Cardiovasc Electrophysiol 1996;7:916 –30. Grogin HR, Lee RJ, Kwasman M, et al. Radiofrequency catheter ablation of atriofascicular and nodoventricular Mahaim tracts. Circulation 1994;90:272– 81. Klein GJ, Guiraudon GM, Kerr CR, et al. “Nodoventricular” accessory pathway: evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties. J Am Coll Cardiol 1988;11:1035 – 40.

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Diagnosis and ablation of typical and reverse typical (type 1) atrial flutter Gregory K. Feld, Ulrika Birgersdotter-Green, and Sanjiv Narayan

Introduction

Definition of atrial flutter terminology

Type 1 atrial flutter (AFL) is a common form of atrial arrhythmia, often occurring in association with atrial fibrillation, which may cause significant symptoms and serious adverse effects, including embolic stroke, myocardial ischemia, and infarction, and rarely tachycardia-induced cardiomyopathy due to rapid atrioventricular conduction. Type 1 AFL results from a combination of underlying electrophysiologic abnormalities, including slow conduction velocity in the cavotricuspid isthmus (CTI), plus anatomical and/or functional conduction block along the crista terminalis and Eustachian ridge. This electrophysiologic milieu produces a sufficiently long reentrant path length relative to the average tissue wavelength to allow for sustained reentry around the tricuspid valve annulus in either a clockwise or counterclockwise direction. The triggers of atrial flutter probably include premature atrial contractions or nonsustained atrial fibrillation, originating from the left atrium and pulmonary veins, which also probably accounts for the fact that type 1 AFL typically manifests clinically as counterclockwise reentry around the tricuspid valve annulus. As a result of its well-defined electrophysiologic and anatomical substrate and its relative resistance to pharmacological suppression, radiofrequency catheter ablation (RFCA) has emerged in the last decade as a safe and effective first-line treatment for type 1 AFL. Although several techniques have been described for ablating type 1 AFL, the most widely accepted and successful is an anatomically guided approach targeting the CTI. Recent technological developments, including three-dimensional eletroanatomical contact and noncontact mapping, and the use of largetip ablation electrode catheters with high-power generators, have produced a high degree of efficacy without increased risk. This chapter reviews the electrophysiology of human type 1 AFL and the techniques currently employed for diagnosing, mapping, and ablating it.

Due to the varied terminology used to describe atrial flutter in humansaincluding type 1 and type 2 AFL, typical and atypical atrial flutter, counterclockwise and clockwise atrial flutter, isthmus-dependent and nonisthmusdependent flutterathe Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology convened and published a consensus document in 2001 in an attempt to develop a generally accepted standardized terminology for atrial flutter [1]. The consensus was that the widely accepted terms “typical” and “type 1” atrial flutter were most commonly used to describe macroreentrant right atrial tachycardia, using the cavotricuspid isthmus (CTI) in either a counterclockwise or clockwise direction. The consensus terminology derived from this conference to describe CTI-dependent right atrial macroreentry tachycardia, in either the counterclockwise or clockwise direction around the tricuspid valve annulus, was therefore “typical” and “reverse typical” AFL, respectively [1]. In this chapter, counterclockwise or clockwise type 1 AFL will therefore be referred to specifically as “typical AFL” and “reverse typical AFL” when being described individually, or as “type 1 AFL” when being referred to in general. Other CTI-dependent atrial flutters with unique electrophysiologic characteristics have been described, including lower-loop reentry and partial isthmus-dependent flutter, and these will also be discussed in this chapter.

Electrophysiologic mechanisms of type 1 atrial flutter The development of successful RFCA techniques for human type 1 AFL was dependent in part on the delineation of the electrophysiologic mechanism involved. Through the use of advanced electrophysiologic techniques, including

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Figure 11.1 Schematic diagrams showing the activation patterns in the typical (A) and reverse typical (B) forms of human type 1 atrial flutter (AFL), as viewed from below the tricuspid valve (TV) annulus, looking up into the right atrium. In the typical form of AFL, the reentrant wavefront rotates counterclockwise in the right atrium, whereas in the reverse typical form, reentry is clockwise. It should be noted that the Eustachian ridge (ER) and crista terminalis (CT) form lines of block, and that an area of slow conduction is present in the isthmus between the inferior vena cava and Eustachian ridge and the tricuspid valve annulus. CS, coronary sinus ostium; His, bundle of His; IVC, inferior vena cava; SVC, superior vena cava; TV, tricuspid valve annulus.

intraoperative and transcatheter activation mapping [2–7], type 1 AFL was determined to be due to a macroreentrant circuit rotating in either a counterclockwise (typical) or clockwise (reverse typical) direction in the right atrium around the tricuspid valve annulus, with an area of relatively slow conduction velocity in the low posterior right atrium (Fig. 11.1). The predominant area of slow conduction in the AFL reentry circuit has been shown to be in the CTI, through which conduction times may reach 80– 100 ms, accounting for one-third to one-half of the AFL cycle length [8 –10]. The CTI is anatomically bounded by the inferior vena cava and Eustachian ridge posteriorly and the tricuspid valve annulus anteriorly (Fig. 11.1), both of which form lines of conduction block or barriers delineating a protected zone of slow conduction in the reentry circuit [11–14]. The presence of conduction block along the Eustachian ridge [11–14] has been confirmed by demonstrating double potentials along its length during AFL (Fig. 11.2A). Double potentials have also been recorded along the crista terminalis [11–14], suggesting that it too forms a line of block separating the smooth septal right atrium from the trabeculated right atrial free wall (Fig. 11.2B). Such lines of block, which may be either functional or anatomic, are necessary to create an adequate path length for reentry to be sustained, even in the presence of an area of slow conduction, and to prevent shortcircuiting of the reentrant wavefront [12–15]. The medial and lateral CTI, respectively, contiguous with the interatrial septum near the coronary sinus ostium and with the low lateral right atrium near the inferior vena cava (Fig. 11.1), correspond electrophysiologically to the exit 174

and entrance to the zone of slow conduction, depending on whether the direction of reentry is counterclockwise (CCW) or clockwise (CW) in the right atrium [2–15]. The path of the reentrant circuit outside the confines of the CTI (Fig. 11.1) consists of a broad activation wavefront in the interatrial septum and right atrial free wall around the crista terminalis and the tricuspid valve annulus [12–15]. The slower conduction velocity in the CTI, relative to the interatrial septum and right atrial free wall, may be caused by anisotropic fiber orientation in the CTI [7–10, 16,17]. This may also predispose to development of unidirectional block during rapid atrial pacing, and account for the observation that typical AFL with CCW reentry is more likely to be induced when pacing from the coronary sinus ostium, and conversely reverse typical AFL with CW reentry is more likely to be induced when pacing from the low lateral right atrium [18,19]. This hypothesis is further supported by direct mapping in animal studies, demonstrating that the direction of rotation of the reentrant wavefront during AFL is dependent on the direction of the paced wavefront producing unidirectional block at the time of its induction [20]. In humans, the typical variety of type 1 AFL predominates, perhaps because atrial ectopic beats or nonsustained atrial fibrillation that often initiate flutter commonly arise from the left atrium or pulmonary veins [21]. Left atrial triggers usually conduct to the right atrium via the coronary sinus or interatrial septum, thus entering the CTI from medial to lateral, favoring clockwise unidirectional block in the CTI with resultant initiation of counterclockwise or typical AFL. Increased dispersion of atrial refractoriness, which is common in the presence of structural heart disease, may increase the likelihood of developing regional conduction block. Shortening of atrial refractoriness as a result of atrial electrical remodeling from rapid rates shortens tissue wavelength, facilitating sustained reentry [22,23]. In the absence of anatomical or functional block across the crista terminalis or Eustachian ridge, conduction through gaps in these structures may lead to the development of lower loop reentry or partial isthmus flutter, respectively [24,25]. Lower loop reentry is a variant CTIdependent flutter in which the caudal-to-cranial limb of the reentrant wavefront crosses through a gap in the crista terminalis in either the clockwise or counterclockwise direction (Fig. 11.3A). The caudal-to-cranial limb of the reentrant wavefront may then collide with a secondary cranial-to-caudal wavefront in the interatrial septum and right atrial free wall. Partial isthmus flutter is another variant CTI-dependent flutter in which the counterclockwise reentrant wavefront circulates between the medial boundary of the Eustachian ridge and the coronary sinus, and then in a clockwise direction around the coronary sinus into the medial CTI, where it collides with the counterclockwise wavefront entering the lateral CTI (Fig. 11.3B).

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Figure 11.2 A. Surface electrocardiography leads I, aVF, and V1, and endocardial electrograms in a patient with typical atrial flutter (AFL), demonstrating double potentials (XY) recorded along the Eustachian ridge by the ablation catheter (RFd). It should be noted that the X and Y potentials straddle the onset of the initial downstroke of the F wave in lead aVF (vertical line), indicating that the X potential is recorded immediately after the activation wavefront exits the subeustachian isthmus and circulates around the coronary sinus above the Eustachian ridge, while the Y potential is recorded after the activation wavefront rotates entirely around the atrium and is proceeding through the subeustachian isthmus below the Eustachian ridge. Double potentials may similarly be recorded along the crista

Diagnosis of type 1 atrial flutter Electrocardiography Surface 12-lead electrocardiography (ECG) is helpful in establishing a diagnosis of type 1 AFL, particularly the typical form. In typical AFL, an inverted saw-tooth F wave pattern is observed in the inferior ECG leads II, III, and aVF, with low-amplitude biphasic F waves in leads I and aVL, an upright F wave in precordial lead V1, and an inverted F wave in lead V6 (Fig. 11.4A). In contrast, in reverse typical AFL, the F wave pattern on the 12-lead ECG is less specific and variable, often with a sine wave pattern in the inferior ECG leads (Fig. 11.4B). The determinants of F wave pattern on ECG are largely dependent on the activation pattern of the left atrium resulting from reentry in the right atrium, with inverted F waves inscribed in the inferior ECG leads in typical AFL as a result of initial activation of the left atrium posteriorly, near the coronary sinus, and upright F waves inscribed in the inferior ECG leads in reverse typical AFL as a result

terminalis. CSp, m, d, electrograms from the proximal, middle and distal electrode pairs on a quadripolar catheter in the coronary sinus with the proximal pair at the ostium; His, electrogram from the bundle of His catheter; RFp, d, electrograms from the proximal and distal electrode pairs of the mapping/ablation catheter, with the distal pair positioned on the Eustachian ridge. B. A schematic diagram of the right atrium indicates where such double potentials (X,Y) may be recorded along the Eustachian ridge and crista terminalis during typical AFL. CS, coronary sinus ostium; CT, crista terminalis; ER, Eustachian ridge; His, bundle of His; IVC, inferior vena cava; SVC, superior vena cava; TV, tricuspid valve annulus.

of initial activation of the left atrium anterior near Bachmann’s bundle [26,27]. However, since typical and reverse typical AFL use the same reentry circuit, but in opposite directions, their rates are often similar in the same patient. The 12-lead ECG pattern in lower loop reentry may resemble typical and reverse typical AFL, but it may also present with subtle differences in the F wave pattern in the inferior leads and V1, depending on the level of breakthrough across the crista terminalis, or varying F waves if there are multiple breakthrough points [24,25]. Partial isthmus-dependent flutter may also resemble typical AFL, but again subtle variations in the F wave pattern may occur, particularly in the inferior ECG leads [24,25]. Algorithms using signal-processing software to assess the stability of the F wave on surface ECG, recently developed in our laboratory, may allow the clinician to determine whether the CTI is a critical zone in the reentry circuit of any AFL observed on ECG, regardless of the F wave pattern [28]. Data from these studies suggest that CTI-dependent AFLaboth the typical and reverse typical formsahas a significantly more stable cycle length and 175

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Figure 11.3 A. Surface electrocardiography (V1) and intracardiac electrogram recordings (top) from a patient with lower loop reentry atrial flutter (AFL), and a schematic of the mechanism (bottom). The collision of wavefronts in the right atrial free wall and the interatrial septum, as a result of the dominant wavefront around the coronary sinus and inferior vena cava and through the cavotricuspid isthmus (CTI), should be noted. Ablation of the CTI will nonetheless cure this uncommon form of isthmus-dependent AFL. CS, coronary sinus; HBE, bundle of His electrogram; IVC, inferior vena cava; SVC, superior vena cava; TA, tricuspid annulus. B. Surface electrocardiography (V1) and electrogram recordings from a patient with partial isthmus AFL (top), and a schematic (bottom). The counterclockwise activation sequence around the tricuspid valve annulus should be noted.

However, in this uncommon form of CTI-dependent AFL, there is a breakthrough of the activation wavefront between the coronary sinus ostium and Eustachian ridge, with circulation of the wavefront around the coronary sinus, resulting in collision of activation wavefronts in the anterior isthmus near the tricuspid valve. Ablation of AFL between the coronary sinus ostium and Eustachian ridge may convert and slow the AFL to a typical AFL requiring complete CTI ablation. (Adapted from [24,25].) The tricuspid annulus (TA) recordings are from a halo catheter positioned as in Fig. 11.6 (see below) with electrode 1 at the inferior portion of the annulus and electrode 10 at the cranial portion of the annulus. CS, coronary sinus; HBE, bundle of His electrogram; IVC, inferior vena cava; SVC, superior vena cava; TA, tricuspid annulus.

activation pattern than atypical forms of AFL (Fig. 11.5). A potential explanation for this observation is that in comparison with atypical AFL, CTI-dependent AFL has a more stable macroreentrant activation pattern, probably due to its anatomically restricted boundaries. This is important mechanistically, and may have clinical implications in planning approaches to mapping and ablation.

in order to confirm the underlying mechanism if RFCA is to be carried out successfully. This is particularly true in the case of reverse typical AFL, which is more difficult to diagnose on 12-lead ECG. For the electrophysiologic study of AFL, activation mapping may be performed using standard multielectrode catheters or a three-dimensional computerized activation mapping system. For standard multielectrode catheter mapping, catheters are typically positioned in the right atrium, bundle of His region, and coronary sinus. To elucidate the endocardial activation sequence more precisely, a Halo 20-electrode mapping catheter (Biosense Webster, Inc., Diamond Bar, California, USA) is commonly positioned in the right atrium around

Electrophysiology and mapping Despite the value of the 12-lead ECG for reaching a presumptive diagnosis of typical AFL, an electrophysiologic study with mapping and entrainment has to be conducted 176

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Figure 11.4 A. Twelve-lead electrocardiogram recorded from a patient with typical atrial flutter (AFL). The typical saw-toothed pattern of inverted F waves in the inferior leads II, III, and aVF should be noted. Typical AFL is also characterized by flat to biphasic F waves in I and aVL, respectively, an upright F wave in V1, and an inverted F wave in V6. B. Twelve-lead

electrocardiogram from a patient with the reverse typical AFL. The F wave in the reverse typical form of AFL has a less distinct sine wave pattern in the inferior leads. In this case, the F waves are upright in the inferior leads II, III, and aVF, biphasic in leads I, aVL, and V1, and upright in V6.

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Figure 11.5 Surface electrocardiography leads aVF, V1, and V5 are shown in the upper panel in this figure, in a patient during transition from type 1 atrial flutter (AFL; left panel, segment 1) to atypical AFL (right panel, segment 2). A template of the F wave is recorded for a single representative atrial cycle and then compared with subsequent cycles for consistency using a computerized algorithm. In the lower panel, an X–Y correlation plot (between leads V5 and aVF) and fast Fourier transform (FFT) of the correlation plot are shown for segments 1 and 2. Atrial temporospatial loops are created, plotting correlation (“r”) values at each time point between the axes to produce the XY atrial and ventricular loops. During

isthmus-dependent atrial flutter (segment 1), the atrial loops are reproducible, approaching the (1,1) coordinate (i.e., they are spatially coherent). During atypical or nonisthmus-dependent atrial flutter (segment 2), the atrial loops are irreproducible and do not approach the (1,1) coordinate (i.e., they are spatially incoherent). The FFT analysis demonstrates a highly repeatable pattern and single dominant frequency for type 1 AFL in comparison with atypical AFL. These findings suggest a very consistent pattern of atrial activation in type 1 AFL, in contrast to that observed in atypical AFL.

Figure 11.6 Left anterior oblique A. and right anterior oblique B. fluoroscopic projections, showing the intracardiac positions of the right ventricular (RV), bundle of His (HIS), coronary sinus (CS), Halo and mapping/ablation catheters (RF). It should be noted that the Halo catheter is positioned around the tricuspid valve annulus, with the proximal electrode

pair at the 1-o’clock position and the distal electrode pair at the 7-o’clock position. The mapping/ablation catheter is positioned in the subeustachian isthmus, midway between the interatrial septum and the low lateral right atrium, with the distal 8-mm ablation electrode near the tricuspid valve annulus.

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the tricuspid valve annulus (Fig. 11.6). Multielectrode recordings obtained during AFL from these catheters are then analyzed to determine the right atrial activation sequence. In patients presenting to the electrophysiology laboratory in sinus rhythm, it is necessary to induce AFL in order to confirm its mechanism. Induction of AFL is accomplished by programmed stimulation from the coronary sinus ostium or low lateral right atrium, with burst pacing at cycle lengths between 180 and 240 ms typically being effective in inducing unidirectional CTI block and AFL. Induction of atrial flutter may occur immediately following the onset of unidirectional CTI isthmus block,

or following a brief period of atrial fibrillation, and the direction of reentry (counterclockwise or clockwise, respectively) may be in part dependent on the pacing site [18,19]. During electrophysiologic study, a diagnosis of either typical or reverse typical AFL is suggested by observing a counterclockwise or clockwise activation sequence in the right atrium, respectively, around the tricuspid valve annulus. For example, as seen in Fig. 11.7A in a patient with typical AFL, the atrial electrogram recorded at the coronary sinus ostium is timed with the initial downstroke of the F wave in the inferior surface ECG leads, followed by caudal-to-cranial activation in the interatrial

Figure 11.7 Endocardial electrograms from the mapping/ablation, Halo, coronary sinus (CS), and His bundle catheters, and surface electrocardiography leads I, aVF, and V1, demonstrating counterclockwise rotation of activation in the right atrium in a patient with typical atrial flutter (AFL) (A) and clockwise rotation of activation in the right atrium in a patient with reverse typical AFL (B). The atrial cycle length was 256 ms for both the typical and reverse typical AFLs. Arrows demonstrate activation sequence. Halo D–P, 10 bipolar electrograms recorded from the distal (low lateral right atrium) to proximal (high right atrium) poles of the 20-pole Halo catheter positioned around the tricuspid valve annulus with the proximal electrode pair at the 1o’clock position and the distal electrode pair at the 7-o’clock position; CSD/CSP, electrograms recorded from the coronary sinus catheter distal/proximal electrode pair positioned at the ostium; HISD/HISP, electrograms recorded from the distal/proximal electrode pair of the His bundle catheter; RF, electrograms recorded from the mapping/ablation catheter positioned with the distal electrode pair in the CTI.

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septum to the His bundle atrial electrogram, and then cranial-to-caudal activation in the right atrial free wall from proximal to distal on the Halo catheter, and finally to the ablation catheter in the CTIaindicating that the underlying mechanism is a counterclockwise macroreentry circuit with electrical activity encompassing the entire tachycardia cycle length. In a patient with reverse typical AFL, the opposite activation sequence is seen (Fig. 11.7B). In addition, confirmation that the reentry circuit uses the CTI requires demonstration of the classical criteria for entrainmentaspecifically, concealed entrainment during pacing from the CTI [5]. Criteria for demonstrating concealed entrainment of AFL include acceleration of the tachycardia to the pacing cycle length without a change in the F wave pattern on surface ECG or in the endocardial atrial activation sequence and electrogram morphology (Fig. 11.8), and the immediate resumption of the tachycardia at the original cycle length upon termination of pacing, including the first post-pacing interval (Fig. 11.8). Concealed entrainment is further confirmed by pacing within the CTI if the stimulus-to-F wave or stimulus-to-reference electrogram interval during pacing and the pacing electrode electrogram-to-F wave or electrogram-to-reference electrogram interval during AFL are equal (Fig. 11.8). In addition, during typical AFL, the stimulus-to-F wave or stimulus-to-proximal coronary sinus electrogram will be shorter when the pacing site is medial, near the exit from the CTI (e.g., 30 –50 ms), and longer when the pacing site is lateral, near the entrance to the CTI (e.g., 80–100 ms), and the converse during reverse typical AFL. In contrast, pacing at sites outside the CTI results in overt entrainment of AFL, with variable degrees of constant fusion of the F wave pattern and endocardial atrial electrograms. Although the activation pattern of lower loop reentry differs from that of typical and reverse typical AFL on standard multielectrode catheter, with collision of wavefronts in the lateral right atrium and septum, its CTI dependence can nonetheless be confirmed by demonstrating concealed entrainment during pacing from the CTI. Concealed entrainment may also be demonstrated in lower loop reentry during pacing from the low lateral right atrium [24,25]. Partial isthmus flutter is confirmed by demonstrating concealed entrainment from the lateral but not the medial CTI, and there will be early coronary sinus activation and evidence of wavefront collision within the CTI [24,25].

Catheter ablation of type 1 atrial flutter Methods for RFCA RFCA of typical and reverse typical AFL is most commonly performed with a steerable mapping/ablation cath180

eter with a distal ablation electrode ranging in length from 4 to 5 mm [2–4,6,29–32]. Successful ablation of the CTI requires a stable temperature of at least 50 – 60 °C, and occasionally 70 °C, while temperatures in excess of 70 °C may cause tissue vaporization (i.e., steam pops) or charring, or formation of blood coagulum on the ablation electrode (resulting in a rise in impedance that limits energy delivery and lesion formation), which may lead to complications such as cardiac perforation or embolization. A larger-curve catheter (e.g., with a mid-distal large curve from Boston Scientific, Natick MA, USA), with or without a preshaped guiding sheath (e.g., SR0, SL1 or ramp sheath from Daig, Inc./St. Jude Medical, St. Paul, Minnesota, USA), may be required for the ablation electrode to reach the tricuspid valve annulus, especially in patients with enlarged right atria. Recently, radiofrequency ablation catheters with either saline-cooled ablation electrodes or large distal ablation electrodes (i.e., 8–10 mm) have been more widely used for the ablation of type 1 atrial flutter (Boston Scientific, Natick MA, USA: Biosense Webster, Diamond Bar, CA, USA; Medtronic, Inc., Minneapolis, Minnesota, USA). During ablation with saline-cooled catheters, use of lower powers and temperature settings is recommended to avoid steam pops [33–36]. Initially, a maximum power of 35–40 W and temperature of 43–45 °C should be used with saline-cooled catheters, although studies have reported use of up to 50 W and 60 °C for ablation of AFL without higher than expected complication rates [33 –36]. In contrast, large-tip (8–10 mm) ablation catheters require a higher power, up to 70–100 W, to achieve the tissue temperatures of 50–70 °C necessary to ablate the CTI isthmus successfully, which has not been associated with an increased risk of complications [36–41]. The preferred target for type 1 AFL ablation is the CTI, which when using standard multipolar electrode catheters for mapping and ablation is localized with a combined fluoroscopically and electrophysiologically guided approach [2–4,6,29–41]. Typically, a steerable mapping/ ablation catheter is positioned initially fluoroscopically (Fig. 11.6) in the CTI, with the distal ablation electrode on or near the tricuspid valve (TV) annulus in the right anterior oblique (RAO) view, and midway between the septum and low right atrial free wall (in the 6-o’clock or 7-o’clock position) in the left anterior oblique (LAO) view. The distal ablation electrode position is then adjusted toward or away from the TV annulus based on the ratio of atrial and ventricular electrogram amplitude recorded by the bipolar ablation electrode. An optimal atrioventricular (AV) ratio is typically 1 : 2 or 1 : 4 at the tricuspid valve annulus, as seen in Fig. 11.7A on the ablation electrode. After the ablation catheter has been positioned on or near the tricuspid valve annulus, it is then gradually withdrawn during ablation toward the inferior vena cava while continuously applying radiofrequency energy, or it

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Figure 11.8 Surface electrocardiogram (ECG) leads I, aVF, and V1 and endocardial electrogram recordings during pacing entrainment from the cavotricuspid isthmus (CTI) in typical atrial flutter (AFL) (A) and reverse typical AFL (B). In both examples, it should be noted that the tachycardia is accelerated to the pacing cycle length and that F wave morphology on surface ECG and endocardial waveforms and activation pattern are unchanged during pacing compared to AFL, indicating concealed entrainment. Furthermore, the stimulus-to-F wave or local electrogram

(CSP) intervals are comparable with the electrogram-to-F wave or local electrogram (CSP) intervals recorded on the mapping/ablation catheter (RFAP) during entrainment and AFL in both examples, indicating concealed entrainment. In A, the post-pacing interval measured at the pacing site is indicated (284 ms) and equals the tachycardia cycle length, consistent with pacing at a site in the circuit. S1, pacing stimulus artifact. All other abbreviations are the same as in previous figures.

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convert the tachycardia to a typical AFL, which will then require complete CTI ablation for cure [24,25].

Procedure end points for RFCA of type 1 atrial flutter

Figure 11.9 Schematic diagram of the right atrium, showing the typical locations for linear ablation of the cavotricuspid isthmus (CTI; line 1), or the tricuspid valve–coronary sinus (line 2) and coronary sinus–inferior vena cava (line 3) isthmuses. CS, coronary sinus ostium; CT, crista terminalis; ER, Eustachian ridge; His, bundle of His; IVC, inferior vena cava; SVC, superior vena cava; TV, tricuspid valve annulus.

can be withdrawn in a stepwise manner a few millimeters at a time (usually the length of the distal ablation electrode) pausing for 30 – 60 s at each location during continuous or interrupted energy application. Electrogram recordings can be used in addition to fluoroscopy to ensure that the ablation electrode is in contact with viable tissue in the CTI throughout each energy application. Ablation of the entire CTI (Fig. 11.9) may require several sequential 30 – 60-s energy applications during a stepwise catheter pullback, or a prolonged energy application of up to 120 s or more during a continuous catheter pull-back. The catheter should be gradually withdrawn until the distal ablation electrode records no atrial electrogram, indicating that it has reached the inferior vena cava, or until the ablation electrode is noted to abruptly slip off the Eustachian ridge fluoroscopically. Radiofrequency energy application should be immediately interrupted when the catheter has reached the inferior vena cava, since ablation in the venous structures may cause significant pain. Alternatively, ablation of the tricuspid valve–coronary sinus and coronary sinus–inferior vena cava isthmuses (Fig. 11.9) can be carried out using an approach similar to that used to ablate the CTI [42]. However, for this approach to be successful, it is often necessary to ablate within the coronary sinus ostium as well, which may be associated with a higher risk of complications, including AV node block. It has also been reported that type 1 AFL may be cured by ablating medially between the tricuspid valve annulus and Eustachian ridge only, which is a potentially narrower isthmus than the CTI [43]. Ablation and cure of lower loop reentry will be accomplished by CTI isthmus ablation, since this arrhythmia is dependent on CTI conduction [24,25]. Partial isthmus flutter in contrast may require ablation of the gap between the Eustachian ridge and coronary sinus, or ablation from the coronary sinus to the inferior vena cava. This may then 182

Ablation can be carried out during sustained AFL or during sinus rhythm. If it is carried out during AFL, the first end point is its termination during energy application (Fig. 11.10). However, even if AFL terminates during ablation, it is not uncommon to find that CTI conduction persists. CTI ablation should be completed, achieving conduction block (see below), before electrophysiologic testing is performed. After CTI ablation is complete, as determined by fluoroscopic and electrophysiologic criteria, observation with programmed stimulation should be continued for at least 30 min to ensure that bidirectional CTI block is persistent and that AFL cannot be reinduced [2–4,6,29–41]. If AFL is not terminated during initial attempts to ablate the CTI, the activation sequence and isthmus dependence of AFL should be reconfirmed and ablation repeated. During repeat ablation, it may be necessary to rotate the ablation catheter away from the initial line of energy application, either medially or laterally in the CTI, in order to create a new line of block, or to use a slightly higher power and/or ablation temperature. In addition, if ablation is initially attempted using a standard 4–5-mm tip electrode and fails, repeat ablation with a larger-tip 8–10-mm electrode catheter or cooled-tip ablation catheter may be successful [33–41]. If AFL is terminated during ablation, pacing should be performed at a cycle length of 600 ms or greater, depending on the sinus cycle length, to determine whether there is a bidirectional conduction block in the CTI (Figs. 11.11–11.14). If ablation is done during sinus rhythm, pacing can be also done during energy application to monitor for development of conduction block in the CTI (Fig. 11.15). The use of this end point for ablation may be associated with a significantly lower recurrence rate of type 1 AFL during the long-term follow-up [44 – 47]. Conduction in the CTI is evaluated by comparing activation sequences in the right atrium around the tricuspid valve annulus, while pacing during sinus rhythm at slow rates (i.e., cycle lengths ≥ 600 ms) from the low lateral right atrium and coronary sinus ostium, before and after ablation. It is important to pace at relatively slow rates during assessment for CTI block, because conduction block across the CTI may be functional and rate-dependent in some patients following ablation. Conduction block across the crista terminalis may also be functional in some patients, and at slow pacing rates conduction across the mid-crista region can result in uncertainty regarding the presence or absence of bidirectional CTI block following ablation [48–50]. Thus, it may be necessary to pace not

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Figure 11.10 Termination of typical atrial flutter (AFL) during radiofrequency energy application using a slow drag technique across the cavotricuspid isthmus (CTI). AFL will usually terminate just as the distal ablation electrode on the mapping/ablation catheter (RFAP) approaches the inferior vena cava. Conduction fails at the CTI, as indicated by block

Figure 11.11 The expected right atrial activation sequence during pacing in sinus rhythm from the coronary sinus ostium, before (A) and after (B) ablation of the cavotricuspid isthmus (CTI). Before ablation, the activation pattern during coronary sinus pacing is caudal-to-cranial in the interatrial septum and low right atrium, with collision of the septal and right atrial wavefronts in the mid-lateral right atrium. After ablation, the activation pattern during coronary sinus pacing is still caudal-to-cranial in the interatrial septum, but the lateral right atrium is now activated in a strictly cranial-to-caudal pattern (i.e., counterclockwise), indicating complete clockwise conduction block in the CTI. CS, coronary sinus ostium; CT, crista terminalis; ER, Eustachian ridge; His, bundle of His; IVC, inferior vena cava; SVC, superior vena cava.

only from the proximal coronary sinus, but also adjacent to the ablation line in the CTI, or in the posterior–inferior right atrial septum, in order to confirm the presence of CTI isthmus block [50]. Bidirectional conduction block in

developing between the low lateral right atrium and coronary sinus in the typical form, and between the coronary sinus and the low lateral right atrium in the reverse typical form (not shown). The power read-out from the radiofrequency energy generator is shown in the bottom three traces. All other abbreviations are the same as in previous figures.

the CTI is confirmed by demonstrating a change from a bidirectional wavefront with collision in the right atrial free wall or interatrial septum before ablation (Figs. 11.11–11.14), to a strictly cranial-to-caudal activation sequence following ablation (Figs. 11.11–11.14) during pacing from the coronary sinus ostium or low lateral right atrium, respectively [44–47]. The presence of bidirectional conduction block in the CTI is also strongly supported by recording widely spaced double potentials (> 90 –110 ms) along the entire ablation line (Fig. 11.15), during pacing from the low lateral right atrium or coronary sinus ostium [51,52]. In order to expedite the assessment of bidirectional conduction block following CTI ablation and to obviate the need for multipolar electrode catheter recordings, several algorithms based on trans-isthmus conduction times, changes in P wave polarity, reversal of electrogram polarity at the ablation line, and use of unipolar electrograms have been employed with varying degrees of accuracy [53–56]. However, in the majority of electrophysiology laboratories, these methods are not relied on solely to confirm the presence or absence of bidirectional CTI conduction block, and they are unlikely to replace the gold standard of multielectrode recordings or three-dimensional activation mapping [2–4,6,29–41]. 183

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Figure 11.12 Surface electrocardiogram (ECG) leads I, aVF, and V1 and endocardial electrograms during pacing in sinus rhythm from the coronary sinus ostium, before (A) and after (B) ablation of the cavotricuspid isthmus (CTI). Tracings include surface ECG leads I, aVF, and V1, and endocardial electrograms from the proximal coronary sinus (CSP), bundle of His (HIS), tricuspid valve annulus at the 1-o’clock position (HaloP) to 7-o’clock position

(HaloD), and high right atrium (HRA or RFA). Before ablation during coronary sinus pacing, there is collision of the cranial and caudal right atrial wavefronts in the mid-lateral right atrium (HALO5). After ablation, the lateral right atrium is activated in a strictly cranial-to-caudal pattern (i.e., counterclockwise), indicating complete medial to lateral conduction block in the CTI. All other abbreviations are the same as in previous figures.

Outcomes and complications of RFCA of type 1 atrial flutter

Figure 11.13 The expected right atrial activation sequence during pacing in sinus rhythm from the low lateral right atrium, before (A) and after (B) ablation of the cavotricuspid isthmus (CTI). Before ablation, the activation pattern during coronary sinus pacing is caudal-to-cranial in the right atrial free wall, with collision of the cranial and caudal wavefronts (i.e., through the CTI) in the mid-septum, with simultaneous activation at the His bundle and proximal coronary sinus. After ablation, the activation pattern during low lateral right atrial sinus pacing is still caudal-to-cranial in the right atrial free wall, but the septum is now activated in a strictly cranial-to-caudal pattern (i.e., clockwise), indicating complete lateral-to-medial conduction block in the cavo-tricuspid isthmus (CTI). CS, coronary sinus ostium; CT, crista terminalis; ER, Eustachian ridge; His, bundle of His; IVC, inferior vena cava; SVC, superior vena cava.

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Early reports [1–6] of RFCA of AFL revealed high initial success rates, but recurrence rates of up to 20 – 45% (Table 11.1). However, as experience with RFCA of AFL has increased [29–41], both acute success rates (defined as termination of AFL and bidirectional isthmus block) and chronic success rates (defined as no recurrence of type 1 atrial flutter) have risen to 85–95% (Table 11.1). Contributing in large degree to these improved results has been the introduction of bidirectional conduction block in the CTI as an end point for successful RFCA of AFL [29 – 41]. In the most recent studies (Table 11.1), using either large-tip (e.g., 8–10 mm) electrode ablation catheters with a highpower radiofrequency generator, or cooled-tip electrode ablation catheters with standard radiofrequency generators, acute success rates as high as 100% and chronic success rates as high as 98% have been reported [38 – 41]. Randomized comparisons of internally cooled, externally cooled, and large-tip ablation catheters suggest slightly better acute and chronic success rates with the externally cooled ablation catheters in comparison with internally

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Figure 11.14 Surface electrocardiogram (ECG) leads I, aVF and V1, and right atrial endocardial electrograms during pacing in sinus rhythm from the low lateral right atrium, before (A) and after (B) ablation of the cavotricuspid isthmus (CTI). Tracings include surface ECG leads I, aVF, and V1, and endocardial electrograms from the proximal coronary sinus (CSP), bundle of His (HIS), tricuspid valve annulus at the 1-o’clock position (HaloP) to

7-o’clock position (HaloD), and high right atrium (HRA or RFA). Before ablation during low lateral right atrial pacing, there is collision of the cranial and caudal right atrial wavefronts in the mid-septum (HIS and CSP). After ablation, the septum is activated in a strictly cranial-to-caudal pattern (i.e., clockwise), indicating a complete lateral-to-medial conduction block in the CTI. All other abbreviations are the same as in previous figures.

cooled ablation catheters or large-tip ablation catheters [33 –36,41]. In addition, in one recent very large study (including 169 patients) of the safety and efficacy of largetip catheters for ablation of type 1 AFL [37–39], it was demonstrated that bidirectional CTI block was achieved acutely with fewer radiofrequency energy applications (10 ± 8 vs.14 ± 8 applications; P = 0.002) and a shorter ablation time (0.5 ± 0.4 vs. 0.8 ± 0.6 h; P = 0.0002) with 10-mm tipped catheters than with 8-mm ones. In nearly all large-scale studies in which CTI ablation has successfully eliminated recurrence of type 1 AFL, there has been statistically significant improvement in quality-of-life scores as a result of reduced symptoms and antiarrhythmic medication use [38 – 40]. Despite the excellent acute and long-term efficacy of RFCA for type 1 AFL, atrial fibrillation and/or atypical atrial flutter may occur in up to 67% of patients in this population over 5 years, especially if there is a history of atrial fibrillation or underlying heart disease before ablation [57,58]. However, ablation of the CTI may also reduce, or in rare cases eliminate, recurrences of atrial fibrillation [58,59], and it is especially effective in patients undergo-

ing pharmacological treatment for atrial fibrillation with antiarrhythmic drug–induced type 1 atrial flutter (i.e., the so-called hybrid therapy approach). Ablation of the CTI may also be required in patients undergoing ablation for atrial fibrillation who also have a history of type 1 atrial flutter [60]. RFCA of the CTI for type 1 AFL is relatively safe, but serious complications can rarely occur, including ablationinduced heart block, cardiac perforation, tamponade, and thromboembolic events leading to pulmonary embolism, stroke, and myocardial infarction. In recent large-scale studies, including those using cooled-tip and large-tip ablation catheters, major complications have been observed in approximately 2.5–3.5% of patients [39– 41]. However, in studies using large-tip ablation electrode catheters, there did not appear to be a relationship between complication rates and the use of higher power (i.e., > 50 W) for ablation of the CTI. Although conversion of AFL to sinus rhythm may be less likely to cause thromboembolic complications such as stroke in comparison with atrial fibrillation, there is still a significant risk, and anticoagulation with warfarin is recommended before ablation in all patients with 185

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Figure 11.15 Surface electrocardiography leads I, aVF, and V1, and endocardial electrograms from the coronary sinus, bundle of His, Halo, mapping/ablation (RF), and right ventricular catheters during RFCA of the cavotricuspid isthmus (CTI), while pacing from the coronary sinus ostium. The progressive change in activation of the lateral right atrium on the Halo catheter from a bidirectional to a unidirectional pattern

should be noted, indicating the development of clockwise block in the CTI. In addition, this was associated with the progressive development of widely spaced (from 100 to 170 ms) double potentials (x and y) on the ablation catheter in the CTI, further confirming medial to lateral conduction block. All abbreviations are the same as in previous figures.

Table 11.1 Success rates of radiofrequency catheter ablation for atrial flutter. Acute and chronic success rates are reported as overall results in randomized or controlled studies.

First author (ref.)

Year

Patients (n)

Electrode

Acute success (%)

Follow-up (months)

Chronic success (%)

Feld [2] Cosio [3] Kirkorian [30] Fischer [29] Poty [44] Schwartzman [45] Cauchemez [46] Tsai [37] Chen [32] Atiga [34] Scavee [35] Feld [39] Calkins [40] Ventura [41]

1992 1993 1994 1995 1995 1996 1996 1995 1996 2002 2004 2004 2004 2004

16 9 22 80 12 35 20 50 65 59 80 169 150 130

4 4 4 4 6/8 8 4 8 8 4 vs cooled 8 vs cooled 8 or 10 8 8 vs cooled

100 100 86 73 100 100 100 92 93 88 80 93 88 100

4±2 2–18 8 ± 13 20 ± 8 9±3 1–21 8±2 10 ± 5 20 ± 11 13 ± 4 15 6 6 14 ± 2

83 56 84 81 92 92 80 100 92 93 98 97 87 98

Acute success: termination of atrial flutter during ablation and/or demonstration of isthmus block following ablation. Chronic success: patients in whom type 1 atrial flutter did not recur during follow-up.

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persistent type 1 AFL [61–63]. This is particularly important in those patients with depressed left ventricular function, mitral valve disease, and left atrial enlargement with left atrial thrombus or spontaneous contrast (i.e., smoke) on echocardiography. As an alternative, the use of transesophageal echocardiography to rule out left atrial thrombus immediately before ablation may be acceptable, but subsequent anticoagulation with warfarin is still recommended due to the fact that atrial stunning may occur after conversion of AFL, as it does with atrial fibrillation [62,63]. In patients with paroxysmal atrial flutter who are in sinus rhythm at the time of ablation, particularly those without structural heart disease, anticoagulation with warfarin is usually not warranted before or after ablation, since these patients’ risk of stroke is low.

Management of difficult cases of AFL ablation Despite the high acute success rates for AFL ablation reported in recent series, difficult cases are occasionally encountered. Several measures can be employed to increase the likelihood of success in these cases. Firstly and most importantly, it is critical to ensure that the mechanism of the spontaneous or induced arrhythmia is typical or reverse typical AFL, or more specifically that it is CTIdependent. If multielectrode catheter mapping with pacing entrainment is not sufficient to confirm this mechanism, then three-dimensional computerized activation mapping may be helpful to rule out other mechanisms of AFL. After the CTI dependence of the AFL has been confirmed, if initial ablation attempts are unsuccessful, it is essential to ensure that the ablation catheter has reached the extreme boundaries of the CTI isthmus, including the tricuspid valve annulus and Eustachian ridge or inferior vena cava. As noted previously, this may require the use of large-curve catheters, or preformed guiding sheaths to ensure catheter contact across the entire CTI [64]. Careful mapping of the CTI with the appropriate catheter may also help identify a gap in an ablation line by demonstrating an area of narrowly spaced double potentials, or continuous fragmented electrical activity, which when ablated may terminate AFL and produce bidirectional CTI conduction block. Gaps in ablation lines resulting in persistent CTI conduction after initial failed ablation may also be identified by three-dimensional computerized activation mapping in some cases when mapping with standard multielectrode catheters is unsuccessful. The authors recommend that ablation should be performed in the 6-o’clock position (in the left anterior oblique view) on the tricuspid valve annulus initially (Fig. 11.6), and if this is unsuccessful, a new ablation line should be created more laterally at the 7-o’clock or 8o’clock position on the tricuspid valve annulus. Large right atrial trabeculae may enter the lateral CTI tangen-

tially, which require ablation to achieve bidirectional conduction block. If this is also ineffective, an ablation line may then be created more medially at the 5-o’clock position, but care has to be taken in this position to monitor AV conduction, as the risk of AV block is increased. Typically, an ablation temperature of 60 °C is initially targeted for CTI ablation, but successful ablation may occasionally require temperatures as high as 70 °C. If standard ablation electrodes of 4 or 5 mm are used initially and ablation fails, the use of a large-tip 8-mm or 10-mm ablation catheter with a high-power generator, or a cooledtip catheter, is then recommended. The authors prefer a large-tip or cooled-tip catheter as the first-line device for CTI ablation, since these catheters have been shown to have greater efficacy than standard catheters in some studies, and to produce CTI block with fewer energy applications and shorter procedure times. The use of temperatures in excess of 70 °C with standard or large-tip ablation catheters, or in excess of 50 °C with cooled-tip catheters, in order to improve success rates is not recommended, due to the increased risk of tissue charring or steam pops, which may rarely cause cardiac rupture.

Computerized three-dimensional mapping in diagnosis and ablation of type 1 atrial flutter The three-dimensional electroanatomical Carto (BioSense Webster, Inc.) and NavX (Endocardial Solutions, Inc./St. Jude Medical) contact activation mapping systems, the EnSite (Endocardial Solutions, Inc./St. Jude Medical) noncontact activation mapping system, and the LocaLisa tracking system (Medtronic, Inc,), while certainly not required for successful ablation of type 1 AFL, have specific advantages that have made them a widely used and accepted technology [64–66]. Although it is not within the scope of this chapter to describe the technological basis of these systems in detail, there are unique characteristics of each system that make them more or less suitable for mapping and ablation of atrial flutter. The EnSite system uses a saline-inflated balloon catheter on which is mounted a wire mesh containing electrodes that are capable of sensing the voltage potential of the surrounding atrial endocardium, without actual electrode– tissue contact, from which the computerized mapping system can generate up to 3000 virtual endocardial electrograms and create a propagation map of the AFL (Fig. 11.16). In addition, a low-amplitude, high-frequency electrical current emitted from the ablation catheter can be sensed and tracked in three-dimensional (3D) space by the mapping balloon, with 3D anatomy being provided by roving the mapping catheter around the right atrial endocardium, onto which the propagation map is superimposed. 187

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Figure 11.16 A three-dimensional anatomical representation of the right atrium in a patient with typical AFL, using the EnSite balloon (St. Jude Medical, St. Paul, Minnesota, USA). This system uses an inflatable wire mesh–coated balloon mounted on a pigtail catheter to record up to 3000 virtual electrograms simultaneously, allowing reconstruction of a virtual anatomy and virtual activation sequence. Virtual electrograms are reconstructed from voltage potentials recorded by the balloon mapping catheter from the endocardial surface. The location of the ablation catheter can also be tracked in three-dimensional space by the system. CSO, coronary sinus ostium; IVC, inferior vena cava; TV, tricuspid valve.

The appropriate ablation target, in this case the CTI, can then be localized and the ablation catheter positioned appropriately and tracked while ablation is performed. After ablation, the mapping system can then be used to assess for bidirectional CTI conduction block during pacing from the low lateral right atrium and coronary sinus ostium. The advantages of the EnSite system include the ability to map the entire AFL activation sequence in one beat, precise anatomical representation of the right atrium, including the CTI and adjacent structures, precise localization of the ablation catheter within the right atrium, and propagation maps of endocardial activation during atrial flutter and pacing after ablation to assess for CTI conduction block. In addition, any ablation catheter system can be used with the EnSite system. The major disadvantage of the EnSite system is the need to use the balloon-mapping catheter, with its large 10-Fr introducer sheath, and the need for full anticoagulation during the mapping procedure. The Carto uses a magnetic sensor in the ablation catheter and a magnetic field generated by a grid placed under the patient and a reference pad on the skin to track the ablation catheter in 3D space, with a computer system to sequentially record the anatomical location and electrograms for online analysis of activation time and computation of isochronal patterns, which are then superimposed 188

on the endocardial geometry (Fig. 11.17A). A live propagation map can also be produced. The advantages of the Carto system include precise anatomical representation of the right atrium, including the CTI and adjacent structures, precise localization of the ablation catheter within the right atrium, and static activation and propagation maps of endocardial activation during atrial flutter and pacing after ablation to assess for CTI conduction block (Fig. 11.17B). The disadvantages of the Carto system include the need to use a magnet, proprietary catheters and ablation generator, and the inability to map the entire endocardial activation sequence in one beat. The NavX electroanatomical activation mapping system combines the advantages of both the Carto and EnSite systems, in that it uses electrical signals between reference ground pads on the patient’s skin, a standard intracardiac reference catheter (e.g., in the coronary sinus), and the roving mapping catheter to determine distance and generate a virtual anatomy of the cardiac chambers, as well as obtain activation timing by point-by-point mapping, similar to the Carto system, while using any available mapping/ablation catheter, and without the need for a magnet attached to the table, a special magnetic catheter, or a balloon electrode array. The 3D computerized mapping systems, again while not being required to map and ablate AFL, may be particularly useful in difficult cases such as patients with unusual mechanisms of CTI-dependent reentry (e.g., lower loop reentry) in whom prior ablation has failed, or in those in whom complex anatomy may be involved, including idiopathic or postoperative scarring, or unoperated or surgically corrected congenital heart disease. For example, a Carto map of the right atrium in a patient with previous failed RFCA for typical AFL shows an area of extensive scar in the CTI (Fig. 11.18). However, near the tricuspid valve annulus, a rim of viable myocardium persists that allows propagation of the macroreentrant through the CTI, perpetuating typical AFL. Ablation in this case required a large-curve ablation catheter to reach the tricuspid valve annulus and successfully ablate AFL. In another example, demonstrating the way in which 3D computerized activation mapping is advantageous for confirming the mechanism of the AFL, a Carto map in a patient with significant idiopathic scarring in the superior and inferior posterior right atrium (Fig. 11.19) revealed a CTI-dependent lower loop reentry, with a conduction gap across the crista terminalis. In addition, 3D activation mapping may be useful in ablation of type 1 AFL, as these systems can mark the location of each ablation performed, thus allowing the operator to reposition the ablation catheter precisely along the ablation line in the event that the catheter moves inadvertently during ablation, or to create a new ablation line adjacent to the previous one if ablation is initially unsuccessful.

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Figure 11.18 A three-dimensional electroanatomical (Carto) map of the right atrium, in a patient who had previously undergone a failed ablation attempt for typical atrial flutter (AFL). An area of extensive scar (gray area) is noted in the cavotricuspid isthmus (CTI) from the previous ablation, but a surviving rim of tissue is observed along the tricuspid valve annulus (TVA), through which an activation wavefront propagates slowly, perpetuating AFL. This narrow rim of surviving tissue was easily ablated and the AFL was cured.

Figure 11.17 A three-dimensional electroanatomical (Carto) map of the right atrium in a patient with typical atrial flutter (AFL), before (A) and after (B) cavotricuspid isthmus (CTI) ablation. The counterclockwise activation pattern around the tricuspid valve during AFL (A) should be noted, which is based on the color scheme indicating activation time from orange (early) to yellow to green to blue to purple (late). After ablation of the CTI (B), pacing from the coronary sinus ostium shows evidence of a medial-to-lateral conduction block in the isthmus, as indicated by juxtaposition of orange (early) and purple (late) colors in the CTI. CS, coronary sinus; IVC, inferior vena cava; TVA, tricuspid valve annulus.

Figure 11.19 A three-dimensional electroanatomical (Carto) map of the right atrium, in a patient with idiopathic scarring of the posterior right atrium, with a gap between the superior and inferior scar resulting in transverse conduction across the crista terminalis and a clockwise lower loop reentry atrial flutter (AFL). Areas of scar can be designated by the mapping system on the basis of very low-amplitude electrograms (e.g., < 0.5 mV) and marked as scar by showing them as gray regions on the map. This AFL was terminated by CTI ablation, confirming that it was isthmus-dependent. IVC, inferior vena cava.

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New energy sources for ablation of type 1 atrial flutter The development of new energy sources for ablation of cardiac arrhythmias is an ongoing effort, largely to the potential disadvantage of the use of radiofrequency energy for ablationaincluding, but not limited to, the risk of coagulum formation, tissue charring, subendocardial steam pops, embolization, failure to achieve transmural ablation, and the long procedure and fluoroscopy times required to ablate large areas of myocardium. Many of these disadvantages of RFCA have been overcome in the case of ablation of type 1 AFL in the past decade, however. Nonetheless, several clinical and preclinical studies have recently been published on the use of catheter cryoablation and microwave ablation of atrial flutter, and other arrhythmias [67–71]. Recent studies have been reported demonstrating that catheter cryoablation of type 1 AFL can be achieved with similar results to radiofrequency ablation [67–71]. The potential advantages of cryoablation include the lack of pain associated with ablation, the ability to produce a large transmural ablation lesion, and the lack of tissue charring or coagulum formation [67–71]. Further clinical research is ongoing with respect to the safety and efficacy of catheter cryoablation for atrial flutter and fibrillation in the USA and Europe (CryoCor, Inc., San Diego, California, USA and CryoCath Technologies, Inc., Montreal, Canada). In addition, preclinical and early work has begun on the use of a linear microwave ablation catheter system (Medwaves Inc., Rancho Bernardo, CA, USA) with antenna lengths up to 4 cm [70–72]. These studies have shown the feasibility of linear microwave ablation, which may have the advantage of very rapid ablation of the CTI with a single energy application over the entire length of the ablation electrode [70–72]. Clinical studies of this system started in Europe and Asia in 2005.

Summary RFCA has become a first-line treatment for type 1 AFL with high success rates and low complication rates. The most effective approach involves combined anatomically and electrophysiologically guided ablation of the CTI, with procedure end points of arrhythmia noninducibility and bidirectional CTI conduction block. The use of large-tip ablation catheters (i.e., 8 –10 mm) with high-output radiofrequency generators (i.e., 100 W), or cooled-tip ablation catheters, is recommended for optimal success rates. Computerized 3D activation mapping is an adjunctive method, which although it is not mandatory to cure AFL may have significant advantages in some cases, resulting in overall improved success rates. New alternative energy 190

sources, including cryoablation and microwave ablation, are under investigation with the hope of further improving procedure times and potentially reducing discomfort and the risk of complications during ablation.

References 1 Saoudi N, Cosio F, Waldo A, et al. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2001;12:852– 66. 2 Feld GK, Fleck RP, Chen PS, et al. RFCA for the treatment of human type 1 atrial flutter: identification of a critical zone in the re-entrant circuit by endocardial mapping techniques. Circulation 1992;86:1233 – 40. 3 Cosio FG, Lopez-Gil M, Goicolea A, et al. Radiofrequency ablation of the inferior vena cava–tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71:705 –9. 4 Lesh MD, Van Hare GF, Epstein LM, et al. RFCA of atrial arrhythmias: results and mechanisms. Circulation 1994;89: 1074 –89. 5 Cosio FG, Goicolea A, Lopez-Gil M, et al. Atrial endocardial mapping in the rare form of atrial flutter. Am J Cardiol 1990;66:715 –20. 6 Tai CT, Chen SA, Chiang CE, et al. Electrophysiologic characteristics and RFCA in patients with clockwise atrial flutter. J Cardiovasc Electrophysiol 1997;8:24 –34. 7 Olshansky B, Okumura K, Gess PG, et al. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardiol 1990;16:1639 – 48. 8 Feld GK, Mollerus M, Birgersdotter-Green U, et al. Conduction velocity in the tricuspid valve–inferior vena cava isthmus is slower in patients with a history of atrial flutter compared to those without atrial flutter. J Cardiovasc Electrophysiol 1997;8:1338 – 48. 9 Kinder C, Kall J, Kopp D, et al. Conduction properties of the inferior vena cava–tricuspid annular isthmus in patients with typical atrial flutter. J Cardiovasc Electrophysiol 1997;8: 727–37. 10 Da Costa A, Mourot S, Romeyer-Bouchard C, et al. Anatomic and electrophysiological differences between chronic and paroxysmal forms of common atrial flutter and comparison with controls. Pacing Clin Electrophysiol 2004;27:1202–11. 11 Feld GK, Shahandeh-Rad F. Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush-injury model. Circulation 1992;86:628 – 41. 12 Olgin JE, Kalman JM, Fizpatrick AP, et al. Role of right atrial endocardial structures as barriers to conduction during human type 1 atrial flutter: activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995;92:1839 – 48. 13 Olgin JE, Kalman JM, Lesh MD. Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy. J Cardiovasc Electrophysiol 1996;7:1112–26.

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Diagnosis and ablation of typical and reverse typical (type 1) atrial flutter

14 Kalman JM, Olgin JE, Saxon LA, et al. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation 1996;94:398 – 406. 15 Tai CT, Huang JL, Lee PC, et al. High-resolution mapping around the crista terminalis during typical atrial flutter: new insights into mechanisms. J Cardiovasc Electrophysiol 2004;15: 406–14. 16 Spach MS, Miller WT III, Dolber PC, et al. The functional role of structural complexities in the propagation of depolarization in the atrium of the dog: cardiac conduction disturbances due to discontinuities of effective axial resistivity. Circ Res 1982;50:175–91. 17 Spach MS, Dolber PS, Heidlage JF. Influence of the passive anisotropic properties on directional differences in propagation following modification of sodium conductance in human atrial muscle: a model of reentry based on anisotropic discontinuous propagation. Circ Res 1988;62:811–32. 18 Olgin JE, Kalman JM, Saxon LA, et al. Mechanisms of initiation of atrial flutter in humans: site of unidirectional block and direction of rotation. J Am Coll Cardiol 1997;29:376 –84. 19 Suzuki F, Toshida N, Nawata H, et al. Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter: analysis of episodes of direct initiation of atrial flutter. J Electrocardiol 1998;31:345–61. 20 Feld GK, Shahandeh-Rad F. Activation patterns in experimental canine atrial flutter produced by right atrial crushinjury. J Am Coll Cardiol 1992;20:441–51. 21 Haïssaguerre M, Sanders P, Hocini M, et al. Pulmonary veins in the substrate for atrial fibrillation: the “venous wave” hypothesis. J Am Coll Cardiol 2004;43:2290 –2. 22 Sparks PB, Jayaprakash S, Vohra JK, et al. Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter. Circulation 2000;102:1807–13. 23 Cha YM, Wales A, Wolf P, et al. Electrophysiologic effects of the new class 3 antiarrhythmic drug dofetilide compared to the class 1a antiarrhythmic drug quinidine in experimental canine atrial flutter: role of dispersion of refractoriness in antiarrhythmic efficacy. J Cardiovasc Electrophysiol 1996;7:809 –27. 24 Yang T, Cheng J, Bochoeyer A, et al. Atypical right atrial flutter patterns. Circulation 2001;103:3092–8. 25 Bochoeyer A, Yang Y, Cheng J, et al. Surface electrocardiographic characteristics of right atrial and left atrial flutter. Circulation 2003;108:60–6. 26 Oshikawa N, Watanabe I, Masaki R, et al. Relationship between polarity of the flutter wave in the surface ECG and endocardial atrial activation sequence in patients with typical counterclockwise and clockwise atrial flutter. J Interv Card Electrophysiol 2002;7:215–23. 27 Okumura K, Plumb VJ, Page PL, et al. Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram. J Am Coll Cardiol 1991;17:509–18. 28 Narayan SM, Feld GK, Hassankhani A, et al. Quantifying intracardiac organization of atrial arrhythmias using temporospatial phase of the electrocardiogram. J Cardiovasc Electrophysiol 2003;14:971–81. 29 Fischer B, Haïssaguerre M, Garrigues S, et al. RFCA of atrial flutter in 80 patients. J Am Coll Cardiol 1995;25:1365 –72.

30 Kirkorian G, Moncada E, Chevalier P, et al. Radiofrequency ablation of atrial flutter: efficacy of an anatomically guided approach. Circulation 1994;90:2804 –14. 31 Calkins H, Leon AR, Deam G, et al. Catheter ablation of atrial flutter using radiofrequency energy. Am J Cardiol 1994; 73:353 –6. 32 Chen SA, Chiang CE, Wu TJ, et al. RFCA of common atrial flutter: comparison of electrophysiologically guided focal ablation technique and linear ablation technique. J Am Coll Cardiol 1996;27:860 –8. 33 Jaïs P, Haïssaguerre M, Shah DC, et al. Successful irrigated-tip catheter ablation of atrial flutter resistant to conventional radiofrequency ablation. Circulation 1998;98:835 –8. 34 Atiga WL, Worley SJ, Hummel J, et al. Prospective randomized comparison of cooled radiofrequency versus standard radiofrequency energy for ablation of typical atrial flutter. Pacing Clin Electrophysiol 2002;25:1172–8. 35 Scavee C, Jaïs P, Hsu LF, et al. Prospective randomized comparison of irrigated-tip and large-tip catheter ablation of cavotricuspid isthmus-dependent atrial flutter. Eur Heart J 2004;25:963 –9. 36 Calkins H. Catheter ablation of atrial flutter: do outcomes of catheter ablation with “large-tip” versus “cooled-tip” catheters really differ? J Cardiovasc Electrophysiol 2004;15: 1131–2. 37 Tsai CF, Tai CT, Yu WC, et al. Is 8-mm more effective than 4mm tip electrode catheter for ablation of typical atrial flutter? Circulation 1999;100:768 –71. 38 Feld GK. Radiofrequency ablation of atrial flutter using largetip electrode catheters. J Cardiovasc Electrophysiol 2004;15: S18 –23. 39 Feld G, Wharton M, Plumb V, et al. RFCA of type 1 atrial flutter using large-tip 8- or 10-mm electrode catheters and a high-output radiofrequency energy generator: results of a multicenter safety and efficacy study. EPT-1000 XP Cardiac Ablation System Investigators. J Am Coll Cardiol 2004;43: 1466 –72. 40 Calkins H, Canby R, Weiss R, et al. Results of catheter ablation of typical atrial flutter. 100 W Atakr II Investigator Group. Am J Cardiol 2004;94:437– 42. 41 Ventura R, Klemm H, Lutomsky B, et al. Pattern of isthmus conduction recovery using open cooled and solid large-tip catheters for radiofrequency ablation of typical atrial flutter. J Cardiovasc Electrophysiol 2004;15:1126 –30. 42 Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter: relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407–24. 43 Nakagawa H, Imai S, Schleinkofer M, et al. Linear ablation from tricuspid annulus to eustachian valve and ridge is adequate for patients with atrial flutter: extending ablation line to the inferior vena cava is not necessary. J Am Coll Cardiol 1997;29:199A. 44 Poty H, Saoudi N, Aziz AA, et al. RFCA of type 1 atrial flutter: prediction of late success by electrophysiologic criteria. Circulation 1995;92:1389 –92. 45 Schwartzman D, Callans D, Gottlieb CD, et al. Conduction block in the inferior caval–tricuspid valve isthmus: association 191

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with outcome of radiofrequency ablation of type 1 atrial flutter. J Am Coll Cardiol 1996;28:1519–31. Cauchemez B, Haïssaguerre M, Fischer B, et al. Electrophysiologic effects of catheter ablation of the inferior vena cava–tricuspid annulus isthmus in common atrial flutter. Circulation 1996;93:284–94. Mangat I, Tschopp DR Jr, Yang Y, et al. Optimizing the detection of bidirectional block across the flutter isthmus for patients with typical isthmus-dependent atrial flutter. Am J Cardiol 2003;91:559–64. Arenal A, Almendral J, Alday JM, et al. Rate-dependent conduction block of the crista terminalis in patients with typical atrial flutter: influence on evaluation of cavotricuspid isthmus conduction block. Circulation 1999;99:2771–8. Liu TY, Tai CT, Huang BH, et al. Functional characterization of the crista terminalis in patients with atrial flutter: implications for radiofrequency ablation. J Am Coll Cardiol 2004;43:1639–45. Anselme F, Savoure A, Ouali S, et al. Transcristal conduction during isthmus ablation of typical atrial flutter: influence on success criteria. J Cardiovasc Electrophysiol 2004;15:184 –9. Tai CT, Haque A, Lin YK, et al. Double potential interval and transisthmus conduction time for prediction of cavotricuspid isthmus block after ablation of typical atrial flutter. J Interv Card Electrophysiol 2002;7:77–82. Tada H, Oral H, Sticherling C, et al. Double potentials along the ablation line as a guide to radiofrequency ablation of typical atrial flutter. J Am Coll Cardiol 2001;38:750 –5. Johna R, Eckardt L, Fetsch T, et al. A new algorithm to determine complete isthmus conduction block after RFCA for typical atrial flutter. Am J Cardiol 1999;83:1666 –8. Hamdan MH, Kalman JM, Barron HV, et al. P-wave morphology during right atrial pacing before and after atrial flutter ablation: a new marker for success. Am J Cardiol 1997;79: 1417–20. Tada H, Oral H, Sticherling C, et al. Electrogram polarity and cavotricuspid isthmus block during ablation of typical atrial flutter. J Cardiovasc Electrophysiol 2001;12:393 –9. Villacastin J, Almendral J, Arenal A, et al. Usefulness of unipolar electrograms to detect isthmus block after radiofrequency ablation of typical atrial flutter. Circulation 2000;102: 3080–5. Gilligan DM, Zakaib JS, Fuller I, et al. Long-term outcome of patients after successful radiofrequency ablation for typical atrial flutter. Pacing Clin Electrophysiol 2003;26:53 –8. Tai CT, Chen SA, Chiang CE, et al. Long-term outcome of RFCA for typical atrial flutter: risk prediction of recurrent arrhythmias. J Cardiovasc Electrophysiol 1998;9:115 –21. Feld GK. New approaches for the management of atrial

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fibrillation: role of ablation of atrial flutter. J Cardiovasc Electrophysiol 1999;10:1188 –91. Scharf C, Veerareddy S, Ozaydin M, et al. Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with atrial fibrillation. J Am Coll Cardiol 2004;43: 2057–62. Welch PJ, Afridi I, Joglar JA, et al. Effect of radiofrequency ablation on atrial mechanical function in patients with atrial flutter. Am J Cardiol 1999;84:420 –5. Prater S, Wades M, Reynerston S, et al. Incidence of atrial thrombus in patients with type 1 atrial flutter undergoing catheter ablation. Circulation 1996;94:I-728. Gronefeld GC, Wegener F, Israel CW, et al. Thromboembolic risk of patients referred for RFCA of typical atrial flutter without prior appropriate anticoagulation therapy. Pacing Clin Electrophysiol 2003;26:323 –7. Schumacher B, Wolpert C, Lewalter T, Vahlhaus C, Jung W, Luderitz B. Predictors of success in radiofrequency catheter ablation of atrial flutter. J Interv Card Electrophysiol 2000;4:121–5. Ventura R, Rostock T, Klemm HU, et al. Catheter ablation of common-type atrial flutter guided by three-dimensional right atrial geometry reconstruction and catheter tracking using cutaneous patches: a randomized prospective study. J Cardiovasc Electrophysiol 2004;15:1157–61. Sporton SC, Earley MJ, Nathan AW, et al. Electroanatomic versus fluoroscopic mapping for catheter ablation procedures: a prospective randomized study. J Cardiovasc Electrophysiol 2004;15:310 –5. Manusama R, Timmermans C, Limon F, et al. Catheter-based cryoablation permanently cures patients with common atrial flutter. Circulation 2004;109:1636 –9. Timmermans C, Ayers GM, Crijns HJ, et al. Randomized study comparing radiofrequency ablation with cryoablation for the treatment of atrial flutter with emphasis on pain perception. Circulation 2003;107:1250 –2. Feld GK, Daubert JP, Weiss R, et al. Acute and chronic efficacy and safety of catheter cryoablation of the cavo-tricuspid isthmus for treatment of atrial flutter [abstract]. Heart Rhythm 2005;2:S238. Adragao P, Parreira L, Morgado F, Bonhorst D, SeabraGomes R. Microwave ablation of atrial flutter. Pacing Clin Electrophysiol 1999;22:1692–5. Liem LB, Mead RH. Microwave linear ablation of the isthmus between the inferior vena cava and tricuspid annulus. Pacing Clin Electrophysiol 1998;21:2079 –86. Iwasa A, Storey J, Yao B, Liem LB, Feld GK. Efficacy of a microwave antenna for ablation of the tricuspid valve: inferior vena cava isthmus in dogs as a treatment for type 1 atrial flutter. J Interv Cardiovasc Electrophysiol 2004;10:191– 8.

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12

Catheter ablation of macroreentrant right and left atrial tachycardias Hiroshi Nakagawa, Warren M. Jackman, Katsuaki Yokoyama, Richard Wu, Karen J. Beckman, Sunny S. Po, Deborah Lockwood, Sameer Oza, Himanshu Shukla, Lisa Herring, and Ralph Lazzara

Introduction Macroreentrant atrial tachycardia (macro-AT) occurs in patients with dilated, severely scarred right or left atria. Macro-AT may be defined either by entrainment pacing or by electroanatomical mapping. When electroanatomical mapping is being used, macro-AT is defined by the recording of continuous atrial activation (“head meets tail”) with a total activation time equal to the tachycardia cycle length (Fig. 12.1) [1]. The substrate for macro-AT is a large heterogeneous atrial scar with surviving myocardial bundles bounded by two or more dense scars, forming protected conduction channels (“arrhythmogenic channels”). During electroanatomical mapping (recorded during the tachycardia or sinus rhythm), the heterogeneous atrial scar is manifested by a large area of low bipolar voltage (≤ 0.5 mV). The dense scars are identified as areas without a recordable atrial potential (≤ 0.03 mV) or as

lines of double atrial potentials signifying conduction block. During electroanatomical mapping, we include any area exhibiting dissociated atrial potentials during macroAT, sinus rhythm, or atrial pacing as a scar since this area is not participating in the circuit. The reentrant impulse propagates through one or more of the arrhythmogenic channels between dense scars (Fig. 12.1). Macro-AT occurs with severe atrial scarring of any etiology, including previous right or left atriotomy, any form of structural heart disease, or following catheter or surgical ablation of atrial fibrillation (Table 12.1). Some macroAT patients present with a large scarred right or left atrium without any other form of structural heart disease, which we refer to as “idiopathic arrhythmogenic atrial myopathy” (Fig. 12.2). We prefer the term “macro-AT” because of the similar patterns of activation during atrial mapping, despite the various etiologies. Other names often used to describe macro-AT include atypical atrial flutter, nonisthmus-dependent atrial flutter, incisional atrial tachycardia, and left atrial flutter (Table 12.1).

Macroreentrant atrial tachycardia Definition by electroanatomical mapping

SVC

RA

1. Continuous activation (head meets tail) 2. Activation time = tachycardia cycle length Substrate 1. Large heterogeneous scar (area of low voltage) 2. Two or more dense scars or areas of block forming at least one narrow isolated channel

IVC

3. Reentrant impulse propagates through a channel rather than propagating around a single scar

Figure 12.1 Definition and schematic diagram of the substrate for macroreentrant atrial tachycardia. IVC, inferior vena cava; RA, right atrium; SVC, superior vena cava.

Table 12.1 Macroreentrant atrial tachycardia. Occurs with severe atrial scarring of any etiology Right atriotomy (repaired congenital heart disease) Left atriotomy (mitral valve surgery) Following catheter or surgical ablation of atrial fibrillation Coronary artery disease (CAD) Hypertrophic cardiomyopathy (HCM) Dilated cardiomyopathy (DCM) Post-myocarditis Idiopathic (“arrhythmogenic atrial myopathy”) Other names Atypical atrial flutter Nonisthmus-dependent atrial flutter Incisional atrial tachycardia Left atrial flutter

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B

A

3.65 mV

RAO projection SVC

Arrhythmogenic channel (1.5 cm)

125 ms Atrial tachycardia CL 355 ms

Bipolar voltage MAP

0.06 mV Scar

Scar

Lines of double potentials

IVC

SVC

Arrhythmogenic channel (1.5 cm)

Activation MAP

RAO projection

-230 ms

Scar

Scar Lines of double potentials

Blind alley

Scar

Scar

Double potentials

Double potentials

Fractionated potential

Fractionated potential

IVC

1.0 cm

1.0 cm

C RAO projection SVC

Ablation Ablation converts converts 22 scars scars into into 11 scar scar continuous continuous with with IVC IVC

125 ms Activation MAP

Ablation (3 RFs)

-230 ms

Scar

Scar Lines of double potentials Scar Double potentials Fractionated potential

Ablation sites

IVC Figure 12.2 Macroreentrant right atrial tachycardia (macro–right AT) in a 57-year-old man with “idiopathic arrhythmogenic right atrial myopathy” (normal coronary arteries and normal left ventricular function). A. Bipolar voltage map of the right atrium in the right anterior oblique (RAO) projection (identified by the angle of the icon of the head and eyes) obtained during a macro–right AT. The bipolar voltage at each mapped site is displayed by color with red at sites of lowest voltage (0.06 mV) and purple at sites of highest voltage (3.65 mV), located on the septum and not displayed in the RAO projection. Sites of no recorded potential (≤ 0.03–0.04 mV) are marked with a gray tag (dense scar). Sites exhibiting double atrial potentials (indicating conduction block) are marked with pink tags. Sites of fractionated atrial potentials are marked with olive-green tags. The entire right atrial free wall exhibits very low bipolar voltage (red and orange), indicating extensive scarring. A narrow (width 1.5 cm) arrhythmogenic channel, formed by the severe scarring, is bounded posteriorly by a dense scar (gray area) extending to the inferior vena cava (IVC) and bounded anteriorly by a linear scar (a line of double potentials, pink tags) continuous with a large anterior dense scar (gray area) that does not extend to the tricuspid annulus. SVC, superior vena cava. B. Activation map of the right atrium (RAO projection), obtained simultaneously with the

voltage map during the macro–right AT. The local activation time at each site is displayed by color, relative to the timing of the reference atrial potential (see Fig. 12.3). Red color indicates earliest activation time within the timing window and purple indicates latest activation time within the timing window. The activation map shows a continuous pattern of activation (red–yellow–green–blue–purple–red, “head meets tail”) around the linear and dense anterior scar and through the arrhythmogenic channel (black arrow). The total activation time around the circuit is equal to the tachycardia cycle length of 335 ms (extending from 230 ms before the reference atrial potential to 125 ms after the reference atrial potential). The dashed arrow shows activation into a “blind alley,” which is surrounded by dense scars with no exit. IVC, inferior vena cava; SVC, superior vena cava. C. Ablation of macro–right AT. Three radiofrequency (RF) applications were delivered across the arrhythmogenic channel, terminating the tachycardia and creating conduction block across the channel. This short ablation line connected the two scars bounding the arrhythmogenic channel and formed a continuous line of conduction block from the large anterior scar (gray area) to the inferior vena cava (IVC). Programmed atrial stimulation after ablation failed to induce any AT. SVC, superior vena cava.

