Cardiac Electrophysiology
Andrea Natale • Amin Al-Ahmad Paul J. Wang • John P. DiMarco (Editors)
Cardiac Electrophysiology Clinical Case Review
Editors Andrea Natale Texas Cardiac Arrhythmia Institute St. David’s Medical Center 1015 East 32nd Street Suite 516, Austin, TX 78705 USA Amin Al-Ahmad School of Medicine Stanford University 300 Pasteur Drive H-2146, Stanford, CA 94305 USA
Paul J. Wang School of Medicine Stanford University 300 Pasteur Drive H-2146, Stanford, CA 94305 USA John P. DiMarco Cardiovascular Division University of Virginia Health System 1215 Lee Street Charlottesville, VA 22908 USA
ISBN 978-1-84996-389-3 e-ISBN 978-1-84996-390-9 DOI 10.1007/978-1-84996-390-9 Springer London Dordrecht Heidelberg New York British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: 2010937972 © Springer-Verlag London Limited 2011 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licenses issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc., in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature. Cover design: eStudioCalamar, Figueres/Berlin Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)
To our wives and families, for the constant support and patience.
Preface
As the field of cardiac electrophysiology continues to evolve and advance, we continue to be challenged to educate new generations of cardiac electrophysiologists with the basics as well as the latest advances in the field. While there are many outstanding books that provide an in-depth review of topics in electrophysiology, there are few case-based books that comprehensively cover clinical electrophysiology, devices, and ablation. Case reviews offer a simple, yet effective way in teaching important concepts, offering insight into both the basic pathophysiology of a problem as well as the clinical reasoning that leads to a solution. In “Cardiac Electrophysiology: Clinical Case Review” we sought to put together the most comprehensive case-based review of electrophysiology that would appeal to all students of the field whether they are fellows, allied professionals, or practicing electrophysiologists. In “Cardiac Electrophysiology: Clinical Case Review” we are fortunate to have many true experts in the field contributing cases that they have encountered and summarizing the important learning objectives in a succinct way. The book covers clinical electrophysiology, device troubleshooting and analysis, as well as intracardiac electrogram analysis and ablation. It is our sincere hope that the readers of “Cardiac Electrophysiology: Clinical Case Review” will find the cases useful as a review of electrophysiology or in their day-to-day interactions with patients. Stanford CA, USA Charlottesville VA, USA Cleveland OH, USA
Amin Al-Ahmad Paul J. Wang John P. DiMarco
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Section 1 Ablation Case 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Amin Al-Ahmad
3
Case 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Haissaguerre
7
Case 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Amin Al-Ahmad
11
Case 4 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Haissaguerre
15
Case 5 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anurag Gupta and Amin Al-Ahmad
19
Case 6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Haissaguerre
23
Case 7 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Haissaguerre
29
Case 8 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Haissaguerre
35
Case 9 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alberto Diaz, Dimpi Patel, William R. Lewis, and Andrea Natale
39
Case 10 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
41
Case 11 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
47
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Case 12 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
51
Case 13 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bradley P. Knight
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Case 14 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
57
Case 15 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
63
Case 16 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
65
Case 17 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bradley P. Knight
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Case 18 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
71
Case 19 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
81
Case 20 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
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Case 21 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bradley P. Knight
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Case 22 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
87
Case 23 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
95
Case 24 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101 Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 25 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 Bradley P. Knight Case 26 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Richard H. Hongo and Andrea Natale
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Case 27 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 28 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 29 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 30 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125 Luis C. Sáenz and Miguel A. Vacca Case 31 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133 Bradley P. Knight Case 32 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Luigi Di Biase, Rodney P. Horton, and Andrea Natale Case 33 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 34 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele Case 35 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 36 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 37 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153 Bradley P. Knight Case 38 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 Luigi Di Biase, Rodney P. Horton, and Andrea Natale Case 39 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 40 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele Case 41 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
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Case 42 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 43 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189 Bradley P. Knight Case 44 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele Case 45 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 46 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 47 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201 Bradley P. Knight Case 48 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele Case 49 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 50 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221 Bradley P. Knight Case 51 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 52 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 53 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233 Bradley P. Knight Case 54 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 55 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar Case 56 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245 Bradley P. Knight
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Case 57 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur Case 58 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253 Roopinder Sandhu, Dimpi Patel, William R. Lewis, and Andrea Natale Case 59 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 60 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267 Matthew D. Hutchinson Case 61 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271 Ronald Lo, Henry H. Hsia, and Amin Al-Ahmad Case 62 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275 Richard H. Hongo and Andrea Natale Case 63 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279 David J. Callans Case 64 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 J. David Burkhardt, Dimpi Patel, and Andrea Natale Case 65 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287 Matthew D. Hutchinson Case 66 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291 Matthew D. Hutchinson Case 67 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295 Matthew D. Hutchinson Case 68 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299 Matthew D. Hutchinson Case 69 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303 Matthew D. Hutchinson Case 70 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307 Matthew D. Hutchinson Case 71 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311 Matthew D. Hutchinson Section 2 Devices Case 72 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317 Amin Al-Ahmad and Paul J. Wang
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Case 73 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319 Amin Al-Ahmad and Paul J. Wang Case 74 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321 Kenneth A. Ellenbogen Case 75 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325 Nora Goldschlager Case 76 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager Case 77 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331 Gregory M. Marcus and Nora Goldschlager Case 78 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 Amin Al-Ahmad and Paul J. Wang Case 79 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 Kenneth A. Ellenbogen and Rod Bolanos Case 80 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 Nora Goldschlager Case 81 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager Case 82 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345 Amin Al-Ahmad and Paul J. Wang Case 83 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 347 Kenneth A. Ellenbogen Case 84 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349 Nora Goldschlager Case 85 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351 Anurag Gupta and Amin Al-Ahmad Case 86 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager Case 87 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357 Kenneth A. Ellenbogen Case 88 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361 Nora Goldschlager Case 89 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 Kenneth A. Ellenbogen, Rod Bolanos, and Mark A. Wood
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Case 90 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager Case 91 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 92 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373 Amin Al-Ahmad Case 93 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 94 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 Kenneth A. Ellenbogen and Rod Bolanos Case 95 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 Byron K. Lee Case 96 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387 Amin Al-Ahmad and Paul J. Wang Case 97 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389 Kenneth A. Ellenbogen and Rod Bolanos Case 98 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 Kenneth A. Ellenbogen Case 99 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Amin Al-Ahmad and Paul J. Wang Case 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 Kenneth A. Ellenbogen Case 101 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 Amin Al-Ahmad and Paul J. Wang Case 102 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 405 Kenneth A. Ellenbogen Case 103 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407 Amin Al-Ahmad and Paul J. Wang Case 104 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411 Kenneth A. Ellenbogen Case 105 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415 Kenneth A. Ellenbogen and Rod Bolanos Case 106 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419 Kenneth A. Ellenbogen
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Case 107 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 423 Paul A. Friedman and Charles D. Swerdlow Case 108 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 427 Paul A. Friedman and Charles D. Swerdlow Case 109 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431 Paul A. Friedman and Charles D. Swerdlow Case 110 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433 Paul A. Friedman and Charles D. Swerdlow Case 111 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 439 Paul A. Friedman and Charles D. Swerdlow Case 112 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 441 Paul A. Friedman and Charles D. Swerdlow Case 113 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 443 Paul A. Friedman and Charles D. Swerdlow Case 114 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447 Paul A. Friedman and Charles D. Swerdlow Case 115 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 Paul A. Friedman and Charles D. Swerdlow Case 116 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Paul A. Friedman and Charles D. Swerdlow Case 117 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455 Paul A. Friedman and Charles D. Swerdlow Case 118 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459 Paul A. Friedman and Charles D. Swerdlow Case 119 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 120 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 469 Paul A. Friedman and Charles D. Swerdlow Case 121 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471 Kenneth A. Ellenbogen Case 122 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473 Anurag Gupta Case 123 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 477 Ronald Lo, Amin Al-Ahmad, and Paul J. Wang
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Case 124 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481 Ronald Lo, Amin Al-Ahmad, and Paul J. Wang Case 125 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483 Ronald Lo, Amin Al-Ahmad, and Paul J. Wang Section 3 Clinical Cases Case 126 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 487 Mehmet K. Aktas, Abrar H. Shah, and James P. Daubert Case 127 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 491 Loren P. Budge and John P. DiMarco Case 128 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495 David J. Callans Case 129 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497 Andrew E. Darby and John P. DiMarco Case 130 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501 Thomas J. Sawyer, Burr W. Hall, and James P. Daubert Case 131 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505 John P. DiMarco Case 132 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509 John P. DiMarco Case 133 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 511 John P. DiMarco Case 134 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513 John P. DiMarco Case 135 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517 John P. DiMarco Case 136 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521 John P. DiMarco Case 137 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 523 John P. DiMarco Case 138 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527 John P. DiMarco Case 139 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529 John P. DiMarco
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Case 140 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 531 John P. DiMarco Case 141 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535 John P. DiMarco Case 142 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 539 John P. DiMarco Case 143 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 545 John P. DiMarco Case 144 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 551 John P. DiMarco Case 145 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555 John P. DiMarco Case 146 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559 Brett A. Faulknier, David T. Huang, and James P. Daubert Case 147 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565 Stefan H. Hohnloser and Joachim R. Ehrlich Case 148 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 567 Joachim Ehrlich and Stefan H. Hohnloser Case 149 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 571 Bradley P. Knight Case 150 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575 Bradley P. Knight Case 151 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 577 Bradley P. Knight Case 152 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 579 Andrew D. Krahn Case 153 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 583 Byron K. Lee, Melvin M. Scheinman, and Zian H. Tseng Case 154 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 585 Srijoy Mahapatra Case 155 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 589 Pamela K. Mason Case 156 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 593 Pamela K. Mason
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Case 157 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595 Pamela K. Mason Case 158 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 597 Pamela K. Mason Case 159 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 599 Lisa G. Umphrey and John Paul Mounsey Case 160 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 603 James A. Reiffel Case 161 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 607 James A. Reiffel Case 162 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 611 Jens Seiler and William G. Stevenson Case 163 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 617 Jens Seiler and William G. Stevenson Case 164 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 625 Jens Seiler and William G. Stevenson Case 165 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 631 J. Jason West and John Paul Mounsey Case 166 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 635 Darren Traub, James P. Daubert, and Spencer Rosero Case 167 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 639 Vikas P. Kuriachan and George D. Veenhuyzen Case 168 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 643 Vikas P. Kuriachan and George D. Veenhuyzen Case 169 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 647 Jeffrey D. Booker and George D. Veenhuyzen Case 170 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 649 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Case 171 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 653 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 655
Section Ablation
I
Case 1 Amin Al-Ahmad
Case Summary A 72-year-old male with a history of aortic sinus of valsalva rupture and repair 30 years prior presents with palpitations. The patient reports having symptoms of shortness of breath and fatigue with palpitations. He is currently taking only aspirin. He has had cardioversions in the past for this arrhythmia and would like to consider ablation. He does not want to take anti-arrhythmic medications. His 12-lead ECG (Fig. 1.1) shows a 2:1 atrial tachyarrhythmia at a rate of approximately 180 bpm. The P-waves in the inferior leads are negative; however there is an isoelectric segment between P-waves.
What maneuvers would be important to elucidate the diagnosis during electrophysiology study and ablation?
Case Discussion This tachycardia may represent a focal atrial tachycardia given the isoelectric segment on the 12-lead ECG. However, in patients with prior cardiac surgery, atrial flutters should be considered. The possibility that this tachycardia is typical isthmus-dependent atrial flutter should be explored using entrainment pacing at the tricuspid valve (TV) to inferior
Fig. 1.1 Twelve-lead ECG showing atrial arrhythmia. Note the negative atrial deflections in the inferior leads and the isoelectric segment between them
A. Al-Ahmad School of Medicine, Stanford University, 300 Pasteur Drive, H-2146, Stanford, CA 94305 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_1, © Springer-Verlag London Limited 2011
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vena cava (IVC) isthmus. Reverse typical atrial flutter would be unlikely given the morphology of the flutter waves. Scarrelated atrial flutters should also be considered. Ablation of all potential atrial flutter circuits in patients post cardiac surgery may reduce the likelihood of recurrence.1
In this case, entrainment at the TV-IVC isthmus demonstrated a near perfect PPI and ablation at the TV-IVC isthmus terminated the atrial flutter (Figs. 1.2 and 1.3). The isoelectric segment between flutter waves likely represents slow atrial conduction in atrial flutter rather than atrial tachycardia.
200ms
I aVF V6 hRA p HIS p HIS d CS 9,10 CS 7,8 CS 5,6 CS 3,4 CS 1,2 RV p ABL
PPI
TCL
ABL d Stim 4
12:22:16 PM
12:22:17 PM
Fig. 1.2 Pacing using the ablation catheter positioned at the tricuspid valve-inferior vena cava (TV-IVC) isthmus. Concealed entrainment and a near perfect post-pacing interval are noted
Case 1
5 500ms
I
aVF hRA p HIS p HIS d CS 9,10 CS 7,8 CS 5,6 CS 3,4 CS 1,2 RV p ABL ABL d Stim 4
1:01:47 PM
1:01:48 PM
1:01:49 PM
Fig. 1.3 Application of RF energy in the TV-IVC area leads to termination of the arrhythmia
Reference 1. Verma A, Marrouche NF, Seshadri N, Schweikert RA, Bhargava M, Burkhardt JD, Kilicaslan F, Cummings J, Saliba W, Natale A. Importance of ablating all potential right atrial flutter circuits in postcardiac surgery patients. J Am Coll Cardiol. July 2004;44(2): 409–414.
1:01:50 PM
1:01:51 PM
Case 2 Michel Haissaguerre
Case Summary A 47-year-old male with a 4-year history of symptomatic, drug-resistant lone paroxysmal atrial fibrillation (AF) was referred for a first ablation procedure. He suffered from daily AF episodes that lasted a maximum of 8 h. Episodes of
AF always started following monomorphic atrial ectopy (Fig. 2.1). A decapolar catheter (Xtrem, ELA Medical, Le-PlessisRobinson, France) was inserted inside the coronary sinus (CS) while the ablation catheter (Thermocool Biosense Webster, Diamond Bar, CA) and a decapolar circumferential
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Fig. 2.1 Twelve-lead ECG. Sinus rhythm and short coupling atrial ectopies (with functional left bundle branch block [LBBB])
M. Haissaguerre Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac 33604, France A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_2, © Springer-Verlag London Limited 2011
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catheter (Lasso, Biosense Webster, Diamond Bar, CA) were introduced through a long sheath in the left atrium (LA). The circumferential catheter was placed in the left superior pulmonary vein (LSPV) and recorded venous and atrial potentials (Fig. 2.2). What mechanism is illustrated and what action is required?
Case Discussion Figure 2.1 shows a recording of atrial ectopics with a short coupling interval (also note the functional left bundle branch block [LBBB]). The P-wave morphology during ectopy is flat in the lateral leads, positive in the inferior leads and in lead V1, suggesting they originate from the LSPV. Endocardial tracings from the LSPV (Fig. 2.2) show two separated potentials during sinus rhythm (Fig. 2.2, first complex). The first potential (white star) represents activation of
the adjacent LA and is synchronous with the second half of the P-wave (in the right PVs it should be the first part of the P-wave). The second potential reflects local activity from the PV striated musculature (black star). When ectopy occurs in the PV (Fig. 2.2, second complex), there is a reversal of the described activation sequence, with the PV potential preceding the atrial potential. This pattern of reverse activation in a dead-end structure during ectopic triggered AF evidence for the arrhythmogenic potential of that PV. Mapping of the earliest site of activity during ectopy allows identification of discrete sites inside the vein, while the atrial exit site is dependent on the anatomy of the PV-LA connecting fascicles. Given that arrhythmia recurrence can occur from either the pulmonary vein that is active at the time of the procedure or any other PV, complete electrical isolation of all PVs has to be carried out with a series of coalescent RF applications using a dedicated PV circumferential catheter to help with mapping. Ablation is performed outside the vein (within 1–2 cm of the PV ostia) for right PVs and for the posterior part
I II V1
PV 1-2 PV 2-3 PV 3-4 PV 4-5 PV 5-6 PV 6-7 PV 7-8 PV 8-9 PV 9-10 CS 1-2 CS 3-4 CS 5-6 CS 7-8 CS 9-10
Fig. 2.2 Endocardial tracings from the left superior pulmonary vein (LSPV). Recording from a decapolar circumferential catheter inserted inside the LSPV (PV 1–2 to PV 9–10) and a decapolar catheter inserted into the coronary sinus (CS 1–2 to CS 9–10). During sinus rhythm (first
complex), there existed the presence of two separated potentials (one atrium, white star followed by one venous, black star). During ectopy (second complex), reversal of the described activation sequence with the PV potential preceding the atrial potential occurred
Case 2
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of the left PVs; however, due to the ridge between the left pulmonary veins and the left atrial appendage (LAA), catheter stability is an issue for ablation of the anterior aspect of the left PV’s, and ablation is often within 1 mm of the veins. In this case, ablation was started at the low anterior LSPV (pole 5) where the earliest activity was located and where a reverse in PV polarity was observed, both criteria pointing at a local anatomical connection (Fig. 2.3, panel A). Ablation at this point delayed the venous potentials (Fig. 2.3, panel B), and a second anatomical breakthrough was subsequently ablated at the upper part of the vein (pole 1). The ectopic beats stopped (Fig. 2.3, panel C) and the venous potentials became dissociated (Fig. 2.4).Ablation of the left inferior PV (LIPV) was performed in the same way. For the right veins,
A
segmental or circumferential ablation with a continuous circular lesion can be performed depending on the operator’s preference. When doing continuous circumferential lesions, it is unusual to achieve PV isolation without further ablation targeting the earliest PV activity or sites of reverse PV polarity as recorded on the circumferential mapping catheter, as in Fig. 2.2, indicating a residual anatomical connection on the line of ablation. After ablation, nine attempts at induction (with bursts up to a cycle length of 200 ms) at three different places (CS and both appendages) could not induce sustained arrhythmia, predicting a favorable clinical outcome. This case illustrates a typical ablation of paroxysmal AF where it was clearly demonstrated that the arrhythmogenic ectopic beats triggering AF originated from the LSPV.
B
C
I II
V1
PV 1-2 PV 2-3 PV 3-4 PV 4-5 PV 5-6 PV 6-7 PV 7-8 PV 8-9 PV 9-10 CS 1-2 CS 3-4 CS 5-6 CS 7-8 CS 9-10
Fig. 2.3 Endocardial tracings recorded during sinus rhythm from the left superior pulmonary (LSPV) vein. Recording from a decapolar circumferential catheter inserted inside the LSPV (PV 1–2 to PV 9–10) and a decapolar catheter inserted into the coronary sinus (CS 1–2 to CS
9–10). During ablation targeting the earliest venous potential (black star), progressive slowing of the conduction to the vein (panel A and B) to the complete block (panel C)
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Fig. 2.4 Endocardial tracings recorded during sinus rhythm from the left superior pulmonary vein (LSPV). Recording from a decapolar circumferential catheter inserted inside the LSPV (PV 1–2 to PV 9–10)
and a decapolar catheter inserted into the coronary sinus (CS 1–2 to CS 9–10). Dissociation of the venous potential (black star) with a slow automatic activity
Bibliography
Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation. 2006;113(5):616-625. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardia using high-density mapping. J Am Coll Cardiol. 2005 December 6;46(11):2088-2099. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophys. 2007;18(1):1-6.
Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation. 2000;102:2463-2465. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of longlasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophys. 2005;16(11):1125-1137.
Case 3 Amin Al-Ahmad
Case Summary A 51-year-old male with a history of pulmonary fibrosis and a single lung transplant is found to have atrial flutter on routine follow-up. Initially he is unaware of this rhythm, but later recalls an increase in fatigue over the previous week. He is referred for evaluation by an electrophysiologist. A Holter monitor shows his heart rate to be approximately 90 on average. He has periods of normal sinus rhythm and periods of atrial flutter. A 12-lead ECG during atrial flutter is shown in Fig. 3.1. Over the next few months his atrial flutter becomes persistent and he continues to complain of fatigue. He is talking multiple medications post transplant to prevent rejection and has some renal insufficiency. Drug therapy with anti-
arrhythmic medications does not seem to be an attractive option given his multiple co-morbid conditions. And despite better rate control he remains symptomatic and is taken to the electrophysiology suite. Where is this tachycardia origin, and what pacing maneuvers may help determine the best area to ablate?
Case Discussion Atrial flutter can be common immediately after lung transplantation. Canine models have suggested a substrate for atrial flutter in the left atrium due to suture lines. In addition,
Fig. 3.1 Twelve-lead ECG of atrial flutter. Note the peaked and strongly positive flutter waves in lead V1
A. Al-Ahmad School of Medicine, Stanford University, 300 Pasteur Drive, H-2146, Stanford, CA 94305 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_3, © Springer-Verlag London Limited 2011
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right-sided atrial flutters may also develop as these patients can commonly have right atrial dilation due to potentially long-standing increased right-sided pressures. To differentiate right- and left-sided atrial flutter, the flutter wave morphology can be useful. In this case a strongly positive flutter wave in the anterior precordial leads suggests that the flutter is left-sided. In addition, entrainment from areas on the right side can be done quickly and can help
determine if the flutter is left-sided or right-sided. Entrainment can further distinguish the critical isthmus for the atrial flutter and help guide ablation. In this case, entrainment on the right side clearly demonstrated that the flutter was not right-sided (Fig. 3.2). Entrainment in the left atrium near the right inferior pulmonary vein was near perfect. Ablation in that area to create a line to the mitral valve caused the flutter to terminate (Figs. 3.3 and 3.4).
200ms
I II V1 V6
S
RA 9,10 RA 7,8 RA 5,6
PPI
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RA 1,2 CS 9,10 CS 7,8 CS 5,6 CS 3,4 CS 1,2 HIS p HIS m
C
HIS d ABL ABL d Stim 3
S1
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S1 9:42:27 AM
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S1 9:42:28 AM
Fig. 3.2 Pacing in the right atrium shows a long post-pacing interval. This was the case from multiple areas in the right atrium
Case 3
13 200ms
I II V1 V6 RA 9,10 RA 7,8 RA 5,6 RA 3,4 RA 1,2 CS 9,10 CS 7,8 CS 5,6
T
CS 3,4 CS 1,2
ABL ABL d Stim 4
PPI
S1 S1 12:55:47 PM
S1
TCL 12:55:48 PM
12:55:49 PM
Fig. 3.3 Pacing in the left atrium near the right inferior pulmonary vein yields a near-perfect PPI
Bibliography Nielsen TD, Bahnson T, Davis RD, Palmer SM. Atrial fibrillation after pulmonary transplant. Chest. August 2004;126(2):496-500.
Fig. 3.4 Right anterior oblique view of the ablation catheter in the left atrium near the right inferior pulmonary vein. CS coronary sinus, ICE intracardiac echo, ABL ablation catheter
Case 4 Michel Haissaguerre
Case Summary A 56-year-old male was referred for ablation of persistent drug-resistant atrial fibrillation (AF). He had a 17-year history of AF, which had been persistent for the last 12 months. The atrial fibrillation cycle length (AFCL) measured during electrophysiological study was 154, 158, and 152 ms on surface ECG, left and right atrial appendages, respectively (Fig. 4.1). Our approach in persistent AF is to first isolate the pulmonary veins (PVs), before targeting complex fractionated atrial
electrograms (CFAEs) and finally performing linear lesions. Any resulting atrial tachycardias (ATs) are mapped and ablated. In this case, following PV isolation there was prolongation of the AFCL to 165 and 159 ms at left and right appendages, respectively. A NavX fractionation map of the LA was performed using a 20-pole high-density mapping catheter. CFAEs were distributed throughout the LA and the CS, as shown in Fig. 4.2. In cases like this, which CFAE should be targeted, and what is the value in measuring AFCL?
I II V1
LAA
Fig. 4.1 Recording from left (LAA) and right (RAA) atrial appendages, and the coronary sinus (CS 1–2 to 9–10). While fractionation is present in the coronary sinus, preventing an easy measurement of the cycle length, potentials at the top of both appendages are almost always of high voltage and unambiguous
RAA CSd
CSp
M. Haissaguerre Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac 33604, France A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_4, © Springer-Verlag London Limited 2011
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M. Haissaguerre 7CFE Mean Map
120 mS 65 mS
0 mS
Fig. 4.2 NavX (EnSite System, St. Jude Medical, MN, USA) fractionation map of the left atrium and coronary sinus after isolation of the four pulmonary veins showing ubiquitous distribution of complex fractionated electrograms
Case Discussion Atrial electrograms in persistent AF are complex and cannot be reliably evaluated in terms of CL except in either right or left appendage. We routinely place a catheter in the right atrial appendage (RAA) and LAA to measure simultaneously the left and right AFCLs at the start of the procedure (Fig. 4.1). Using custom analysis software (Bard EP, Lowell, MA, USA), the mean AFCL for the selected window is calculated. The electrogram annotation is then verified manually online to ensure accuracy (Fig. 4.1). The electrograms measured at the top of both appendages are almost always discrete and of high amplitude, thereby facilitating unambiguous automatic annotation. In the absence of this software, the mean AFCL can be easily estimated by measuring the total duration required for 10–30 cycles (or longer) and then dividing that number by the number of cycles. Often, the AFCL is also reasonably estimated from V1 on the 12-lead ECG. Following PV isolation and throughout the procedure, the circumferential mapping catheter is placed within the RAA, and the ablation catheter in the LAA, and the AFCL may then be assessed simultaneously to measure the impact of ablation in both chambers. Initial AFCL has been shown to be the strongest predictor of success for AF ablation (AF of less than 5 years
continuous duration). AFCL of less than 140 ms is associated with AF termination in less than 69%, while a higher AFCL like in our case is associated with more than 89% of AF termination. Furthermore, the impact of ablation of each region during electrogram-based ablation can be quantified in both atria by AFCL monitoring. After each step of ablation, a gradual prolongation of AFCL is usually observed (a change in AFCL greater than 6 ms is considered significant). Conversion to sinus rhythm or AT occurs when AFCL reaches between 180 and 200 ms and, conversely, rarely occurs when the AFCL is shorter than this. Concerning the appropriate sequence of ablation during the electrogram-based part of the procedure, the main issue is to distinguish active from passive patterns, which still remains one of the major obstacles to minimal effective ablation of persistent AF. This is particularly striking when there are multiple CFAEs distributed throughout the atrium, as in this case. From a purely anatomic perspective, in addition to PVs, ablation at structures annexed to the LA, namely the interface between the inferior LA and the CS and the base of the LAA, have been shown to have the greatest impact on the AF, as measured by AFCL.1 The endpoint of ablation during electrogram-based ablation remains imprecise; however, the organization and slowing of local potentials by ablation seems for us to be preferable to complete elimination of local potentials. In this case, following PV isolation, ablation started along the inferior LA where continuous activity was recorded (Fig. 4.3, panel A). Ablation at the endocardial interface of the CS aims at interrupting the muscular fascicles connecting the LA and the CS and organizing the chaotic activity recorded within the CS. This resulted in a prolongation of the AFCL to 171 ms in the LAA and 168 ms in the RAA. The following step consisted of the ablation at the posterior part of the LAA, where consistent distal-to-proximal electrograms suggesting centrifugal activation were recorded (Fig. 4.3, panel B); this resulted in a prolongation of both AFCLs to 176 ms. Ablation was performed along the roof of the LA where almost continuous electrograms were recorded (Fig. 4.3, panel C), and the AFCL was prolonged to 188 and 183 ms in the right and left appendages, respectively. Finally, ablation of continuous electrical activity at the anteroseptal LA resulted in restoration of sinus rhythm (Fig. 4.4). During sinus rhythm, PV isolation was confirmed and the roofline was completed.
Case 4
Fig. 4.3 Recording of the ablation catheter (RF) and the coronary sinus (CS 1–2 to 9–10). Panel A: Ablation along the inferior left atrium targeting continuous electrical activity. Panel B: Ablation at the posterior part of the left atrial appendage targeting centrifugal activation with
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consistent distal-to-proximal fractionated electrograms. Panel C: Ablation was then performed along the roof targeting almost continuous fractionated electrograms
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RFp CS 1-2
RFd CS 3-4
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Fig. 4.4 Recording of the ablation catheter (RF) and the coronary sinus (CS 1–2 to 9–10). Ablation of fractionated electrical activity at the anterseptal LA (left panel) resulted in direct restoration of sinus rhythm (right panel, black star)
Bibliography Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation. 2000;102:2463-2465. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of longlasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophys. 2005;16(11):1125-1137.
Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation. 2006;113(5):616-625. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophys. 2007; 18(1):1-6. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardia using high-density mapping. J Am Coll Cardiol. 6 December 2005;46(11):2088-2099.