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Catheter ablation of macroreentrant right and left atrial tachycardias

Table 12.2 Comparison between macroreentrant right atrial and left atrial tachycardias. Channel width (cm) Channel voltage (mV) RF per channel (n) 8 mm/irrigated electrode Acute ablation success

Macro–right AT (50 patients/109 channels)

Macro–left AT (50 patients/106 channels)

P

0.5–2.7 (median 1.5) 0.05–1.48 (median 0.18) 1–15 (median 3) 22/50 (44%) patients 50/50 patients

0.8–6.0 (median 2.3) 0.05–2.84 (median 0.60) 1–41 (median 6) 40/50 (80%) patients 47/50 patients

< 0.01 < 0.01 < 0.01 < 0.01 n.s.

AT, atrial tachycardia; RF, radiofrequency.

Macroreentrant right atrial tachycardia In macroreentrant right atrial tachycardia (macro–right AT), the heterogeneous atrial scar usually involves almost all of the right atrial free wall, which is manifested by low bipolar voltage (≤ 0.5 mV) during electroanatomical mapping (Fig. 12.2A). The reentrant circuit propagates around at least one dense scar and through a narrow channel between two sites of conduction block (dense scars, Fig. 12.2B). In 50 patients, the width of 109 right atrial channels forming a macroreentrant circuit was only 0.5 –2.7 cm (median 1.5 cm; Fig. 12.2B and Table 12.2) [1,2]. Channels larger than 3.0 cm in width generally do not support macro–right AT, except for the subeustachian isthmus, supporting typical atrial flutter (reentry around the tricuspid annulus) [1,3,4].

Ablation of macro–right AT Several approaches have been used for ablation of macro– right AT. The first approach targeted sites exhibiting an isolated diastolic atrial potential, presumably originating from a zone of slow conduction [5,6]. Entrainment pacing was used to confirm that the tissue generating the isolated diastolic atrial potential was located within the reentrant circuit. In one series of patients with macro–right AT following surgical repair of congenital heart disease, ablation of the isolated potentials successfully eliminated at least one of the patient’s atrial tachycardias in 73% of the patients [5]. However, atrial tachycardia recurred in 53% of the patients with acute success (mean time to recurrence 4.1 months) [6]. A second approach was based on the concept that macro– right AT results from reentry around an atriotomy scar or other scar, but not necessarily propagating through a narrow channel [7,8]. Catheter ablation was used to create a transmural linear lesion between the scar and an anatomical barrier (tricuspid annulus, inferior vena cava, or superior vena cava) to interrupt the reentrant circuit [7,8]. The scar was defined as an area without an atrial potential, or with double atrial potentials separated by an isoelectrical baseline, indicating a line of conduction block [7–9]. In

two studies using this approach, ablation acutely eliminated at least one atrial tachycardia in 83% and 93% of patients, with recurrence of atrial tachycardia in 33% and 46%, respectively, of the patients with acute ablation success [7,8]. Two limitations of this approach are: firstly, adjacent scars may allow multiple circuits; and secondly, the difficulty in creating a long, continuous, transmural linear atrial lesion. The optimal ablation approach is to identify the narrow arrhythmogenic channel providing the critical component of the macroreentrant circuit and create a short transmural linear lesion across the channel. This converts the two scars forming the arrhythmogenic channel into a single scar. Since one of the scars is usually connected to the inferior or superior vena cava, the ablation eliminates any reentrant circuit associated with either of the two scars (Fig. 12.2C). Ablation across the right atrial channels is generally accomplished without difficulty, due to the narrow width and thin tissue. In 50 patients, 1–15 (median three) radiofrequency (RF) applications were required to create conduction blocks across 109 channels (Table 12.2).

Factors affecting mapping and ablation of macro–right AT (Table 12.3) An electroanatomical map provides the endocardial location, the timing of activation, and the voltage at each mapped site [1,3,10]. The electroanatomical mapping system (Carto, Biosense Webster, Inc., Diamond Bar, California, USA) used for the data and figures in this chapter uses three magnetic fields to provide the catheter tip location relative to the location of a reference sensor positioned on the skin overlying the left posterior chest [10]. A reference atrial potential is obtained from another catheter positioned at a stable site within the coronary sinus or right atrium. A window of time equal to the atrial tachycardia cycle length is established around the timing of the reference atrial potential (Fig. 12.3) [3]. The local activation time, recorded from the mapping catheter at each endocardial site, is measured relative to the timing of the reference atrial potential. The timing of activation at each site is displayed in color. The earliest time within the window is shown in red and latest time shown in purple (activation 195

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Supraventricular tachycardia

Table 12.3 Factors affecting mapping and ablation of macroreentrant atrial tachycardia. • Accurate identification of the circuit and localization of the margins of the arrhythmogenic channels requires a high-density electroanatomical map • Voltage of potentials recorded in arrhythmogenic channels may be extremely low (< 0.1 mV), mimicking dense scar (hiding the location of the arrhythmogenic channel) • Atrial potentials with identical activation time recorded at two or more separate sites indicate double-loop reentry or blind alleys • Timing of activation in arrhythmic channels (ablation sites) is variable relative to the P wave, not just “mid-diastolic” • Limitations of entrainment — Sites outside an isolated channel can exhibit isolated “mid-diastolic” potentials and entrainment pacing, producing concealed fusion and PPI = AT CL (ablation at that site will fail) — Entrainment pacing may terminate the atrial tachycardia or change to another atrial tachycardia • Most patients have multiple atrial tachycardias, some unmappable (nonsustained, not reinducible, or changing atrial activation sequence) • Confirmation of complete conduction block across all potential arrhythmogenic channels following ablation

Figure 12.3 Selection of the timing window for the electroanatomical map of the right atrium during the macro–right AT shown in Fig. 12.2. The reference atrial electrogram was recorded from the coronary sinus (CS). The timing window must be equal to the tachycardia cycle length (355 ms) and was arbitrarily selected to extend from 230 ms before the reference atrial potential to 125 ms after the reference atrial potential. Other tracings are electrocardiogram leads II, V1, and the atrial electrogram recorded from the mapping catheter (MAP). A, atrial electrogram.

map, Fig. 12.2B). Since activation is continuous in macroAT, the spectrum of colors on the activation map is present in continuous pattern with “earliest” atrial activation (red) directly adjacent to the site of “latest” atrial activation (purple, “head meets tail”). The voltage of the bipolar atrial Figure 12.4 (opposite) Macro–right AT formed by a small circuit with markedly low-amplitude atrial potentials in a 36-year-old man, 10 years after a Fontan procedure for repair of pulmonary atresia and a hypoplastic right ventricle. A. The activation map shows activation around a small dense scar within an area constrained by large upper and low dense scars (gray areas). Although the entire length of the circuit is only 6–7 cm, activation is continuous throughout the tachycardia cycle length of 435 ms, confirming the macroreentrant circuit. Activation with timing similar to the tachycardia circuit is shown anterior to the heavily scarred area. However, activation in this region is not continuous throughout the tachycardia cycle length, indicating an incomplete “entrained loop” rather than the macroreentrant circuit for this tachycardia. CL, cycle length; IVC, inferior vena cava; RA-PA, right atrium-pulmonary artery; SVC, superior vena cava. B. Voltage map of the macro–right AT shows extremely low bipolar voltage (red color 0.04 mV) involving most of the right atrial free wall, including all of the area of the reentrant circuit. If an arbitrary voltage criterion is used for dense scar, such as areas = 0.1 mV, the entire right atrial free wall would be colored gray. This would obscure the entire reentrant circuit and eliminate the ability to ablate the arrhythmogenic channel. The reentrant circuit can be localized only by annotating any atrial potential with constant timing within the tachycardia cycle length, regardless of low amplitude. A single RF

196

potential recorded at each site is also displayed in color, with the lowest voltage represented in red and greatest voltage represented in purple (voltage map, Fig. 12.2A). A very high-density electroanatomical map (usually with more than 300 mapped points) is critical for accurately localizing the entire reentrant circuit and the arrhythmogenic channels. Distances of 2–4 mm between mapped sites may be required to differentiate a small macroreentrant circuit from a focal atrial tachycardia (Fig. 12.4A). Similar resolution is required to delineate the margins of the arrhythmogenic channel for ablation. Activation of surviving myocardial bundles within the scar often produces potentials with extremely low bipolar voltage (0.04–0.06 mV), mimicking a dense scar (Fig. 12.4B). Our approach is to assign a timing of activation for every recordable bipolar potential, regardless of how small (Fig. 12.4C, D). Many of the narrow channels between dense scars would be obscured (and shown as a single continuous scar) if scar were to be defined by an arbitrary voltage criterion (e.g., < 0.1 mV). application (RF1) was delivered within the narrow (1.5 cm) arrhythmogenic channel between the small central scar and large lower scar. The atrial potential amplitude at the ablation site was only 0.06 mV. CL, cycle length; IVC, inferior vena cava; RA-PA, right atrium, posteroanterior; SVC, superior vena cava. C. Bipolar electrogram (ABL, 30–500 Hz) and unipolar electrograms (Uni 1 tip electrode and Uni 2 second electrode, 1–500 Hz), recorded from the ablation catheter during the macro–right AT at the site of the first RF application (RF1), showing an extremely low atrial potential amplitude (0.06 mV, arrows), simulating a dense scar. This small potential was recorded within the P wave, which was 315 ms (72% of the tachycardia cycle length) before the onset of next P wave. Other tracings from the top are electrocardiogram leads aVL, I, II, III, and V1, and electrograms recorded around the tricuspid annulus (Halo 10 anterior, Halo 1 posterior) and right atrium (RA). D. The first RF application was delivered at this site, immediately lengthening the tachycardia cycle length from 435 ms to 455 ms and terminating the macro–right AT after 2.2 s at a power of 17 W. The black arrows indicate the low-amplitude atrial potential recorded at the ablation site. Elimination of this potential (white arrow) was associated with the termination of tachycardia. RA, right atrium (Adapted from [1] with permission from Lippincott, Williams and Wilkins.)

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Catheter ablation of macroreentrant right and left atrial tachycardias B

A 85 ms

Atrial tachycardia CL 435 ms

SVC

Activation MAP

RA-PA conduit

Right posterior oblique projection

Scar

Scar

- 350 ms

Atrial tachycardia CL 435 ms Right posterior oblique projection

Entrained loop (head does not meet tail)

SVC RA-PA Conduit

Bipolar voltage MAP Scar 0.04 mV

Scar

Scar

Small macroreentrant circuit (head meets tail)

6.41mV

Scar

RF1

1.0 cm

1.0 cm

Scar

IVC

Scar (no potential) Double potentials Fractionated potential SVC, IVC

Channel width 1.5 cm voltage 0.06 mV

Scar

Scar (no potential) Double potentials Fractionated potential SVC, IVC Ablation site

C

D

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Supraventricular tachycardia

During macro-AT, the electroanatomical map often shows multiple sites across the right atrium with similar timing (color). This may be found in double-loop reentry (Fig. 12.5A), an entrained loop (incomplete or slower circuit, Fig. 12.4A) or activation into a dead-end pathway (“blind alley,” Fig. 12.2B). The reentrant circuit is identified by tracing activation times (colors) and locating a continuous activation pattern (“head meets tail”). In previous studies on ablation of macroreentrant atrial or ventricular tachycardia, the combination of an electrogram exhibiting a mid-diastolic potential plus entrain-

ment pacing showing concealed fusion with a post-pacing interval equal to the tachycardia cycle length has been considered to be located within a “protected isthmus” and therefore an ideal ablation site [6,7,11,12]. Since a majority of the macro-AT cycle length consists of conduction outside of the arrhythmogenic channel but within the large heterogeneous scar, many sites outside of the isolated arrhythmogenic channel exhibit very low-amplitude, fractionated, or double atrial potentials. The potentials within the arrhythmogenic channels are no more frequently “mid-diastolic” than occurring within or shortly before

B AP projection

A Right lateral projection

C LAO projection

128 ms

128 ms

128 ms

-100ms

-100ms

-100ms

AT AT CL CL 228ms 228ms Entrain sites 1,2,3 Concealed fusion PPI = AT CL

Entrain site 4 Concealed fusion PPI = AT CL

Channel width 1.8 cm voltage 0.08 mV

Common segment 4.2 cm, 3.17 mV

D Right lateral projection

Entrain Site 6 Concealed Fusion PPI = AT CL + 60ms

3RFs

E LAO projection

F Right lateral projection

128 ms

128 ms

190 ms

-100ms

-100ms

55 ms

Entrain site 7 Concealed fusion PPI = AT CL

198

Entrain site 5 Concealed fusion PPI = AT CL

8 RFs

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Catheter ablation of macroreentrant right and left atrial tachycardias

Figure 12.6 Characteristics of the atrial potential in the arrhythmogenic channel at the site of successful ablation in 40 macro–right ATs in 32 patients. Fractionated atrial potentials (squares) were recorded at only 11 sites (27%), while a single atrial potential (circles) was recorded at 14 (35%) sites and double atrial potentials (triangles) were recorded at 15 (38%) sites. A. Timing of the atrial potential within the arrhythmogenic channel (successful ablation site) relative to the onset of the next P wave. A “mid-diastolic” timing (preceding the P wave by 33–66% of the tachycardia

cycle length) was present at only 14 (35%) of the 40 sites. The atrial potential preceded the P wave by 0–33% of the tachycardia cycle length (“presystolic”) at 12 (30%) of the 40 sites, and the atrial potential occurred within the P wave (“systolic”) at 14 (35%) of the 40 sites. AT, atrial tachycardia; ECG, electrocardiogram. B. The bipolar voltage of the atrial potential within the arrhythmogenic channel ranged from 0.05 mV to 0.41 mV (median 0.15 mV). The voltage was very small (= 0.10 mV), mimicking a dense scar, at 15 (38%) of the 40 sites.

the P wave (Fig. 12.6). In addition, the atrial potentials at successful ablation sites within arrhythmogenic channels are variable in morphology and amplitude as well as timing relative to the P wave (Fig. 12.6) [1].

The use of entrainment pacing to select an ablation site in macro-AT has two major limitations. Entrainment pacing produces the identical atrial activation sequence and P wave (concealed fusion) with a post-pacing interval equal

Figure 12.5 (opposite) Double-loop macro–right AT in a 16-year-old girl who had undergone surgical repair of pulmonary valve stenosis at the age of 2 days and repair of atrial septal defect (ASD) at the age of 13 years. A–C. Activation maps during double-loop macro–right AT, cycle length (CL) 228 ms, in the right lateral projection (A), anteroposterior projection (B), and left anterior oblique (LAO) projection (C). A. In the right atrial free wall, activation is continuous (black arrow) around an area of conduction block formed by lines of double atrial potentials (pink tags), and propagates through a channel between the lines of double potentials and the inferior vena cava (IVC; channel width 1.8 cm, voltage 0.08 mV), with total activation time equal to the tachycardia cycle length (AT CL 228 ms). Entrainment pacing at four right atrial free wall sites (yellow tags, entrain sites 1–4) around the lines of double potentials produced concealed fusion with a post-pacing interval (PPI) equal to the tachycardia cycle length (PPI = AT CL), confirming macroreentry around the lines of double potentials. B, C. Activation is also continuous around the tricuspid annulus in the counterclockwise direction, as viewed in the LAO projection. Entrainment pacing in the subeustachian isthmus (yellow tag, entrain site 5) also produced concealed fusion with PPI = AT CL, confirming macroreentry around the tricuspid annulus and double-loop reentry. The two circuits have a common segment (width 4.2 cm) on the right atrial free wall between the lines of double potentials and the tricuspid annulus (white arrow in B). D. Two options were available for ablation for the double-loop macro–right AT. Ablation across the common segment (B) would eliminate both reentrant circuits. However, this segment was wide (width 4.2 cm) and the voltage was high (3.17 mV), suggesting potential difficulty in creating a continuous transmural lesion. It was elected to ablate two circuits

separately. Three radiofrequency (RF) applications were delivered across the channel between the lines of double potentials and the IVC. The tachycardia continued with the same cycle length. However, electrograms in the channel changed from a single atrial potential to two widely separated potentials. Entrainment pacing at site 6 (close to entrain site 2), posterior to the lines of double potentials, still produced concealed fusion, but the postpacing interval was 60 ms longer than the AT CL, confirming elimination of the right atrial free-wall loop. E. After ablation of the right atrial free-wall channel, entrainment pacing within the subeustachian isthmus (entrain site 7) still produced concealed fusion with PPI = AT CL, confirming continuation of reentry around the tricuspid annulus. Eight RF applications were delivered across the subeustachian isthmus, which terminated the tachycardia. F. Repeat right atrial map during proximal CS pacing, following ablation of both channels. The new activation times (measured from the CS pacing stimulus), represented by color superimposed over a gray shell (“re-map”), shows atrial activation propagating around a new line of conduction block formed by the original area of double potentials (pink tags) and the right atrial free-wall ablation line (brown tags). The area on the opposite side of the right atrial free-wall channel shows marked delay (purple area, 190 ms after the CS pacing stimulus) and a reversal in the direction of activation (anterior to posterior), confirming complete conduction block across the channel. Complete conduction block across the ablation line in the subeustachian isthmus is also demonstrated (late activation and reversal in the direction of activation). Recordings at sites that previously showed double atrial potentials continued to show double potentials (pink tags), consistent with fixed anatomical block. Programmed atrial stimulation failed to induce any other tachycardia.

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to tachycardia cycle length at many sites within the circuit in the large heterogeneous scar, but outside of an isolated arrhythmogenic channel. A single point ablation at these sites is unlikely to eliminate the tachycardia (Fig. 12.7). Successful ablation at that site would require creating an ablation line on each side of this site to a fixed anatomical obstacle (such as another scar, tricuspid annulus, or inferior vena cava). Another limitation is that entrainment pacing occasionally terminates the tachycardia or changes it to another tachycardia. Occasionally, the original tachycardia can not be reinduced. Since entrainment pacing is just confirmat-

A

Voltage map

2.43 mV

ory in the presence of a complete atrial map, we currently utilize entrainment pacing to confirm double-loop reentry (Fig. 12.5A) [13] or identify components of the reentrant circuit when the activation map does not exhibit a clear, single macroreentrant circuit. Multiple macro–right ATs are induced by stimulation or catheter manipulation during the ablation procedure in the majority of patients. Many of these tachycardias are unmappable (nonsustained, not reinducible, or changing atrial activation sequence). In 50 consecutive patients with macro–right ATs, a median of four atrial tachycardias was induced [1,2,14]. A single atrial tachycardia was induced

Activation map

B

190 ms

SVC

0.07 mV

-180 ms

Scar Entrain site 3 Concealed fusion PPI = AT CL + 146 ms

RF 2 (success) Entrain site 4

Entrain site 1

No capture

RF 1 (failed) RF 2 (success)

Entrain site 2

RF 1 (failed)

Concealed fusion PPI = AT CL

Figure 12.7 Limitation of entrainment pacing in identifying an isolated arrhythmogenic channel. A, B. Voltage map (A) and activation map (B) in the right anterior oblique (RAO) projection of a macro–right AT in a 47-year-old man who had undergone closure of an atrial septal defect at the age of 7 years. There is a very long isolated channel between the large upper dense scar (with line of conduction block, pink tags) and smaller lower dense scar (gray tags) extending to the inferior vena cava (IVC). Entrainment pacing at entrain site 1, which exhibited a low-amplitude, mid-diastolic atrial potential (C), resulted in concealed fusion (identical atrial activation sequence and P wave) and a post-pacing interval (PPI) equal to the atrial tachycardia cycle length (PPI = AT CL), suggesting an ideal ablation site. However, ablation at this site (RF 1) failed to terminate the tachycardia. The activation map and voltage map show that this site was located just beyond the exit of the isolated channel. Entrainment pacing at entrain site 2, just before the entrance to the isolated channel, also exhibited concealed fusion and PPI = AT CL. Entrainment pacing at entrain site 3, between the lines of block, produced concealed fusion, but the PPI was 146 ms longer than the AT CL, indicating a location within a “blind alley.” The site for the second RF application (RF 2) was selected from the activation and voltage maps to be located within the isolated channel.

200

Concealed fusion PPI = AT CL

IVC

Scar

1.0 cm

Although entrainment pacing at this site (entrain site 4) failed to capture atrial myocardium, the single RF application (RF 2) eliminated the tachycardia. (Adapted with permission from Circulation [1].) C. Electrograms recorded before RF 1 at entrain site 1 during the macro–right AT. The distal bipolar electrogram recorded at the site of RF 1 (ABLd) has a low amplitude (0.20 mV) and is recorded 126 ms (34% of the AT CL) before the onset of the P wave. Other tracings from the top are electrocardiography leads aVL, I, II, III, aVF, and V1, electrograms recorded from the high right atrium (RA), electrograms from the proximal bipolar electrodes of the ablation catheter (ABLp), and electrograms recorded from the coronary sinus (CSd–CS7). D. Electrograms recorded before RF 2 at entrain site 4. The bipolar electrogram recorded at the site of RF 2 (ABLd) has a low amplitude (0.16 mV) and is recorded 166 ms (45% of the AT CL) before the onset of the P wave. E. RF 2 at entrain site 4 resulted in immediate lengthening of the tachycardia cycle length, with termination of the tachycardia at 2.0 s after the onset of RF energy (20 W), despite the failure of entrainment pacing to capture the atrial myocardium at this site. The black arrows indicate the low-amplitude bipolar atrial potential recorded from the ablation catheter. Elimination of this potential (white arrow) was associated with termination of the tachycardia.

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Figure 12.7 (continued)

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Figure 12.8 Numbers of macro–right ATs induced during the ablation procedure in 50 consecutive patients (see text).

in only eight of the 50 patients (16%), while seven or more atrial tachycardias were induced in 14 patients (28%) (Fig. 12.8). Our strategy is to obtain a very high-density electroanatomical map during a stable macro-AT and ablate the arrhythmogenic channels involved in that tachycardia (resulting in termination of the tachycardia). Then, during either sinus rhythm or atrial pacing, we ablate all of the other potential arrhythmogenic channels (< 3.0 cm in width)

A

6.41mV RA-PA conduit Channel Channel 22 width width 1.8 1.8 cm cm voltage voltage 0.06 0.06 mV mV

Voltage MAP

SVC Scar

Ablation Ablation converts converts 44 scars scars into into 11 scar scar connected connected to to IVC+SVC IVC+SVC

6.41mV SVC

Voltage MAP Scar

0.04 mV

Scar

Scar (no potential) Double potentials Fractionated potential SVC, IVC

Scar 1.0 cm

Figure 12.9 The strategy for ablation of multiple unmappable macro–right ATs in a 36-year-old man following a Fontan procedure (the same patient as in Fig. 12.4). During the ablation procedure, two mappable and four unmappable (nonreproducible, nonsustained, or changing atrial activation sequences) ATs were induced. A single high-density electroanatomical map of the right atrium was obtained during one of the mappable macro–right ATs (Fig. 12.4). A. The voltage map identifies three arrhythmogenic channels

202

B

0.04 mV

Channel Channel 33 width width 1.9 1.9 cm cm voltage voltage 0.06 0.06 mV mV

Scar

Channel Channel 11 width width 1.5 1.5 cm cm voltage voltage 0.06 0.06 mV mV

identified on the original map (Fig. 12.9A) [1,2,14,15]. The location of the channels should be similar to the tachycardia during sinus rhythm or atrial pacing, since the channels are anatomically fixed (scar-induced) rather than functional, and due to the minimal contraction of the right atrial free wall (as a result of extensive scarring) during macro-AT and sinus rhythm (Fig. 12.5). Conduction block across each ablated channel is confirmed by obtaining a repeat electroanatomical map during atrial pacing on one side of the ablated channel and recording a reversal of activation on the opposite side (Fig. 12.5F). Ablation of all of the potential arrhythmogenic channels converts multiple scars into a single continuous scar connected to either the inferior vena cava or superior vena cava (Fig. 12.9), eliminating the substrate for unmappable as well as mappable macro–right ATs [1,14]. Testing for the inducibility of any remaining atrial tachycardias is performed after ablation of all potential arrhythmogenic channels. If a stable atrial tachycardia is induced, a repeat electroanatomical map during this tachycardia is recommended because a focal atrial tachycardia may also be present. The presence of a focal atrial tachycardia in combination with multiple macro–right ATs is most common in patients following a Fontan procedure. In patients with only unmappable macro–right ATs, we obtain a high-density electroanatomical map during atrial pacing or sinus rhythm, and then ablate all of the potential arrhythmogenic channels [1,14]. In 50 patients with

2 RFs

3 RFs

Scar

Scar

2 RFs

Scar (no potential) Double potentials Fractionated potential SVC, IVC

IVC

Scar

Ablation site

(width 1.5–1.9 cm and voltage 0.06 mV). IVC, inferior vena cava; RA-PA, right atrium-pulmonary artery; SVC, superior vena cava. B. Radiofrequency (RF) ablation across channel 1 (two RFs), channel 2 (three RFs), and channel 3 (two RFs) connected four separate dense scars into a single dense scar connected to both the superior vena cava (SVC) and inferior vena cava (IVC), eliminating all arrhythmogenic channels. Programmed atrial stimulation following ablation failed to induce any form of atrial tachycardia.

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Catheter ablation of macroreentrant right and left atrial tachycardias

A Activation (a) Activation MAP MAP

B Voltage (b) Voltage MAP MAP

146 ms

SVC

Pacing

Double potentials

4 ms

≥ 2.5 mV

≤ 0.10 mV

5.0 cm

TA

IVC

1.0 cm RAO projection

RAO projection

Right lateral projection

Figure 12.10 Activation map (A) and voltage map (B) during right atrial pacing in a 33-year-old man following surgical repair of tetralogy of Fallot (at the age of 14) without “postoperative right atrial myopathy” or macro–right AT. The patient was undergoing catheter ablation of both supraventricular tachycardia (found to be atrioventricular nodal reentrant tachycardia) and ventricular tachycardia. A. The atrial activation sequence during pacing from the right atrial free wall is normal, with no sites of

significant conduction block. IVC, inferior vena cava; RAO, right anterior oblique (projection); SVC, superior vena cava; TA, tricuspid annulus. B. The bipolar voltage in the right atrium is preserved, and the two right atrial scars are small (pink tags). The large distance (5.0 cm, white arrow) and high voltage between the two small scars explain the absence of substrate for macro–right AT (“no channel, no macroreentry”).

macro–right AT associated with different forms of heart disease, 60 stable mappable macro–right ATs were induced in 47 of the 50 patients and 123 unmappable macro–right ATs were induced in 35 of the 50 patients. An arrhythmogenic channel was identified and ablated in all 60 mappable macro–right ATs. After ablation of all potential arrhythmogenic channels, post-ablation testing induced only 21 of the 123 unmappable macro–right ATs, in 14 of the 50 patients. During the follow-up period (6–97 months, median 56 months), atrial tachycardia recurred in only five of the 50 patients (10%). It is important to note that patients with macro–right AT following atriotomy do not simply have a discrete linear scar at the site of the atriotomy surrounded by relatively normal atrial myocardium (bipolar voltage > 1.0 mV). In our experience, all of these patients have a large area of markedly reduced voltage (< 0.5 mV) in the right atrial free wall. The etiology of this “atrial myopathy” is unclear. Possible explanations include interruption of the right atrial arterial supply and/or insufficient protection of the right atrial free wall during cardioplegia. The tachycardia frequently develops 10 or more years after surgery, suggesting that remodeling may play a role in creating

the substrate for macroreentry. The “atrial myopathy” is not present in all patients who have undergone right atriotomy (Fig. 12.10; i.e., no channel, no macroreentry). In patients with macro–right AT, the decrease in voltage is less severe along the septum than on the right free wall. In 21 patients with previous atrial septal defect (ASD) closure, reentry confined within the septum (or around the ASD patch) was not observed (Fig. 12.11) [1,16]. An arrhythmogenic channel may not be created on the septum due to the relatively large distance (usually > 3.0 cm) between the ASD patch and the closest area of conduction block (the tricuspid annulus, crista terminalis, or inferior vena cava) and the preserved voltage.

Macroreentrant left atrial tachycardia The substrate for macroreentrant left atrial tachycardia (macro–left AT) differs significantly from that of macro– right AT [2,15,17,18]. The pulmonary veins (PVs) provide additional anatomical obstacles in the left atrium, frequently supporting double-loop reentry with circuits around the right or left PVs and around the mitral annulus 203

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A

Activation Activation Map Map

Free-Wall

115 ms

B

SVC

-155 ms

Free-Wall

Channel 3 2 RFs

Voltage Voltage Map Map 4.49 mV

C

Septum

0.04 mV Channel 2 3 RFs

Septum

3.7 cm

IVC

Right lateral projection

RF 1

Right lateral projection

Channel 1 2 RFs

PA projection

1.0 cm

Figure 12.11 Comparison of the voltage abnormality between the atrial septum and right atrial free wall in a 40-year-old woman who had undergone repair of an atrial septal defect (ASD) at the age of 27. A. Activation map (right lateral projection) during a macro–right AT, showing propagation through a long channel bounded inferiorly and posteriorly by a dense scar continuous with the inferior vena cava (IVC; gray tags) and continuous with a line of conduction block (double potentials, pink tags). The channel is bounded anteriorly by another line of conduction block (pink tags). This tachycardia was terminated by a linear radiofrequency (RF) application (8 mm in length) across the channel near its entrance (RF 1). One extra RF application was delivered at the same site. Following ablation, this tachycardia could not be reinduced, but six other atrial tachycardias were induced, which were either nonsustained or could not be reinduced (unmappable). Ablation was then carried out across two other channels (channels 2 and 3 in B) located between other lines of block on the free wall, which were identified from the activation and voltage maps obtained

during the original tachycardia. Following ablation of the three channels on the free wall, programmed atrial stimulation failed to induce any form of atrial tachycardia. SVC, superior vena cava. B. Voltage map of the right atrial free wall during the macro–right AT. Voltage is very low (red–orange) across almost all of the free wall (diffuse scar) with multiple lines of double potentials (pink tags) and a dense scar (gray tags). C. Voltage map of the septum. In comparison with the free wall, the voltage on the septum is greater and fractionated, or double atrial potentials are less frequent. The septum exhibited an area of double potentials in the region of the fossa ovalis (site of the ASD repair). However, the distance between the ASD repair and the closest area of block near the IVC is 3.7 cm. Since all of the atrial tachycardias were eliminated by ablation of the three channels on the free wall, it is unlikely that this area of double potentials is able to support macroreentry. (Adapted from [1] with permission from Lippincott, Williams and Wilkins.)

(Fig. 12.12), around the right PVs and around the left PVs, or two separate circuits around the PVs and the mitral annulus (Fig. 12.13). The arrhythmogenic channels in macro–left AT are wider and have greater bipolar voltage, suggesting thicker atrial myocardium (Table 12.2, Fig. 12.12B). Creating a continuous transmural lesion across left atrial channels requires a greater number of RF applications, often with greater RF power (Table 12.2, Fig. 12.12B). Currently, we use a saline-irrigated electrode (NaviStar ThermoCool, Biosense Webster, Inc.) for ablation in the left atrium to maintain adequate RF power (in low bloodflow areas) and minimize thrombus formation at the electrode–tissue interface to reduce the risk of a thromboembolic event [19–22]. Ablation is guided by electrogram attenuation. RF energy is delivered beginning at 20–25 W. The RF power is increased in 5-W increments until the unfiltered unipolar electrogram recorded from the ablation

tip electrode shows a decrease of more than 80% in the atrial potential amplitude and/or atrial potential splits into two low-amplitude potentials, consistent with transmural necrosis (Fig. 12.14) [23]. In order to prevent a steam pop, which could perforate the left atrial wall, we limit RF power to 35 W when the catheter tip is orientated perpendicular to the endocardium. It is common to induce at least one unmappable macro–left AT. Unlike macro–right AT, the arrhythmogenic channels of the unmappable ATs may not be apparent on a map obtained during another tachycardia or during atrial pacing, because reentry may be occurring around the PVs or mitral annulus rather than through a narrow, low-voltage channel. Empirically creating continuous transmural linear lesions between the PVs and the mitral annulus or between the right and left PVs may be difficult due to the longer distance and higher voltage than

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A 130 ms

Double-loop reentry

LSPV

Activation MAP

RSPV

Wide arrhythmogenic channel

Double potentials

≤ 0.10 mV

Left atriotomy

Fractionated potential

RIPV

Voltage MAP

RSPV

- 120 ms

AT CL 250 ms

≥ 3.0 mV

LSPV

Double potentials Fractionated potential Ablation

RIPV Mitral annulus

Left atriotomy (Waterston incision)

Mitral annulus

1.0 cm

AP projection

Annular suture site

1.0 cm

width 4.1 cm voltage 0.76 mV 41 RFs

Annular suture site

Figure 12.12 Double-loop macroreentrant left atrial tachycardia (macro–left AT) with a wide common arrhythmogenic channel in a 70-year-old man, 4 years after mitral valve repair. A. Activation map of the left atrium in the anteroposterior (AP) projection. A line of conduction block (pink tags) is present in front of the right pulmonary veins (left atriotomy, Waterston incision). A second line of block is located around the septal aspect of the mitral annulus (pink tags). Activation propagates around the right pulmonary veins (PVs) in the clockwise direction and around the mitral annulus in the counterclockwise direction. Both circuits have the same activation time (250 ms), which is identical to the atrial tachycardia cycle length (AT CL), confirming double-loop reentry. Both circuits share the same

wide arrhythmogenic channel located between the lines of conduction block in front of the right PV and adjacent to the mitral annulus. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, orifice of the right superior pulmonary vein. B. The voltage map shows relatively preserved left atrial voltage, except for the regions around the two lines of conduction block and the septal region. The common channel on the septum was wide (4.1 cm), with relatively high voltage (0.76 mV). Ablation across this channel, requiring 41 radiofrequency applications using a nonirrigated ablation electrode, terminated the tachycardia and prevented its reinduction. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, orifice of the right superior pulmonary vein.

the arrhythmogenic channels in the right atrium. In addition, incomplete linear lesions may create new arrhythmogenic channels and new macro–left ATs [24,25]. The difficulty in ablating potential arrhythmogenic channels in the left atrium is probably a major factor in the higher recurrence rate of macro–left AT than macro–right AT (Table 12.2). In 50 patients with macro–left AT associated with either prior left atriotomy (10 patients), prior catheter or surgical ablation atrial fibrillation (18 patients), or without prior left atriotomy or catheter ablation (22 patients), 82 stable mappable macro–left ATs were induced in 49 of the 50 patients and 169 unmappable macro–left ATs were induced in 49 of the 50 patients. An arrhythmogenic channel was identified and ablated in all 82 mappable macro–left ATs. After ablation of all identified arrhythmogenic channels, post-ablation testing induced only 18 of the 169 unmappable macro–left ATs, in only 16 of the 50 patients. During the follow-up period (1–92 months, median 42.5 months), atrial tachycardia recurred in 10 (20%) of the 50 patients (Table 12.2).

to 10 or more years for macro–right AT following surgical repair of congenital heart disease. The left atriotomy is usually placed just anterior to the right PVs (Waterston incision), creating a line of conduction block in front of the right PVs. This line of conduction block forms an anchor for reentry around the right PVs, through wide channels with relatively high voltage (little scarring, Fig. 12.12). In eight patients studied, at least one arrhythmogenic channel was bounded by the line of conduction block in front of the right PVs and either the mitral annulus suture site (Fig. 12.12) or another scar between this line of block and the mitral annulus (Fig. 12.13). A total of 10 macro–left ATs were mapped in the eight patients: 1) single-loop reentry propagating around the right PVs in three ATs; 2) single-loop reentry propagating around the mitral annulus in three ATs; and 3) double-loop reentry with one circuit propagating around the right PVs and the other circuit extending around the mitral annulus in four ATs (Fig. 12.15A) [15,18].

Macro–left AT following left atriotomy

Macro–left AT following catheter and surgical ablation of atrial fibrillation

Macro–left AT following left atriotomy for mitral valve surgery usually begins 2–5 years after surgery, compared

Macro–left AT may result from arrhythmogenic channels created during catheter ablation of atrial fibrillation (AF). 205

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A 3.81 mV

Channel 1 width 1.6 cm voltage 0.39 mV

Voltage Voltage MAP

LSPV

RSPV

230 ms

AT # 1 CL 430 ms

LSPV

4 RFs

RSPV

-200 ms

0.04 mV

Double potentials

Left atriotomy (Waterston Incision) Channel 2 width 2.1 cm voltage 0.39 mV

Mitral annulus

Fractionated potential

Mitral annulus Left atriotomy (Waterston Incision)

1.0 cm

AP projection

C

1.0 cm

AP projection

Double potentials Fractionated potential Ablation

170 ms

AT # 2 CL 270 ms

LAA

Activation MAP

-100 ms

RSPV

Double potentials Fractionated potential Ablation

Mitral annulus Left atriotomy (Waterston Incision)

4 RFs

AP projection

1.0 cm

Figure 12.13 Macro–left atrial tachycardias (ATs) in a 54-year-old woman with rheumatic heart disease, 4 years after mitral and aortic valve replacement. A. Voltage map of the left atrium in an anteroposterior (AP) projection, recorded during the first macro–left AT, showing extensive scarring (markedly low voltage, red) with large areas of conduction block (double potentials, pink tags) and fractionated atrial potentials (olive tags), involving almost all of the septum and anterior wall. The areas of conduction block form two long arrhythmogenic channels (channel 1 and channel 2). LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein. B. Activation map during the first macro–left atrial tachycardia (AT #1) with a cycle length (CL) of 430 ms. Activation propagates around the right pulmonary veins (clockwise direction) and through channel 1 between the left atriotomy scar

and the area of block (pink tags) on the anterior wall. Four radiofrequency applications across channel 1 terminated AT #1. LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein. C. Programmed atrial stimulation after ablation of atrial tachycardia no. 1 (AT #1) induced a second macro–left AT (AT #2), with a cycle length (CL) of 270 ms. The activation map shows reentry around the mitral annulus in the counterclockwise direction through channel 2. Four radiofrequency applications across channel 2 terminated AT #2. Programmed atrial stimulation after ablation across channel 2 failed to induce any atrial tachycardia. It should be noted that the activation map during AT #2 confirms conduction block across channel 1 at the previous ablation site. AP, anteroposterior; LAA, left atrial appendage; RSPV, right superior pulmonary vein.

Macro–left AT was inducible after (but not before) segmental isolation of the PV ostia in 9–10% of patients [26,27]. These patients generally had other scars in the left atrium that contributed to the arrhythmogenic channels. Some of these macro–left ATs have a very short cycle length (160–200 ms), mimicking AF (Fig. 12.16).

Most of the recent AF ablation approaches extend the ablation lesions posteriorly outside the PV ostia (to the PV antrum), and some approaches include left atrial linear lesions [28,29]. The inducibility of macro–left AT has increased (more than 30%) with these approaches for two reasons. First, the larger areas of conduction block

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Figure 12.14 Use of atrial potential attenuation during radiofrequency (RF) application to identify achievement of transmural necrosis. Recordings from the left atrial (LA) ablation catheter are the proximal (Bip 3–4) and distal (Bip 1–2) bipolar electrograms and the unfiltered (1–500 Hz) unipolar electrograms from the second electrode (Uni 2) and ablation tip electrode (Uni 1). A. Recordings before ablation show a large single atrial potential in the distal bipolar and unipolar electrograms. B. During RF application at 25 W, the atrial potential amplitude in the distal unipolar electrogram has decreased by 80% (first arrow) and a second potential is beginning to emerge. C. Later in the RF application (30 W), the distal unipolar electrogram shows two low-amplitude atrial potentials (split potentials), consistent with transmural necrosis at the ablation site.

produced by PV antrum isolation facilitates reentry around the PVs and mitral annulus (Fig. 12.17). Second, the absence of complete conduction block in either the PV isolation lesions or linear lesions creates multiple narrow arrhythmogenic channels that support smaller and more complex macroreentrant circuits. In our experience, the “carina” between the superior and inferior PVs often provides the arrhythmogenic channel for a small macroreentrant circuit (reentry around one PV, Fig. 12.18). Complete PV antrum isolation may prevent many of the small macroreentrant circuits [30]. In contrast, these small macroreentrant circuits appear to occur more frequently when the criterion for successful circumferential ablation is a reduction in voltage within the ablated region rather than complete PV antrum isolation (either no potential or dissociated atrial/PV potentials) [28,29]. For single-loop (large circuit) macro–left AT propagating around either the right PVs, left PVs, or mitral annulus, a relatively long linear lesion is required between the isolated PVs (or PV antrum) and the mitral annulus. For reentry around the right PVs, the linear lesion between the isolated right PVs and the mitral annulus is usually created along the anterior wall (Fig. 12.15C). This ablation line is created anterior to the His bundle to avoid AV block. This line is sometimes difficult to create due to the relatively long length and higher voltage close to Bachmann’s bundle. Another limitation in creating this ablation line is the difficulty in maneuvering an ablation catheter close to the transseptal site. After ablation, complete conduction block between the right PVs and mitral annulus can be confirmed by a repeat left atrial map during proximal coronary sinus (CS) pacing (Fig. 12.15C).

For reentry around the left PVs, the linear lesion is usually created between the isolated left inferior PV and the mitral annulus, an area referred to as the “mitral isthmus” or “left atrial isthmus” [24]. This ablation line is also long and may have to be created through regions of high voltage close to the left atrial appendage. The greatest difficulty is creating complete block near the mitral annulus due to conduction over the CS myocardium, which is connected to the left atrium on both sides of the ablation line. Ablation within the CS may help achieve complete conduction block. However, there is a small risk of injury to the left circumflex coronary artery by ablation within the CS [31,32]. Placing the ablation line more superiorly within the mitral isthmus reduces the likelihood of CS myocardium close to the mitral annulus, but this region of the mitral isthmus usually has greater voltage, which often correlates with greater difficulty in producing transmural lesions. Alternative locations for the linear lesion include: 1) between the isolated left PVs and isolated right PVs; and 2) along the anterior wall between the left superior PV and mitral annulus, septal to the left atrial appendage. For reentry around the mitral annulus, any of the linear lesions described above between the left or right PVs and the mitral annulus can be used. Selection of the location of the ablation line is based on shorter length, lower voltage, areas of block from prior ablation, location of the CS myocardium, and ease of catheter manipulation in that region. For double-loop reentry around the mitral annulus and either the right PVs or left PVs, a linear lesion between the isolated PVs and the mitral annulus eliminates both circuits of the macro–left AT. For double-loop reentry around the right PVs and around the left PVs, a linear lesion between the isolated right PVs and left PVs will eliminate this tachycardia (Fig. 12.17). The choice between a superior location for the ablation line (connecting the right and left superior PVs, Fig. 12.17) or an inferior/ posterior location (connecting the right and left inferior PVs) is based on shorter length, lower voltage, and the location of the esophagus (to reduce the risk of a left atrioesophageal fistula) [33]. Creating a transmural necrosis is generally easier on the posterior left atrial wall than the anterior or superior left atrium. Using a 3.5-mm saline-irrigated electrode, transmural necrosis in the posterior wall, identified by electrogram attenuation (Fig. 12.14), is often achieved using RF power of ≤ 35 W. We generally limit RF power to 20–25 W at sites close to the esophagus. Linear ablation between the isolated right and left PVs may facilitate macroreentry around the mitral annulus. Similarly, linear ablation between the mitral annulus and either the isolated right or left PVs may facilitate macroreentry around the left or right PVs, respectively. Therefore, the creation of two linear ablation lines is recommended 207

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A

Single-loop macroreentrant left AT Around right PVs Line of block

Around mitral annulus

Around left PVs LAA

LS

Small circuit LS

LS

RS

LI

LI

LI

RI Line of block

Mitral annulus LAO projection

AP projection

Post left atriotomy (n=10)

3

0

3

0

Post AF ablation (n=18)

3

4

1

4

No surgery or no ablation (n=24)

5

3

5

2

B

Double-loop macroreentrant left AT Around right PVs and mitral annulus

Around left PVs and mitral annulus

Line of block

Around right PVs and mitral annulus

LS

LS RS

RS

LI LI LI

RI

RI Mitral annulus AP projection

Line of block LAO projection

PA projection

Post left atriotomy (n=10)

4

0

0

Post AF ablation (n=18)

4

1

1

No surgery or no ablation (n=24)

5

1

3

Figure 12.15 Schematic representation of the location of the macroreentrant circuits in 52 mapped macro–left atrial tachycardias (ATs) in 38 patients. A. Single-loop macroreentrant circuits. B. Double-loop circuits. Of the 10 macro–left ATs (in eight patients) following left atriotomy, the arrhythmogenic channel was bounded by the left atriotomy scar, located in front of the right pulmonary veins (PVs), with the circuit extending around the right PVs in three ATs, around the mitral annulus in three, and in a double loop around the right PVs and around the mitral annulus in four. Twelve of the 18 macro–left ATs in 13 patients with previous catheter ablation (12 patents) or surgical ablation (one patient) of atrial fibrillation (AF) were single-loop reentry. The circuit extended around the right PVs in three ATs, left PVs in four, and around the mitral annulus in one AT. A small complex reentrant circuit propagating through the carina (between the superior and inferior PVs) and around one PV produced three ATs in patients following catheter ablation of AF (see Fig. 12.18). A small complex reentrant

circuit between the left inferior pulmonary vein and mitral annulus produced AT in one patient following surgical AF ablation (see Fig. 12.19). Six of the 18 ATs had double-loop reentry, which propagated around the right PVs and around the mitral annulus (four ATs), around the left PVs and around the mitral annulus (one AT) and around the right PVs and left PVs (one AT). Of the 24 macro–left ATs in 17 patients without prior left atriotomy or catheter ablation, 15 ATs were single-loop around the right PVs (five ATs), around the left PVs (three ATs), around the mitral annulus (five ATs), or associated with a small complex reentrant circuit (two ATs). The remaining nine macro–left ATs were double-loop reentry, which propagated around the right PVs and around the mitral annulus (five ATs), around the left PVs and around the mitral annulus (one AT), and around the right PVs and left PVs (three ATs). AP, anteroposterior; LAO, left anterior oblique; LI, left inferior; LS, left superior; PA, posteroanterior; RI, right inferior; RS, right superior.

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A

B

AT CL 160 ms

C

Activation MAP

post-ablation Verification of conduction block postablation

60 ms

74 ms

LSPV

RSPV

RSPV

LSPV

Bachmann’s bundle region

- 100 ms

12 ms

LAA RIPV

Mitral annulus

LAA

RIPV HB

Mitral annulus Double potentials Ablation

Double potentials

1.0 cm

AP projection

Figure 12.16 Rapid macro–left atrial tachycardia (AT) in a 53-year-old woman following catheter ablation of atrial fibrillation (AF) (pulmonary vein segmental isolation). A. Twelve-lead electrocardiography of the rapid macro–left AT, simulating AF. B. Activation map during macro–left AT with a cycle length (CL) of 160 ms in the anteroposterior (AP) projection. Activation propagates around the right pulmonary veins (PVs) (clockwise direction) and through the channel between the isolated right PVs (double potentials, pink tags) and the mitral annulus. Linear ablation across the channel (shown in C) terminated tachycardia. LAA, left atrial appendage;

Pacing LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. C. Activation map following ablation and during left atrial pacing from the proximal coronary sinus. Above the ablation line, activation occurred in the superior-to-inferior direction (blue to purple), confirming complete conduction block across the ablation line (brown tags). HB, bundle of His; LAA, left atrial appendage; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

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A

100 ms

AT CL 200 ms

B

110 ms

RFA1-A7 RFA1 Term AT

LSPV

LSPV

RSPV

RSPV 15 ms

-100 ms

RIPV LIPV

RIPV LIPV Scar (no potential) Double potentials

Scar (no potential) Double potentials

RF B1-B12

Ablation

RF B1-B12

Ablation

1.0 cm

PA projection

Pacing

LPO projection

C

1.0 cm

150 ms

LSPV

RSPV 115 ms

RIPV LIPV Scar (no potential) Double potentials Ablation

RF B1-B19

Pacing

LPO projection Figure 12.17 Incessant double-loop macro–left atrial tachycardia (AT) in a 47-year-old man following two catheter ablation procedures for atrial fibrillation (pulmonary vein segmental isolation). A. Activation map in a posteroanterior (PA) projection, demonstrating double-loop macro–left AT with a cycle length (CL) of 200 ms, with reentry around the right pulmonary veins (PVs) in the clockwise direction and around the left PVs in the counterclockwise directions (bold black arrows), using a common channel in the posterior left atrium between the right and left PVs. One radiofrequency application (RFA1) in the center of the common channel terminated the tachycardia. Six additional RF applications were delivered across the channel to produce complete conduction block. Programmed atrial stimulation then induced two unmappable ATs. Another ablation line was created during coronary sinus pacing between the mitral annulus and a line of double atrial potentials extending inferiorly from the isolated left inferior pulmonary vein (LIPV) using 12 RF applications (RF B1–B12). It should be noted that the PV potentials were recorded in the right superior (RSPV), right inferior (RIPV), and left superior (LSPV) pulmonary veins. Only the left inferior pulmonary

210

1.0 cm

vein (LIPV) was isolated. B. Activation map following radiofrequency (RF) application B12, during left atrial pacing from the posterolateral coronary sinus in the left posterior oblique (LPO) projection. Conduction (black arrows) was occurring across the ablation line (brown tags) and across the original line of double atrial potentials (pink tags) extending inferiorly from the isolated left inferior pulmonary vein (LIPV). Seven additional RF applications were delivered across the areas of conduction. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. C. Activation map following radiofrequency (RF) application B19, during left atrial pacing from the same site in the posterolateral coronary sinus (CS). Activation above the ablation line is now occurring in the superior-to-inferior direction with the late activation (purple area, 150 ms after the CS pacing stimulus), confirming complete conduction block across the ablation line (mitral isthmus). Programmed atrial stimulation then failed to induce any atrial tachycardia. LIPV, left inferior pulmonary vein; LPO, left posterior oblique; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

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Catheter ablation of macroreentrant right and left atrial tachycardias B

>2.8 mV

AT#1 (CL 310 ms)

105 ms

AT#1 (CL 310 ms)

Voltage MAP

LSPV

LSPV-LIPV carina

RSPV

LSPV

- 205 ms

<0.1 mV

RSPV Double potentials Fractionated potential Scar (no potential)

RIPV Channel Channel #1 #1 2.5 2.5 cm cm 1.48 1.48 mV mV 33 RFs RFs 30-35 30-35 watts watts (irrigated (irrigated electrode) electrode)

RIPV LIPV 1.0 cm

PA projection C

LIPV 1.0 cm

LPO projection

Double potentials Fragmented potential Scar (no potential) Ablation

260 ms

AT#2 (CL 370 ms) 1 RF

Entrain site 1 concealed fusion PPI=ATCL + 50

LSPV

- 110 ms

RSPV RIPV

Entrain site 2 concealed fusion PPI=ATCL + 50 1.0 cm

LIPV

LPO projection

Figure 12.18 Incessant small-circuit macro–left atrial tachycardia (AT) in a 45-year-old woman, 13 months after the second catheter ablation procedure for atrial fibrillation. The first procedure was pulmonary vein (PV) segmental isolation and the second was wide circumferential ablation with left atrial linear lesions. A. Voltage map in a posteroanterior (PA) projection during incessant AT (AT#1) shows markedly low voltage (red, < 0.1 mV) with double atrial potentials (pink tags) and fractionated atrial potentials (olive tags) in a large area surrounding the PVs and between the right and left PVs. PV potentials were recorded in all four PVs, indicating incomplete PV isolation. CL, cycle length; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. B. Activation map in a left posterior oblique (LPO) projection during atrial tachycardia no. 1 (AT#1) with a cycle length (CL) of 310 ms, demonstrating a small circuit propagating through the carina between the left superior pulmonary vein (LSPV) and left inferior pulmonary vein (LIPV) and around the LIPV (bold black arrows). Ablation between the line of conduction block at the anterior margin of the LIPV and the mitral annulus (width 2.5 cm, greatest voltage 1.48 mV) using three radiofrequency (RF) applications with a saline-irrigated electrode (30–35 W) lengthened the tachycardia cycle length to 370 ms and changed the local

Double potentials Fragmented potential Scar (no potential) Ablation

atrial activation sequence (AT#2). RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. C. Activation map during atrial tachycardia no. 2 (AT#2) shows continuing activation through the carina and now around the left superior pulmonary vein (LSPV; bold black arrows). Entrainment pacing with a cycle length (CL) of 355 ms on both sides of the carina (entrain site 1 and entrain site 2) produced the same atrial activation sequence as the tachycardia (concealed fusion). The post-pacing interval (PPI) was the same at both sites (50 ms longer than the tachycardia cycle length), indicating that both sites were within (or equally close to) the reentrant circuit, confirming conduction across the carina as the arrhythmogenic channel. The 50-ms delay in the post-pacing interval probably resulted from the 15-ms shorter pacing cycle length in comparison with the tachycardia cycle length. A single radiofrequency (RF) application on the carina terminated AT#2. One additional RF application was delivered within the carina, producing complete conduction block between the LSPV and left inferior pulmonary vein (LIPV). Another linear lesion was created on the superior left atrium between the right superior pulmonary vein (RSPV) and LSPV to prevent macroreentry around the right PVs. LPO, left posterior oblique; RIPV, right inferior pulmonary vein.

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(between the right and left PVs and between the mitral annulus and the right or left PVs, Fig. 12.17). Smaller and complex macroreentrant circuits may not be eliminated by the empiric use of the two linear ablation lines described above. For example, in the patient shown in Fig. 12.18, the initial macroreentrant circuit propagated around the left inferior PV. The carina between the left superior PV and left inferior PV formed the arrhythmogenic channel. Ablation between the left inferior PV and

1.30 mV

Voltage MAP

A

the mitral annulus (mitral isthmus ablation line) converted the initial macro–left AT to a second macro–left AT propagating around the left superior PV and through the carina. A single RF application on the carina (arrhythmogenic channel) eliminated the second tachycardia. Focal left atrial tachycardia also occurs following AF ablation [25]. The most common sites for these focal atrial tachycardias are the region anterior to the right PVs (septum or anterior wall) and the roof of the left atrium septal

B

Activation MAP (AT CL 220 ms) RSPV

LSPV

LSPV

RSPV ≤ 0.10 mV

LIPV

RIPV

LIPV

Double potentials Fractionated potential

1.0 cm

PA projection

No potential or dissociated potentials

Figure 12.19 Incessant small-circuit macro–left atrial tachycardia (AT) in a 36-year-old man 22 months after surgical ablation of atrial fibrillation (Cox maze III) and 11 months after an unsuccessful attempt at catheter ablation of the AT using two empirical linear left atrial lesions between the left inferior pulmonary vein (LIPV) and mitral annulus (mitral isthmus) and between the right superior pulmonary vein (RSPV) and mitral annulus. A. Voltage map in a posteroanterior (PA) projection during incessant AT shows no potentials or dissociated potentials (gray tags) in any of the four pulmonary veins (PVs) or most of the posterior left atrium surrounding the PVs. The remaining left atrium exhibited markedly low voltage (red, < 0.1 mV) with double atrial potentials (pink tags) and fractionated atrial potentials (olive tags). LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein. B. Activation map in a left anterior oblique (LAO) projection during AT with a cycle length (CL) of 220 ms, showing activation originating in the narrow band between the isolated left inferior pulmonary vein (LIPV) and the mitral annulus and propagating around the mitral annulus in both the clockwise and counterclockwise directions. This pattern excludes macroreentry around the mitral annulus and, without higher-density mapping, suggests a focal pattern of atrial activation. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein. C. Higher-density mapping in a left posterior oblique (LPO)–caudal projection within the markedly low-voltage area below the left inferior pulmonary vein (LIPV)

212

Mitral annulus LAO projection identified a small macroreentrant circuit around a line of double potentials (white line with pink tags). The AT was terminated by the first radiofrequency application (RF #1) delivered within the narrow channel (1.5 cm, voltage only 0.05 mV) between the line of double potentials and a small scar adjacent to the mitral annulus. Three additional RF applications were delivered, producing complete conduction block across the channel. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. D. Recordings during atrial tachycardia at the site of radiofrequency application no.1 (RF#1; LA-Map), showing extremely low bipolar voltage (0.05 mV, arrows). During tachycardia at a cycle length of 220 ms, a 2 : 1 conduction block was present between the left atrium and right atrium (right atrial cycle length 440 ms). The absence of atrial potentials in the lateral coronary sinus (CSd to CS6) should be noted. HB, His bundle region; RAA, right atrial appendage; TA, electrograms around the tricuspid annulus. E. Electrograms recorded during radiofrequency application no. 1 (RF#1). The tachycardia cycle length increased to 270 ms and then 280 ms, followed by termination of the atrial tachycardia. It should be noted that the increase in the left atrial cycle length resulted in 1 : 1 conduction from the left atrium to the right atrium. CS, coronary sinus; HB, His bundle region; LA, left atrial; RAA, right atrial appendage; TA, electrograms around the tricuspid annulus.

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C

115 ms

LSPV

RSPV LIPV

- 105 ms

RIPV Mitral annulus RF #1

1.0 cm

LPO-caudal projection

Double potentials Fractionated potential No potential or dissociated potentials Ablation

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to the left superior PV. We obtain a high-density left atrial map during a stable tachycardia because of the possibility of a focal left atrial tachycardia or a small complex macroreentrant circuit. These two forms of tachycardia would not be expected to be eliminated by an empiric ablation line between the right PVs and left PVs or between the mitral annulus and either the right or left PVs. Similarly, reentry around the right PVs will not be eliminated by an empiric linear lesion across the mitral isthmus. Macro–left AT occurs in some patients following surgical ablation of AF. Unlike patients with macro–left AT following catheter ablation, the posterior left atrial wall and PVs are isolated following the Cox maze operation (Fig. 12.19). Macroreentry most commonly propagates around the mitral annulus due to recovery of the surgical lesion extending to the mitral annulus. However, a small complex macroreentrant circuit may be present and an empiric ablation line between the isolated area (posterior wall and PVs) and the mitral annulus will fail to eliminate the tachycardia (Fig. 12.19).

with any form of structural heart disease, and may even occur in patients without apparent structural heart disease. The areas of low voltage, sites of conduction block and the locations of the macroreentrant circuits are similar to (and often indistinguishable from) those found in patients with prior left atriotomy or catheter ablation (Fig. 12.20). The approach to mapping and ablation is the same. Ablation of macro–left AT is most difficult in patients with hypertrophic cardiomyopathy. Creating transmural necrosis often requires a greater number of RF applications and higher RF power, consistent with thicker left atrial myocardium (Fig. 12.21). When a nonirrigated electrode is being used, the higher RF power and greater number of RF applications may be associated with a higher incidence of thrombus formation at the electrode–tissue interface.

References 1 Nakagawa H, Shah N, Matsudaira K, et al. Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channel between scars allow “focal” ablation. Circulation 2001;103:699 –709. 2 Nakagawa H, Matsudaira K, Beckman K, et al. Anatomical differences between right and left macroreentrant atrial tachy-

Macro–left AT in patients without prior catheter ablation or surgery in the left atrium Macro–left AT may occur in patients without prior catheter ablation or surgery in the left atrium, but with left atrial scarring. The left atrial scarring may be associated

A

B 2.81 mV

Scar

Channel width 2.0 cm voltage 0.24 mV

Voltage MAP

LAA RSPV

0.04 mV

LSPV

RSPV

AT CL 405 ms Scar LAA

205 ms

Activation MAP - 200 ms

LSPV

3 RFs

Double potentials Fragmented potential Scar (no potential)

Scar (no potential)

Ablation

RIPV

Double potentials Fragmented potential

RIPV AP projection

1.0 cm

Mitral annulus

Figure 12.20 Macro–left atrial tachycardia (AT) in a 79-year-old woman with restrictive cardiomyopathy. A. Voltage map in an anteroposterior (AP) projection during AT shows very low voltage over almost all of the left atrium (except the left atrial appendage, LAA) with areas of double potentials (pink tags), fractionated potentials (olive tags), and no potential (gray tags). LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; B. Activation map in an anteroposterior (AP) projection during atrial tachycardia (AT) with a cycle length (CL) of 405 ms, showing reentry around the right pulmonary veins

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Mitral annulus

AP projection

1.0 cm

(PVs) and through a channel between the area of double atrial potentials in front of the right PVs and an area of double potentials and dense scar on the anterior wall. The location of this channel is similar to that seen in patients with macro–left AT following left atriotomy. Extensive scarring results in late activation around the mitral annulus in the counterclockwise direction (“blind alley”). Three radiofrequency (RF) applications were delivered across the channel, terminating the tachycardia and producing complete conduction block. LAA, left atrial appendage; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

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A

LSPV

AT CL 230 ms

RSPV

130 ms

Activation MAP

LAA

LSPV

AT CL 230 ms

RSPV

≥ 3.0 mV

Voltage MAP

LAA

- 100 ms

0.09 mV

RIPV

LIPV

LIPV 1.0 cm

1.0 cm

RIPV

Double potentials Fractionated potential

Channel width 4.0 cm voltage 1.72 mV 25 RFs RF11 term AT (35 watts)

Mitral annulus

AP projection

Double potentials Fractionated potential Ablation site

Mitral annulus AP projection

D

C

RSPV

LSPV

145 ms

Previous ablation line

Activation MAP - 100 ms

LIPV

LSPV

RSPV

LAA

145 ms

- 100 ms

AT #2 CL 245ms

1.0 cm Double potentials Fractionated potential

AT #2 CL 245ms LAO projection

Mitral annulus

1.0 cm

LIPV

Mitral annulus

Double potentials Fractionated potential

Left posterior oblique projection

Figure 12.21 Macro–left AT in a 60-year-old man with hypertrophic cardiomyopathy. A. Activation map in an anteroposterior (AP) projection during atrial tachycardia (AT) with a cycle length (CL) of 230 ms, showing reentry around the mitral annulus in the counterclockwise direction and through a wide channel between an area of double atrial potentials at the septal base of the left atrial appendage (LAA) and an area of double potentials anterior to the mitral annulus. LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein. B. Voltage map in an anteroposterior (AP) projection during atrial tachycardia (AT) shows much higher voltages across the left atrium than usually seen in patients with macro–left AT. The wide (4.0 cm) and high-voltage (1.72 mV) channel required 11 radiofrequency (RF) applications using a saline-irrigated electrode to terminate the tachycardia, and a total of 25 RF applications to produce complete conduction block. The RF power was limited to 35 W to minimize the risk of deep steam pop and left atrial perforation. Programmed atrial stimulation after ablation failed to induce any AT. CL, cycle length; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior

pulmonary vein. C, D. The patient underwent a repeat ablation procedure 4 months later after the recurrence of AT. Activation maps of the new atrial tachycardia (AT#2) with a cycle length (CL) of 245 ms in the left anterior oblique (LAO, C) and left posterior oblique projections (D) show doubleloop reentry around the previous ablation line and around the left pulmonary veins PVs (black arrows). One should note the conduction block across the previous ablation line on the anterior wall (top white line). LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein. E. Voltage map (left posterior oblique projection) during atrial tachycardia no. 2 (AT#2) shows an area of low voltage (red) and a line of double potentials (pink tags) extending inferiorly from the left inferior pulmonary vein (LIPV). For ablation, 25 radiofrequency (RF) applications were delivered across the channel (2.8 cm, 1.89 mV) between the line of double potentials below the LIPV and the mitral annulus. This terminated AT#2 and produced complete conduction block across the channel. It should be noted that the voltage at other sites is relatively preserved. AT did not recur in this patient during a follow-up period of 4 years. CL, cycle length; LAA, left atrial appendage; LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein.

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E

≥ 3.0 mV

RSPV

LSPV

Voltage Voltage MAP MAP

LAA

0.08 mV

AT #2 CL 245ms Channel width 2.8 cm voltage 1.89 mV

1.0 cm

25 RFs term AT (35 watts)

Double potentials Fractionatedpotential Ablation site

Left posterior oblique projection

Figure 12.21 (continued )

3

4

5

6

7

8

9

10

11

cardia following atriotomy [abstract]. Pacing Clin Electrophysiol 2000;23:625. Nakagawa H, Jackman WM, Use of a 3-dimensional, nonfluoroscopic mapping system for catheter ablation of typical atrial flutter. Pacing Clin Electrophysiol 1998:21:1279 – 86. Nakagawa H, Lazzara R, Khastgir T, et al. The role of the tricuspid annulus and the eustachian valve/ridge in atrial flutter: relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996;94:407–24. Triedman JK, Saul P, Weindling SN, Walsh EP. Radiofrequency ablation of intra-atrial reentrant tachycardia after surgical palliation of congenital heart disease. Circulation 1995;91:707–14. Triedman JK, Bergau FD, Saul P, Epstein MR, Walsh EP. Efficacy of radiofrequency ablation for control of intraatrial reentrant tachycardia in patients with congenital heart disease. J Am Coll Cardiol 1997;30:1032–8. Kalman JM, VanHare GF, Olgin JE, Saxon LA, Stark SI, Lesh MD. Ablation of “incisional” reentrant atrial tachycardia complicating surgery for congenital heart disease. Circulation 1996;93:502–12. Baker BM, Lindsay BD, Bromberg B, Frazier DW, Cain ME, Smith JM. Catheter ablation of intraatrial reentrant tachycardias resulting from previous atrial surgery: location and transecting the critical isthmus. J Am Coll Cardiol 1996;28:411–7. Feld GK, Shahandeh-Rad F. Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush injury model. Circulation 1992;86:628 – 41. Gepstein L, Evans S. Electroanatomical mapping of the heart: basic concepts and implications for the treatment of cardiac arrhythmias. Pacing Clin Electrophysiol 1998;21:638 – 48. Morady F, Kadish A, Rosenheck S, et al. Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction. J Am Coll Cardiol 1991;17:678–89.

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12 Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infraction. Circulation 1993;88:1647–70. 13 Shah D, Jaïs P, Takahashi A, et al. Dual-loop intra-atrial reentry in humans. Circulation 2000;101:631–9. 14 Nakagawa H, Matsudaira K, Overholt E, et al. Successful ablation of unstable macroreentrant right atrial tachycardias following a Fontan procedure by targeting all narrow channels between scars [abstract]. Circulation 2000;102:II-572. 15 Nakagawa H, Beckman K, Spector P, et al. Characterization of the reentrant circuit in macroreentrant left atrial tachycardia [abstract]. Circulation 2001;104:II-460. 16 Jaïs P, Shah DC, Haïssaguerre M, Clementy J, Leveque H. Mapping and ablation of atrial arrhythmias following surgical atrial septal defect closure [abstract]. Circulation 1998;98: I-281. 17 Jaïs P, Shah D, Haïssaguerre M, et al. Mapping and ablation of left atrial flutter. Circulation 2000;101:2928 –34. 18 Ouyang F, Ernst S, Vogtmann T, et al. Characterization of reentrant circuits in left atrial macroreentrant tachycardia: critical isthmus block can present atrial tachycardia recurrence. Circulation 2002;105:1934 –42. 19 Nakagawa H, Yamanashi WS, Pitha JV, et al. Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation. Circulation 1995;91:2264 –73. 20 Jaïs P, Haïssaguerre M, Shah D, et al. Successful irrigated tip catheter ablation of atrial flutter resistant to conventional radiofrequency ablation. Circulation 1998;98:835 –8. 21 Matsudaira K, Nakagawa H, Wittkampf et al. High incidence of thrombus formation without impedance rise during radiofrequency ablation using electrode temperature control. Pacing Clin Electrophysiol 2003;26:1227–37. 22 Yokoyama K, Nakagawa H, Wittkampf FH, Pitha JV, Lazzara R, Jackman WM. Comparison of electrode cooling between internal and open irrigation in radiofrequency ablation lesion depth and incidence of thrombus and steam pop. Circulation 2006;113:11–9. 23 Nakagawa H, Yamanashi WS, Imai S, et al. Use of atrial potential attenuation to identify endpoint of radiofrequency application for continuous, transmural linear atrial ablation [abstract]. Circulation 1997;96:I-451. 24 Jaïs P, Hocini M, Hsu L, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004;110:2996–3002. 25 Pappone C, Manguso F, Vicedomini G, et al. Prevention of iatrogenic atrial tachycardia after ablation of atrial fibrillation: a prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004;110:3036 – 42. 26 Nakagawa H, Aoyama H, Beckman KJ, et al. Incidence and location of the reentrant circuit in macroreentrant left atrial tachycardia following pulmonary vein isolation [abstract]. Pacing Clin Electrophysiol 2003;26:970. 27 Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000;102:2463 –5.

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28 Oral H, Scharf C, Chugh A, et al. Catheter ablation for paroxysmal atrial fibrillation: segmental pulmonary vein ostial ablation vs. left trail ablation. Circulation 2003;108:2355 – 60. 29 Pappone C, Oreto G, Rosanio S, et al. Atrial electroanatomic remodeling after circumferential radiofrequency pulmonary vein ablation: efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation. Circulation 2001;103:2539–44. 30 Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atrial tachyarrhythmias after complete circular isolation of pulmonary veins: lessons from double lasso technique. Circulation 2005; 111:127–35.

31 Takahashi Y, Jaïs P, Hocini M, et al. Acute occlusion of the left circumflex coronary artery during mitral isthmus linear ablation. J Cardiovasc Electrophysiol 2005;16:1104 –7. 32 Aoyama H, Nakagawa H, Pitha JV, et al. Comparison of cryothermia and radiofrequency current in safety and efficacy of catheter ablation within the canine coronary sinus close to the left circumferential coronary artery. J Cardiovasc Electrophysiol 2005;16:1218 –26. 33 Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 2004;109:2724 – 6.

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13

Circumferential ablation of the pulmonary veins Carlo Pappone and Vincenzo Santinelli

The aim of this chapter is to summarize not only the epidemiological aspects but also the development over the last 10 years of transcatheter ablative therapy for atrial fibrillation. Catheter ablation strategies for the treatment of atrial fibrillation (AF) have been in a process of continuous development since 1996, and catheter ablation is now regarded as an established therapeutic approach to this frequent form of arrhythmia [1–51]. According to a recent study in the USA, AF affects one in 25 adults aged 60 or over and nearly one in 10 adults aged 80 or over. Due to symptoms and the risk of ischemic stroke in elderly patients, this type of arrhythmia is a source of considerable concern, and its impact is likely to increase as the number of individuals affected by AF rises nearly 2.5-fold during the next 50 years. The economic repercussions on national health systems around the world will be considerable. AF patients require frequent clinical visits for adjustment of their medication and monitoring of anticoagulation treatment. This type of arrhythmia is also associated with increased numbers of emergency room visits, hospitalizations, and numerous procedures. Even in comparison with patients matched for age and the presence of cardiovascular disease, AF patients have medical costs that are approximately $2500 higher per patient-year. These observations show that it is imperative to promote coordinated efforts on behalf of cardiologists, electrophysiologists, neurologists, and primary-care providers to meet the increasing challenge of stroke prevention and rhythm management in the growing population of patients with atrial fibrillation.

The AFFIRM issue The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study demonstrated that a rhythm control strategy conferred no survival advantage over rate control in patients with AF who had risk factors for stroke [52,53]. However, drug inefficacy or

adverse drug effects, or both, could easily account for the absence of a survival benefit with rhythm control. In 2003, we reported that circumferential pulmonary vein ablation (CPVA) is associated with advantages with regard to mortality and morbidity rates in comparison with medical therapy alone [33]. It was found that in both the ablation and antiarrhythmic groups, sinus rhythm (SR) maintenance was associated with significantly lower mortality and adverse event rates. This called into question the results of three recent AF trialsathe Pharmacological Intervention in AF (PIAF), AFFIRM, and Rate Control versus Electrical Cardioversion (RACE) studiesathat demonstrated, contrary to prevailing practice, that rhythm control conferred no advantage over heart rate control by drugs [52–55]. On the one hand, these conflicting results could be explained by the fact that it is difficult to compare our study directly with others, as the patient populations were inevitably different. The RACE and AFFIRM studies only enrolled older patients with one or more risk factors for stroke, most of whom had persistent AF. Younger patients with structurally normal hearts and paroxysmal arrhythmia were disproportionately poorly represented in these trials, and the results cannot be generalized to a broader AF population. Curing AF and maintaining SR may therefore still be the goal, at least in some groups of patients. On the other hand, it is intrinsically unlikely that SR is per se harmful to the patient’s life, and one could argue that the warning trend toward a higher risk of death in the rhythm-control groups in both the RACE and AFFIRM studies could be attributable to the means used to achieve SR or to the means used for long-term maintenance of it. We therefore believe that the quest for safer and more effective catheter ablation techniques for curing AF will continue. In the meantime, although this cohort follow-up study suggests that pulmonary vein ablation can be attempted not only in patients with severe, drugrefractory AF, the purpose it really serves is to provide encouragement for a prospective multicenter randomized clinical trial to confirm our findings. 221

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Left atrial versus pulmonary vein isolation There are currently two main approaches, based on the elimination of the triggers that initiate AF: pulmonary vein isolation (PVI) and CPVA, which is based on both trigger and substrate elimination [2,13,17,44]. There have been two randomized studies comparing PVI and CPVA, with differing results [42,56]. In the first study, by the Michigan group, segmental ostial ablation to isolate the pulmonary veins (PVs) was compared with the circumferential left atrial ablation strategy in 80 patients with paroxysmal AF [42]. The end point of the study was freedom from symptomatic AF in the absence of drug therapy after a single ablation procedure. In this study, symptomatic paroxysmal AF was eliminated more reliably by left atrial ablation that encircled the PVs than by segmental ostial ablation of the four PVs, with success rates at 6 months of 87% and 67%, respectively [42]. The average procedure duration with both approaches was approximately 2.5 h, although 50% shorter fluoroscopy times were reported. Notably, at 6 months, 67% of the patients randomly assigned to segmental ablation of the PV had sinus rhythm without any repeat procedures, and 88% of those randomly assigned to circumferential PV ablation. Interestingly, among patients with recurrent AF after segmental isolation who were subsequently treated with the left atrial approach, the Michigan group did not observe any patients relapsing into AF. In the second study, Karch et al. reported no superiority of left atrial ablation when comparing CPVA with PV isolation [56]. Surprisingly, the authors did not carry out left atrial ablation in the way it is currently performed in Milan, despite several published articles [17,44,45], so that fair comparison with appropriate conclusions is not possible. On the basis of our initial experience in more than 250 patients [17], we emphasized that the percentage of the encircled area is crucial in predicting the success of CPVA. In our initial experience [13,17], encircled lesions were made at a distance of 5 mm, but patients who had postablation AF recurrences showed significantly smaller encircled areas in comparison with those who did not. Subsequently, we demonstrated that only the percentage of the ablated area (hazards ratio 0.723; 95% confidence interval, 0.657– 0.796; P < 0.001) and vagal denervation (HR 0.025; 95% CI, 0.014–0.750; P < 0.025) are predictive of the outcome in patients undergoing CPVA [45]asuggesting that large lesions are needed, including reentrant wavelets, rotors, wave mothers, and vagal ganglia, all of which contribute to maintaining AF. Since 2002, therefore, circumferential lines are delivered at a distance of at least 15 mm from the PV ostia, when possible, to include more substrate without the risk of PV stenosis [44]. In all probability, 222

Karch et al. [56] applied smaller ablated areas, as they created lesions at a shorter distance from the PV ostia (> 5 mm), and this could account for the higher recurrence rate of AF associated with significant PV stenosis. Another important point in our strategy not reported in this study is that we also eliminate residual atrial potentials within the ablated area after ablation, as larger encircled lesions frequently require further radiofrequency (RF) applications inside the ablation lines in order to eliminate residual gaps completely. Also, Karch et al. [56] did not use posterior lines in any patient, further reducing the possibility of including much more substrate in the AF ablation strategy. Finally, the mitral isthmus line, if incomplete, may be proarrhythmic, which may account for the high incidence of atrial tachyarrhythmias reported by Karch et al. with both approaches. In our experience [44] and that of the Bordeaux group, a minimum double potential of 150 ms is required to prevent iatrogenic left atrial tachycardia after ablation. If Karch et al. carried out “partial” CPVA in their first 50 patients, therefore, their results are not surprising; they may represent a learning curve effect, but no conclusions can be drawn from the study. The superiority of left atrial ablation may result from several key points, as CPVA eliminates both the initiating triggers and the substrate [5,13,17,44,45,47,49 – 51]. CPVA eliminates: • Anchor points for rotors or mother waves that drive AF. • The vein of Marshall, which has a left atrial insertion in close proximity to the left superior PV and which may be a source of triggers for AF. • Sources of AF that arise on the posterior wall of the left atrium, as up to 30% of the left atrial myocardium is excluded by the encircling lesions, thus limiting the area available for circulating wavelets. • Vagal ganglia, as demonstrated by abolition of vagal reflexes following RF applications around PV ostia, which results in significant vagal attenuation up to 6 months after ablation. These effects are incremental to the effects of segmental ostial ablation alone and may account for the greater efficacy of left atrial ablation in eliminating both paroxysmal and permanent AF. These findings also suggest that CPVA is preferable to PV isolation alone as the first approach in patients with AF who are appropriate candidates for catheter ablation.

Patient selection More than 7000 patients with either paroxysmal or permanent AF, many of whom have structural heart disease, have now been treated at our department (Fig. 13.1). In our series, the presence of heart failure, coronary artery

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Cumulative milan experience (n = 4177 pts) From Jan 1998 to Jun 2004

Baseline features CHF 21%

Prior stroke 11%

CAD 25%

Valve disease 17%

HTN 39%

Male 54% DCM 17%

LVH 21%

Figure 13.1 Characteristics of patients who underwent pulmonary vein ablation in our electrophysiology laboratories from 1998 to 2004. CAD, coronary artery disease; CHF, congestive heart failure; DCM, dilated cardiomyopathy; HTN, hypertension; LVH, left ventricular hypertrophy.

disease, and mechanical prosthetic valves did not affect the outcome (Figs. 13.2–13.4). Inclusion and exclusion criteria are listed in Table 13.1.

Circumferential ablation of the pulmonary veins

visualizing the complex anatomy (Fig. 13.8). Anatomic variability in the pulmonary veins may have potential implications for the choice of the ablation approach. In patients with anatomic variations in the PVs, the circumferential approach is preferable. One such variation is the presence of a common ostium of the left PVs, which is encountered in up to 32% of patients undergoing PV isolation. Common ostia of this type are usually too large to allow stable positioning of the circumferential mapping catheter. Another anatomic variation is the presence of a right middle lobe PV, present in up to 21% of patients. When present, this vein is typically separated from the right superior and right inferior PVs by a narrow rim of atrial tissue. This leads to a tendency for the ablating catheter to slide into the PV during ablation. Another anatomic finding that makes an extraostial isolation more favorable is an ostial diameter of less than 10 mm. RF applications at a small ostium would carry a higher risk of PV stenosis.

AF mechanisms: implications for the ablation procedure Anatomic considerations: implications for the ablation procedure Magnetic resonance imaging is the gold standard for reconstructing the complex anatomy (Figs. 13.5–13.7), and threedimensional techniques are a relatively simple method of

The mechanisms involved in AF are complex and have not yet been well defined (Fig. 13.9). Improvements in catheter ablation techniques will depend to a great degree on a better understanding of the mechanisms of this arrhythmia. Permanent AF is a highly heterogeneous and

Subgroup analysis – Heart failure 1,0

0,8

AF freedom

CHF 21% Baseline features

0,6 11%

21%

25% 17%

0,4

No HF HF

0,2

39%

54% 21%

17%

0,0 0

180

360

540

720

900

1080

Follow-up (days) Figure 13.2 Subgroup analysis relative to the occurrence of heart failure (HF). No significant differences were observed, with all subgroups achieving

a cure rate approaching 80%. AF, atrial fibrillation; CHF, congestive heart failure.

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Subgroup analysis – Coronary artery disease 1,0

CAD 25%

AF Freedom

0,8

Baseline Features

0,6

Prior stroke 11%

CHF 21%

CAD 25%

Valve disease 17%

0,4

CAD No CAD

0,2

HTN 39% Male 54%

LVH 21%

DCM 17%

0,0 0

180

360

540

720

900

1080

Follow-up (days) Figure 13.3 Subgroup analysis relative to the occurrence of coronary artery disease. No significant differences were observed, with all subgroups achieving a cure rate approaching 80%. AF, atrial fibrillation; CAD, coronary

artery disease; CHF, congestive heart failure; DCM, dilated cardiomyopathy; HTN, hypertension; LVH, left ventricular hypertrophy.

Figure 13.4 Anteroposterior (AP) and right anterior oblique (RAO) views of a patient with a mechanical mitral valve who underwent circumferential pulmonary vein ablation. In our experience, the presence of mechanical valves did not have a negative impact on the outcome in patients with either paroxysmal or chronic atrial fibrillation. Cath, catheter; CS, coronary sinus; LIPV, left inferior pulmonary vein; LMPV, left middle pulmonary vein; MV, mitral valve; RSPV, right superior pulmonary vein; RV, right ventricular.

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Table 13.1 Patient selection. Inclusion criteria • At least one monthly episode of persistent symptomatic atrial fibrillation • At least one weekly episode of paroxysmal atrial fibrillation • Permanent atrial fibrillation • At least one failed trial of antiarrhythmic drugs • More than one anti-arrhythmic drug to control symptoms Exclusion criteria • New York Heart Association (NYHA) functional class IV • Age > 80 years Contraindications to anticoagulation therapy • Presence of left atrial thrombus • Left atrial diameter (LAD) ≥ 65 mm • Thyroid dysfunction • Recent updates • Patients with mitral and/or aortic metallic prosthetic valves are not excluded. • Previous repair of atrial septal defects is not an absolute contraindication.

complex condition, and different mechanisms may operate in different patients. However, it has become increasingly evident that AF is a disease of the posterior wall of the left atrium. As mentioned above, there are several possible mechanisms of action for the current CPVA strategy, which includes additional ablation lines in the posterior left atrium and mitral isthmus: • PV isolation, at least to some degree. • Elimination of anchor points for the mother waves or rotors that may generate AF, at or near the left atrial–PV junction.

Circumferential ablation of the pulmonary veins

• Ablation of other potential trigger sites, such as the vein of Marshall and the posterior left atrial wall. • Ablation of right–left atrial connections, which may play a role in generating AF. • Atrial debulking, to provide less space for circulating wavelets. • Complete PV vagal denervation. Some or all of these factors may explain why the circumferential left atrial ablation strategy is more effective than segmental ostial ablation for both paroxysmal and permanent AF. We have recently demonstrated and localized vagal fibers and/or ganglia around PV ostia at the venoatrial junction. During the follow-up, CPVA results in a shift in the sympathovagal balance toward parasympathetic withdrawal, particularly in patients in whom vagal reflexes were elicited and abolished by RF applications (Fig. 13.10). Intensive follow-up recording is crucial for assessing AF recurrences after AF ablation, regardless of the ablation strategies used, and this is essential for establishing the true success rate. In our approach, symptomatic or asymptomatic AF recurrences are assessed using at least four transtelephonic strips per day for 1 year and at least 48-h Holter recordings scheduled before and 1 week after CPVA and once monthly thereafter until the end of follow-up, usually at 12 months [45]. Almost all patients in whom it is possible to elicit and abolish vagal reflexes (overall, 30% of the patients in our series) are free from both symptomatic and asymptomatic AF recurrences after 12 months of follow-up, as documented by intensive postablation electrocardiographic monitoring [45].

Figure 13.5 Magnetic resonance imaging–based anatomical reconstruction of the left atrium with tributary pulmonary veins. The branching system of the pulmonary veins is reconstructed with a high degree of fidelity.

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Figures 13.6 and 13.7 Using magnetic resonance imaging–based techniques, the pulmonary vein–left atrial junction can be reconstructed to determine the size and orientation of the pulmonary veins. As can be seen

Ablation technique Catheter placement Three catheters are usually used: a standard bipolar or quadripolar catheter in the right ventricular apex to provide back-up pacing; a quadripolar catheter in the coronary sinus to allow pacing of the left atrium; and a deflectable ablation catheter with an 8-mm tip, which is advanced

Figure 13.8 Comparison between three-dimensional pulmonary vein–left atrial junction reconstruction obtained using the Carto system (Biosense Webster, Diamond Bar, California, USA) (A), contrast magnetic resonance angiography (B), and EnSite (Endocardial Solutions/St. Jude Medical, St. Paul, Minnesota, USA) (C). There is a high degree of correlation between

226

in these two images from the same patient, there is considerable variability in the size and pattern of entry in the left atrium.

through the transseptal sheath [5,17,44,45,47,51]. A pigtail catheter is temporarily positioned above the aortic valve to act as a landmark at the time of transseptal puncture. A reference patch is also placed on the patient’s back. After the transseptal puncture, the Mullins sheath is withdrawn into the right atrium, leaving only the 8-mm F- or D-curve ablation catheter in the left atrium. During navigation and ablation, both the power and impedance, as well as electrical activity, are continuously and accurately monitored (Fig. 13.11).

the morphology and size of the left atrial chamber and pulmonary veins as assessed by the two three-dimensional imaging techniques. LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein.

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Electrophysiological EndPoints Microreeentrant circuits Sueda Ann Thorac Surg 1997

LOM Hwang Circulation 2000

Figure 13.9 Overview of the electrophysiological substrate in the posterior left atrial wall, amenable to catheter ablation using an extensive approach. LOM, legament of Marshall; PV, pulmonary vein. Data from Sueda et al. [59], Haïssaguerre et al. [2], Hwang et al. [60], Mandapati et al. [61], and Pappone et al. [44].

Vagal ganglia Pappone Circulation 2004

PV foci Haissaguerre NEJM 1998

Dominant spiral wave

Mandapati Circulation 2000

Figure 13.10 Heart rate variability analysis before and after ablation in a patient in whom vagal reflexes were elicited near the left inferior pulmonary vein. Abolition of the vagal reflexes by radiofrequency energy results in a shift in the sympathovagal balance toward parasympathetic withdrawal. A. Before circumferential pulmonary vein ablation (CPVA). B. One week after CPVA. HF, high frequency; LF, low frequency; VLF, very low frequency.

Mapping process A real-time three-dimensional replica of the left atrium is created with an electroanatomical mapping system [5,17,44,45,47,51]. Tubular models of the PVs and the outline of the mitral valve annulus are also depicted as anatomical landmarks for the navigation system, and we create the map by entering each PV in turn (Figs. 13.12, 13.13). Three locations are recorded along the mitral annulus to tag the valve orifice. To acquire PVs, we use criteria based

on fluoroscopy, impedance, and electrical activity. Entry into the vein is clearly identified as the catheter leaves the cardiac shadow on fluoroscopy, the impedance usually rises above 140–150 Ω, and the electrical activity disappears. Due to the orientation of some veins and the limitations of catheter shape, it can be difficult to enter deep into some veins, but the impedance still rises when it is in the mouth of the vein. To allow better differentiation between the PVs and the left atrium, we use voltage criteria (fractionation of the local bipolar electrogram) and impedance 227

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Figure 13.11 Impedance maps. As can be seen, the impedance rises as the catheter approaches the pulmonary vein ostia, with values < 90 Ω characterizing the left atrial body. AP, anteroposterior; LAA, left atrial

appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; LL, left lateral; MV, mitral valve; PA, posteroanterior; RIPV, right inferior pulmonary vein; RL, right lateral; RSPV, right superior pulmonary vein.

(a rise of > 4 Ω above the mean left atrial impedance) to define the PV ostium. Clearly, the anatomical appearance provides added confirmation of catheter entry into the PV ostium, and a deflectable catheter with an 8-mm tip is used for mapping and ablation. The mapping and ablation procedures are carried out using the coronary sinus (CS) atrial signal if the patient is in SR, or the right ventricular signal if the patient is in AF, as the synchronization trigger for the Carto system (Biosense Webster, Diamond Bar, California, USA). Each endocardial location is recorded while a stable catheter position is maintained, as assessed by both end-diastolic stability (a distance of 2 mm between two successive locations) and local activation time (LAT) stability (an interval of 2 ms between two successive LATs). If spontaneous ventricular rates during AF are too low, we usually pace the right ventricle at higher rates to increase the Carto system sampling rates. If the patient is in SR, we map during continuous CS pacing to increase the refresh

rate. Atrial volumes are calculated at the end of diastole independently of the underlying rhythm (AF or SR). The mapping catheter is introduced into the left atrium under fluoroscopic guidance, and its location is recorded relative to the location of the fixed reference. Usually, 100 points are required to create adequate maps of the left atrium and PVs and up to 200 points for accurate mapping of left atrial tachycardia. Intracardiac ultrasound is used only for investigational purposes.

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Mapping system The anatomic reconstruction of the left atrium obtained with the Carto system (Biosense Webster) or EnSite system (Endocardial Solutions/St. Jude Medical, St. Paul, Minnesota, USA) is reliable in comparison with magnetic resonance imaging. As the catheter is moved inside the heart, the mapping system continuously analyzes its

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Circumferential ablation of the pulmonary veins

Figure 13.12 Electroanatomical left atrial maps (posteroanterior view). A. Preablation voltage map. B. Postablation voltage map. The lesion set should be noted. Circular radiofrequency lesions are deployed around each pulmonary vein (PV) ostium, constituting the standard ablation set. Additional linear lesions connect the right inferior PV and the mitral annulus

(mitral isthmus line) and the contralateral superior and inferior PVs (posterior lines) to prevent LA incisional tachycardia. The blue spheres represent hot spots for eliciting vagal reflexes. LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MV, mitral valve; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

Figure 13.13 Solid gray map of the left atrium, in a posteroanterior view. The red spheres represent radiofrequency lesions and color tubes depict the pulmonary veins (PVs). A. Standard circumferential pulmonary vein ablation (CPVA). B. After 2001, the standard approach was modified, with

additional lines connecting the left inferior PV to the mitral annulus and the superior and inferior contralateral PVs. LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MV, mitral valve; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

location and orientation and displays it on the monitor of a graphic workstation, allowing navigation without the use of fluoroscopy. The mapping procedure is carried out by moving the catheter to numerous sequential points within the left atrium and PVs and acquiring the location

in three-dimensional space, together with the local unipolar and bipolar voltages and the LAT relative to the chosen reference interval. The system continuously monitors the quality of catheter–tissue contact and LAT stability to ensure the validity and reproducibility of each local 229

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Figure 13.14 A frame from a propagation map in a patient suffering from incessant palpitations after circumferential pulmonary vein ablation due to incisional left atrial flutter. One should note the circular movement of the activation front around the mitral annulus. The arrhythmia was terminated by radiofrequency delivery at the mitral isthmus. LA, left atrial; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

measurement. The acquired information is then colorcoded and displayed (Figs. 13.12, 13.13). As each new site is acquired, the reconstruction is updated in real time to progressively create a three-dimensional chamber geometry color-coded with the activation time. In addition, the collected data can be displayed as voltage maps, depicting the magnitude of the local peak voltage in a three-dimensional model. The chamber geometry is reconstructed in real time by interpolation of the acquired points. Local activation times can be used to create activation maps, which are of enormous importance when attempting to map and ablate focal or macroreentrant atrial tachycardias (Fig. 13.14), but are not used during ablation treatment in patients with AF.

Ablation strategy Our initial strategy was to encircle the four PVs by creating circumferential lines of conduction block around each PV. These lines consisted of contiguous focal lesions deployed at a distance > 5 mm from the ostia. However, since 2002, we now create circumferential lesions at a distance at least 15 mm from the ostia when possible, in order to include much more substrate. Also, additional lesion lines (Fig. 13.13) are made on the posterior wall connecting the superior and inferior PVs and the mitral annulus to the left inferior PV (mitral isthmus line) to avoid iatrogenic left atrial flutters [44,50,51]. Once the main PVs and left atrium have been adequately reconstructed, radiofrequency current is applied with a target temperature of 55– 65 °C and a maximum power of 100 W to create circumferential lines of conduction block. The encircling ablation lines are then connected with two ablation lines 230

in the posterior left atrium. RF energy is applied in the posterior wall with a maximum power of 50 W and a temperature target of 55 °C to reduce the risk of injury to the surrounding structures [46,47]. If there is an impedance rise, or if the patient has a cough or burning pain, RF delivery is stopped. The gray location map is used for the ablation procedure, as it avoids presenting the operator with unnecessary information. RF energy is applied continuously on the circumferential planned ablation lines, as the catheter is gradually dragged along the line. Continuous catheter movement, often in a to-and-fro fashion over a point, helps keep the catheter tip temperature down due to passive cooling. The end point of ablation is voltage abatement of the local atrial electrogram by 90%, or to less than 0.05 mV. In some patients, additional ablation lines are created if necessary along the left atrial roof, septum/anterior wall, or along the posterior mitral annulus. On average, a total of 10–15 s of RF is required. If the catheter position deviates significantly from the planned line, or falls into a PV (usually associated with a sudden rise in impedance of > 4 Ω), RF application is immediately terminated until the catheter is returned to a suitable location. Circumferential ablation lines are usually made starting at the lateral mitral annulus and withdrawing posteriorly and then anterior to the left-sided PVs, passing between the left superior pulmonary vein (LSPV) and the left atrial appendage (LAA) before completing the circumferential line on the posterior wall of the left atrium. The “ridge” between the LSPV and LAA can be identified by fragmented electrograms due to collision of activity from the LAA and LSPV/left atrium. The appendage is identifiable by a significantly higher impedance (> 4 Ω above the left atrium mean), a high-voltage local bipolar electrogram, with characteristically organized activity in fibrillating patients. The right PVs are isolated in a similar fashion, and then a posterior line connecting the two circumferential lines is created to reduce the risk of macroreentrant atrial tachycardias [44]. Usually, four discrete orifices are identified, which permit separate ablation lines be performed around each vein. However, a single circular line around two ipsilateral veins is created in the presence of ostia less than 20 mm apart from each other, a common ostium with early branching, or a separately branching PV. As a result, we can easily tailor the lesion set on the basis of the varying PV–left atrium junction morphology. Termination of AF is observed during the procedure in approximately one-third of the patients. If AF does not terminate during RF, then transthoracic cardioversion is carried out at the end of the procedure. If there are immediate recurrences of AF after the cardioversion, then the completeness of the lines is reassessed. Once SR is restored either by RF or cardioversion, attempts to reinduce AF by rapid atrial pacing, with or without infusion of isoproterenol, are only made for investigational

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purposes in selected patients. Ablation is carried out in the cavotricuspid isthmus in patients with a history of typical atrial flutter, and cavotricuspid isthmus–dependent atrial flutter is induced by atrial pacing. We do not isolate the superior vena cava for the treatment of AF, but have had to do so in some cases of atrial tachycardia.

Assessment of PV innervation Potential vagal target sites, now regarded as one of the most important targets for the CPVA strategy, were first described by our group [45]. They are usually identified during the procedure in at least one-third of the patients. Vagal reflexes are considered to include sinus bradycardia (< 40 beats/min), asystole, atrioventricular block, or hypotension that occurs within a few seconds of the onset of RF application [45,47]. If a reflex is evoked, then RF energy is delivered until such reflexes are abolished, or for up to 30 s. The end point for ablation at these sites is termination of the reflex, followed by sinus tachycardia or AF. Failure to reproduce the reflexes with repeat RF is considered as confirming denervation. Complete local vagal denervation is defined by the abolition of all vagal reflexes. The most common sites are tagged on electroanatomical maps (Fig. 13.12). CPVA induces vagal attenuation after the procedure (as demonstrated by heart rate variability analysis), which persists for up to 6 months after ablation (Fig. 13.10). Our seminal observations on the role of the vagal ganglia around the PVs and their ablation by RF applications in patients with atrial fibrillation [45] have been confirmed by recent studies by the Oklahoma and Bordeaux groups, thus opening up new avenues in atrial fibrillation ablation strategies.

Remap process and lesion validation Among patients in SR, postablation remapping is carried out, using the preablation map for the acquisition of new points to allow accurate comparison of the pre-RF and post-RF bipolar voltage maps (Fig. 13.12). Among patients in AF, after restoration of SR, postablation remapping is carried out using the anatomic map acquired during AF, to provide the same landmarks and lesion tags for accurate lesion validation [47]. There are no significant intrapatient differences between the anatomic map of a fibrillating atrium and the map obtained during pacing, as location points are recorded at end-diastole. Usually, we do not validate circumferential lesions around PVs by pacing maneuvers, but validate the bipolar voltage abatement within the encircled areas simply by performing a voltage remap by acquiring new points on the existing geometry to provide voltage measurements (Fig. 13.11). The end point for circumferential left atrial ablation is a reduction in voltage of > 90% within the isolated regions.

Circumferential ablation of the pulmonary veins

Only one postablation voltage map is therefore usually required to validate circumferential lesions around each PV, without the need for time-consuming conventional mapping studies. In addition, all points inside and around the lesions with an amplitude of < 0.1 mV can be selected and tagged, and the software can calculate the surface area in square millimeters of the three-dimensional reconstruction inside the marked region of interest. Conversely, the completeness of additional lesion lines, particularly at the mitral isthmus, is critical in preventing postablation macroreentrant left atrial tachycardias, which in the majority of cases are mitral isthmus–dependent and incessant [44]. Gaps are defined as breakthroughs in an ablated area, and identified by sites with single potentials and by early local activation. The completeness of the mitral isthmus line is usually demonstrated during coronary sinus pacing by endocardial and coronary sinus mapping, with a search being conducted for widely spaced double potentials across the line of block, which are confirmed by differential pacing. In our series, the minimum double potential interval at the mitral isthmus during coronary sinus pacing after block has been achieved is 150 ms, depending on the atrial dimensions and the extent of scarring and lesion creation [44]. After the planned lines of block have been created, the left atrium is remapped, and the preablation and postablation activation maps are compared (Fig. 13.12). Incomplete block is revealed by impulse propagation across the line; in these cases, further RF applications are given to complete the line of block. Although this strategy does not require PV isolation, CPVA is usually associated with PV isolation in about 80% of the patients. Among patients who are in AF at the beginning of the procedure, RF ablation is carried out without an initial attempt at cardioversion. If AF does not terminate during circumferential atrial ablation or during the linear ablation in additional lines including the mitral isthmus, cardioversion is carried out at the end of the procedure. At the end of procedure, protamine is injected to allow removal of the sheaths. After 30 min, heparin infusion is restarted for 12–18 h to keep the activated clotting time between 200 and 250 s. Since we first started conducting this procedure 6 years ago, the procedure time has declined substantially, and is currently less than 90 min from the time of femoral sheath insertion [47].

Safety The most common complications of circumferential left atrial ablation are reported in Table 13.2. Postablation left atrial flutters are relatively common, but usually they do not require a repeat procedure, as most of them resolve spontaneously within 5 months after the index procedure [47]. Atrio-esophageal fistula is very rare, but 231

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Table 13.2 Complication rates following circumferential pulmonary vein ablation. Death Pericardial effusion Stroke Transient ischemic attack Tamponade Atrio-esophageal fistula Pulmonary vein stenosis Incisional left atrial tachycardia

0% 0.1% 0.03% 0.2% 0.1% 0.03% 0% 6%

its occurrence is dramatic and devastating [46]. A lower RF energy application is recommended during ablation on the posterior wall of the left atrium, and we now make the line on the posterior wall near the roof of the left atrium, where the left atrium is not in direct contact with the esophagus. None of the patients has developed symptoms suggestive of PV stenosis, and none of those who underwent repeat magnetic resonance imaging had PV stenosis.

this is associated with both electrical and mechanical changes. In patients with mitral regurgitation who undergo ablation, the anatomic remodeling is more pronounced and, interestingly, is associated with reduced mitral regurgitation and improved left ventricular function in comparison with patients in whom SR is maintained by drugs alone.

Efficacy The success rates are approximately 90% for patients with paroxysmal AF and 80% for those with permanent AF [5,17,44,45,47,51]. In patients with paroxysmal AF in whom vagal reflexes are elicited and abolished by RF applications, the long-term success rate is approximately 100% [45]. Early recurrence of AF or iatrogenic left atrial tachycardia may develop within the first few months after the procedure, but usually these are transient phenomena that do not require a repeat procedure, as they resolve spontaneously during the long-term follow-up [44].

Future directions Anatomic remodeling after the procedure Restoration of SR after ablation (usually at the 5-month follow-up examination) results in “reverse” electrical and mechanical atrial remodeling and improved atrial function (Fig. 13.15). Enlarged atria may become smaller, and

Figure 13.15 Anatomical remodeling in a patient in whom a repeat procedure was performed to abolish left atrial flutter. A. After ablation. LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MV, mitral valve; RIPV, right inferior pulmonary vein; RSPV, right superior

232

The current technology has some limitations (Fig. 13.16). An alternative methodology is represented by the EnSite system. The anatomic reconstruction is acquired from an electrical field that is applied across the thoracic cavity from “patch” electrodes placed on the body surface.

pulmonary vein. B. The follow-up findings after 5 months. There is shrinkage of the left atrial body due to reduction in the extent of the left atrial posterior wall.

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Limitations of current technology

Fluoroscopy








X-ray exposure 2-D projection imaging Limited anatomy Inability to visualize catheter–tissue catheter-tissue interface Inability to visualize lesions

Electroanatomical mapping systems Virtual reconstruction
Relevant learning curve effect
Limited information on PV branching system


Figure 13.16 Summary of the limitations of current technologies. Abl, ablation catheter; TSP, “tran septal puncture” sheath; LI, left inferior; LS, left superior; PV, pulmonary vein; RI, right inferior; RS, right superior.

Figure 13.17 A simultaneous noncontact high-density activation mapping technology, the EnSite Array system, is being investigated (Endocardial Solutions/St. Jude Medical, St. Paul, Minnesota, USA). LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

Figure 13.18 A map obtained with the EnSite system (Endocardial Solutions/St. Jude Medical, St. Paul, Minnesota, USA). The anatomical reconstruction of the left atrial surface is improved.

The real-time physical locations of multiple electrodes inside the chamber are derived from the measured impedance generated by the applied electric field. There are two modes of operation: simultaneous noncontact high-

density reconstruction of “virtual” electrograms, known as EnSite Array (Fig. 13.17); and sequential direct acquisition of contact electrograms, known as EnSite NavX (Fig. 13.18). 233

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exposes the patient to less risk. Finally, special attention should be given to the relative efficacy, safety, and ease of performing each ablation technique. To maximize success rates and minimize complications in patients with either paroxysmal or chronic AF, an electroanatomical approach should be regarded as the first-line therapy.

References

Figure 13.19 A novel and promising approach to transcatheter ablation of atrial fibrillation is remote magnetic technology (RMT) control of the catheter using an electrical-field guidance system (Carto-RMT, Biosense Webster, Diamond Bar, California, USA).

Remote magnetic navigation for atrial fibrillation ablation A new technique for mapping and ablation of atrial fibrillation has been successfully carried out for the first time in our laboratory (Fig. 13.19). The technique involves magnetic field guidance of the catheter tip [57,58]. The technique has also been incorporated into a new mapping system, with displays on separate screens (Carto-RMT, Biosense Webster). The early results from our laboratory indicate that remote magnetic navigation is safe and feasible, with a short learning curve, suggesting that AF ablation could be carried out even by less experienced operators, reducing the fluoroscopic exposure time in all cases, particularly for the operator. While the manual approach may well be operator-dependent, the remote approach does not depend solely on a single operator, but requires a well-trained team. In addition, magnetic catheter navigation can be quantified, including counterclockwise rotation or the deflection angle and advancement or withdrawal lengths in millimeters. It may therefore be easier to share experience among users. We strongly believe that this could become an important technique in the future in ablation treatment for atrial fibrillation.

Conclusions Circumferential pulmonary vein ablation can be safely performed in the majority of patients with AF, with high success rates that are maintained in the longer term. With practice and technological advances, procedure times can be very short, so that the procedure is well tolerated and 234

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35 Oral H, Ozaydin M, Chugh A, et al. Role of the coronary sinus in maintenance of AF. J Cardiovasc Electrophysiol 2003;14: 1329 –36. 36 Lin WS, Tai CT, Hsieh MH, et al. Catheter ablation of paroxysmal AF initiated by non-PV ectopy. Circulation 2003;107:3176 –83. 37 Scharf C, Sneider M, Case I, et al. Anatomy of the PVs in patients with AF and effects of segmental ostial ablation analyzed by computed tomography. J Cardiovasc Electrophysiol 2003;14:150 –5. 38 Kato R, Lickfett L, Meininger G, et al. PV anatomy in patients undergoing catheter ablation of AF: lessons learned by use of magnetic resonance imaging. Circulation 2003;107:2004 –10. 39 Saad EB, Marrouche NF, Saad CP, et al. PV stenosis after catheter ablation of AF: emergence of a new clinical syndrome. Ann Intern Med 2003;138:634– 8. 40 Marchlinski FE, Callans D, Dixit S, et al. Efficacy and safety of targeted focal ablation versus PV isolation assisted by magnetic electroanatomic mapping. J Cardiovasc Electrophysiol 2003;14:358 –65. 41 Marchlinski FE, Callans D, Dixit S, et al. Efficacy and safety of targeted focal ablation versus PV isolation assisted by magnetic electroanatomic mapping. J Cardiovasc Electrophysiol 2003;14: 358 –65. 42 Oral H, Scharf C, Chugh A, et al. Catheter ablation for paroxysmal AF: segmental PV ostial ablation vs. left atrial ablation. Circulation 2003;108:2355 –60. 43 Arora R, Verheule S, Scott L, et al. Arrhythmogenic substrate of the PVs assessed by high-resolution optical mapping. Circulation 2003;107:1816 –21. 44 Pappone C, Manguso F, Vicedomini G, et al. Prevention of iatrogenic atrial tachycardia after ablation of atrial fibrillation: a prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004;110:3036 –42. 45 Pappone C, Santinelli V, Manguso F, et al. PV denervation enhances long-term benefit after circumferential ablation for paroxysmal AF. Circulation 2004;109:327–34. 46 Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of AF. Circulation 2004;109: 2724 – 6. 47 Pappone C, Santinelli V. The who, what, why, and howto guide for circumferential pulmonary vein ablation. J Cardiovasc Electrophysiol 2004;15:1226 –30. 48 Pappone C, Santinelli V. Segmental pulmonary vein isolation versus the circumferential approach: is the tide turning? Heart Rhythm 2004;1:326 – 8. 49 Pappone C, Santinelli V. Prevention of atrial fibrillation: how important is transseptal atrial conduction in humans? J Cardiovasc Electrophysiol 2004;15:1118 –9. 50 Pappone C, Santinelli V. Towards a unified strategy for atrial fibrillation ablation? Eur Heart J 2005;26:1687–8. 51 Lang CC, Santinelli V, Augello G, et al. Transcatheter radiofrequency ablation of atrial fibrillation in patients with mitral valve prostheses and enlarged atria: safety, feasibility, and efficacy. J Am Coll Cardiol 2005;45:868 –72. 52 Wyse DG, Waldo AL, DiMarco JP, et al. AF Follow-up Investigation of Rhythm Management (AFFIRM) investigators: a comparison of rate control and rhythm control in patients with AF. N Engl J Med 2002;347:1825 –33. 235

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53 Corley SD, Epstein AE, DiMarco JP, et al. Relationships between SR, treatment, and survival in the AF Follow-Up Investigation of Rhythm Management (AFFIRM) study. Circulation 2004;109:1509–13. 54 Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent AF. N Engl J Med 2002;347:1834 – 40. 55 Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in AFaPharmacological Intervention in AF (PIAF): a randomised trial. Lancet 2000;356:1789–94. 56 Karch MR, Zrenner B, Deisenhofer I, et al. Freedom from atrial tachyarrhythmias after catheter ablation of atrial fibrillation: a randomized comparison between 2 current ablation strategies. Circulation 2005;11:2875–80. 57 Faddis MN, Lindsay BD. Magnetic catheter manipulation. Coron Artery Dis 2003;14:25–7.

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58 Faddis MN, Blume W, Finney J, et al. Novel, magnetically guided catheter for endocardial mapping and radiofrequency catheter ablation. Circulation 2002;106:2980 –5. 59 Sueda T, Nagata H, Orihashi K, et al. Efficacy of a simple left atrial procedure for chronic atrial fibrillation in mitral valve operations. Ann Thorac Surg 1997;63:1070 –5. 60 Hwang C, Wu TJ, Doshi RN, Peter CT, Chen PS. Vein of Marshall cannulation for the analysis of electrical activity in patients with focal atrial fibrillation. Circulation 2000;101: 1503 –5. 61 Mandapati R, Skanes A, Chen J et al. Stable microreentrant sources as a mechanism of atrial fibrillation in the isolated sheep heart. Circulation 2000, Jan 18; 101:194–9.

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14

Long linear lesions in the treatment of atrial fibrillation Li-Fern Hsu, Prashanthan Sanders, Mélèze Hocini, Michel Haïssaguerre, and Pierre Jaïs

Introduction Atrial fibrillation (AF), the most common form of cardiac arrhythmia, is associated with a wide range of manifestations, the most serious of which are heart failure, thromboembolic events, and increased mortality risk [1,2]. Although these adverse consequences can be overcome in part by anticoagulation and ventricular rate control, the goal of therapy should be the restoration and maintenance of sinus rhythm in order to eliminate them. Although antiarrhythmic drugs have been the mainstay of treatment for such patients, their limited efficacy and potential for significant adverse effects led to renewed interest in rate-control measures, stimulated by the publication of the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study [3], the Rate Control versus Electrical Cardioversion (RACE) study [4], and the Pharmacological Intervention in Atrial Fibrillation (PIAF) [5] trial, which suggested equivalent outcomes for pharmacological rhythm and rate-control strategies. However, these findings merely highlighted the fact that the benefits of sinus rhythm can be negated by the deleterious effects of antiarrhythmic drugs, as demonstrated by a further analysis of the AFFIRM results, demonstrating that sinus rhythm was associated with a 47% lower risk of death, while the use of antiarrhythmic drugs significantly increased the mortality risk by 49% [6]. Thus, the restoration and maintenance of sinus rhythm is of potential benefit if it can be achieved without the use of antiarrhythmic drugs, and this view has continued to drive the development of techniques for catheter ablation to maintain sinus rhythm.

as triggers and substrate. The role of spontaneous electrical activity originating from the thoracic veins, particularly the pulmonary veins (PVs), in the initiation and maintenance of AF has been well demonstrated [7–9], and PV isolation is now an integral part of most strategies for catheter ablation of AF. However, despite the exclusion of this predominant source of triggers, most patients with persistent or permanent AF and approximately 20 – 40% of patients with paroxysmal AF have further episodes of AF [10–12]. In a series of 15 patients (seven with structural heart disease) with chronic AF (5 ± 4 months’ duration), selected on the basis of frequent ectopy causing early reinitiation after cardioversion, isolation of the arrhythmogenic PVs following cardioversion resulted in 60% of patients remaining in sinus rhythm without antiarrhythmic drugs at 11 ± 8 months [11]. In unselected patients, these results may be significantly less attractive. In a series in which empirical electrical isolation of only the right and left superior PVs was carried out in patients with persistent AF, only 21% of the patients continued in sinus rhythm without antiarrhythmic medication at 29 ± 8 months of follow-up [12]. Similarly, Oral and co-workers reported that PV isolation in patients with persistent AF resulted in arrhythmia suppression in only 22% of cases [10]. Among our patients with paroxysmal AF, approximately 70% have remained free of arrhythmias without the need for antiarrhythmic or anticoagulant therapy at 1 year after ablation. Thus, it has become clear that in patients with chronic or persistent AF and 20–30% of patients with paroxysmal AF, PV isolation alone is insufficient to maintain sinus rhythm.

Catheter ablation to modify the substrate Pulmonary vein ablation The development of AF is dependent on a complex interaction between several mechanisms, broadly categorized

The role of the appropriate substrate in maintaining AF has increased in prominence following improved understanding of the mechanisms of AF. These areas of slow conduction, usually located in close proximity to the 237

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initiating source, promote the transformation of ectopic activity to reentrant circuits or rotors, perpetuating and maintaining fibrillatory activity [13]. Present evidence suggests that the substrate for AF may be related to diffuse atrial structural remodeling and its electrophysiological consequences [14–18]. The conceptual basis for substrate modification by compartmentalization of the atria is based on the multiple wavelet hypothesis of Moe and Abildskov, which suggested that AF is maintained by multiple reentrant wavelets propagating simultaneously in the atria, and that a minimum mass of electrically continuous myocardium must be present to sustain the wavelets on reentry [19]. The presence of such wavelets has been observed in experimental and clinical mapping studies during AF [20,21]. In addition, surgical procedures designed to create anatomical barriers to interrupt the potential reentrant circuits, notably the maze operation developed by Cox et al. [22], further highlighted the importance of this hypothesis with their success in suppressing further AF. These compartmentalization procedures, which are now predominantly restricted to the left atrium (LA), have been highly successful in restoring sinus rhythm (with an 80–99% longterm cure rate for AF with antiarrhythmic agents) [23]. This has fueled interest in the development of catheterbased techniques to modify the substrate for AF in an attempt to reproduce a similar long-term cure of AF without the need for an open-chest procedure.

Clinical electrophysiology of linear lesions The cornerstone of linear ablation is to join anatomical structures or regions of scar to anatomical structures in order to interrupt the mass of continuous tissue available for arrhythmia propagation. The creation of a linear conduction block has been the most important predictor of a successful clinical outcome after linear ablation. Complete linear block enforces an obligatory activation detour, whereas slow conduction through gaps in the line allows an additional activation wavefront across it and creates the substrate for further arrhythmias, notably reentrant tachyarrhythmias. Several electrophysiological criteria can be used to assess linear conduction. During AF, linear conduction block can be evidenced by dissociated activities on either side of the line and can be suspected on the basis of an electrogram amplitude decrease along the line, but these criteria need to be to be further verified during pacing, therefore necessitating conversion to sinus rhythm. The atrial activation wavefront relative to the line is of crucial importance to elicit evidence of conduction block. This is optimized by pacing to produce the maximal 238

difference in activation times on opposite sides of the line. Because atrial activation is approximately radial in two-dimensional atrial tissue, it produces simultaneous alternative wavefronts, and the line of conduction block must interfere with very early activation to produce the maximal detour. Sinus rhythm is therefore often inappropriate, and specific pacing sites adjacent to the line are required to demonstrate regional intra-atrial block. If the line is connected to a larger barrier (atrioventricular ring), the pacing site has to be moved near this connection (that is, close to the tricuspid or mitral annulus). The right atrium differs significantly from the LA, with a preexisting long slow-conducting area formed by the crista terminalis, which expands the activation detour produced by other lines. By mapping on or around the line, it is possible to establish linear conduction block using various criteria (see below).

Atrial activation detour An activation detour created by linear conduction block depends on several factors: the site of origin of activation; the length of the line or interconnection with other lines; the connection of the line to an anatomical barrier; and the conduction velocity along different parts of the detour pathway. Comprehensive isochronal mapping is easier using simultaneous rather than sequential recordings. Conventional multielectrode catheters, basket catheters, or threedimensional mapping systems can be used for mapping, but require coverage of the full activation detour to demonstrate the characteristic cascading configuration when linear block is achieved. However, if far from the line, activation detour mapping may miss small gaps that specifically require closer or local recordings. Recording two sitesathe earliest and the latestaprovides a simplified overview of the activation detour. This simple assessment can be carried out sequentially at both points straddling the line, by comparison with a reference (the stimulus artifact), by a multielectrode catheter crossing the line, or by a single bipole over the line. In the LA, the coronary sinus offers the most practical and efficient means of assessing lines connected to the mitral annulus. Provided the multielectrode catheter brackets the line, dynamic changes in conduction can be appreciated during the procedure just by monitoring local potentials facing the line extremity. The difference in activation times indicates the conduction time of the activation detour around the line or through gaps in the line. A threshold of conduction time can be determined that defines incomplete linear conduction block below it; for example, a complete conduction block with mitral isthmus ablation (see below) in patients with paroxysmal AF results in an activation detour and

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conduction time of 151 ± 26 ms (longer for chronic AF), while complete block has not been observed in our laboratory in association with a conduction time < 100 ms. A gap in the line creates a short circuit of activation and anticipation of the final potential, which is more marked if the gap is situated close to the pacing site. The absolute value is therefore less specific for excluding a gap and it can never guarantee the completeness of the block.

Local electrograms and vector mapping The morphology of electrograms on either side of the line provides important information about the wavefront direction. Unipolar and bipolar recordings obtained on the line provide information about activities occurring sequentially on either side (near-field activities) as well as across the line. A complete activation detour provides a fully negative unfiltered unipolar electrogram at the initial (pacing) site and a fully positive electrogram at the final site. Bipolar electrograms can also show polarity reversal, provided the wavefront and bipole orientation are unchanged. The presence of double potentials separated by an isoelectric interval is highly suggestive of significant linear conduction delay or block, whether anatomical or functional (Fig. 14.1). An isoelectric interval between double potentials is equal to the activation detour conduction time from one side to the other. As a corollary, the presence of gaps in a linear lesion can be recognized by the presence of narrow or fractionated electrograms spanning the isoelectric interval of adjacent double potentials (Fig. 14.1). Such on-line mapping is able to disclose slowconducting gaps at any point on the line, which can be missed by all other activation detour criteria. However, at the thickest parts of the atria, gaps may also be related to deep crevices, resulting in misleadingly wide double potentials on endocardial recordings.

Differential pacing techniques Conduction through a gap may be slow enough to allow the activation wavefront around the line to reach the other side first, thus creating the appearance of conduction block. Besides an optimal pacing site, full on-line mapping with careful analysis of electrogram characteristics and differential pacing producing contrasting results in slow conduction versus linear conduction block should be used [24]. Differential pacing is performed by sequentially pacing from the distal then proximal bipoles of a catheter placed close to the suspected gap and parallel to atrial activation while recording potentials on the line (Fig. 14.2). Switching from distal to proximal bipole pacing increases the activation time from the stimulus to the first potential. The time to the second potential increases (with a similar increment) if there is slow conduction directly

Figure 14.1 A. The presence of double potentials separated by an isoelectric interval is indicative of functional or anatomical linear conduction block. CS, coronary sinus. B. Gaps in a linear lesion can be recognized by the presence of fractionated electrograms spanning the isoelectric interval of adjacent double potentials.

linking the first and second potentials; it decreases if the second potential is activated by a detour around the linear conduction block.

Electrocardiographic changes Lines required in the treatment of AF are frequently long enough to divert atrial activation to the point of changing the surface P wave morphology, as in atrial flutter ablation [25]. Again, the proximity of the line and activation origin is important to maximize the impact on the surface P wave. A line in the cavotricuspid isthmus or in the lateral LA (for example, left inferior PV to mitral annulus) cannot be expected to change the P wave in sinus rhythm because both lines are situated close to terminal activation by fusing wavefronts in their respective chambers, and therefore pacing is necessary. Lines interfering early in atrial activation wavefronts, such as the superior vena cava to the anterior tricuspid annulus in the right atrium and to Bachmann’s bundle endings in the LA, modify the P wave during sinus rhythm. The most demonstrative electrocardiogram (ECG) leads are dependent on the site of the line; for example, in leads II, III, and aVF for lines oriented vertically to the tricuspid or mitral annulus. An abrupt and significant P wave change usually accompanies the completion of linear conduction block, whereas intermediate or no changes are observed in the case of persistent slow conduction. Therefore, further validation 239

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Figure 14.2 Evaluation of the anterior line (transecting the anterior left atrium). A. Complete conduction block along the line is demonstrated by recording a corridor of double potentials along the line while pacing the anterior left atrial wall lateral to the line. B. Differential pacing to assess the conduction block. Changing the site of pacing from the distal (CSD) to the proximal (CSP) bipole of the coronary sinus catheter results in a shorter conduction delay recorded on the map catheter (positioned on the line) due to the shorter distance traveled by the activation wavefront around the mitral annulus. AP, anteroposterior; CS, coronary sinus; LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein.

by electrophysiological criteria is often required initially. However, once the pattern of P wave change is identified, P wave morphology can be subsequently monitored to confirm stability of linear conduction block without the need for endocardial recordings.

Technological assistance for linear ablation Various technical means of achieving linear transmural continuous lesions are being explored in different laboratories. These techniques employ either sequential ablation resulting in coalescing multiple punctate lesions by a graduated withdrawal of a regular catheter (guided by various shaped sheaths), or the simultaneous creation of large, confluent lesions using multiple or long electrodes (with or without a guiding sheath). Different configurations of multiple, closely spaced ring electrodes, coils, ribbons, and balloons have been investigated for this purpose, some with additional features such as saline irrigation, simultaneous multielectrode energy delivery to “cover” the interelectrode spacing, or different modes of energy [26,27]. Designing multielectrode catheters suitable for positioning at all desired locations in such a way as to ensure contact along the electrode surface and to deliver enough energy through the electrode to ensure lesion continuity and transmurality without formation of 240

thrombi or char has been challenging. These techniques currently remain investigational and are not in clinical use. In comparison, catheter technology to create punctate lesions has developed significantly, particularly with the development of an irrigation system that cools the distal tip, allowing higher power delivery if needed with a lower risk of char or coagulum formation on both the electrode and the endocardium, consequently reducing the risk of embolic events during ablation in the LA. The externally irrigated ablation catheter is routinely used in our laboratory for ablation of right and left atrial flutter and AF. Linear ablation may also be facilitated by the development of anatomical and catheter tracking mapping systems, and intracardiac echocardiography to guide linear ablation [28]. These nonfluoroscopic systems, by allowing on-line monitoring of catheter and lesion positioning and tracking, have been shown to reduce procedural and fluoroscopic times and RF energy application. Technological advances and technical refinements have been such that catheter-based linear ablation should now be viewed as a “closed-heart surgical procedure.”

Clinical experience with catheter linear ablation The development of effective and broadly applicable percutaneous linear ablation techniques and strategies for AF

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began in 1994 with Swartz et al. [29] and Haïssaguerre et al. [30]. Conceived as a replication of the surgical maze procedure, the procedure by Swartz deployed specifically tailored long sheaths to facilitate fluoroscopically guided RF applications to create a set of predetermined ablation lines in both atria. Long-term follow-up in 40 patients with chronic AF demonstrated the excellent efficacy of this procedure, with 90% in sinus rhythm. However, it was associated with a prolonged procedure duration (up to 15 h) and a very high (22%) incidence of major complications, including stroke, pericardial tamponade, and PV occlusion [31]. Subsequently, various combinations of more limited linear lesions have been attempted in the search for the ideal configuration that combines technical ease and safety with cure of AF, to be applicable to the majority of patients.

two of the 32 patients, including patients with right atrial transection. While these studies have clearly demonstrated a limited benefit of linear ablation isolated to the right atrium for the cure of AF, it is important to recognize that there may be a small subgroup of patients in whom the dominant substrate for AF may be structures within the right atrium, such as the crista terminalis [37], or in whom the right atrium may be an additional source of triggers when AF recurs following LA ablation, who may benefit from procedures limited to the right atrium. Studies have also suggested a decrease in the subsequent incidence of AF after successful ablation of the cavotricuspid isthmus, indicating that AF was favored by flutter or that conduction through the isthmus may be due to a single macroreentrant circuit with fibrillatory conduction.

Efficacy of isolated right atrial linear ablation

Left atrial linear ablation

For safety reasons, linear ablation was initially performed in the right atrium at our center. In an early series, increasingly complex right atrial linear ablations were carried out in three consecutive groups of 15 patients [32]. Right atrial ablation organized local atrial activity and led to stable sinus rhythm during the procedure in 18 patients (40%). However, linear conduction block was observed in only four of a total of 90 lines (5%), highlighting the main problem of creating linear lesions. In 40 of the 45 patients, sustained AF continued to be inducible. A previously undiagnosed typical atrial flutter was observed in 70% of cases, requiring subsequent ablation targeting the cavotricuspid isthmus. Although 24 patients (53%) had some improvement in the medium term, after 26 ± 5 months of follow-up only 11% were free of AF without drugs [33]. Interestingly, four of the patients with documented recurrent AF reported no sensation of further episodes. In 10 patients with symptomatic recurrence, LA ablation was carried out [32]. This allowed the initial recognition of PV foci, which were ablated in addition to linear ablation, but again complete linear block using conventional catheters could not be achieved. Gaita and co-workers reported 16 patients with paroxysmal AF who underwent right atrial linear ablation, resulting in 56% remaining without recurrence at 11 ± 4 months following ablation [34]. Garg and co-workers performed right atrial linear ablation in 12 patients with paroxysmal AF, with only a single patient having no recurrence of AF at 13 ± 13 months [35]. Ernst and coworkers used electroanatomical mapping guidance to create right atrial linear lesions in 32 patients [36]. Postprocedural line validation was carried out in 27 patients, demonstrating a complete isthmus line in 16 patients (59%), an anterior line in 12 patients, and an intercaval line in four patients. Recurrence of AF was observed in all but

Linear ablation isolated to the LA alone has yielded varying results. Using multiple linear lesions in the LA, Packer and co-workers studied 18 patients with chronic AF [38]. Acute success was obtained in 15 patients (83%), and after several repeat procedures in some patients, long-term elimination of AF was achieved in 14 patients (78%). These procedures were associated with prolonged procedure duration (8–15 h) and fluoroscopy times (30 –210 min). In contrast, of 13 patients in whom electroanatomical mapping guidance was used to create a circular line to isolate the PV ostia and then a second line to connect this with the mitral annulus, all of the patients had recurrent AF after a median follow-up period of 26 days (range 1– 47 weeks) [35]. In another study using electroanatomical guidance, Ernst and co-workers tested four different LA line designs in 84 patients, with systematic use of electrophysiological criteria to assess the completeness of conduction block across the ablation lines [39]. Ablation was performed using catheters with standard 4-mm electrodes. Complete lesions were difficult to achieve using this conventional radiofrequency current technology, ranging from 5% to 66% in the different groups. However, complete lesions were associated with maintenance of sinus rhythm in 74% of patients, while incomplete lesions resulted in a high rate of AF recurrence or gap-related reentrant tachycardia.

Extensive biatrial linear ablation In contrast to the transcatheter maze procedure described by Swartz and colleagues [29,31], Jaïs and co-workers reported biatrial linear ablation in 44 patients with predominantly paroxysmal AF (four with chronic AF and 11 with structural heart disease) [40]. In the right atrium, ablation was limited to a septal line and the cavotricuspid 241

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isthmus. In the LA, ablation joined the two superior PVs posteriorly to the mitral annulus, including the inferior PVs in their course, a horizontal line in the roof of the LA connecting the two superior PVs, and an additional septal line connecting the right superior PV to the fossa ovalis [40]. These patients required 2.7 ± 1.3 sessions, with a cumulative procedure duration of 615 ± 345 min, a fluoroscopy time of 171 ± 94 min, and 104 ± 56 min of radiofrequency applications. Complete conduction block was achieved from the right superior PV to the mitral annulus in 13 patients, across the roof in four patients, and from the left superior PV to the mitral annulus in one patient. Left atrial flutters were observed in 31 patients, mostly due to macroreentry propagating through incomplete ablation lines, and 29 patients had triggering foci, predominantly from the PVs. Using this approach, the success rate for maintaining sinus rhythm was 57% without antiarrhythmic drugs, increasing up to 84% when a previously ineffective antiarrhythmic was reintroduced. However, significant procedural complications were observed, with pericardial effusion in five patients, pulmonary embolism in one, inferior myocardial infarction in one, left PV occlusion in one, and a reversible stroke in one. Using electroanatomical mapping Pappone and coworkers created three right atrial lines (cavotricuspid isthmus, intercaval, and anterior septal) together with a long line encircling the PVs [41]. The procedure duration was 312 ± 103 min, with a fluoroscopy time of 107 ± 44 min. After 10 ± 3 months, 16 of the 27 patients were asymptomatic (with four receiving antiarrhythmic drugs). Ernst and colleagues used electroanatomical mapping and a similar configuration of linear lesions in 12 patients, but were unable to recreate similar results, reporting complete linear conduction block in a single patient and recurrence of AF in all patients [36]. These studies on extensive biatrial linear ablation have demonstrated the difficulty of creating complete linear lesions and the associated prolonged procedural and fluoroscopic durations. Patients frequently require further ablation procedures for LA flutters that arise due to incomplete lines. Finally, such ablation is associated with significant procedural complications. In addition to pericardial tamponade, death due to atrio-esophageal fistulas has recently been reported after circumferential PV ablation, associated with high temperature and energy delivery [42].

Limited biatrial linear ablation In view of the difficulties encountered with extensive biatrial ablation, we have evaluated the efficacy of limited biatrial linear ablation in combination with PV isolation for AF. Various configurations of LA lines in addition to

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systematic electrical PV isolation and cavotricuspid isthmus ablation have been tested with the aim of improving clinical outcomes and allowing more practical and widespread application of catheter ablation techniques for AF.

Transection of the anterior LA Animal models suggest a crucial role of the interatrial connections in the substrate for AF [43,44]. The effects of transecting the anterior LA were evaluated in 24 patients with paroxysmal (16 patients) or chronic AF (eight patients) resistant to PV isolation alone [45]. To achieve this, two linear lesions were created: one line joining the two superior PVs (roof line), and one line connecting the roof line to the anterior mitral annulus (Fig. 14.2). Ablation of the roof line was carried out by linear ablation joining the two superior PVs. The ablation catheter was introduced through a long sheath for stability, and ablation commenced at the left superior PV. Using a dragging technique with clockwise torque of the assembly, ablation was continued to the right superior PV. In some cases, to achieve stability during the ablation, the catheter was looped around the lateral inferior septal walls to reach the left superior PV. Dragging in this instance was carried out by gradually withdrawing the catheter. During dragging, ablation was performed for approximately 30– 60 s at each point. Further application was performed if mapping suggested the presence of a gap at these sites. Radiofrequency energy was delivered with power limited to 40 W using irrigation rates of 5–60 mL/min to achieve the desired power delivery. Temperature was limited to 50 °C. Validation of the linear lesion was performed by the demonstration of a corridor of double potentials along the ablation line during pacing at the anterior LA (Fig. 14.3). Anterior LA pacing could be achieved by: • Advancing the quadripolar catheter quite distally into the coronary sinus, to capture the anterior wall. • Pacing the LA appendage by introducing the quadripolar catheter transseptally to this structure. • Or by pacing the high septal right atrium when activation proceeded over the anterior interatrial connections to the anterior septal LA. In our experience, the best site for pacing appeared to be at the left appendage. Following ablation of the roof line, anterior line ablation was carried out. The ablation catheter was curved and advanced to the anterior mitral annulus, where the atrioventricular electrogram showed a 1–2 : 1 ratio, to begin ablation. Gradual anticlockwise torque of the sheath with release of the catheter curvature was used to drag the electrode to the roof line, with 30–60 s of radiofrequency energy at each point. The stability of the ablation catheter during ablation determined the location of this line, but it

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Figure 14.3 Evaluation of the roof line (joining the two superior pulmonary veins). Complete conduction block along the line is demonstrated by recording a corridor of double potentials along the line during pacing from the anterior left atrial wall (either from the distal coronary sinus, left atrial appendage, or high septal right atrium). AP, anteroposterior; CS, coronary sinus; LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein.

was created as septally as feasible. Radiofrequency energy was delivered with power limited to 40–45 W using irrigation rates of 5 – 60 mL/min to achieve the desired power delivery. Temperature was limited to 50 °C. Complete linear block was validated by: • Demonstrating a corridor of double potentials along the line during pacing lateral to the line (Fig. 14.2A). • Differential pacing techniques, by pacing lateral to the lineashifting the pacing site from the distal to proximal bipoles, without moving the catheter, lengthens conduction time to the opposite side of the line in the presence of conduction, while it shortens it in the presence of conduction block (Fig. 14.2B). • Activation mapping to demonstrate an activation detour during either pacing in the LA lateral to the ablation line (as described above) or during high septal right atrial pacing, when the earliest LA activation was anterior and septal to the ablation line. Twenty patients were in AF at the time of the ablation, which terminated during transection of the anterior LA in 12 patients. However, complete linear lesions could only be demonstrated in 14 patients (58%), with a procedure duration of 187 ± 102 min and fluoroscopy time of 54 ± 26 min, including 42 ± 16 min of radiofrequency energy application. Of the 14 patients with successful anterior LA transection, nine (64%) remained free of arrhythmia without antiarrhythmics, in comparison with three of the 10 patients (30%) with incomplete transection, at 28 ± 4 months following their last procedure. While this approach was found to be effective in terminating AF, this configuration of linear lesions is technically challenging to complete, and the modest long-term arrhythmia suppression may be attributable to the high incidence of incomplete linear lesions. In addition, it is associated with incoordinated and delayed LA activation

as observed on the surface ECG during sinus rhythm, which may be hemodynamically undesirable.

Mitral isthmus ablation The mitral isthmus, defined as the narrow region spanning the left inferior PV to the mitral annulus, is an attractive target for substrate modification, as it is short and its proximity to the coronary sinus allows optimal positioning of catheters to confirm linear conduction block [46]. Mitral isthmus ablation was carried out in 100 patients with drug-refractory paroxysmal AF as an adjunct to our standard procedure of PV electrical isolation and cavotricuspid isthmus ablation [47]. Ablation commenced at the ventricular aspect of the lateral mitral annulus, and a linear lesion was created by dragging the ablation catheter endocardially to the ostium of the left inferior PV (Fig. 14.4A). The ablation catheter, bent with a 90–180° curve and introduced through the long sheath to achieve good contact and stability, was first positioned at the ventricular edge of the lateral mitral annulus, where the atrioventricular electrogram showed a 1 : 1 to 2 : 1 ratio, to begin ablation. The sheath and catheter assembly were then rotated clockwise to extend the lesion posteriorly, ending at the ostium of the left inferior pulmonary vein. RF energy was delivered for 90–120 s at each site using power limited to 40 W, with irrigation rates of 5 – 60 mL/ min to achieve the desired power delivery. Near the ostium of the PV or the left atrial appendage, the catheter was manipulated cautiously to avoid inadvertent displacement into these structures. Ablation was monitored by the on-site appearance of double potentials (progressive delay of potentials during pacing from the coronary sinus, Fig. 14.4B). Bidirectional block was verified by demonstrating the direction of

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Figure 14.4 A. Position of the mitral isthmus on fluoroscopy (anteroposterior view). The coronary sinus is highlighted by angiography, while the dashed circle denotes the position of the left inferior pulmonary vein. CS, coronary sinus; LIPV, left inferior pulmonary vein. B. Ablation performed during proximal coronary sinus (CSP) pacing. Progressive endocardial and epicardial conduction delay is seen on the ablation catheter (Abl) and distal coronary sinus (CSD) electrograms, respectively (arrows).

Figure 14.5 Bidirectional conduction block after mitral isthmus ablation. A. Differential pacing from the coronary sinus medial to the line of block. Changing the site of pacing from the distal (CSD) to the proximal (CSP) bipole of the coronary sinus catheter results in a shorter conduction delay recorded on the map catheter along the ablation line, due to the greater distance traveled by the activation wavefront around the mitral annulus. AP, anteroposterior. B. Reversal of activation during pacing with the map catheter lateral (and anterior) to the line of block (usually from the left atrial appendage). This results in proximal-to-distal coronary sinus activation. AP, anteroposterior; LAA, left atrial appendage; LAO, left anterior oblique.

activation detour during pacing on either side of the line and by differential pacing techniques (Fig. 14.5). Ablation of the endocardial aspect of the mitral isthmus was performed using 20 ± 10 min of RF energy and resulted in complete bidirectional block in 32 patients (32%); more than 30 min of RF had to be delivered in 20 patients. In 68 patients (68%), persisting epicardial conduction after endocardial ablation was evidenced by early electrograms with high voltage in the coronary sinus, 244

contrasting with the corresponding endocardial aspect (Fig. 14.6A). Ablation from within the coronary sinus (Fig. 14.6B) resulted in complete isthmus block in 57 patients (84%) using a mean of 5 ± 4 min of RF energy (Fig. 14.6C). Overall, mitral isthmus ablation with confirmed conduction block (Fig. 14.7) was achieved in 92 patients (92%). The procedure duration, fluoroscopy time, and total RF delivery time were 179 ± 56, 51 ± 21, and 65 ± 26 min, respectively.

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Figure 14.6 A. Persistent epicardial conduction after endocardial ablation. The endocardial map catheter (Endo) showed a marked conduction delay, not reflected on the corresponding CS electrode facing the line (CSD), which showed only a slight conduction delay (arrows). Ablation within the coronary sinus is therefore indicated. B. The position of the ablation catheter during radiofrequency (RF) energy delivery in the coronary sinus. C. Conduction block achieved on the epicardial side after coronary sinus ablation, as evidenced by the significant conduction delay on the coronary sinus electrode (CSD, arrows).

Figure 14.7 Activation map after a complete mitral isthmus ablation line, created during coronary sinus (CS) pacing. There is a complete activation detour around the mitral annulus and the left pulmonary veins, indicating a complete conduction block along the line. LIPV, left inferior pulmonary vein.

After the initial procedure, 32 patients (32%) had at least one recurrence of atrial arrhythmia. All underwent a second procedure, with four requiring a third one (a total of 36 repeat ablation procedures). LA macroreentry, as defined by activation and entrainment mapping and/ or electroanatomical mapping, was observed to occur through an incomplete or recovered mitral isthmus line in five patients (Fig. 14.8A) or around the right PVs in four patients (Fig. 14.8B). These were successfully ablated by RF application at gaps along the mitral isthmus or with a linear lesion along the LA roof connecting the two

superior PVs (roof line, see above). Cavotricuspid isthmus– dependent flutter was observed in two patients. In 22 procedures, repeat ablation was performed for AF recurrence. Conduction recovery was observed in at least one PV in all patients, and non-PV foci (not observed during the index procedure) were identified in 12. At 1 year following the last procedure, 87 patients (87%) were arrhythmia-free without the need for antiarrhythmics [47,48]. Importantly, there was no change in atrial activation in sinus rhythm after mitral isthmus ablation, despite a significant activation detour during pacing from the coronary sinus, suggesting that atrial hemodynamic function had not been negatively affected. However, the significant complication with this procedure has been pericardial tamponade developing during the procedure, requiring drainage in six patients (3.6%). This occurred during catheter manipulation in the LA in two patients, during endocardial mitral isthmus ablation with high power in three patients (two with an audible pop), and in one patient during cavotricuspid ablation. All of the cases were related to a high level of power delivery of > 45 W during ablation. The rate of tamponade decreased to less than 1.5% with the reduction of maximal power delivery to ≤ 40 W. While ablation within the coronary sinus raises concern, particularly with regard to damage to the coronary arteries [46], all patients were screened after ablation with maximal exercise stress tests or coronary angiography, with no features suggesting stenosis. In chronic AF, preliminary data on 70 patients using this limited linear ablation procedure have been less favorable. In comparison with paroxysmal AF, conduction block at the mitral isthmus could be achieved in a similar proportion of patients (92%), in most cases with less RF energy applications and reduced need for ablation within the coronary sinus, suggesting a more dilated or diseased LA in such patients [49]. After a relatively short follow-up period of 8 ± 4 months, 51 patients (73%) remained in sinus rhythm without the use of antiarrhythmic drugs. 245

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Figure 14.8 Common types of reentrant tachycardia after PV and mitral isthmus ablation. A. Perimitral flutter, often resulting from an incomplete or a recovered mitral isthmus ablation line. LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein. B. Flutter around the right pulmonary veins. LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

Future directions With the role of the substrate in AF becoming increasingly important, it would theoretically be desirable in every patient to supplement PV isolation with the appropriate linear lesions in order to reduce the critical mass of substrate and to prevent macroreentry after ablation. However, the advantage of this approach is tempered by the possibility of increasing the complications of ablation, the challenging nature of LA linear ablation, as well as prolonged procedure time and radiation exposure. In addition, the potential for macroreentrant atrial arrhythmias due to incomplete lesions or conduction recovery is increased, especially in the presence of significantly dilated left atria. It is therefore important to identify which patients are capable of benefiting from additional substrate modification by linear ablation rather than PV electrical isolation alone.

Individualized approach to substrate modification after PV isolation Paroxysmal atrial fibrillation. We have observed that patients with sustained episodes of AF lasting > 24 h and large LA (longitudinal diameter > 57 mm) were more likely to have AF recurrence despite successful PV isolation [50]. In addition, the inducibility or persistence of sustained AF after PV isolation was associated with a greater propensity for clinical recurrence of AF. These patients subsequently required substrate modification to achieve the clinical elimination of AF. In contrast, noninducibility after the index procedure was associated with significantly lower arrhythmia recurrence, predominantly due

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to recovered PV conduction [51]. The results of an ongoing prospective study at our institution evaluating AF inducibility after PV isolation as a guide to further substrate modification have been encouraging (Fig. 14.9). Using this approach, in which LA linear ablation was performed only if AF lasting > 10 min was inducible after PV isolation, linear ablation was only required in 22 of 46 patients (48%), as AF had been rendered noninducible in the others after PV isolation. A single linear lesion was carried out in 17 patients, while the other five received a second linear lesion due to persistent AF or inducibility after the first lesion. At the end of this staged approach, noninducibility of AF was achieved in 44 patients (96%). After a follow-up period of 6 ± 5 months, 42 of the 46 patients (91%) were arrhythmia-free without requiring antiarrhythmic therapy [50,52]. On the basis of these results, an individualized approach to substrate modification in patients with paroxysmal AF, guided by inducibility of sustained AF or alternatively clinical recurrence of AF after PV isolation, may be useful in identifying patients in whom further substrate modification is required. Chronic atrial fibrillation. Ablation of chronic AF is challenging and involves substrate modification in almost all cases. In addition, multiple procedures are often required. Ablation is therefore restricted to the most symptomatic patients in many centers. However, an emerging and potentially important indication for the procedure in these patients is the presence of heart failure. In a recent study, the combination of PV isolation and limited LA linear ablation incorporating the mitral isthmus and roof lines was effective in maintaining sinus rhythm in 78% of patients with chronic AF and heart failure (69% without the need for drugs). Importantly, left ventricular function

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Figure 14.9 An individualized approach to the selection of patients requiring further substrate modification following pulmonary vein (PV) isolation, using inducibility of sustained atrial fibrillation (AF) after each procedural stage as a criterion. PAF, paroxysmal atrial fibrillation.

improved significantly, even in patients with coexisting structural heart disease or those who were adequately rate-controlled before ablation [53].

Conclusion The last decade has seen significant developments in our understanding of AF and has led to important advances in its management, especially with the development of catheter ablation techniques that have demonstrated the potential for achieving cure. It has become evident that PV ablation alone is associated with a success rate limited to approximately 70% in paroxysmal AF and much less in persistent and permanent AF. These results can be improved by additional substrate modification. While the value of linear ablation has been demonstrated, such lesions are technically challenging and are limited by their potential to produce left atrial reentrant arrhythmias as well as their higher complication rate. In addition, the ideal number and configuration of lesions sufficient to cure AF has yet to be established. Rather than applying a pre-specified ablation strategy to all patients, it is likely that an individualized approach to substrate modification, starting by identifying those patients who may need linear ablation after PV isolation, followed by customizing the lesion sets for each patient based on mapping, AF inducibility, or other parameters, could potentially offer the best balance between cure of AF and procedural risks.

References 1 Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991;22:983 – 8. 2 Benjamin EJ, Wolf PA, D’Agostino RB, et al. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 1998;98:946 –52. 3 Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825 –33. 4 Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002;347:1834 – 40. 5 Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillationaPharmacological Intervention in Atrial Fibrillation (PIAF): a randomised trial. Lancet 2000;356:1789 – 94. 6 Corley SD, Epstein AE, DiMarco JP, et al. The AFFIRM Investigators. Relationships between sinus rhythm, treatment and survival in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study. Circulation 2004;109:1509 –13. 7 Jaïs P, Haïssaguerre M, Shah DC, et al. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation 1997;95:572 – 6. 8 Haïssaguerre M, Jaïs P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659 – 66.