Case 5 Anurag Gupta and Amin Al-Ahmad
Case Summary A 21-year-old male with Wolf–Parkinson–White syndrome is referred for electrophysiology study given worsening episodes of palpitations. A 12-lead electrocardiogram (ECG) during sinus rhythm shows pre-excitation (Fig. 5.1). Diagnostic electrode catheters are then placed for recording in the His bundle area and right ventricle, as well as a 20-pole Halo catheter for recording in the right atrium adjacent to the tricuspid valve annulus. Ventricular pacing shows the retrograde atrial
activation sequence (Fig. 5.2). Can this patient be treated with a single application of radiofrequency energy? What maneuvers may be helpful in determining this?
Case Discussion Analysis of the delta waves) on the 12-lead ECG during sinus rhythm (Fig. 5.1), including R/S <1 in V2, negative D in III, positive D in V1, and negative D in aVF, is suggestive
Fig. 5.1 Twelve-lead ECG during sinus rhythm showing ventricular pre-excitation
A. Gupta (*) and A. Al-Ahmad Cardiac Electrophysiology Service, Division of Cardiology, Department of Medicine, Stanford University Hospital and Clinics, 300 Pasteur Drive, Room H2146, Stanford, CA e-mail:
[email protected];
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_5, © Springer-Verlag London Limited 2011
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Fig. 5.2 Ventricular pacing from the RV apex. Note the change in the retrograde activation sequence. In the first beat, earliest atrial activation is at pole RA 9,10. However, in the following beat, atrial activation at pole 9,10 is late, whereas atrial activation recorded from the His bundle catheter is earliest. TV tricuspid valve, CS coronary sinus, RA right atrium, HBE His bundle electrogram, P proximal electrode pair, M middle electrode pair, D distal electrode pair, RVA right ventricular apex
Fig. 5.3 Induced SVT. Note the change in the retrograde atrial activation. The SVT continues at the same rate. Is this evidence for another accessory pathway?
of a right posterior/right posterolateral accessory pathway. During electrophysiology study, initiation of orthodromic AVRT is observed at the end of atrial extrastimuli testing; the retrograde atrial activation is observed to change spontaneously during tachycardia (Fig. 5.3). A VPC during the period that the His bundle is refractory advances the following atrial beat and resets the tachycardia. With RF application near Halo RA 9,10 at approximately 8:00 with reference to the left anterior oblique view with the
tricuspid valve depicted as a clockface, the SVT is terminated and pre-excitation is eliminated. However, a second supraventricular tachycardia is subsequently induced with atrial extrastimuli testing. The second SVT has a concentric retrograde activation pattern consistent with the other retrograde pattern seen intermittently during the initial SVT. Para-Hisian pacing is performed (Fig. 5.4).Ventricular pacing next to the His bundle and proximal to the right bundle branch at high output directly captures the His bundle, thus
Case 5
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Fig. 5.4 Para-Hisian pacing is performed. The first QRS complex obtained with highoutput pacing is narrow, while the second QRS complex obtained with low-output pacing is wide with LBBB morphology and longer activation time of RV apex, which is indicative of the loss of His bundle capture. While earliest retrograde activation occurs at the proximal His bundle electrogram in both cases, conduction over an accessory pathway is indicated by minimal change in stimulus to atrial interval and in atrial activation sequence
activating the ventricles through the His–Purkinje system with resultant narrow QRS complex. Ventricular pacing at low output does not capture the His–Purkinje system, as evidenced by left bundle branch block (LBBB) QRS morphology with later activation of the RV apex. However, despite loss of His bundle capture, there is minimal change in the stimulus to atrial interval and activation sequence, which is indicative of another retrograde accessory pathway. RF application of an anteroseptal pathway terminated the tachycardia, and no further SVT was inducible.
Bibliography Chiang CE, Chen SA, Teo WS, et al. An accurate stepwise electrocardiographic algorithm for localization of accessory pathways in patients with Wolff–Parkinson–White syndrome from a comprehensive analysis of delta waves and R/S ratio during sinus rhythm. Am J Cardiol. 1995;76:40-46. 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;94:1027-1035.
Case 6 Michel Haissaguerre
Case Summary A 62-year-old male was referred for a second ablation of persistent atrial fibrillation (AF). He had a 5-year history of AF, which had been persistent for the previous 5 months. The first procedure consisted of pulmonary vein (PV) isolation, ablation of the inferior left atrium (LA) and coronary sinus (CS), electrogram-based ablation at the posterior and anterior LA and a linear lesion at the LA roof. This terminated the AF to an intermediate atrial tachycardia (AT), which was subsequently ablated anterior to the ostium of the left atrial appendage (LAA) with subsequent restoration of sinus rhythm. Unfortunately, a few days later, he had a recurrence, which was considered to be AF (Fig. 6.1). There was relatively organized atrial activity in V1, and the atrial cycle length was 230 ms with slight irregularity and variability in the F-wave morphology. A quadripolar catheter was placed into the CS and this demonstrated a consistent proximal-todistal activation pattern during arrhythmia. A quadripolar cooled-tip ablation catheter was then inserted into the LA. LA endocardial activation was sequentially mapped and appeared to be organized most of the time (Figs. 6.2–6.4). What inferences can be made from Figs. 6.1–6.4 with relevance to the mechanism of atrial arrhythmia?
time period. Mapping of such organized AF can be performed conventionally and allows in most cases to determinate the atrial area from which the centrifugal activation emanates. Then, the area is closely mapped to find either a discrete site of early activity (focal point), or a small circuit (where “early” and “late” cannot, therefore, be defined) representing localized re-entry. In our case, global activation demonstrated a consistent septal-to-lateral activation sequence anteriorly and posteriorly (Fig. 6.2, panel A), a high-to-low activation sequence in the anterior (Fig. 6.3, panel A) and septal LA (Fig. 6.2, panel A), and a low-to-high sequence in the posterior LA (Fig. 6.3, panel B). This activation sequence was compatible with centrifugal activation from a localized source located anterior and septal to the roofline in the presence of roofline block. (A macro re-entrant AT was excluded by the irregularity of the cycle length.) The ablation catheter was placed at the high anteroseptal LA (Fig. 6.4) where the electrograms showed a significant conduction delay between the distal and proximal bipoles. Furthermore, a pause in electrical activity confirmed that the first electrogram to show variation was the distal electrode
I II III
Case Discussion Organized AF may be defined as AF displaying irregular atrial cycle lengths with beat-to-beat variations of ³20 ms, but with discrete atrial complexes having a consistent activation sequence for (arbitrarily) ³75% of the time over a 10-min
AVR AVL AVF VI V2 V3 V4 V5
M. Haissaguerre Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac 33604, France
V6
Fig. 6.1 Electrocardiogram of the atrial arrhythmia with relatively organized atrial activity in V1 despite slight irregularity
A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_6, © Springer-Verlag London Limited 2011
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A
B LAA Septum
Fig. 6.2 Schematic representation of the LA including the left septum and the left atrial appendage (LAA), after the first atrial fibrillation ablation. Representation of previous encirclement of the right (RPV) and left (LPV) pulmonary veins (continuous lines), and the previous ablation of the roofline (dotted line). Electrograms on distal (RFd) and proximal (RFp) poles of the ablation at the mouth of the left appendage (panel A), and at the left septum (panel B). Recording of V1 and electrogram on distal coronary sinus (CS)
M. Haissaguerre
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pair of the mapping catheter, while the other electrograms followed with the same activation sequence. After these observations, other electrograms were recor ded within 10–15 mm of the original site, and the whole span of the cardiac cycle was mapped in this area: the initial part of the circuit, the second part of the circuit, and throughout the circuit (Fig. 6.5). These findings were compatible with a localized re-entrant circuit with centrifugal activation of the LA, except for the posterior wall because of the roofline block. Ablation at this site slowed and terminated the tachycardia. Conduction block over the roofline was confirmed in sinus rhythm. Localized sources perpetuating AF have been described during ablation procedures as persistent fibrillatory activity confined within isolated LA areas after restoration of sinus rhythm. These sources play an important role in AF maintenance, in addition to pulmonary vein (PV) activity and re-entrant loops. After pulmonary vein isolation (PVI) and linear lesions, ablation of these sources remains the last step of substrate elimination and results in AT conversion or restoration of sinus rhythm.
A localized source may be a discrete point or a small area. During organized AF, when atrial activation mapping converges towards the origin of activity, a small area displaying centrifugal activation and including the localized source can be analyzed. This area may include a discrete point – harboring less than 75% of the cycle length (CL) – which allows tracking of the earliest activity and where local electrograms display centrifugal activation with or without one-to-one conduction to the adjacent atrium (i.e., the same or faster cycle length of the source compared to the atrial fibrillation cycle length [AFCL], respectively). In the majority of cases, the source is not a discrete point but a small area of localized re-entry, as in this case. This area of earliest activation displays electrical activity covering 75–100% of the cycle length, suggesting a localized small circuit. By mapping with a conventional quadripolar ablation catheter, local potentials will display either continuous activity spanning most of the CL or temporally alternating potentials between distal and proximal bipoles (depending on the re-entrant circuit size and properties). By mapping with a high-density 20-pole catheter, local activity will span most or all of the CL.
Case 6
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Fig. 6.3 Same graphic as Fig. 6.2, with the addition of an anterior wall. Ablation catheter positioned at the anterior (panel A) and posterior (panel B) left atrium
A
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Indeed, irregularity was >15% of the CL (inset ECG) suggesting, in fact, focal AT. Furthermore, post pacing interval (PPI) at the posterior wall was short (+20 ms), but the anterior PPI was very long (+200 ms), ruling out macro re-entrant roof-dependant AT. Since the roofline was previously blocked, it suggested a focal origin from the high posterior LA. Mapping this area close to the roof line revealed very low voltage local activity spanning most of the CL at three different spots very close to each other (Fig. 6.3, POST 1–3). This voltage was only 0.04 mV, which can be easily hidden in case of electrical noise. Ablation of a very low voltage continuous activity site located in between the three described spots terminated the tachycardia (Fig. 6.4). This case emphasizes the importance of localized re-entrant AT in the context of prior AF ablation. In this context, 53% of AT are focal, and localized re-entries are the
most frequent AT mechanism, representing 71% of focal ATs (and 37% of total ATs). The preferential regions for focal ATs are the PV–LA junction, left septum, and the mouth of the LAA. Focal ATs are generally localized to sites targeted during electrogram-based AF ablation. Injury or oedema to the atrial tissue induced by RF applications could generate the substrate for further arrhythmia by creating an anchoring point potentially able to maintain re-entry. Therefore the mechanism of AT after AF ablation may be different to that of spontaneous AT. The presence of pre-existing LA scar (which may be idiopathic or related to underlying structural heart disease) may also result in local slow conduction areas predisposing to re-entry. Mapping and ablation of focal or macro re-entrant AT is a crucial step in the AF ablation process, and often represents the difference between procedural success and failure.
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Fig. 6.4 Same graphic as Fig. 6.2. Ablation catheter positioned a nterior and septal to the roofline
LAA LPV
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Fig. 6.5 Scanning the area within 10–15 mm of the site showed in Fig. 6.4: Electrograms show activation compatible with the entire circuit (initial part in RF2, second part in RF3 and throughout the circuit in RF1). These data are most compatible with left atrial activation coming centrifugally from a small re-entrant source central to the excursion of the catheter in this small area
RPVs
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Case 6
Bibliography Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation. 2006;113(5):616-625. Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation. 2000;102:2463-2465.
27 Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of longlasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophys. 2005;16(11):1125-1137. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardia using high-density mapping. J Am Coll Cardiol. 6 December 2005;46(11):2088-2099. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophys. 2007;18(1):1-6.
Case 7 Michel Haissaguerre
Case Summary A 67-year-old male with an 8-year history of persistent atrial fibrillation (AF) and three external direct current (DC) cardioversions was referred for ablation. The inital procedure consisted of pulmonary vein (PV) isolation, extensive ablation based on fractionated electrograms in the left atrium (LA) and the right atrium (RA), and linear lesions at the roof and the left mitral isthmus. AF was not terminated and an external cardioversion was required. Linear lesions (left atrial roofline and mitral isthmus line) were completed during sinus rhythm. Early recurrence of AT necessitated a second ablation procedure one month later. A decapolar catheter was placed into the CS and showed a proximal-to-distal activation pattern. A quadripolar cooled-tip ablation catheter was then inserted into the LA. AT cycle length was 260 ms with 10% irregularity. PV isolation was confirmed. Extensive anterior scar was noted, and anterior endocardial activation was difficult to assess, but it appeared to be septal to lateral. Post pacing interval (PPI) at the RA was long (+130 ms), PPI at the posterior LA was long (+120 ms). PPI in the LAA was long (+60 ms), while PPI at the anterior LA was good (+10 ms). The anterior part of the LAA showed almost continuous activity (Fig. 7.1). Can this site be considered for ablation?
Case Discussion In the case of extensive scarring or ablation, mapping of AT can be challenging with the practical algorithm. In this situation, three methods can be used to facilitate identification
and ablation of the AT (Fig. 7.2). Entrainment manoeuvres performed during the arrhythmia point towards a focal origin by demonstrating long return cycle lengths around the mitral annulus, the roofline or the tricuspid annulus except at sites adjacent to the focus (by definition, less than two segments). For localized re-entry, local activity spanning all of the AT CL can be demonstrated at the area of earliest activity. For focal point AT, an area of early activity may exhibit middiastolic potential. These tracings illustrate a case with prior extensive LA ablation including the left mitral isthmus line. Conduction around the mitral annulus was compatible with a perimitral circuit (lateral to septal anteriorly and septal-to-lateral posteriorly). The PPI was <30 ms at the anterior annulus, but >30 ms at the CS, which made a macro re-entrant peri-mitral circuit unlikely and suggested a focal AT located lateral to the complete left mitral isthmus line. Mapping was performed in this area where a site displaying most of the CL was found at the anterior mouth of the LAA (Fig. 7.1); however, the PPI was 100 ms at this site, suggesting it was far from the origin of the AT. A second site displaying most of the CL with an activation gradient on the electrogram recording and a short PPI (10 ms) was mapped on the anterior LA (Fig. 7.3). A threedimensional reconstruction of this spot with activation mapping confirmed that the activity spanned all the cycle lengths in a very localized region (Fig. 7.4). Ablation at this site restored sinus rhythm, and a local double potential was visualized after ablation (Fig. 7.5, arrows) in sinus rhythm. This case illustrates how useful the PPI can be in difficult cases. During entrainment, attention must be paid to avoid induction of AF at short CLs and one must be aware of the possibility of conversion to another AT.