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9 Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 1999;100:1879–86. 10 Oral H, Knight BP, Tada H, et al. Pulmonary vein isolation for paroxysmal and persistent atrial fibrillation. Circulation 2002; 105:1077–81. 11 Haïssaguerre M, Jaïs P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol 2000;11:2–10. 12 Kanagaratnam L, Tomassoni G, Schweikert R, et al. Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a three-dimensional nonfluoroscopic mapping system: long-term follow-up. Pacing Clin Electrophysiol 2001;24:1774–9. 13 Allesie MA, Boyden PA, Camm AJ, et al. Pathophysiology and prevention of atrial fibrillation. Circulation 2001;103:769 –77. 14 Sanders P, Morton JB, Davidson NC, et al. Electrical remodeling of the atria in congestive heart failure: electrophysiological and electroanatomic mapping in humans. Circulation 2003;108:1461–8. 15 Morton JB, Sanders P, Vohra JK, et al. Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect. Circulation 2003;107:1775 – 82. 16 Sanders P, Morton JB, Kistler PM, et al. Electrophysiological and electroanatomical characterization of the atria in sinus node disease: evidence of diffuse atrial remodeling. Circulation 2004;109:1514–22. 17 Kistler PM, Sanders P, Fynn SP, et al. Electrophysiologic and electroanatomical changes in the human atrium associated with age. J Am Coll Cardiol 2004;44:109–16. 18 Verheule S, Wilson E, Everett T 4th, et al. Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation. Circulation 2003;107:2615–22. 19 Moe GK, Abildskov JA. Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Am Heart J 1959;58:59–70. 20 Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation, 2: intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406–26. 21 Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665–80. 22 Cox JL, Schuessler RB, Lappas DG, et al. An 81/2-year clinical experience with surgery for atrial fibrillation. Ann Surg 1996;224:267–75. 23 Cox JL, Ad N, Palazzo T, et al. Current status of the maze procedure for the treatment of atrial fibrillation. Semin Thorac Cardiovasc Surg 2000;12:15–9. 24 Shah D, Haïssaguerre M, Takahashi A, et al. Differential pacing for distinguishing block from persistent conduction through an ablation line. Circulation 2000;102:1517–22. 25 Hamdan MH, Kalman JM, Barron HV, et al. P-wave morphology during right atrial pacing before and after atrial flutter

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ablation: a new marker for success. Am J Cardiol 1997;79: 1417–20. Mackey S, Thornton L, He DS, et al. Simultaneous multielectrode radiofrequency ablation in the monopolar mode increases lesion size. Pacing Clin Electrophysiol 1996;19:1042 – 8. Nakagawa H, Yamanashi WS, Pitha JV, et al. Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation. Circulation 1995;91:2264 –73. Olgin JE, Kalman JM, Chin M, et al. Electrophysiological effects of long, linear atrial lesions placed under intracardiac ultrasound guidance. Circulation 1997;96:2715 –21. Swartz JF, Pellersels G, Silvers J, et al. A catheter based curative approach to atrial fibrillation in humans [abstract]. Circulation 1994;90 (Suppl):I35. Haïssaguerre M, Gencel L, Fischer B, et al. Successful catheter ablation of atrial fibrillation. J Cardiovasc Electrophysiol 1994;5: 1045 –52. Cannom DS. Atrial fibrillation: nonpharmacological approaches. Am J Cardiol 2000;84:25D–35D. Haïssaguerre M, Jaïs P, Shah DC, et al. Right and left atrial radiofrequency catheter therapy of paroxysmal atrial fibrillation. J Cardiovasc Electrophysiol 1996;7:1132 – 44. Jaïs P, Shah DC, Takahashi A, Hocini M, Haïssaguerre M, Clementy J. Long-term follow-up after right atrial radiofrequency catheter treatment of paroxysmal atrial fibrillation. Pacing Clin Electrophysiol 1998;21:2533 – 8. Gaita F, Riccardi R, Calo L, et al. Atrial mapping and radiofrequency catheter ablation in patients with idiopathic atrial fibrillation: electrophysiological findings and ablation results. Circulation 1998;97:2136 – 45. Garg A, Finneran W, Mollerus M, et al. Right atrial compartmentalization using radiofrequency catheter ablation for management of patients with refractory atrial fibrillation. J Cardiovasc Electrophysiol 1999;10:763 –71. Ernst S, Schluter M, Ouyang F, et al. Modification of the substrate for maintenance of idiopathic human atrial fibrillation: efficacy of radiofrequency ablation using nonfluoroscopic catheter guidance. Circulation 1999;100:2085 –92. Liu TY, Tai CT, Chen SA. Treatment of atrial fibrillation by catheter ablation of conduction gaps in the crista terminalis and cavotricuspid isthmus of the right atrium. J Cardiovasc Electrophysiol 2002;13:1044 – 6. Packer DL. Linear ablation for atrial fibrillation: the pendulum swings back. In: Zipes DP, Haïssaguerre M, eds. Catheter Ablation of Arrhythmias, 2nd ed. Armonk, NY: Futura, 2002: 107–28. Ernst S, Ouyang F, Lober F, et al. Catheter-induced linear lesions in the left atrium in patients with atrial fibrillation. J Am Coll Cardiol 2003;42:1271– 82. Jaïs P, Shah DC, Haïssaguerre M, et al. Efficacy and safety of septal and left-atrial linear ablation for atrial fibrillation. Am J Cardiol 1999;84:139R–146R. Pappone C, Oreto G, Lamberti F, et al. Catheter ablation of paroxysmal atrial fibrillation using a 3D mapping system. Circulation 1999;100:1203 – 8.

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42 Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 2004;109:2724 – 6. 43 Kumagai K, Uno K, Khrestian C, Waldo AL. Single site radiofrequency catheter ablation of atrial fibrillation: studies guided by simultaneous multisite mapping in the canine sterile pericarditis model. J Am Coll Cardiol 2000;36:917–23. 44 Betts TR, Roberts PR, Morgan JM. Feasibility of a left atrial electrical disconnection procedure for atrial fibrillation using transcatheter radiofrequency ablation. J Cardiovasc Electrophysiol 2001;12:1278–83. 45 Sanders P, Jaïs P, Hocini M, et al. Electrophysiologic and clinical consequences of linear catheter ablation to transect the anterior left atrium in patients with atrial fibrillation. Heart Rhythm 2004;1:176–84. 46 Becker AE. Left atrial isthmus: anatomic aspects relevant for linear catheter ablation procedures in humans. J Cardiovasc Electrophysiol 2004;15:809–12. 47 Jaïs P, Hocini M, Hsu LF, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004;110: 2996–3002.

Long linear lesions in the treatment of atrial fibrillation

48 Jaïs P, Hsu LF, Hocini M, et al. The left atrial isthmus: from dissection bench to ablation lab. J Cardiovasc Electrophysiol 2004;15:813 – 4. 49 Takahashi Y, Jaïs P, Hocini M, et al. Achievement of mitral isthmus block is easier in chronic versus paroxysmal atrial fibrillation [abstract]. Heart Rhythm 2004;1:S166. 50 Hsu LF, Jaïs P, Sanders P, et al. Catheter ablation of pulmonary vein atrial fibrillation: electrophysiologically guided procedure. In: Chen SA, Haïssaguerre M, Zipes DP, editors. Thoracic Vein Arrhythmias. Malden, MA: Blackwell, 2004: 248 – 62. 51 Haïssaguerre M, Sanders P, Hocini M, et al. Changes in atrial fibrillation cycle length and inducibility during catheter ablation and their relation to outcome. Circulation 2004;109: 3007–13. 52 Jaïs P, Hocini M, Hsu LF, et al. Individualized atrial fibrillation ablation with the end-point of non-inducibility: a prospective study [abstract]. Heart Rhythm 2004;1:S266. 53 Hsu LF, Jaïs P, Sanders P, et al. Catheter ablation for atrial fibrillation in congestive heart failure. N Engl J Med 2004;351:2373 – 83.

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Mapping the electrophysiologic substrate to guide atrial fibrillation ablation Koonlawee Nademanee, Mark Schwab, Joshua Porath, and Aharon Abbo

In 1994, Swartz and co-workers spurred interest in the use of catheter ablation to cure atrial fibrillation (AF) by introducing the catheter-based maze procedure [1]. Shortly thereafter, many prominent electrophysiology centers around the world began searching for the best approach for ablating AF [2–5]. The watershed observation by Haïssaguerre et al. that pulmonary veins are an important source of triggering foci for paroxysmal AF drew electrophysiologists’ attention to the pulmonary veins as important target sites for AF ablation [2]. Although the initial approach was to use focal ablation of the culprit pulmonary vein that was identified as the triggering site initiating AF [2,3], this approach was quickly abandoned due to numerous limitations: firstly, it is difficult to map and search for the triggering focus, due to a paucity of spontaneous AF occurrences; secondly, it is a time-consuming process, since triggering arrhythmia often requires multiple provocations and is generally quite inconsistent; thirdly, mapping multiple triggering foci is a daunting task; and fourthly, multiple cardioversions are often needed for patients whose AF has become persistent. Changing the strategy, electrophysiologists began to isolate the electrical connections of all four veins from the left atrial muscle. Various techniques were used to achieve electrical isolation of the pulmonary veins (PVs): • Segmental isolation, introduced by Haïssaguerre and colleagues [6]. • PV isolation at the antrum of the pulmonary veins, at the atrium–venous junction, using intracardiac ultrasound guidance [5]. • Electroanatomical mapping and circumferential pulmonary vein ablation, popularized by Pappone et al. [4]. However, total isolation of all four veins poses a risk of pulmonary vein stenosis. In addition, this strategy assumes that pulmonary veins are virtually the primary source of triggers or perpetuators of AF and thus that all AF patients can essentially be treated in the same way, guided by an anatomical scheme rather than electrophysiological mapping. It is therefore not surprising to observe 250

that electrical isolation of PVs has a variable success rate in the treatment of patients with all types of AF [7– 9]. Since AF is not homogeneous and the electrophysiologic mechanisms underlying it may vary from one patient to another, it is not likely that a single anatomical ablative design will fit all types of AF. Logically, it is best to search for an approach capable of identifying target sites for AF ablation in a given patient by identifying the substrates that perpetuate AF. It was previously thought that AF substrates could not be mapped, as the conventional wisdom suggested that reentrant circuits underlying the AF substrate were random and were not amendable to point-to-point mapping or endocardial mapping. However, recent studies have indicated that it is possible to identify AF substrates that serve as “AF perpetuators” by searching for areas that have complex fractionated atrial electrograms (CFAEs) [10]. Ablating these areas that have persistent CFAEs eliminates AF. With this observation, we have proposed a new approach to AF ablation, as described below.

Characteristics of atrial electrograms during atrial fibrillation When both atria are mapped during atrial fibrillation, it is found that there are three types of atrial electrogram characteristics [10–13]: • A single potential atrial electrogram. • Double potential electrograms, defined as two discrete atrial electrograms with an interval between the two atrial deflections shorter than 70 ms. As previously described, a double potential atrial electrogram is commonly seen in areas exhibiting a line of block. • Complex fractionated atrial electrograms (CFAEs), which are defined as follows: a) atrial electrograms that have fractionated electrograms composed of two deflections or more, and/or have a perturbation of the baseline with continuous deflection of a prolonged activation

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Figure 15.1 Examples of complex fractionated atrial electrograms (CFAEs). A. Fractionated electrograms with continuous prolonged activation complexes over the posterior septal areas. CS, coronary sinus.

B. Another type of CFAE at the left atrial (LA) roof, where electrograms with a very short cycle length in comparison with the rest of the atria were recorded. RAA, right atrial appendage.

complex over a 10-s recording period (Fig. 15.1A); b) atrial electrograms with a very short cycle length (≤ 120 ms) (Fig. 15.1B) averaged over a 10-s recording period. In general, CFAEs are usually low-voltage multiple potential signals between 0.05 and 0.25 mV. It is noteworthy that in some AF patients, CFAEs may exhibit signals with a very short cycle length (< 100 ms) without clear-cut multiple prolonged potentials. However, in comparison with the rest of the atria, this site has the shortest cycle length, which drives the rest of the atria. More importantly, the distribution of these electrograms in the right and left atria is vastly different from one area to another [10,11]. On the other hand, even though there are regional differences in the distribution of these atrial electrograms, individual types of atrial electrogram stay surprisingly stable and do not change from one area to another. In other words, the presence of these atrial electrograms in each region allows relative spatial and temporal stability. Point-to-point mapping of these electrogram regions can therefore be carried out, and they can be linked to the electroanatomical map to display their distributions in the atria. In addition, it is becoming evident that patients with atrial fibrillation are not homogeneous with respect to the pattern of these regional distributions of atrial electrograms during AF. For example, patients who have chronic atrial fibrillation tend to have a higher CFAE distribution in more areas of the atria than is seen in patients with paroxysmal AF [10].

tials (CFAEs) observed during intraoperative mapping of human AF were found mostly in areas of slow conduction and/or at pivot points, where the wavelets turn around the end of the arch of the functional block [12,13]. Such areas of CFAE during AF therefore represent either continuous reentry of the fibrillatory waves into the same area or an overlap between different wavelets entering the same area at different times. Quan et al. showed that electrical stimulation of cardiac ganglia near the pulmonary vein orifices significantly shortened the atrial refractoriness close to the site of the stimulation and that the effects diminished at distances > 2 cm away from this site [14]. More importantly, electrograms recorded from these areas consistently show CFAEs. This observation raises the possibility that neurotransmitter releasesae.g., of acetylcholineaat preganglionic and/or postganglionic terminals may contribute to the genesis of CFAEs. This may also play a role in the differences in the CFAE regional distribution in the atria during AF. Scherlag et al. have convincingly demonstrated that areas in the left atrium in which ganglionic plexuses are identified by highfrequency stimulation almost always allow CFAEs to be recorded after the high-frequency stimulation initiates atrial fibrillation [15]. The authors suggest that marked shortening of the action potential duration initiates the formation of early repolarization, resulting in sustained AF. Finally, CFAEs may represent an area of focal reentry using pathological or functional anisotropic propagation in the areas of CFAE recording; this phenomenon is commonly observed in ischemic myocardium or around the border zone of scar myocardium [16]. It is possible that all of the above electrophysiological changes are the underlying causes. However, regardless of the mechanism underlying CFAEs, it is very likely that CFAEs represent substrate areas in which AF is perpetuated.

Electrophysiologic mechanisms underlying CFAEs The elegant studies by Konings et al. showed that the complex, multiple-component fractionated electrical poten-

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Technique of AF substrate mapping guided by point-to-point mapping of CFAEs Conventional mapping Our mapping technique is straightforward and is always done during AF. For recording and stimulation, multipolar electrode catheters are positioned in the coronary sinus and/or right atrium. AF is induced in patients who have paroxysmal AF, but who are in normal sinus rhythm during the time of study. Patients with premature atrial contractions are first given isoproterenol infusions; if sustained AF is not provoked, then rapid atrial pacing is performed, with or without isoproterenol infusion. For patients with infrequent premature atrial contractions, programmed atrial stimulation and rapid atrial pacing is carried out with or without isoproterenol. Once AF has been sustained for over 5 min, the patients undergo nonfluoroscopic electroanatomical mapping with the Carto navigation and mapping system (Biosense Webster, Inc., Diamond Bar, California, USA) [16,17], as do patients with chronic AF. The coronary sinus or right atrial appendage recording is used for electrical reference during Carto mapping. Intracardiac recordings are simultaneously recorded with the Carto and a computerized multichannel recording system (EPWorkMate, EPMedSystems, Inc., West Berlin, New Jersey, USA). Tachycardia cycle lengths are monitored and recorded from both the reference and the mapping catheter. The Carto system creates biatrial replicas in the form of a three-dimensional map. Carto allows navigation within the cardiac chamber with little fluoroscopic exposure and combines three-dimensional endocardial anatomy with electrical activation wavefronts. The physician is then able to locate, tag, and later revisit relevant sites. Heparin (5000 U bolus followed by 1500 U every hour) is used for anticoagulation. During AF, the local activation time of the arrhythmia is of no value in guiding the activation sequence mapping, as we do not simultaneously map multiple sites in both atria. However, Carto provides an invaluable endocardial shell and enables the operator to associate areas of CFAE with the anatomy of both atria. We use bipolar recording filtered at 30 –500 Hz and define CFAEs as mentioned above. Using the three-dimensional anatomic guide, areas with CFAEs can be located and ablated. Radiofrequency (RF) energy is delivered between the distal electrode of the locatable mapping catheter and a large patch electrode placed on the patient’s back. RF applications are delivered with a maximal temperature of 55 – 60 °C at the catheter tip. 252

The primary end points during RF ablation of AF are either complete elimination of the areas with CFAEs or conversion of AF to normal sinus rhythm. When the areas with CFAEs are completely eliminated but the arrhythmias continue as organized atrial flutter or atrial tachycardia, the atrial tachyarrhythmias are mapped and ablated (occasionally in conjunction with ibutilide 1 mg for 10 min to revert the arrhythmias to sinus rhythm). If the arrhythmias are not successfully terminated, external cardioversion is carried out. Figure 15.2A shows a Carto map from a physician who had had a history of persistent AF for over 2 years and in whom flecainide treatment had failed; he had undergone multiple cardioversions. The voltage map shows areas of low-voltage signals from CFAEs at the interatrial septum, left superior pulmonary vein, posterolateral aspect of the mitral annulus, and proximal coronary sinus at the coronary sinus os; the cycle length at the os (CS p in Fig. 15.2B) was short at 75 ms in comparison with the rest of the coronary sinus recording and the right superior pulmonary vein (RSPV) recording, where the electrograms were very organized. After ablation along these areas (as shown in Fig. 15.2B), the tachycardia cycle lengths along the distal coronary sinus recording significantly increased in comparison with the findings before ablation. It should be noted that there were also distinct differences in the cycle length between the electrograms recorded from the distal coronary sinus and those from the proximal coronary sinus at the coronary sinus os. The tachycardia cycle length at the coronary sinus os was four times shorter than those at the coronary sinus recording distal to the os (Fig. 15.2B); this suggests either 4 : 1 conduction or a conduction block from these localized areas that still have focal AF at this site. Thus, the effects of the ablations on the CFAE areas at the interatrial septum and the left superior pulmonary vein to the mitral annulus resulted in eliminating fibrillatory conduction in those areas, and in turn changing the overall AF substrate to become localized only at the proximal CS. When RF energy was applied at the proximal coronary sinus areas, as shown in Fig. 15.2B, AF terminated. The patient remained free of symptoms and arrhythmia during the long-term follow-up. It is important to emphasize that the tachycardia cycle length almost always lengthens progressively before termination. If there is no change in the tachycardia cycle length, the ablation may not be effective and one must reevaluate the findings to determine whether the RF energy is being delivered adequately or whether remapping of the CFAEs may be warranted.

Mapping with CFAE software Using the operator’s eye to identify and tag CFAEs to the atrial shell is subjective and heavily dependent on the

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Figure 15.2 A. A posteroanterior view of Carto voltage mapping in a physician with chronic atrial fibrillation (AF), showing areas of complex fractionated atrial electrograms (CFAEs) along the septum and the mouth of the left inferior pulmonary vein (LIPV) and proximal coronary sinus (CS). This voltage map shows that the CFAE areas correspond to the low-voltage areas before ablation. The color scale ranges from red as the lowest voltage (0.08 mV) to magenta as the highest (1 mV). The red dots are the ablation points. Tracing 1: CFAEs from the LIPV; tracing 2: CFAEs from CS os; tracing 3: normal electrograms at the right superior pulmonary vein; tracing 4:

CFAEs at the upper septum. B. In the same patient, the map is seen here in the mesh fashion to highlight the ablation areas. The effect of the ablations before the last application at the coronary sinus os on the atrial fibrillation cycle length in the coronary sinus recording is demonstrated in the tracings on the lower left. The tracing on the lower right shows CFAEs at the proximal coronary sinus (cycle length 75 ms). While the cycle length at the distal coronary sinus increased significantly from 215 to 265 ms, the tachycardia cycle length at the coronary sinus os remained short at 69 and 92 ms. The last ablation at this site terminated the atrial fibrillation.

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Figure 15.3 A complex fractionated atrial electrogram (CFAE) map of a patient with paroxysmal atrial fibrillation shows a posteroanterior view of the left atrium. The map was created during atrial fibrillation. The map shows CFAE areas in relation to the shortest cycle length of the fractionated electrogram. Red areas have the shortest cycle length; in this patient, the right superior pulmonary vein (RSPV) has the shortest cycle length (< 70 ms). The electrograms in this area are shown in the inset (arrow); the bottom tracing is recorded from the mid-coronary sinus (CS) and has a much longer cycle length, without fractionation. The red dots are the radiofrequency application points (see text).

operator’s level of experience. Success or failure depends on accurately and thoroughly identifying areas with consistent CFAEs and clearly illuminating their locations. To improve the accuracy of CFAE mapping, software has been developed featuring algorithms capable of associating the anatomical shell of both atria with areas of complex fractionated electrograms. To allow easy recognition of the CFAE map, areas of CFAEs are displayed in colorcoded areas depending on the degree of fractionated signals and their cycle lengths. Figure 15.3 shows an example of a CFAE map from a patient with daily symptomatic paroxysmal atrial fibrillation (PAF). The map shows a posteroanterior view of the left atrium, with electroanatomical map clearly showing the CFAE area located exclusively around the right superior pulmonary vein (RSPV), as shown in red. The rest of the left atrium was relatively organized and activated with a relatively much longer cycle length. The software displays areas in which no CFAEs are found as gray. The colors show the areas according to the cycle lengths of the CFAEs. In this case, the RSPV has the shortest cycle length among the CFAEs (< 70 ms) and serves as the prime target for ablation. A few RF applications (red dots) terminated the AF and rendered it noninducible. The map shows that the RSPV is the only site perpetuating AF; in this case, it would also be possible to use a different ablation strategy, by isolating this RSPV from the left atrium. This would probably yield similarly successful results as eliminating all CFAEs in this area. The other important aspect of CFAE mapping is the persistence of the CFAE recording. To be of any significance in perpetuating AF, CFAE areas have to be not temporary, but stable. We have therefore also created an algorithm for 254

recognizing the persistence of CFAEs, which can be displayed as a “confidence interval map,” taking into account the number of CFAEs repetitively recorded during the span of the recording period. The higher the confidence interval, the more CFAEs are detected. Figure 15.4 shows electroanatomical mapping of the left atrium in a patient with persistent AF, with both shortest complex interval and confidence interval maps. It should be noted that both maps display the prime target sites in almost identical areas of the left atrium; the shortest interval map shows the areas with the shortest interval around 70 ms along the antrum of the left and right superior pulmonary veins and along the posterior aspect of the left atrial roof. It was confirmed that these sites had high levels of repetitiveness by a confidence interval ranging from medium to high confidence. These maps guided ablation to the corresponding areas (red dots), resulting in termination of AF. Since the patient reverted to sinus rhythm, the end point of the ablation, we did not proceed to ablate all of the CFAE areas that had a relatively short cycle length and a fairly high confidence interval. After treatment, the patient did well and had no recurrent AF. The excellent results of the ablation in this patient again clearly suggest that mapping of CFAEs is an effective method of guiding AF substrate ablation and that it significantly improves the long-term outcome.

Evidence that CFAE areas represent AF substrates Recent research has provided support for the hypothesis that CFAE areas are critical in perpetuating AF and that

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A

Mapping the electrophysiologic substrate to guide atrial fibrillation ablation B

Figure 15.4 Two electroanatomical complex fractionated atrial electrogram (CFAE) maps in a patient with persistent atrial fibrillation, with the shortest complex interval (A) and confidence interval (B). Both maps show the left atrial area in a posterior superior oblique view. The cycle lengths of the shortest complex interval range from 70 to 120 ms. The red color represents the shortest interval and the magenta represents the

longest interval (120 ms); the area in which cycle length is longer than 120 ms is shown in gray. The confidence interval map (B) shows the area with the highest number of CFAEs, with the confidence interval ranging from the highest (7.2–12, red) to the lowest (2, magenta). The red dots are radiofrequency application sites for both maps. (See text for details.)

radiofrequency ablation over these areas leads to the termination of AF and renders the atria incapable of sustaining AF. The findings are summarized below.

ablation; 18 (28%) required concomitant ibutilide treatment. The remaining six patients with chronic AF (9%) needed external cardioversion with ibutilide to attain normal sinus rhythm. As shown in the above example, after radiofrequency application over the CFAE areas, most atrial electrograms either disappeared or were drastically reduced in amplitude, resulting in complete elimination of CFAEs in virtually all of the patients, often associated with organization of the atrial electrograms in the areas adjacent to the ablated ones. The elimination of CFAEs always uniformly increased tachycardia cycle lengths before AF termination, even though the cycle lengths were measured from the electrical reference from the area remote from the ablation sites. The overall tachycardia cycle length increased from 172 ± 26 ms at baseline to 237 ± 42 ms (P < 0.05). At the 1-year follow-up, 92 of the 121 patients (76%) had only one ablative session and were free of arrhythmia; 47 had PAF (two of whom required amiodarone therapy) and 45 had chronic AF (three requiring amiodarone and two requiring sotalol). Ten patients with PAF and 19 patients with chronic AF required a second ablation procedure, after which seven patients with PAF (one of whom required amiodarone) and 11 patients with chronic AF (two of whom required amiodarone) became free of arrhythmia. However, the remaining 11 patients (eight with

Previously published study [10]. We studied 121 patients (92 men, 29 women; mean age 63 ± 12 years), 64 of whom had chronic AF (26 with persistent AF and 38 with permanent AF) and 57 of whom had paroxysmal AF. Paroxysmal AF is self-terminating within 7 days of the onset; persistent AF is not self-terminating within 7 days, or is terminated by either electrical or pharmacological conversion; permanent AF is AF that cannot be terminated by cardioversion. Most of the patients had a long history of AF (4 ± 3.3 years) and treatment with at least two previous antiarrhythmic drugs had failed (mean 2.4 ± 1.3 agents). Seventy-nine patients had structural heart disease: 42 had coronary artery disease, 17 had cardiomyopathy, 14 had valvular heart diseases, and six had congenital disease. The mean size of the left atrium was 42 ± 6 mm. All of the patients underwent biatrial Carto mapping. The mean procedure time was 3.1 ± 0.85 h and the fluoroscopy time was 14.7 ± 4.8 min. During the ablative procedure, all 57 PAF patients went into normal sinus rhythm and AF was rendered noninducible; eight (14%) required concomitant ibutilide treatment. Fifty-eight patients with chronic AF had AF converted to sinus rhythm during

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chronic AF, three with PAF) continued to have recurrent atrial tachyarrhythmias; four of these patients required amiodarone, and seven were treated with an atrial defibrillator. Overall, 110 patients (91%) were free of arrhythmia and symptoms, without any late complications. Clearly, the above findings suggest that CFAE areas are indeed the substrates that perpetuate AF. The above findings also emphasize the fact that this ablation approach is very effective and yields excellent long-term outcomes, showing that by eliminating CFAE areas, the substrate is also removed and the atria are no longer able to fibrillate. Recent study. The above study was recently expanded to include more patients with both paroxysmal and chronic atrial fibrillation. A total of 302 patients were included (209 men, 93 women; mean age 62 ± 13 years), 161 of whom had chronic atrial fibrillation and 141 had paroxysmal AF. Most of the patients had a long history of AF (5 ± 4.2 years) and treatment with at least two previous antiarrhythmic drugs (mean 2.2 ± 1 agents) had failed. A total of 188 of the patients had heart diseases: 92 had coronary artery disease, 72 had cardiomyopathy, 16 had valvular heart disease, and eight had congenital disease. Figure 15.5 shows the effects of ablation over the areas of fractionated atrial electrograms for the overall population. Of the 141 patients with PAF, 117 patients had their AF terminated during ablations, and AF was rendered noninducible. The remaining 24 patients required a concomitant ibutilide infusion for AF termination; no reinduction was attempted in these patients. Of the 161 patients with chronic AF, 144 had AF terminated during RF applications over the CFAE areas (93 without ibutilide and 51

Figure 15.5 The flow chart shows the effects of radiofrequency ablation guided by complex fractionated atrial electrogram (CFAE) mapping on the termination of atrial fibrillation (AF). NSR, normal sinus rhythm; PAF, paroxysmal atrial fibrillation.

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with ibutilide infusion). Only 17 patients with chronic AF required external cardioversion to convert the rhythm to AF. The fact that ablating CFAE areas terminated AF in over 90% of this patient population strongly suggests that these CFAE areas contribute substantially to the perpetuation of AF. These findings suggest that CFAE mapping can precisely identify AF substrates of this type that maintain AF. Interestingly, these AF substrates tend to be located in specific parts of the atria, as shown by regional differences in distribution of the CFAEs.

Regional distribution of CFAEs To characterize AF in humans using biatrial Carto mapping, the right and left atria were divided into nine areas (Fig. 15.6). The interatrial septum, the pulmonary veins, and the coronary sinus were the most common sites in which CFAEs were located. The advent of Carto mapping not only made it possible to navigate freely in both atria but also allowed us to revisit the areas of interest in which CFAEs were regularly found. The distribution of CFAEs, while regionally different, was not temporary and tended to be confined to the same locations. As a result, mapping demonstrated that AF is heterogeneous and can be divided into three types on the basis of the regional distribution of CFAEs:

Figure 15.6 The regional distribution of complex fractionated atrial electrograms (CFAEs). On the basis of Carto mapping, the biatrial replica can be divided into nine distinct areas: 1) the septum, including the Bachmann’s bundle; 2) the left posteroseptal mitral annulus and coronary sinus os; 3) the pulmonary veins; 4) the roof of the left atrium; 5) the mitral annulus; 6) the cavotricuspid isthmus; 7) the crista terminalis; 8) the right and left atrial appendages; and 9) the superior vena cava–right atrial junction. The numbers shown in each region represent the number of patients whose CFAEs were found and needed to be ablated in that region. (See text for further details). LAO, left anterior oblique; PA, posteroanterior.

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A

Figure 15.7 A. Electroanatomical complex fractionated atrial electrogram (CFAE) maps in a patient with permanent atrial fibrillation. The maps show in left anterior oblique (LAO) and posteroanterior (PA) views of CFAEs areas with color-coded confidence intervals; red represents the highest repetitiveness of CFAEs and gray represents no CFAEs in these areas. Abl-d, ablation distal bipolar electrode; CS, coronary sinus. B. The effects of the ablations on areas with high confidence interval recordings of CFAEs, resulting in drastic alteration in the tachycardia cycle lengths and eventual conversion from AF to atrial tachycardia, localized at the mitral annulus. The composite compares intracardiac recordings between the first

radiofrequency application (RF1) (top) and the 43rd RF application (RF43). The conversion of atrial fibrillation to atrial tachycardia during the 43rd RF application is shown in the lower panel. The asterisk denotes the time at which RF is switched on. C. The earliest site that activated the atrial tachycardia. The ablation distal bipolar electrode recorded electrograms at the anterior mitral annulus; it should be noted that it is 105 ms earlier than the P wave. RF ablation at this site reverted atrial tachycardia to sinus rhythm. The top panel was recorded at the speed of 100 ms, whereas the lower panel showing termination was recorded at the speed of 75 ms.

• Type 1. The CFAEs are only located in one area, and the rest of the atria displays discrete, organized atrial electrograms. Typically, the cycle length of the CFAE area is much shorter than other areas in the rest of the atria (Fig. 15.3). When RF applications are applied to these areas, they result in the elimination of the CFAEs, terminating the AF. • Type 2. The CFAEs are located in two areas and ablations are required in both areas to terminate AF. For the purposes of definition, we classify the pulmonary veins as one area, regardless of how many veins are involved. • Type 3. The CFAEs are distributed over three or more areas. Figure 15.7A shows an example of a type 3 CFAE distribution in a patient with chronic permanent AF. The map shows left anterior oblique and posteroanterior views of the CFAE map. The maps show that the CFAEs are distributed mainly along the anterior and posterior aspects of the left superior pulmonary vein. Ablation of these areas (after 43 RF applications; Fig. 15.7B) converted AF to atrial tachycardia. The atrial tachycardia focus was at the mitral annulus, where the last RF application was delivered, resulting in termination of the tachycardia (Fig. 15.7C). The

patient did well up to 6 months after the ablation, with no antiarrhythmic treatment, and had no recurrences of AF.

Long-term outcomes Figure 15.8 summarizes the effects of the ablations guided by CFAEs on the long-term clinical outcome. Of the 141 PAF patients, 129 (91%) had no AF recurrenceaonly 13 patients (10%) required concomitant antiarrhythmic drugs. However, several patients required multiple ablations: 28 patients underwent two ablations and nine had three ablations. Of the 161 patients with chronic AF, 137 patients (85%) became free of arrhythmia and did very well; 25 patients required concomitant antiarrhythmic treatment. Fortysix patients had two ablations and 18 patients had three ablations. These findings emphasize the fact that this approach to ablation is very effective and yields an excellent long-term outcome. This in turn indicates that when CFAE areas are eliminated, the substrate is also removed and the atria can no longer fibrillate. 257

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B

C

Figure 15.7 (continued )

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Each of the 12 patients who developed isthmusdependent atrial flutter underwent successful ablation of the cavotricuspid isthmus, resulting in the elimination of recurrent arrhythmias. Atrial tachyarrhythmias that occurred after ablation in some patients may have been multifactorial. It is possible that the ablation procedure itself caused the arrhythmias, as is commonly seen after the maze surgical procedure [19], due to electrophysiological changes that occur during the healing process and disappear once healing is complete. Further evidence for this theory was provided by the fact that many of the atrial arrhythmias that occurred in these patients following ablation ended 12 weeks after the ablation. Another possibility is that some of the arrhythmias were the primary arrhythmias that induced AF via fibrillatory conduction. Once the atria could no longer fibrillate after the ablations, due to the substrates for AF having been eliminated, the primary arrhythmia manifested itself again. Many of the patients who had cavotricuspid isthmusdependent atrial flutter as the recurrent arrhythmia did not have this area ablated at the initial session, supporting this supposition. However, 15 patients with atypical atrial flutter had the reentrant circuits clearly defined in the areas in which RF applications were performed; these patients most likely developed ablation-related macroreentrant tachycardia.

Figure 15.8 The flow charts show the long-term clinical outcomes for patients with paroxysmal and chronic atrial fibrillation. AA, antiarrhythmic agent; AF, atrial fibrillation; NSR, normal sinus rhythm; PAF, paroxysmal atrial fibrillation.

Atrial tachyarrhythmias after CFAE ablation Among the 302 patients, 151 experienced recurrent atrial tachyarrhythmias, but the majority of the arrhythmias were not AF. Of the 142 patients with early recurrent atrial arrhythmias, 96 became free of arrhythmia and symptoms 12 weeks after the initial ablation. Forty-six of the 55 patients who were continuing to have atrial tachyarrhythmias 3 months after the initial ablations underwent a second ablation for the following arrhythmias: 15 had atypical left atrial flutter (eight in the interatrial septum, four with mitral isthmus-dependent atrial flutter, and three in the roof of the left atrium); 12 had atrial flutter dependent on the cavotricuspid isthmus; 11 had atrial tachycardia (three at the left superior pulmonary vein, three at the right superior pulmonary vein, one at the superior vena cava, and four at the coronary sinus os); and eight had AF. Nine patients who continued to have AF after the first ablation session did not undergo a second ablation.

Procedure-related complications Among the 302 patients, 17 (6%) experienced major complications. Two patients had a cerebrovascular accident 24 h after the ablation. Six patients had cardiac tamponade, one had a complete atrioventricular block, and two had transient severe pulmonary edema. Six patients developed groin complications, with femoral arteriovenous fistulas or pseudoaneurysms.

Conclusions These data clearly demonstrate that CFAEs represent a strong surrogate of AF substrates that are crucial for sustaining AF. These areas can be readily mapped using electroanatomical point-to-point mapping of the CFAEs. It is noteworthy that these CFAEs, once found in specific areas, do not meander and tend to be confined in the same areas, suggesting that AF substrates have temporal and spatial stability, allowing point-to-point mapping of the substrates. This supposition is further supported by the fact that RF ablation over the CFAE areas resulted in termination of the AF and/or rendered AF noninducible afterward. The long-term outcomes with this approach are excellent, with a relatively low complication rate. 259

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References 1 Swartz JF, Pellersels G, Silvers J, Patten L, Cervantez D. A catheter based curative approach to atrial fibrillation [abstract]. Circulation 1994;90(Suppl I):I-335. 2 Haïssaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659– 66. 3 Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 1999;100:1879–86. 4 Pappone C, Oreto G, Lamberti F, et al. Catheter ablation of paroxysmal atrial fibrillation using a 3D mapping system. Circulation 1999;100:1203–8. 5 Marrouch NF, Dresing T, Cole C, et al. Circular mapping and ablation of the pulmonary vein for treatment of atrial fibrillation. J Am Coll Cardiol 2002;40:464–74. 6 Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000;102:2463–5. 7 Pappone C, Rosanio S, Augello G, et al. Mortality, morbidity and quality of life after circumferential pulmonary vein ablation for atrial fibrillation: outcomes from a controlled randomized long-term study. J Am Coll Cardiol 2003;42:185 –97. 8 Oral H, Scharf C, Chugh A, et al. catheter ablation for paroxysmal atrial fibrillation: segmental pulmonary vein ostial ablation versus left atrial ablation. Circulation 2003;108:2355 – 60. 9 Cappato R, Calkins H, Chen S, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100 –5.

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10 Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044 – 53. 11 Jaïs P, Haïssaguerre M, Shah DC, et al. Regional disparities of endocardial atrial activation in paroxysmal atrial fibrillation. Pacing Clin Electrophysiol 1996;19:1998 –2003. 12 Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665 – 80. 13 Konings KTS, Smeets JLRM, Penn OC, et al. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans. Circulation 1997;95:1231– 41. 14 Quan KJ, Lee JH, Van Hare GF, Biblo LA, Mackall JA, Carlson MD. Identification and characterization of atrioventricular parasympathetic innervation in humans. J Cardiovasc Electrophysiol 2002;13:735 – 9. 15 Scherlag BJ, Nakagawa H, Jackman WM, et al. Electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation. J Interv Card Electrophysiol 2005;13(Suppl 1): 37– 42. 16 de Bakker JM, van Capelle FJ, Janse MJ et al. Slow conduction in the infarcted human heart “zigzag” course of activation. Circulation 1993;88:1872 – 87. 17 Khongphatthanyothin A, Kosar E, Nademanee K. Nonfluoroscopic three-dimensional mapping for arrhythmia ablation: tool or toy? J Cardiovasc Electrophysiol 2000;11:239 – 43. 18 Shpun S, Gepstein L, Hayam G, et al. Guidance of radiofrequency endocardial ablation with real-time three-dimensional magnetic navigation system. Circulation 1997;96:2016 –21. 19 Cox JL, Schuessler RB, Lappas DG, et al. An 81/2-year clinical experience with surgery for atrial fibrillation. Ann Surg 1996;224:267–75.

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Ablation for rate control of atrial fibrillation Harish Doppalapudi and G. Neal Kay

Introduction Atrial fibrillation (AF) affects more than 2 million people in the U.S. The ideal goal in the treatment of AF is to keep the patient in sinus rhythm. Restoration of sinus rhythm and prevention of AF are often difficult, even with vigorous antiarrhythmic therapy. The secondary goal is to maintain good control of the ventricular rate during AF. This can be achieved by drugs that block the atrioventricular (AV) node or by catheter ablation. It is estimated that about 12% of patients with AF have a ventricular rate that is refractory to medical therapy. These patients may suffer intractable symptoms and have a severely diminished quality of life. Radiofrequency (RF) catheter ablation of the AV node followed by permanent pacemaker implantation is a recognized treatment to alleviate symptoms in many of these patients. Catheter ablation of the AV junction for treatment of uncontrollable atrial arrhythmias was first proposed in 1982 by Scheinman et al. [1] and Gallagher et al. [2]. Early AV junction ablation was achieved by direct current (DC) shock. The application of thermal energy with RF electrical current (dessication) has now replaced high-energy endocavitary DC shock (fulguration). DC ablation results in a high temperature (1700 °C) and high pressure (140 atm) at the tip of the catheter, and the lesions are large, imprecise, and arrhythmogenic. By contrast, RF ablation results in a minimal temperature rise and creates smaller, homogeneous, and weakly arrhythmogenic lesions. Equivalent AV blocks are created with both modalities, but fewer sessions are required for RF. There are also fewer major complications with RF.

Rate-control strategy Physiology of atrial fibrillation Atrial fibrillation is characterized by an irregular, and

usually rapid, ventricular rate, which can lead to hemodynamic deterioration acutely and to tachycardia-mediated cardiomyopathy in the long run. Hemodynamic deterioration in AF is manifested as palpitations, dizziness, dyspnea, and poor exercise capacity. The hemodynamic consequences of AF can result from a rapid ventricular rate, from an irregular R–R interval, or from loss of AV synchrony. The effect of rapid ventricular rates in decreasing cardiac output is well recognized. Irregularity of the ventricular rate by itself has been shown to result in reduced coronary flow [3,4] and decreased cardiac output [5–7]. Tachycardia-induced cardiomyopathy is a well-recognized complication of long-standing tachyarrhythmias, including AF [8]. The diagnosis of tachycardia-induced cardiomyopathy is made when left ventricular systolic function improves to a normal or near-normal level after rate control in patients with tachyarrhythmias. The incidence of tachycardia-induced cardiomyopathy has been noted to be around 25% in several studies of AF [9–13].

Determinants of ventricular rate Physiologically, the AV node is a slow-response tissue, since the generation of its action potential depends on calcium ions flowing through a kinetically slow channel. The activation and reactivation characteristics of these calcium channels normally result in slow conduction through the AV node. The AV node is richly supplied by both components of the autonomic nervous systemathe sympathetic nerves facilitating, and the parasympathetic nerves slowing, AV nodal conduction. In the typical patient with untreated AF, the ventricular rate during the day varies between 100 and 160 beats/min. A ventricular rate below 60 beats/min may be seen with a high vagal tone (as in athletes), with AV nodal disease (which is often associated with sinus node disease), or in the presence of drugs that block AV nodal conduction. A ventricular rate above 200 beats/min may occur in the presence of an accessory pathway (preexcited AF), hyperthyroidism, catecholamine 261

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excess, or parasympathetic withdrawal. There is also a circadian variation in the ventricular response rate, caused by a circadian rhythm for both AV nodal refractoriness and concealed conduction [14]. This variation is attenuated in patients with heart failure, in whom autonomic tone is characterized by sympathetic activation and vagal withdrawal.

Optimal rate control and strategies What constitutes optimal rate control in AF? In the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) trial [15], the targets for the ratecontrol arm were a resting heart rate < 80 beats/min, a 24-h Holter average of < 100 beats/min with no rate > 110% of the age-predicted maximum, and a heart rate < 110 beats/min during a 6-min walk. The pharmacologic options for rate control include AV node-blocking drugs such as digoxin, beta-blockers, and calcium-channel blockers. Nonpharmacologic options include AV node ablation and AV node modification. Radiofrequency energy is almost universally used during ablation nowadays, making DC shock an obsolete modality.

Outcomes after AV node ablation Clinical outcomes Clinical outcomes after RF ablation of the AV node in patients with medically refractory atrial tachyarrhythmias have been investigated in several nonrandomized studies. These studies compared the patients’ condition before ablation with their condition after a variable duration of follow-up. However, only a few trials have been conducted in a randomized fashion. A recent meta-analysis of 21 studies from 1989 to 1998 (19 nonrandomized studies, two randomized trials), including a total of 1181 patients, examined the effects of AV node ablation and pacing therapy on the clinical outcome in patients with medically refractory atrial tachyarrhythmias, primarily atrial fibrillation [16]. The outcome analysis included 642 patients in 15 studies. The average duration of follow-up ranged from 48 days to 2.3 years. Thirteen studies were nonrandomized trials, and two compared ablation and pacing therapy with pharmacological therapy or RF modification of AV nodal conduction. Nineteen measures of clinical outcomea including symptoms, quality of life, exercise duration, ventricular function, and health-care useawere derived from the studies. Significant improvement was demonstrated after ablation and pacing therapy in all outcome measures except echocardiographic fractional shortening, which demonstrated a trend toward improvement 262

(P = 0.08). Cardiac symptom scores, quality-of-life measures and health-care use showed improvement in all individual studies. Exercise duration was unchanged in four of seven studies, and the ejection fraction was unchanged in five of 11 studies. However, the meta-analysis results showed significant improvement in both of these measures. A few randomized trials have compared the effects of ablation and pacemaker implantation with medical therapy and/or pacemaker implantation. As in the metaanalysis, these trials showed a significant reduction in symptoms, especially palpitations, with AV node ablation and pacemaker implantation in comparison with medical therapy. However, except in one study [17], the quality of life, exercise duration, and ventricular function improved equally with either ablation and pacemaker implantation or medical therapy, so that there were no significant differences between the two groups. In a short-term study by Brignole et al. [18], 23 patients with medically refractory atrial fibrillation or flutter were randomly assigned to either RF ablation of the AV junction and pacemaker implantation, or pacemaker implantation alone. After 15 days, palpitations, effort dyspnea, exercise intolerance, and asthenia were significantly reduced in the ablation group in comparison with the group who received a pacemaker alone. In another study, Brignole et al. [19] randomly assigned 43 patients with medically refractory paroxysmal AF to atrioventricular junction ablation and a DDDR modeswitching pacemaker or to medical therapy. At 6 months, the ablation group showed significantly greater improvement in palpitations, effort dyspnea, exercise intolerance, easy fatigue, and score on a heart failure questionnaire in comparison with the medical therapy group. Symptomatic improvement has been specifically documented in the subset of patients with chronic AF and congestive heart failure (CHF). Brignole et al. [20] randomly assigned 66 patients with clinical heart failure, AF, and a resting rate > 90 beats/min to pharmacologic AV nodal blockade or AV nodal ablation and implantation of a VVIR pacemaker. After a 12-month follow-up period, patients who had undergone AV nodal ablation and pacemaker implantation had significant reductions in palpitations, dyspnea with exertion, exercise intolerance, easy fatigability, and chest discomfort in comparison with those receiving pharmacologic therapy. There was no difference in the overall quality of life, New York Heart Association functional class, or objective measures of cardiac function. Cardiac performance remained stable over time in both groups. Levy et al. [21] randomly assigned 36 patients with permanent AF and normal left ventricular function to either His bundle ablation and VVIR pacemaker or VVI pacemaker and pharmacologic rate control. Although the exercise duration and quality of life significantly improved

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from the baseline in both groups, there were no differences in outcomes between the groups. Left ventricular function was equally preserved by both treatments during the follow-up. Marshall et al. [22] randomly assigned 56 patients with a history of drug-resistant paroxysmal AF to continued medical therapy or to AV nodal ablation plus pacing. After a 6-week run-in period of DDDR pacing, paced patients were randomly assigned to DDDR/MS or VVIR and subsequently crossed over [22]. Overall symptoms, palpitations, dyspnea, and psychological general wellbeing were significantly better with ablation and DDDR/ MS pacing in comparison with medical therapy. DDDR/ MS was more effective than VVIR. At 6 weeks, more patients with ablation and pacing developed persistent AF (32% versus 0% with medical therapy). Ueng et al. [17] randomly assigned 50 patients with AF alone to AV node ablation and VVIR pacemaker (21 patients) or medical therapy (29 patients). After 12 months, the ablation group showed significantly better scores for general quality of life, overall symptoms, and overall activity scale, and a significant increase in the left ventricular ejection fraction in comparison with the baseline. No significant difference was found in the group treated with drugs. The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial (AIRCRAFT) [23] compared AV junction ablation and pacing with pharmacologic rate control in 99 patients with symptomatic permanent AF in whom ventricular rate control had not been achieved with previous pharmacologic therapy. At 1 year, there were no differences between the two groups in left ventricular ejection fraction or exercise duration on treadmill testing. However, the symptoms were significantly reduced and the peak ventricular rate was significantly lower with AV junction ablation than with pharmacologic rate control, both during exercise (112 vs. 153 beats/min) and during activities of daily life (117 vs. 152 beats/min).

Effects on specific measures of clinical outcome Symptoms. Atrioventricular node (AVN) ablation and pacemaker implantation have been shown to result in a significant improvement in symptoms, especially palpitations. The incremental benefit in comparison with ratecontrolling medical therapy is probably due, at least in part, to regularization of the ventricular rate and elimination of the adverse effects of drug therapy. Effect on quality of life (QOL). Several indicesasuch as the Quality of Life Index, Health Status Questionnaire, and Minnesota Living with Heart Failure Questionnairea have been used in different studies to estimate QOL. AVN

Ablation for rate control of atrial fibrillation

ablation and pacemaker implantation have been shown to improve the QOL as measured by all of these indices. Effect on consumption of health resources. AVN ablation has been shown to reduce the consumption of health-care resources, including a decrease in emergency room visits, hospitalization, and antiarrhythmic drug use. Effect on cardiac performance and exercise tolerance. The mechanism of improved exercise duration is probably related to the salutary effects of strict heart-rate control on ventricular systolic function, diastolic function, filling time, and cardiac output. Effect on left ventricular function (ejection fraction). In the meta-analysis by Wood et al. [16], the ejection fraction was unchanged in five of 11 studies. However, the metaanalysis results showed significant improvement. In studies stratifying patients by ejection fraction before therapy, the mean left ventricular function improved significantly in those patients with baseline impairment, but it remained unchanged or decreased slightly in those with normal ventricular function. The fractional shortening showed a trend toward improvement, but did not reach statistical significance, in the meta-analysis. Improved ventricular function may be attributed to enhanced diastolic filling times, improved cardiac mechanics, the withdrawal of negative inotropic drugs, and the reversal of tachycardiainduced cardiomyopathy. The benefit of restoring adequate rate control and resolution of tachycardia-mediated cardiomyopathy is at least partly offset by impairment in ventricular function and worsening of mitral regurgitation by right ventricular (RV) pacing.

Survival analysis The average 1-year total mortality rate after AV node ablation and pacemaker implantation has ranged from 3.8% to 7.4% per year in various studies. In the meta-analysis by Wood et al. [16], 1073 patients from 16 studies were included in the mortality analysis. The average follow-up period ranged from 3 months to 2.3 years. Calculated monthly and 1-year total mortality rates after ablation and pacing therapy were 1.4% and 6.3%, respectively. The calculated monthly and 1-year sudden death rates were 0.7% and 2.0%, respectively. Ozcan et al. [24] reported a series of 350 patients from the Mayo Clinic who underwent ablation and pacemaker implantation. At a mean follow-up of 3 years, 78 patients had died, yielding a 1-year mortality of 7.4%. Yeung-Lai-Wah et al. [25] followed 359 patients with drug-refractory atrial fibrillation who underwent radiofrequency catheter ablation of the atrioventricular junction and pacemaker implantation. During a mean followup period of 41 months, 46 patients died. The actuarial 263

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survival probability for all patients was 0.953 and 0.827 at 1 and 5 years, respectively (average 1-year mortality 3.8%). Darpo et al. [26] studied 220 patients with AF who underwent RF ablation of the AV junction followed by pacing at > 70 beats/min for 1–3 weeks. There were a total of 31 deaths during a mean follow-up period of 31 months, yielding a 1-year mortality of 5.5%. The long-term survival for patients with atrial fibrillation was found to be similar whether they receive ablation or drug therapy. In the study by Ozcan et al. [24], the observed survival rate among the 350 patients who underwent ablation was found to be similar to that among 229 controls with atrial fibrillation who received drug therapy. Increased mortality after ablation was mostly limited to patients with structural heart disease. Survival among patients without underlying heart disease who underwent ablation was found to be similar to the expected survival in the general population. Several predictors of mortality were identified in various studies. Previous myocardial infarction, a history of congestive heart failure, and treatment with cardiac drugs after ablation were found to be independent predictors of death in the study by Ozcan et al. [24]. The observed survival among patients without these three risk factors was similar to the expected survival. None of the 26 patients with atrial fibrillation alone died during the follow-up period in the study. Yeung-Lai-Wah et al. [25] found four clinical variables, but no ablation variables, to be independent predictors of death: age ≥ 65 years, the presence of heart failure, coexisting diabetes, and fractional shortening ≤ 20%. There were 20 deaths among 28 patients with three or more risk factors and four deaths in 115 patients with no risk factors. In the study by Darpo et al. [26], 11 patients, all with structural heart disease, died suddenly (1.9% per year).

Procedure The procedure of RF ablation of the AV junction involves ablating the distal AV node and requires implanting a permanent pacemaker for ventricular rate support. Both ablation and pacemaker implantation are typically carried out in the same session, with the pacemaker being implanted first. After intravenous sedation, a steerable ablation catheter is positioned across the tricuspid annulus to record a His bundle electrogram (HBE). A second electrode catheter is placed at the apex of the right ventricle for temporary pacing. The optimal site for ablation is then located. Ablation with RF energy is aimed at the compact AV node in order to preserve automaticity of the His bundle.

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Figure 16.1 The region of the septal leaflet of the tricuspid valve (TV) annulus is divided into 10 sites. Site 1 represents the apex of the Koch’s triangle, and site 10 is located at the level of the floor of the coronary sinus. The ideal site for AV node ablation is site 5. CFB, central fibrous body.

Although several terminologies have been introduced for indicating the location of the ablation electrode relative to the region of the AV node, our scheme divides the region of the septal leaflet of the tricuspid valve annulus into 10 sites, with site 1 representing the apex of Koch’s triangle and site 10 at the level of the floor of the coronary sinus (Fig. 16.1). The AV node is ablated at site 5. The electrogram recorded from the ablation electrode at this site (Figs. 16.2 and 16.3) has a characteristic large atrial deflection and a small His deflection. For patients in atrial fibrillation, the target is chosen as the point where the His potential is small, with distinct F waves, as the catheter is withdrawn from the ventricular cavity into the atrium. Once an appropriate target site has been identified, RF current is delivered for 60–120 s with a target temperature of 60 °C. Wide-tipped electrodes (4 – 8 mm) have been shown to increase the surface area and depth of the lesions. If AV conduction remains unchanged, the catheter is repositioned and a repeat attempt is made. The right-sided (venous) approach described above is preferred in most cases (approximately 90%). In case of failure to achieve AV block with the venous approach, the left-sided route should be used [27–29]. The AV junction is approached from the left side in a retrograde aortic fashion. The ablation catheter is passed retrogradely across the aortic valve into the left ventricle and positioned immediately below the noncoronary cusp of the aortic valve to record a His bundle deflection, as well as

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A

B

Figure 16.2 A. The ideal fluoroscopic position of the ablation catheter in the anteroposterior projection. B. The electrogram recorded from the ablation catheter at this site has a large atrial deflection and a small His deflection.

atrial and ventricular deflections. RF energy is then delivered in standard fashion. A supravalvular noncoronary aortic cusp approach has also been described, but is rarely necessary [30].

Procedural success The overall success rate for AV junction ablation with RF is nearly 100%. Occasional recurrences (approximately 2%) after apparent successful ablation have been observed,

and are amenable to repeat ablation attempts. Longterm results are usually obtained immediately with RF (as opposed to DC shock), but a few cases of late recovery have been reported. The North American Society for Pacing and Electrophysiology (NASPE) Prospective Catheter Ablation Registry [31] included 646 patients who underwent atrioventricular (AV) junctional ablation. The success rate was 97.4%. The incidence of recurrent AV node conduction during the follow-up was 3.5%.

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B

Figure 16.3 A. The fluoroscopic anteroposterior image shows an ablation catheter that is positioned too distally. B. The electrogram recorded from the ablation catheter at the same site shows a large ventricular deflection and a small or absent atrial deflection.

In the Ablate and Pace Trial (APT) [32], AV node ablation was successful in 155 of 156 patients who underwent the procedure. Persistent complete heart block was observed in 96%.

Early complications Early complications include those that are common to all invasive ablative procedures, such as bleeding at the site of venous access, pneumothorax (with subclavian vein puncture), deep venous thrombosis, pericardial effusion 266

or cardiac tamponade, and respiratory compromise from intravenous sedation. Complications specific to AV node ablation and pacemaker implantation include ventricular tachycardia or fibrillation leading to sudden death, and occasional acute hemodynamic decompensation, probably due to dyssynchrony induced by RV apical pacing. Major complicationsaincluding mortality related to the procedure, ventricular tachycardia or fibrillation, pulmonary embolism, and cardiac tamponadeaare rare and are significantly less frequent with RF ablation in comparison with DC ablation of the AV node. Brignole and Menozzi summarized the early complications from DC

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and RF ablation in a review [33]. The NASPE Prospective Catheter Ablation Registry [31] included 646 patients who underwent AV junction ablation. Significant complications occurred in five patients, including one procedure-related death due to pacemaker malfunction. While the number of AV junction ablations was higher for those > 60 years of age, there was no significant difference in the success rate or incidence of complications when patients aged 60 or over were compared with those under 60 years of age. In addition, there were no differences in the success or complication rates between large-volume centers (> 100 ablations/year) and lower-volume centers, or between teaching and nonteaching hospitals. The Multicentre European Radiofrequency Survey [34] included 900 patients who underwent AV junction ablation between 1987 and 1992. Procedure-related complications occurred in 29 patients (3.2%). Most of the complications were minor local complications of venous cannulation (hematomas, phlebitis, etc.). Major complications such as pericardial effusion and ventricular arrhythmias were rare, and the procedural mortality rate was < 0.1%. Moreover, patients who underwent AV junction ablation were shown to have the lowest incidence of complications in comparison with patients who underwent other RF ablation procedures.

Sudden death and ventricular arrhythmias Sudden death and ventricular arrhythmias have been observed in the early phase after AV node ablation. This could potentially be related to an effect of the procedure itself (ablation and/or pacing), to pacing system failure or an inadequate lower pacing rate, or to preexisting heart disease. Ozcan et al. [35] evaluated the incidence of sudden death in 334 patients with AF who underwent radiofrequency ablation at the Mayo Clinic. They found that nine patients (2.7%) had sudden cardiac death. Four of these (1.2%) occurred within 4 days and were considered likely to be related to the procedure; three (0.9%) occurred between 4 days and 3 months and were thought to be possibly related; and two occurred late and were thought to be unrelated. Diabetes, New York Heart Association functional class (II or higher), preprocedural ventricular arrhythmia, mitral or aortic stenosis, aortic regurgitation, and chronic obstructive pulmonary disease were found to be independent predictors for sudden death. A specific risk for polymorphic VT and early sudden death after AV node ablation and pacing appears to be related to absolute or relative bradycardia in comparison with the ventricular rate during AF. Pacing at relatively rapid rates (80 –90 beats/min) for 1–2 months after the procedure appears to dramatically decrease this risk. Peters et al. [36] described a patient who developed recurrent VF immediately after AV node ablation. VF was noted to be pause-dependent and bradycardia-dependent

Ablation for rate control of atrial fibrillation

and was suppressed by rapid ventricular pacing at 90 beats/min. Geelen et al. [37] studied 235 patients who underwent radiofrequency ablation of the AV node for drug-refractory atrial arrhythmias. In the first 100 patients, in whom the post-ablation pacing rate was less than 70 beats/min, the incidence of VF or sudden death was 6% at 1 year, with all cases occurring in the first month after ablation. In the next 135 patients, in whom a pacing rate of 90 was used for 1–3 months after the ablation, there were no episodes of VF or sudden death at 1 year. Recent studies using high-rate pacing have reported no sudden deaths at up to 25 months of follow up. In a study of 220 patients with AF who underwent RF ablation of the AV junction followed by pacing at > 70 beats/min for 1–3 weeks, Darpo et al. [26] reported no early sudden deaths or ventricular arrhythmias. Jensen et al. [38] reported no ventricular arrhythmias in 50 patients after AV junction ablation for treatment-resistant atrial fibrillation or flutter, followed by pacing at 80 beats/min for 1 week after the ablation. Brignole et al. [19] reported no complications related to ablation or pacemaker at 6 months in 21 patients after AV node ablation followed by pacing at a lower limit of 70 beats/min. Further insights into the relationship between bradycardia and early sudden death or ventricular arrhythmias have been provided by other studies. Repolarization abnormalities have been shown to occur at lower pacing rates in the first few days after ablation, especially in patients with structural heart disease. Cellarier et al. [39] studied 11 patients with chronic rapid atrial fibrillation who underwent AV node ablation and VVI pacemaker implantation and compared them with a control group of patients with chronic complete heart block who had a pacemaker programmed in the VVI mode. The group undergoing ablation exhibited a prolonged paced QT interval at rates less than 75 beats/min for the first 2 days after ablation, with the abnormality resolving completely thereafter. Raj et al. [40] showed that QT dispersion increased after AV node ablation during a sudden rate drop from 80 to 40 beats/min in patients with reduced left ventricular (LV) function, but not in patients with normal LV function. Activation of the sympathetic nervous system and prolongation of the action potential duration have been demonstrated early after ablation at low pacing rates, which may predispose to early afterdepolarizations that can lead to ventricular arrhythmias. These changes have been shown to be suppressed by pacing at higher rates. Hamdan et al. [41] studied 10 patients with chronic AF undergoing RF ablation of the AV junction. Sympathetic nerve activity was increased significantly after ablation at a pacing rate of 60, but not with pacing at 90 beats/min. Also, the cardiac action potential and right ventricular effective refractory period increased after ablation. 267

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Worsening of heart failure Although the majority of well-selected patients improve hemodynamically following AV junction ablation and right ventricular pacemaker implantation, some patients worsen after the procedure. RV pacing is known to cause dyssynchronous ventricular activation, which can lead to worsening of heart failure (HF). In addition, in patients with chronic AF and severe mitral regurgitation, RV apical pacing may exacerbate the mitral regurgitation by causing failure of mitral regurgitation leaflet apposition. Pacing of the right ventricular outflow tract, His bundle, or biventricular pacing may reduce this risk. Vanderheyden et al. [42] reported that eight of 108 patients (7.4%) undergoing ablation of the AV node for drug-refractory AF developed hemodynamic deterioration related to worsening mitral regurgitation. Acute pulmonary edema occurred in three patients and congestive heart failure in five patients at a mean of 3 and 8 weeks, respectively, after the procedure. Patients with marked left ventricular enlargement and/or more severe mitral regurgitation at baseline were at greater risk. Twidale et al. [43] conducted hemodynamic studies before and after the procedure. They concluded that mitral regurgitation was a complication of RV pacing and not of RF ablation itself. Moreover, changing the pacing site to the right ventricular outflow tract reduced the amount of mitral regurgitation.

Consequences of AV junction ablation Pacemaker dependency Although most patients have been shown to have some type of either junctional or idioventricular escape rhythm after AV junction ablation, patients should be considered pacemaker-dependent. A permanent pacemaker is usually implanted at the time of the procedure. The type of pacemaker, mode of pacing, and the occasional need for an implantable cardioverter-defibrillator (ICD) are important issues in this regard, which are discussed in more detail in the next section.

Thromboembolism The risk of cerebral vascular events or transient cerebral ischemia remains unchanged after AV junction ablation. While AV nodal ablation results in adequate heart rate control, it does not stop the atria from fibrillating. As a result, there continues to be a need for long-term anticoagulation treatment, similar to that in patients with permanent AF whose heart rate control is achieved pharmacologically. Gasparini et al. [44] reviewed 585 patients who underwent AV nodal ablation and pacemaker implantation. 268

Antiplatelet agents were used in 202 patients and warfarin in 187. After a follow-up period of 34 months, the actuarial rates for thromboembolism at 1, 5, and 7 years were 1%, 4.2%, and 7.4%, respectively, which compared favorably with the incidence among patients treated with pharmacologic AV nodal blockade. The only predictor of a thromboembolic event was the presence of permanent atrial fibrillation. AV node ablation does not protect against thromboembolism.

Risk of permanent AF AV node ablation and pacemaker implantation have been shown to be associated with more recurrences of paroxysmal AF and a higher rate of progression to permanent AF. Brignole et al. [19] reported that 24% of 21 patients developed permanent AF 6 months after AV node ablation, in comparison with none of 18 patients randomly assigned to medical therapy. Marshall et al. [22] showed that 32% of 37 patients developed permanent AF within 6 weeks after AV node ablation and DDDR pacemaker implantation, in comparison with none of 19 patients randomly assigned to medical therapy. The incidence of AF after AV node ablation and pacemaker implantation has been shown to increase over time. Of 62 patients with paroxysmal AF who underwent AV node ablation in a study by Gribbin et al. [45], 42% had developed permanent AF by 30 months. The estimated incidence of permanent AF after 7 years was 75%. Gianfranchi et al. [46] estimated that the actuarial progression rate to permanent AF was 22%, 40%, and 56% at 1, 2, and 3 years after ablation in 63 patients with paroxysmal AF. Permanent cardiac pacing may worsen cardiac function and may increase the frequency of atrial fibrillation in patients who are in sinus rhythm. Right ventricular pacing has been shown to be associated with an increased risk of recurrences and of developing permanent AF. Post hoc analysis of data from the MOde Selection Trial (MOST) [52] that evaluated those participants with a baseline QRS duration < 120 ms demonstrated that regardless of pacing mode, patients with a higher cumulative percentage of ventricular paced beats had a significantly greater incidence of subsequent HF hospitalizations and subsequent development of atrial fibrillation. Biventricular pacing (cardiac resynchronization) may be preferred in such patients, particularly those with significant left ventricular dysfunction. In addition to the effect of ventricular pacing, the risk of developing permanent AF is probably also related to the discontinuation of antiarrhythmic drugs. AV nodeblocking drugs can be stopped after ablation, but class I or III antiarrhythmic medications need to be continued if sinus rhythm is to be maintained. Withdrawal of antiarrhythmic medications has been shown to be associated

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with a greater probability of developing permanent AF. However, continuation of antiarrhythmic drugs may diminish some of the benefit seen in the quality of life or in symptom control. It has been shown that maintaining sinus rhythm after ablation may not lead to a better outcome. Brignole et al. [48] randomly assigned 137 patients to antiarrhythmic drug therapy or no antiarrhythmic drug therapy after AV node ablation. Even though the group with drug therapy had a 43% relative risk reduction of developing permanent AF (21% vs. 37%), the outcome was similar between the 40 patients who developed permanent AF and the 97 who did not. Moreover, the drug therapy group had more episodes of heart failure and hospitalizations.

Post-ablation device implantation Escape rhythm Most patients have been shown to have some type of either junctional or idioventricular escape rhythm after the procedure. Several studies report that 25–35% of patients never develop an escape rhythm after RF. The presence of an escape rhythm after ablation is a positive predictive factor for long-term escape. Patient survival obviously depends on the presence of an escape rhythm in case of defective pacemaker function. In the APT trial [32], 67% of patients (104 of 155) had some type of escape rhythm after successful AV junction ablation. However, the average heart rate in these escape rhythms was 39 ± 10 beats/min, and only 31% had a rate greater than 40 beats/min. Thus, the majority of patients are pacemaker-dependent after AV junction ablation, as defined by the lack of an escape rhythm or the presence of an escape rhythm less than 40 beats/min. A permanent pacemaker is typically implanted at the same time as AV junction ablation.

Mode of pacing The presence of chronotropic incompetence after ablation requires a rate-responsive pacemaker. In patients with permanent AF, a VVIR pacemaker with a rate-adaptive sensor is implanted. Among patients with paroxysmal AF, better relief of symptoms may be achieved with DDDR pacemakers with mode switching, since this maintains AV synchrony during periods of sinus rhythm. One concern with DDDR pacemakers is that recurrent or persistent AF may result in very rapid ventricular responses, due to tracking of the atrial electrogram. Automatic mode switching can eliminate atrial tracking when a rapid increase in rate is sensed. Atrial sensing recognizes a return to normal sinus rhythm and the automatic mode

Ablation for rate control of atrial fibrillation

switching returns function to a DDD mode. In older pacemakers that do not have a mode-switching capability, a simple approach is to limit the atrial tracking rate by setting the pacemaker to a relatively low upper rate limit. However, this reduces the maximal pacing response to sinus rhythm, and sequential AV pacing may be lost with a sinus tachycardia. Another option is the DDIR mode. Although DDIR is nontracking, the rate-adaptive sensor can be programmed to allow a rate higher than the sinus rate, which gives rise to AV synchrony. However, DDIR is best reserved for patients with concomitant sinus node dysfunction. The benefit of DDDR/MS pacing after AV node ablation in patients with paroxysmal AF has been shown in randomized trials. Kamalvand et al. [49] studied 48 patients with a history of paroxysmal atrial tachyarrhythmias and heart block using a randomized, crossover design. The DDDR/MS pacemaker significantly improved symptoms and exercise time more effectively than conventional DDDR or VVIR pacing. Even in the subgroup of 17 patients with AV node ablation, DDDR/MS was better than VVIR in terms of symptom control and exercise time. Marshall et al. [22] randomly assigned 56 patients with a history of drug-resistant paroxysmal AF to continued medical therapy or to AV nodal ablation plus pacing. Follow-up over 18 months included a 6-week run-in period of DDDR pacing in paced patients, after which they were randomly assigned to DDDR/MS or VVIR and subsequently crossed over after 6 weeks. DDDR/MS was more effective in controlling the overall symptoms and dyspnea and in improving the QOL than VVIR. Patients who undergo AV node ablation for paroxysmal AF have a high risk of progression to permanent AF. It has been postulated that DDDR pacing (pacing the atrium) may prevent or delay progression to permanent AF. In a randomized trial of 67 patients with paroxysmal AF, Gillis et al. [50] compared the outcomes with DDDR and VDD pacing after AV junction ablation. Although both are physiologic pacing modalities and maintain AV synchrony, DDDR pacing provides the ability to pace the atrium, allowing evaluation of the potential benefits of atrial pacing. After a 6-month follow-up period, there were no differences between the two groups with regard to the time to the first episode of AF, the AF burden, or the incidence of permanent AF (35% versus 32%).

Biventricular pacing The detrimental effects of RV apical pacing, especially in patients with a left ventricular ejection fraction (LVEF) < 40%, are well known from the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial [51]. RV pacing causes the RV to contract before the LV, simulating the effects of left bundle branch block. For patients with 269

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normal interventricular conduction prior to pacemaker placement, the loss of ventricular synchrony from pacing may actually worsen cardiac function. Sweeney et al. [52] conducted a post hoc analysis of data from the MOST trial that evaluated those participants with a baseline QRS duration < 120 ms. Regardless of the pacing mode, patients with a higher cumulative percentage of ventricular paced beats had a significantly greater incidence of subsequent HF hospitalization and subsequent development of atrial fibrillation. Acute studies have shown the benefit of LV or biventricular (BiV) pacing over RV pacing in patients with AF undergoing AV node ablation. Puggioni et al. [53] compared RV pacing to LV pacing within 24 h after AV node ablation in 44 patients with permanent AF. The ejection fraction (EF) was found to improve after AV node ablation with both RV and LV pacing, probably as a result of rhythm regularization. LV pacing provided an additional modest but favorable hemodynamic effect, as reflected by a greater increase in EF (17.6% vs. 11.2%) and reduction of mitral regurgitation (16.7% vs. 0%). In another acute study, Simantirakis et al. [54] showed that LVbased pacing significantly improved LV contractile function and LV filling in comparison with RV apical pacing in 12 patients after AV node ablation for drug-refractory AF. Patients who have moderate to severe heart failure definitely seem to benefit from biventricular pacing. Leon et al. [47] studied 20 consecutive patients with severe HF, AF, and AV ablation. They found that upgrading from right ventricular pacing to biventricular pacing significantly increased the left ventricular ejection fraction from 22% to 31% in association with symptomatic improvement. The Post-AV Nodal Ablation Evaluation (PAVE) trial, which was recently completed, compared outcomes in 102 patients with chronic AF who were randomly assigned to biventricular pacing or RV pacing after AV node ablation. At 6 months, the BiV-paced group had a significant improvement in 6-min walking, peak VO2 max, and exercise duration in comparison with the RVpaced group. The mean LVEF remained at the baseline value of 46% in the BiV-paced group after 6 months, whereas it decreased from 44.9% to 40.7% in the RV-paced group. Further analysis of the results suggests that patients with a baseline LVEF < 0.35 had better functional status and LVEF with biventricular pacing. In contrast, patients with preserved LVEF at baseline showed no significant benefit from biventricular pacing.

When is a defibrillator appropriate? On the basis of data from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), patients with AF and congestive heart failure with a left ventricular ejection fraction 270

of less than 35% will benefit from an ICD. However, care should be taken to exclude patients with tachycardiamediated LV dysfunction, who will improve with rate control alone.

Indications and contraindications The ideal candidate for AV node ablation would be a patient who is symptomatic with rapid ventricular rates and has poor rate control despite medical therapy. Symptomatic patients who are either intolerant to ratecontrolling medications or have comorbid illnesses that limit medical therapy should also be considered for ablation. Patients who have ventricular dysfunction that is thought to be tachycardia-induced may show improvement after ablation. Patients with paroxysmal AF who develop rapid hemodynamic deterioration, syncope, or ischemia during episodes of AF would also make good candidates. On the other hand, asymptomatic patients who are adequately rate-controlled do not benefit from AV node ablation. Patients who remain symptomatic despite adequate rate control with drugs may show some benefit from ablation due to regularization of the rate, but may not be affected if their symptoms are due to loss of AV synchrony. The American College of Cardiologists and American Heart Association recommend that rate-controlling drugs should be tried first before AV node ablation is considered.

AV node modification The aim of AV node modification in AF is to slow the ventricular rate by selectively damaging the AV node to modify, rather than completely abolish, AV node conduction, thus eliminating or decreasing the need for AV node–blocking drugs without causing complete heart block. There is evidence that dual AV nodal physiology may exist in a significant percentage of the population, even in those without AV nodal reentrant tachycardia. RF ablation of one of these inputs (especially the slow pathway), analogous to that used to ablate atrioventricular node reentry tachycardia (AVNRT), can reduce the number of impulses that reach the infranodal conduction system and the ventricles during AF. Modulating the rapid pathway in the compact node lengthens the AH interval without significantly affecting the anterograde refractory period of the AV node and the Wenckebach cycle. Ablation of the slow pathway has no effect on the AH interval, but lengthens the refractory period and the Wenckebach cycle. Hence, the slow pathway is the preferred target for AV node modification.

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The technique is similar to that used in slow pathway ablation of AVNRT. RF energy is delivered along the posteroseptal portion of the tricuspid annulus. Successive applications are given, starting in the medioseptal area and working towards the compact node. From initial settings of 15–30 W for 60 s, the energy level is gradually lowered as the ablation site approaches the compact node. When the rate suddenly changes, RF application is stopped. The target decrease is < 100 at baseline and < 120 during adrenergic stimulation. The success rate is lower than with AV node ablation, since the end point is harder to achieve. Moreover, the ventricular rate commonly tends to increase after several months. A bimodal RR interval distribution during AF suggests the presence of dual AV node physiology and predicts a better outcome of RF ablation of the slow pathway [55]. Loss of dual-pathway physiology after ablation has been shown to have a high positive predictive value for slowing the ventricular rate during AF [56]. However, simple elimination of the slow pathway may be inadequate to control the ventricular rate in patients with little difference in conduction properties between the fast and slow pathways [57], or in patients with a short Wenckebach cycle length in the fast pathway [58]. It may also not provide adequate rate control during periods of excessive sympathetic stimulation, which can enhance conduction through the fast pathway [59]. The main advantage of AV node modification over AV node ablation is that there may be no need for a pacemaker. However, inadvertent destruction of the fast pathway results in up to a 20% need for a permanent pacemaker acutely or during follow-up. The main drawback in comparison with AV node ablation is that, even if successful, the ventricular rate remains irregular. Feld et al. [60] attempted AV node modification in 10 patients by RF catheter ablation in the region of the AV nodal slow pathway. The procedure was successful in seven patients (70%), who had a reduction in the maximum ventricular rate from a mean of 164 to 123 beats/min (P < 0.01) and a reduction in the average ventricular rate from a mean of 128 to 83 beats/min after the ablation. A mean of 17 RF applications was required. All seven patients remained symptom-free during a mean followup period of 14 months. Three patients remained off all AV node–blocking drugs, three remained on digoxin, and one patient remained on beta-blocker treatment due to a history of angina. No late AV block or symptomatic bradycardia was observed in these seven patients. Williamson et al. [61] attempted AV node modification in 19 patients with chronic or paroxysmal AF refractory to multiple medical trials. The procedure was initially successful in 17 patients; one patient had an inadvertent complete AV block, and an AV block was deliberately

Ablation for rate control of atrial fibrillation

carried out in another patient after the modification procedure was unsuccessful in slowing the ventricular rate. The mean number of RF applications was 11. Three of the 17 patients with initial successful AV nodal modification developed complete AV block within 3 days after the procedure, yielding a success rate of 74% (14 of 19 patients). The 14 patients who had successful modification of conduction had persistent reductions in maximal ventricular rate during exercise (rate at 3 months, 126 ± 24 beats/min; P < 0.01). During a mean follow-up period of 8 months, only one of the 14 patients had recurrent symptomatic AF with a rapid rate; the patient responded to a second modification procedure. One patient with dilated cardiomyopathy died suddenly 5 months after a successful procedure. Della Bella et al. [62] attempted slow AV node pathway ablation in 14 patients with drug-refractory paroxysmal atrial flutter or fibrillation. RF current was delivered in six patients during sinus rhythm, in six during atrial flutter, and in two during atrial fibrillation. In the six patients who were in sinus rhythm, the mean anterograde effective refractory period was prolonged from 270 ms to 390 ms (P = 0.005) and the mean Wenckebach cycle from 346 ms to 458 ms (P = 0.004). In the six patients in atrial flutter, the mean AV conduction ratio increased from 1.6 to 3 (P = 0.02). In the two patients with AF, the mean ventricular rate decreased from 157 to 67 beats/min. Complete AV block occurred in two patients. During a mean follow-up period of 5.8 months, 11 patients experienced symptomatic or asymptomatic recurrences of atrial tachyarrhythmias. None of the patients experienced a high-degree AV block during the follow-up period. Luderitz et al. [63] were able to achieve successful AV nodal modification in nine of 10 patients (90%) with uncontrolled AF. In one patient, AV junction ablation was carried out because rate control was not achieved with AV node modification. Morady et al. [64] followed 62 patients with symptomatic drug-refractory AF and an uncontrolled ventricular rate after AV node modification. The procedure was acutely successful in 50 patients (81%). Ten patients (16%) developed inadvertent high-degree AV block. During a follow-up period of 19 months in the 50 patients with successful acute results, five (10%) had a symptomatic recurrence of an uncontrolled rate during AF. Overall, long-term adequate rate control at rest and during exercise was achieved in 45 of 62 patients (73%). Among 37 patients with successful modification, LVEF increased from 0.44 to 0.51. Complications other than AV block included polymorphic ventricular tachycardia early after ablation in two patients with predisposing factors, and sudden cardiac death 1 and 5 months after the procedure, respectively, in two patients with idiopathic dilated cardiomyopathy. 271

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Comparison with AV node ablation A few studies compared the effects of RF modulation and RF ablation of the AV node on quality of life and cardiac performance. One of the major differences between the two procedures is the regularity of the heart rate. This could explain the mild palpitations encountered in patients with successful AV modulation and the favorable impact on quality of life and LVEF reported with AV node ablation. Lee et al. [65] randomly assigned 60 patients with medically refractory AF to atrioventricular junction (AVJ) ablation or AVJ modification. They found a significant improvement in the general quality of life and a significant reduction in the frequency of major symptoms and symptoms during attacks after 1 and 6 months of follow-up in both groups. However, patients who underwent complete AV node ablation had a significantly greater improvement in QOL and symptoms. In patients with depressed LV function, the two methods were similarly efficacious in improving LVEF and daily life activity scores. Twidale et al. [66] compared the two approaches in 44 patients with CHF and uncontrolled AF. Quality of life, LVEF, and exercise tolerance significantly improved in patients with ablation, while there were no significant changes in LVEF or quality of life, and a small increase in exercise tolerance, in patients with modulation. However, the success rate of modulation was only 32% after 4 weeks of clinical follow-up, which may at least in part explain the failure of this procedure to improve the status of the patients. Proclemer et al. [67] compared AV ablation and modulation in 120 patients with either paroxysmal or chronic drug-refractory AF. The two procedures, when successful, appeared to be equally effective in achieving long-term ventricular rate control and symptom score improvement. There were no further complaints of major symptoms in any of the patients in either treatment group. Ablation of the AV node showed a higher acute success rate (100%) than AV node modulation (57– 63% success). Knight et al. [68] showed that AV junction modification was more cost-effective than AV junction ablation, even when costs for repeat procedures and eventual permanent pacemaker implantation were included.

ablations. Among the many competing therapies for atrial fibrillation, AV junction ablation has a definite, though limited, role. In our present practice, AV junctional ablation is offered to patients who have atrial fibrillation with a rapid ventricular response who also have such significant comorbid conditions that curative therapies are either contraindicated or associated with increased risk. For example, patients who are quite elderly or who have significant structural heart disease, such as rheumatic valvular disease, that is not amenable to surgical repair are most likely to be offered AV junctional ablation. These patients must be quite symptomatic from a rapid, irregular ventricular response to atrial fibrillation, and ratecontrolling medications must have failed for them. For patients with hemodynamically significant restrictions on diastolic filling, such as severe left ventricular hypertrophy or restrictive cardiomyopathy, all efforts should be made to restore sinus rhythm and atrial contractility. AV junctional ablation is often poorly tolerated in these individuals, and catheter ablation or surgical treatment of the atrial fibrillation may offer better long-term results. In addition, patients who have symptomatic, medically refractory atrial fibrillation who have a concomitant indication for cardiac surgery should be considered for surgical ablation. An important group of patients who appear to benefit significantly from AV junctional ablation are those with systolic left ventricular dysfunction due to ischemic or idiopathic dilated cardiomyopathies. These patients may significantly improve with AV junctional ablation and biventricular implantation of a cardioverterdefibrillator. Great care should be taken to exclude patients who have a tachycardia-mediated cardiomyopathy, for whom rate control may be expected to improve or reverse the impaired ventricular function. There appears to be little role for biventricular pacing aloneacardiac resynchronization therapy (CRT)aas there are usually indications for cardioverter-defibrillator implantation (CRT-D) in this population. Patients who have atrial fibrillation may be better served with primary atrial fibrillation ablation, especially if they are under the age of 70. Importantly, atrial flutter or atrial tachycardia are virtually never considered for AV junctional ablation, as catheter ablation of the atrial mechanism is associated with a very high likelihood of success. Finally, we see no role at present for AV nodal modification without pacemaker implantation as a rate-control strategy.

Perspective In the era of pulmonary vein isolation (PVI) and other curative ablative strategies for AF, where does AV node ablation stand? A look at the number of procedures conducted in our own institution, for instance, shows a progressive decline in the number of AV node ablations over time, with a simultaneous increase in the number of AF 272

References 1 Scheinman MM, Morady F, Hess DS, Gonzalez R. Catheterinduced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA 1982;248: 851– 5.

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2 Gallagher JJ, Svenson RH, Kasell JH, et al. Catheter technique for closed-chest ablation of the atrioventricular conduction system. N Engl J Med 1982;306:194–200. 3 Kochiadakis GE, Skalidis EI, Kalebubas MD, et al. Effect of acute atrial fibrillation on phasic coronary blood flow pattern and flow reserve in humans. Eur Heart J 2002;23:734 – 41. 4 Nanthakumar K, Kay GN. The deleterious effects of an irregular RR interval. Eur Heart J 2002;23:695– 6. 5 Clark DM, Plumb VJ, Epstein AE, Kay GN. Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation. J Am Coll Cardiol 1997;30:1039 – 45. 6 Daoud EG, Weiss R, Bahu M, et al. Effect of an irregular ventricular rhythm on cardiac output. Am J Cardiol 1996;78: 1433–6. 7 Herbert WH. Cardiac output and the varying R–R interval of atrial fibrillation. J Electrocardiol 1973;6:131–5. 8 Shinbane JS, Wood MA, Jensen DN, Ellenbogen KA, Fitzpatrick AP, Scheinman MM. Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol 1997;29:709–15. 9 Redfield MM, Kay GN, Jenkins LS, Mianulli M, Jensen DN, Ellenbogen KA. Tachycardia-related cardiomyopathy: a common cause of ventricular dysfunction in patients with atrial fibrillation referred for atrioventricular ablation. Mayo Clin Proc 2000;75:790–5. 10 Rodriguez LM, Smeets JL, Xie B, et al. Improvement in left ventricular function by ablation of atrioventricular nodal conduction in selected patients with lone atrial fibrillation. Am J Cardiol 1993;72:1137–41. 11 Brown CS, Mills RM Jr, Conti JB, Curtis AB. Clinical improvement after atrioventricular nodal ablation for atrial fibrillation does not correlate with improved ejection fraction. Am J Cardiol 1997;80:1090–1. 12 Edner M, Caidahl K, Bergfeldt L, Darpo B, Edvardsson N, Rosenqvist M. Prospective study of left ventricular function after radiofrequency ablation of atrioventricular junction in patients with atrial fibrillation. Br Heart J 1995;74:261–7. 13 Ozcan C, Jahangir A, Friedman PA, et al. Significant effects of atrioventricular node ablation and pacemaker implantation on left ventricular function and long-term survival in patients with atrial fibrillation and left ventricular dysfunction. Am J Cardiol 2003;92:33–7. 14 Hayano J, Sakata S, Okada A, Mukai S, Fujinami T. Circadian rhythms of atrioventricular conduction properties in chronic atrial fibrillation with and without heart failure. J Am Coll Cardiol 1998;31:158–66. 15 Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825–33. 16 Wood MA, Brown-Mahoney C, Kay GN, Ellenbogen KA. Clinical outcomes after ablation and pacing therapy for atrial fibrillation: a meta-analysis. Circulation 2000;101:1138 – 44. 17 Ueng KC, Tsai TP, Tsai CF, et al. Acute and long-term effects of atrioventricular junction ablation and VVIR pacemaker in symptomatic patients with chronic lone atrial fibrillation and normal ventricular response. J Cardiovasc Electrophysiol 2001;12:303–9. 18 Brignole M, Gianfranchi L, Menozzi C, et al. Influence of atrioventricular junction radiofrequency ablation in patients

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with chronic atrial fibrillation and flutter on quality of life and cardiac performance. Am J Cardiol 1994;74:242 – 6. Brignole M, Gianfranchi L, Menozzi C, et al. Assessment of atrioventricular junction ablation and DDDR mode-switching pacemaker versus pharmacological treatment in patients with severely symptomatic paroxysmal atrial fibrillation: a randomized controlled study. Circulation 1997;96:2617–24. Brignole M, Menozzi C, Gianfranchi L, et al. Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study. Circulation 1998;98:953 – 60. Levy T, Walker S, Mason M, et al. Importance of rate control or rate regulation for improving exercise capacity and quality of life in patients with permanent atrial fibrillation and normal left ventricular function: a randomised controlled study. Heart 2001;85:171– 8. Marshall HJ, Harris ZI, Griffith MJ, Holder RL, Gammage MD. Prospective randomized study of ablation and pacing versus medical therapy for paroxysmal atrial fibrillation: effects of pacing mode and mode-switch algorithm. Circulation 1999;99:1587– 92. Weerasooriya R, Davis M, Powell A, et al. The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial (AIRCRAFT). J Am Coll Cardiol 2003;41:1697–702. Ozcan C, Jahangir A, Friedman PA, et al. Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with atrial fibrillation. N Engl J Med 2001;344:1043 –51. Yeung-Lai-Wah JA, Qi A, Uzun O, Humphries K, Kerr CR. Long-term survival following radiofrequency catheter ablation of atrioventricular junction for atrial fibrillation: clinical and ablation determinants of mortality. J Interv Card Electrophysiol 2002;6:17–23. Darpo B, Walfridsson H, Aunes M, et al. Incidence of sudden death after radiofrequency ablation of the atrioventricular junction for atrial fibrillation. Am J Cardiol 1997;80:1174–7. Sousa J, el-Atassi R, Rosenheck S, Calkins H, Langberg J, Morady F. Radiofrequency catheter ablation of the atrioventricular junction from the left ventricle. Circulation 1991;84: 567–71. Souza O, Gursoy S, Simonis F, Steurer G, Andries E, Brugada P. Right-sided versus left-sided radiofrequency ablation of the His bundle. Pacing Clin Electrophysiol 1992;15:1454 –9. Trohman RG, Simmons TW, Moore SL, Firstenberg MS, Williams D, Maloney JD. Catheter ablation of the atrioventricular junction using radiofrequency energy and a bilateral cardiac approach. Am J Cardiol 1992;70:1438 – 43. Cuello C, Huang SK, Wagshal AB, Pires LA, Mittleman RS, Bonavita GJ. Radiofrequency catheter ablation of the atrioventricular junction by a supravalvular noncoronary aortic cusp approach. Pacing Clin Electrophysiol 1994;17:1182 –5. Scheinman MM, Huang S. The 1998 NASPE prospective catheter ablation registry. Pacing Clin Electrophysiol 2000;23: 1020 – 8. Curtis AB, Kutalek SP, Prior M, Newhouse TT. Prevalence and characteristics of escape rhythms after radiofrequency ablation of the atrioventricular junction: results from the registry for AV junction ablation and pacing in atrial fibrillation. 273

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Ablate and Pace Trial Investigators. Am Heart J 2000;139: 122–5. Brignole M, Menozzi C. Control of rapid heart rate in patients with atrial fibrillation: drugs or ablation? Pacing Clin Electrophysiol 1996;19:348–56. Hindricks G. The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart J 1993;14:1644–53. Ozcan C, Jahangir A, Friedman PA, et al. Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation. J Am Coll Cardiol 2002;40: 105–10. Peters RH, Wever EF, Hauer RN, Wittkampf FH, Robles de Medina EO. Bradycardia dependent QT prolongation and ventricular fibrillation following catheter ablation of the atrioventricular junction with radiofrequency energy. Pacing Clin Electrophysiol 1994;17:108–12. Geelen P, Brugada J, Andries E, Brugada P. Ventricular fibrillation and sudden death after radiofrequency catheter ablation of the atrioventricular junction. Pacing Clin Electrophysiol 1997;20:343–8. Jensen SM, Bergfeldt L, Rosenqvist M. Long-term follow-up of patients treated by radiofrequency ablation of the atrioventricular junction. Pacing Clin Electrophysiol 1995;18:1609 – 14. Cellarier G, Deharo JC, Chalvidan T, et al. Prolonged QT interval and altered QT/RR relation early after radiofrequency ablation of the atrioventricular junction. Am J Cardiol 1999;83:1671–4, A7. Raj SR, Gillis AM, Mitchell B, et al. Paced QT dispersion and QT morphology after radiofrequency atrioventricular junction ablation: impact of left ventricular function. Pacing Clin Electrophysiol 2003;26:662–8. Hamdan MH, Page RL, Sheehan CJ, et al. Increased sympathetic activity after atrioventricular junction ablation in patients with chronic atrial fibrillation. J Am Coll Cardiol 2000;36:151–8. Vanderheyden M, Goethals M, Anguera I, et al. Hemodynamic deterioration following radiofrequency ablation of the atrioventricular conduction system. Pacing Clin Electrophysiol 1997;20:2422–8. Twidale N, Manda V, Holliday R, et al. Mitral regurgitation after atrioventricular node catheter ablation for atrial fibrillation and heart failure: acute hemodynamic features. Am Heart J 1999;138:1166–75. Gasparini M, Mantica M, Brignole M, et al. Thromboembolism after atrioventricular node ablation and pacing: long term follow up. Heart 1999;82:494–8. Gribbin GM, Bourke JP, McComb JM. Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias. Heart 1998;79:548 – 53. Gianfranchi L, Brignole M, Menozzi C, Lolli G, Bottoni N. Progression of permanent atrial fibrillation after atrioventricular junction ablation and dual-chamber pacemaker implantation in patients with paroxysmal atrial tachyarrhythmias. Am J Cardiol 1998;81:351–4.

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47 Leon AR, Greenberg JM, Kanuru N, et al. Cardiac resynchronization in patients with congestive heart failure and chronic atrial fibrillation: effect of upgrading to biventricular pacing after chronic right ventricular pacing. J Am Coll Cardiol 2002;39:1258 – 63. 48 Brignole M, Menozzi C, Gasparini M, et al. An evaluation of the strategy of maintenance of sinus rhythm by antiarrhythmic drug therapy after ablation and pacing therapy in patients with paroxysmal atrial fibrillation. Eur Heart J 2002;23:892 – 900. 49 Kamalvand K, Tan K, Kotsakis A, Bucknall C, Sulke N. Is mode switching beneficial? A randomized study in patients with paroxysmal atrial tachyarrhythmias. J Am Coll Cardiol 1997;30:496 – 504. 50 Gillis AM, Connolly SJ, Lacombe P, et al. Randomized crossover comparison of DDDR versus VDD pacing after atrioventricular junction ablation for prevention of atrial fibrillation. The atrial pacing peri-ablation for paroxysmal atrial fibrillation (PA (3)) study investigators. Circulation 2000;102:736 – 41. 51 Wilkoff BL, Cook JR, Epstein AE, et al. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA 2002;288:3115 –23. 52 Sweeney MO, Hellkamp AS, Ellenbogen KA, et al. Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation 2003;107:2932 –7. 53 Puggioni E, Brignole M, Gammage M, et al. Acute comparative effect of right and left ventricular pacing in patients with permanent atrial fibrillation. J Am Coll Cardiol 2004;43:234 – 8. 54 Simantirakis EN, Vardakis KE, Kochiadakis GE, et al. Left ventricular mechanics during right ventricular apical or left ventricular-based pacing in patients with chronic atrial fibrillation after atrioventricular junction ablation. J Am Coll Cardiol 2004;43:1013 – 8. 55 Tebbenjohanns J, Schumacher B, Korte T, Niehaus M, Pfeiffer D. Bimodal RR interval distribution in chronic atrial fibrillation: impact of dual atrioventricular nodal physiology on long-term rate control after catheter ablation of the posterior atrionodal input. J Cardiovasc Electrophysiol 2000;11:497– 503. 56 Blanck Z, Dhala AA, Sra J, et al. Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and after a selective slow-pathway ablation. Circulation 1995;91:1086 – 94. 57 Chen SA, Lee SH, Chiang CE, et al. Electrophysiological mechanisms in successful radiofrequency catheter modification of atrioventricular junction for patients with medically refractory paroxysmal atrial fibrillation. Circulation 1996;93: 1690 –701. 58 Kreiner G, Heinz G, Siostrzonek P, Gossinger HD. Effect of slow pathway ablation on ventricular rate during atrial fibrillation: dependence on electrophysiological properties of the fast pathway. Circulation 1996;93:277–83. 59 Strickberger SA, Weiss R, Daoud EG, et al. Ventricular rate during atrial fibrillation before and after slow-pathway ablation. Effects of autonomic blockade and beta-adrenergic stimulation. Circulation 1996;94:1023 – 6.

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60 Feld GK, Fleck RP, Fujimura O, Prothro DL, Bahnson TD, Ibarra M. Control of rapid ventricular response by radiofrequency catheter modification of the atrioventricular node in patients with medically refractory atrial fibrillation. Circulation 1994;90:2299–307. 61 Williamson BD, Man KC, Daoud E, Niebauer M, Strickberger SA, Morady F. Radiofrequency catheter modification of atrioventricular conduction to control the ventricular rate during atrial fibrillation. N Engl J Med 1994;331:910 –7. 62 Della Bella P, Carbucicchio C, Tondo C, Riva S. Modulation of atrioventricular conduction by ablation of the “slow” atrioventricular node pathway in patients with drug-refractory atrial fibrillation or flutter. J Am Coll Cardiol 1995;25: 39–46. 63 Luderitz B, Pfeiffer D, Tebbenjohanns J, Jung W. Nonpharmacologic strategies for treating atrial fibrillation. Am J Cardiol 1996;77:45A–52A. 64 Morady F, Hasse C, Strickberger SA, et al. Long-term followup after radiofrequency modification of the atrioventricular

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node in patients with atrial fibrillation. J Am Coll Cardiol 1997;29:113 –21. Lee SH, Chen SA, Tai CT, et al. Comparisons of quality of life and cardiac performance after complete atrioventricular junction ablation and atrioventricular junction modification in patients with medically refractory atrial fibrillation. J Am Coll Cardiol 1998;31:637– 44. Twidale N, McDonald T, Nave K, Seal A. Comparison of the effects of AV nodal ablation versus AV nodal modification in patients with congestive heart failure and uncontrolled atrial fibrillation. Pacing Clin Electrophysiol 1998;21:641– 51. Proclemer A, Della Bella P, Tondo C, et al. Radiofrequency ablation of atrioventricular junction and pacemaker implantation versus modulation of atrioventricular conduction in drug refractory atrial fibrillation. Am J Cardiol 1999;83:1437–42. Knight BP, Weiss R, Bahu M, et al. Cost comparison of radiofrequency modification and ablation of the atrioventricular junction in patients with chronic atrial fibrillation. Circulation 1997;96:1532 – 6.

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IV

Ventricular tachycardia

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17

Ablation of idiopathic right ventricular tachycardia David J. Wilber and Sandeep Joshi

Ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) in the absence of overt structural heart disease is a common entity, representing up to 10% of all ventricular tachycardias evaluated by specialized arrhythmia services [1]. The clinical presentation is variable, with symptom onset typically between the ages of 20 and 40 years. The arrhythmia appears to be more common in women [2]. Nonsustained VT is more frequent, representing 60 –92% of cases in reported series [3 – 6]. Episodes most often occur as repetitive salvos (the pattern of repetitive monomorphic VT) [7,8]. Occasionally, runs of VT are incessant, and premature ventricular beats form a substantial proportion of all QRS complexes in a 24 -h period. Less commonly, patients present with paroxysmal sustained tachycardia, separated by relatively long intervals of infrequent premature ventricular beats [9 –12]. Episodes tend to increase in frequency and duration during exercise and emotional stress. In more than 80% of patients, the QRS configuration is a left bundle pattern with an inferior axis, reflecting an origin in the RVOT.

Diagnostic evaluation and prognosis The diagnosis of idiopathic RVOT VT is one of exclusion. The early stages of right ventricular structural disease, including arrhythmogenic right ventricular dysplasia or arrhythmogenic right ventricular cardiomyopathy (ARVC), may not be detected during routine clinical examination and diagnostic testing [13 –16]. VT associated with ARVC usually shows multiple QRS configurations during different episodes, including tachycardias with a superior QRS axis (both uncommon in idiopathic right ventricular tachycardia). However, many patients with ARVC present with a left bundle inferior QRS axis tachycardia alone (Fig. 17.1a) [17,18]. Exclusion of ARVC in patients being considered for catheter ablation is critical, since both the long-term prognosis [18 –20] and the response to catheter ablation [20 –22] may be less favorable in these cases.

The diagnosis of ARVC remains problematic. The 1994 European Society of Cardiology Task Force criteria provide widely accepted guidelines [23]. In patients with overt ARVC, the echocardiogram, particularly with quantitative techniques, is abnormal [24]. However, the diagnostic value of echocardiography in early or mild forms of the disease is less clear. An abnormal signal-averaged electrocardiogram (SAECG) is uncommon in patients with idiopathic RVOT VT, while an abnormal time or frequency-domain SAECG is present in 50 – 80% of patients with ARVC [25,26]. In idiopathic right ventricular VT, the 12-lead electrocardiogram is usually normal. T wave inversion in the anterior precordial leads extending to lead V3 is rare in normal adults, and its presence, along with incomplete or complete right bundle branch block (Fig. 17.1b), should prompt a more thorough investigation for ARVC [20]. Cine magnetic resonance imaging (MRI) and radionuclide right ventriculography provide useful information regarding right ventricular size and function. However, several groups have reported a substantial incidence of MRI abnormalities (65–76%) in patients with idiopathic RVOT VT without other evidence of ARVC [27–29]. These abnormalities included focal thinning and segmental contraction abnormalities, and were equally distributed between the outflow tract and the anterior free wall. In addition, focal fatty infiltration was observed in approximately 25% of patients. The clinical significance of these abnormalities, both in the pathogenesis of tachycardia and as prognostic markers, is uncertain. The diagnosis of ARVC based on MRI alone should be made with caution. “Idiopathic” left bundle superior axis tachycardias are much less frequently observed. In contrast to tachycardias with an inferior QRS axis, a superior axis is associated with a very high incidence of occult structural abnormalities. Mehta et al. found right ventricular structural abnormalities on echocardiography in all of six patients with left bundle superior axis sustained ventricular tachycardia. In addition, five of the six patients had > 10% fibrous 279

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A

B

Figure 17.1 A. Electrocardiogram of ventricular tachycardia arising from the right ventricular outflow tract in a patient ultimately diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC). B. Sinus rhythm electrocardiogram in the same patient. There are T wave inversions in leads V1–V3, and a QRS duration of 115 ms with an incomplete right bundle branch block pattern, suggestive of ARVC.

replacement of myocardium on morphometric analysis of biopsy specimens [30]. In a subsequent study, these investigators found an abnormal SAECG in seven of nine patients with left bundle superior axis tachycardias [31]. The probability of an abnormal SAECG was strongly correlated with the degree of fibrosis found in biopsy specimens. Wellens et al. reported progression from a normal right ventricular structure to typical right ventricular cardiomyopathy on serial echocardiograms during the longterm follow-up in two of five patients with left bundle superior axis tachycardias [16]. Collectively, these observations underscore the importance of close follow-up in this group of patients. 280

The long-term prognosis in patients with truly idiopathic RVOT VT is excellent, despite frequent recurrences of tachycardia [3–12,32]. Sudden death is rare in patients with initially normal left and right ventricular function; in such patients, occult cardiomyopathy is usually identified in the postmortem examination. Similarly, progression to diffuse cardiomyopathy is rare. However, in patients presenting with at least some evidence of structural heart disease (right ventricular contraction abnormalities on echocardiography or angiography, abnormal biopsy, abnormal SAECG), progression to a more generalized cardiomyopathy within the initial 6 months of clinical presentation, as well as sudden death, may occur [4,33].

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CHAPTER 17

Electrophysiologic evaluation The large majority of idiopathic outflow tract tachycardias are due to cyclic adenosine monophosphate (AMP)mediated triggered activity [10,12,34]. In contrast, tachycardias associated with ARVC are commonly due to reentry [20,21]. Adenosine rarely influences tachycardias due to reentry [34,35], and in particular has no effect on VT associated with ARVC. In patients who present with sustained VT, the tachycardia usually can be reproduced by programmed stimulation [12,35 –37]. Burst pacing is usually more effective than ventricular extrastimuli. A critical range of paced cycle lengths for induction is often observed, which may shift with changing levels of adrenergic activation. The tachycardia may be induced in the baseline state, but catecholamine infusion is generally required to facilitate induction. Occasionally, epinephrine or phenylephrine is more effective than isoproterenol. Tachycardia induction may be inconsistent [12], reflecting the complex interplay between heart rate, degree of adrenergic activation, and coupling intervals during ventricular pacing. Aminophylline and atropine, though theoretically useful in facilitating triggered activity, are rarely effective. Sedation may suppress this VT, particularly the use of benzodiazepines and propofol. In a small number of patients, idiopathic right ventricular (RV) tachycardias may be due to catecholamineenhanced automaticity or reentry. These mechanisms appear to be an uncommon cause of sustained RVOT VT, but may be observed more frequently in tachycardias originating from other RV sites. Typically, enhanced automaticity is initiated by catecholamine infusion, but not programmed stimulation [11]. Pacing during tachycardia may result in transient suppression, but not termination. Convincing evidence of a reentrant mechanism is available in only a few cases. Aizawa et al. reported on three patients with idiopathic RV tachycardia localized to the septal portion of the inflow tract within 1 cm of the His bundle, one of whom also had an additional right bundle tachycardia [38]. All of the tachycardias were initiated and terminated by programmed stimulation in the absence of isoproterenol, and entrainment was demonstrated in each. Similar tachycardias have been reported by others [39,40]. In patients presenting clinically with at most nonsustained runs of VT, induction of sustained tachycardia during programmed stimulation is considerably less common [3,5,6,30,41,42]. The QRS morphology during RVOT VT typically has a left bundle configuration, with QS or rS patterns in leads V1 and V2, and a right or left inferior axis (Figs. 17.2, 17.3). Minor variations in the QRS morphology between complexes during tachycardia may occur, associated with minor variations in local electrograms recorded near the

Ablation of idiopathic right ventricular tachycardia

site of tachycardia origin [43]. However, multiple morphologically distinct VTs due to triggered activity are uncommon, and should raise a suspicion of alternative mechanisms and occult underlying heart disease.

Endocardial mapping Optimal techniques for localizing the site of origin of idiopathic RVOT VT have received considerable attention. As expected for focal rhythms, endocardial activation at successful ablation sites tends to be only modestly early, ranging from 10 to 60 ms before the onset of the surface QRS [40,43–47]. Bipolar endocardial electrograms have high amplitudes and rapid slew rates (Fig. 17.4). Recent data suggest that three-dimensional voltage maps of the right ventricle in either sinus rhythm or tachycardia may be useful in distinguishing between idiopathic right ventricular VT and ARVC, on the one hand, and nonspecific cardiomyopathy on the other [48]. Patients with idiopathic RV VT rarely if ever have electrograms with amplitudes < 1.5 mV. Widespread findings of low-voltage, fractionated electrograms and diastolic potentials are rarely seen and suggest the diagnosis of ARVC (Fig. 17.5). The morphology of the unipolar electrogram is potentially useful for localizing focal sources of activation. Amerendral and Peinado [45] found that a QS complex was highly sensitive in identifying successful ablation sites. However, nearly 70% of unsuccessful sites also manifested a QS unipolar complex. Man et al. examined the unipolar electrogram morphology at various distances from the site of origin of mechanically induced RV premature complexes [49]. A QS complex was recorded at the origin of the premature complex in all patients, but was also recorded from electrodes located > 1 cm away in 65% of patients. Soejima and colleagues reported a QS complex in 100% of successful RVOT ablation sites, but also in 25% of unsuccessful sites [50]. Thus, unipolar electrogram morphology recorded with standard ablation electrodes is a highly sensitive but nonspecific marker of optimal ablation sites in this group of patients. Initial endocardial activation away from the site of origin is rapid. In a recent series of patients undergoing three-dimensional electroanatomical mapping during RVOT VT, the mean area of myocardium activated within the first 10 ms was 3.0 ± 1.6 cm2, ranging from 1.3 to 6.4 cm2 [51] (Figs. 17.6, 17.7). Given interobserver variability of up to 5 ms or more in the manual assignment of activation time, it is not surprising that single-site activation times are reported to be of relatively limited value as predictors of successful ablation sites. However, highdensity simultaneous display of the activation time and anatomic location with three-dimensional electroanatomical mapping systems facilitates discrimination between 281

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RIGHT

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FW

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Figure 17.2 A. Electrocardiogram of idiopathic right ventricular tachycardia arising from the anterior (leftward) septum. Note the QS complex in lead I, QRS duration of 130 ms, absence of R wave notching in the inferior leads, and R > S in lead V3. B–D. Electroanatomical maps acquired during this tachycardia, shown in 45° right anterior oblique (RAO),

45° left anterior oblique (LAO), and coronal projections. The color-coded isochrones represent activation times during tachycardia, with peak QRS voltage in lead II as the fiducial point. Earliest activation times are shown in red. FW, free wall; SEP, septum.

minor differences in timing and “smooths over” potential measurement errors. Ablation directed at the center of the early activation area is highly effective in eliminating tachycardia (Figs. 17.2, 17.3, 17.6–17.8). Three-dimensional activation mapping with noncontact arrays [52–54] and multielectrode basket catheters [55] have been similarly effective in identifying target sites. Pace-mapping was initially believed to be more useful for localizing target sites. Most investigators reported successful ablation at sites with identical or near-identical matches in all 12 surface leads [12,40,44,45,47]. The use of body surface mapping [56] and computerized algorithms for comparison of paced and tachycardia QRS configurations [57] may improve the precision of pace-mapping. Kadish et al. examined the spatial resolution of unipolar pacing with respect to the degree of pace-map matching [58]. Pacing at a site 5 mm from the index pacing site resulted in minor differences in configuration (notching, new small components, change in the amplitude of individual components, or overall change in the QRS shape) in at least one lead in 24 of 29 patients. In contrast, if only

major changes in the QRS configuration were considered, pacing sites separated by as much as 15 mm could appear similar. Current strength up to 10 mA had little effect on the unipolar paced electrocardiogram configuration. These results suggested that in optimal conditions, the spatial resolution of an exact pace-map match may be less than 5 mm. Bipolar pacing introduces additional variability into the RV paced electrocardiogram, but these changes can be minimized by low pacing outputs and small interelectrode distances (≤ 5 mm) [59]. Goyal and colleagues demonstrated that significant changes in paced QRS configuration occur during bipolar pacing at the same RV site when differences in the paced cycle length exceed 80 ms [60]. Rate-dependent aberration due to increasing degrees of incomplete repolarization and fusion with the preceding T wave during shorter cycle lengths may both play a role. These data suggest that pace-mapping should be carried out as close as possible to the cycle length of the spontaneous tachycardia. Azegami and co-workers used electroanatomical mapping to compare activation mapping and pace-mapping

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A

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Figure 17.3 A. Electrocardiogram of a tachycardia arising from the midposterior (rightward) free wall. One should note the positive QRS in lead I, a QRS duration of 160 ms, prominent R wave notching in the inferior leads, and R < S in lead V3. B–D. Electroanatomical maps acquired during this tachycardia, shown in 45° right anterior oblique (RAO), 45° left anterior

oblique (LAO), and coronal projections. The color-coded isochrones represent activation times during tachycardia, with peak QRS voltage in lead II as the fiducial point. Earliest activation times are shown in red. FW free wall, SEP, septum.

Figure 17.4 Surface electrocardiograms and intracardiac electrograms during idiopathic right ventricular outflow tract tachycardia. A. Electrograms from the ablation site (ABL) have rapid slew rates, with onset 28 ms before the surface QRS. B. Radiofrequency energy application at this site resulted in termination of the tachycardia within 4 s.

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Figure 17.5 Electroanatomical maps of the right ventricle, displaying voltage amplitude during sinus rhythm in the same patient as in Fig. 17.1. Amplitudes > 1.5 mV are displayed in purple. One should note the extensive lowvoltage areas in the right ventricular outflow tract and anterior and inferior tricuspid valve area, typical of arrhythmogenic right ventricular cardiomyopathy. RAO, right anterior oblique.

Tricuspid annulus

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Figure 17.6 A. An electroanatomical isochronal activation map of a mid free-wall tachycardia, illustrating the site of successful ablation (yellow dots) with selected pacemapping sites (white and green dots). There is rapid activation away from the site of origin, with activation during the first 10 ms encompassing an area of 3.7 cm2. B. Twelvelead electrocardiograms during ventricular tachycardia and during sinus rhythm pacemapping. Pacing near the site of origin (site 1) resulted in an exact match, with scores of 20, 18, and 15, as the distance of the pacing site from the site of origin increased. AP, anteroposterior; PV, pulmonary vein. (Reproduced with permission from [51].)

Site1

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Figure 17.7 A. Electroanatomical isochronal activation map of a low posterior free-wall tachycardia arising near the bundle of His, illustrating the site of successful ablation (yellow dot) with selected pace-mapping sites (white and green dots). There is rapid activation away from the site of origin, with activation during the first 10 ms encompassing an area of 4.0 cm2. B. Twelve-lead electrocardiograms during ventricular tachycardia and during sinus rhythm pace-mapping. The best pace-map score was 23, obtained near the site of origin (site 1). Pace-map scores progressively diminished at more remote sites, from 20, to 17 and finally 12 at a site near the pulmonary valve. PV, pulmonary vein; RAO, right anterior oblique. (Reproduced with permission from [51].)

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A First 10 ms isochrone = 1.3 cm2

Ablation of idiopathic right ventricular tachycardia

B First 10 ms isochrone = 5.5 cm2

ANGULATED LPO

LPO PV

PV

HIS HIS ABL Site

Best PM Site

Other PM Site

Figure 17.8 Electroanatomical isochronal activation maps of right ventricular outlet tract (RVOT) tachycardia, illustrating the sites with the best pace-map match (white dots), clustered around the site of successful ablation (yellow dot). Green dots represent other pacing sites in the RVOT. A. A map from a patient with a tachycardia arising from the high septum, adjacent to the pulmonary valve. This patient had a small early activation area (EAA) (1.3 cm2), and the best pace-map match sites were also confined to a small area, generally within the first 10-ms isochrone. LPO, left posterior

oblique; PV, pulmonary vein. B. A map from another patient with septal tachycardia. This patient had a large EAA (5.5 cm2) and also had a greater number of sites with best pace-map matches, spread over a broader area (but still within the first 10-ms isochrone). It should be noted that the total activation time for the RVOT was twice as long in A (approximately 60 ms) in comparison with B (approximately 30 ms). LPO, left posterior oblique; PV, pulmonary vein. (Reproduced with permission from [51].)

in RVOT tachycardias [51]. They found that the spatial resolution of pace-mapping in the RVOT is modest at best, and highly variable between patients. While the probability of obtaining an exact pace-map match diminishes with increasing distance from the site of origin (Figs. 17.6, 17.7), exact matches could be obtained from multiple sites in all patients, some at points more than 2 cm distant from the site of origin (Fig. 17.8). Isoproterenol infusion diminished the spatial resolution of pace-mapping. Moreover, pace-mapping and activation mapping were highly correlated, such that pace-mapping added little additional precision to sites selected on the basis of three-dimensional activation mapping alone.

ior and posterior, which typically refer to the location of a site in the right anterior oblique radiographic projection. These directions are more accurately referred to as leftward (toward the left arm) for “anterior” locations, and rightward (toward the right arm) for “posterior” locations. These relationships are summarized in Fig. 17.10. Initial reports suggested that VT invariably arose from a relatively well-circumscribed area on the superior septal, mid-septal, and anterior septal surface, just under the pulmonary valve [46]. However, an early report of surgical cryoablation of adenosine-sensitive RVOT tachycardia identified a mid free-wall focus [62]. Subsequently, a freewall site of origin has been reported in 20–30% of patients undergoing ablation of RVOT VT [43,45,47,63–66]. The vast majority of RVOT VTs, both septal and free-wall, originate from myocardium within 1–2 cm of the pulmonary valve. In our laboratory, 72 patients have undergone highdensity electroanatomical mapping of the RVOT during tachycardia, allowing more precise localization of the site of origin (Fig. 17.11) [67]. A free-wall focus was identified in 34% (Figs. 17.3, 17.6, 17.7). Several investigators have used pace-mapping as a tool to evaluate the potential value of surface electrocardiography characteristics for localizing the site of VT origin within the outflow tract. A QS complex in lead I suggests an anterior (leftward) focus, while an R or qR indicates a more posterior (rightward) focus [66,68]. The precordial

Location of tachycardia focus and role of the 12-lead electrocardiogram The reported origin of VT within the RVOT varies widely. An important confounding factor is confusion regarding the appropriate terminology for the complex anatomy of the RVOT. The right coronary cusp is located near the level of the His bundle. A substantial portion of the dorsal outflow tract has no true septum, but rather arches anteriorly over the aortic root [61] (Fig. 17.9). It is this interface that is often designated, if imprecisely, as the septal surface. Confusion also arises with respect to the terms anter-

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A

B

Figure 17.10 Schematic demonstrating the orientation of the right ventricular outflow tract in the chest cavity as viewed in a coronal projection. AO, aorta; LAO, left anterior oblique, RAO, right anterior oblique; RVOT, right ventricular outflow tract.

286

L

Figure 17.9 Right anterior oblique (A) and anteroposterior (B) views of a perfusion-fixed heart, demonstrating the relationship of the right ventricular outflow tract to the great vessels and left ventricle. It should be noted that the intraventricular septum does not extend to the vast majority of the dorsal outflow tract immediately beneath the pulmonary valve (right in A). APM, anterior papillary muscle; IPM, inferior papillary muscle; LA, left atrium; LAA, left atrial appendage; LPA, left pulmonary artery; LSPV, left superior pulmonary vein; LV, left ventricle; PA, pulmonary artery; PT, pulmonary trunk; RA, right atrium; RAO, right anterior oblique; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; RV, right ventricle; s, SPM, superior papillary muscle; SVC, superior vena cava; TV, tricuspid valve; x, island of anterior wall of the right ventricle; 1, parietal band; 2, septal band; 3, moderator band. (Adapted with permission from [61].)

Figure 17.11 Schematic of the right ventricular outflow tract (RVOT) endocardium opened along the junction between the free wall and the anterior septum. The schematic is divided into 16 segments to characterize the locations of successful ablation sites (and site of origin of ventricular tachycardia) in 72 patients undergoing electroanatomical mapping of idiopathic RVOT ventricular tachycardia. The numbers inside each segment indicate the number of tachycardias localized to that segment. EAT, earliest activation time. (Reproduced with permission from [67].)

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Table 17.1 Evaluation of electrocardiographic criteria for localizing the origin of right ventricular outflow tract tachycardia.

Ablation of idiopathic right ventricular tachycardia

Sensitivity

Specificity

PPV

Free wall vs. septal sites QRS duration > 140 ms R wave notching in inferior leads Lead V3 R/S ratio < 1

0.74 0.79 1.00

0.93 0.99 0.74

0.88 0.94 0.73

Anterior (leftward) vs. posterior (rightward) sites Negative or isoelectric QRS in lead I

0.96

0.67

0.77

Caudal (> 2 cm from PV) vs. cranial sites Isoelectric or positive QRS in lead aVL

0.86

1.00

1.00

PPV, positive predictive value; PV, pulmonary valve.

lead transition (R ≥ S) moves leftward as the origin moves caudally from the pulmonary valve, or away from the septum [66,68]. Wider QRS duration and notching of the R wave in the inferior leads are associated with free-wall VT. Finally, VT arising within 2 cm of the pulmonary valve virtually always has a negative QRS in lead aVL [66]; the amplitude in lead aVL is generally greater in tachycardias of septal origin relative to free-wall tachycardias. In a series of 46 patients with RVOT VT presenting for catheter ablation, we prospectively examined the potential role of several electrocardiographic criteria in predicting the location of successful ablation sites [67]. QRS amplitude, notching, duration, and polarity were evaluated for their ability to predict the site of origin along three perpendicular anatomic axes: septal–free wall, cranial–caudal, and leftward–rightward. Five variables were found to be significant predictors of location (P < 0.001), and the sensitivity, specificity, and positive predictive value of each are presented in Table 17.1. A QRS duration ≥ 140 ms and R wave notching in two or more of leads II, III, and aVF were highly specific, but somewhat less sensitive in predicting a free-wall origin (Figs. 17.3, 17.6, 17.7). An R/S

ratio ≤ 1 in lead V3 (reflecting a more leftward precordial transition) was highly sensitive, but less specific for a freewall origin. QRS polarity in lead I (negative or isoelectric) was a sensitive, but less specific predictor of an anterior (leftward) site of origin. Finally, an isoelectric or negative QRS in lead aVL strongly predicted a site caudally in the outflow tract, adjacent to the His bundle (Fig. 17.7). This latter group of tachycardias, constituting approximately 10% of all RVOT VTs, has similar mechanisms and electrophysiologic properties to those arising closer to the pulmonary valve. Localization algorithms based on similar criteria have been reported by others [69 –71]. Timmermans and co-workers reported that tachycardias with an apparent RVOT QRS configuration could also originate from a muscular sleeve investing the proximal pulmonary artery above the valve [72] (Fig. 17.12). A more recent study suggests that with careful angiographic localization of the ablation electrode relative to the pulmonary valve at the successful ablation site, such tachycardias may account for approximately 15% of all idiopathic VTs with a left bundle branch block–inferior QRS configuration [73]. A majority of these are located

Figure 17.12 Posterior view of a perfusionfixed heart with the majority of the pulmonary artery dissected away to reveal a broad band of circumferential muscle fibers (orange hatching in the right panel) investing the proximal pulmonary artery at the level of the valve leaflets, nearly extending to the commissures. LAL, left anterior leaflet; LV, left ventricle; P, posterior leaflet; RAL, right anterior leaflet; RV, right ventricle. (Reproduced with permission from [61].)

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along the “septal” surface of the pulmonary artery adjacent to the aorta, and are within 1.5 cm of the valve. Rarely, they may originate several centimeters above the valve. In the absence of simultaneous imaging of the pulmonary valve, such sites could easily be presumed to lie beneath the valve. Intracardiac echocardiography provides a simple alternative to angiography for imaging of electrode locations relative to the valve (Fig. 17.13). A lowamplitude ventricular electrogram (< 1 mV), an associated atrial electrogram, and the requirement for high pacing outputs to capture the ventricle are clues that the recording site is actually located above the valve. Surface electrocardiograms from VT arising above the valve tend to have greater R wave voltage in the inferior leads, a larger R/S ratio in V2, and greater aVL/aVR Q wave ratio in comparison with RVOT VT of endocardial origin. However, there is a large overlap in these parameters between the two groups, limiting their ability to discriminate sites of origin. An important implication of suspecting a pulmonary

artery focus is that power titration should be more cautious within the thin-walled artery, which is also located close to the origins of the coronary arteries. Left bundle–shaped tachycardias with an inferior QRS axis and prominent R waves in V1 or V2 (R/S amplitude ratio ≥ 0.5 and R wave duration/QRS duration ratio ≥ 0.3) usually arise from the left ventricular outflow tract (endocardium, aortic sinuses of Valsalva, or epicardium adjacent to the anterior interventricular vein) [73–76] (Fig. 17.14). Mapping of the aortic sinuses, the endocardial left ventricular outflow tract, and the coronary venous system should be strongly considered in these patients before attempted ablation in the RVOT. Algorithms for distinguishing between right-sided and left-sided origins of VT arising from the outflow tract have recently been reported [70,77], and prospective validation of these is awaited. Collectively, these data indicate that the surface electrocardiogram contains important and practical clues for localizing RV outflow tachycardias, but must be interpreted

C C

A

LCC

B Figure 17.13 Intracardiac echocardiographic images of the normal right ventricular outflow tract (RVOT), pulmonary valve (PV), and pulmonary artery (PA). It should be noted that the planes of the valve annuli are at nearly 90° to each other. A. In systole, demonstrating both aortic and pulmonary valve leaflets in the open position. B. Apposition of the valve

288

D D leaflets in diastole. C. The mapping electrode (arrow) positioned at the septal outflow tract, immediately beneath the pulmonary valve. D. The mapping electrode (arrow) advanced beyond the valve into the pulmonary artery. AV, aortic valve; LCC, left coronary cusp; RCC, right coronary cusp.

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Figure 17.14 Electrocardiogram from a tachycardia arising from the left sinus of Valsalva. The prominent and broad R waves in V1 and V2 should be noted.

B

A

RAO Figure 17.15 A. Electroanatomical map of an idiopathic right ventricular tachycardia arising adjacent to the anterior tricuspid valve annulus. The orange dot represents the site of His bundle activation. B. Twelve-lead

electrocardiogram of the tachycardia, demonstrating a left superior axis and late precordial transition, typical of this location.

carefully. Specific characteristics in individual leads may not be associated with a single unique site. Differences in the orientation of the heart within the thoracic cavity introduce additional variability. In our own experience and that of others [47,66], these criteria provide a reliable first approximation for localizing tachycardias within the outflow tract. Idiopathic RV tachycardias with a superior QRS axis are generally located in the body of the right ventricle on the anterior free wall, mid-septum, and distal septum, or along the tricuspid valve annulus (Fig. 17.15).

endocardial electrogram is recorded. As noted above, this site may be located above the pulmonary valve and may be a potential site of VT origin. Once a large-amplitude ventricular electrogram is recorded without an associated atrial electrogram, gentle torque is applied to the catheter for circumferential mapping of the outflow tract within 1 cm of the pulmonary valve, with a minimum of four sites (left and right septal, and left and right free wall, as determined by biplanar fluoroscopy and/or threedimensional mapping. The plane of the septum in the left anterior oblique (LAO) projection is nearly perpendicular to the imaging plane (Fig. 17.16), with slight variability introduced by the exact degree of angulation and the anatomical orientation of the heart. The catheter is then withdrawn in 1-cm increments, and the process repeated. On the basis of the mapping results at these initial sites, and with guidance from the surface QRS configuration,

Approach to catheter ablation We generally begin mapping by placing the ablation catheter in the proximal pulmonary artery and slowly withdrawing it into the outflow tract until the first local

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Figure 17.16 A perfusion-fixed heart, demonstrating the disposition of the right ventricular outflow tract in the 45° left anterior oblique (LAO) imaging plane. The right ventricular free wall has been dissected free, leaving only the attachments to the septum and tricuspid and pulmonary annuli. It should be noted that the entire septal surface of the outflow tract in this projection is to the right of the His bundle region (red star). As the imaging plane moves toward the 60° LAO, the septum becomes nearly

perpendicular to the imaging plane, but because of the septal curvature as one moves closer to the pulmonary valve, septal points remain to the right or at most vertical to the His bundle region. LA, left atrium; LIPV, left inferior pulmonary vein; LPA, left pulmonary artery; LSPV, left superior pulmonary vein; LV, left ventricle; TV, tricuspid valve; VMS, ventricular membranous septum; 1, right anterolateral; 2, left anterolateral; 3, posterior. (Adapted with permission from [61].)

attention is then directed to specific regions of early activation. A catheter positioned at the proximal His bundle and/or mid-anterior septum aids in accurate anatomic localization, as septal sites are nearly always within the same vertical plane or further rightward relative to these catheter positions in the LAO projection, even accounting for slight leftward bulging of the septum (Figs. 17.17, 17.18). It is our practice to use three-dimensional activation mapping as the primary localization technique for selecting target sites for ablation. Once the center of the early activation area is identified, pacing from this site invariably produces an excellent or exact pace-map match (Fig. 17.7).

Temperature-guided radiofrequency (RF) application is important, as cooling of the catheter tip by circulating blood flow is relatively poor in some regions of the RV; electrode tip temperature may increase rapidly with relatively low power applications. In our experience, and that of Wen and colleagues [65], termination of tachycardia at ultimately successful sites generally occurs within 10 s (Fig. 17.4). Acceleration of the tachycardia during RF application, followed by gradual slowing or abrupt termination may also be observed [12] (Fig. 17.19). Application of radiofrequency energy in sinus rhythm at sites near the tachycardia origin also may result in the induction of repetitive responses or tachycardia with QRS characteristics

Figure 17.17 Catheter positions at the successful ablation site for the septal tachycardia illustrated in Fig. 17.2. A. Left anterior oblique, 60°. B. Right anterior oblique, 30°. The open arrow indicates the ablation catheter and the closed arrow the His catheter. The third catheter is positioned on the midanterior septum. The position of the ablation electrode to the right of the His position in the left anterior oblique projection should be noted.

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Figure 17.18 Catheter positions at the successful ablation site for the free-wall tachycardia illustrated in Fig. 17.3. A. Left anterior oblique, 60°. B. Right anterior oblique, 30°. The open arrow indicates the ablation catheter and the closed arrow the His catheter. The third catheter is positioned on the midanterior septum. The position of the ablation electrode to the left of the His position in the left anterior oblique projection should be noted.

Figure 17.19 Onset of radiofrequency application during sustained ventricular tachycardia, indicated by the bold line above the right ventricular outflow tract (RVOT) electrogram. There is an initial acceleration of the

tachycardia, followed by progressive slowing and irregularity. After 14 s, the tachycardia terminates and does not recur. (Reproduced with permission from [12].)

similar to those seen during spontaneous VT [78]. These observations may be due to thermal facilitation of triggered activity [79], but may also simply reflect thermally induced abnormal automaticity [80]. Neither phenomenon is a specific marker for a successful ablation site. Persistent difficulty in identifying optimal target sites or in eliminating VT during ablation is uncommon, but may arise for several reasons. The induced VT may not be of RVOT origin [81]. Occasionally, preexcited tachycardia with antegrade conduction through a right-sided accessory atrioventricular connection (either passively or as the antegrade limb of atrioventricular reciprocating tachycardia) may cause diagnostic confusion, particularly when preexcitation is intermittent or latent [82]. Finally, a small number of RVOT VTs with typical left bundle (QS or minimal R wave in leads V1 and V2) inferior QRS patterns and a QS complex in lead aVLamimicking a typical anteroseptal

locationamay originate on the epicardium near the anterior interventricular vein [76] (Fig. 17.20).

Outcome of ablation Table 17.2 summarizes the available data with respect to the outcome of radiofrequency catheter ablation of RVOT VT [22,40,43–47,52,54,55,63–67,70,83]. Series with more than 10 patients were included if adequate outcome data were provided. Acute procedural success was reported in 93% of the patients. In patients with successful ablation, 5% had recurrent VT during variable follow-up periods. The majority of recurrences were within the first year, and patients underwent repeat ablation with long-term freedom from additional recurrences. Recurrence more than 1 year after ablation was rare, despite follow-up periods 291

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A

D

B

C

E

RV

LAO

LV

RAO

Figure 17.20 A. Electrocardiogram of a proximal anterior interventricular vein (AIV) tachycardia. C. Electroanatomical endocardial activation maps of ventricular tachycardia (VT). The earliest activation was on the septal right ventricular tract, 18 ms before the onset of QRS, where endocardial ablation failed to terminate the VT (pink dots). LAO, left anterior oblique; LV, left ventricle; RV, right ventricle. D. Recordings from the multipolar epicardial venous mapping catheter, demonstrating earliest epicardial activation 48 ms before the onset of QRS (arrow). B. A right anterior oblique (RAO) radiograph, demonstrating the placement of an 18-pole

3.5-Fr microcatheter positioned in the distal great cardiac vein and proximal anterior interventricular vein (small arrows). A quadripolar ablation catheter (large arrowhead) is positioned at the site of earliest endocardial activation. E. A right anterior oblique radiograph immediately before ablation, demonstrating the positions of the ablation electrode in the proximal anterior interventricular vein (large arrowhead), a Judkins catheter positioned at the left coronary artery ostium (small arrow), and a diagnostic catheter in the right ventricular outflow tract at the earliest site of endocardial activation (double arrows).

of several years in a substantial number of patients. Procedural variables influencing the probability of recurrence after initially successful ablation were examined by Wen et al. Poor pace-map matches (< 12/12), later activation at the target site, and reliance on pace-mapping alone were all significant predictive factors for recurrence [65]. Serious complications occur in approximately 1% of patients, usually related to cardiac perforation. Published data regarding outcome in non-outflow tract idiopathic RV tachycardia is limited, as these patients

represent < 10% of reported patients with RV tachycardias undergoing ablation. Available data are listed in Table 17.3 [38,40,63,84]. In general, ablation of these tachycardias has been less successful, reflecting a greater diversity of underlying mechanisms, as well as a greater likelihood of occult structural heart disease. Ablation of frequent, highly symptomatic, single premature ventricular complexes arising from the RV has been reported by several centers [85–89]. The techniques and outcome are similar to those reported for RV tachy-

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Table 17.2 Outcome of radiofrequency catheter ablation in patients with idiopathic right ventricular outflow tachycardia. First author (ref.)

Year

Patients (n)

Acute success

Mean follow-up (months)

Recurrences† (n)

Calkins [40] Coggins [64] Mandrola [63] Movsowitz [46] Gumbrielle [44] Chinushi [43] Rodriguez [47] Amerendral [45] Wen [65] Aiba [55] Lee [83] Friedman [52] O’Donnell [22] Ribbing [54] Ito [70] Joshi [67]

1993 1994 1995 1996 1997 1997 1997 1998 1998 2001 2002 2002 2003 2003 2003 2005

10 20 35 18 10 13 35 15 44 50 35 10 33 33 109 72

10/10 17/20 35/35* 16/18 10/10 13/13 29/35 13/15* 39/44 47/50 30/35 9/10 32/33 27/33 106/109 71/72

8 10 24 12 16 28 30 21 41 n.a. n.a. 11 56 54 21 51

0/10 1/17 0/35 5/16 0/10 1/13 4/28 1/13 4/39 n.a. n.a. 2/9 1/32 1/27 0/106 2/71

542

504/542 (93%)

Total

22/426 (5%)

* Acute success determined at hospital discharge, with one or more patients undergoing repeat procedures due to early recurrence or initial failure. In all other series, success was determined at the end of the initial procedure. † After initially successful ablation.

Table 17.3 Outcome of radiofrequency catheter ablation in patients with idiopathic right ventricular tachycardia from non-outflow sites. First author (ref.)

Year

Aizawa [38] Calkins [40] Mandrola [63] Vohra [84] Present authors

1993 1993 1995 1996 2005

Total

Acute success 3/3 2/4 5/8 1/3 7/10

Location

Recurrences

IT 3 IT 2, PB 1, AFW 1 IT 6, AFW 2 RVA 2, AFW 1 RVA 2, TVA 5, AFW 3

0/3 0/2 0/5 0/1 0/7

18/28 (64%)

0/18

AFW, anterior free wall; IT, inflow tract; PB, posterobasal; RVA, right ventricular apex; TVA, tricuspid valve annulus.

cardias. While reassurance and judicious use of antiarrhythmic drugs are often sufficient for managing the symptoms, this approach merits consideration in patients disabled by symptomatic ectopic beats who are unresponsive or intolerant to drug therapy. Patients with frequent or incessant tachycardia from the right ventricle are at risk for tachycardiomyopathy, which may be reversible after successful ablation [90–93]. More recently, it has been appreciated that this phenomenon may be operative even in patients with frequent premature ventricular complexes alone [88,89]. In such patientsa with impaired ventricular function and/or ventricular dilation in the absence of other apparent causesasuccessful ablation of ectopic beats reduces the ventricular size

and normalizes ventricular function. While these patients frequently have a substantial ectopic burden before ablation (> 20% of all QRS complexes), improvement in ventricular function has also been demonstrated in patients with less frequent ventricular ectopy [89]. The value of catheter ablation in asymptomatic patients with frequent ventricular ectopy and normal left ventricular dimensions and function remains to be demonstrated, and the procedure cannot be recommended routinely. Ablation of idiopathic RV tachycardias can be carried out safely and effectively in children and adolescents [94 –96]. Safety in the very young has not been established, and experimental data raise concerns with regard to lesion enlargement over time after radiofrequency application in 293

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the immature heart [97]. Limited data also suggest that idiopathic right ventricular VT with onset in infancy has a high probability of spontaneous resolution [98]. Which patients with idiopathic RV tachycardias should undergo ablation? Experience with currently available antiarrhythmic drug therapy indicates that 30–40% of patients will experience recurrent symptoms or VT during the long-term follow-up [6,99]. In patients with hemodynamic compromise associated with tachycardia (syncope and presyncope), ablation should be considered as the primary therapy. When symptoms are less severe, multiple factors, including side effects and inconvenience associated with long-term drug therapy, frequency of symptoms, response to prior drug trials, and the patient’s preferences need to be balanced against the small risk of procedural complications. For many of these patients, catheter ablation may also be chosen as the primary therapy. Ablation should also be considered in patients with concomitant unexplained left ventricular dysfunction, given the high probability of improved ventricular function following elimination of the arrhythmia. With current technology, and in experienced centers, catheter ablation of idiopathic RV VT can be accomplished with low morbidity and an excellent immediate and long-term outcome. These results approach those reported for supraventricular tachycardia.

9

10

11

12

13

14

15

16

References 17 1 Brooks F, Burgess H. Idiopathic ventricular tachycardia. Medicine 1988;67:271–94. 2 Nakagawa M, Takahashi N, Nobe S, et al. Gender differences in various types of idiopathic ventricular tachycardia. J Cardiovasc Electrophysiol 2002;13:633–8. 3 Buxton AE, Waxman HL, Marchlinski FE, Simson MB, Cassidy D, Josephson ME. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1983;68: 917–27. 4 Pietras RJ, Lam W, Bauernfeind R, et al. Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: clinical, hemodynamic, and angiographic findings. Am Heart J 1983;105:357–71. 5 Ritchie AH, Kerr CR, Qi A, Yeung-Lai-Wah JA. Nonsustained ventricular tachycardia arising from the right ventricular outflow tract. Am J Cardiol 1989;64:594–8. 6 Lemery R, Brugada P, Bella PD, Dugernier T, van den Dool A, Wellens HJ. Nonischemic ventricular tachycardia: clinical course and long-term follow-up in patients without clinically overt heart disease. Circulation 1989;79:990 – 9. 7 Zimmermann M, Maisonblanche P, Cauchemez B, Leclercq JF, Coumel P. Determinants of spontaneous ectopic activity in repetitive monomorphic idiopathic ventricular tachycardia. J Am Coll Cardiol 1986;7:1219–27. 8 Coumel P, Leclercq JF, Slama R. Repetitive monomorphic idiopathic ventricular tachycardia. In: Zipes DP, Jalife J, eds. 294

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42 Brodsky MA, Orlov MV, Winters RJ, et al. Determinants of inducible ventricular tachycardia in patients with clinical ventricular tachyarrhythmia and no apparent structural heart disease. Am Heart J 1993;126:1113 –20. 43 Chinushi M, Aizawa Y, Takahashi K, Kitazawa H, Shibata A. Radiofrequency catheter ablation for idiopathic right ventricular tachycardia with special reference to morphological variation and long term outcome. Heart 1997;78:255 – 61. 44 Gumbrielle TP, Bourke JP, Doig JC, et al. Electrocardiographic features of septal location of right ventricular outflow tract tachycardia. Am J Cardiol 1997;79:213 – 6. 45 Amerendral J, Peinado R. Radiofrequency catheter ablation of idiopathic right ventricular outflow tract tachycardia. In: Farre J, Concepcion M, eds. Ten Years of Radiofrequency Catheter Ablation. Armonk, NY: Futura, 1998: 249 – 62. 46 Movsowitz C, Schwartzman D, Callans DJ, et al. Idiopathic right ventricular outflow tract tachycardia: narrowing the anatomic location for successful ablation. Am Heart J 1996; 131:930 – 6. 47 Rodriguez LM, Smeets JL, Timmermans C, Wellens HC. Predictors for successful ablation of right- and left- sided idiopathic ventricular tachycardia. Am J Cardiol 1997;79:309 – 14. 48 Corrado D, Basso C, Leoni L, et al. Three-dimensional electroanatomic voltage mapping increases accuracy of diagnosing arrhythmogenic right ventricular cardiomyopathy/ dysplasia. Circulation 2005;111:3042 –50. 49 Man KC, Daoud EG, Knight BP, et al. Accuracy of the unipolar electrogram for identification of the site of origin of ventricular activation. J Cardiovasc Electrophysiol 1997:8:774 –9. 50 Soejima Y, Aonuma K, Iesaka Y, Isobe M. Ventricular unipolar potential in radiofrequency catheter ablation of idiopathic nonreentrant ventricular outflow tachycardia. Jpn Heart J 2004;45:749 – 60. 51 Azegami K, Wilber DJ, Arruda M, Lin AC, Denman RA. Spatial resolution of pacemapping and activation mapping in patients with idiopathic right ventricular outflow tract tachycardia. J Cardiovasc Electrophysiol 2005;16:823 – 9. 52 Friedman PA, Asirvatham SJ, Grice S, et al. Noncontact mapping to guide ablation of right ventricular outflow tract tachycardia. J Am Coll Cardiol 2002;39:1808 –12. 53 Fung JW, Chan HC, Chan JY, Chan WW, Kum LC, Sanderson JE. Ablation of nonsustained or hemodynamically unstable ventricular arrhythmia originating from the right ventricular outflow tract guided by noncontact mapping. Pacing Clin Electrophysiol 2003;26:1699 –705. 54 Ribbing M, Wasmer K, Monnig G, et al. Endocardial mapping of right ventricular outflow tract tachycardia using noncontact activation mapping. J Cardiovasc Electrophysiol 2003;14:602 – 8. 55 Aiba T, Shimizu W, Taguchi A, et al. Clinical usefulness of a multielectrode basket catheter for idiopathic ventricular tachycardia originating from right ventricular outflow tract. J Cardiovasc Electrophysiol 2001;12:518 –20. 56 Klug D, Ferracci A, Molin F, et al. Body surface potential distributions during idiopathic ventricular tachycardia. Circulation 1995;91:2002–9. 57 Gerstenfeld EP, Dixit S, Callans DJ, Rajawat Y, Rho R, Marchlinski FE. Quantitative comparison of spontaneous and paced 12-lead electrocardiogram during right ventricular 295

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73 Sekiguchi Y, Aonuma K, Takahasi A, et al. Electrocardiographic and electrophysiologic characteristics of ventricular tachycardia originating within the pulmonary artery. J Am Coll Cardiol 2005;45:887– 95. 74 Callans DJ, Menz V, Schwartzman D, Gottlieb CD, Marchlinski FE. Repetitive monomorphic tachycardia from the left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin. J Am Coll Cardiol 1997;29:1023 –7. 75 Ouyang F, Fotuhi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002;39:500 – 8. 76 Daniels DV, Lu Y, Morton JB, Santucci PA, Akar JG, Green A, Wilber DJ. Idiopathic Epicardial Left Ventricular Tachycardia Originating Remote From the Sinus of Valsalva: Electrophysiologic Characteristics, Catheter Ablation, and Identification from the 12 lead Electrocardiogram. Circulation 2006;113(13): 1659 –66. 77 Yang Y, Saenz LC, Varosy PD, et al. Analyses of phase differences from surface electrocardiogram recordings to distinguish the origin of outflow tract tachycardia [abstract]. Heart Rhythm 2005;2:580. 78 Chinushi M, Aizawa Y, Ohhira K, et al. Repetitive ventricular response induced by radiofrequency ablation for idiopathic ventricular tachycardia originating from the outflow tract of the right ventricle. Pacing Clin Electrophysiol 1998;21:669 –78. 79 Mugelli A, Cerbai E, Amerini S, Visentin S. The role of temperature on the development of oscillatory afterpotentials and triggered activity. J Mol Cell Cardiol 1986;18:1313 – 6. 80 Nath S, Lynch C 3rd, Whayne JG, Haines DE. Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle. Circulation 1993;88:1826 –31. 81 Krebs ME, Krause PC, Engelstein ED, Zipes DP, Miles WM. Ventricular tachycardias mimicking those arising from the right ventricular outflow tract. J Cardiovasc Electrophysiol 2000;11:45 –51. 82 Goldberger JJ, Pederson DN, Damle RS, Kim YH, Kadish AH. Antidromic tachycardia utilizing decremental, latent accessory atrioventricular fibers: differentiation from adenosine-sensitive ventricular tachycardia. J Am Coll Cardiol 1994;24:732 – 8. 83 Lee SH, Tai CT, Chiang CE, et al. Determinants of successful ablation of idiopathic ventricular tachycardias with left bundle branch block morphology from the right ventricular outflow tract. Pacing Clin Electrophysiol 2002;25:1346 –51. 84 Vohra J, Shah A Hua W, et al. Radiofrequency ablation of idiopathic ventricular tachycardia. Aust N Z J Med 1996;26: 186 – 94. 85 Gursoy S, Brugada J, Souza O, et al. Radiofrequency ablation of symptomatic but benign ventricular arrhythmias. Pacing Clin Electrophysiol 1992;15:738 – 41. 86 Zhu D, Maloney JD, Simmons TW, et al. Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity. J Am Coll Cardiol 1995;26:843 – 9. 87 Seidl K, Schumacher B, Hauer B, et al. Radiofrequency catheter ablation of frequent monomorphic ventricular ectopic activity. J Cardiovasc Electrophysiol 1999;10:924 –34. 88 Takemoto M, Yoshimura H, Ohba U, et al. Radiofrequency catheter ablation of premature ventricular complexes from

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94 O’Conner BK, Case CL, Sokoloski MC, et al. Radiofrequency catheter ablation of right ventricular outflow tachycardia in children and adolescents. J Am Coll Cardiol 1996;27:869 –74. 95 Smeets JL, Rodriguez LM, Timmermans C, Wellens HJ. Radiofrequency catheter ablation of idiopathic ventricular tachycardias in children. Pacing Clin Electrophysiol 1997;20:2068 –71. 96 Tanel RE, Walsh EP, Triedman JK, Epstein MR, Bergau DM, Saul JP. Five-year experience with radiofrequency catheter ablation: implications for management of arrhythmias in pediatric and young adult patients. J Pediatr 1997;31:878 – 87. 97 Saul JP, Hulse JE, Papagiannis J, et al. Late enlargement of radiofrequency lesions in infant lambs: implications for ablation procedures in small children. Circulation 1994;90:942 – 9. 98 Pfammatter JP, Paul T. Idiopathic ventricular tachycardia in infancy and childhood: a multicenter study on clinical profile and outcome of the Working Group of Dysrhythmias and Electrophysiology of the Association for European Pediatric Cardiology. J Am Coll Cardiol 1999;33:2067–72. 99 Gill JS, Mehta D, Ward DE, Camm AJ. Efficacy of flecainide, sotalol, and verapamil in the treatment of right ventricular tachycardia in patients without overt cardiac abnormality. Br Heart J 1992;68:392 –7.

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18

Idiopathic left ventricular tachycardias Akihiko Nogami and Hiroshi Tada

Introduction Sustained monomorphic ventricular tachycardia (VT) is most often related to myocardial structural heart disease, including healed myocardial infarction and cardiomyopathies. However, no apparent structural abnormality is identified in approximately 10% of all sustained monomorphic VTs in the United States [1] or 20% of those in Japan [2]. These VTs are referred to as “idiopathic.” Idiopathic VTs usually occur in specific locations and have specific QRS morphologies, whereas VTs associated with structural heart disease have a QRS morphology that tends to indicate the location of the scar. This idiopathic VT includes multiple discrete subtypes that are best differentiated by their mechanism, QRS morphology, and site of origin. There are four types of idiopathic left VT: • Reentrant fascicular VT • Focal Purkinje VT • Mitral annular VT • Left ventricular outflow tract VT This chapter focuses on the assessment and nonpharmacological treatment of these types of VT.

Classification of idiopathic left VT Idiopathic left VT has been classified into three subgroups relative to the mechanism (Table 18.1). We have also classified idiopathic VT according to its site of origin (Table 18.2) [3]: • Verapamil-sensitive fascicular VT (reentry). • VT with a focal origin in the distal Purkinje system (triggered activity or automaticity). • VT from the mitral annulus (triggered activity, reentry, or automaticity).

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Table 18.1 Classification of ventricular tachycardia (VT) relative to the mechanism. I II III

Verapamil-sensitive VT (reentry) Adenosine-sensitive VT (triggered activity) Propranolol-sensitive VT (automaticity)

Table 18.2 Classification of ventricular tachycardia (VT) relative to the site of origin. I

Verapamil-sensitive fascicular VT (reentry) Left posterior fascicular VT Proximal type (mid-septum) Distal type (apical inferior septum) Left anterior fascicular VT Proximal type (mid-septum) Distal type (anterolateral wall) Left upper septal fascicular VT (upper septum) II Focal Purkinje VT (triggered activity or automaticity) III Mitral annular VT (triggered activity, reentry, or automaticity) IV Left outflow tract VT (triggered activity, reentry, or automaticity) Endocardial origin Mediosuperior aspect of mitral annulus (aortomitral continuity) Superior basal septum (His bundle area) Epicardial origin Aortic sinus approach Coronary venous approach Pulmonary artery approach Direct epicardial approach

• Left ventricular outflow tract VT (triggered activity, reentry, or automaticity). While the mechanism of verapamil-sensitive fascicular VT is reentry, the mechanisms of other forms of VT are not homogeneous.

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Left posterior fascicular VT is common; left anterior fascicular VT is uncommon; and left upper septal fascicular VT is very rare.