M. Haissaguerre Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac 33604, France A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_7, © Springer-Verlag London Limited 2011
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RFd
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CS 1-2 CS 3-4 CS 5-6 CS 7-8 CS 9-10
Fig. 7.1 Recordings of the radiofrequency RF ablation catheter and a decapolar catheter inserted into the coronary sinus (CS 1–2 to 9–10). Site of high-voltage continuous electrograms displaying almost all the cycle length
PPI to assess number of segment(s) involved
Fig. 7.2 Approach to atrial tachycardia in the context of atrial fibrillation (AF), in the case of extensive scar or ablation. See text for details
≤2 segments FOCAL
>2 segments MACRO RE-ENTRY
• EGM spanning all the AT cycle length in the involved segment(s) • Mid diastolic potentials
Activation compatible with: • Perimitral macro re-entry • Roof dependant macro re-entry • Peritricuspid macro re-entry More complex macro re-entry
Case 7
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Fig. 7.3 Recordings of the RF ablation catheter and a decapolar catheter inserted into the coronary sinus (CS 1–2 to 9–10). Site of complex fractionated electrograms with a gradient of activation between the proximal and distal bipoles (black arrows)
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Fig. 7.4 NavX (EnSite System, St. Jude Medical, MN, USA) activation map (antero-posterior view) showing local activity spanning all the cycle lengths in a very localized region below the left atrial appendage
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Fig. 7.5 Recordings of the RF ablation catheter and a decapolar catheter inserted into the coronary sinus (CS 1–2 to 9–10). After restoration of sinus rhythm, local double potential visualized after ablation
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Case 7
Bibliography Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation. 2000;102:2463-2465. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of longlasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophys. 2005;16(11):1125-1137.
33 Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation. 2006;113(5):616-625. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophys. 2007;18(1):1-6. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardia using high-density mapping. J Am Coll Cardiol. 2005 December 6;46(11):2088-2099.
Case 8 Michel Haissaguerre
Case Summary A 54-year-old female with persistent atrial fibrillation (AF) for 12 months, a 10-year history of AF, a dilated left atrium (LA) (54 mm diameter), and having failed five external cardioversions and amiodarone, was referred for ablation. Baseline AF cycle length (CL) before ablation was 135 ms in the left atrial appendage (LAA) and 132 ms in the right atrial appendage (RAA). The first procedure consisted of PV isolation, extensive ablation based on electrograms in the LA, and linear lesions at the roof and the left mitral isthmus. Then electrogram-based ablation in the RA resulted in a transient conversion to atrial tachycardia (AT). Early recurrence of AF
I II V1
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required external cardioversion to restore sinus rhythm. During sinus rhythm, both linear lesions were assessed and completed. Four months later, the woman developed an AT and she therefore had a second ablation procedure. A decapolar catheter was placed into the coronary sinus (CS) and demonstrated a colliding activation pattern in the proximal CS. A quadripolar cooled-tip ablation catheter was then inserted into the LA. AT cycle length was 271 ms with irregularity reaching 22% of the mean AT cycle length. Pulmonary vein isolation (PVI) was confirmed, and the endocardial activation was determined by moving the ablation catheter sequentially in the anterior LA (Fig. 8.1, panel A, low anterior; and
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M. Haissaguerre Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac, 33604, France A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_8, © Springer-Verlag London Limited 2011
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Fig. 8.1, panel B, high anterior) and in the posterior LA (Fig. 8.1, panel C, high posterior; and Fig. 8.1, panel D, low posterior). Activation was ascending in the anterior wall (Fig. 8.1, panels A and B) and descending at the posterior wall (Fig. 8.1, panels C and D) with the activation sequence covering all the AT cycle length. What inferences can be made from Fig. 8.1 with relevance to the mechanism of AT, and what maneuver has to be done to confirm the diagnosis?
Case Discussion First, for the purposes of describing the approach to ATs arising in the context of catheter ablation of AF, the following definitions are employed: macro re-entry is defined as a circuit involving more than three atrial segments, usually greater than 2 cm in diameter and where more than 75% of the circuit is mapped. Focal point tachycardia is defined as centrifugal activation originating from a discrete site and includes automaticity, triggered activity, and re-entrant mechanisms where <75% of the cycle can be mapped in the chamber of interest. Localized re-entry constitutes a circuit involving one or two adjacent segments, usually smaller than 2 cm in diameter and spanning more than 75% of the CL within the involved segment(s). A diagnostic algorithm has been developed by our group to allow easy and accurate mapping of AT arising in the context of prior AF ablation (Fig. 8.2). After confirmation of PVI, it consists of 1. Assessment of AT cycle length variability: if >15%, suggestive of focal AT and if <15%, not of discriminating value (CL variability is calculated by dividing the CL range by the mean CL averaged over 30 cycles)
Yes
CL Irregularity >15%
No
Focal
Focal or macroreentry
Map earliest region
Activation compatible with: • Perimitral macro re-entry • Roof dependant macro re-entry • Peritricuspid macro re-entry
• Localized re-entry • Focal point AT No
• ~100% cycle • Entrainment Yes Macro re-entry
Fig. 8.2 Practical approach to atrial tachycardia (AT) in the context of atrial fibrillation (AF) ablation. See text for details
2. Macro re-entry is first investigated by assessing the activation in the LA, in order to determine the likelihood of perimitral, roof-dependent, or peritricuspid circuit (entrainment maneuvers are used to confirm the diagnosis) 3. In the case of the absence of macro re-entrant AT, focal point/area AT is determined by tracking the earliest area of activity (entrainment maneuvers can be used to evaluate the site of origin). In the case of localized re-entry, long-duration fractionated potentials spanning most or all of the CL are tracked. Otherwise, the earliest activity is targeted 4. In the case of nonconsistency, more complex tachycardia are investigated, or a change in AT (mechanical or due to stimulation) is searched In our case, the activation front was consistent with a roofdependent macro-re-entry (from A to D): ascending the anterior wall (solid line, A to B) and descending the posterior wall (dashed line, C to D). The mapped activity spanned the entire CL (potentially compatible with roof dependent AT), but slow conduction in the anteroseptal area (A) could be misleading. Indeed, irregularity was >15% of the CL (inset ECG), suggesting in fact focal AT. Furthermore, PPI at the posterior wall was short (+20 ms), but the anterior PPI was very long (+200 ms), ruling out macro re-entrant roof-dependant AT. Because the roof line was previously blocked, it suggested a focal origin from the high posterior LA. Mapping this area close to the roof line revealed very low voltage local activity spanning most of the CL at three different spots very close to each other (Fig. 8.3, POST 1 to 3). This voltage was only 0.04 mV, which can be easily hidden in case of electrical noise. Ablation of a very low voltage continuous activity site located in between the three described spots terminated the tachycardia (Fig. 8.4). This case emphasizes the importance of localized re-entrant AT in the context of prior AF ablation.1 In this context, 53% of AT are focal and localized re-entries are the most frequent AT mechanism, representing 71% of focal ATs (and 37% of total ATs). The preferential regions for focal ATs are the PV–LA junction, left septum, and the mouth of the LAA. Focal AT are generally localized to sites targeted during electrogram-based AF ablation. Injury or edema to the atrial tissue induced by RF applications could generate the substrate for further arrhythmia by creating an anchoring point potentially able to maintain re-entry. Therefore the mechanism of AT after AF ablation may be different to that of spontaneous AT. The presence of preexisting LA scar (which may be idiopathic or related to underlying structural heart disease) may also result in local slow conduction areas predisposing to re-entry. Mapping and ablation of focal or macro re-entrant AT is a crucial step in the AF ablation process, and often represents the difference between procedural success and failure.
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Fig. 8.3 Antero-posterior fluoroscopic view of the left atrium (LA). Mapping of three close posterior spots (post 1–3). Local activity (within red rectangles) spanning the entire CL (pink bars)
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Fig. 8.4 Antero-posterior fluoroscopic view of the left atrium (LA) with a decapolar catheter placed into the coronary sinus (CS). Panel A: Ablation catheter (Abl) placed in the posterior LA and recording a very low voltage
(<0.05 mV) signal spanning all of the CL. Panel B: Change of the atrial tachycardia (AT) (black star) during radiofrequency application at this posterior wall
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Bibliography Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation. 2000;102:2463-2465. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of longlasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophys. 2005;16(11):1125-1137.
M. Haissaguerre Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial fibrillation organized by prior ablation. Circulation. 2006;113(5):616-625. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophys. 2007;18(1):1-6. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachycardia using high-density mapping. J Am Coll Cardiol. 2005 December 6;46(11):2088-2099.
Case 9 Alberto Diaz, Dimpi Patel, William R. Lewis, and Andrea Natale
Case Summary The patient is a 55-year-old male with a history of hypertension, left ventricular hypertrophy, and paroxysmal atrial fibrillation (AF) since 2001; both Flecainide and Sotalol had failed. He underwent AF ablation in August 2007. He was placed on Sotalol after radiofrequency ablation (RFA). A month later he had recurrent palpitations that required electrical cardioversion. His arrhythmia was exacerbated after trying to come off the Sotalol. He was evaluated for a repeat ablation. His echocardiogram showed a normal left ventricular ejection fraction (LVEF), normal left atrial size, no valvular abnormalities. His adenosine stress test showed no evidence of ischemia with a LVEF of 74%. He was brought to the EP lab. A catheter was placed in the CS via the internal jugular vein; two transseptal sheaths were used to advance the ablation catheter and the Lasso catheter. The right and left superior pulmonary veins (RSPV and LSPV) appeared to have recovered and were re-ablated (Figs. 9.1 and 9.2.).
Following ablation, isoproterenol was given up to a dose of 20 mcg/kg/min. Following that, the PVs were mapped again to check for electrical isolation. The EGMs below were observed placing the Lasso catheter in the RSPV and the LSPV. Based on the recordings, what would you consider? a) Ablate the left superior PV b) Ablate the right superior PV c) Ablte both PVS d) No additional ablation
Case Discussion Both left and right PVs showed dissociated firing, which confirms both entry and exit blocks. During isoproternol infusion, AF started inside the right upper PV without affecting the atrial chambers, which remained in sinus rhythm. This confirms that there is no reason for additional ablation.
A. Diaz () Heart and Vascular Department, Metro Health Medical Center, 2500 Metro Health Drive, Cleveland, OH, 44109 e-mail:
[email protected] D. Patel St. David’s, Texas Cardiac Arrhythmia Institute, 1015 E. 32nd St, #516, OH Austin, TX 78705 W.R. Lewis Clinical Cardiology, Case Western Reserve University, Heart and Vascular Center, MetroHealth Medical Center, 2500 MetroHealth Drive, Suite H322, Cleveland, OH 44109 A. Natale Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32nd Street, Suite 516, Austin, TX 78705
A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_9, © Springer-Verlag London Limited 2011
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Fig. 9.1 Lasso in the left superior pulmonary vein (LSPV)
Fig. 9.2 Lasso in the right superior pulmonary vein (RSPV)
A. Diaz et al.
Case 10 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary The patient is a 13-year-old male with prior 8-year history of palpitations during exercise. No structural heart disease. The transesophageal EP study easily demonstrated the induction of sustained SVT during minimal effort (AA300ms). The echocardiography evaluation was normal and 24 h-ECG Holter documented two episodes of SVT which began after a physiologic increase in heart rate.
After examining Figs. 10.1–10.3, what is the likely diagnosis?
Case Discussion This case demonstrates a narrow complex tachycardia that is not 1:1; with A > V. This excludes AVRT and makes AVNRT less likely unless there is block below the lower common pathway (see Figs. 10.4–10.8).
Fig. 10.1 12-lead resting ECG (paper speed 25 mm/s) showing normal sinus rhythm with a ventricular rate of 66 bpm and a normal PR interval (136 ms) and a QRS width of 100 ms
A. Rossillo (), S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_10, © Springer-Verlag London Limited 2011
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Fig. 10.2 Panel A: 12-lead ECG taken during atrial tachycardia (paper speed 25 mm/s). Panel B: a detail of lead D2, aVL, and V1
Case 10 Fig. 10.3 Intracardiac recordings taken during the electrophysiology study (paper speed 100 mm/s) revealing SVT with a cycle length of 300 ms. Four surface ECG leads (I, aVF, V1, V6), three bipolar recordings from the His bundle region (distal= HIS D, intermediate = HIS I, and proximal = HIS P), two bipolar recordings from the coronary sinus (CS prox = proximal coronary sinus and CS dist = distal coronary sinus), and the unipolar (MC U-CATH) and the distal bipolar recording of the mapping catheter (MC D)
Fig. 10.4 The electroanatomical mapping of the tachycardia showed the origin of the arrhythmia coming from the His bundle region (the red area in the LAO view). The orange tags show the area where it was possible to record the His bundle potentials
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Fig. 10.5 Electroanatomical mapping with CARTO: detailed remap of the area of interest; the orange tag shows the His bundle potential and the blue tag shows the site of earliest activation during tachycardia
Fig. 10.6 Electroanatomical mapping with CARTO: detailed remap of the area of interest; the orange tag reflects the His bundle potential, the blue tag shows the site of earliest activation during tachycardia, and the red tag shows where a single RF lesion is applied
Case 10 Fig. 10.7 Intracardiac recordings taken at the ablation site (paper speed 100 mm/s). Same display as that shown in Fig. 10.3. A atrium, V ventricle
Fig. 10.8 Intracardiac recordings taken at the ablation site (paper speed 100 mm/s) during RF application. A single RF application of 30 s with titration of the power starting from 30 W resulted in sinus rhythm restoration. RF energy was stopped as soon as the His bundle potential appeared on the ablation catheter. Same display as that shown in Fig. 10.3. A atrium, V ventricle, H His bundle
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Bibliography Chen SA, Chiang CE, Yang CJ, Cheng CC, et al. Sustained atrialtachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90:1262-1278. Frey B, Kreiner G, Gwechenberger M, Gossinger H. 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. Kalman JM, Olgin JE, Karch MR, et al. “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol. 1998;31:451-459. Kay GN, Chong F, Epstein AE, Dailey SM, Plumb VJ. Radiofrequency ablation for treatment of primary atrial tachycardias. J AM Coll Cardiol. 1993;21:901-909. 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;33:775-781.
A. Rossillo et al. Lai LP, Lin GL, Chen TF, et al. Clinical electrophysiological characteristics and radiofrequency catheter ablation of atrial tachicardia near the apex of Koch’s triangle. PACE. 1998;21:367-374. Lesh MD, Van Hare GF, Epstein LM, et al. Radiofrequency Catheter ablation of atrial arrhythmias: results and mechanisms. Circulation. 1994;89:1074-1089. Pappone C, Stabile G, De Simone A, et al. Role of catheter-induced mechanical trauma in localisation of target sites of radiofrequency ablation of automatic atrial tachycardia. J Am Coll Cardiol. 1996;27:1090-1097. Poty H, Saudi N, Haissaguerre M, et al. Radiofrequency catheter ablation of atrial tachycardias. Am Heart J. 1996;131:481-489. Tang CW, Scheinmann MM, Van Hare GF, et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol. 1995;26:1315-1324. 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;21:910-917.