Classification Verapamil-sensitive fascicular VT is the most common form of idiopathic left VT. This form of idiopathic VT was first recognized as an electrocardiographic entity in 1979 by Zipes et al. [4], who identified the characteristic diagnostic triad: • Induction with atrial pacing. • Right bundle branch block (RBBB) and left axis configuration. • Manifestation in patients without structural heart disease. In 1981, Belhassen and co-workers [5] were the first to demonstrate the verapamil-sensitivity of the tachycardia, the fourth identifying feature. In 1988, Ohe et al. [6] reported another variant of this type of tachycardia, RBBB with a right axis deviation. Shimoike et al. [7] described the upper septal form of this tachycardia in 2000. Depending on the QRS morphology, verapamil-sensitive left fascicular VT can be classified into three subgroups: • Left posterior fascicular VT, with an RBBB configuration and superior axis (Fig. 18.1). • Left anterior fascicular VT, with an RBBB configuration and right axis deviation (Fig. 18.2). • Upper septal fascicular VT, with a narrow QRS configuration and normal or right axis deviation (Fig. 18.3).

Anatomy and mechanism The anatomic basis of this type of tachycardia has attracted considerable interest. Some data suggest that the tachycardia may originate from a false tendon or fibromuscular band in the left ventricle [8–11]. Suwa et al. [9] described a false tendon in the left ventricle of a patient with idiopathic VT in whom the VT was eliminated by surgical resection of the tendon. Using transthoracic and transesophageal echocardiography, Thakur et al. [10] found false tendons extending from the posteroinferior left ventricle to the basal septum in all of 15 patients with idiopathic left VT, but in only 5% of control patients. Maruyama et al. [11] recorded sequential diastolic potentials bridging the entire diastolic period from a false tendon extending from the mid-septum to the inferoapical septum in a single case. Lin and colleagues reported the presence of a fibromuscular band in 17 of 18 patients with idiopathic fascicular VT, but also in 35 of 40 control patients without VT [12]. They concluded that the fibromuscular band was a common echocardiographic finding, although the potential role of the band as a substrate for VT could not be excluded. Small fibromuscular bands, trabeculae carneae, or small papillary muscles cannot be detected by echocardiography. We believe that the

Figure 18.1 Twelve-lead electrocardiogram of verapamil-sensitive left posterior fascicular ventricular tachycardia. (Reproduced with permission from [3].)

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Figure 18.2 Twelve-lead electrocardiogram of verapamil-sensitive left anterior fascicular ventricular tachycardia. (Reproduced with permission from [19].)

Purkinje networks in these small anatomic structures are important when considering the reentry circuit of verapamil-sensitive left fascicular VT.

Left posterior fascicular VT

Figure 18.3 Twelve-lead electrocardiogram of verapamil-sensitive left upper septal ventricular tachycardia (VT). The QRS morphology during the VT was relatively narrow (100 ms) and showed an R wave transition at V3. (Reproduced with permission from [3].)

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The electrocardiogram (ECG) in this type of VT shows RBBB and a superior axis (left axis deviation or north-west axis) (Fig. 18.1). This is the common type of verapamilsensitive fascicular VT. The tachycardia can be initiated and terminated by programmed stimulation, and importantly can be entrained from multiple sites, consistent with reentry as the mechanism. To explore the nature of the reentrant circuit, we performed left septal mapping with an octapolar electrode in 20 patients with left posterior fascicular VT [13] (Fig. 18.4). In 15 of the 20 patients, two distinct potentials, P1 and P2, were recorded during the VT from the mid-septum (Fig. 18.5). The mid-diastolic potential (P1) was recorded earlier from the proximal electrode than from the distal electrode, while the fused presystolic Purkinje potential (P2) was recorded earlier from the distal than from the proximal electrodes. During sinus rhythm at the same sites, P2 was recorded after the His bundle potential and before the onset of the QRS complex; however, the sequence of P1 and P2 was the reverse of that seen during the VT. The tachycardia could be entrained from both the

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Figure 18.4 An octapolar electrode catheter positioned at the left ventricular septum, as viewed fluoroscopically in the right anterior oblique (RAO, A) and left anterior oblique (LAO, B) projections. The distance between electrodes 1 and 8 on the octapolar electrode catheter was approximately 25 mm. HBE, His bundle electrogram; LV, left ventricle; RVA, right ventricular apex; RVOT, right ventricular outflow tract. (Reproduced with permission from [13].)

Figure 18.5 Intracardiac recordings from an octapolar electrode catheter. A. During left posterior fascicular ventricular tachycardia, a diastolic potential (P1) and a presystolic Purkinje potential (P2) were recorded. While P1 was recorded earlier from the proximal than the distal electrodes, P2 was recorded earlier from the distal than the proximal electrodes. B. During

sinus rhythm, recording at the same site demonstrated the P2, which was recorded before the onset of the QRS complex. HBE, His-bundle electrogram; RVO, right ventricular outflow tract; LV, left ventricle. (Reproduced with permission from [13].)

atrium and ventricle. Entrainment pacing from the atrium and ventricle captured P1 orthodromically and reset the VT. The interval from the stimulus to P1 was prolonged as the pacing rate was increased. Both the P1–P2 and P2–P1 intervals were proportionally prolonged following intravenous administration of a small dose of verapamil. However, the P2–QRS interval remained unchanged. These findings demonstrated that P1 was a critical component of the circuit in verapamil-sensitive left posterior fascicular VT. The findings also confirm the presence of a

macroreentry circuit involving the normal Purkinje system, as well as abnormal Purkinje tissue displaying decremental properties and verapamil sensitivity. While the critical role of the diastolic potential (P1) in the antegrade limb of the reentrant circuit was demonstrated, it remains unclear whether the left posterior fascicle or Purkinje fiber (P2) were obligate components [11,14]. Ouyang et al. [15] suggested that idiopathic left fascicular VT might be a relatively small circuit consisting of one anterograde Purkinje fiber with a Purkinje potential, one retrograde Purkinje 301

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fiber with retrograde Purkinje potential, and the ventricular myocardium as the bridge. As the diastolic potential (P1) appears to be a critical potential in the VT circuit, it may serve as an effective target for ablation. Nakagawa et al. [16] first reported the potential role of Purkinje potentials in the ablation of VT. Tsuchiya et al. [17] reported successful ablation targeting the late diastolic potential (same potential as P1). However, their successful ablation sites differed from each other. The ablation sites described by Tsuchiya et al. were at the basal septal regions closer to the main trunk of the left bundle branch, while those described by Nakagawa et al. were at the left ventricular apical–inferior septum. These findings suggest that any P1 during VT can be targeted for catheter ablation. It is our preference to target the apical third of the septum in order to avoid producing a left bundle branch block (LBBB) or atrioventricular block (Fig. 18.6). In our study, radiofrequency (RF) energy ablation was successfully performed at the site where P1 was recorded during VT in the 15 patients in whom P1 was detected. During ablation, the P1–P2 interval gradually prolonged and VT terminated when block was observed between P1 and P2 [13] (Fig. 18.7). After termination of the VT, P1 was observed to follow the QRS complex during sinus rhythm, while the P2 was unchanged, occurring prior to the QRS complex (Fig. 18.8). After successful ablation, the P1

Figure 18.6 Recordings from the site of successful ablation during left posterior fascicular ventricular tachycardia. A diastolic potential (P1) and presystolic Purkinje potential (P2) were recorded in the mid-septal area. The proximal two electrodes of the ablation catheter recorded the diastolic

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occurred after the QRS complex, with an identical activation sequence to that observed during the VT, and exhibited decremental conduction during atrial pacing and/or ventricular pacing. Intravenous verapamil significantly prolonged the H–P1 interval during sinus rhythm (Fig. 18.9). Pace-mapping at the successful ablation site often results in poor matches, because the selective pacing of P1 is difficult and there is an antidromic activation of the proximal P1 potentials. Pace-mapping after successful ablation may be better, because the antidromic activation of P1 is blocked [18]. In the five patients in whom the diastolic potential (P1) could not be detected during VT, a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients. It may be speculated that in these patients, the circuit may be smaller, involving less of the Purkinje system, or that the area of slow conduction was not close to the endocardial surface.

Left anterior fascicular VT The uncommon type of verapamil-sensitive fascicular VT is a left anterior fascicular VT. The QRS morphology exhibits an RBBB configuration and right axis deviation [6,19] (Fig. 18.2). In six patients with this form of VT, the mean cycle length of the VT was 390 ± 62 ms and the mean

potential (P1) 15 ms earlier than the distal pair of electrodes. HRA, high right atrum; HBE, His-bundle electrogram; LV, left ventricle. (Reproduced with permission from [13].)

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Figure 18.7 An application of radiofrequency (RF) current during left posterior fascicular ventricular tachycardia (VT). During the energy application, the P1–P2 interval gradually became longer, and the VT was terminated by

block between P1 and P2. After the ablation, the P1 occurred after the QRS complex during sinus rhythm. ABL, ablation catheter. HBE, His-bundle electrogram. (Reproduced with permission from [13].)

Figure 18.8 Intracardiac recordings during sinus rhythm before and after the successful ablation of left posterior fascicular ventricular tachycardia (VT). A. Before the ablation, no diastolic potential was observed during sinus rhythm. B. After the ablation, the P1 occurred after the QRS complex. The

activation sequence of P1 was identical to that observed during the VT shown in Fig. 18.15. H, His-bundle potential, HBE, His-bundle electrogram; RVA, right ventricular outflow apex; LV, left ventricle. (Reproduced with permission from [13].)

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Figure 18.9 Verapamil sensitivity of P1, which occurred after the QRS complex. A. The H–P1 interval during sinus rhythm was 370 ms. B. The H–P1 interval became significantly longer after intravenous administration of 10 mg of verapamil. SCL, sinus cycle length. ABL, ablation catheter; H,

His-bundle potential; HRA, high right atrium; HBE, His-bundle electrogram; RVA, right ventricular outflow apex; LV, left ventricular; SCL, sinus cycle length. (Reproduced with permission from [18].)

QRS axis was 120° ± 16°. Endocardial mapping during left anterior fascicular VT identified the earliest activation in the anterolateral wall of the left ventricle. RF current delivered to this site suppressed the VT in three patients (patients nos. 1–3). A fused Purkinje potential was recorded that preceded the QRS by 20 –35 ms, and pace-mapping exhibited an optimal match with the clinical VT in each. These patients were considered to have the distal form of anterior fascicular reentry. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, a diastolic Purkinje potential was recorded during VT at the mid-anterior left ventricular septum. The potential preceded the QRS during the VT by 56 – 66 ms; catheter ablation at these sites was successful (patients nos. 4 – 6). These patients were considered to have the proximal form of anterior fascicular reentry. Figure 18.10A shows intracardiac recordings at the VT exit site in patient no. 4 at the anterolateral wall. The Purkinje potential preceded the QRS (P–QRS) by 25 ms during the VT, and pace-mapping at that site produced a similar QRS complex, with an interval between the pacing stimulus and QRS (S–QRS) of 25 ms, equal to the P–QRS interval during the VT. While RF current at this site terminated the VT, it could still be reinduced. Figure 18.10D shows the intracardiac recordings during VT from a catheter posi-

tioned in the mid-septal area, where the diastolic Purkinje potential was recorded. At this site, pace-mapping produced a similar QRS complex, with a longer S– QRS interval of 66 ms, equal to the P–QRS interval during the VT. Ablation at this site terminated VT and prevented further reinduction. Patients with the two forms of anterior fascicular VT demonstrated significant differences in the 12-lead ECGs. While the distal type of left anterior fascicular VT showed a QS or rS morphology in leads I, V5, and V6, the proximal type of VT exhibited an RS or Rs morphology in those leads. Idiopathic VT with an RBBB right axis QRS configuration arising through a different mechanism has also been reported. Yeh et al. [20] reported four patients with this QRS morphology, which was adenosine-sensitive and could be successfully ablated from the anterobasal left ventricle. The chest leads showed an atypical RBBB configuration, with a broad monophasic R wave configuration in all of the leads. Crijns et al. [21] reported a rare case of interfascicular reentrant VT with an RBBB configuration and right axis deviation. In this patient, the VT circuit used the anterior fascicle as the anterograde limb and the posterior fascicle as the retrograde limb. In this form of VT, a His bundle potential can usually be recorded during diastole, as well as posterior fascicular potentials during tachycardia. However, it may be difficult to distinguish this tachycardia from verapamilsensitive anterior intrafascicular VT [19].

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Figure 18.10 Intracardiac electrograms during left anterior fascicular ventricular tachycardia (VT). A. During the VT, the Purkinje potential preceded the QRS (P–QRS) by 25 ms at the VT exit site. B. During the basal rhythm (atrial fibrillation), a Purkinje potential was recorded after the His bundle potential and before the QRS complex. C. Pace-mapping at that site produced a similar QRS complex, with an interval between the pacing stimulus and QRS (S–QRS) of 25 ms, equal to the P–QRS interval during the VT. The radiofrequency (RF) current delivered at that site terminated the VT, but VT was still induced. D. During the VT, the Purkinje potential

Left upper septal fascicular VT The last type of verapamil-sensitive fascicular VT is an upper septal fascicular VT. This rare form of VT shows a relatively narrow QRS configuration, with a normal or right axis deviation (Fig. 18.3) [3,7]. In this form of VT, the retrograde His bundle activation precedes the QRS complex (Fig. 18.11). If retrograde ventriculoatrial conduction is also present, it may mimic atrioventricular nodal reentry or atrioventricular reciprocating tachycardia. To avoid

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preceded the QRS (P–QRS) by 66 ms at the zone of slow conduction. E. During atrial fibrillation, a Purkinje potential was recorded after the His bundle potential and before the QRS complex, and a late potential (LP) was also recorded after the QRS complex. F. Pace-mapping at that site produced a similar QRS complex with an interval between the pacing stimulus and QRS (S–QRS) of 66 ms, equal to the P–QRS interval during the VT. The RF current delivered at that site terminated the VT and suppressed reinduction of the VT. (Reproduced with permission from [19].)

a misdiagnosis, recognition of the sequence of the His bundle activation and measurement of the H–V interval during tachycardia are important. In upper septal fascicular VT, a potential is recorded from the upper left ventricular septum that precedes the His bundle potential, at a site where the left bundle potential is recorded during sinus rhythm. Figure 18.11 shows the intracardiac electrograms at the successful ablation site of the upper septal fascicular VT. At a left upper septal site, a left bundle branch potential was recorded during sinus rhythm, and 305

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Figure 18.11 Intracardiac electrograms at the successful ablation site of a left upper septal fascicular ventricular tachycardia (VT). During the VT, there was retrograde activation of the His bundle. The activation sequence of the His bundle potentials was the reverse of that during sinus rhythm. The H–V interval is short during the VT. The VT was successfully ablated at the left

ventricular upper septum. At that site, a left bundle branch (LF) potential was recorded during sinus rhythm and the potential preceded the QRS by 35 ms during the VT. Radiofrequency application eliminated the VT without creating a left bundle branch block or atrioventricular block. (Reproduced with permission from [3].)

during VT preceded the QRS by 35 ms. Ablation at this site eliminated the VT without LBBB or atrioventricular block. A potentially similar VT was reported by Shimoike et al. [7]. The latter case differed in that the QRS morphology had a left bundle normal QRS axis during VT. However, the QRS was narrow and the successful ablation site was similar to ours.

Purkinje potentials were recorded from an octapolar electrode catheter placed at the left ventricular septum. Diastolic Purkinje potentials were recorded earlier from the proximal than the distal electrodes, and fused presystolic Purkinje potentials were recorded earlier from the distal than the proximal electrodes. During sinus rhythm, recording at the same site demonstrated fused Purkinje potentials before the onset of the QRS. After RF energy applications, VPCs nos. 1 and 2 were eliminated, and polymorphic VT became noninducible. During a 4-year follow-up period in which the patient received no drug therapy, no episodes of syncope or VF recurrence occurred. In this patient, VF appears to have been triggered from Purkinje tissue. However, suppression of VF was achieved by catheter ablation of the Purkinje network, not the earliest Purkinje potential. Further studies are needed to evaluate the mechanisms of this type of arrhythmia.

Focal Purkinje VT While focal tachycardia from the distal Purkinje system is usually observed in patients with ischemic heart disease [22], it is also observed in patients with structurally normal hearts [23]. Recently, monomorphic ventricular premature contractions (VPCs) have been shown to initiate ventricular fibrillation (VF) in patients with no structural heart disease [24,25] and ischemic cardiomyopathy [26]. Figure 18.12 shows the initiation of polymorphic VT in a patient with idiopathic VF [25]. The first VPC (VPC no. 1) had a right bundle branch block configuration with right axis deviation, and the second one (VPC no. 2) was a right bundle branch block pattern with a north-west axis. During the polymorphic VT, diastolic and presystolic 306

Mitral annular VT We recently reported on 19 patients with idiopathic VT or VPC originating from the mitral annulus [27]. Among

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Figure 18.12 Catheter mapping during polymorphic ventricular tachycardia (PVT). During the PVT, the diastolic Purkinje potential (Pd) and presystolic Purkinje potential (Pp) were recorded from the left ventricular septum. During sinus rhythm, fused Purkinje potentials (P) were recorded

these, the origin was from the anteroseptal portion of the mitral annulus in 11 patients (58%), from the posterior portion in two (11%), and there was a posteroseptal origin in the remaining six (31%). RF catheter ablation from the endocardium was effective in eliminating the VT. Figure 18.13 shows the intracardiac recordings from the successful ablation site in a patient with verapamil-sensitive mitral annular VT. The ablation catheter was positioned at the anterolateral mitral annulus. During sinus rhythm, the atrial and ventricular potentials were recorded, and a delayed potential was also observed after the QSR complex. During the VT, a diastolic potential preceded the QRS by 70 ms. Pace-mapping at that site produced a similar QRS complex during the VT. RF current delivered at this site terminated the VT and suppressed the reinduction of the VT. As suggested in previous reports concerning left atrial tachycardia from the mitral annulus [28,29], a remnant of the atrioventricular conduction system close to the aortic–mitral continuity, such as a “dead-end” tract [30], may be important in the genesis of the mechanism for tachycardia. Remnants of the atrioventricular ring, as specialized tissue in the posterior or posteroseptal mitral annulus, might also be related to the genesis of posterior and posteroseptal mitral annular VT [31]. In a different series of six mitral annular VTs, we observed a reentrant mechanism and verapamil sensitivity in three patients (50%) [32].

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before the onset of the QRS. HBE, His bundle electrogram; HRA, high right atrium; LV, left ventricle; P, Purkinje potential during sinus rhythm; Pd, diastolic Purkinje potential; Pp, presystolic Purkinje potential; SAP, atrial pacing stimulus. (Reproduced with permission from [25].)

Left ventricular outflow tract VT Classification The mechanism of left ventricular outflow tract VT is most probably adenosine-sensitive triggering activity. The VT cannot be entrained and demonstrates sensitivity to adenosine, verapamil, Valsalva maneuver, carotid sinus pressure, edrophonium, and beta-blockadeafindings consistent with a triggered mechanism [1,33,34]. In patients with adenosine-sensitive VT, only 10% have a left ventricular site of origin [1]. Callans et al. [35] estimated the origin of repetitive monomorphic VT in 33 consecutive patients and found that VT originated at the endocardial left ventricular outflow tract in four patients. Yeh et al. [20] also reported on four patients with adenosine-sensitive left ventricular outflow tract VT, which was successfully ablated from the anterior aspect of the left ventricle just below the mitral annulus. Since then, variants of this form of VT, originating from the left ventricular outflow tract, have been identified increasingly often. Shimoike et al. [36] and Sadanaga et al. [37] reported on patients with repetitive monomorphic VT who underwent successful RF ablation from the left coronary cusp. However, in some patients, catheter ablation with the conventional endocardial or coronary cusp approach is unsuccessful. This has raised the possibility of an epicardial origin of this type of 307

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Figure 18.13 Intracardiac recordings from the successful ablation site in a patient with verapamil-sensitive mitral annular ventricular tachycardia (VT). The ablation catheter was positioned at the anterolateral mitral annulus. A. During sinus rhythm, the atrial and ventricular potentials were recorded, and a delayed potential (DP) was also observed after the QSR complex. B. During the VT, a diastolic potential preceded the QRS by 70 ms. C. Pacemapping at that site produced a similar QRS complex during the VT. ABL, ablation site; CS, coronary sinus; LAO, left anterior oblique; RAO, right anterior oblique.

VT, remote from the aortic sinus [38]. Da Paola et al. [39] reported mapping and ablation through the coronary venous system, and Tomassoni et al. [40] reported successful mapping and ablation of this type of VT by direct epicardial instrumentation. Recently, Tanner et al. [41] described six different anatomic approaches for successful ablation of outflow tract VT with R/S transition in lead

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V3. Of 33 patients with such VT, RF ablation was successfully performed from right ventricular outflow tract in 20 (61%), left ventricular outflow tract in 5 (15%), aortic sinus of Valsalva in 2 (6%), coronary sinus in 3 (9%), the main trunk of the pulmonary artery in 1 (3%), and the epicardium via pericardial puncture in 2 (6%). We have classified left ventricular outflow tract VT into five

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subgroups relative to the catheter ablation approach used (Table 18.2) [3]: • Endocardial approach. • Aortic sinus approach. • Coronary venous approach. • Pulmonary artery approach. • Direct epicardial approach.

Endocardial approach A left ventricular outflow tract origin is suggested by an RBBB morphology in lead V1 or an atypical LBBB morphology associated with an early precordial transition in lead V2. In comparison with right outflow tract VT, the distinctive QRS characteristics of left outflow tract VT with endocardial origin were an S wave in I and tall R waves in leads V1 and V2. Small S waves were also observed in leads V5 and V6 [42]. Left ventricular outflow tract VT most often originates from the superior basal region of the left interventricular septum, inferior to the aortic valve in the posterior region of the left ventricular outflow tract (region of the aortomitral continuity). Another type of left ventricular outflow tract VT has an origin in the superior basal septum [35]. In this type of VT, care should be exercised to exclude a His bundle potential at the site of ablation. Failures of catheter ablation are caused either by an inability to induce the arrhythmia in the laboratory, preventing adequate mapping, or by a location of the focus deep in the septum, beyond the reach of endocardial RF ablation lesions.

Aortic sinus approach Previous studies have shown that epicardial left ventricular outflow tract VT can be successfully ablated from the coronary cusp, although the aortic valve and coronary artery represent potential risks [36 –38,42–49]. This type of VT is sometimes considered to have a coronary cusp “origin.” However, we have postulated that RF energy application from the coronary cusp would not ablate the valve itself, but the epicardium above the septum [42]. Figure 18.14 shows a 12-lead ECG of left coronary cusp “origin” VT and the position of the catheters during successful RF ablation with left coronary angiography. The QRS morphology during VT showed tall R waves in the inferior leads, rS in lead I, and no S wave in leads V5 and V6. R/S transition was between V2 and V3. The ventricular electrogram at the pulmonary artery was 25 ms before the QRS, and pace-mapping at this site produced a similar QRS during VT. However, coronary angiography revealed that this site in the pulmonary artery was adjacent to the left coronary artery. The ventricular electrogram at the left coronary cusp preceded the QRS by 30 ms. RF current

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delivered at this site immediately abolished VT. It is sometimes difficult to differentiate between coronary cusp “origin” VT and right ventricular outflow tract VT, as they are so close each other. Ouyang et al. [44] reported that the R/QRS wave width ratio and R/S wave amplitude ratio in V1 and V2 were significantly lower in right ventricular outflow tract VT than in right or left coronary cusp “origin” VT. Coronary angiography should be carried out before ablation to ensure that there is more than 10 mm between the ablation catheter and the ostium of the left main coronary artery, and the left main coronary artery should be cannulated as a marker and for prevention during RF energy delivery. Right coronary angiography should also be carried out before RF energy application. Hiratsuji et al. [45] reported a patient who had transient ST elevation in the inferior leads during RF energy application from the left sinus of Valsalva. In their case, selective right coronary angiography revealed an anomalous origin of the right coronary artery from the left sinus of Valsalva. While this kind of anomaly affects about 1% of the general population, selective angiography of both coronary arteries should be carried out to avoid potential risks. On the basis of their animal studies, Hachiya et al. [46] recommended that the tip temperature of the ablation catheter should be kept at 55 °C during energy delivery in order to prevent aortic valvular damage.

Epicardial origin In some patients, catheter ablation with the conventional endocardial or coronary cusp approach is unsuccessful. In these cases, the earliest ventricular activation is recorded from the electrodes at the transitional area from the great cardiac vein to the anterior interventricular vein [38,47]. Da Paola et al. [39] reported mapping and successful ablation through the coronary venous system. However, this approach is limited by the anatomy of the coronary venous tree and the ability to cannulate these branches consistently for mapping and ablation purposes. Mapping and ablation of this type of VT has been successfully and safely carried out by percutaneous epicardial instrumentation [40,43,48]. Kanagaratnam et al. [43] performed simultaneous epicardial mapping in patients with left coronary cusp “origin” VT. Interestingly, they found an earlier activation on the epicardial surface. This finding suggests that left coronary cusp “origin” VT also has an epicardial origin.

Electrocardiographic algorithms to predict the site of origin Electrocardiographic characteristics have been described for differentiating the origin of outflow tract VT

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Figure 18.14 Twelve-lead electrocardiogram of the left coronary cusp “origin” and the position of catheters during successful radiofrequency (RF) ablation with left coronary angiography. The QRS morphology during VT showed tall R waves in the inferior leads, rS in lead I, and no S wave in leads V5 and V6. The R/S transition was between V2 and V3. The ventricular electrogram at the pulmonary artery (PA) preceded the QRS by 25 ms, and

pace-mapping at this site produced a similar QRS during VT. However, coronary angiography revealed that this site in the pulmonary artery was adjacent to the left coronary artery. The ventricular electrogram at the left coronary cusp (LCC) preceded the QRS by 30 ms. RF current delivered at this site immediately abolished VT. LAO, left anterior oblique; RAO, right anterior oblique. (Reproduced with permission from [3].)

[35,42,44,49]. Callans et al. [35] reported that VT with a precordial R wave transition at or before lead V2 is consistent with a left ventricular origin. However, this could not identify an origin remote from the right ventricular outflow tract and left ventricular outflow tract. Hachiya et al. [42] emphasized the S wave in leads V5 and V6. They reported that in 88% of VTs with a coronary cusp origin, no S wave was observed in either V5 or V6. In contrast, an Rs pattern was observed in both V5 and V6 in 100% of patients with endocardial left ventricular outflow VT. Ouyang et al. [44] reported that the QRS morphology of idiopathic VT from the aortic sinus of Valsalva is similar to that of right ventricular outflow tract VT and that a longer R wave duration and a higher R/S wave amplitude in leads V1 and V2 was present in VT originating in the aortic sinus of Valsalva. We have developed a precise electrocardiographic algorithm for classifying idiopathic outflow tract VT relative to the site of origin, allowing localization of the VT origin in six different outflow tract sites using seven steps of analysis [49]. The six divisions are based on the results of catheter ablation (Fig. 18.15):

• Septum of the right ventricular outflow tract. • Free wall of the right ventricular outflow tract. • Near the His bundle region in the right ventricular outflow tract. • Endocardium of the left ventricular outflow tract. • Left sinus of Valsalva. • Left ventricular epicardium remote from the left sinus of Valsalva. The overall sensitivity of this algorithm (Fig. 18.16) was 88%, with a specificity of 95%. The positive and negative predictive values were 88% and 96%, respectively.

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Conclusions Previous studies have shown that “idiopathic” left VT actually consists of multiple discrete subtypes that are best differentiated by their mechanism, VT morphology, site of origin, and the successful ablation site. Recognition of the heterogeneity of this type of VT and its unique characteristics should facilitate appropriate diagnosis and therapy.

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Figure 18.15 Twelve-lead electrocardiograms of premature ventricular contractions originating from the outflow tract. The six different outflow tract sites were: A. The septum of the right ventricular outflow tract. B. The free wall of the right ventricular outflow tract. C. Near the His bundle region

Idiopathic left ventricular tachycardias

in the right ventricular outflow tract. D. The endocardium of the left ventricular outflow tract. E. The left sinus of Valsalva. F. The left ventricular epicardium remote from the left sinus of Valsalva. (Reproduced with permission from [49].)

References

Figure 18.16 Stepwise electrocardiographic algorithm for determining the location of the origin of outflow tract ventricular tachycardia VT. LSV, left sinus of Valsalva; LV end, left ventricular endocardium; LV epi, left ventricular epicardium remote from the left sinus of Valsalva; near His, near the His bundle region; RV, right ventricular. (Reproduced with permission from [49].)

1 Lerman BB, Stein KM, Markowitz SM. Mechanism of idiopathic ventricular tachycardia. J Cardiovasc Electrophysiol 1997; 8:571– 83. 2 Okumura K, Tsuchiya T. Idiopathic left ventricular tachycardia: clinical features, mechanism and management. Card Electrophysiol Rev 2002;6:61–7. 3 Nogami A. Idiopathic left ventricular tachycardia: assessment and treatment. Card Electrophysiol Rev 2002;6:448 –57. 4 Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol 1979;44:1– 8. 5 Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 1981;46:679 – 82. 6 Ohe T, Shimomura K, Aihara N, et al. Idiopathic sustained left ventricular tachycardia: clinical and electrophysiological characteristics. Circulation 1988;77:560 – 8. 7 Shimoike E, Ueda N, Maruyama T, Kaji Y. Radiofrequency catheter ablation of upper septal idiopathic left ventricular tachycardia exhibiting left bundle branch block morphology. J Cardiovasc Electrophysiol 2000;11:203 –7.

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8 Gallagher JJ, Selle JG, Svenson RH, et al. Surgical treatment of arrhythmias. Am J Cardiol 1988;61:27A– 44A. 9 Suwa M, Yoneda Y, Nagao H, et al. Surgical correction of idiopathic paroxysmal ventricular tachycardia possibly related to left ventricular false tendon. Am J Cardiol 1989;64:1217–20. 10 Thakur RK, Klein GJ, Sivaram CA, et al. Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93: 497–501. 11 Maruyama M, Terada T, Miyamoto S, Ino T. Demonstration of the reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia: direct evidence for macroreentry as the underlying mechanism. J Cardiovasc Electrophysiol 2001; 12:968 –72. 12 Lin FC, Wen MS, Wang CC, Yeh SJ, Wu D. Left ventricular fibromuscular band is not a specific substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:525 –7. 13 Nogami A, Naito S, Tada H, et al. Demonstration of diastolic and presystolic Purkinje potential as critical potentials on a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol 2000;36:811–23. 14 Kuo JY, Tai CT, Chiang CE, et al. Is the fascicle of left bundle branch involved in the reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia? Pacing Clin Electrophysiol 2003;26:1986–92. 15 Ouyang F, Cappato R, Ernst S, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional block and macroreentry within the Purkinje network. Circulation 2002;105:462–9. 16 Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993;88: 2607–17. 17 Tsuchiya T, Okumura K, Honda T, Iwasa A, Ashikaga K. Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia. Circulation 1999;99:2408–13. 18 Tada H, Nogami A, Naito S, et al. Retrograde Purkinje potential activation during sinus rhythm following catheter ablation of idiopathic left ventricular tachycardia. J Cardiovasc Electrophysiol 1998;9:1218–24. 19 Nogami A, Naito S, Tada H, et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients. J Cardiovasc Electrophysiol 1998;9:1269–78. 20 Yeh SJ, Wen MS, Wang CC, Lin FC, Wu D. Adenosine-sensitive ventricular tachycardia from the anterobasal left ventricle. J Am Coll Cardiol 1997;30:339–45. 21 Crijns HJ, Smeets JL, Rodriguez LM, Meijer A. Cure of interfascicular reentrant ventricular tachycardia by ablation to anterior fascicle of the left bundle branch. J Cardiovasc Electrophysiol 1995;6:486–92. 22 Lopera G, Stevenson WG, Soejima K, et al. Identification and ablation of three types of ventricular tachycardia involving the His–Purkinje system in patients with heart disease. J Cardiovasc Electrophysiol 2004;15:52–8. 23 Gonzalez RP, Scheinman MM, Lesh MD, Helmy I, Torres V, Van Hare GF. Clinical and electrophysiologic spectrum of fascicular tachycardias. Am Heart J 1994;128:147– 56.

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24 Haïssaguerre M, Shoda M, Jaïs P, et al. Mapping and ablation of idiopathic ventricular fibrillation. Circulation 2002;106:962–7. 25 Nogami A, Sugiyasu A, Kubota S, Kato K. Mapping and ablation of idiopathic ventricular fibrillation from the Purkinje system. Heart Rhythm 2005;2:646 –9. 26 Bansch D, Oyang F, Antz M, et al. Successful catheter ablation of electrical storm after myocardial infarction. Circulation 2003;108:3011–16. 27 Tada H, Ito S, Naito S, et al. Idiopathic ventricular arrhythmia arising from the mitral annulus: a distinct subgroup of idiopathic ventricular arrhythmias. J Am Coll Cardiol 2005;45:877– 86. 28 Kistler PM, Sanders P, Hussin A, et al. Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol 2003;41: 2212 –9. 29 Nogami A, Suguta M, Tomita T, et al. Novel form of atrial tachycardia originating at the atrioventricular annulus. Pacing Clin Electrophysiol 1998;21:2691– 4. 30 Kurosawa H, Becker AE. Dead-end tract of the conduction axis. Int J Cardiol 1985;7:13–20. 31 Anderson RH, Davis MJ, Becker AE. Atrioventricular specialized tissue in the normal heart. Eur J Cardiol 1974;2:219 –30. 32 Arima H, Nogami A, Kowase S, et al. Mitral annular tachycardia with verapamil-sensitivity: a new entity of verapamilsensitive ventricular tachycardia [abstract]. Heart Rhythm 2005;2:S253. 33 Kobayashi Y, Kikushima S, Tanno K, Baba T, Katagiri T. Sustained left ventricular tachycardia terminated by dipyridamole: camp-mediated triggered activity as a possible mechanism. Pacing Clin Electrophysiol 1944;17:377– 85. 34 Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine: evidence for myocardial receptor-mediated effects. Circulation 1993;87:382 – 90. 35 Callans DJ, Menz V, Schwartzman D, Gottlieb CD, Marchlinski FE. Repetitive monomorphic ventricular tachycardia from the left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin. J Am Coll Cardiol 1997;29:1023 –7. 36 Shimoike E, Ohnishi Y, Ueda N, Maruyama T, Kaji Y. Radiofrequency catheter ablation of the left ventricular outflow tract tachycardia from a coronary cusp: a new approach to the tachycardia focus. J Cardiovasc Electrophysiol 1999;10:1005 –9. 37 Sadanaga T, Saeki K, Yoshimoto T, Funatsu Y, Miyazaki T. Repetitive monomorphic ventricular tachycardia of the left coronary cusp origin. Pacing Clin Electrophysiol 1999;22: 1553 – 6. 38 Tada H, Nogami A, Naito S, et al. Left ventricular epicardial outflow tract tachycardia: new distinct subgroup of outflow tract tachycardia. Jpn Circ J 2001;65:723 –30. 39 Da Paola AV, Melo WDS, Tavora MZP, Martinez EE. Angiographic and electrophysiological substrates for ventricular tachycardia mapping through the coronary veins. Heart 1998; 79:59 – 63. 40 Tomassoni G, Stanton M, Richey M, Leonelli FM, Beheiry S, Natale A. Epicardial mapping and radiofrequency catheter ablation of ischemic ventricular tachycardia using a three-

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41

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dimensional nonfluoroscopic mapping system. J Cardiovasc Electrophysiol 1999;10:1643–8. Tanner H, Hindricks G, Schirdewahn P, et al. Outflow tract tachycardia with R/S transition in lead V3: six different anatomic approaches for successful ablation. J Am Coll Cardiol 2005;45:418–23. Hachiya H, Aonuma K, Yamauchi Y, et al. Electrocardiographic characteristics of left ventricular outflow tachycardia. Pacing Clin Electrophysiol 2000;23:1930–4. Kanagaratnam L, Tomassoni G, Schweikert R, et al. Ventricular tachycardia arising from the aortic sinus of Valsalva: an under-recognized variant of left outflow ventricular tachycardia. J Am Coll Cardiol 2001;37:1408–14. Ouyang F, Fotuhi P, Yen S, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002;39:500–8.

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45 Hiratsuji T, Tada H, Naito S, Oshima S, Taniguchi K. Transient ST elevation during radiofrequency energy application from the left sinus of Valsalva. J Cardiol 2003;41:297– 300. 46 Hachiya H, Aonuma K, Yamauchi Y, Igawa M, Nogami A, Iesaka Y. How to diagnose, locate, and ablate coronary cusp ventricular tachycardia. J Cardiovasc Electrophysiol 2002;13:551–6. 47 Ito S, Tada H, Naito S, et al. Simultaneous mapping in the left sinus of Valsalva and coronary venous system predicts successful catheter ablation from the left sinus of Valsalva. Pacing Clin Electrophysiol 2005;28:S150 –S154. 48 Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003;108:1329 –35. 49 Ito S, Tada H, Naito S, et al. Development and validation of an ECG algorithm for identifying the optimal ablation site for idiopathic ventricular outflow tract tachycardia. J Cardiovasc Electrophysiol 2003;14:1280 – 6.

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19

Catheter ablation of stable ventricular tachycardia after myocardial infarction William G. Stevenson

The mapping and ablation approach to ventricular tachycardia (VT) is determined by the underlying heart disease and the nature of the VT. Most VTs that are associated with structural heart disease are due to reentry involving regions of infarction or ventricular scar. Approximately 8% are due to reentry or automaticity involving the Purkinje system [1]. A smaller number have a focal origin in regions of abnormal myocardium.

Infarct-related VT circuits Patients with scar-related VTs often have multiple potential reentry circuits, giving rise to more than one morphology of inducible monomorphic VT. In most patients, three or four different VTs are inducible [2–4]. VTs that are hemodynamically well tolerated and inducible are commonly referred to as stable or “mappable.” The majority of patients have one or more VTs that are unstable and not amenable to extensive mapping, due to poor hemodynamic tolerance, frequent changes to other VT morphologies during attempted mapping, or inconsistent inducibility. Substrate mapping approaches that identify target regions for ablation during stable sinus rhythm often allow ablation of these tachycardias (see Chapter 20). Stable VTs in patients with scars are most commonly due to relatively large, stable reentry circuits, which can have a variety of configurations [5–8]. An isthmus (channel) of surviving myocardium within the region of the infarct or scar is often critical to the maintenance of reentry (Fig. 19.1). Depolarization of this isthmus is not detected in the surface electrocardiogram (ECG). The QRS complex is inscribed when the reentry wavefront leaves the isthmus at its exit and propagates across the ventricle. Thus, the QRS morphology indicates the location of the reentry circuit exit. When VT is stable for mapping, a systematic approach seeking to identify critical portions of the reentry circuit can be used (Fig. 19.2). This approach is particularly useful 314

for patients with incessant VT and recurrent episodes of well-defined slow VT.

Pre-ablation assessment Before the procedure, the underlying heart disease should be adequately defined, including the severity of coronary artery disease and valvular heart disease. These considerations are important for assessing the risks of the procedure and for guiding management in the event of unexpected hemodynamic deterioration. An echocardiogram is useful to assess areas of wall motion abnormality that suggest the infarct location and to assess the presence of mobile left ventricular thrombus, which is a contraindication to endocardial left ventricular mapping due to the potential risk of embolization. Access to the left ventricle is occasionally limited by peripheral vascular disease. A transeptal approach to the left atrium and through the mitral valve to the left ventricle is required in some patients.

Initial electrophysiologic assessment Unless complete atrioventricular (AV) block is present, a catheter is placed at the His bundle to assist in confirming the diagnosis and to facilitate detection of bundle branch reentry VT. If VT is not incessant, programmed stimulation is used to induce tachycardia before mapping, for several reasons. The diagnosis of VT is confirmed. Demonstration that VT is inducible makes interpretation of the results of programmed stimulation after ablation more easily interpretable. Occasionally, VT is no longer inducible after initial mapping, before any ablation is performed, possibly due to mechanical trauma, systemic absorption of local anesthetic, or sedation. The QRS morphology of the VT is recorded, which is particularly useful when a 12-lead ECG is not available, as is common for patients with implantable cardioverter-defibrillators (ICDs), which

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Catheter ablation of stable ventricular tachycardia after myocardial infarction

Figure 19.1 Theoretical reentry circuits. In each panel, gray regions are areas of conduction block from dense scar or the mitral annulus (at the top). A. Components of the reentry circuit are labeled. The reentry circuit has an isthmus with an exit, central, and proximal portions. The excitation wavefront emerges from the exit to propagate across the ventricles producing the QRS complex. From the exit, the excitation wavefront propagates through two loops to return to the isthmus. The loop along the border of the infarct scar is an outer loop. The loop through the infarct region is an inner loop. Bystander regions that are not involved in this reentry circuit, but from which abnormal and diastolic electrograms may be recorded, are also indicated. B, C. Ablation (black circle) in an outer or inner loop failed to terminate ventricular tachycardia here. D. An ablation lesion in the common isthmus prevents reentry through this circuit.

Figure 19.2 The approach to mapping and ablation for stable ventricular tachycardia. CS, coronary sinus; LBBB, left bundle branch block; PPI, post-pacing interval; RF, radiofrequency; RV, right ventricle; VT, ventricular tachycardia.

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Figure 19.3 Initial mapping data from a patient with an old anterior wall infarct. The ventricular tachycardia (VT) has a left bundle branch block configuration in lead V1, raising the possibility of bundle branch reentry or a right ventricular origin. A His deflection is not evident in relation to VT, and entrainment occurs with a post-pacing interval of 490 ms, which is 100 ms longer than the VT cycle length, thus excluding bundle branch reentry and making a left ventricular origin of the VT more likely. Fusion is present during entrainment, but is relatively subtle. RVA, right ventricular apex.

usually terminate VT before an ECG can be obtained. Initial induction of VT is usually followed by entrainment from the right ventricle (RV) and, in most cases, pacing to terminate VT (Fig. 19.3). A post-pacing interval (PPI) approximating the VT cycle length (within 30 ms) from the RV apex suggests that the right ventricle is involved in the VT, with either RV scar, septal scar, or bundle branch reentry [9].

QRS morphology The QRS morphology of the induced VT suggests the location of the VT exit (Fig. 19.4). As the exit or pacing site during pace-mapping moves closer to the positive ter-

minal of the ECG recording bipole (e.g., the left arm for lead I and aVL), that lead becomes more negative in polarity (losing R waves and gaining S waves). VT that has a dominant S wave in V1 is referred to as having a left bundle branch block-like configuration (VT-1 in Figs. 19.5 and 19.6). Bundle branch reentry, RV origin, or left ventricle (LV) septal origin of the VT should be considered. VTs that have a dominant R wave in V1 originate from the left ventricle (VT-2 in Fig. 19.5), although rare exceptions occur for some RV tachycardias when the RV is severely dilated. A frontal plane axis directed inferiorly, with dominant R waves in II, III, and aVF, suggests an exit in the cranial aspect of the ventricle. A superiorly directed frontal plane axis suggests origin on the diaphragmatic aspect of the ventricle (VT-1 in Fig. 19.5). The mid-precordial leads,

Figure 19.4 The relation of the reentry circuit exit (or pace-mapping site) to the QRS morphology. LBBB, left bundle branch block; LV, left ventricle; RV, right ventricle.

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Figure 19.5 Mapping data from a patient with an old anterior wall infarction. From the left are 12-lead electrocardiograms (ECGs) of VT-1, VT-2, and a pace-mapping site. VT-1 has a left bundle branch block configuration in V1 and a dominant R wave in V1, suggesting a septal or RV origin. The frontal plane axis is directed superiorly, consistent with an exit on the inferior wall. Dominant S waves are present across the precordium, suggesting that the exit is near the apex. The post-pacing interval at the right ventricular apex was long (cf. Fig. 19.3). This constellation of findings suggests an exit at the left ventricular (LV) inferoapical septum, and pacemapping (not shown) at that region site indicated in Fig. 19.6, matched the VT morphology. VT-2 has a right bundle branch block configuration in V1

and an inferiorly directed frontal plane axis, consistent with an exit on the anterior wall of the left ventricle. The right panel shows pace-mapping at a site on the anterior wall of the left ventricle, shown on the voltage map in Fig. 19.6 (site 11–2 in the Josephson numbering scheme). The pacing cycle length is 600 ms. The paced QRS matches VT-2, suggesting that this is an exit region for the VT. An interval of 90 ms (arrow) is present between the stimulus and QRS onset, consistent with slow conduction away from the pacing site. The inset on the lower right shows an enlargement of ECG lead V5 and the bipolar electrogram recorded at this site during sinus rhythm. A low-amplitude late potential extends beyond the end of the QRS complex (arrow).

V3 and V4, provide an indication of the exit location relative to the apex and base (AV groove) of the heart. Dominant S waves in these leads indicate an apical location (VT-1 in Fig. 19.5). Dominant R waves indicate a location close to the base of the heart (VT-2 in Fig. 19.5). A rightward frontal plane axis suggests a left lateral position, which can also be apical. A dominant R wave in lead I often indicates a septal or RV location (VT-1 in Fig. 19.5).

ize the time spent in VT while still targeting an isthmus. If VT is slow and well tolerated, initial mapping is performed in VT.

Catheter mapping If the patient is in sinus rhythm, initial mapping is carried out to assess sinus rhythm electrograms and pace-mapping to identify a likely region containing the reentry circuit exit. The ablation catheter is then left at a site with favorable characteristics, and tachycardia is induced for inspection of electrograms at the site during tachycardia and entrainment mapping. This approach attempts to minim-

Sinus rhythm electrograms and voltage maps Bipolar electrograms recorded from regions of infarction have a peak-to-peak amplitude < 1.5 mV (1 mm interelectrode spacing with a 4-mm distal electrode and filtered at 10–400 Hz) [10–13]. Anatomic maps of electrogram amplitude (voltage maps) can be used to identify regions of infarction that are likely to contain reentry circuits (Fig. 19.5). In patients with VT, these infarct regions are typically large, with a circumference exceeding 20 cm [2]. The QRS morphology of VT, pace-mapping, and additional sinus rhythm electrogram characteristics are therefore of interest in suggesting the region of the scar that is likely to contain the reentry circuit isthmus. 317

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Figure 19.6 Mapping data from the same patient as in Figs. 19.5 and 19.7. A. A voltage map of the left ventricle as viewed from an anteroposterior projection. The colors represent peak-to-peak electrogram amplitudes (purple > 1.5 mV, red < 0.1 mV). A large anteroseptal lowvoltage infarct is present. Sites in which pace-mapping matched VT-1 and VT-2 are indicated (arrows). B. An activation map of VT-2 (QRS shown in Fig. 19.5). The complete reentry circuit was defined in this case, with early (red) meeting latest (purple) activation at the anteroseptal region. A long isthmus is present (yellow arrow) with an exit region at the superior aspect of the

low voltage region, consistent with the site of the pace-map match for VT-2 (Fig. 19.5). Entrainment from a site in the isthmus is shown in Fig. 19.7. After emerging from the exit, the black arrows indicate propagation of the excitation wavefronts around the region, returning to the isthmus at its inferior septal location. Blue tags indicate double potential regions that are likely areas of block in the ventricular tachycardia circuit. In this case, dense unexcitable scar was not present in this region. Dark red tags are initial ablation sites. Ablation at the superior and inferior regions of the infarct abolished both VT-1 and VT-2.

Late potentials during sinus rhythm (Fig. 19.5) and isolated potentials during VT (Fig. 19.7) are usually present within these low-amplitude regions and are often produced by conduction through potential conduction channels in the infarct. These types of potential also occur at some

bystander regions, so that they are not sufficiently specific targets for ablation if only a single stable VT is being targeted with a limited number of ablation lesions [14 –17]. More extensive ablation of all potentials may be effective and useful when VT is not stable for mapping [13,16].

Figure 19.7 Entrainment from the central isthmus of VT-2 shown in Fig. 19.6B. During ventricular tachycardia (VT), a large potential is present at the mapping site, followed by a lowamplitude isolated potential, best seen in the enlarged electrogram inset. VT is entrained with concealed fusion. The large potential is evident during pacing, indicating that it is a far-field potential (see Chapter 4). The postpacing interval measured to the low-amplitude isolated potential matches the VT cycle length of 480 ms, indicating that the site is in the circuit. The S–QRS of 180 ms also matches the electrogram-to-QRS interval (not labeled), and is consistent with a central site in the circuit.

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Pace-mapping provides three pieces of information: capture, the paced QRS morphology, and an indication of abnormal or slow conduction. We prefer unipolar pacing between the distal mapping catheter electrode and a remote electrode in the inferior vena cava, rather than bipolar pacing between the distal and proximal electrodes, to avoid capture at the proximal electrode [5]. Whether unipolar pacing is better for mapping than bipolar pacing from closely spaced electrodes has not, however, been established, and most laboratories use bipolar pacing. Capture indicates that the pacing electrode is in contact with electrically active tissue. We mark areas of high pacing threshold > 10 mA at a 2-ms pulse width as unexcitable scar [5]. These are likely areas of dense fibrosis that are often borders of reentry circuits.

Regions in which the QRS morphology resembles that of an induced VT suggests the approximate location of the VT exit [12,18,19]. Comparison of pace-mapping data and the VT QRS morphology sometimes reveals a marked discrepancy between the anticipated VT exit location based on the QRS morphology and the pace-map. Anatomic distortions from ventricular remodeling and regions of conduction block from scar are likely causes. A discrepancy in the QRS morphology between VT and the pace-map does not necessarily indicate that the region is remote from the VT circuit [18,20]. Even when the catheter is at a reentry circuit isthmus, pace-mapping during sinus rhythm may produce a QRS morphology different from that of the VT (Fig. 19.8). During VT, entrainment at that site may occur with concealed fusion, howeverawith a completely different QRS morphology from the morphology present during pace-mapping, because the stimulated antidromic

Figure 19.8 Mapping data from a patient with an old inferior wall infarction. A. Entrainment of ventricular tachycardia (VT). VT has a right bundle branch block configuration and superior axis configuration, consistent with an inferior left ventricular wall exit. Pacing from an inferobasal site at a cycle length of 520 ms entrains VT with concealed fusion. During entrainment, two discrete potentials remain visible in the mapping catheter recordings, indicating that these are far-field potentials. The post-pacing interval (PPI) is measured to the third potential, which is absent during entrainment, and is consistent with pacing from a reentry circuit site with a PPI of 540 ms, which matches the VT cycle length.

The S–QRS is 270 ms, consistent with a proximal site in the circuit. The potential mechanism of these findings is shown below the tracing. B. Pace-mapping from the same site. Pacing produces a QRS morphology that is markedly different from that of the VT, with an S–QRS interval of 65 ms. The mechanism of the discrepant QRS despite pacing at a site that is in the VT circuit is shown in the diagram beneath the tracing. During entrainment (diagram in A), the antidromic wavefronts are contained near the circuit by returning orthodromic wavefronts. In the absence of VT, stimulated wavefronts exit from the infarct region through other paths, producing a different QRS configuration (see text).

Pace-mapping

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wavefronts are confined in or near the circuit by collision with circulating wavefronts and areas of block that are not present in the absence of VT. Long S– QRS intervals exceeding 40 ms during pacemapping indicate the presence of regions of slow conduction that are often associated with reentry circuit isthmuses, but can also occur in bystander regions [18,19,21]. In some patients, the reentry circuit isthmus can be traced using pace-mapping. At the exit region, the paced QRS resembles that of VT with a relatively short S–QRS interval. As the catheter is moved to more proximal sites, the QRS morphology remains the same, but the S–QRS interval increases, consistent with slow conduction between the pacing site and the exit region [19].

Electrograms during VT The reentry circuit isthmus is depolarized before the QRS onset, typically giving rise to diastolic electrical activity at these sites. Isolated potentials preceding the QRS are common and are associated with reentry circuit isthmuses, but can also originate from bystander regions [22–25]. Dissociation of the potential from the VT is clear evidence that the tissue is not critical to the VT circuit, but entrainment may be required to distinguish bystander sites with diastolic potentials from reentry circuit sites. It is also important to recognize that some VT circuits can be successfully ablated at sites in which diastolic or presystolic potentials are not present [26]. Sites that are proximal in the isthmus are depolarized very early relative to the QRS onset, or during the end of the QRS, and are often overlooked (Fig. 19.8A). Entrainment is useful for identifying these regions (see below).

Entrainment mapping Isthmus sites are recognized during entrainment by entrainment with concealed fusion and a post-pacing interval that approximates the VT cycle length (within 30 ms) [8,22]. In addition, the S– QRS indicates the conduction time from the pacing site and the circuit exit: short near the exit, and progressively longer at isthmus sites that are further from the exit. Thus, the electrogram-to-QRS interval at these sites matches the S– QRS during entrainment. From the reentry circuit exit, the circulating reentry wavefront returns to the proximal portion of the isthmus by propagating through one or more loops. Outer loops exist along the border of the scar. Activation at these sites typically occurs during inscription of the QRS complex. The PPI indicates that the site is in the circuit, but QRS fusion is present and the S– QRS is usually short (typically < 40 ms). Inner loops are confined within the infarct or scar region. Activation typically occurs during the QRS or at the end of the QRS complex. The PPI indicates that the 320

site is in the circuit. Entrainment occurs with concealed fusion with a long S–QRS > 70% of the VT cycle length. Focal ablation lesions terminate VT at fewer than 10% of reentry circuit loop sites. The loop may be broad, such that interruption is difficult. Interruption of one loop will not terminate reentry if multiple loops are present. Ablation therefore seeks to identify a reentry circuit isthmus. At isthmus sites, application of radiofrequency usually terminates VT within 20 s. Occasionally, a series of radiofrequency (RF) lesions is required if the isthmus is broad. Occasionally, a stimulus terminates tachycardia without producing an excitation wavefront that propagates beyond the scar, with no QRS complex following the stimulus [27]. This finding can be mimicked by a fortuitous tachycardia termination; it is important to demonstrate reproducibility. Stimuli applied at longer coupling intervals may reset the tachycardia with concealed fusion, suggesting that stimuli can capture the site. Stimulus capture followed by block of all propagating wavefronts within the scar is the likely mechanism of tachycardia termination. The stimulus site is likely to be in or near the tachycardia circuit. The application of RF current often terminates tachycardia at such sites. The phenomenon is more easily recognized with scanning single stimuli than with trains of pacing stimuli, and searching for this phenomenon is time-consuming. Catheter manipulation may terminate and render VT noninducible through mechanical trauma. If the site of catheter trauma is known, ablation should be considered if the VT is not immediately inducible, as recovery is not predictable and may not occur during the procedure.

Ablation lesion placement and assessing the effects of ablation Termination of VT during ablation provides further confirmation that the site is critical to the maintenance of tachycardia, provided that ablation or catheter movement does not produce premature beats that terminate the arrhythmia. With RF ablation at critical isthmus sites, VT usually terminates abruptly within 15 s, but occasionally termination is preceded by gradual slowing. Termination of VT after long durations of RF application and preceded by gradual slowing often indicates that the reentry path extends to the margin of the region of effective heatingaoften intramural or epicardial in location. Recurrent inducible VT is common. When RF application fails to terminate VT at a site that appears to be in the reentry circuit, the site may be a bystander, or the size of the RF lesion may not be sufficient to interrupt conduction. Application of RF current should be targeted to sites likely to be in the circuit, and should generally be confined to regions with abnormal electrograms in order to avoid damaging contractile myocardium [28].

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Figure 19.9 Findings in a patient with an old anterior wall infarct and stable ventricular tachycardia (VT). The voltage map (B) is viewed from the right anterior oblique and diaphragmatic position. The colors represent peak-to-peak electrogram amplitudes (purple > 1.5 mV, red < 0.1 mV). Gray areas are electrically unexcitable scarring, in which the pacing threshold exceeds 10 mA at a pulse width of 2 ms. It should be noted that this defines potential channels for conduction. In the 12-lead electrocardiogram (A), the VT has a right bundle branch block configuration, with a superiorly directed frontal plane axis. Pace-mapping at the inferoapical site in the low-amplitude scar indicated by the arrow reproduces the VT QRS morphology, suggesting that this region contains the exit for that VT. The S–QRS of 80 ms indicates abnormal conduction and suggests that the pacing site may be in the isthmus. Catheter manipulation at this site terminated the VT, and radiofrequency ablation rendered it no longer inducible.

When a reentry circuit isthmus is identified, we apply RF lesions at the site until the pacing threshold at the site exceeds 10 mA at a 2-ms pulse width, in the hope of insuring an adequate lesion [5,29]. We favor ablation with a saline-irrigated or 8-mm electrode catheter, as these create larger lesions than 4 –5-mm electrode catheters and the ablation often targets a broad, deep region [30,31]. Because of the frequent coexistence of multiple tachycardias and multiple potential reentry circuits, we generally enlarge the initial ablation region. For inferior wall infarcts, ablation lesions are commonly extended to the mitral annulus, to interrupt potential circuits using an isthmus of tissue beneath the mitral annulus [7,32]. Lesions are also extended to any adjacent regions of electrically unexcitable scar, which often form the border of reentry paths (Fig. 19.9) [5]. The length of the ablation region typically averages 3 cm. After the creation of the ablation lesion, programmed stimulation is repeated to assess the presence of other inducible VTs. One of three outcomes is observed: • No inducible VT. • The same VT is inducible, with clear failure to abolish the reentry circuit. • The initial VT is not inducible, but other morphologies of VT are inducible. The latter response indicates that the reentry substrate has been modified. Whether these VTs are targeted for ablation varies among laboratories. Our practice is to target all

VTs that have cycle lengths approximating those that have occurred spontaneously, or are slowed. Whether slower VTs are indications of damaged circuits from ablation or preexisting slow circuits is usually not clear at the time of the procedure. During the follow-up, approximately 20% of patients rendered free of VT, or who have modified reentry circuits, experience recurrent VT [2,33]. In patients with ICDs, the frequency of VT episodes is often markedly reduced, even among patients with recurrences. In 20–30% of patients ablation fails and frequent recurrences persist.

Intramural and epicardial reentry circuits When ablation of a stable VT is unsuccessful, it is usually due to absence of an identifiable reentry circuit isthmus on the endocardium. In some cases an apparent exit region on the endocardium reflects endocardial breakthrough from an epicardial or intramural circuit. Current ablation technologies may not produce lesions sufficient to interrupt tachycardia at broad, deep portions of the reentry path [34]. This situation is often suspected when ablation repeated slows or transiently terminates VT, with subsequent recovery of inducible VT. Intramural and epicardial reentry circuits are major causes for failure of 321

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endocardial ablation. Failure of ablation was not predicted by the infarct.

Epicardial mapping and ablation The technique developed by Sosa and colleagues for percutaneous epicardial mapping and ablation has been used by several groups [35,36]. In 14 patients with VT due to inferior wall infarction, seven of 30 VTs had a portion of a reentry circuit identified and ablated from the epicardium [35]. In another series, epicardial ablation was successful in eight of 10 patients with incessant VT in whom endocardial ablation failed or who were unable to undergo endocardial ablation due to limited ventricular access or LV thrombi [37]. Berruezo et al. hypothesized that slower epicardial, compared with endocardial, propagation away from epicardial reentry circuits would produce QRS findings suggesting epicardial reentry circuits for right bundle branch block-type VTs [38]. These features, corroborated in a series of cases, included: a pseudodelta wave (from the onset of the QRS to the beginning of the earliest rapid deflection in any precordial lead) of ≥ 34 ms, a time from QRS onset to the peak of the R wave in V2 (intrinsicoid deflection time) of ≥ 85 ms (Fig. 19.10), or a precordial RS interval > 120 ms.

Identical methods for obtaining voltage maps, pacemapping, and entrainment mapping can be carried out from the epicardium, although pacing thresholds can be higher than on the endocardium and epicardial fat can be a limiting factor [39,40]. In some cases, epicardial fat may mimic low-voltage scar [39]. Risks include damage to epicardial coronary arteries, or left phrenic nerve as it courses along the left ventricle, and pericardial bleeding. Coronary angiography is performed before ablation, and ablation not generally attempted if there is a large vessel in the proximity of the ablation electrode. It has been suggested that cryoablation might be associated with a lower risk of coronary artery injury, but efficacy for percutaneous epicardial ablation has not been tested in humans. In patients with prior cardiac surgery, the pericardial space may be fibrosed, preventing percutaneous access. Creation of a subxiphoid pericardial window in the electrophysiology laboratory can allow pericardial access for ablation in some patients, although when adhesions are dense, access is likely to be limited to the inferior surface of the ventricles with this approach [40].

Transcoronary ethanol ablation The blood supply to intramural and epicardial reentry circuits can be potentially identified by selective and subselective cannulation of coronary artery branches and terminating VT with the injection of cold saline during VT. Infarction of the region can then be accomplished with injection of absolute ethanol [41,42]. Early experience with the technique demonstrated that large infarcts could be created and that reflux of ethanol into branches could produce larger infarcts than desired. Development of collateral blood flow into the region allowed recurrent VT in some patients after the initial procedure occluded the primary circulation to the region. With advances in angioplasty techniques and increasing experience with use of ethanol ablation for treating hypertrophic cardiomyopathy, this technique has been used for ablation of intraseptal reentry circuits.

Outcomes of ablation for mappable VT after myocardial infarction

Figure 19.10 Electrocardiogram of sustained ventricular tachycardia (VT) in a patient with an old anterior wall infarction. This VT had a broad endocardial exit and outer loop endocardial sites, but endocardial ablation was unsuccessful. The onset of the QRS is relatively slurred, and the interval from QRS onset to the peak of V2 is 110 ms, consistent with an epicardial origin. Reproduced with permission from [38].

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Outcomes of ablation for stable mappable VT have been reported from series of patients selected specifically for this type of arrhythmia; these are the minority of patients with VT after myocardial infarction. The targeted mappable VT is no longer inducible after ablation in 68% to more than 90% of patients [6,12,25,34,43 – 47]. Interpretation of the results is complicated by the frequent presence of other VTs that are inducible, including VTs that are hemodynamically unstable, but often not described, in the

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majority of patients. Following an acutely successful ablation for a mappable VT, 20 – 44% of patients have a recurrence of VT during the follow-up [12,43,46,47]. Many of these are detected and terminated by ICDs, and might have terminated spontaneously otherwise, but are nonetheless of concern. Some recurrent VTs are similar to an ablated VT, suggesting healing of the initial RF ablation lesions. Spontaneous occurrence of VT that was inducible at the initial procedure, but deemed “nonclinical” and not targeted for ablation, also occurs. In addition, new morphologies of VT are occasionally observed late after ablation, suggesting some modification of the recovered arrhythmia substrate. Della Bella et al. performed catheter ablation in 124 patients with stable VT late after myocardial infarction [43]. Ablation abolished the targeted VT in 73% of patients. Amiodarone and/or beta-blockers were continued in the majority of patients. Only 11 patients received ICDs. During the follow-up, 60% of those in whom VT remained inducible at the end of the procedure had a spontaneous VT recurrence. Of those with an acutely successful ablation procedure, 27% suffered a recurrence. Although the recurrence rate was substantial, only three patients (2.5%) died suddenly. Thus, in selected patients who have hemodynamically tolerated VT, the risk of sudden death is low, raising the question of whether an ICD can be avoided in some patients. The potential for recurrences and frequent presence of depressed LV function will warrant continued ICD use for most patients.

Complications Patients with VT due to prior infarction are a high-risk group who have depressed ventricular function and are usually referred for ablation when VT is difficult to control. In a multicenter trials of 146 patients, procedurerelated mortality was 2.7% [3]. Uncontrollable VT with hemodynamic deterioration leading to death, often without ablation attempts, was the most common cause of procedure-related mortality in a trial of saline-irrigated ablation with an externally irrigated catheter [48]. Stroke occurred in 2.7% of patients in one multicenter trial in which mapping and ablation with an internally irrigated ablation catheter were used [3]. A recent multicenter trial using an externally irrigated catheter observed no strokes in 226 patients [48]. Cardiac perforation with tamponade and damage to the aortic and mitral valve apparatus are infrequent complications, occurring in less than 1–2% of patients. AV block is not uncommon if ablation of VT originating from the basal septum is attempted. The most common complications are related to vascular access, including femoral hematomas, pseudoaneurysms, and AV fistulas. The volume load administered with externally

irrigated ablation catheters requires careful monitoring, as it can lead to pulmonary edema.

Summary Catheter ablation is a good option for controlling recurrent episodes of VT late after myocardial infarction, particularly in patients with ICDs and frequent symptomatic therapies. When VT is sufficiently stable to allow mapping, or is incessant, a systematic approach to identifying an isthmus for ablation can be used to insure that the VT which is problematic is ablated. Other VTs are usually present, so that ablation extending over a region containing the identified isthmus is often reasonable. An approach combining substrate mapping with limited activation sequence and entrainment mapping can be used to identify VT circuit isthmuses for ablation.

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radiofrequency ablation of ventricular tachycardia. Circulation 1997;95:183 –90. Kocovic DZ, Harada T, Friedman PL, Stevenson WG. Characteristics of electrograms recorded at reentry circuit sites and bystanders during ventricular tachycardia after myocardial infarction. J Am Coll Cardiol 1999;34:381– 8. El-Shalakany A, Hadjis T, Papageorgiou P, et al. Entrainment/mapping criteria for the prediction of termination of ventricular tachycardia by single radiofrequency lesion in patients with coronary artery disease. Circulation 1999;99:2283 –9. Bogun F, Knight B, Goyal R, et al. Discrete systolic potentials during ventricular tachycardia in patients with prior myocardial infarction. J Cardiovasc Electrophysiol 1999;10:364–9. Podczeck A, Borggrefe M, Martinez-Rubio A, Breithardt G. Termination of re-entrant ventricular tachycardia by subthreshold stimulus applied to the zone of slow conduction. Eur Heart J 1988;9:1146 –50. Khan HH, Maisel WH, Ho C, et al. Effect of radiofrequency catheter ablation of ventricular tachycardia on left ventricular function in patients with prior myocardial infarction. J Interv Card Electrophysiol 2002;7:243 –7. Delacretaz E, Soejima K, Brunckhorst CB, et al. Assessment of radiofrequency ablation effect from unipolar pacing threshold. Pacing Clin Electrophysiol 2003;26:1993 – 6. Soejima K, Delacretaz E, Suzuki M, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct-related ventricular tachycardias. Circulation 2001;103:1858 – 62. Nabar A, Rodriguez LM, Timmermans C, Wellens HJ. Use of a saline-irrigated tip catheter for ablation of ventricular tachycardia resistant to conventional radiofrequency ablation: early experience. J Cardiovasc Electrophysiol 2001;12:153 –61. Hadjis TA, Stevenson WG, Harada T, et al. Preferential locations for critical reentry circuit sites causing ventricular tachycardia after inferior wall myocardial infarction. J Cardiovasc Electrophysiol 1997;8:363 –70. Stevenson WG, Friedman PL, Kocovic D, et al. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction. Circulation 1998;98:308 –14. Ouyang F, Bransch D, Schaumann A, et al. Catheter ablation of subepicardial ventricular tachycardia using electroanatomic mapping. Herz 2003;28(7):591–7. Sosa E, Scanavacca M, d’Avila A, et al. Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction. J Am Coll Cardiol 2000;35:1442–9. Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003;108:1329 –35. Brugada J, Berruezo A, Cuesta A, et al. Nonsurgical transthoracic epicardial radiofrequency ablation: an alternative in incessant ventricular tachycardia. J Am Coll Cardiol 2003;41: 2036 – 43. Berruezo A, Mont L, Nava S, et al. Electrocardiographic recognition of the epicardial origin of ventricular tachycardias. Circulation 2004;109:1842–7. Dixit S, Narula N, Callans DJ, Marchlinski FE. Electroanatomic mapping of human heart: epicardial fat can mimic scar. J Cardiovasc Electrophysiol 2003;14:1128.

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40 Soejima K, Couper G, Cooper JM, et al. Subxiphoid surgical approach for epicardial catheter-based mapping and ablation in patients with prior cardiac surgery or difficult pericardial access. Circulation 2004;110:1197–201. 41 Kay GN, Epstein AE, Bubien RS, et al. Intracoronary ethanol ablation for the treatment of recurrent sustained ventricular tachycardia. J Am Coll Cardiol 1992;19:159– 68. 42 Brugada P, de Swart H, Smeets JL, Wellens HJ. Transcoronary chemical ablation of ventricular tachycardia. Circulation 1989;79:475–82. 43 Della Bella P, De Ponti R, Uriarte JA, et al. Catheter ablation and antiarrhythmic drugs for haemodynamically tolerated post-infarction ventricular tachycardia; long-term outcome in relation to acute electrophysiological findings. Eur Heart J 2002;23:414–24. 44 Delacretaz E, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with coronary heart disease, 2: clinical aspects, limitations, and recent developments. Pacing Clin Electrophysiol 2001;24:1403–11.

45 Borger van der Burg AE, de Groot NM, van Erven L, et al. Long-term follow-up after radiofrequency catheter ablation of ventricular tachycardia: a successful approach? J Cardiovasc Electrophysiol 2002;13:417–23. 46 Gonska BD, Cao K, Schaumann A, et al. Catheter ablation of ventricular tachycardia in 136 patients with coronary artery disease: results and long-term follow-up. J Am Coll Cardiol 1994;24:1506 –14. 47 Della Bella P, Riva S, Fassini G, et al. Incidence and significance of pleomorphism in patients with postmyocardial infarction ventricular tachycardia: acute and long-term outcome of radiofrequency catheter ablation. Eur Heart J 2004; 25:1127–38. 48 Stevenson WG, Wilber DJ, Natale A, et al. Multicenter trial of irrigated RF ablation with electroanatomic mapping for ventricular tachycardia after myocardial infarction. Circulation 110:17(Suppl): 1869 abstr.

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20

Substrate-based ablation of postinfarction ventricular tachycardia David J. Wilber

Introduction The last decade has brought about substantial changes in the conceptualization and approach to the ablation of ischemic ventricular tachycardia (VT). Data from surgical and catheter mapping suggest that the reentrant circuits of postinfarction VT are relatively large [1–3]. The most vulnerable component of the circuit appears to be a slow conduction channel (SCC) insulated from surrounding myocardium either anatomically by fibrosis, or functionally due to collision of wavefronts or incomplete recovery from depolarization. As discussed in the previous chapter, the response to pacing during VT at multiple sites within the circuitaparticularly those demonstrating activation during the diastolic or presystolic phaseais useful in identifying this vulnerable channel, which can subsequently be targeted for ablation [4]. Sites with short postpacing intervals are within the reentrant circuit. Those that additionally demonstrate concealed entrainment are within the SCC. Longer stimulus–QRS and electrogram (EGM)–QRS intervals suggest a more proximal location in the SCC, while shorter times suggest a location more distally, near the exit to normal myocardium, coincident with the onset of the surface QRS. Physicians undertaking VT ablation face multiple challenges. A majority of VTs (approximately 80%) are hemodynamically unstable and will not permit mapping during prolonged periods of tachycardia. Most patients also have multiple spontaneous or induced VT morphologies. While many of these may partially share a single SCC, repetitive spontaneous or pacing-induced changes in morphology can hamper mapping efforts. Often clinical tachycardias cannot be reproduced during electrophysiological testing. The SCC may be narrow and easily transected with a small number of radiofrequency lesions, but can also be relatively broad (> 2–3 cm). For these reasons, activation and entrainment mapping has been increasingly supplemented and/or replaced by approaches that 326

target the underlying substrate abnormalities responsible for VT. This chapter outlines the current state and future development of substrate-based VT ablation.

Characterization of the substrate for postinfarction VT Histopathology The substrate of VT complicating remote myocardial infarction (MI) is well characterized. Surviving muscle bundles, commonly located in the subendocardium, but also in the mid-myocardium and epicardium, traverse the borders and penetrate deeper scar (Fig. 20.1). Action potential characteristics of surviving myocytes late after infarction are near-normal [5]. However, these bundles are characterized by decreased gap junction density, as well as alterations in distribution, composition, and function [6]. Increased spatial separation of surviving fibers occurs, with larger amounts of collagen and connective tissue between bundles. Surviving fibers can be connected side to side in regions in which the collagenous sheaths are interrupted, resulting in a zigzag pattern of transverse conduction along a pathway lengthened by branching and merging bundles of surviving myocytes [5,7,8]. The pattern of fibrosis may be important in determining the degree of conduction delay: patchy fibrosis between strands of surviving muscle produces greater delay than diffuse fibrosis [9]. There is also evidence of ongoing ionchannel remodeling within scar, at least early after MI, resulting in regional reductions in INa and ICaL [10]. While each of these aspects of scar remodeling alone may be inadequate to produce sufficient conduction delay for VT [11], in combination they contribute to formation of SCC.

In vivo scar definition Three-dimensional mapping has provided an opportunity

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A

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B

C

Figure 20.1 A. Top Photomicrograph of infarcted human papillary muscle demonstrating surviving subendocardial muscle bundles (light areas) and scar (dark areas). Bottom: Magnification of the subendocardial region emphasizing the interdigitation of fibrous sheathes between surviving muscle bundles. B. Schematic of a short axis section from a human heart with posterior lateral infarction demonstrating surviving muscle (dark

regions) interspersed within fibrosis (light region). C. Three dimensional reconstruction of a cross section from the same heart as B in a region of transmural infarction. A tract of surviving muscle fibers traverses the scar in a zig-zag pattern connecting noninfarcted posterior and lateral myocardium (adapted from de Bakker JM et al., reference 8 [A] and 7 [B,C], with permission).

for improved imaging of the myocardial substrate. Pathological, echocardiographic, and statistical data all suggest that myocardial scar can be detected by reduced voltage of the bipolar or unipolar EGM. EGM voltage has proved useful as an index of myocardial scar. In normal left ventricular endocardium, 95% of sampled sites are reported to have a bipolar voltage > 1.5 mV [12,13], though a lower cut-off (1.0 mV) has been reported by others [14]. In experimental animal models of myocardial infarction, the lowvoltage endocardial surface area determined by in vivo three-dimensional mapping demonstrated excellent correlation with the infarct area determined by postmortem histological analysis [15–19], although the optimal voltage cut-off ranged from 1.0 to 2.5 mV. Endocardial bipolar voltage is strongly influenced by local scarring in the immediate vicinity of the recording electrode, as evidenced by an increase in mean voltage at scar sites following subendocardial resection [20]. However, in experimental models, endocardial bipolar voltage also correlates with the transmural extent of infarction: lower voltages (generally < 1.0 mV) reflect greater transmurality (usually > 50%), but with considerable overlap [17]. Whether similar relationships exist in clinical scars awaits correlation studies with high-resolution imaging techniques. Adequate electrode contact must be ensured in order to obtain accurate voltage determinations at individual sites. EGM durations < 40 –50 ms may be useful in distinguishing sites

with low voltage obtained from normal myocardium due to poor electrode contact [13,16,18]. Unipolar voltage correlates poorly with bipolar voltage and with pathologic indices of scar [16,17]. Findings regarding the correlation between bipolar voltage and other in vivo indices of myocardial scar, such as perfusion scintigraphy or delayed enhancement magnetic resonance imaging, have not yet been reported. Preliminary reports of a good correlation between unipolar voltage and these indices suggest that this line of investigation may provide future refinements in the use of bipolar voltage for endocardial scar definition [21,22]. Myocardial scar is also characterized by lower impedance, and scar areas determined by impedance mapping correlate well with voltage criteria and postmortem pathology [17,23]. Bipolar voltage may be influenced by differences in the direction of activation (ventricular tachycardia, sinus rhythm, ventricular pacing), but the available data suggest that these differences have only a minor influence on endocardial scar dimensions using the voltage criterion of 1.5 mV [24,25]. Finally, pacing may be used as an index of viability by identifying electrically unexcitable regions (inability to capture with high-output pacing stimuli). Pacing thresholds correlate with bipolar voltage amplitude, but the technique appears particularly useful for distinguishing viable from nonviable myocardium at very low voltage sites [26]. While physicians performing 327

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ablation should be cognizant of the limitations of voltage criteria reviewed above, the use of 1.5 mV as an initial criterion for scar, and 0.5 mV for dense scar, is reasonable and widely accepted.

Electrogram characteristics Beyond voltage, the morphologic characteristics of local EGMs within scar during basal rhythms can be useful in narrowing the number of sites that may harbor potential SCC. Classification of scar EGMs has been variable, with overlapping categories and often incomplete character-

ization [20,27–35]. For the purpose of this and subsequent discussion, the definitions given in Table 20.1 are used, and typical examples illustrated in Fig. 20.2. Multicomponent potentials indicate asynchronous activation of the myocardium under the recording electrode, with conduction block and/or delay between myocyte bundles. As discussed in detail below, some types of sinus rhythm multicomponent potentials, particularly isolated potentials (IPs), may identify sites within the SCC during VT (Fig. 20.3). IPs are typically low-voltage signals (typically 0.05 – 0.30 mV) that require careful control of recording noise

Table 20.1 Definitions of sinus rhythm scar electrograms (EGMs). Multipotential EGM

EGM demonstrating more than one discrete potential, with individual potentials separated by an isoelectric interval > 20 ms (often referred to as split or double potentials)

Isolated potential (IP)

The second and subsequent potentials of a multipotential electrogram, separated from the primary ventricular electrogram by an isoelectric interval of at least 20 ms (up to 50 ms [30])

Isolated diastolic potential (IDP)

An isolated potential that occurs after completion of the surface QRS complex

Fractionated EGM

Low-amplitude (< 0.5 mV), long-duration EGM (> 130 ms) without a significant isoelectric interval

Late potential (LP)

Any distinct EGM component that occurs after completion of the surface QRS, including IDP, or long-duration EGMs continuing after completion of the surface QRS

IP (early)

IP (late – IDP)

Fractionated Figure 20.2 Representative examples of abnormal electrograms recorded from subendocardial scar. See table 1 for abbreviations and definitions.

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A

B

Figure 20.3 Surface ECG and intracardiac electrograms from a patient during sinus rhythm (A) and during ventricular tachycardia (B), with the ablation catheter (ABL) positioned at the same site during both recordings.

Note the isolated diastolic potential 120 ms after QRS offset during sinus rhythm, which precedes QRS onset by 120 ms during ventricular tachycardia (arrows). CS = coronary sinus; RVA = right ventricular apex.

if they are to be properly detected. The duration of IP (measured from the onset of the initial deflection to the offset of the last deflection) ranges from 100 to 400 ms or more, with the greatest delays usually, but not invariably, in dense scar (Figs. 20.4, 20.5); they often occur as clusters [31,34]. They are equally distributed between border and dense scar sites [30,36]. The presence or absence of IPs at specific scar sites may vary in some instances, depending on the direction of activation during the baseline rhythm (sinus rhythm or ventricular pacing) [30], and they are more likely to be manifest during paced rhythms [24,30,37]. The frequency of IPs at scar sites in patients with spontaneous VT is increased nearly twofold in comparison with scars in patients without VT, independently of the scar area, ejection fraction, and New York Heart Association functional class [36]. Even amongst patients with sustained VT, IP and isolated diastolic potential (IDP) frequency and distribution varies over a broad spectrum. Although frequency is not influenced by scar size, ejection fraction, or other clinical variables, IDPs are more common in patients with longer ventricular volumes older scars, and multiple infarctions [37]. There is also evidence that the degree of IDP delay may increase as a function of time from myocardial infarction in patients presenting with ventricular tachycardia [34,37]. Evidence that IPs represent local and relatively superficial endocardial activation at the site of the recording electrode, while the initial potential coincident with the surface QRS represents far-field or deeper myocardial activation, is supported by the disappearance

of IPs with endocardial resection [20] or catheter ablation [35] without a change in the morphology of the initial component. As a broad category, sinus rhythm late potentials (LPs) are common in scar, and are poor guides for ablation of VT [29,33]. However, some IPs may serve as markers for an SCC capable of supporting VT [30–33,35,38,39]. Their detection during sinus or paced rhythm suggests the presence of an SCC that is anatomically fixed, and that conduction to adjacent myocardium is constrained by fibrosis. During sinus rhythm, these sites are activated from the borders of the endocardial scar, or potentially from viable intramural or epicardial fibers. During VT, there is a reversal in the order of potentials, with the IDP preceding global ventricular activation and the onset of the surface QRS (Fig. 20.5). Several investigators have undertaken retrospective analysis of sinus rhythm EGMs at or near sites that had previously been demonstrated by a variety of mapping techniques to be in the SCC during sustained VT. In nearly all patients, IPs during sinus rhythm were found [31,33,35]. While the sensitivity of sinus rhythm IPs for SCC appears to be high, when more extensive mapping of the scar is performed, IPs overall appear to have poor specificity. Brunckhorst and colleagues found that of all IPs identified within scar, only 31% were located within the vicinity of a critical isthmus during VT [30]. Many IPs are generated by sites representing areas of fixed conduction block in bystander or dead-end pathways. However, the finding of 329

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Figure 20.4 Electroanatomical voltage map in the right anterior oblique projection from a patient with a large anteroapical infarction acquired during baseline atrioventricular pacing. Normal myocardium with voltage > 1.5 mV is displayed in purple, with dense scar (≤ 0.5 mV) shown in red. Sites

SCC EXIT EGMS Sinus

0.5 mv

VT

with isolated diastolic potentials (IDP) are indicated by red and blue tags. In this patient, IDP were identified at 30% of scar sites, broadly distributed between dense scar and border sites.

CENTRAL SCC EGMS

Sinus

VT 330

VP in SR

VT

Figure 20.5 Sinus rhythm (SR) electroanatomical voltage map from a patient with an apical infarction (bottom, center) displayed in a format similar to the previous figure. During ventricular tachycardia (VT), a slow conduction channel was identified (dashed lines) with an exit near the scar border and a central isthmus deeper in the apical scar, confirmed by entrainment mapping (not shown). Electrograms (EGMS) from both the exit site (top panel) and central isthmus (right panel) are displayed. Both sites demonstrate isolated diastolic potentials during SR, suggesting activation from the border of the scar to the interior. During VT, the order of potentials is reversed, with the low amplitude diastolic potentials preceding QRS onset. Ventricular pacing (VP) during SR at the exit site reproduces the QRS morphology during VT.

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very long IP durations improves specificity [30,31,34,39]. Similarly, pace-mapping during sinus rhythm from IP sites produces long stimulus–QRS delays, and good electrocardiography (ECG) matches to VT also improve specificity [31,32,35,38,40]. A potential limitation of these data is that most correlations of VT SCC to sinus rhythm EGM have been examined in patients with frequent spontaneous VT and relatively slow, if not always stable, tachycardias. It is not known whether these findings can be generalized to patients in whom VT is infrequent, has not yet occurred spontaneously, or shows very rapid rates. Finally, not all SCCs associated with VT are anatomically determined [41,42]. The boundaries of the channel may be functional, emerging only when the direction and/or coupling interval of the basal rhythm or premature beat produces conduction block between poorly coupled myocardial fibers within the scar, with maintenance of block and the boundaries of the SCC perpetuated only during tachycardia. Such functional circuits have been well characterized in

animal models [43,44]. The implication of these observations with regard to substrate ablation will be discussed in detail below.

Relationship of VT circuits to sinus rhythm electrograms and scar geometry We recently investigated the geometry of the reentrant circuit with particular reference to the scar and scar border, defined electroanatomically in 35 stable VTs from 28 patients with post-MI VT [45]. All of the patients initially underwent sinus rhythm mapping, followed by activation and entrainment mapping during VT to define various components of the circuit and their relation to scar geometry (Fig. 20.6). After identification of the exit site (entrainment with concealed fusion, postpacing interval similar to the VT cycle length, and S–QRS during entrainment < 30% of the VT cycle length), the VT was terminated and pacing was performed during sinus rhythm at the previously identified exit site. Finally, short linear ablation lesions

Outer Loop Site ME, PPI = TCL EGM–QRS = -20

Bystander Site CE, PPI > TCL

APEX APEX

MVA MVA VP in SR

Caudal Caudal Central SCC Site

Exit Site

CE, PPI = TCL, EGM-QRS = -120

CE, PPI = TCL, EGM-QRS = -44

Figure 20.6 Electroanatomical maps (caudal projection) from a patient with ventricular tachycardia (VT) and a large inferior infarction. Left panel: Electroanatomical activation map during VT. Selected sites where entrainment mapping was performed are indicated by brown tags. The results of entrainment mapping at these sites are summarized in the surrounding boxes. Red indicates earliest activating sites, and purple the latest activating sites. The map depicts a large figure of eight circuit exiting toward the septum. Right panel: Electroanatomical voltage map displayed in a format similar to previous figures. The sites of entrainment mapping

VT

during VT are superimposed on this map (white circles). Note the location of the central SCC in dense scar. The path of the SCC is oriented tangential to the scar border, with the exit site at the scar border. Ventricular pacing at the exit site during sinus rhythm (far right panel) reproduces the observed QRS morphology during VT. CE = concealed entrainment; EG,EGM = electrogram; ME = manifest entrainment; MVA = mitral valve annulus; PPI = postpacing interval, SCC = slow conduction channel; TCL = tachycardia cycle length.

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were performed parallel to the scar border, incorporating the exit site, followed by attempts to reinduce the VT. In 32 of 35 VTs, the exit site was identified within 1.5 cm of the scar border (either mitral annulus or 1.5 mV isopotential line). An excellent pace-map during sinus rhythm was obtained at the same site for all VTs in which the exit site could be determined (Figs. 20.5, 20.6B). In addition, for 20 VTs (63%), sinus rhythm IPs were found at or within 1 cm of the exit site. Overall, the SCC defined by entrainment was oriented perpendicularly or tangentially to the scar border. For VT circuits arising adjacent to the mitral valve annulus, the SCC is oriented adjacent and parallel to the annulus (Fig. 20.7), similar to the observations reported by de Chillou et al. [3]. Importantly, linear lesions parallel to the scar border (or perpendicular to the mitral annulus, in the case of perimitral VT) prevented VT reinduction. Hsia and colleagues reported similar data from their experience with entrainment mapping of stable VT [46]. Of 48 VTs, 44 (92%) had endocardial exit sites in regions of scar (< 1.5 mV), the majority in “border zone” voltage sites (> 0.5 mV). Verma and co-workers reported the sites of successful ablation in 86 VTs from 46 patients with post-MI VT [47]. Ablation was directed at critical isthmus sites defined by activation and entrainment mapping. Successful ablation was achieved in 68% of VTs at sites with “border zone” voltage and in 18% at sites within dense scar. In this study, no attempt was made to initially ablate at VT exit sites, so that the proportion of successful ablation at exit sites was likely underestimated. Collectively, these data indicate that in a large majority of postMI VTs, the exit of the SCC is near the scar border and can be identified by pace-mapping.

Ablation of slow conduction channels during sinus rhythm Endocardial substrate ablation in dense scar Several methods have been proposed for targeting SCC during sinus rhythm, either within dense scar, or closer to the scar border (Table 20.2). Soejima et al. used highoutput pacing to define electrically unexcitable regions within dense scar in 14 patients [26]. Linear lesions were placed between these regions, guided by entrainment mapping or sinus rhythm pacing. All inducible VTs were eliminated in 71% of cases, with a marked reduction in the VT frequency during follow-up. Two prospective studies of ablation guided by IDP in dense scar have been reported. Arenal et al. performed ablation targeting IDP, corroborated by pace-mapping, in 18 patients in whom the previously documented clinical VT could not be reproduced during programmed stimulation, or the induced VT was unstable [31]. During a mean follow332

up period of 9 months, 72% of the patients were free of recurrent ventricular arrhythmias. Nakagawa and co-workers performed ablation guided by elimination of all IDPs within dense scar in 22 patients with frequent unmappable VT [39]. During a 2-year follow-up, 17 patients (80%) remained free of recurrent VT, with a marked reduction in VT frequency in the remaining patients. A smaller scar area and a longest IDP delay of < 230 ms were predictors of recurrence. Arenal et al. introduced the concept of manipulating voltage filters of electroanatomical maps to identify corridors of higher voltage within dense scar that could represent putative SCC [48]. They found such corridors in 75% of patients, corroborated by IP and/or pace-mapping in most patients. Hsia et al. identified such “corridors” in approximately 50% of VTs [46]. While this novel method offers an alternative for identifying SCC, the high-voltage corridors were identified retrospectively in most patients, with prior knowledge of the region of interest. The utility of the method prospectively applied in patients with unstable VT in whom there is little prior knowledge of the potential sites of origin remains unclear. One potential limitation of sinus rhythm (SR) pacemapping in central scar is that the boundaries of the SCC may be partly functional, so that global ventricular activation during pacing in sinus may differ substantially from VT if the areas of functional block during each are not identical (Fig. 20.8). Even if pacing is performed in an anatomically constrained SCC, if the pacing site is closer to the entrance rather than the exit of the channel, then antidromic activation of the channel may activate normal myocardium near the entrance rather than the exit, resulting in a very different QRS morphology. These limitations do not apply when pace-mapping is performed at exit sites.

Endocardial substrate ablation in the scar border zone In our own laboratory, we have focused on targeting the exit sites of the SCC at the scar border. Based on the previous excellent outcomes of surgical cryoablation at the scar border [49,50], and consistent with the geometry of VT circuits relative to the scar border, we hypothesized that linear ablation of the scar border would provide an effective SR substrate ablation strategy. Pace-mapping during the basal rhythm is used to define the exit sites for all induced VTs, both stable and unstable. A substantial proportion of these sites also demonstrate SR diastolic potentials. Short linear lesions (3–4 cm) are placed parallel to the scar border, centered on the exit site defined by the pace-map match. These lesions are placed 1–2 cm inside the 1.5-mV isopotential line (voltage usually < 0.5 mV) to minimize the risk of injury to normal myocardium and to avoid the potential “fanning out” of the SCC at its junction with normal myocardium (Figs. 20.9, 20.10). This approach

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VT #1 RB - RSA

VT # 2 LB - LSA

Voltage Map In SR

Activation Map in VT #2 CAUDAL

CAUDAL

Sept

Sept

FW FW

S-QRS=90ms EGM-QRS=80ms VT SR PACE

SR PACE

VT

Figure 20.7 Electroanatomical maps (format similar to previous figures) and tracings from a patient with an inferior infarction and both left and right bundle ventricular tachycardias (VT) arising adjacent to the mitral valve annulus. The voltage map displays a large scar abutting the annulus, with an area of higher voltage perpendicular and immediately adjacent to the annulus. Pacing in sinus rhythm (SR) adjacent to the annulus exactly

reproduces the QRS morphologies of the two VTs. An activation map displayed in the far right panel during the left bundle VT demonstrates a SCC parallel to the annulus, exiting toward the septum. The SR pacemap match site (white tag) for the left bundle VT was near the exit site demonstrated on the activation map and confirmed by entrainment. Abbreviations as in previous figures.

Table 20.2 Approaches to substrate ablation.

VT episodes of more than 90%. Similarly favorable outcomes have been obtained by other investigators using scar border ablation techniques [12,13,52].

Technique 1 Ablation transecting slow conduction channels (SCCs) in dense scar a Definition of electrically inexcitable zones, with linear ablation between zones b Identification and ablation of isolated diastolic potentials (IDPs) c Identification and transection of high-voltage corridors 2 Ablation transecting SCC exits near scar border Target chamber 1 Left ventricular endocardium 2 Right ventricular endocardium 3 Epicardium

has been highly effective in eliminating both stable and unstable VT in patients with advanced ischemic cardiomyopathy and frequent multidrug-resistant VT [51]. There have been no adverse effects on ventricular function as measured by echocardiography 24 hours after the procedure. We have now used this technique in 120 consecutive patients with postinfarction VT, 91% of whom had at least one unstable VT, and 55% of whom had only unstable VT. After 2 years of follow-up, the actuarial incidence of freedom from any VT/V recurrence was 80%. Of the remaining 23 patients, 19 had a reduction in monthly

Epicardial substrate ablation In patients with stable VT, the SCC is epicardially located in approximately 10% of those with postinfarction VT [47,53,54], although the results of surgical mapping suggest a somewhat greater frequency [2,55]. Percutaneous epicardial mapping is feasible using the subxiphoid approach [56]. Voltage criteria for defining epicardial scar are similar to the endocardial EGM criteria [57], although some concern has been raised regarding the potential for the insulating effect of myocardial fat to produce falsely low voltage over relatively normal myocardium [58]. Substrate mapping of the epicardium is feasible, including pace-mapping and detection of IP. Overall, the epicardial scar area is smaller than that of the endocardium in most patients with ischemic cardiomyopathy [58]. Prior surgical revascularization poses a technical challenge to percutaneous epicardial access in this population, due to pericardial adhesions and fibrosis, which can be overcome in some instances by limited direct surgical access to the epicardial space [59]. An example of a patient with 333

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Pacing during VT in SCC Figure 20.8 Pacing from dense scar at a central SCC site during entrainment of VT (left panel) and during sinus rhythm from the same site after termination of VT. There are considerable differences in QRS

Pacing in SR at same site morphology between the two circumstances, suggesting the presence of functional block during VT not present in sinus rhythm. See text for details. Abbreviations as in previous figures.

VT

VT

VP

LAO

334

VP

Figure 20.9 Linear scar border ablation in a patient with a large anteroapical infarction. The voltage map is displayed in a format similar to previous figures. The patient had 3 different induced QRS morphologies, each reproduced during sinus rhythm pacing at specific sites around the circumference of the scar border. Short linear ablation lesions (white tags) parallel and inside the scar border, incorporating the pacemap match sites, resulted in noninducibility of any ventricular tachycardia, and long term freedom from recurrences. VT = ventricular tachycardia; VP = ventricular pacing in sinus rhythm.

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RAO

VT VP

VT VP

INFERIOR Figure 20.10 Linear scar border ablation in a patient with a large inferoseptal infarction. The voltage maps (left panels) are displayed in a format similar to previous figures. The patient had 3 different induced QRS morphologies, each reproduced during sinus rhythm pacing at specific sites around the circumference of the scar border. Short linear ablation lesions (white tags) parallel and inside the scar border, incorporating the pacemap match sites, resulted in noninducibility of any ventricular tachycardia, and

long term freedom from recurrences. Of note, the VT morphology arising adjacent to the mitral annulus was not reproduced at the lateral scar border, but rather 2 cm more medial. Linear ablation at the lateral scar border did not eliminate this VT, but a linear lesion perpendicular to the annulus at the site of the best pacemap match was effective. VT = ventricular tachycardia; VP = ventricular pacing in sinus rhythm.

successful ablation of an unstable epicardial VT associated with an anteroapical aneurysm is shown in Fig. 20.11. In this patient, percutaneous access was not feasible due to extensive pericardial adhesions, and access was obtained by a limited lateral thoracotomy.

morphologies that share the same SCC as the mapped VT. While not obligatory, display of activation and pacing data on three-dimensional maps is very useful in interpreting the relationship of the SCC to scar geometry and potential anatomic boundaries such as the mitral annulus. Once VT is terminated, extension of the ablation region by short linear lesions perpendicular to the long axis of the SCC is prudent, given the relatively broad width of some channels. Extension of the linear lesion to the mitral annulus for periannular circuits, or between potential anatomic boundaries (electrically unexcitable regions, or dense scar areas), and elimination of local sinus rhythm IDP may improve the durability and long-term success of ablation.

Practical approach to substrate ablation for post-MI VT In patients with stable sustained VT, targeting the SCC by traditional activation and entrainment mapping remains useful and effective as an initial step. This approach also has the potential advantage of eliminating other VT

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Endocardium

Epicardium

Figure 20.11 Ablation of epicardial VT in a patient with a large anteroapical aneurysm and two previous surgical revascularizations. The voltage maps (bottom panels) are displayed in a format similar to previous figures. Pacemapping along the lateral apical border of dense endocardial scar produced fair, but not exact matches to the induced VT morphology, and a linear lesion (white tags) adjacent to the scar border was not effective. Percutaneous access to the epicardium via a subxyphoid approach was not successful due to scarring related to prior surgery. A small lateral

thoracotomy enabled access to the lateral epicardium. Note that the area of epicardial scar was smaller and patchy relative to endocardial scar (lower left panel). A pacemap near the epicardial scar border reproduced the VT morphology. A short epicardial linear lesion incorporating the pacemap site resulted in elimination of inducible VT and absence of recurrence during long-term follow-up. The pacemap match site was located just lateral to visually identified dense white epicardial scar (upper left panel).

In this sense, traditional mapping techniques serve to localize the region of interest, with the final lesion set enhanced and extended by knowledge of the sinus rhythm substrate properties. Controversy continues regarding the need to eliminate all unstable VT morphologies during an ablation session. In patients presenting only with stable or mappable spontaneous VT, elimination of this form alone is typically associated with a high degree of freedom from recurrent VT over a follow-up period of 1–2 years. However, unstable

VTs not targeted during the initial ablation session represent a significant proportion of subsequent episodes in those patients in whom VT does recur. In our laboratory, we attempt to target all VT morphologies, in addition to those clinically documented. The rationale for this approach is in part secondary to the limited clinical information available from implantable defibrillator logs regarding QRS morphology, and the inconsistent relationship between spontaneous and induced VT rates for the same morphology (the latter generally more rapid). In patients who

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present with only unstable spontaneous VT, or in whom both stable and unstable clinical VT coexists, substrate mapping approaches are required to successfully treat VT. The selection of substrate-based technique may be dictated by the specific properties of the scar. We currently begin an ablation session with a detailed three-dimensional substrate map of the left ventricle in sinus rhythm, delineating the scar boundaries (1.5 and 0.5 mV isopotential lines) and marking IDPs using color-coded tags (making particular reference to long-duration IDPs > 200 ms, which may be more specific for SCC). In experienced hands, this should take no more than 15–30 minutes to obtain. Regions of normal voltage can be mapped with low density, but a greater density of points should be obtained within scar. If stable VT can be induced, a separate activation map is performed, and sites of entrainment (exit and central SCC) tagged. Once VT is terminated by ablation, these tags can subsequently be superimposed on the basal rhythm substrate map to assist deployment of the final lesion set. As discussed previously, the scar borders can be

reasonably extrapolated by voltages obtained during VT, but other information from a substrate map will not be available to guide ablation of remaining unstable VT. We then perform pace-mapping around the scar border. Close pace-map matches can be obtained in 70–80% of all induced VT morphologies. These sites are then ablated by linear lesions near the scar border as described above. When adequate pace-map matches cannot be obtained by scar border pacing, and the spontaneous or induced VT has a left bundle configuration, a substrate map and pacemapping is subsequently performed in the right ventricle (Fig. 20.12). Rarely, the morphology of spontaneous or induced VT can only be reproduced by pacing in deeper scar. In patients without inducible VT, or in whom the clinical VT is slow but only very rapid VT of a different morphology is induced, we target IDP within the scar (Fig. 20.13). Since an isolated epicardial source of VT is relatively uncommon in postinfarction VT, we generally reserve epicardial mapping for patients in whom endocardial target sites for clinical VT cannot be found, or were

RV

LV

SPONTANEOUS VT

PACEMAP Figure 20.12 Ablation of ischemic VT originating from the right ventricle. The patient had frequent episodes of spontaneous VT with a left bundle superior QRS morphology (upper left panel), but VT could not be induced during electrophysiological study. Left ventricular endocardial electroanatomical mapping revealed a discrete inferior scar (displayed in a caudal view, right panel). Extensive pacemapping around the scar border during sinus rhythm (green tags) failed to reproduce the spontaneous VT

morphology. Right ventricular electroanatomical mapping demonstrated a small inferior apical scar; pacemapping at the border of the RV scar reproduced the spontaneous QRS configuration (lower left panel). A short linear ablation lesion (brown tags) was made at the scar border. There has been no recurrence of VT during more than two years of follow-up. LV = left ventricle, RV = right ventricle, VT = ventricular tachycardia.

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CAUDAL 1.5 mv line

RV LV

Figure 20.13 Ablation of noninducible VT associated with inferior infarction guided by substrate mapping. The patient had frequent ICD shocks from VT at a cycle length of 350 ms. No VT could be induced during electrophysiological testing. No 12 lead ECG of spontaneous VT was available. Endocardial electroanatomical maps of the right and left ventricles were generated (right panel). In this example, the upper voltage filter was set at 0.4 mV in order to permit identification of a “high voltage” corridor

transecting the basal half of the inferior scar. The total scar area (≤ 1.5 mV) is enclosed by the yellow dashed line. Low amplitude isolated diastolic potentials were detected during sinus rhythm from a limited region in the center of the higher voltage corridor (left panel). Regional ablation around this site resulted in freedom from recurrent VT over 18 mo of follow-up. LV = left ventricle, RV = right ventricle, VT = ventricular tachycardia.

ineffective. This often requires a separate ablation session, given difficulties in accessing the pericardium in this patient population. Our approach to substrate mapping is summarized in Table 20.3.

The optimal approach for substrate ablation remains to be defined. Ablation near the scar border requires the generation and evaluation of multiple pace-maps, which can be time-consuming (but generally less than 30 minutes). Ablation in central scar has the potential advantage of eliminating a single central channel with multiple exit sites, but requires high-density mapping (and potentially pacing) of the entire central scar. A relatively large number of lesions may be required to eliminate all IDPs. In published data to date, there appears to be little difference in the total number of radiofrequency lesions delivered to eliminate VT between the various methods, and none of the approaches appears to have a significant deleterious effect on ventricular function. Based on specific clinical presentation and scar properties, different strategies or combinations of strategies may be most appropriate in individual patients.

Table 20.3 Approach to Substrate Mapping 1)

2) 3)

4)

5)

Detailed LV electroanatomical substrate map in basal rhythm – voltage thresholds set at 0.5 and 1.5 mV to define scar – tag sites with isolated diastolic potentials – higher density mapping in low voltage areas (minimum fill threshold 1 cm) Programmed stimulation. If stable VT induced, generate separate activation map – entrainment during VT, tag sites within SCC – terminate VT by ablation at SCC site – import tags into substrate map, additional ablation based on substrate map as appropriate If unstable VT induced, pacemap in border zone around circumference of LV scar and tag matches to induced VT – if no pacemap match obtained, and LB VT morphology, substrate and pacemapping in RV – linear ablation inside and parallel to scar border incorporating pacemap match sites – if no matches obtained by scar border pacing, ablation at selected IDP sites (with or without corroborative pacemapping and/or search for high voltage corridors) Epicardial mapping usually reserved for separate session unless high degree of clinical suspicion

See text for details IDP = isolated diastolic potential; LB = left bundle; LV = left ventricle; RV = right ventricle; SCC = slow conduction channel; VT = ventricular tachycardia

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The future of substrate-based ablation Further refinements in the definition and display of myocardial scar will facilitate substrate-based mapping and ablation. Both magnetic resonance imaging and computed tomography of the ventricle with delayed contrast enhancement provide high-resolution discrimination of normal myocardium from chronic infarction and allow improved definition of the transmural distribution of scar. Such images may also provide a more accurate template onto which the electrical characteristics of the ventricles can be mapped [60,61]. Practical, automated online algorithms for identifying optimal pace-map matches to induced or

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Figure 20.14 Example of automated comparison and display of sinus rhythm pacemapping (62). Pacemaps are acquired and compared to induced VT by an automated cross correlation algorithm which generates a correlation coefficient for individual leads and for the overall ECG match.

spontaneous VT would greatly shorten procedure time and are currently under development (Fig. 20.14) [62]. Finally, more sophisticated computer algorithms for predicting potential VT SCCs based on sinus rhythm activation parameters appears feasible [63], but requires prospective validation. As substrate approaches are refined and user-friendly applications software for processing anatomic and electrophysiological data becomes available, the future also holds the prospect of wider application. Currently, ablation is limited largely to patients with advanced disease, limited functional capacity, and extremely frequent episodes despite multiple combinations of antiarrhythmic drugs. Preliminary data indicate that substrate-based ablation applied earlier in the patient’s clinical course, soon after initial presentation with VT, may have a favorable impact on the long-term risk of recurrence and mortality [64].

These results can be displayed as electroanatomical maps of the spatial distribution of degree of pacemap correlations (upper left panel) or superimposed on voltage maps (upper right panel).

Acknowledgment Research for this chapter was supported in part by a grant from the George M. Eisenberg Foundation.

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34 Bogun F, Krishnan S, Siddiqui M, et al. Electrogram characteristics in postinfarction ventricular tachycardia: effect of infarct age. J Am Coll Cardiol 2005;46:667–74. 35 Bogun F, Good E, Reich S, et al. Isolated potentials during sinus rhythm and pace-mapping within scars as guides for ablation of post-infarction ventricular tachycardia. J Am Coll Cardiol 2006;47:2013–9. 36 Oza SR, Porter M, Akar J, et al. Electroanatomical substrate of ischemic cardiomyopathy with and without spontaneous ventricular tachycardia. Heart Rhythm 2006;3:S238. 37 Oza SR, Cahoon K, Brysiewicz N, Akar JG, Santucci P, Vorma N, Spear W, Shapira A, Pandya K, Wilber DJ. Frequency and determinants of isolated diastolic potentials in patients with ventricular tachycardia associated with prior myocardial infarction. Circulation 2007; in press (abstract). 38 Kottkamp H, Wetzel U, Schirdewahn P, et al. Catheter ablation of ventricular tachycardia in remote myocardial infarction: substrate description guiding placement of individual linear lesions targeting noninducibility. J Cardiovasc Electrophysiol 2003;14:675–81. 39 Nakagawa H, Singh D, Beckman KJ, et al. Ablation of unmappable post MI ventricular tachycardia using substrate mapping during sinus rhythm. Heart Rhythm 2004;1:S36. 40 Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH, Friedman PL, Stevenson WG. Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation 2004;110:652–9. 41 Callans DJ, Zardini M, Gottlieb CD, Josephson ME. The variable contribution of functional and anatomic barriers in human ventricular tachycardia: an analysis with resetting from two sites. J Am Coll Cardiol 1996;27:1106 –11. 42 Downar E, Kimbler S, Harris L, et al. Endocardial mapping of ventricular tachycardia in the intact human heart: evidence for multiuse reentry in a functional sheet of surviving myocardium. J Am Coll Cardiol 1992;20:869–78. 43 Dillon S, Allessie M, Ursell P, Wit A. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone. Circ Res 1988;63:182–206. 44 Assadi M, Restivo M, Gough WB, el-Sherif N. Reentrant ventricular arrhythmias in the late myocardial infarction period: 17. Correlation of activation patterns of sinus and reentrant ventricular tachycardia. Am Heart J 1990;119:1014 –24. 45 Wilber DJ, Morton JB, Cai J, et al. Relationship of post infarction ventricular tachycardia exit sites to the scar border: implications for catheter ablation [abstract]. Heart Rhythm 2004;1:S36. 46 Hsia HH, Lin D, Sauer WH, Callans DJ, Marchlinski FE. Anatomic characterization of endocardial substrate for hemodynamically stable reentrant ventricular tachycardia: identification of endocardial conducting channels. Heart Rhythm 2006;3:503–12. 47 Verma A, Marrouche NF, Schweikert RA, et al. Relationship between successful ablation sites and the scar border zone defined by substrate mapping for ventricular tachycardia postmyocardial infarction. J Cardiovasc Electrophysiol 2005;16:465–71. 48 Arenal A, del Castillo S, Gonzalez-Torrecilla E, et al. Tachycardia-related channel in the scar tissue in patients with sustained monomorphic ventricular tachycardias: influence of the voltage scar definition. Circulation 2004;110:2568 –74. 49 Ostermeyer J, Breithardt G, Borggrefe M, Godehardt E, Siepel I, Bircks W. Surgical treatment of ventricular tachycardias.

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Ablation of ventricular tachycardia associated with nonischemic structural heart disease Jason T. Jacobson, David Lin, Ralph Verdino, Joshua Cooper, and Francis E. Marchlinski

Introduction Most experience with catheter ablation for ventricular tachycardia (VT) with structural heart disease has been in the setting of coronary artery disease. This chapter discusses radiofrequency ablation in the adult patient with noncoronary structural heart disease, specifically: • Arrhythmogenic right ventricular cardiomyopathy. • Repaired tetralogy of Fallot. • “Idiopathic” dilated cardiomyopathy. • Other infiltrative myopathies, such as sarcoidosis and Chagas’ disease. We begin by providing an overview of the general approach to the patient undergoing catheter ablation in this setting. For each specific disease process, we describe the epidemiological considerations related to the development of sustained VT. We also describe the anatomic substrate and the electrophysiological nature of this substrate, both in sinus rhythm and with the development of VT. Our own experienceaas well as previously published experience with radiofrequency ablation for VT in these disease processesais presented, with an emphasis on special considerations that apply to each unique disease substrate and VT syndrome. The chapter concludes with a summary and a description of recommendations for future research that may make ablative therapy for VT associated with noncoronary structural heart disease more widely applicable.

General approach to the patient with nonischemic cardiomyopathy Successful ablation is critically dependent on a clear definition of the electrophysiologic substrate and identification of the origin of the VT. Both are facilitated by preprocedural 342

assessment of the location of the anatomic abnormality and a careful analysis of all electrocardiographic (ECG) information related to spontaneous VT events. In patients with nonischemic structural heart disease, echocardiography, magnetic resonance imaging, fast computed tomography (CT) imaging, and nuclear perfusion scans may all help in identifying anatomic abnormalities. Twelve-lead ECG recordings of the “clinical” arrhythmia are important for identifying the region of origin for more detailed mapping [1–3]. Typical morphologies of VT that are associated with the different arrhythmia syndromes are discussed with each syndrome below. In lieu of the 12-lead electrocardiogram, single-lead or multiple-lead telemetry monitoring can help identify the bundle branch block morphology and QRS axis if leads V1 and V2 are used for monitoring. Recordings from an implantable cardioverter-defibrillator (ICD) can also be very helpful in providing some insight into spontaneous arrhythmias. The electrogram morphology recorded from the ICD lead system frequently produces a characteristic signature [4]. This allows some assessment of the number of spontaneous VT morphologies and can be used to create a template for determining whether induced arrhythmias are likely to mimic spontaneous ones in the absence of more detailed recordings. Whenever possible, device recordings are transferred into our recording/mapping system during the ablation procedure to facilitate such comparisons. Comparison of VT rates must take into account any drug therapy at the time of the recordings. Our approach in the laboratory also typically follows a standard protocol. We believe that a bipolar voltage map is an important imaging tool for defining the presence of significant fibrosis and the anatomic substrate [1,2,5]. We routinely perform detailed endocardial and, if appropriate, epicardial mapping in most patients with documented or suspected nonischemic structural heart disease and VT. A confluent area of low voltage will identify

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the anatomic substrate for VT. Most frequently, threedimensional electroanatomical mapping is used to collect bipolar electrograms throughout the chamber of interest. The fill threshold is typically maintained at 15 mm or less to insure adequate sampling. Bipolar electrograms are typically filtered at 30 –150 Hz. A three-dimensional computerized color display of the detailed voltage map is displayed, with confluent areas of low voltage identifying “abnormal myocardium.” On the basis of recordings obtained in patients without structural heart disease, we established the appropriate color range for identifying abnormal myocardium [6,7]. Typically, we use a value of 1.5 mV to define normal in the right ventricle and a value of 1.8 mV (2.0 mV if a history of ventricular hypertrophy is present) in the left ventricle [2]. If both chambers are displayed, the 1.5-mV value is used, with minimal risk of understating the degree of abnormality in a hypertrophied left ventricle. In an attempt to define areas of very dense scar, we set the lower limit of the color range at 0.5 mV. Occasionally, if appropriate, we try to further adjust the color range in the area of dense scar to identify channels of viable myocardium. This can be done by scanning the color range in 0.1-mV increments from 0.1 to 0.5 mV, or by identifying and tagging areas with very low signal amplitude and an inability to capture with up to 10–20 mA output in order to highlight tissue between these unexcitable areas [8]. Mapping is most often done with a mapping and ablation catheter with a 4-mm tip, although catheters with an 8-mm tip have also been used. While there are few data on the differences in electrogram characteristics between catheters with 4-mm and 8-mm tips, it has been our experience that it is more difficult to localize high-frequency, low-voltage signals (e.g., Purkinje potentials, late potentials, mid-diastolic potentials during VT, and viable channels of myocardium in dense scar) using a catheter with an 8-mm tip. We therefore suggest that voltage mapping should be carried out with an electrode catheter with a 4-mm tip whenever possible. After the substrate is defined, we attempt VT induction. The ECG morphology of all induced VTs is compared to spontaneous events to document a match. The approach to mapping and ablation depends on the hemodynamic stability of the arrhythmia, as discussed below. If the arrhythmia is tolerated hemodynamically, detailed activation and entrainment mapping of the VT is performed. For VT that is poorly tolerated or becomes unstable in response to pacing, a more aggressive and extensive approach to ablation is used, with linear lesions targeting the specific anatomic substrate and targets within the defined substrate being guided by pace-mapping, available activation mapping, and channel identification. Because of the frequent epicardial origin of VT, a low threshold for accessing the pericardial space for more detailed mapping and ablation has now become standard.

Arrhythmogenic right ventricular cardiomyopathy Pathological, epidemiological, and diagnostic considerations. Right ventricular cardiomyopathy involves replacement of myocardium to a variable extent by fatty and fibrous tissue [9]. The arrhythmogenic subset, characterized by relatively frequent and recurrent VT, was first described by Fontaine et al. in 1977 [10]. Pathologically, arrhythmogenic right ventricular cardiomyopathy (ARVC) predominantly affects three areas of the right ventricle (known as the “triangle of dysplasia”): the anterior infundibulum, the apex, and the basal inferior wall [11]. The histological appearance may vary from myocyte degeneration and necrosis with foci of inflammation to myocardial replacement with fibrous or lipomatous tissue [11,12]. Although the right ventricle is primarily affected, left ventricular involvement can occur as well [5–10]. Our own experience has emphasized the importance of perivalvular fibrosis as the anatomic substrate and source of arrhythmogenesis in most patients [1]. Epidemiologically, ARVC usually affects males and can be sporadic [3–11] or familial [13–19]. It is unknown whether the disease process represents a genetically determined degenerative process or a pathologic reaction to an environmental pathogen that may be potentiated by a genetic predisposition. Owing perhaps to the heterogeneous nature of the disease, the clinical course is variable. ARVC may be present in as many as 20% of people under 35 years of age who experience sudden death [12]. Conversely, 10% of ARVC patients experienced sudden death in one series [20]. Despite the suggestion of a more benign prognosis in patients presenting with VT who are subsequently treated with antiarrhythmic agents [21,22], the 5-year recurrence of arrhythmic events may be as high as 40%. Recurrent VT appears to correlate with the extent of the disease, the presence of late potentials, and inducible VT [23]. The diagnosis of ARVC is suggested by three features of the 12-lead ECG: • Incomplete or complete right bundle branch block (RBBB; 50% of affected individuals). • Inverted T-waves in V1–V3 (90% of affected individuals). • “Epsilon” waves (Fig. 21.1) in the anterior precordial leads (15–60% of affected individuals) [11,22,24 –26]. Notably, epsilon waves may not be present or may be confined to the anterior precordial leads. We have observed lead-specific changes on the 12-lead ECG that reflect the distribution of low-voltage regions in patients with ARVC (Fig. 21.2). The signal-averaged ECG is typically abnormal in patients with ARVC [27,28]. Echocardiography may show diffuse right ventricular dilatation or localized aneurysmal segments [29,30]. Metaiodobenzylguanidine-123 343

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ARVC, in comparison with 0% of age-matched and sexmatched controls [36]. However, the right ventricular free wall is a relatively thin structure, and normal epicardial fat overlying this area may be easily misinterpreted as fatty infiltration, particularly if imaging experience is lacking. In another series from the Johns Hopkins group, only 27% of 89 patients previously diagnosed with ARVC based on MRI findings of intramyocardial fat/wall thinning actually met the Task Force criteria [37]. Notably, none of the patients who had a repeat MRI examination (84%) displayed any evidence of a right ventricular (RV) myopathic process. Thus, it is imperative that the diagnosis should rest not solely on limited or magnetic resonance evaluation, but that Task Force criteria should be met and/or abnormalities in the sinus rhythm RV bipolar voltage should be present. Figure 21.1 Surface electrocardiography leads V1 through V6 in a patient with arrhythmogenic right ventricular cardiomyopathy, showing classic T wave abnormalities and epsilon waves (arrows) in the anterior precordial leads.

(123MIBG) scintigraphy, which quantifies myocardial sympathetic activity by measuring presynaptic norepinephrine uptake, shows regional sympathetic denervation in 83% of patients with ARVC [31]. Magnetic resonance imaging (MRI) may be helpful, but requires cautious interpretation by an experienced reader [32–34]. The Johns Hopkins group found high intramyocardial fat on MRI in 75% of patients meeting the Task Force criteria [35] for

Baseline ECG with inferior epsilon waves

Bipolar voltage map and late potentials

V6 Abl V6 Abl V6 Abl

344

Electrophysiological considerations. During sinus rhythm, local ventricular electrograms of areas involved with ARVC typically show broadened deflections and late, sharp, high-frequency terminal deflections representing delayed myocardial activation and slow conduction [11]. These late electrograms, which correlate with epsilon waves on the surface ECG or late potentials on the signalaveraged electrocardiogram (SAECG), should be differentiated from the “late” electrograms observed in the right ventricular infundibulum of normal hearts (Fig. 21.2). In patients with ARVC, areas of delayed myocardial activation and slow conduction provide the anatomic substrate for reentry, one of the mechanisms for ventricular

Figure 21.2 Epsilon waves localized to the inferior leads (arrows) in a patient with arrhythmogenic right ventricular cardiomyopathy. The bipolar voltage map demonstrated perivalvular voltage abnormalities (signal amplitude < 1.5 mV) consistent with endocardial involvement localized to the inferior right ventricle, surrounding the tricuspid valve. Late potentials (blue arrows) were recorded from the mapping catheter in the region surrounding the inferior aspect of the tricuspid valve.

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tachycardia due to ARVC. A previous series of threedimensional electroanatomical mapping with the Carto system showed areas of low unipolar and bipolar voltage that corresponded to affected areas noted on echocardiography or MRI [38]. Affected areas were limited to the apex, lateral wall, infundibulum, and outflow tract. The septum was invariably spared. In our experience [39], the electrophysiologic abnormalities in ARVC are predominantly

perivalvular (tricuspid and/or pulmonary) and can extend over large areas of the free wall (Figs. 21.2–21.8). The apex is usually spared, although extension from the perivalvular area can approach this region. Septal extension around the perivalvular region is also the rule in patients who present with VT. On the basis of our experience, we believe that the sinus rhythm voltage map is one of the most reliable ways of confirming the diagnosis of

AP AP View PV Figure 21.3 The characteristic pattern of endocardial bipolar voltage abnormalities in a patient with marked right ventricular (RV) cardiomyopathy and multiple morphologies of ventricular tachycardia. An anteroposterior (AP) view, highlighting the free wall, and a posteroanterior (PA) view, highlighting the septum, are shown. Peritricuspid and peripulmonary regions of low voltage are present. The RV apical region demonstrates a normal signal amplitude, and some septal involvement is evident (arrows) in addition to the extensive free wall abnormalities. PV, pulmonary valve; TV, tricuspid valve.

AP PA View PV

PV

Normal

>1.5mV

APEX

RV

TV

RV

PV

Septal

TV

TV

A b n o r m a l

Septal APEX

APEX

Pattern 1

<0.5mV

Pattern 2

RAO

AP

Normal

PV

>1.5mV

RV RV

TV Figure 21.4 Characteristic patterns of endocardial bipolar voltage abnormalities in two patients with arrhythmogenic right ventricular (RV) cardiomyopathy and ventricular tachycardia. The right anterior oblique (RAO), left anterior oblique (LAO), anteroposterior (AP), and posteroanterior (PA) views are shown. Low-voltage regions are typically adjacent to the tricuspid valve (TV), pulmonary valve (PV), or both valves. The distribution of abnormal electrograms always extends from the perivalvular regions. The RV apical region rarely demonstrates an abnormal signal amplitude. Recognition of perivalvular abnormalities allows one to focus on these regions for more detailed mapping and ablation.

TV APEX

LAO

PA

PV

Septum

RV

RV TV APEX

APEX APEX

A b n o r m a l

TV <0.5mV

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RVOT VT

ARVCM and VT

APEX

BOTTOM

APEX

BOTTOM

Normal

>1.8mV

LV

RV RV

LV

TV Bipolar endocardial voltage maps of RV and LV

MV

TV

LAO CORONAL

RIGHT POSTERIOR

PV

RV LV

RV

MV

TV

LV

APEX

A b n o r m a l

RV <0.5mV

patient with idiopathic RVOT VT. The entire endocardial surface is purple (normal amplitude) and only isolated noncontiguous sites have loweramplitude signals, represented by other colors. The right panel shows bottom and right posterior view voltage maps from a patient with arrhythmogenic RV cardiomyopathy and VT. The left ventricular endocardium is purple (normal amplitude electrograms), but the right ventricular endocardium is abnormal, with cone-shaped areas of abnormality extending from the tricuspid and pulmonary valve regions to involve extensive areas of the endocardium. LAO, left anterior oblique; MV, mitral valve; TV, tricuspid valve.

Figure 21.5 Contrast of bipolar endocardial voltage maps of the right ventricle (RV) and left ventricle (LV) in a patient with idiopathic right ventricular outflow tract (RVOT) ventricular tachycardia (VT) only (left panels) and in a patient with arrhythmogenic right ventricular cardiomyopathy (ARVCM) and VT (right panels). The color scale on the right identifies normal endocardium, represented by the color purple (signal amplitude > 1.8 mV) with abnormal endocardium being represented by the rest of the color range. The most markedly abnormal areas, with an electrogram amplitude < 0.5 mV, are red. The left panel shows bottom and left anterior oblique coronal views of the RV and LV voltage maps from a

PV LV MV

AV RV

LV TV

Right posterior view

RV

RV and LV LV VT #1

cardiomyopathy

Figure 21.6 Bipolar endocardial voltage maps of the right ventricle (RV) and left ventricle (LV), showing the location of abnormal RV and LV endocardium and the origin of ventricular tachycardia (VT) in a patient with right and left ventricular cardiomyopathy (left ventricular ejection fraction 35%) and VT. A right posterior view of the RV and LV is shown, with the valvular structures highlighted. The color scale on the right identifies normal endocardium, represented by the color purple (signal amplitude > 2.0 mV), with abnormal endocardium represented by the rest of the color range.

RV VT #1

RV VT #2

Both the LV endocardium and RV endocardium show sizable low-amplitude areas extending from the tricuspid and pulmonary valves and the mitral valve (solid arrows). On the basis of activation and pace-mapping, the right bundle branch block type of VT originated from the perivalvular mitral valve (dashed arrows) and the left bundle branch block type of VT originated from the perivalvular tricuspid valve (dashed arrows). Both regions were targeted for ablation. AV, aortic valve; MV, mitral valve; PV, pulmonary vein; TV, tricuspid valve.

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RV -AP BIPOLAR

Normal >1.5mV

APEX

BIPOLAR

RV - LAO

A b n o r m TV a l

RV L - AO

Mesh showing distribution of lesions

<0.5mV

TV APEX

VT with idiopathic RVCMÐscar on voltage map with many VTs Figure 21.7 The typical distribution of linear ablation lesions in a patient with right ventricular cardiomyopathy (RVCM) and multiple morphologies of ventricular tachycardia (VT) that could not be mapped using conventional activation and entrainment mapping techniques. Multiple point-by-point

ablation lesions (brown circles) were applied to create lines that tend to transect the abnormal endocardium and reach the valve annuli. AP, anteroposterior; LAO, left anterior oblique; RV, right ventricle; TV, tricuspid valve.

VT

PM

PV

Figure 21.8 Linear ablation lesions (brown circles) guided by a pace-map match (PM) of ventricular tachycardia (VT) in a patient with arrhythmogenic right ventricular cardiomyopathy. The lesions extend from the edge of the normal myocardium, defined by the color purple, to the tricuspid valve annulus through the well-defined region of low voltage with signal amplitudes < 1.5 mV. PA, posteroanterior; PV, pulmonary vein; RF, radiofrequency; TV, tricuspid valve.

TV

PA view Linear RF 347

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ARVC. A confluence of endocardial low voltage (< 1.5 mV) should be present in patients who present with ventricular tachycardia due to ARVC (Figs. 21.2–21.8). Multiple arrhythmogenic mechanisms have been described in ARVC. Both reentrant and focal VT have been suggested on the basis of mapping, entrainment, and cycle length stability characteristics [40]. VT may or may not demonstrate either mid-diastolic potentials or continuous electrical activity [41,42]. In electrophysiological examinations, over 90% of patients have VT inducible with programmed stimulation [11,22,29,43], which appears to be highly reproducible over time [44]. The relationship of exercise to arrhythmogenesis is well documented in patients with ARVC [11,19,21,45,46]. Haïssaguerre and colleagues have shown that continuous infusion of highdose isoproterenol can induce VT in the majority of patients with ARVC (85%), in comparison with 2% of control individuals [47]. It is important to distinguish between VT due to ARVC, induced in this manner, and catecholamineinduced idiopathic right ventricular outflow tract (RVOT) VT; the former is characteristically reentrant, while the latter is triggered or automaticaalthough automatic or triggered foci can also be seen with ARVC, especially with triggers around the perivalvular regions. Typically, multiple morphologies of tachycardia can be induced in the same individual, but almost all VTs have left bundle branch block (LBBB) morphology, poor R wave progression across the precordial leads, and a variable frontal plane axis consistent with a site of origin in the right ventricular free wall sites described (Fig. 21.5) [11]. Importantly, the morphology of VT associated with perivalvular pulmonary valve scarring may mimic typical idiopathic RVOT VT. The presence of abnormal perivalvular electrograms coupled with multiple VT morphologies makes it clear that the diagnosis is not idiopathic VT (Fig. 21.5). Occasionally, VT with RBBB morphology may be seen, presumably reflecting left ventricular involvement; however, the majority of ARVC VTs map to the right ventricular outflow tract, basal inferior wall, or anterior infundibulum in proximity to the tricuspid valve (Fig. 21.6). In our experience, patients with nonfamilial ARVC display late potentials (LPs) in the perivalvular areas, concordant with “scar” on three-dimensional electroanatomical mapping (Fig. 21.2). These LPs are frequently recorded very late after the surface QRS during sinus rhythm (narrow complex and RBBB) and RV apical pacing. The distribution of LPs helps explain characteristic surface and signal-averaged ECG changes (Fig. 21.2). We believe these perivalvular LPs may also contribute to the arrhythmogenesis responsible for VT. Experience with catheter ablation. Early attempts at definitive treatment of ARVC VT included surgical (cryoablation and incisional disarticulation) and direct-current catheter 348

ablation [48 – 54]. These techniques were generally associated with a high rate of recurrence despite additional antiarrhythmic therapy [21,55], while disarticulation was associated with a substantial rate of perioperative mortality. Many small series have investigated the efficacy of radiofrequency catheter ablation. These reports have achieved a high acute success rate (67–87%) and excellent mid-term to long-term (7–24 months) freedom from VT [40,56 –58]. Most patients with acute success had no recurrences during the follow-up period, while in one of these series, ICD therapy decreased from 49 episodes per month to 0.3 episodes per month. In contrast to these promising results, Haverkamp and colleagues have reported a 60% recurrence rate in 14 patients with drug-refractory VT in whom radiofrequency ablation was acutely successful using both earliest detectable endocardial activation and pace-mapping [59]. Notably, only five of their patients had VT inducible by programmed stimulation, and nine required catecholamine infusion. The difference in outcome compared with the previously mentioned series may be related to the small number of patients, site of origin of the targeted tachycardia (e.g., infundibulum versus inferior wall), differences in mapping end points for energy delivery, and, possibly, disease progression causing new tachycardias. In our experience, loss of the late, fractionated electrograms at the tachycardia site of origin recorded in sinus rhythm is sometimes observed following acutely successful radiofrequency ablation; the specificity and predictive value of this finding in relation to tachycardia recurrence is unknown (Fig. 21.9). In selected patients with ARVC and poorly tolerated arrhythmias, we applied a linear lesion approach that had proved successful in patients with coronary artery disease [6]. The VT substrate was defined, characterized by extensive sites of low voltage (< 1.5 mV). Using 12-lead ECG analysis and pace-mapping, regions of interest were defined and linear ablation lesions created that extended from densely scarred myocardium with a voltage amplitude of 0.5 mV through abnormal endocardium extending to the tricuspid and/or pulmonary valve annuli (Figs. 21.7, 21.8). This ablation strategy has proved very effective in controlling arrhythmia. In a recent report, we provided detailed characterization of the arrhythmogenic substrate and outcome with ablation therapy [1]. A striking observation was that perivalvular low-voltage regions, consistent with scarring as the arrhythmogenic substrate, were present in all patients with ARVC (Fig. 21.10). The site of origin of almost all VTs was associated with this perivalvular substrate. In the perivalvular region, we have been able to apply radiofrequency energy using an irrigated-tip catheter with a great deal of success and without complications. The ability to administer aggressive ablative treatment safely is probably related to the degree of fibrosis noted, especially in

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Loss of late potential with RF PRE

POST

Figure 21.9 Tracing from a patient with arrhythmogenic right ventricular cardiomyopathy, showing two late potentials (arrows) before ablation (Pre), recorded from two different mapping catheters in the right ventricle. After

radiofrequency (RF) ablation using an irrigated tip at a site near the tricuspid annulus (Post), the first late potential is abolished (black arrow), while the second remains (open arrow).

Normal >2.0 mV

Figure 21.10 Bipolar endocardial voltage maps of the left ventricle (LV, top left) and right ventricle (RV, top right) coupled with gross anatomy of the LV and RV endocardium from hearts explanted at the time of transplantation from a patient with LV cardiomyopathy (left) and RV cardiomyopathy (right). These patients had ventricular tachycardia from the LV and RV, respectively. Areas of low voltage in proximity to the mitral and tricuspid valve are evident on the color displays of the voltage map on top (yellow arrows) and correlate with the location of the pathological changes suggesting perivalvular fibrosis (bottom, yellow arrows). PA, posteroanterior; RAO, right anterior oblique.

A b n o r m a l

LV cardiomyopathy PA view bipolar voltage map

Mitral valve

RV cardiomyopathy

RV

RAO bipolar voltage map Tricuspid valve

LV

<0.5mV

LV

Perivalvular endocardial scarring

RV

RV Mitral valve annulus

Tricuspid valve annulus

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Ventricular tachycardia

Table 21.1 Ablation outcome for frequent (median > 30 ventricular tachycardias per month), unmappable ventricular tachycardia using substrate mapping, and endocardial linear lesions guided by pace-mapping in 61 patients. The median follow-up period was 14 months (range 1–56 months).

Outcome

Patients (n)

No recurrence

Infrequent VT < 1/3 months) (<

Frequent VT > 1/3 months) (>

Overall CAD RVCM LVCM

61 36 13 12

37 (61%) 23 (64%) 10 (77%) 4 (33%)

15 (25%) 9 (25%) 3 (23%) 3 (25%)

9 (14%) 4 (11%) 0 5 (42%)

CAD, coronary artery disease; LVCM, left ventricular cardiomyopathy; RVCM, right ventricular cardiomyopathy; VT, ventricular tachycardia.

the perivalvular regions (Fig. 21.10). Energy delivery of this type should be used with caution as one moves away from the perivalvular region. In summary, the limited data available suggest that radiofrequency ablation for VT associated with ARVC can be accomplished safely with a relatively high acute success rate, and with good long-term freedom from VT. Taking particular care to focus on perivalvular regions of the right ventricle is critical in identifying the likely site of origin. Activation/entrainment mapping for tolerated arrhythmias is appropriate. For multiple changing VT morphologies and/or rapid VTs, an ablation approach that incorporates the use of linear lesions that extend through abnormal endocardium to valvular structures appears to be successful. The location of the ablation lines appears to be effectively guided by analysis of the 12-lead ECG of VT and pace-mapping data (Table 21.1). Targeting regions with late potentials for pace-mapping and potential ablation may also be helpful. Despite the success rates for ablation of VT in ARVC, this treatment modality should be considered adjunctive to the implantation of a cardioverterdefibrillator in most patients. Certainly, patients who have a history of very rapid and poorly tolerated VTs, multiple VT morphologies, an extensive anatomic substrate defined by voltage mapping, or marked left ventricular (LV) involvement are best served by conservative management with an ICD.

VT associated with repaired tetralogy of Fallot Epidemiological considerations. Tetralogy of Fallot is the most common cyanotic congenital heart lesion, found in 6% of patients with congenital cardiac lesions at birth [60]. The tetrad consists of infundibular stenosis, an overriding aorta, a ventricular septal defect, and right ventricular 350

hypertrophy. In 1955, the first patient with tetralogy of Fallot had the defect corrected by open intracardiac surgery [61]. Currently, complete repair is associated with an excellent long-term prognosis [62], with actuarial survival rates approaching those of the normal population. The major late complication or risk after surgical repair appears to be VT and/or sudden death [63 – 65]. In older reported series, sudden death accounted for 30 –75% of late deaths [65–68]. Even in patients without bifascicular block or transient complete heart block immediately following surgery, retrospective data suggest a 1–6% incidence of sudden death, probably due to malignant ventricular arrhythmias [63,65,67]. Patients with ventricular ectopy, depressed cardiac index, pulmonary or tricuspid regurgitation, or outflow tract aneurysm appear to have a higher incidence of VT [69]. Electrophysiological considerations. Complete repair of tetralogy of Fallot involves patching of the ventricular septal defect and a right ventriculotomy or infundibulotomy. Subsequent scarring and fibrosis from the incisions and patching provides the anatomic substrate for macroreentrant VT observed late after surgery [70–74]. During sinus rhythm in these patients, fractionated and late local electrograms may be recorded from the region of the ventriculotomy or near the ventricular septal defect patch [72, 73,75]. With initiation of tachycardia, further electrogram fragmentation, mid-diastolic potentials, and continuous electrical activity may be observed in these areas [70,72, 73,75–77]. Typically, the VT circuit is associated with the right ventriculotomy or infundibulotomy scar [70 –72,74, 76–78]; less commonly, reentry is associated with the septal patch [73,74]. In either case, VT can invariably be initiated and terminated by programmed stimulation, and can be entrained [70,72,79]. Intraoperative mapping has shown that creating a line of unidirectional block located in the vicinity of the ventriculotomy scar is part of the arrhythmogenic substrate that allows VT initiation [70]. During ongoing ventriculotomy-associated tachycardia, intraoperative mapping studies by Josephson have shown a zone of slow conduction extending superiorly from the ventriculotomy scar to the pulmonary valve (Fig. 21.11) [75]. Clockwise rotation about the ventriculotomy scar generally results in an inferior axis tachycardia with LBBB QRS morphology, although RBBB morphologies have been described, presumably representing conduction into the left ventricle and a potentially larger reentrant circuit (Fig. 21.11). Counterclockwise rotation usually causes an LBBB superior axis tachycardia [75]. Patch-associated tachycardia is usually RBBB in morphology, with a superiorly directed frontal plane axis [73]. Radiofrequency ablation considerations. Early surgical ablation approaches advocated for VT associated with repaired

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Target for ablation

Ventriculotomy scar

Site of entrainment

Figure 21.11 Right ventricular voltage map and tracings from a patient with repaired tetralogy of Fallot and recurrent ventricular tachycardia (VT). An extensive area of low voltage involves large segments of the right ventricle (RV) beyond the typical ventriculotomy scar. Macroreentry involving the entire RV was identified using entrainment criteria. Pacing

during VT (right) shows perfect entrainment criteria and inferior axis, despite pacing at a site in the inferior aspect of the RV. A critical isthmus was identified at the top of the ablation scar, where a line of ablation lesions from ventriculotomy incision scar to the pulmonary valve terminated the VT. AP, anteroposterior; PV, pulmonary vein; TV, tricuspid valve.

tetralogy of Fallot included transmural ventriculotomy from the region of the previous ventriculotomy scar to the pulmonary valve and elimination of myocardium with cryoablation at sites of earliest activation [70–77]. Published data describing radiofrequency ablation are limited to case reports and small series. The first successful ablations were described in two patients by Burton and Leon in 1993 [64]. The investigators used pace-mapping during tachycardia (entrainment) and during sinus rhythm to identify likely sites for delivery of radiofrequency energy; successful ablation sites demonstrated entrainment with concealed fusion (surface 12-lead) during tachycardia and a 12/12 perfect pace-map during sinus rhythm. Multiple radiofrequency lesions were necessary. Other investigators have also reported success using pace-mapping in sinus rhythm. Once again, multiple radiofrequency lesions were necessary to achieve arrhythmia control [78]. In our experience as well as that of others, mid-diastolic potentials during tachycardia may be more useful to identify likely slow conduction zone targets for radiofre-

quency energy delivery [76]. However, at least for ventriculotomy-associated tachycardia, the slow conduction zone may be too broad to be spanned by discrete anatomic lesions [77]. Instead, an “anatomic approach” may be required in order to create a fixed line of block connecting the ventriculotomy scar to an anatomic boundary (i.e., the pulmonary or tricuspid valve) [80,81]. This anatomic approach, similar in principle to older surgical approaches, is analogous to radiofrequency ablation of type 1 atrial flutter, where an anatomic line of block is created across the “isthmus” (Fig. 21.11) that the flutter wavefront traverses in an obligatory fashion. To date, however, there are no data regarding which subsets of patients with ventriculotomy-associated tachycardia might benefit from such an anatomic approach, regarding the way in which block should be determined in these patients, or whether complete anatomic block is even necessary to prevent tachycardia recurrence. Furthermore, there has been no systematic appraisal of other methods’ relative value in determining targets for delivery of radiofrequency energy 351

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Ventricular tachycardia

(pace-mapping, entrainment, mid-diastolic potentials, or, potentially, exit-site criteria analogous to those developed for VT associated with coronary artery disease). However, regardless of the method used for targeting ablation sites, preliminary data suggest that acute procedural success, as indexed by noninducibility of VT, is associated with a good medium-term outcome, with no recurrent ventricular tachycardia during a mean follow-up period of up to 15 months [74,82,83]. In summary, ventricular arrhythmias are a known late complication following successful repair of tetralogy of Fallot. These arrhythmias have been shown to be reentrant in mechanism. In most cases, tachycardia originates from the vicinity of the ventriculotomy scar; however, septal origins corresponding to the ventricular septal defect patch have also been described. Importantly, it appears that with annular free wall patches now extending across the pulmonary valve annulus at time of surgical repair, a decreased risk of reentrant VT around the patch may be anticipated. It is always prudent to review the specifics of the patient’s anomaly, and the operative report from the surgical repair, to orient oneself to the anatomical possibilities dictating the VT circuit. Although there are limited data, radiofrequency ablation using pace-mapping/entrainment, mid-diastolic potentials, or anatomic considerations may be successful in acutely eliminating VT. Selected focal lesions or a linear lesion from an anatomic valve boundary to the ventriculotomy septal patch appear effective. Acute procedural success seems to suggest a good medium-term outcome, but until long-term follow-up data are scrutinized, ICD implantation should be considered. The status of LV function, the arrhythmia presentation, and the inducibility of VT after the ablation procedure may all play a role in decision-making regarding the ICD implant. Notably, when patients are being considered for ablative therapy, some authors suggest that those with significant pulmonary valve regurgitation should undergo surgical valve replacement and intraoperative cryoablation of the VT [84].

Nonischemic dilated cardiomyopathy Nonischemic dilated cardiomyopathy may be caused by a myriad of conditions. Any discussion regarding tachyarrhythmia disturbances and their treatment with radiofrequency ablation is therefore limited by the heterogeneity of the disease processes involved. VT-induced cardiomyopathy and bundle branch reentry VT are important considerations in nonischemic cardiomyopathy that are discussed elsewhere in this text. This section focuses on VTs of myocardial origin associated with idiopathic dilated cardiomyopathy. 352

VT of myocardial origin in dilated cardiomyopathy Epidemiological and pathological considerations. Ventricular tachyarrhythmias are quite frequent in dilated cardiomyopathy, with between 42% and 60% of patients showing at least nonsustained VT on 24-h Holter monitoring [85 – 87]. However, the value of electrophysiology studies in stratifying the risk for sudden death in these patients is limited, with lower sensitivity and specificity than for patients with coronary artery disease [88–90]. Signal-averaged ECG may be helpful in predicting adverse outcomes with the development of sustained VT [91], but this is controversial. In idiopathic cardiomyopathy, the degree of fibrosis (as detected by biopsy) has been associated with spontaneous VT on 48-h Holter monitoring [92]. In addition, the degree of myocyte hypertrophy and myofibrillar degeneration has been shown to strongly correlate with spontaneous ventricular ectopy and nonsustained VT [93]. In contrast, ejection fraction, wall stress, and left ventricular mass and dimension are less well correlated with spontaneous arrhythmogenesis [92]. Patchy myocardial fibrosis is extremely common in patients with idiopathic dilated cardiomyopathy. In a large autopsy series including over 150 patients, grossly visible scars were identified in 14% of patients, and histologically evident fibrosis was noted in 57%. Generally, the left ventricle is more affected by fibrosis [94]. Myocardial fibrosis and myofibrillar destruction, which may be variably located, provide the anatomic substrate for sustained VTs. This fibrosis tends to predominate in perivalvular areas in patients with sustained unimorphic ventricular tachycardia and coincides with the well-described anatomic substrate in these patients (Figs. 21.10, 21.12–21.14). Electrophysiological considerations. Endocardial mapping studies during sinus rhythm have shown that abnormal, fractionated, and/or late electrograms are less frequently seen in patients with dilated cardiomyopathy and ventricular arrhythmia than in patients with coronary artery disease [95]. Notably, the overall incidence of abnormal epicardial electrograms roughly equals the incidence of abnormal endocardial electrograms in patients with dilated cardiomyopathy and monomorphic VT [96]. Importantly, endocardial abnormalities predominate in some patients, while epicardial abnormalities predominate in others. These electrogram abnormalities correspond to areas of focal fibrosis and myofibrillar destruction, which provide the substrate for tachycardia. As a result, VTs associated with dilated myopathy may have deep myocardial or epicardial routes of reentrant conduction in focal origin instead of, or in addition to, an endocardial origin more typically associated with infarct-related VT. This may help explain the relatively reduced success rate of standard endocardial

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Inferior

Lateral

Figure 21.12 Bipolar endocardial voltage map from a patient with nonischemic left ventricular cardiomyopathy and ventricular tachycardia. The low-voltage area extends along the inferior and lateral aspects of the mitral valve.

catheter ablation in patients with dilated myopathies compared to those with ischemic cardiomyopathy. A subxiphoid pericardial approach that accesses the epicardium has become routine at our institution in attempting to identify and ablate epicardial VT in this setting (Fig. 21.15). While some animal models of dilated cardiomyopathy have shown VT that is not due to reentry [97,98], in humans reentry is an important mechanism for at least some monomorphic VTs [99,100]. In patients presenting with sustained VT, clinical VTs can usually be induced by programmed stimulation [88–90,101,102]. Induced tachycardias may manifest mid-diastolic potentials and demonstrate entrainment [99]. Delacretaz et al. [103] noted three mechanisms of VT in dilated cardiomyopathy: myocardial reentry (62%), bundle branch/fascicular reentry (19%), and focal VT (27%). More recent data from the same institution included epicardial mapping in select patients [104], with these mechanisms being found in similar frequencies. Although most VTs appear to arise from the left ventricle, perhaps due to the relative predominance of interstitial fibrotic changes compared to the right ventricle, VTs originating from the basal RV septum and free wall have been noted in patients with cardiomyopathy involving both ventricles (Fig. 21.6) [94,99]. Recent evidence from

our institution has shown that scarring is seen most commonly at the base of the LV (100%; 5% also had apical scar), frequently involving the mitral annulus (Figs. 21.12–21.14) [105]. In addition, most VTs (88%) were found to be reentrant and originated from the basal LV. Similarly, Soejima and colleagues [104] found that scarring was most frequently adjacent to a valve annulus (63%) and that scars mapped both endocardially and epicardially had a larger epicardial surface area. Ablation considerations. Early experience with endocardial radiofrequency ablation has been less successful in the cohort of patients with idiopathic cardiomyopathy in comparison with infarct-associated VT, although in selected patient subgroups, acute ablation success rates may be higher. Acute success rates of 67–85%, with no recurrence of successfully ablated VT, have been reported [99,100]. Ablation sites were selected based on mid-diastolic potentials, earliest presystolic electrical activity, entrainment mapping, and pace-mapping in these series. More recently, Soejima et al. [104] attempted ablation in 20 of 22 patients with myocardial reentrant VT. Isthmus sites in mappable VT and exit/closest sites in unmappable VT were targeted for radiofrequency (RF) ablation. Eighteen of these patients had RF delivered to the 353

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PART IV

Ventricular tachycardia

Idiopathic LVCM – scar on voltage map and many VTs

Sinus rhythm voltage map

VT1

PM

VT2

VT3

Linear ablation lines

Figure 21.13 Voltage map and location of linear lesions (brown circles) in a patient with left ventricular cardiomyopathy (LVCM) and multiple poorly tolerated ventricular tachycardias (VTs). The top right panel shows a coronal view of the LV, with a large area of low voltage extending from the

perivalvular mitral and aortic valves. The three VT morphologies and the location of the region of the best pace-map match for one of the VTs are shown. Lines of multiple point lesions extending through the abnormal myocardium to the valve structures are shown in the lower right panel.

endocardium, and five patients had RF delivered to the epicardium at a second session as well. The other two patients had endocardial ablation attempts at other institutions and underwent only epicardial ablation in this series. Six patients underwent successful ablation from the endocardium only, with four other patients considered to have had their VT modified. Failure from the endocardium occurred in 10 patients. Of these, seven underwent epicardial ablation attempts using the technique developed by Sosa and colleagues [106], six of which were successful. During a follow-up period of 334 ± 280 days, 54% of the patients with myocardial reentrant VT remained arrhythmiafree, despite frequent episodes before ablation. At our institution, we used both focal ablation and linear lesion formation to target 39 of 57 VTs in 19 patients

[105]. Thirty VTs were rendered noninducible acutely (in 14 patients). After a follow-up period of 22 ± 12 months, five patients were alive and without VT, eight were alive with rare VT (< 1 event per 6 months), four had died, and two had undergone transplantation. Nearly all VTs were localized to the LV perivalvular region. Our strategies for ablating VT that is poorly tolerated resemble those used in patients with RV and coronary artery disease, with the outcome using endocardial linear lesions being less successful than with the other disease processes (Table 21.1). The less effective outcome has been attributable to an epicardial substrate for VT in selected patients. Unfortunately, the presence of extensive epicardial fat and coronary vasculature precludes simple application of endocardial bipolar voltage criteria to define the extent of the epicardial scar (Fig. 21.16).