Case 11 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary
Case Discussion
A 17-year-old male with a normal heart has an electrocardiogram (ECG) showing intermittent pre-excitation suggestive of left free-wall accessory pathway (AP) and supraventricular tachycardia (SVT). The induced tachycardia is a narrow QRS regular tachycardia (Fig. 11.1) with ST depression in inferior leads. The patient is taken to the electrophysiological (EP) lab. In Fig. 11.2 the ablation catheter is positioned at the lateral tricuspid annulus (9 o’clock). Where is the site of the successful ablation?
The first two complexes show earliest A in CS 1-2 and in RFD; after this the coronary sinus (CS) activation reverses, but the A remains earliest in Radiofrequency Distal (RFD), suggesting that the orthodromic atrioventricular reentrant tachycardia (AVRT) is mediated by a right free-wall AP with a bystander left-lateral AP. Ablation of the right-sided AP resulted in success.
Y.Y. Lokhandwala () KEM Hospital, Parel, Mumbai, India A.K. Gupta Apollo Hospital, Ahmedabad, India R.K. Thakur Thoracic and Cardiovascular Institute Sparrow Health System, Michigan State University 405 West Greenlawn, Suite 400, Lansing, MI 48910 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_11, © Springer-Verlag London Limited 2011
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I II III AVR AVL AVF V1 V2 V3 V4 V5 V6 10 mm/mV 25 mm/s
Fig. 11.1 The electrocardiogram (ECG) shows induced tachycardia
Case 11
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AVF V1 V6 CS910 CS78 CS56 CS34 CS12 HISD HISP RFD RFP 10 mm/mV 200 mm/s
Fig. 11.2 Intracardiac recordings. CS 1-2 is distal. The ablation catheter (RFD) is placed along the lateral tricuspid annulus
Case 12 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 59-year-old male with ischemic cardiomyopathy who underwent heart transplantation three years earlier was repeatedly hospitalized for atrial flutter (AFL) (Fig. 12.1, panel A) refractory to rate control and antiarrhythmic drugs. Left ventricular ejection fraction was normal by echocardiography. He was referred for electrophysiology study and ablation. Intracardiac recordings showed AFL with tachycardia cycle length 268 ms and earliest left atrial activation from the distal coronary sinus (CS), consistent with a left atrial circuit (Fig. 12.1, panel B). Entrainment pacing from the mid-CS A
performed during flutter demonstrated a long post-pacing interval of 442 ms. Noteworthy was that during entrainment pacing from the high right atrial (HRA) catheter, 2:1 block of right-to-left atrial conduction was observed without terminating the tachycardia (Fig. 12.1, panel C). Where is the likely circuit of this flutter?
Case Discussion Based on Fig. 12.1, which shows the left atrium dissociated from the flutter circuit during tachycardia, left AFL was excluded from the differential diagnosis. Electroanatomic
B
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Fig. 12.1 Cardiac tracings recorded during the clinical atrial flutter (AFL). Panel A: Surface 12-lead ECG recorded during AFL. Panel B: Intracardiac tracings and ECG leads II, V2, and V5 showing earliest left atrial activation in the distal CS. Panel C: Intracardiac tracings and ECG leads II, V2, and V5 showing entrainment pacing from the HRA, and 2:1 block of the right-to-left atrial conduction. CS coronary sinus, HRA high right atrium, CS (HB) d,p the distal and proximal electrode pairs of the coronary sinus (His bundle) catheter
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_12, © Springer-Verlag London Limited 2011
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mapping of the right atrium (RA) showed large areas of lowvoltage scar (colored gray in Fig. 12.2). Activation mapping revealed a macro-reentrant AT utilizing a channel in the lateral wall of the RA (Fig. 12.2). A line of ablation along the lateral RA wall, shown in Fig. 12.2, successfully terminated the tachycardia. It is known that conduction from RA to LA
occurs over multiple septal pathways, including Bachmann’s bundle, the foramen ovale, and CS.1 In this case, due to scarring over a large part of the RA, conduction through Bachmann’s bundle was more rapid than the lower septal sites, resulting in distal to proximal of LA activation as seen in the CS catheter.
200 ms
Fig. 12.2 Electroanatomic map of the right atrium during the clinical AFL. Red areas indicate earliest endocardial activation; orange, yellow, green, blue, and purple indicate progressively delayed activation. The scar is shown in gray (<0.1 mV). White tags indicate the ablation sites. The black solid arrows show the activation sequence within the tachycardia circuit, and the black dotted arrows show bystander activation of right atrium as well as left atrium via Bachmann’s bundle. TA tricuspid annulus, RA right atrium, AFL atrial flutter
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Reference 1. Roithinger FX, Cheng J, SippensGroenewegen A, et al. Use of electroanatomic mapping to delineate transseptal atrial conduction in humans. Circulation. 1999;100:1791-1797.
Conduction via Bachmann’s bundle
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Case 13 Bradley P. Knight
Case Summary A 54-year-old female with mental retardation presented to the emergency department with a recurrent supraventricular tachycardia (SVT) at 180 bpm. An electrophysiology (EP) study was performed. The baseline rhythm was sinus rhythm without ventricular preexcitation. Her clinical tachycardia was induced when an atrial extrastimulus was delivered with a coupling interval of 340 ms during a drive train with a cycle length (CL) of 550 ms (Fig. 13.1). There was a one-to-one relationship between the atrium and the ventricle. The ventriculoatrial (VA) interval associated with the first beat of the tachycardia is nearly identical to the remaining VA intervals. Can atrial tachycardia be excluded?
is “VA linking.” This observation strongly suggests that the atrial depolarization is dependent on the ventricular depolarization, meaning that the atrial rhythm is dependent on VA conduction. This should not be present with an atrial tachycardia, because the first beat of the tachycardia should have no relationship to the prior QRS, which was a result of conduction of the atrial extrastimulus to the ventricle. This observation can be useful, but it is important to recognize that it is not absolute and should be reproducible. There is always a small chance that the first VA interval will be the same or similar as that during tachycardia by chance alone. Indeed, in this case the tachycardia was actually a left atrial septal tachycardia. Figure 13.2 shows a spontaneous initiation of the same tachycardia that is shown in Fig. 13.1 by a premature atrial beat during sinus rhythm. This event shows that at times the tachycardia does not have a constant VA interval and occasionally displays Wenckebach AV block.
Case Discussion When a tachycardia with a constant VA interval is induced with an atrial premature beat and the first VA interval is the same as the subsequent VA intervals, it can be said that there
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_13, © Springer-Verlag London Limited 2011
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Fig. 13.1 Induction of a supraventricular tachycardia with a single atrial extrastimulus. Shown are surface electrograms from leads I, II, V1, and V6, and the intracardiac electrograms from the high right
atrium (HRA), the ablation catheter (ABL) positioned at the His bundle location, and the right ventricular apex (RVA)
Case 13
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Fig. 13.2 A different induction of the same supraventricular tachycardia shown in figure 13.1 showing a variable ventriculo-atrial relationship. The format is the same as in Figure 13.1
Case 14 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
Case Summary A 27-year-old male complained of multiple episodes of palpitations. His echocardiogram (ECG) and baseline ECG were within normal limits. His palpitations were captured with the 12-lead ECG shown in Fig. 14.1. In the electrophysiology (EP) lab, the same tachycardia was induced. After pacing from the right ventricle during the tachycardia shown in Fig. 14.1, the rhythm changed to the ECG shown in Fig. 14.2. During the ventricular programmed stimulation, the results shown in Fig. 14.3 were observed. The tachycardia was initiated in the lab with the atrial programmed stimulation shown in Fig. 14.4. Two ventricular extrastimuli were performed from the right ventricular apex during the tachycardia, showing the results in Fig. 14.5. Three ventricular extrastimuli were performed during the tachycardia, which showed the results in Fig. 14.6. What can be excluded? What is the diagnosis?
Case Discussion The initial presentation of this healthy young male is a wide complex tachycardia with right bundle branch block (RBBB) morphology and right axis deviation. The duration of the QRS is 145 ms. It is difficult to assess if there are P-waves. If the small deflection between the two QRS complexes is a P-wave, there is an AV association. Interestingly, there is an obvious electrical alternans present, occurring simultaneously with a CL alternans. These findings favor supraventricular tachycardia (SVT) rather than ventricular tachycardia (VT) or atrial flutter (AFL). However, we cannot exclude any of the possibilities.
M.E. Mortada (*), J.S. Sra, and M. Akhtar Department of Electrophysiology, Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke’s Medical Centers, University of Wisconsin School of Medicine and Public Health, 2801 W. Kinnickinnic River Parkway, #777, Milwaukee, WI 53215
After pacing from the right ventricle, the QRS narrows down to a normal duration (72 ms). The electrical alternans remains the same. However, the CL of the tachycardia accelerates from 259 to 240 ms. This indicates the presence of an accessory pathway (AP) ipsilateral to the bundle branch block (right), which is part of the electrical circuit of the tachycardia. Hence the tachycardia is due to orthodromic AV reentry with aberrancy. The aberrancy disappears due to early activation of the right bundle by pacing from the right ventricle, leading to a break-in-the-link phenomenon and early recovery of the right bundle, in readiness for anterograde activation from the next beat, causing narrow QRS morphology.1 The narrow complex tachycardia (Fig. 14.2) has an incomplete RBBB with QRS at 80 ms and a rate of 240 beats per minute. The P-wave is in the ST-T segment, suggestive of short RP tachycardia. The most likely diagnosis is either AP-mediated tachycardia or atrial tachycardia. Though, one cannot exclude AV-nodal reentry tachycardia or para-Hisian ventricular tachycardia with one-to-one VA conduction — but this phenomenon is very rare. During ventricular pacing (Fig. 14.3), the VA conduction was retrograde over the AV node during the first two beats. When a ventricular extrastimuli was introduced (third beat), the VA conduction continued retrogradely over the AV node with a longer VA duration, due to the decremental property of the AV node rather than to a jumping phenomenon (dual physiology). The fourth ventricular beat is either a ventricular repetitive response or a bundle branch reentry beat, which does not result in retrograde atrial activation. The absence of VA conduction over an AP during ventricular pacing and at the time of AV nodal block makes it less likely that AP-mediated tachycardia is the cause – but it does not exclude the possibility. Some APs have multiple fibers at their ventricular insertion sites where they might interact during the electrical propagation, leading to block and prevention of retrograde conduction over the AP.2, 3 The possibility that this VT is para-Hisian in origin is less likely, due to the weak retrograde conduction over the AV node. Therefore, none of the findings in Fig. 14.3 help define the cause of the tachycardia.
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Fig. 14.1 The patient’s palpitations were captured with this 12-lead ECG
Fig. 14.2 The same tachycardia was induced in the electrophysiology lab. After pacing from the right ventricle during the tachycardia, the patient’s rhythm changed, as shown in this ECG
Case 14
Fig. 14.3 Tracing of patient’s response to ventricular programmed stimulation with one ventricular extrastimuli. The recording in this figure and other figures are (from top to bottom): surface ECG with leads I, II and V1, high right atrial recording, proximal coronary sinus (CS
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9,10) to distal coronary sinus (CS 1, 2), His bundle recording and right ventricular recording. HRA: high right atrium; CS: coronary sinus; HISp: proximal His, HISm: middle His; HISd, distal His, RVa: apical right ventricle
Fig. 14.4 Tracing demonstrating the initiation of the tachycardia with atrial programmed stimulation
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Fig. 14.5 Two ventricular extrastimuli during the tachycardia
Fig. 14.6 Three ventricular extrastimuli during the tachycardia
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Case 14
One extrastimuli from the high right atrium (HRA) induced tachycardia with right bundle branch block morphology and right axis deviation (Fig. 14.4). The activation sequence of the tachycardia is: left atrium (LA) to right atrium (RA), then His, followed by ventricular activation (VA). The most likely cause for this rhythm is left atrial tachycardia or orthodromic AV reentry tachycardia (AVRT) via the left free-wall AP. Antidromic AVRT, in which the electrical activation should be V-H-A, is ruled out in this case due to the sequence of the electrical activation (A-H-V) and the fact that the tachycardia is initiated by antegrade activation over the AV node. Induction of VT via extrastimuli at the high right atrium (HRA) can be seen in bundle branch reentry or fascicular ventricular tachycardia. Atrial eccentric activation usually does not rule out AVNRT. Six to eight percent of AVNRTs display eccentric atrial activation.4, 5 However, the eccentric activation occurs with earliest atrial activation coming from an area not more than 4 mm from the AV node. Hence, AVNRT can be ruled out in this case because the earliest atrial activation was at CS 1-2 (left atrial free wall), which is more than 4 mm away from the AV node. A study of the ventricular extrastimuli present during supraventricular tachycardia (SVT) at the time of His refractoriness is sometimes helpful in defining the cause of the tachycardia. In this case (Fig. 14.5), two extrastimuli are seen. The first was late and fused with the QRS of the tachycardia. The second came a few milliseconds prior to the His activation (His refractory period). If the next atrial activation occurred earlier, the presence of AP could be confirmed. However, the atrial activation did not change, as occurs in both atrial tachycardia and AVNRT.
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AP-mediated tachycardia cannot be excluded, because the distance from the right ventricular apex to the assumed AP, which should be on the left ventricular free wall in this scenario, far from the tachycardia circuit. Therefore, pacing with one or two extrastimuli, from the right ventricular apex, may not enter and entrain the tachycardia circuit. Three ventricular extrastimuli were performed at cycle lengths of 210 ms to entrain the tachycardia (cycle length, 245 ms), which showed VAV response, thus atrial tachycardia was excluded. The post-pacing interval was 330 ms, thus the pacing site is near to the circuit and the diagnosis is orthodromic AVRT via the left ventricular free-wall AP.