354

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Linear RF

Pacemap VT

Figure 21.14 Lateral view of a left ventricular endocardial bipolar voltage map. Poorly tolerated ventricular tachycardia (VT) was successfully eliminated by identifying the pace-map site matching the VT and creating a

linear lesion that crossed a channel of larger-amplitude signals surrounded by lower-amplitude signals and then extended to the mitral valve annulus. RF, radiofrequency.

In summary, radiofrequency ablation for VT in patients with dilated cardiomyopathy can be successful in highly selected subgroups. Emerging technology for mapping, energy delivery, and targeting epicardial surfaces may help improve success rates. Because of the limited data available, optimal criteria for ablation and site selection for ablation are not firmly established. However, it is clear that a VT origin in proximity to the LV valvular structures is common and should be the initial target region for mapping. Aggressive ablation attempts may be required in regions of dense endocardial scar, and an irrigated-tip RF ablation catheter may be required. An epicardial site of origin should be suspected in the absence of an extensive endocardial substrate. ECG clues suggesting an epicardial origin include a QS complex in lead 1 for VT originating from the basal perivalvular region [3]. Other clues can be identified by assessing the morphologic features of the VT in comparison with endocardial pace-maps. VT marked by a wider QRS, a delayed nadir of an S wave, or a more negative QRS complex in leads 1 and aVL in comparison with endocardial pacing sites, creating comparable QRS

morphologies, are definite clues that epicardial mapping and ablation may be required. The role of epicardial fat in confounding substrate assessment at the time of epicardial mapping [107] is becoming more evident. Epicardial ablation should target sites identified on the basis of activation mapping, with care being taken to avoid the coronary arteries. A substrate-based ablation strategy based on the electrogram amplitude to identify abnormal epicardium awaits investigation in determining the effect of fat and coronary vasculature on bipolar signal amplitude parameters (Fig. 21.16).

Infiltrative myopathies: sarcoidosis and Chagas’ disease Sarcoidosis Epidemiological and pathological considerations. Sarcoidosis, a multisystemic granulomatous disease of unknown origin, most frequently presents with mediastinal, pulmonary, and skin or eye involvement. The incidence of clinically 355

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B.A

Epicardial site of origin of VT Epicardial activation early

B

VT

* Endocardial activation late

C

Mid diastolic electrograms

Figure 21.15 Ventricular tachycardia (VT) originating from the left ventricular (LV) epicardium in a patient with nonischemic cardiomyopathy. A. Activation maps of the LV endocardium and epicardium. At the earliest site of activation (identified with the color red and the yellow asterisk on the LV epicardium), a mid-diastolic potential is recorded (shown in B) and

perfect entrainment (not shown) was demonstrated. B. The QS complex in electrocardiogram leads I and aVL suggests an epicardial origin. C. Cine angiography confirmed that the catheter was positioned away from major coronary arteries. Catheter ablation at this epicardial region successfully eliminated the VT.

apparent cardiac abnormalities in sarcoid patients is relatively low (5–13%) [108,109]. Pathological cardiac involvement at autopsy has been demonstrated in 27–60% of patients with systemic sarcoidosis [109,110]. Clinical cardiac manifestations of sarcoidosis include conduction disturbances, paroxysmal arrhythmias, and far less frequently, heart failure. Sudden death due to bradyarrhythmias and tachyarrhythmias has been observed in as many as two-thirds of patients with documented cardiac sarcoidosis [108,110]. Cardiac sarcoid lesions are usually microscopic, consisting of either focal granulomas or discrete areas of fibrosis [109,110]. Because of the patchy nature of involvement, cardiac sarcoid may be missed by endomyocardial biopsy [111]. Various imaging modalities (e.g., nuclear studies,

MRI) may be more useful for monitoring disease activity [112–114]. Patients with widespread granulomas and myocardial fibrosis generally have arrhythmias and often die suddenly [109,115], but even asymptomatic patients with previously electrically “silent” lesions may experience ventricular tachyarrhythmias [108,109,116]. Rarely, sustained VT and congestive cardiomyopathy may be the only signs of systemic sarcoidosis with cardiac involvement [117]. There are no studies that specifically address the electrophysiological risk stratification of asymptomatic cardiac sarcoid patients.

356

Electrophysiological considerations. There are few data describing the electrophysiological characteristics of ventricular arrhythmias associated with cardiac sarcoidosis.

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Voltage maps suggesting epicardial scar

Figure 21.16 Epicardial fat confounding the interpretation of epicardial electrogram voltage characteristics when attempting substrate mapping for ventricular tachycardia (VT) in a patient with left ventricular cardiomyopathy. A. The voltage map from the endocardium demonstrated normal left ventricular electrograms (purple with a signal amplitude greater than 2.0 mV). LAO, left anterior oblique. B. The epicardial voltage map obtained via subxiphoid pericardial puncture (C) demonstrated extensive areas of low voltage, including the apical segment. AP, anteroposterior. D. The heart, obtained from cardiac transplantation, shows large areas of thick epicardial fat, but no scar. The effect of epicardial fat and the coronary vasculature on the epicardial voltage criteria needs to addressed if voltage mapping is to be used as an effective tool for targeting the epicardial substrate for VT using the same linear lesion approach applied successfully for endocardial VTs. RF, radiofrequency.

A

> 2.0mV

B

A b n o r m a l

Normal

LAO Endocardial

C

D Epi RF lesion

< 0.5mV

AP Epicardial

It is speculated that ventricular myocardial scarring produced by sarcoid granulomas provides the substrate for reentrant arrhythmias [115,116]. Inducibility of monomorphic VT with programmed stimulation in at least some of these patients also supports a reentrant mechanism [115,118,119]. The surface electrocardiogram morphology of inducible VT in cardiac sarcoidosis varies. Varying morphologies and cycle lengths have been described [116,118,119]. We have seen recurrent VT in cardiac sarcoid patients with minimal ventricular dysfunction. In these patients, multiple morphologies of tachycardia were inducible, all arising from the basal septum or the posterolateral left ventricle with corresponding 201Tl defects (unrelated to coronary artery disease) in these anatomic distributions. Unfortunately, there are no data describing radiofrequency ablation methods, acute success, and/or long-term success in patients with cardiac sarcoid. Given the diffuse and often progressive nature of the disease process, one might speculate that tachyarrhythmia recurrence would prove the rule. In addition, similar to other nonischemic cardiomyopathies, an effort to characterize in detail the endocardial and epicardial substrate and target epicardial

Endo RF lesion

Epicardial fat PA

LOW VOLTAGE - EPICARDIAL FAT

VT sites of origin should be anticipated. In our experience, patients with sarcoid or sarcoidosis and VT have lowvoltage areas mapped to the basal ventricle (right or left). VT is often mapped to these areas and can be successfully ablated.

Chagas’ disease Epidemiological and pathological considerations. Chagas’ disease is a major cause of cardiac dysfunction in Latin America. The causative parasite, Trypanosoma cruzi, is spread to humans via an insect vector, the reduviid bug. Recent data suggest that 16 million people, or more than 4% of the population, are infected in Latin American countries. In certain areas, seropositivity as assayed by blood donors exceeds 60% [120]. In North America, the incidence of Chagas’ disease has been increasing, owing perhaps to increasing immigrant populations. Seropositivity is observed in one in 7500 voluntary blood donors in Los Angeles and in one in 9000 in Miami [121]. Following acute infection, most patients are asymptomatic. After a latent period that can last decades, 10–40% of seropositive patients develop chronic heart disease. 357

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Manifestations can include congestive heart failure, conduction abnormalities, bradyarrhythmias, tachyarrhythmias, syncope, and sudden death [122,123]. The latter may account for up to 30% of deaths in patients with Chagas’ disease. Interestingly, patients with Chagas’ disease who present with hemodynamically tolerated monomorphic ventricular tachycardia usually do not have severe myocardial disease and appear to have a relatively good prognosis [124]. In contrast, patients who present with recurrent syncope that is ascribed to VT on the basis of electrophysiological study generally have a poorer prognosis [122]. The causative role of the parasite in chronic chagasic cardiomyopathy is not fully clarified. Active parasitemia is not a prominent feature, leading to the speculation that autoimmune, neurogenic, and microvascular processes are involved in the development of chagasic cardiomyopathy. However, Bellotti et al. have demonstrated that detection of T. cruzi antigen correlates with the presence of moderate or severe myocarditis both in autopsy specimens and in patients undergoing MRI-guided endomyocardial biopsy [125]. Furthermore, using a Langendorff-perfused rabbit heart model, de Carvalho and colleagues have shown that exposure of adult rabbit hearts to sera from chronic chagasic rabbits results in acute abnormalities of sinus node automaticity and conduction [126]. It is not known whether these findings also apply in humans. Electrophysiological considerations. Patients with Chagas’ disease who present with hemodynamically tolerated VT usually have baseline ventricular premature depolarizations, ST and T wave abnormalities, and left axis deviation. Unlike “classic” patients with chronic chagasic cardiomyopathy, right bundle branch block is often not present at baseline, and left ventricular function is usually not severely depressed [124]. In the majority of patients, the clinical arrhythmia can be reproducibly initiated with programmed stimulation, implying a reentrant mechanism. The surface ECG QRS morphology during ventricular tachycardia may vary from patient to patient [127,128]. Not unlike ARVC and idiopathic cardiomyopathy, a basal site of VT origin appears common even in patients who have apical aneurysmsaspecifically, the inferolateral wall, near the mitral annulus (Fig. 21.17) [129]. There are limited but growing data regarding catheter ablation of VT associated with Chagas’ disease. In a very small group, electrical fulguration controlled the clinical arrhythmia in approximately 50% of patients [129–131]. One case report describes the use of intracoronary ethanol to successfully ablate a VT [132]. Endocardial RF ablation was described in a case series of 11 consecutive patients with 14 clinical tachycardias [133]. In this small group, sites of RF ablation using a catheter with an 8-mm tip were classified as “successful” or “unsuccessful” depending on whether tachycardia terminated during RF energy delivery. In 358

Chagas’ disease Location of LV site of origin of sustained VT

Mapped LV VT: 82

65 VT (79.3%) 11 VT (13.4%) 6 VT (7.3%)

Figure 21.17 Distribution of the left ventricular sites of origin of ventricular tachycardia (VT) in patients with Chagas’ disease. Most VTs originate near the perivalvular regions, consistent with other forms of nonischemic cardiomyopathy. LV, left ventricle. (Adapted with permission from [134], courtesy of Dr. Andre d’Avila.)

comparison with unsuccessful sites (n = 99), successful sites (n = 38) were more likely to show: entrainment or concealed entrainment (74% vs. 48%; P < 0.05); a post-pacing interval tachycardia cycle length difference of < 20 ms (32% vs. 21%); and smaller-amplitude local ventricular electrograms (0.44 ± 0.35 mV vs. 0.54 ± 0.52 mV). Neither local ventricular electrogram duration nor presystolic activity was predictive of successful versus unsuccessful sites, although all successful sites had at least 30 ms of presystolic activity. In the overall group of 11 patients with 14 clinical tachycardias, nine tachycardias were rendered noninducible (a 64% acute success rate); one of these recurred during the follow-up period of 12 ± 7 months. Ten patients remained on antiarrhythmic therapy. Scanavacca et al. [134] described successful RF ablation by interruption of an isthmus between the mitral annulus and perivalvular myocarditic scar. The technique of percutaneous subxiphoid pericardial puncture for epicardial access was introduced for mapping and ablation of chagasic VT [106]. Recent data suggest that acute ablation success rates may be higher if epicardial mapping and ablation are used. Sosa and colleagues reported 10 consecutive patients with Chagas’ disease and 18 mappable VTs in whom percutaneous epicardial mapping and RF ablation were carried out [135]. Coronary angiography was performed at the time of the study to avoid potential complications from RF energy delivery on or near major epicardial arteries. In 14 of the VTs, an epicardial circuit was seen (defined as earliest activation in comparison with the endocardium, concealed entrainment with similar return cycle only seen in the epicardium, mid-diastolic potentials and/or continuous electrical activity, and inducible VT abolished by RF

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ablation). RF energy was delivered to the epicardial surface in six patients and to the endocardial surface in four patients (guided by epicardial mapping). In the latter four patients, the clinical VT was still inducible at the end of the procedure. In contrast, in the six patients in whom RF energy was delivered to the epicardial surface, the targeted VT was no longer inducible following ablation. There were no recurrences in this group after 4–9 months. One patient experienced hemopericardium after withdrawal of the epicardial catheter, which was drained without incident. In summary, the limited data suggest that RF ablation of VT associated with chagasic cardiomyopathy may be acutely successful in at least half of the patients. If acutely successful, ablation is usually associated with freedom from recurrence of the clinical tachycardia for at least the medium term. The optimal strategy for targeting sites for RF energy delivery includes assessment of the endocardial and epicardial substrate, anticipation of a perivalvular endocardial VT origin in most cases, and the common occurrence of epicardial origin. An aggressive approach to endocardial and epicardial activation mapping and ablation appears effective.

Conclusions and future directions In comparison with the literature describing RF ablation of VT associated with coronary artery disease, the published data on patients with nonischemic structural heart disease are limited, but are growing. The presence of perivalvular abnormalities providing an arrhythmia substrate is a common theme across many of these diseases. Ablation strategies targeting these areas have shown promise. The introduction of a percutaneous epicardial mapping and ablation technique by Sosa and colleagues [135] has revolutionized the approach to these patients. The further success of ablation for VT in nonischemic cardiomyopathy may very well depend on the development of more effective ablation modalities.

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85 Huang SK, Messer JV, Denes P. Significance of ventricular tachycardia in idiopathic dilated cardiomyopathy: observations in 35 patients. Am J Cardiol 1983;51:507–12. 86 Meinertz T, Hofmann T, Kasper W, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984;53:902–7. 87 von Olshausen K, Schafer A, Mehmel HC, Schwarz F, Senges J, Kubler W. Ventricular arrhythmias in idiopathic dilated cardiomyopathy. Br Heart J 1984;51:195 –201. 88 Milner PG, Dimarco JP, Lerman BB. Electrophysiological evaluation of sustained ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy. Pacing Clin Electrophysiol 1988;11:562–8. 89 Poll DS, Marchlinski FE, Buxton AE, Josephson ME. Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy. Am J Cardiol 1986;58:992–7. 90 Chen X, Shenasa M, Borggrefe M, et al. Role of programmed ventricular stimulation in patients with idiopathic dilated cardiomyopathy and documented sustained ventricular tachyarrhythmias: inducibility and prognostic value in 102 patients. Eur Heart J 1994;15:76–82. 91 Mancini DM, Wong KL, Simson MB. Prognostic value of an abnormal signal-averaged electrocardiogram in patients with nonischemic congestive cardiomyopathy. Circulation 1993;87:1083–92. 92 Pelliccia F, Critelli G, Cianfrocca C, et al. Interstitial fibrosis as a substrate of spontaneous nonsustained ventricular tachycardia in idiopathic dilated cardiomyopathy [abstract]. J Am Coll Cardiol 1994;23:340A. 93 Lo YS, Billingham M, Rowan RA, Lee HC, Liem LB, Swerdlow CD. Histopathologic and electrophysiologic correlations in idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmia. Am J Cardiol 1989;64:1063 –6. 94 Roberts WC, Siegel RJ, McManus BM. Idiopathic dilated cardiomyopathy: analysis of 152 necropsy patients. Am J Cardiol 1987;60:1340–55. 95 Cassidy DM, Vassallo JA, Miller JM, et al. Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias. Circulation 1986;73:645–52. 96 Perlman R, Miller J, Kindwall K, Buxton A, Josephson M, Marchlinski F. Abnormal epicardial and endocardial electrograms in patients with idiopathic dilated cardiomyopathy: relationship to arrhythmias [abstract]. Circulation 1990;82:I708. 97 Pogwizd SM. Nonreentrant mechanisms underlie spontaneously occurring ventricular arrhythmias in dilated cardiomyopathy [abstract]. Circulation 1993;88:I326. 98 Pogwizd S, McKenzie J, Cain M. Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy. Circulation 1998;98: 2404–14. 99 Kottkamp H, Hindricks G, Chen X, et al. Radiofrequency catheter ablation of sustained ventricular tachycardia in idiopathic dilated cardiomyopathy. Circulation 1995;92:1159 –68. 100 Wilber D, Glascock D, Kail J, et al. Radiofrequency catheter ablation of sustained ventricular tachycardia associated with idiopathic dilated cardiomyopathy [abstract]. Circulation 1995;92:I684. 362

101 Constantin L, Martins JB, Kienzle MG, Brownstein SL, McCue ML, Hopson RC. Induced sustained ventricular tachycardia in nonischemic dilated cardiomyopathy: dependence on clinical presentation and response to antiarrhythmic agents. Pacing Clin Electrophysiol 1989;12:776 – 83. 102 Liem LB, Swerdlow CD. Value of electropharmacologic testing in idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmias. Am J Cardiol 1988;62:611– 6. 103 Delacretaz E, Stevenson W, Ellison K, Maisel WH, Friedman PL. Mapping and radiofrequency catheter ablation of the three types of sustained monomorphic ventricular tachycardia in nonischemic heart disease. J Cardiovasc Electrophysiol 2000;11:11–7. 104 Soejima K, Stevenson W, Sapp J, Selwyn A, Couper G, Epstein LM. Endocardial and epicardial radiofrequency ablation of ventricular. J Am Coll Cardiol 2004;43:1834 –42. 105 Hsia HH, Callans DJ, Marchlinski FE. Characterization of endocardial electrophysiological substrate in patients with nonischemic cardiomyopathy and monomorphic ventricular tachycardia. Circulation 2003;108:704–10. 106 Sosa E, Scanavacca M, d’Avila A, Pilleggi F. A new technique to perform epicardial mapping in the electrophysiology. J Cardiovasc Electrophysiol 1996;7:531– 6. 107 Dixit S, Narula N, Callans D, Marchlinski FE. Electroanatomic mapping of human heart: epicardial fat can mimic scar. J Cardiovasc Electrophysiol 2003;14:1128. 108 Mayock RL, Bertrand P, Morrison CE, Scott JH. Manifestations of sarcoidosis: analysis of 145 patients, with a review of nine series selected from the literature. Am J Med 1963;35:67–89. 109 Silverman KJ, Hutchins GM, Bulkley BH. Cardiac sarcoid: a clinicopathologic study of 84 unselected patients with systemic sarcoidosis. Circulation 1978;58:1204 –11. 110 Matsui Y, Iwai K, Tachibana T, et al. Clinicopathological study of fatal myocardial sarcoidosis. Ann N Y Acad Sci 1976;278:455 –69. 111 Fleming HA. Sarcoid heart disease. Br Heart J 1980;43:366. 112 Tawarahara K, Kurata C, Okayama K, Kobayashi A, Yamazaki N. Thallium-201 and gallium-67 single photon emission computed tomographic imaging in cardiac sarcoidosis. Am Heart J 1992;124:1383 – 4. 113 Alberts C, van der Schoot JB, Groen AS. 67Ga scintigraphy as an index of disease activity in pulmonary sarcoidosis. Eur J Nucl Med 1981;6:205 –12. 114 Kinney EL, Jackson GL, Reeves WC, Zelis R. Thallium-scan myocardial defects and echocardiographic abnormalities in patients with sarcoidosis without clinical cardiac dysfunction: an analysis of 44 patients. Am J Med 1980;68:497–503. 115 James TN. Clinicopathologic correlations. De subitaneis mortibus. XXV. Sarcoid heart disease. Circulation 1977;56: 320 – 6. 116 Paz HL, McCormick DJ, Kutalek SP, Patchefsky A. The automated implantable cardiac defibrillator: prophylaxis in cardiac sarcoidosis. Chest 1994;106:1603 –7. 117 Lopez JA, Hogan PJ, Fish RD, Capek P, Perin EC. Cardiac sarcoidosis: an unusual form of acute congestive cardiomyopathy. Tex Heart Inst J 1995;22:265 –7. 118 Winters SL, Cohen M, Greenberg S, et al. Sustained ventricular tachycardia associated with sarcoidosis: assessment of the underlying cardiac anatomy and the prospective utility

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Ablation of ventricular tachycardia associated with nonischemic structural heart disease

of programmed ventricular stimulation, drug therapy and an implantable antitachycardia device. J Am Coll Cardiol 1991;18:937–43. Huang PL, Brooks R, Carpenter C, Garan H. Antiarrhythmic therapy guided by programmed electrical stimulation in cardiac sarcoidosis with ventricular tachycardia. Am Heart J 1991;121:599–601. Personal Perspective: New initiative will halt Chagas disease in six years. WHO: TDR news. August 1992;40:3 –5. Leiby DA, Herron RM Jr, Read EJ, Lenes BA, Stumpf RJ. Trypanosoma cruzi in Los Angeles and Miami blood donors: impact of evolving donor demographics on seroprevalence and implications for transfusion transmission. Transfusion 2002;42:549–55. Martinelli Filho M, Sosa E, Nishioka S, Scanavacca M, Bellotti G, Pileggi F. Clinical and electrophysiologic features of syncope in chronic chagasic heart disease. J Cardiovasc Electrophysiol 1994;5:563–70. Andrade Z. Mechanisms of myocardial damage in Trypanosoma cruzi infection. In: Cytopathology of Parasitic Disease: Organized by the Ciba Foundation, London, U.K., in Partnership with the Centro Me´dico Docente la Trinidad, Caracas, Venezuela. London: Pitman, 1983: 214–33. (Ciba Foundation symposium, 99.) Bestetti RB, Santos CR, Machado-Junior OB, et al. Clinical profile of patients with Chagas’ disease before and during sustained ventricular tachycardia. Int J Cardiol 1990;29:39– 46. Bellotti G, Bocchi EA, de Moraes AV, et al. In vivo detection of Trypanosoma cruzi antigens in hearts of patients with chronic Chagas’ heart disease. Am Heart J 1996;131:301–7. de Carvalho AC, Masuda MO, Tanowitz HB, Wittner M, Goldenberg RC, Spray DC. Conduction defects and arrhythmias in Chagas’ disease: possible role of gap junctions and

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humoral mechanisms. J Cardiovasc Electrophysiol 1994;5:686– 98. Mendoza I, Camardo J, Moleiro F, et al. Sustained ventricular tachycardia in chronic chagasic myocarditis: electrophysiologic and pharmacologic characteristics. Am J Cardiol 1986;57:423 –7. Giniger AG, Retyk EO, Laino RA, Sananes EG, Lapuente AR. Ventricular tachycardia in Chagas’ disease. Am J Cardiol 1992;70:459 –62. Rosas F, Velasco V, Arboleda F, et al. Catheter ablation of ventricular tachycardia in Chagasic cardiomyopathy. Clin Cardiol 1997;20:169 –74. Galvao S, Medeiros J, Santos RA. Treatment of recurrent ventricular tachycardia by endocardial catheter fulguration in patients with Chagas’ cardiomyopathy [abstract]. European Journal of Cardiac Pacing and Electrophysiology 1992;2:153. Sosa E, Scalabrini A, Rati M, et al. Successful catheter ablation of the “origin” of recurrent ventricular tachycardia in chronic chagasic heart disease. J Electrophysiol 1987;1:58 –61. de Paola AA, Gomes JA, Miyamoto MH, Fo EE. Transcoronary chemical ablation of ventricular tachycardia in chronic chagasic myocarditis. J Am Coll Cardiol 1992;20:480 –2. de Paola A, Tavora M, Silva R, et al. Radiofrequency catheter ablation of sustained ventricular tachycardia in patients with chronic chagasic cardiomyopathy [abstract]. Pacing Clin Electrophysiol 1996;19:693. Scanavacca M, Sosa E, d’Avila A, De Lourdes Higuchi M. Radiofrequency ablation of sustained ventricular tachycardia related to the mitral isthmus in Chagas’ disease. Pacing Clin Electrophysiol 2002;25:368 –71. Sosa E, Scanavacca M, D’Avila A, et al. Endocardial and epicardial ablation guided by nonsurgical transthoracic epicardial mapping to treat recurrent ventricular tachycardia. J Cardiovasc Electrophysiol 1998;9:229 –39.

363

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Index

ablation see catheter ablation ablation catheters diode laser balloon, 44 large-tip, 24 see also ultrasound ablation catheters ablation electrodes radiofrequency energy dissipation, 21–2 temperature distribution, 20–1 tip size, 24 ablative lesions, assessment, 80 accessory pathways (APs), 91, 93 anatomy, 151 catheter ablation, 92, 93, 149–72 complications, 165 outcomes, 165 in pediatric patients, 94 preprocedure evaluation, 149 risk factors, 149 troubleshooting, 162–3 classification, 151 clinical presentation, 149 comorbidities, 151 cryoablation, 164 definition, 149 electrocardiographic characteristics, 149–51 electrophysiological evaluation, 152–5 localization, 149–51 midseptal, 163–4 multiple, 164 nomenclature, 149, 151 nonatrioventricular, 165–6 radiofrequency ablation, 160–2 see also anteroseptal accessory pathways; atriofascicular pathways; free-wall accessory pathways; posteroseptal accessory pathways; right-sided accessory pathways activation mapping, 63, 64, 66 and pace-mapping compared, 282–5 three-dimensional, 290–1

activation sequence mapping, 49, 68 paced, 112–13 procedures, 50–1 acute marginal vein, 14 adenosine, 105–6 AF see atrial fibrillation (AF) AFFIRM see Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) AFL see atrial flutter (AFL) anatomic imaging, 64–5 in electrophysiology, 73 anatomy accessory pathways, 151 arrhythmias and, 72–3 cytoskeleton, 25–6 mammalian cells, 25–6 mapping systems, 64–5 nucleus, 26 plasma membrane, 25 verapamil-sensitive fascicular ventricular tachycardia, 299 –300 see also heart anatomy; integrated, anatomy-based mapping anterior descending coronary artery, 13 anterior left atrium, transection, 242–3 anterior septum, 9, 10 anteroseptal accessory pathways, 152, 163 – 4 characterization, 164 anticoagulation, 94 antidromic reciprocating tachycardia (ART), 149 antidromic wavefronts, 56 aorta, 4, 5, 12 aortic mound, 7 aortic root, 4 imaging, 77, 83 aortic sinuses, 12–13 aortic valve, 4, 10, 11, 12 imaging, 75 APs see accessory pathways (APs)

arrhythmias and anatomy, 72–3 catheter ablation, 3 in congenital heart disease, 95 –6 physiology, 72–3 ventricular, 267 see also atrial arrhythmias arrhythmogenesis origins, 72–3 and right atrium, 81 arrhythmogenic right ventricular cardiomyopathy (ARVC), 280, 281 diagnosis, 279, 281 multiple arrhythmogenic mechanisms, 348 prevalence, 343 and radiofrequency catheter ablation, 342 and ventricular tachycardia radiofrequency catheter ablation, 343 –50 diagnostic issues, 343 – 4 electrophysiological issues, 344 – 8 epidemiology, 343 – 4 outcomes, 350 pathology, 343– 4 studies, 348–50 arrhythmogenic right ventricular dysplasia, diagnosis, 279 ART (antidromic reciprocating tachycardia), 149 ARVC see arrhythmogenic right ventricular cardiomyopathy (ARVC) atrial activation detour, 238 –9 atrial arrhythmias ablation, 80–3 and anatomy, 72 atrial biopsies, cryoablation, 36 –7 atrial chambers anatomy, 4–9 see also left atrium (LA); right atrium (RA) 365

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Index atrial epicardial lesions, infrared coagulator studies, 45–6 atrial fibrillation (AF), 7, 219–75 and atrioventricular junction ablation, 268–9 catheter ablation, 81–3, 205–6 development, 221 electrophysiological substrate mapping, 250–60 remote magnetic navigation, 234 catheter ablation energy sources, 35 characterization, 261 chronic, 246–7 complex fractionated atrial electrogram ablation guidance, 250–60 complications, 259 long-term outcomes, 257 and complex fractionated atrial electrograms, 254–6 costs, 221 cryoablation, 37 electrocardiographic changes, 239–40 electrograms, 250–1 and ganglion plexuses, 65– 6 linear lesions in treatment of, 237–49 mechanisms, 60, 227 implications for ablation, 223–5 microwave catheter ablation, 39– 40 physiology, 261 prevalence, 221, 237, 261 and pulmonary veins, 64, 67, 72–3 rate control ablation, 261–75 optimal, 262 strategies, 261–2 and stroke, 221 substrate, 65–7 substrate mapping, 252–4 conventional, 252 three-dimensional mapping, 60–71 future trends, 69–70 triggers, 65–7 ventricular rate, determination, 261–2 see also paroxysmal atrial fibrillation (PAF) Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM), 237 findings, 221 issues, 221 atrial flutter (AFL) catheter ablation, management of difficult cases, 187 cryoablation, 38 entrainment mapping, 53, 54 macroreentrant, 50, 51 nomenclature, 173 type 2, 173 366

voltage mapping, 61–2, 63 see also lower loop reentry atrial flutter; reverse typical atrial flutter; type 1 atrial flutter; typical atrial flutter atrial septum, anatomy, 8–9 atrial tachyarrhythmias, and complex fractionated atrial electrogram ablation guidance, 259 atrial tachycardias (ATs) activation sequence mapping, 50–1 annular, 115 anteroseptal, 107 and crista terminalis, 81 entrainment mapping, 58 midseptal, 107 posteroseptal, 108 septal, 115 see also ectopic atrial tachycardia (EAT); focal atrial tachycardia; intra-atrial reentrant tachycardia (IART); macroreentrant atrial tachycardias (macro-ATs); macroreentrant left atrial tachycardia; macroreentrant right atrial tachycardia atrio-esophageal fistulas, in atrial fibrillation ablation, 85 atriofascicular (Mahaim) fibers, 93 atriofascicular pathways, 149 catheter ablation, 167–9 electrocardiographic properties, 166 –7 electrophysiological properties, 166 –7 mapping, 167–9 atrioventricular block, 164 ultrasound catheter ablation studies, 41 atrioventricular conduction bundle of His, 15, 16 atrioventricular conduction system, anatomy, 14–16 atrioventricular junction ablation, 31, 261 complications, 266–8 consequences, 268–9 future trends, 272 and pacemaker dependency, 268 and permanent atrial fibrillation, 268 –9 post-ablation device implantation, 269 –70 and thromboembolism, 268 see also atrioventricular node (AVN) ablation atrioventricular junctions, anatomy, 9 –10

atrioventricular nodal lesions, reversibility studies, 36 atrioventricular nodal reentrant tachycardia (AVNRT) catheter ablation, 120 – 48 circuits, 120 cryoablation studies, 36, 37– 8 definition, 120, 121 diagnosis, 120 entrainment mapping, 58 fast pathway, 6 lower common pathway, 130 –2, 145 – 6 prevalence, 120 slow pathway, 6 types of, 120 see also fast/slow atrioventricular nodal reentrant tachycardia; slow/fast atrioventricular nodal reentrant tachycardia; slow/slow atrioventricular nodal reentrant tachycardia atrioventricular node (AVN), 10, 15 anatomy, 15–16 injury risk minimization, 97 atrioventricular node (AVN) ablation and atrioventricular node modification compared, 272 complications, 266 – 8 contraindications, 270 effects on cardiac performance, 263 on exercise tolerance, 263 on health resource consumption, 263 on left ventricular function, 263 on quality of life, 263 on symptoms, 263 future trends, 272 and heart failure, 268 indications, 270 outcomes, clinical, 262–3 post-ablation device implantation, 269 –70 procedures, 264– 6 success rates, 265– 6 and sudden death, 267 survival analysis, 263 –4 and ventricular arrhythmias, 267 atrioventricular node (AVN) modification, 270 –2 advantages, 271 and atrioventricular node ablation compared, 272 atrioventricular pathways, use of term, 149 AVN see atrioventricular node (AVN) AVN ablation see atrioventricular node (AVN) ablation

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Index AVN modification see atrioventricular node (AVN) modification AVNRT see atrioventricular nodal reentrant tachycardia (AVNRT) Bachmann’s bundle, 14 balloon catheters diode laser, 44 fiberoptic, 44 intracardiac ultrasound guidance, 82 basket catheters, 111 bilateral linear ablation extensive, 241–2 limited, 242 bioheat transfer equation, 22 biological tissues, heat transfer models, 22 bipolar mapping, 342–3 bipolar pacing, 58, 282 biventricular pacing, 269–70 blood flow, and hyperthermia, 29 body surface mapping, 110–11 Boston Children’s Hospital (US), 97, 98 Brockenbrough puncture technique, 92 cAMP (cyclic adenosine monophosphate), 281 cardiac anatomy see heart anatomy cardiac chambers atrial, 4–9 spatial relationships, 4, 5 ventricles, 10–13 see also left atrium (LA); right atrium (RA) cardiac conduction system, anatomy, 14–16 cardiac electrophysiology field of study, 72 intracardiac echocardiography in, 72–90 cardiomyopathy idiopathic dilated, 342 nonischemic, and ventricular tachycardia radiofrequency catheter ablation, 342–3 see also arrhythmogenic right ventricular cardiomyopathy (ARVC); infiltrative myopathies; nonischemic dilated cardiomyopathy Carto mapping, 64, 67, 113 atrial fibrillation, 252 left atrium, 228–9 type 1 atrial flutter, 187, 188, 189 catheter ablation accessory pathways, 92, 93, 149–72 alternative energy sources, 35–48 cryoablation, 35–8 infrared, 44–6

laser, 43–4 microwave, 38–40 ultrasound, 41–3 atrioventricular nodal reentrant tachycardia, 120–48 children, 293– 4 focal atrial tachycardia, 105–19 and heart anatomy, 3–19 idiopathic right ventricular outflow tract ventricular tachycardia, 279 –97 left ventricular outflow tract ventricular tachycardia, 309 macroreentrant atrial tachycardias, 193 –217 mapping for, 49–59 in pediatric patients, 91–101, 293–4 post-myocardial infarction ventricular tachycardias, 314–25 radiofrequency energy, electrical characteristics, 20–2 reverse typical atrial flutter, 173–92 substrate modification, 237–8 tachycardias, 91 typical atrial flutter, 173–92 in young patients, 91–101, 293–4 atrioventricular node injury risk minimization, 97 biophysics and safety issues, 96 –7 catheter manipulation, 92 congenital heart disease issues, 93 – 4, 95 –6, 98 –9 electrophysiological issues, 94 –6 immature myocardium features, 96 –7 incessant tachycardias with secondary cardiomyopathy, 94 –5 indications, 98–9 natural history of accessory pathways, 94 outcomes, 97–8 patient characteristics, 97 sedation, 91–2 technical issues, 91–4 vascular access, 92 see also cryoablation; infrared catheter ablation; laser catheter ablation; microwave catheter ablation; radiofrequency catheter ablation (RFCA); ultrasound catheter ablation catheter ablation for cardiac arrhythmias, field of study, 3 catheters basket, 111 deflectable, 92

intrapericardial, 86 ultrathin, 92 see also ablation catheters; balloon catheters; cryocatheters catheter-tip thermometry, 79 catheter–tissue interface, 21 cavotricuspid isthmus (CTI), 173, 174, 175 – 6, 184 ablation, 180 –3, 185, 186 –7, 190 block, 179, 185, 186 cell killing, heat-induced, 26 –7 cellular electrophysiology and hyperthermia, 27–8 in vitro studies, 27–8 cellular metabolism, and hyperthermia, 27 CFAEs see complex fractionated atrial electrograms (CFAEs) Chagas’ disease etiology, 357–8 prevalence, 357 and ventricular tachycardia radiofrequency catheter ablation, 342, 357–9 electrophysiological issues, 358 –9 epidemiological issues, 357– 8 pathological issues, 357– 8 CHD see congenital heart disease (CHD) children, catheter ablation, 91–101, 293 – 4 chronic atrial fibrillation, substrate modification, 246 –7 circumferential pulmonary vein ablation (CPVA), 221–36 advantages, 221 anatomic issues, 223 catheter placement, 226 complications, 231–2 efficacy, 232 future trends, 232– 4 lesion validation, 231 mapping process, 227– 8 mapping system, 228 –30 patient selection, 222–3, 224, 225 postoperative anatomic remodeling, 232 pulmonary vein innervation assessment, 231 and pulmonary vein isolation compared, 222 remap process, 231 safety issues, 231–2 strategies, 230–1 techniques, 226–31 circumflex artery, 13 coagulum formation, 23, 24 removal, 23– 4 367

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Index complex fractionated atrial electrogram ablation guidance atrial fibrillation, 250– 60 and atrial tachyarrhythmias, 259 complications, 259 complex fractionated atrial electrograms (CFAEs), 250 and atrial fibrillation substrates, 254–6 definition, 250–1 electrophysiological mechanisms, 251 persistence, 254 point-to-point mapping, 252–4 regional distribution, 256–7 software, 252–4 congenital heart disease (CHD) and catheter ablation in young patients, 93– 4, 98–9 and postoperative arrhythmias, 17 postoperative arrhythmias, 95–6 preoperative arrhythmias, 95–6 cooled-tip ablation technologies, 24 coronary arteries anatomy, 13 cryoablation studies, 36 coronary sinus, 6, 7, 9 accessory pathways, 162 coronary veins, anatomy, 13–14 CPVA see circumferential pulmonary vein ablation (CPVA) crista terminalis, and atrial tachycardias, 81 cryoablation, 35–8, 135 accessory pathways, 164 adoption issues, 46 advantages, 36, 38 clinical studies, 36–8 disadvantages, 38 and heart block risk, 38 and ice mapping, 36, 38 mechanisms, 35 preclinical studies, 36 and pulmonary vein stenosis, 36, 38 time limitations, 38 tissue injury mechanisms, 35 type 1 atrial flutter, 190 cryocatheters development, 37 studies, 37–8 cryomapping, 36, 38 CTI see cavotricuspid isthmus (CTI) cyclic adenosine monophosphate (cAMP), 281 cytoskeleton anatomy, 25–6 and hyperthermia, 25–6 DC (direct current) ablation, 261 dead-end tract, 16 368

defibrillators appropriate use of, 270 implantable cardioverter, 96, 314–16 deflectable catheters, 92 denatured proteins accumulation, 23–4 see also coagulum differential pacing, techniques, 239 diode laser balloon ablation catheters, 44 diode lasers, 43 preclinical studies, 44 see also laser catheter ablation direct current (DC) ablation, 261 dispersive electrodes, 20–1 diverticula, 158, 159 DNA synthesis, inhibition, 26 Doppler imaging, 77 spectral, 83 Doppler tissue acceleration (DTA) imaging, 80 Doppler tissue energy (DTE) imaging, 80 Doppler tissue velocity (DTV) imaging, 80 EAT see ectopic atrial tachycardia (EAT) Ebstein’s anomaly, and accessory pathways, 151, 163 Ebstein’s malformation, 93, 95 ECG see electrocardiography (ECG) echocardiography diagnostic value of, 279 signal-averaged, 279, 280 transesophageal, 73–4 see also intracardiac echocardiography (ICE) ectopic atrial tachycardia (EAT), 94–5 sedation issues, 92 EGMs see electrograms (EGMs) electroanatomical mapping, 61, 62, 69, 250, 282–5 intra-atrial reentrant tachycardia, 95 left atrium, 227–8 limitations, 233 macroreentrant right atrial tachycardia, 195–8 three-dimensional, 163, 342 ventricular tachycardias, 96 electrocardiography (ECG), 72 atrial fibrillation, 239–40 see also twelve-lead surface electrocardiography electrode–tissue interface temperature, 22, 23 cooling, 24 mean, 31 peak, 24

electrogram recording methods development, 60 electrodes, 50 filtered, 50 for mapping, 49–50 unfiltered, 50 electrograms (EGMs) atrial fibrillation, 250 –1 fractionated, 66–7 high-frequency, 66 –7 local, 239 post-myocardial infarction ventricular tachycardias, 328 –31 see also complex fractionated atrial electrograms (CFAEs); sinus rhythm electrograms electromagnetic mapping, 113 see also Carto mapping electrophysiological substrate mapping, atrial fibrillation catheter ablation guidance, 250 – 60 electrophysiology anatomic imaging in, 73 linear lesions, 238 – 40 see also cardiac electrophysiology endocardial activation mapping, 111 endocardial mapping, idiopathic right ventricular outflow tract ventricular tachycardia, 281– 5 energy titration, guidance imaging, 79 EnSite mapping, 113, 228 –9, 233 type 1 atrial flutter, 187– 8 see also noncontact mapping entrainment with concealed fusion, 56–7 entrainment mapping, 49, 54, 55 applications, 51, 57– 8 classification scheme, 57 limitations, 57 post-myocardial infarction ventricular tachycardias, 320 procedures, 51–3 requirements, 51, 53 entrainment pacing, 195, 198 –200 entrainment response (ER), 55 epicardiac neural plexus, ganglionated subplexuses, 16, 17 epicardial mapping and ablation, postmyocardial infarction ventricular tachycardias, 322 ER (entrainment response), 55 erythrocytes, fragmentation, 26 escape rhythms, 269 esophagus, 4, 5, 8 European Society of Cardiology Task Force, 279 Working Group of Arrhythmias, 173 eustachian ridge, 137, 138 eustachian valve, 5, 7, 8, 137

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Index false tendons, 12, 16 fast/slow atrioventricular nodal reentrant tachycardia, 120, 145–6, 147 catheter ablation, 146 fat pads, 16, 17 fiberoptic balloon catheters, 44 flap valve, 8, 9 fluoroscopic guidance, 78 fluoroscopy, 72, 76, 82 biplanar, 85, 93 limitations, 233 flutter (inferior) isthmus, 5, 6 focal atrial tachycardia, 212–14 catheter ablation, 105–19 complications avoidance, 114–17 outcomes, 114, 115–16 techniques, 113–17 clinical characteristics, 105 definition, 105 diagnostic criteria, 106 electrophysiological characteristics, 105–6 mapping methods, 108–13 intracardiac echocardiography, 110, 113 invasive, 111–13 noninvasive, 108–11 mechanisms automatic, 105 microreentry, 105 triggered activity, 105 pharmacological responses, 105–6 sites of origin, 106–8 focal Purkinje ventricular tachycardia, 298, 306 Fontan operation, 95 fractionated electrograms, and threedimensional mapping, 66–7 free-wall accessory pathways mapping, 160 right, 149 use of term, 149 see also left free-wall accessory pathways Freezor Xtra (cryocatheter), 37 fusion entrainment with concealed, 56–7 and entrainment mapping, 51–3 ganglia, 16 ganglionated subplexuses, 16, 17 ganglion plexuses, and atrial fibrillation, 65–6 general anesthetics, for pediatric patients, 91–2 gray-scale imaging, two-dimensional, 80 great cardiac vein, 3, 4, 5, 7, 10, 13 greater coronary venous system, 13

Hansen catheter manipulation system, 69 heart, in situ, 3 heart anatomy and catheter ablation, 3–19 orientational issues, 3 heart block and cryoablation, 38 see also atrioventricular block heart failure, and atrioventricular node ablation, 268 heart rate variability analysis, 227 heart valves eustachian, 5, 7, 8, 137 pulmonary, 4, 10, 11, 12 see also aortic valve; mitral valve; tricuspid valve heat shock proteins, 27 heat transfer, in biological tissues, 22 heparin, 94 heterotaxy syndrome, 93 high-frequency electrograms, and threedimensional mapping, 66–7 hilum, anatomy, 16 His bundle refractoriness, 152, 153 Hsp70, 27 hyperthermia effects on blood flow, 29 on cellular electrophysiology, 27–8 on cellular metabolism, 27 on cytoskeleton, 25–6 on nucleus, 26–7 on plasma membrane, 25 IART see intra-atrial reentrant tachycardia (IART) ICDs (implantable cardioverter defibrillators), 96, 314–16 ICE see intracardiac echocardiography (ICE) ice mapping, and cryoablation, 36, 38 idiopathic arrhythmogenic atrial myopathy, 194 use of term, 193 idiopathic dilated cardiomyopathy, and radiofrequency catheter ablation, 342 idiopathic left ventricular tachycardias, 298 –313 classification, 298 prevalence, 298 idiopathic right ventricular outflow tract ventricular tachycardia catheter ablation, 279–97 approaches, 289–91 indications, 294 outcomes, 291–4 diagnosis, 280

electrophysiology, 281 endocardial mapping, 281–5 etiology, 281 prognosis, 280 tachycardia focus location, 285 –9 IDPs see isolated diagnostic potentials (IDPs) implantable cardioverter defibrillators (ICDs), 96, 314 –16 inappropriate sinus tachycardia (IST), 110 catheter ablation, 116 definition, 108 inferior caval vein, 4, 5, 6, 7 inferior isthmus, 5, 6 infiltrative myopathies, and ventricular tachycardia radiofrequency catheter ablation, 342, 355 –9 inflammatory responses, radiofrequency lesions, 29–31 infrared catheter ablation, 44 – 6 advantages, 46 disadvantages, 46 mechanisms, 46 tissue injury mechanisms, 44 –5 infrared coagulators, 45 – 6 preclinical studies, 45 – 6, 47 innervation, 16 integrated, anatomy-based mapping, 67–9 development, 67 validation, 67–8 internodal tracts, specialized, 14 interpolation obliteration, 60 –1 intra-atrial reentrant tachycardia (IART), 95 – 6 electroanatomical mapping, 95 intracardiac echocardiography (ICE) ablation-related complications monitoring, 84 –5 ablative lesion assessment, 80 atrial arrhythmia ablation, 80 –1 atrial fibrillation ablation, 81–3 in cardiac electrophysiology, 72 –90 early studies, 74 focal atrial tachycardia mapping, 110, 113 future trends, 85–6 image-guided catheter manipulation, 78 imaging to guide energy titration, 79 intracardiac imaging venues, 75 –7 limitations, 85 linear ablation guidance, 82 mechanical single-element imaging, 74 microbubble imaging, 79 –80 and microwave catheter ablation, 39 phased-array imaging, 74 –5 and three-dimensional imaging, 86 –7 369

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Index intracardiac imaging venues, 75–7 intracardiac mechanical single-element imaging, 74 intracardiac ultrasound, applications, 67 intracardiac ultrasound–computed tomography fusion, 68–9 intrapericardial catheters, positioning, 86 IPs (isolated potentials), 328–31 isoflurane, 92 isolated diagnostic potentials (IDPs), 329, 330, 332, 335, 337 elimination, 338 isolated potentials (IPs), 328–31 isoproterenol, 135 IST see inappropriate sinus tachycardia (IST) Koch’s triangle see triangle of Koch LA see left atrium (LA) LAA (left atrial appendage), 230 LAO (left anterior oblique) projection, 121, 122, 123, 127, 289–90 LASER see light amplification by stimulated emission of radiation (LASER) laser balloon ablation catheters, 44 laser catheter ablation, 43– 4 advantages, 44 clinical studies, 44 diffusing needle tips, 44 disadvantages, 44 mechanisms, 43 preclinical studies, 43–4, 45, 46 tissue injury mechanisms, 43 late potentials (LPs), 329 Latin America, Chagas’ disease, 357 left anterior fascicular ventricular tachycardia, 302–4 left anterior oblique (LAO) projection, 121, 122, 123, 127, 289–90 left atrial ablation, vs. pulmonary vein isolation, 222 left atrial appendage (LAA), 230 left atrial linear ablation, efficacy, 241 left atrial ridge, 7, 8 left atrial slow/fast atrioventricular nodal reentrant tachycardia, 120, 146–7 catheter ablation, 139– 41 left atrium (LA), 4, 5, 214 anatomy, 7–8 anterior, transection, 242–3 electroanatomical mapping, 227–8 imaging, 75, 76 mapping, 60 three-dimensional mapping, 65 370

left bundle superior axis tachycardias, 279 left coronary sinus, 13 left free-wall accessory pathways, 155–8, 163 occurrence, 149 retrograde approach, 155–6 complications, 165 transseptal approach, 156–8 transseptal vs. retrograde approach, 155 left inferior pulmonary vein, 4, 5, 7 and arrhythmogenesis, 81 left parietal junction, 9–10 left phrenic nerve, 3 left posterior fascicular ventricular tachycardia, 300–2 left-sided posteroseptal accessory pathways, 151 left superior pulmonary vein (LSPV), 4, 5, 230 and arrhythmogenesis, 81 left upper septal fascicular ventricular tachycardia, 305–6 left ventricle, 4, 5 anatomy, 12–13 left ventricular outflow tract ventricular tachycardia, 298, 307–10 catheter ablation, 309 aortic sinus approach, 309 coronary venous approach, 309 direct epicardial approach, 309 endocardial approach, 309 pulmonary artery approach, 309 classification, 307–9 electrocardiography, 309–10, 311 epicardial origin, 309 left ventricular outlet, 12 leftward inferior extension slow/fast atrioventricular nodal reentrant tachycardia, 120, 146 catheter ablation, 137–9 lesion formation via radiofrequency catheter ablation, 20 –34 see also radiofrequency (RF) lesion formation lesions ablative, 80 atrial epicardial, 45–6 atrioventricular nodal, 36 see also linear lesions; myocardial lesions; radiofrequency (RF) lesions light amplification by stimulated emission of radiation (LASER) direct pulsed, 43– 4 mechanisms, 43 sources, 43

see also diode lasers; laser catheter ablation linear ablation, 64 clinical experience, 240 –5 future trends, 246 –7 intracardiac echocardiography guidance, 82 left atrial, 241 right atrial, 241 technological assistance, 140 see also bilateral linear ablation linear lesions atrial activation detour, 238 –9 electrophysiology, 238 – 40 local electrograms, 239 in treatment of atrial fibrillation, 237– 49 vector mapping, 239 linear microwave ablation, type 1 atrial flutter, 190 lower common pathway, in atrioventricular nodal reentrant tachycardia, 130 –2, 145 –6 lower loop reentry atrial flutter, 175, 176 catheter ablation, 182 LPs (late potentials), 329 LSPV see left superior pulmonary vein (LSPV) macro-ATs see macroreentrant atrial tachycardias (macro-ATs) macroreentrant atrial flutter, activation sequence mapping, 50, 51 macroreentrant atrial tachycardias (macro-ATs) catheter ablation, 193 –217 definition, 193 entrainment mapping, 58 occurrence, 193 use of term, 193 macroreentrant left atrial tachycardia, 195, 203 –16 following left atriotomy, 205 following catheter ablation of atrial fibrillation, 205 –14 following surgical ablation of atrial fibrillation, 205 –14 in patients without prior catheter ablation or surgery in left atrium, 214 macroreentrant right atrial tachycardia, 194, 195 –203, 195 catheter ablation, 195 factors affecting, 195 –203 mapping, 195–203 magnetic resonance (MR), pulmonary vein studies, 65 magnetic resonance imaging (MRI), 279 anatomic reconstruction, 223, 225 – 6

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Index Mahaim fibers, 93 mammalian cells anatomy, 25– 6 hyperthermia effects, 25–8 mapping bipolar, 342–3 body surface, 110–11 for catheter ablation, 49–59 conventional, 252 cryomapping, 36, 38 electrogram recording methods, 49–50 electromagnetic, 113 electrophysiological substrate, atrial fibrillation catheter ablation guidance, 250–60 endocardial, 281–5 endocardial activation, 111 NavX, 64, 67, 188 noncontact, 50, 113, 114 post-myocardial infarction ventricular tachycardias, 317–20 scar, 61 vector, 239 see also activation mapping; activation sequence mapping; Carto mapping; electroanatomical mapping; EnSite mapping; entrainment mapping; integrated, anatomy-based mapping; pacemapping; three-dimensional mapping mapping systems anatomy characterization, 64–5 development, 60 image-guided interventions, 69 interpolation obliteration, 60–1 requirements, 60–7 Marshall (oblique left atrial) vein, 13 microbubble imaging, 79–80 microreentry circuits, mapping, 61, 62 microvascular blood flow, radiofrequency ablation microwave catheter ablation, 38– 40 advantages, 39, 40 antenna design, 39 clinical studies, 39–40 disadvantages, 40 feedback control, 39 mechanisms, 39 preclinical studies, 39 tissue injury mechanisms, 38 midazolam, 92 middle cardiac vein, 13–14 midseptal accessory pathways, 163– 4 effects, 29 mitral annular ventricular tachycardia, 298, 306–7 mitral annulus, 4, 207

mitral isthmus, 7, 8 ablation, 243–5 mitral leaflets, 12 mitral valve, 4, 7, 8, 9, 10, 12 imaging, 75, 77 surgery, 36–7, 205 MR (magnetic resonance), pulmonary vein studies, 65 multimodality imaging technologies, 69 multiple wavelet hypothesis, 238 muscular ventricular septum, 12 Mustard operation, 95 myocardial ablation, 22 myocardial conduction, in vitro studies, 27–8 myocardial infarction, catheter ablation of stable ventricular tachycardia after, 314–25 myocardial injury, thermally induced, 28 myocardial lesions microwave-induced, 40 three-dimensional mapping, 326– 8 myocardial substrate, in vivo scar definition, 326– 8 myocardium abnormal, 343 immature, 96–7 narcotics, 92 NavX mapping, 64, 67, 188 nodofascicular pathways, 149, 169–70 nodoventricular pathways, 149, 169–70 noncontact mapping, 50, 113, 114 noncoronary sinus, 12, 13 nonischemic cardiomyopathy, and ventricular tachycardia radiofrequency catheter ablation, 342–3 nonischemic dilated cardiomyopathy and ventricular tachycardia radiofrequency catheter ablation, 352–5 ablation issues, 353–5 electrophysiological issues, 352–3 epidemiological issues, 352 pathological issues, 352 nonischemic structural heart disease, with ventricular tachycardias, radiofrequency catheter ablation, 342– 63 North American Society of Pacing and Electrophysiology, 99, 173 nucleus anatomy, 26 and hyperthermia, 26–7 oblique left atrial vein, 13 orthodromic reciprocating tachycardia (ORT), 149, 152–3, 163

and radiofrequency energy, 161 os, 7, 8 oval fossa, 8, 9, 15 owl’s eyes, imaging, 75, 76 paced activation sequence mapping, 112–13 pacemaker dependency, and atrioventricular junction ablation, 268 pacemaker implantation, 263 pace-mapping, 49, 282, 292, 333, 337 and activation mapping compared, 282–5 multiple, 338 optimal, 338–9 post infarction ventricular tachycardias, 319 –20 sinus rhythm, 331, 332 pacing bipolar, 58, 282 biventricular, 269–70 differential, 239 entrainment, 195, 198 –200 mode of, 269 unipolar, 58 see also post-pacing interval (PPI) pacing cycle lengths, 57–8 PAF see paroxysmal atrial fibrillation (PAF) PAPCA (Prospective Assessment after Pediatric Cardiac Ablation), 97–8 papillary muscles, 10 –11, 12 para-Hisian pacing limitations, 154–5 procedures, 153– 4 paroxysmal atrial fibrillation (PAF) mapping, 254 pulmonary vein ostial dimensions, 81 substrate modification, 246 pathways atrioventricular, 149 lower common, 130 –2, 145 – 6 nodofascicular, 149, 169 –70 nodoventricular, 149, 169 –70 septal, 149 see also accessory pathways (APs); atriofascicular pathways pectinate muscles, intracardiac imaging, 75 Pediatric Electrophysiology Society (US), 97 pediatric patients catheter ablation, 91–101, 293 –4 general anesthetics, 91–2 radiofrequency ablation, 91 tachycardia mechanisms, 97 pericardial effusions, detection, 84 pericardium, anatomy, 3, 4 371

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Index permanent junctional reciprocating tachycardia (PJRT), 94–5, 159, 160 Pharmacological Intervention in Atrial Fibrillation (PIAF), 237 issues, 221 phased array imaging, 74–5 phospholipids, 25 PIAF see Pharmacological Intervention in Atrial Fibrillation (PIAF) PJRT (permanent junctional reciprocating tachycardia), 94–5, 159, 160 plasma membrane anatomy, 25 and hyperthermia, 25 polycythemia, 94 posterior descending coronary artery, 13 posterior interventricular artery, 13 posterior septum, 9, 10 posteroseptal accessory pathways, 151 catheter ablation, 158–9 complications, 165 left-sided, 151 nomenclature, 151 right-sided, 151 post-MI VTs see post-myocardial infarction ventricular tachycardias (post-MI VTs) post-myocardial infarction ventricular tachycardias (post-MI VTs) catheter ablation, 314–25 assessment, 320–1 complications, 323 lesion placement, 320–1 outcomes, 322–3 electrograms, 320 electrophysiological assessment, 314–15 entrainment mapping, 320 epicardial mapping and ablation, 322 mappable, 322–3 mapping, 317–20 pace-mapping, 319–20 pre-ablation assessment, 314 QRS morphology, 316–17 reentry circuits, 315 epicardial, 321–2 intramural, 321–2 sinus rhythm electrograms, 317–18 stable, 322–3 substrate characterization, 326–32 electrogram characteristics, 328–31 histopathology, 326 in vivo scar definition, 326– 8 substrate ablation, 326– 41 approaches, 333, 335–8 future trends, 338–9 372

slow conduction channels during sinus rhythm, 332–8 transcoronary ethanol ablation, 322 voltage maps, 317–18 postoperative arrhythmias, and congenital heart disease, 17 post-pacing interval (PPI), 53–6, 57 assessment, 58 determination, 53 far-field vs. local potentials, 55–6 power amplitude, and radiofrequency lesion size, 22, 23 power ramping protocols, 31 PPI see post-pacing interval (PPI) preexcitation, 149–50, 152 propofol, 92 propranolol, 105 Prospective Assessment after Pediatric Cardiac Ablation (PAPCA), 97–8 pseudo-three-dimensional flower catheter, 65 pulmonary arteries, 7, 8 pulmonary trunk, 4, 5 pulmonary valve, 4, 10, 11, 12 pulmonary vein ablation, 237 see also circumferential pulmonary vein ablation (CPVA) pulmonary vein isolation (PVI), 250 and circumferential pulmonary vein ablation compared, 222 efficacy issues, 237 postoperative substrate modification, 246 –7 vs. left atrial ablation, 222 pulmonary vein ostial dimensions, 81 pulmonary veins (PVs), 7, 8, 205 –14 anatomical mapping, 64–5 and atrial fibrillation, 64, 67, 72–3 imaging, 75, 76, 78, 81–2 mapping, 60–1 right inferior, 4, 5 right superior, 4, 5 ultrasound catheter ablation studies, 42 see also circumferential pulmonary vein ablation (CPVA); left inferior pulmonary vein; left superior pulmonary vein (LSPV) pulmonary vein stenosis and cryoablation, 36, 38 mitigation, 84–5 Purkinje fibers, 15, 16 Purkinje network, 12 PVI see pulmonary vein isolation (PVI) PVs see pulmonary veins (PVs) QRS complexes, 51, 53, 56 QRS fusion, 57

QRS morphologies, 72 post-myocardial infarction ventricular tachycardias, 316 –17 QS complexes, 50 RA see right atrium (RA) RACE see Rate Control versus Electrical Cardioversion (RACE) radiofrequency catheter ablation (RFCA) advantages, 35 biological effects, 32 cellular effects, 25 –8 disadvantages, 35 electrical characteristics, 20 –2 in vitro models, 31 lesion formation, 20 –34 pediatric patients, 91 and RF lesion formation, 25 –8 safety issues, 96–7 thermodynamics, 22–5 tissue effects, 29–31 type 1 atrial flutter, 173, 180 –7 ventricular tachycardia associated with nonischemic structural heart disease, 342–63 radiofrequency (RF) current density, 20–1 radiofrequency (RF) energy electrical characteristics, during catheter ablation, 20 –2 operating frequencies, 20 optimum delivery duration, 24 –5 phase offsets, 21 properties, 20 radiofrequency (RF) lesion formation assessment, 80 biophysics, 20–5 pathophysiology, 25 –8 tissue effects, 29–31 radiofrequency (RF) lesions depth control, 23, 24 inflammatory responses, 29 –31 in pediatric patients, 96 –7 small, 22–3 and ultrastructural changes, 31 volume control, 23 radiofrequency (RF) lesion size control, 22, 24 and steady-state power amplitude, 22, 23 and temperature, 22, 23 radionuclide right ventriculography, 279 RAO (right anterior oblique) projection, 123, 127, 141 rate control, of atrial fibrillation, ablation, 261–75

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Index Rate Control versus Electrical Cardioversion (RACE), 237 issues, 221 reentrant fascicular ventricular tachycardia, 298 reentry circuits activation sequence mapping, 51 entrainment mapping, 51, 52, 54, 55, 56 epicardial, 321–2 intramural, 321–2 microreentry circuits, 61, 62 post-myocardial infarction ventricular tachycardias, 315, 321–2 and post-pacing interval, 53 ventricular tachycardias, 314 remote magnetic navigation, for atrial fibrillation ablation, 234 repetitive monomorphic ventricular tachycardia, 12, 279 retrograde fast pathway conduction, 123 –5, 126 retrograde slow pathway conduction, 126 –9, 130 reverse typical atrial flutter catheter ablation, 173–92 diagnosis, 179–80 electrocardiograms, 175, 177 nomenclature, 173 RFCA see radiofrequency catheter ablation (RFCA) RF energy see radiofrequency (RF) energy RF lesion formation see radiofrequency (RF) lesion formation RF lesions see radiofrequency (RF) lesions RF lesion size see radiofrequency (RF) lesion size right anterior oblique (RAO) projection, 123, 127, 141 right anterolateral accessory pathways, 162 right atrial linear ablation, efficacy, 241 right atrium (RA), 4, 5 anatomy, 5–7 and arrhythmogenesis, 81 as intracardiac imaging venue, 75 medial wall, 7 schematic diagram, 182 right coronary arterial dominance, 13 right coronary sinus, 13 right free-wall accessory pathways, occurrence, 149 right inferior pulmonary vein, 4, 5 right parietal junction, 9, 10 right posterior accessory pathways, 160, 161

right-sided accessory pathways atrial insertion mapping, 160 catheter ablation, 159–60, 163 complications, 165 ventricular insertion mapping, 159 – 60 right-sided posteroseptal accessory pathways, 151 right superior pulmonary vein, 4, 5 right ventricle, 4, 5 anatomy, 10–12 right ventricular outflow tract (RVOT), imaging, 77 right ventricular outflow tract ventricular tachycardia (RVOT VT) activation sequence mapping, 50–1 prevalence, 279 see also idiopathic right ventricular outflow tract ventricular tachycardia right ventricular outlet, 12 rightward inferior extension slow/fast atrioventricular nodal reentrant tachycardia, 120, 146 catheter ablation, 132–7 reentrant circuits, 129–32 ring of fire, 72 Ross procedure, 12 RVOT (right ventricular outflow tract), 77 RVOT VT see right ventricular outflow tract ventricular tachycardia (RVOT VT) SAECG (signal-averaged echocardiography), 279, 280 sarcoidosis incidence, 355– 6 and ventricular tachycardia radiofrequency catheter ablation, 342, 355 –7 electrophysiological issues, 356–7 epidemiological issues, 355–6 pathological issues, 355–6 scar mapping, 61 SCCs see slow conduction channels (SCCs) sedation, for catheter ablation in young patients, 91–2 segmental isolation, 250 semilunar areas of myocardium, 11, 12 Senning operation, 95 septal isthmus, 5– 6 septal leaflet, 11 septal pathways, use of term, 149 septoparietal trabeculations, 12

septum anterior, 9, 10 atrial, 8–9 muscular ventricular, 12 posterior, 9, 10 signal-averaged echocardiography (SAECG), 279, 280 sinotubular junction, 13 sinus of Keith (subeustachian sinus), 5, 6 sinus nodal reentrant tachycardia, definition, 106 –8 sinus node, 5, 6, 13 anatomy, 14 discovery, 7 sinus rhythm electrograms, 328 –31 definitions, 328 and ventricular tachycardia circuits, 331–2 sinus rhythm maintenance, 237 sinus rhythm pace-mapping, 331, 332 sinus rhythm restoration, 237 microwave catheter ablation, 39 – 40 sinus tachycardias, 106 –8 catheter ablation, 116 see also inappropriate sinus tachycardia (IST) slow conduction channels (SCCs), 326, 328, 329 –31 substrate ablation, 332– 8 slow/fast atrioventricular nodal reentrant tachycardia, 120, 122, 123 – 41, 142, 146 –7 catheter ablation, 132– 41 definition, 121 reentrant circuits, 129 –32 retrograde fast pathway conduction, 123 –5 slow atrioventricular nodal pathway conduction, 126 –9 see also left atrial slow/fast atrioventricular nodal reentrant tachycardia; leftward inferior extension slow/fast atrioventricular nodal reentrant tachycardia; rightward inferior extension slow/fast atrioventricular nodal reentrant tachycardia slow/slow atrioventricular nodal reentrant tachycardia, 120, 122, 141–5, 147 catheter ablation, 143 –5 definition, 121 small cardiac vein, 13, 14 Stereotaxis system, 69 stroke, and atrial fibrillation, 221 subeustachian sinus, 5, 6 subpulmonary muscular infundibulum, 11, 12 373

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Index substrate ablation endocardial in dense scar, 332 in scar border zone, 332–3 epicardial, 333–5 post-myocardial infarction ventricular tachycardias, 326– 41 approaches, 333, 335–8 future trends, 338–9 substrate modification individualized approaches, 246–7 via catheter ablation, 237–8 sudden death, 149, 165, 343, 350, 352 and atrioventricular node ablation, 267 and Chagas’ disease, 358 and sarcoidosis, 356 superior caval vein, 6, 7 supraventricular crest, 11, 12, 13 supraventricular tachycardia (SVT), 94, 103–217 recurrent, 95 sustained monomorphic ventricular tachycardia, 298 SVT see supraventricular tachycardia (SVT) tachycardia cycle length (TCL), 53– 4, 55, 57, 58 tachycardias and accessory pathways, 149, 152–3 antidromic reciprocating, 149 catheter ablation, 91 incessant, with secondary cardiomyopathy, 94–5 left bundle superior axis, 279 mechanisms, pediatric patients, 97 permanent junctional reciprocating, 94–5, 159, 160 see also atrial tachycardias (ATs); atrioventricular nodal reentrant tachycardia (AVNRT); orthodromic reciprocating tachycardia (ORT); sinus tachycardias; supraventricular tachycardia (SVT); ventricular tachycardias (VTs) TCL (tachycardia cycle length), 53– 4, 55, 57, 58 TEE (transesophageal echocardiography), 73–4 temperature and radiofrequency lesion size, 22, 23 see also electrode–tissue interface temperature tendon of Todaro, 5, 6 terminal crest, 6, 7 tetralogy of Fallot repair, 96 prevalence, 350 374

and ventricular tachycardia radiofrequency catheter ablation, 342, 350 –2 ablation issues, 350–2 electrophysiological issues, 350 epidemiological issues, 350 thermal injuries, clinical studies, 31 thoracic veins, atrial tachycardia ablation from, 116 three-dimensional electroanatomical mapping, 163, 342 three-dimensional imaging, and intracardiac echocardiography, 86 –7 three-dimensional mapping, 72 anomaly detection issues, 61–3 in atrial fibrillation, 60–71 future trends, 69–70 data acquisition issues, 61 electroanatomical, 163, 342 image-guided interventions, 69 imaging issues, 61 intervention site cataloging, 63 mechanical event displays, 63 myocardial lesions, 326– 8 noncontact, 65 type 1 atrial flutter, 187–9 validation, 67–8 thromboembolism, and atrioventricular junction ablation, 268 thrombus formation, cryoablation vs. radiofrequency ablation, 36 transcatheter ablation see catheter ablation transcatheter lasers, 43–4 transcoronary ethanol ablation, postmyocardial infarction ventricular tachycardias, 322 transesophageal echocardiography (TEE), 73– 4 transseptal catheterization, 78 transseptal puncture, 8–9 transseptal technique, 92 triangle of Koch, 5–6 activation, 133, 134 anatomy, 15, 16 tricuspid valve, 4, 5, 6, 9, 10 Ebstein’s malformation, 93 intracardiac imaging, 75 Trypanosoma cruzi (parasite), 357–8 twelve-lead surface electrocardiography, 108 –10, 111 roles, 285–9 twin atrioventricular nodes, 93 two-catheter technique, 111 type 1 atrial flutter ablation, new energy sources, 190 cryoablation, 190 diagnosis, 175–80

computerized three-dimensional mapping, 187–9 electrocardiography, 175 – 6, 178 electrophysiological mechanisms, 173 – 4 electrophysiology, 176 – 80 etiology, 173 linear microwave ablation, 190 mapping, 176–80 nomenclature, 173 occurrence, 173 radiofrequency catheter ablation, 180 –7 complications, 184–7 computerized three-dimensional mapping, 187–9 management of difficult cases, 187 methods, 180–2 outcomes, 184–7 procedure end points, 182– 4 see also reverse typical atrial flutter; typical atrial flutter type 2 atrial flutter, nomenclature, 173 typical atrial flutter catheter ablation, 173 –92 diagnosis, 179–80 electrocardiograms, 175, 177 nomenclature, 173 typical slow/fast atrioventricular nodal reentrant tachycardia see rightward inferior extension slow/fast atrioventricular nodal reentrant tachycardia ultrasound, intracardiac, 67, 68 –9 ultrasound ablation catheters development, 42 double-balloon focused, 42 ultrasound catheter ablation, 41–3 advantages, 42–3 clinical studies, 42 disadvantages, 42–3 mechanisms, 41 preclinical studies, 41–2 tissue injury mechanisms, 41 ultrasound imaging, ventricular tachycardias, 83 – 4 ultrastructural changes, and radiofrequency lesions, 31 unipolar pacing, 58 vagus nerve, 14 Valsalva (aortic) sinuses, 12–13 vector mapping, linear lesions, 239 vein of Galen (acute marginal vein), 14 venoatrial junctions, 7– 8 venography, 82 ventricles, anatomy, 10 –13

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Index ventricular arrhythmias, and atrioventricular node ablation, 267 ventricular myocardium, ultrastructural changes, 30, 31 ventricular preexcitation, Wolff– Parkinson–White variant, 9 ventricular rate, determination, 261–2 ventricular tachycardia circuits and scar geometry, 331–2 and sinus rhythm electrograms, 331–2 ventricular tachycardias (VTs), 13, 277–363 activation sequence mapping, 50–1 associated with nonischemic structural heart disease, radiofrequency catheter ablation, 342–63 classification, 298 electroanatomical mapping, 96 entrainment mapping, 51–3, 55, 58 focal Purkinje, 298, 306 idiopathic ablation, 83 infarct-related, 314

laser catheter ablation, 44 late postoperative, 96 left anterior fascicular, 302–4 left posterior fascicular, 300–2 left upper septal fascicular, 305– 6 mappable, 314 mitral annular, 298, 306–7 mitral isthmus-dependent, 72 outflow tract, 72 QRS fusion, 57 reentrant fascicular, 298 reentry circuits, 314 repetitive monomorphic, 12, 279 scar-dependent, ablation, 83–4 sedation issues, 92 stable, 314, 315 sustained monomorphic, 298 ultrasound imaging, 83–4 unstable, 314 see also idiopathic left ventricular tachycardias; idiopathic right ventricular tachycardia; left ventricular outflow tract

ventricular tachycardia; postmyocardial infarction ventricular tachycardias (post-MI VTs); right ventricular outflow tract ventricular tachycardia (RVOT VT); supraventricular tachycardia (SVT); verapamil-sensitive fascicular ventricular tachycardia verapamil, 105 verapamil-sensitive fascicular ventricular tachycardia, 299 –306 anatomy, 299–300 classification, 299 mechanisms, 299–300 Vieussens’ valve, 13 VTs see ventricular tachycardias (VTs) Wolff–Parkinson–White syndrome, 94, 165 Wolff–Parkinson–White variant, 9 young patients, catheter ablation, 91–101, 293 –4

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