References 1. Lehmann MH, Denker S, Mahmud R, Addas A, Akhtar M. Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits. Circulation 1985;71:254-265. 2. Rordorf R, Vicentini A, Petracci B, Landolina M. Intermittent ratedependent retrograde conduction over a concealed atrioventricular accessory pathway: what is the mechanism? Europace 2008;Dec 3(epub ahead of print). 3. Bai R, Tritto M, Di Biase L, Salerno-Uriarte JA. Pacing site and bradycardia dependent retrograde conduction block over an atrioventricular accessory pathway. Europace 2006;8:438-442. 4. Ong MG, Lee PC, Tai CT, Lin YJ, Hsieh MH, Chen YJ, Lee KT, Tsao HM, Kuo JY, Chang SL, Chen SA. The electrophysiologic characteristics of atrioventricular nodal reentry tachycardia with eccentric retrograde activation. Int J Cardiol 2007; 120:115-122. 5. Katritsis DG, Ellenbogen KA. Eccentric retrograde atrial activation in atrioventricular nodal reentrant tachycardia. Heart Rhythm 2005;2:1394-1395.
Case 15 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary
Case Discussion
A 75-year-old male with history of orthotopic heart transplantation with a cavo-caval anastomosis initially developed atrial flutter 13 years post-transplantation with an episode of mild rejection. He was successfully treated for rejection and a right atrial cavotricuspid isthmus dependent atrial flutter was ablated. Two years later, presented with palpitations and shortness of breath and was found to have recurrent atrial flutter. Cardiac catheterization and biopsy did not show evidence of transplant coronary artery vasculpathy or acute rejection. What is the most likely mechanism of atrial flutter in this patient?
Electroanatomic mapping demonstrated recurrent cavotricuspid isthmus dependent atrial flutter (Fig. 15.1) and an ablation line from the inferior vena cava to the tricuspid valve terminated the tachycardia. He has had no recurrence in 3 years of follow-up. Atrial flutter is the most common arrhythmia in post-cardiac transplant patients. Of all supraventricular tachycardias occurring in stable transplant patients without evidence of rejection or vasculopathy, cavotricuspid isthmus dependent atrial flutter is most common. Furthermore, the type of anastomosis at the time of transplant, whether cavo-caval or atrio-atrial, does not affect the incidence of atrial flutter in these patients.
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
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A
B
Fig. 15.1 (Panel A) Activation map: this patient, despite a cavo-caval anastomosis, developed atrial flutter. The activation map demonstrated a right atrial flutter with the wave-front propagating superiorly along the interatrial septum, around the annulus, and inferiorly along the lateral wall of the right atrium. (Panel B): A duodecapolar catheter was
placed in the right atrium with bipole D10 placed along the lateral wall and D1 along the interatrial septum, showing propagation from D1 to D10 in the right atrium. D duodecapolar, LAO left atrium, RAO right atrium, CS coronary sinus
Case 16 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary
Case Discussion
The patient is a 27-year-old women with a history of palpitations. No heart disease was documented. Event recorder documented sustained SVT. Examine Figs. 16.1–16.3. What are the likely possibilities?
This patient has a normal 12-lead ECG. The induced narrow complex tachycardia is regular. The possibilities include AVNRT, AT, and AVRT. The atrial activation sequence during SVT is eccentric indicating either a left-sided AT or a left-sided AP. In this case a left-sided AP was successfully ablated (Figs. 16.4–16.6).
Fig. 16.1 Twelve-lead resting ECG (paper speed 25 mm/s) showing normal sinus rhythm
A. Rossillo (*), S. Themistoclakis, A. Bonso, A. Corrado and A. Raviele Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_16, © Springer-Verlag London Limited 2011
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Fig. 16.2 Twelve-lead ECG taken during SVT (paper speed 25 mm/s)
Fig. 16.3 Intracardiac recordings taken during the electrophysiology study (paper speed 100 mm/s). Five surface ECG leads (II, III, aVF, V1, V6), two bipolar recordings from the pacing catheter placed in right atrium or ventricle (HRA), three bipolar recordings from the His bundle
region (HIS PROX, MED, and DIST), five bipolar recordings from the coronary sinus (CS), and a bipolar recording from the distal mapping catheter (MAP D). AVRT (cycle length 408 ms) with earliest activation on CS 1-2. A atrium, V ventricle, H His
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Fig. 16.4 Intracardiac recordings taken during RF energy delivery (paper speed 100 mm/s). Same display as shown in Fig. 16.3. The red arrow showed termination of the tachycardia. A atrium, V ventricle, H His
Fig. 16.5 Intracardiac recordings taken during RF energy delivery (paper speed 12.5 mm/s). Same display as shown in Fig. 16.3. The red arrows point at the restoration of sinus rhythm after 5 s of RF delivery
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Fig. 16.6 Intracardiac recordings (paper speed 100 mm/s) taken during programmed ventricular stimulation showing the absence of VA conduction (paper speed 100 mm/s). Same display as shown in Fig. 16.3. A atrium, V ventricle
Bibliography Calkins H, Langberg J, Sousa J, et al. Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients. Abbreviated therapeutic approach to Wolff-Parkinson-White syndrome. Circulation. 1992;85:1337-1346. 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.
Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324:1605-1611. Scheinman MM, Wang YS, Van Hare GF, Lesh MD. Electrocardio graphic and electrophysiologic characteristics of anterior, midseptal and right anterior free wall accessory pathways. J Am Coll Cardiol. 1992;20:1220-1229.
Case 17 Bradley P. Knight
Case Summary A 14-year-old male underwent an electrophysiology procedure for recurrent left atrial tachycardia (AT). A prior attempt at ablation was unsuccessful. After transeptal catheterization, an electroanatomic map of the left atrium (LA) and left atrial appendage (LAA) was created during AT. The mechanism of the tachycardia did not appear to be macroreentrant. The origin of the tachycardia appeared to be the left atrial appendage. However, the electroanatomic map showed a relatively broad area of early activation and failed to identify a clear focus of origin. What additional strategy could be used to increase the likelihood of successful ablation?
Case Discussion
Fig. 17.1 Fluoroscopic view during ablation of a left atrial appendage tachycardia. The view is left anterior oblique. A coronary sinus electrode catheter can be seen placed from a superior approach. An ablation catheter and the 20-electrode circular mapping catheter positioned in the appendage, placed via double transseptal catheterization, can also be seen
A multielectrode circular mapping catheter, which is usually used to map pulmonary vein (PV) ostia, was subsequently placed in the LAA (Fig. 17.1). Using the bipolar signals from this catheter, the LAA was explored until the earliest activation site was identified. Figure 17.2 shows the earliest atrial activation recorded from bipole 13–14. The ablation catheter was then positioned adjacent to the earliest bipole and radiofrequency current was delivered. The tachycardia terminated and was noninducible. Advanced computerized three-dimensional (3D) mapping systems have greatly improved the ability to tackle
complex tachycardias. However, it is important to recognize the limitations of such systems, and to occasionally confirm the findings using conventional mapping techniques. In this case, the complex structure of the LAA and its trabeculations proved to be a challenge for the electroanatomic contact mapping system to reconstruct the chamber accurately enough to provide a clear ablation target. The circular mapping catheter may have also distended the appendage and moved trabeculations that may have interfered with localization.
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_17, © Springer-Verlag London Limited 2011
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Fig. 17.2 This tracing was recorded during ablation of a left atrial appendage tachycardia. Shown are the surface tracings from leads I and V5, and the bipolar intracardiac electrograms from the ablation catheter,
B.P. Knight
20-electrode circular mapping catheter positioned in the appendage, and the octapolar electrode catheter placed in the coronary sinus. Note termination of the atrial tachycardia during delivery of radiofrequency current
Case 18 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary
Case Discussion
The patient is a 73-year-old female with a long history of palpitations and hypertension. Echo reveals normal LVEF with an LA diameter of 38 mm. The transesophageal EP study revealed SVT, which was induced with minimum effort (Figs. 18.1 and 18.2). What is the likely mechanism of the SVT?
Although the patient is elderly, the ECG shows a regular narrow complex tachycardia. Atrial tachycardia, AVNRT, and AVRT should all be considered. In this case, no visible P waves are seen during the SVT. This suggests either AVNRT or AT with a long PR interval. In this case, AVNRT was induced in the EP lab and successfully ablated (Figs. 18.3–18.16).
Fig. 18.1 The 12-lead resting ECG (paper speed 25 mm/s) showed sinus rhythm with a ventricular rate of 80 bpm a short PR interval (102 ms) and a QRS width of 80 ms
A. Rossillo (*), S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_18, © Springer-Verlag London Limited 2011
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72 Fig. 18.2 12-lead ECG taken during SVT (paper speed 25 mm/s) with a heart rate of 186 bpm
Fig. 18.3 Intracardiac recordings taken at baseline during the electrophysiology study (paper speed 200 mm/s). Four surface ECG leads (I, aVF, V1, V6), one bipolar recording from the high right atrium (HRA), three bipolar recordings from the His bundle region (distal = HIS D, intermediate = HIS I and proximal = HIS P), two bipolar recordings from the coronary sinus (CS prox = proximal coronary sinus and CS dist = distal coronary sinus), and the distal bipolar recording of the mapping catheter (MC D). A atrium, V ventricle, H His bundle
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Case 18 Fig. 18.4 (a, b). Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s). Same display that is shown in Fig. 18.3. (a) With a coupling interval of 410 ms the AH interval is 188 ms and (b) with a coupling interval of 280 ms it suddenly increased to 307 ms (ERP of the fast pathway with a jump of 120 ms) A atrium, V ventricle, H His bundle
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74 Fig. 18.5 Intracardiac recordings taken during programmed atrial stimulation with two beats with retrograde conduction through the fast pathway (S slow pathway and F fast pathway) (paper speed 100 mm/s). Same display as that shown in Fig. 18.3
Fig. 18.6 Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s) showing the atrial ERP with a coupling interval of 200 ms. Same display as that shown in Fig. 18.3. A atrium, V ventricle, H His bundle
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Case 18 Fig. 18.7 Intracardiac recordings taken during continuous atrial stimulation (paper speed 100 mm/s) with induction of non-sustained AVNRT. A atrium, V ventricle, H His bundle
Fig. 18.8 Intracardiac recordings taken during programmed atrial stimulation with an infusion of isoproterenol IV (paper speed 100 mm/s) showing induction of AVNRT (cycle length 300 ms). Same display as shown in Fig. 1.19.3. A atrium, V ventricle, H His bundle
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76 Fig. 18.9 Intracardiac recordings (paper speed 200 mm/s). Same display as shown in Fig. 18.3. Pace mapping of the anteroseptal region of Koch’s triangle with a stim-H interval of 78 ms. St pacing, A atrium, V ventricle, H His bundle
Fig. 18.10 Intracardiac recordings (paper speed 200 mm/s). Same display as Fig. 1.19-3. Pace mapping of the midseptal region of Koch’s triangle with a stim-H interval of 81 ms. St pacing, A atrium, V ventricle, H His bundle
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Case 18 Fig. 18.11 Intracardiac recordings (paper speed 200 mm/s). Same display as shown in Fig. 18.3. Pace mapping of the posteroseptal region of Koch’s triangle with a stim-H interval of 106 ms. St pacing, A atrium, V ventricle, H His bundle
Fig. 18.12 Intracardiac recordings (paper speed 200 mm/s). Same display as shown in Fig. 18.3. Ablation site slow pathway potential
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78 Fig. 18.13 Intracardiac recordings during radiofrequency delivery (paper speed 100 mm/s) with induction of slow junctional beats in fusion with a sinus beat. Same display as shown in Fig. 18.3
Fig. 18.14 Intracardiac recordings taken during programmed atrial stimulation with infusion of isoproterenol IV (paper speed 100 mm/s) with a very slow anterograde conduction (AH interval 280 ms). Same display as shown in Fig. 18.3. A atrium, V ventricle, H His bundle
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Fig. 18.15 Intracardiac recordings taken during continuous atrial stimulation with an infusion of isoproterenol IV (paper speed 100 mm/s) showing the Wenckebach point and without induction of tachycardia. Same display as shown in Fig. 18.3. A atrium, V ventricle, H His bundle
Fig. 18.16 RAO and LAO of mapping catheter at the ablation site in the posteroseptal part of Koch’s triangle
RAO
Bibliography Delise P, Gianfranchi L, Paparella N, et al. Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation. Am J Cardiol. 1997;79:1421-1423. Delise P, Sitta N, Bonso A, et al. Pace mapping of Koch’s triangle reduces risk of atrioventricular block during ablation of atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol. 2005;16:30-35. Haissaguerre M, Gaita F, Fischer B, et al. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to
LAO
guide application of radiofrequency energy. Circulation. 1992;85: 2162-2175. Haïssaguerre M, Jaïs P, Shah DC, et al. Analysis of electrophysiological activity in Koch’s triangle relevant to ablation of the slow AV nodal pathway. Pacing Clin Electrophysiol. 1997;20:2470-2481. 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;327:313-318. Natale A, Greenfield RA, Geiger MJ, et al. Safety of slow pathway ablation in patients with long PR interval: further evidence of fast and slow pathway interaction. Pacing Clin Electrophysiol. 1997;20: 1698-1703.
Case 19 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary A 50-year-old female with a normal heart presents with a wide complex tachycardia (Fig. 19.1). The patient is taken to the electrophysiology (EP) lab (Fig. 19.2). What clues to the diagnosis are present in the electrocardiogram (ECG)? Is this supraventricular tachycardia (SVT) or ventricular tachycardia (VT)? What is the mechanism of the tachycardia?
Case Discussion The tachycardia has right bundle branch block (RBBB) morphology with QRS axis +90. There is a sudden change in cycle length (CL), but it is not a multiple of the shorter
CL. The bundle branch block has a typical morphology and R > S in V6. Hence, this is SVT, not VT. The diagnosis of SVT confirmed, note that the HV interval is normal. The first two complexes show A-waves in the coronary sinus (CS) simultaneous with the QRS, suggesting that this is most likely slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). Then, two premature atrial complexes (PACs) are delivered from CS 5-6. The first PAC does not reset the tachycardia. The second PAC conducts with a longer AH interval, and subsequently the tachycardia has a longer CL, but the retrograde atrial activation remains the same, suggesting the presence of a different slow pathway. There is baseline RBBB. The patient has slow–fast AVNRT with two slow pathways, participating in AVNRT; hence, she has two CLs.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India A.K. Gupta Apollo Hospital, Ahmedabad, India R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910
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I II III AVR AVL AVF V1 V2 V3 V4 V5 V6 10 mm/mV 25 mm/s
Fig. 19.1 Electrocardiogram (ECG) of wide complex tachycardia
2008070 I AVF V1 V6 CS910 CS78 CS56 CS34 CS12 HISD HISP
Fig. 19.2 Intracardiac recordings. CS 1-2 is distal
Case 20 Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 21-year-old female with a history of viral cardiomyopathy status post orthotopic heart transplantation (OHT) in June 2002 presented with recurrent palpitations three years post transplant. She had received a right atrio–atrial anastomosis at the time of transplantation. She was found to have an atrial flutter (AFL) on surface electrocardiogram (ECG) that proved refractory to medications. Her cardiac catheterization and biopsy showed no evidence of transplant coronary artery vasculopathy or acute rejection, respectively. She was referred for ablation of her AFL.Fluoroscopic position of the duodecapolar catheter in the right anterior oblique (RAO) view and the corresponding ECG recordings are shown in
A
Fig. 20.1 Panel A: Fluoroscopic RAO view shows the position of the duodecapolar catheter. Panel B: Intracardiac activation sequence. CS coronary sinus, D1–D10 duodecapolar bipoles 1–10, DDC duodecapolar catheter, RV right ventricle, LV left ventricle
Fig. 20.1. Duodecapolar bipoles 6–9 were positioned more posteriorly at the native atrium. What type of AFL is demonstrated by the intracardiac duodecapolar ECGs? Is there activation of the native atrium? What is the rate of the native atrial rhythm?
Case Discussion The duodecapolar recordings from the donor atrium showed a typical tricuspid annulus dependent counterclockwise AFL; Fig. 20.2 (top panels). This is the most common type of supraventricular tachycardia (SVT) in stable OHT patients.1
B I AVF V1 V6 D10 D9 D8 D7 D6 D5 D4 D3 D2 D1
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M. Vaseghi (*), N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_20, © Springer-Verlag London Limited 2011
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84 Fig. 20.2 Panel A: Fluoroscopic RAO view shows the position of the duodecapolar catheter with the distal bipoles (D1–D3) along the tricuspid valve isthmus and the proximal electrode (D10) along the superior aspect of the interatrial septum. Panel B: Intracardiac activation sequence in the donor atrium confirms counterclockwise activation. CS coronary sinus, D1–D10 duodecapolar bipoles 1–10, DDC duodecapolar catheter, RV right ventricle, LV left ventricle
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Fig. 20.3 Electroanatomic maps of atrio-atrial anastamosis (gray areas identify native atrial tissue). The flutter wavefront involves the donor atrium only and is propagating in a counterclockwise fashion along the tricuspid annulus
Poles D6–D9 are in contact with the native atrial tissue, which is not in flutter, and is in a dissociated regular bradycardic rhythm of 40 bpm (beats per minute) (arrow), separate from the tachycardia. A critical isthmus is noted on the intracardiac ECGs at duodecopolar position D5. The activation map is shown in Fig. 20.3. An inferior vena cava (IVC) – tricuspid isthmus ablation line terminated the donor atrial tachycardia. No ablation was performed on the native atrium.
Reference 1. Vaseghi M, Boyle NG, Kedia R, et al. Supraventricular tachycardia following orthotopic heart transplantation. J Am Coll Cardiol. 2008;51:2241-2249.
Case 21 Bradley P. Knight
Case Summary A young man underwent an electrophysiology (EP) procedure for recurrent supraventricular tachycardia (SVT). The recording obtained after induction of the tachycardia is shown in Fig. 21.1. Surface intracardiac recordings from the His bundle electrogram (HBE), mapping catheter (Map), coronary sinus (CS), and right ventricle (RV) are shown. What is the mechanism of the tachycardia?
Case Discussion The initial part of the tracing shows a wide complex tachycardia with a cycle length (CL) of 320 ms. There is a His-bundle recording before the QRS complex, which has a typical left bundle branch block (LBBB) pattern. Therefore, the tachycardia is consistent with a supraventricular mechanism. The
earliest atrial activation can be seen in the proximal CS at electrode pair CS 3-4. The QRS complex, however, normalizes during the second part of the recording. An important measurement to make – whenever a SVT is associated with both a normal QRS complex and a bundle branch block – is the VA interval. The reason for this is that when the tachycardia mechanism is orthodromic reentrant tachycardia (ORT), and a rate-related bundle branch block develops on the same side as the accessory pathway (AP), the reentrant circuit will increase in length (due to transeptal conduction) and results in a longer VA interval during the ipsilateral bundle branch block. In this case, the VA interval is clearly longer during the LBBB compared to when the QRS complex normalizes. This is diagnostic for ORT using a left-sided AP. This case is also interesting, because the tachycardia CL does not change significantly during the LBBB, despite an increase in the VA interval. This is because there is a compensatory decrease in the AH interval during the LBBB.
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_21, © Springer-Verlag London Limited 2011
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B.P. Knight I II III V1 V5 HBE d HBE p Map d Map p CS 1-2 CS 3-4 CS 5-6 CS 7-8 CS 9-10 RV d Stim
Fig. 21.1 This tracing was obtained during an ablation procedure for supraventricular tachycardia. Note the change in the ventricular atrial interval when the wide-QRS complex normalizes. The vertical line
depicts the onset of the surface QRS complex in each case and the arrow points to the earliest intracardiac atrial activation
Case 22 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary
Case Discussion
The patient was a 34-year-old female with a history of palpitations. No heart disease was documented. Two months prior to the ablation the arrhythmia episodes became more frequent. After examining Figs. 22.1–22.4, will ablation at a single site eliminate the patient’s palpitations?
In this case, catheter manipulation induced AVNRT. Ventricular pacing demonstrated retrograde conduction via a left-sided accessory pathway. AVRT was also easily induced and was consistent with the clinical tachycardia. Ablation of the left-sided AP and the slow pathway were performed (see Figs. 22.5–22.11).
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Fig. 22.1 Twelve-lead resting ECG (paper speed 25 mm/s) showing short PQ interval with ventricular pre-exitation with an early transition of R wave between lead V1 and V2 and negative wave in leads III and aVF
A. Rossillo (), S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_22, © Springer-Verlag London Limited 2011
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Fig. 22.2 Intracardiac recordings at baseline during the electrophysiology study (paper speed 100 mm/s). Four surface ECG leads (I, aVF, V1, V6), two bipolar recordings from the pacing catheter placed in right
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atrium or ventricle (HRA), three bipolar recordings from the His bundle region (HIS PROX, MED, and DIST), and five bipolar recordings from the coronary sinus (CS). A Atrium, V Ventricle, H His bundle
Fig. 22.3 Intracardiac recordings taken during SVT induced with catheter manipulation (paper speed 100 mm/s, cycle length 330 ms). Same display as that shown in Fig. 22.2. A Atrium, V Ventricle, H His bundle
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Fig. 22.4 Intracardiac recordings taken during programmed ventricular stimulation with induction of SVT (paper speed 100 mm/s, cycle length 290 ms) with earliest activation on CS 3. Same display as that shown in Fig. 22.2. A Atrium, V Ventricle
Fig. 22.5 Intracardiac recordings taken during AVRT (paper speed 100 mm/s, cycle length 264 ms). Same display as that shown in Fig. 22.2 and a bipolar recording from the distal mapping catheter (ABL dist).
A spontaneous ventricular ectopic beat reduced the cycle length of the tachycardia and the anterograde conduction after the ectopic beat is through nodal decremental fibers
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Fig. 22.6 Intracardiac recordings taken during sinus rhythm (paper speed 100 mm/s). Same display as that shown in Fig. 22.5. Ablation site
III aVF V1 V6 HRA 1-2 HRA 3-4 HIS PROX HIS MED HIS DIST CS 1 CS 2 CS 3 CS 4 CS 5 ABL dist
Fig. 22.7 Intracardiac recordings taken during RF energy delivery (paper speed 100 mm/s). Same display as that shown in Fig. 22.5. The red arrows show the absence of the ventricular pre-excitation
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Fig. 22.8 Intracardiac recordings taken during RF energy delivery (paper speed 25 mm/s). Same display as that shown in Fig. 22.5. The red arrows show the absence of ventricular pre-excitation
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Fig. 22.9 Intracardiac recordings (paper speed 100 mm/s) taken during programmed ventricular stimulation showing a decremental VA conduction (paper speed 100 mm/s). Same display as that shown in Fig. 22.5. A Atrium, V Ventricle
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Fig. 22.10 Intracardiac recordings (paper speed 100 mm/s) taken during programmed atrial stimulation with two extrastimuli showing the ERP of the AV node (paper speed 100 mm/s). Same display as that shown in Fig. 22.5. A Atrium, V Ventricle
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Fig. 22.11 12-lead resting ECG (paper speed 25 mm/s) showing normal PQ interval with the absence of ventricular pre-excitation with negative T waves in the inferior leads
Case 22
Bibliography Calkins H, Langberg J, Sousa J, et al. Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients. Abbreviated therapeutic approach to Wolff-Parkinson-White syndrome. Circulation. 1992;85:1337-1346. Haïssaguerre M, Dartigues JF, Warin JF, Le Metayer P, Montserrat P, Salamon R. Electrogram patterns predictive of successful catheter
93 ablation of accessory pathways. Value of unipolar recording mode. Circulation. 1991;84:188-202. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324:1605-1611. Scheinman MM, Wang YS, Van Hare GF, Lesh MD. Electrocardio graphic and electrophysiologic characteristics of anterior, midseptal and right anterior free wall accessory pathways. J Am Coll Cardiol. 1992;20:1220-1229.
Case 23 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary
Case Discussion
The patient is a 58-year-old male with a normal heart. The resting electrocardiogram (ECG) is normal. He has a narrow QRS tachycardia. He is taken to the electrophysiology (EP) lab; see Figs. 23.1 and 23.2. What is the likely mechanism of this tachycardia?
The ventriculo-atrial (VA) conduction pattern and VA time are different in the two beats in Fig. 23.1. The first retrograde A is bracketed, earliest in coronary sinus (CS) 3-4 and 5-6; the second retrograde A is also bracketed, but earliest in CS 5-6 and 7-8. Figure 23.2 shows para-Hisian pacing. The VA
Fig. 23.1 Ventricular pacing
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India A.K. Gupta Apollo Hospital, Ahmedabad, India R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_23, © Springer-Verlag London Limited 2011
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Fig. 23.2 Para-Hisian pacing
time clearly is shortest with His bundle capture (second complex). The VA pattern of the first complex is different from the other two complexes. The first retrograde A is earliest in CS 5-6. The second and third retrograde A are earliest in CS 7-8. Thus the second and third retrograde A are via the AV node; the first is likely via a left AP. The tachycardia displays varying degrees of right bundle branch block (RBBB) during SVT (Fig. 23.3) (normal HV). The earliest retrograde A is consistently in CS 5-6, with a constant VA interval. CS 9-10 was at CS os (ostium). Thus the retrograde A is via a concealed left posterior AP.
In Fig. 23.4, tachycardia has a left bundle branch block (LBBB) morphology. Compared to the previous tracing, the VA time is clearly longer in this case. This is consistent with our prior diagnosis of a left-sided AP. Ablation was performed during right ventricular (RV) pacing (Fig. 23.5) because this allows for catheter stability. If ablation is performed during reentrant tachycardia, the catheter may move suddenly when RT terminates during RF application. So, catheter stability can be obtained by entraining the RT at 10–20 ms faster than the tachycardia CL. The VA conduction during RV pacing changes from left AP to AV node.
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Fig. 23.3 Development of a right bundle branch block (RBBB)
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Fig. 23.4 Development of a left bundle branch block (LBBB)
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Fig. 23.5 Ablation of AP
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Case 24 Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary
graphy demonstrated a normal ejection fraction at the time of arrhythmia. Surface electrocardiogram (ECG) was consistent with atypical atrial flutter (AFL). The patient was taken to the electrophysiology (EP) laboratory. Intracardiac ECGs along with location of the catheters are shown in (Fig. 24.1). What is the likely mechanism of this arrhythmia based on the duodecapolar and coronary sinus (CS) catheter recordings?
A 60-year-old male status post orthotopic heart transplantation (OHT) in June 1999 presented with drug refractory palpitations 8 years after his transplantation. Cardiac catheterization and biopsy showed no evidence of transplant vasculopathy or acute rejection, respectively. Echocardio
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Fig. 24.1 Panel A: Fluoroscopic LAO view: The position of the duodecapolar and CS catheters are shown in right atrium. Panel B: Intracardiac tracings obtained from the duodecapolar and CS catheters are shown.
CS coronary sinus, D1–D10 duodcapolar bipoles 1–10, LAO left anterior oblique, RVa RV catheter bipole
M. Vaseghi (*), N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
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Case Discussion Although typical clockwise AFL is the most common type of supraventricular tachycardia (SVT) in stable post-OHT patients, this patient’s intracardiac tracings show earliest activation in the distal CS consistent with a left AFL. Further, the flutter pattern spreads from the distal CS to the proximal CS and then to the right atrium where D10 (or septal activation is earliest). This is followed by activation
Fig. 24.2 Activation map: the flutter circuit begins in the inferior wall of the LA (pink) close to the CS 3-4 bipole, and then propagates across to the RA and around the tricuspid annulus, as well as around and over the mitral annulus. LA left atrium, LAA left atrial appendage, LIPV left inferior pulmonary vein, LSPV left superior pulmonary vein, RA right atrium, RSPV right superior pulmonary vein, SVC superior vena cava
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around the tricuspid annulus. Hence this left AFL spreads in a figure-eight fashion around both the tricuspid and mitral annuli. Mapping with ablation catheters showed earliest activation at CS 1-2 and ostium of the left inferior pulmonary vein. The activation map obtained via the ablation catheter and the ablation line, which successfully terminated the tachycardia, are shown in (Fig. 24.2). The patient has been without recurrence during the 10 months of follow-up.
Case 25 Bradley P. Knight
Case Summary A female marathon runner without structural heart disease had a documented regular wide complex tachycardia (Fig. 25.1). At the time of electrophysiology (EP) testing, she had normal sinus and atrioventricular (AV) node function, no ventricular preexcitation, and no inducible ventricular tachycardia (VT). A wide complex tachycardia was induced with an atrial premature extrastimulus during sinus rhythm (Fig. 25.2). The QRS morphology was a right bundle branch block (RBBB) pattern with an inferior axis. There was not His-bundle potential recordable before the QRS during the tachycardia. What is the most likely diagnosis?
tachycardia was induced by an atrial premature beat that conducts to the ventricle, with a QRS morphology that is the same as that during tachycardia, makes VT very unlikely. SVT with aberrancy can also be excluded because a Hisbundle potential could not be recorded before the QRS complex. Therefore, the most likely diagnosis is ART. In a patient with no preexcitation during sinus rhythm, the most common mechanism of ART is a slowly conducting, right-sided atriofascicular accessory pathway (AP). A study of 384 patients with a single AP found that anterograde decremental conduction was seen only in the right free wall location. However, the QRS morphology in this patient is not consistent with a right-sided AP. In this case, the earliest ventricular activation was along the mitral annulus where ablation was successful (Fig. 25.3). This represents a very unusual location for a slowly conducting anterograde AP.
Case Discussion The differential of a wide complex tachycardia includes VT, supraventricular tachycardia (SVT) with aberrancy, and antidromic AV reentrant tachycardia (ART). The fact that this
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_25, © Springer-Verlag London Limited 2011
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Fig. 25.1 Shown is a two lead rhythm strip showing the onset of a sustained wide-QRS complex tachycardia. The tracing was recorded from an ambulatory event recorder
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Fig. 25.2 This tracing was recorded during an ablation procedure in a patient with a wide complex tachycardia. Shown are surface electrograms from leads I, II, V1, and V3, and the intracardiac electrograms from the high right atrium (HRA), the ablation catheter (ABL) posi-
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tioned at the His bundle location, and the right ventricular apex (RVA). Note the initiation of a wide complex tachycardia with a single atrial extrastimulus delivered during sinus rhythm
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Fig. 25.3 This tracing was recorded after the ablation catheter was positioned along the mitral annulus at the site of the earliest ventricular local activation. The format is the same as figure 25.2
Case 26 Richard H. Hongo and Andrea Natale
Case Summary The patient is a 53-year-old woman with recurrent palpitations since age 16 with documented episodes of tachyarrhythmia (Fig. 26.1). Discrete P-waves at a rate of approximately 180 bpm have been apparent with atrioventricular (AV) node blockade from adenosine (Fig. 26.2).
She has been treated with a variety of antiarrhythmic agents including verapamil, sotalol, and amiodarone with variable success. She presented for electrophysiology (EP) study with possible catheter ablation because of highly symptomatic episodes of atrial arrhythmia that continued to recur despite medical therapy. High-dose isoproterenol infusion (20 mcg/min)
Fig. 26.1 Continuous 3-lead (II, V1, V5) ECG capturing recurrent episodes of narrow-complex regular tachyarrhythmia at a rate of approximately 180 bpm
R.H. Hongo Sutter Pacific Medical Foundation, California Pacific Medical Center, 2100 Webster Street, Suite 521, San Francisco, CA 94115, USA e-mail:
[email protected] A. Natale () Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32nd Street, Suite 516, Austin, TX 78705 e-mail:
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during EP study induced a tachyarrhythmia with a ventricular rate of 150 bpm (Fig. 26.3). Double transseptal puncture was performed and a 20-mm 10-electrode lasso catheter and a 3.5-mm F-curve saline irrigated ablation catheter were advanced into the left atrium (LA). Intracardiac activation of the atrial arrhythmia was recor ded (Fig. 26.4) with the lasso catheter at the os of the right superior pulmonary vein (RSPV) and the ablation catheter approximately 6 mm within the same vein (Fig. 26.5). A 20-electrode deflectable catheter was introduced from the right internal jugular vein and placed along the lateral wall of the right atrium (RA) with the distal 10 electrodes in the coronary sinus (CS). What is the tachyarrhythmia based on the surface electrocardiogram (ECG) before and during adenosine, and assuming it is the same arrhythmia induced with isoproterenol? What is the tachyarrhythmia based on the intracardiac ECGs? What is the most appropriate next step?
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Case Discussion AV block during adenosine infusion (Fig. 26.2) uncovers discrete P-waves most consistent with atrial tachycardia. Distinct isoelectric segments between the P-waves in all twelve leads of the ECG during isoproterenol infusion (Fig. 26.3) makes both typical and atypical flutter less likely. Loss of 1:1 AV association eliminates atrioventricular reciprocating tachycardia (ART) as a diagnosis. Intracardiac ECGs (Fig. 26.4) reveal the earliest activation to be at the distal ablation catheter positioned within the RSPV (Fig. 26.5), clearly before the activation around the lasso catheter at the vein os. The most appropriate ablation strategy is to isolate the RSPV. Ablation at the earliest activation site within the vein should be avoided because of the risk of PV stenosis. If either atrial fibrillation (AF) or typical atrial flutter (AFL) were observed clinically, isolation of all four pulmonary veins and cavotricuspid isthmus ablation, respectively, would also be appropriate.
Fig. 26.2 Continuous 3-lead (II, V1, V5) ECG during adenosine-induced AV block. Uncovered discrete P-waves are most consistent with atrial tachycardia
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Fig. 26.3 12-lead ECG during isoproterenol infusion (20 mcg/min) demonstrates sustained atrial tachyarrhythmia. Distinct isoelectric PR segments are seen in all leads I
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Fig. 26.4 Simultaneous surface and intracardiac ECGs during the atrial tachyarrhythmia reveal the earliest activation to be at the distal electrode pair of the ablation catheter (ABL d), clearly in front of the activation seen on the Lasso catheter. HRA = high right atrial catheter; CS = coronary sinus catheter; Ls = Lasso catheter
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Fig. 26.5 Fluoroscopic image in shallow LAO projection, showing the position of the catheters that correspond with the intracardiac ECGs from Fig. 26.4. The Lasso catheter is placed at the right superior pulmonary vein (RSPV) os. The ablation catheter is shown positioned within the RSPV
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Case 27 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
Case Summary A 63-year-old female with a history of tachycardia 7 years ago with the electrocardiogram (ECG) shown in Fig. 27.1 presented complaining of recurrent palpitations with the tachycardia shown in Fig. 27.2. During an electrophysiology (EP) study, the responses from premature ventricular beat and ventricular pacing were recorded during the tachycardia, as shown in Figs. 27.3 and 27.4. What is the diagnosis?
Case Discussion The presenting tachycardia is characterized by a long RP, narrow complex tachycardia, with low septal to high atrial activity (negative P-wave in lead II and positive P-waves in leads aVR and aVL). Therefore, the differential diagnoses include: low septal atrial tachycardia, atypical AV nodal reentry tachycardia (AVNRT), and persistent junctional reciprocating tachycardia.
Seven years prior to this presentation, the patient had short RP and narrow complex tachycardia. The differential diagnoses of that rhythm include: typical AVNRT, atrial tachycardia (AT) with long PR interval, and AV reentry tachycardia via an accessory pathway (AP). The presence of both rhythms in one patient means this is probably AVNRT. The first rhythm was probably a typical tachycardia. The patient now presents with atypical AVNRT. The first intracardiac tracing reveals earliest atrial activation is in the proximal coronary sinus (CS), suggesting an AT originating in the lower septum, retrograde activation over the AV node, or retrograde activation over a septal AP. A spontaneous premature ventricular capture (PVC) during the tachycardia, at the time of the His refractory, was observed. At that time, the tachycardia cycle length (CL) was not changed. The presence of a PVC reduces the likelihood that the mechanism is an AV reentry tachycardia via a septal AP. The second intracardiac tracing illustrates ventricular entrainment during the tachycardia. Post–ventricular pacing shows a V-A-V response, excluding the diagnosis of a low septal AT. Thus, the diagnosis is atypical AVNRT.
M.E. Mortada (*) J.S. Sra, and M. Akhtar Department of Electrophysiology, Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke’s Medical Centers, University of Wisconsin School of Medicine and Public Health, 2801 W. Kinnickinnic River Parkway, #777, Milwaukee, WI 53215 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_27, © Springer-Verlag London Limited 2011
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Fig. 27.1 Surface ECG of the tachycardia seven years prior to the current presentation
Fig. 27.2 Surface ECG of the current tachycardia
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Fig. 27.3 Spontaneous PVC during the tachycardia at the His refractory period. From top to bottom: surface ECG with leads I, II and V1, followed by intracardiac tracing of HRA, proximal to distal CS, and finally His catheters
Fig. 27.4 Response from ventricular entrainment of the tachycardia
Case 28 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary A 21-year-old female with a normal heart comes to the electrophysiology (EP) lab because of palpitations. A diagnosis of typical atrioventricular reentrant tachycardia (AVNRT) is made (Fig. 28.1). However, after atrial pacing, long PR and sudden left bundle branch block (LBBB) – like morphology is seen (Figs. 28.2 and 28.3). What maneuver is being performed? What does this say about the tachycardia mechanism?
during tachycardia; this caused advancement of the next QRS. The QRS advancement by a “His-refractory” APD proves the presence of an extranodal (atriofascicular or atrioventricular accessory pathway) (Fig. 28.4). The HA during tachycardia is identical to HA during RV pacing; thus the Mahaim-like accessory pathway is not a bystander. Final diagnosis: (1) Right lateral Mahaim-like AP with true antidromic AVRT and (2) slow–fast, typical AVNRT (Figs. 28.5 and 28.6).
Case Discussion An atrial premature depolarization (APD) was delivered from a radiofrequency (RF) catheter in the right atrium (RA),
Y.Y. Lokhandwala () KEM Hospital, Parel, Mumbai, India A.K. Gupta Apollo Hospital, Ahmedabad, India R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910
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Case 28 RUBY HALL CLINIC 2008051 I II III AVR AVL AVF V1 V2 V3 V4 V5 V6 10 mm/mV 25 mm/s
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Case 291 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary
Case Discussion
A 57-year-old female with recurrent atrial flutter (AFL) was referred for catheter ablation. The surface electrocardiogram (ECG) suggested clockwise AFL with positive F-waves in II, III, and AVF, and negative F-wave in V1. The complete absence of an R-wave in lead I was noted. The chest x-ray demonstrated dextrocardia, and echocardiography established complete situs inversus with otherwise normal intracardiac anatomy. Based on the ECG, what is the likely diagnosis?
A duodecapolar (DD) catheter was positioned around the tricuspid annulus in the anatomical right atrium (RA) with the distal tip located at the medial cavotricuspid isthmus (Fig. 29.1). Electrophysiological mapping of the AFL demonstrated earliest activation in the electrogram recorded from DD poles 19,20 and latest activation at DD poles 1,2. Top left image shows an LAO view of the heart (camera in the RAO position relative to the torso) and direction of flutter (white arrows) as shown by
Fig. 29.1 Fluoroscopy of intracardiac catheters. Top left panel shows LAO view of the heart (camera in the RAO position relative to the torso). Top right panel shows the RAO view of the heart (camera in the
LAO position relative to the torso). CS coronary sinus catheter, Abl ablation catheter, HRA high right atrial catheter, His His bundle catheter
This case is adapted from heart rhythm volume 2, issue 6, pages 673-674 (June 2005)
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E. Buch (), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center,David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
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the intracardiac tracings, demonstrating early activation in DD19, 20 and counterclockwise rotation of flutter in the RA (Fig. 29.2). Entrainment pacing demonstrated that the
tricuspid valve – inferior vena cava (IVC) isthmus was a part of the circuit and this tachycardia was cured by ablation of the isthmus.
I II III aVF V1 HRA DD19,20 DD17,18 DD15,16 DD13,14 DD11,12 DD9,10 DD7,8 DD5,6 DD3,4 DD1,2 HIS p HIS m HIS d CS 9,10 CS 7,8 CS 5,6 CS 3,4 CS 1,2 RVa Stim 3
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Fig. 29.2 Intracardiac electrograms. In this patient with mirror-image dextrocardia, typical flutter was counterclockwise (CCW) in the RA, as demonstrated by the wave front of activation on duodecapolar (DD) catheter. However, the inferior leads of the EKG inscribe F-waves that are positive, which is suggestive of clockwise (CW) flutter. This discrepancy
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is attributed to the fact that in the situs inversus heart, because of the rotated position of the atria and ventricles (mirror image of a situs solitus heart), CCW flutter appears CW (its mirror image) on the surface EKG. Hence, the position of the heart in the thorax must be kept in mind when evaluating CW versus CCW flutter based on a surface EKG
Case 30 Luis C. Sáenz and Miguel A. Vacca
Case Summary The patient is a 5-year-old male with a past medical history significant for paroxysmal palpitations which became incessant 8 months ago despite taking various anti-arrhythmic agents (AADs). The patient had worsening congestive heart failure and was hospitalized. He had no other significant past medical history. The tachycardia EKG taken in the emergency room is showed in Fig. 30.1. His echocardiogram showed left ventricular dilatation and ejection fraction of 38%. While the patient was in the hospital another tracing was taken showing spontaneous changes in his electrical rhythm (Fig. 30.2a and b). Variable atrioventricular conduction during the tachycardia with an isoelectric interval between the p waves is showed in Fig. 30.2a suggesting an atrial tachycardia as the mechanism of the arrhythmia. After
increasing the doses of the AAD medications, a transitory and regular rhythm with “1 per 1” atrioventricular conduction was registered, and is showed in Fig. 30.2b. Considering tachycardiomyopathy and the failure of the AAD to prevent arrhythmia recurrences, the patient was brought to the electrophysiology lab for ablation. CARTO was used during the procedure. A decapolar multielectrode catheter was introduced into the coronary sinus for mapping. In Fig. 30.3, the coronary sinus channels are showed from proximal (SC5) to distal (SCD). The third coronary sinus channel is not showed due to electrical noise. The intra-cardiac electrograms from the roving CARTO mapping and ablation catheter are showed as RFD and RFP for the bipolar electrograms that were taken from the distal1,2 and proximal3,4 par of electrodes, respectively. The unipolar electrogram from the electrodes 1 and 3 of the CARTO roving catheter are showed as 1 and 3, respectively. A CARTO
Fig. 30.1 EKG of tachycardia taken in the emergency room L.C. Sáenz (*) Jefe Servicio de Electrofisiología, Cardiólogo-Electrofisiólogo, Fundación Cardio Infantil-Instituto de Cardiología, Calle 163A No 28-60, Bogotá, Colombia M.A. Vacca Cardiac Electrophysiologist, Centro Internacional de Arritmias FCI, Fundacion Cardioinfantil, Instituto de Cardiologia, Calle 163 A No. 13B-60, Bogota, Colombia A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_30, © Springer-Verlag London Limited 2011
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Fig. 30.2 (a and b) Spontaneous changes in the electrical rhythm
right atrial and superior vena cava activation map was constructed during the tachycardia and shown in Fig. 30.3. The CARTO map suggested a focal origin of the tachycardia and showed the site of earliest electrical activation (in red) of the mapped chambers over the posterior aspect of the superior vena cava where fractionated and almost double electrograms were found and marked as blue points, Fig. 30.3.
Remarkably, the electrograms registered from the coronary sinus are almost isochronic with the electrograms taken from the earliest CARTO zone in the posterior aspect of the superior vena cava, Fig. 30.3. In order to simplify the case, the CARTO activation and the sequence of the propagation maps (from left to right) of the right atrium, superior vena cava, and coronary sinus is shown in Fig. 30.4.
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Fig. 30.3 Right atrium and superior vena cava CARTO activation map and intra-cardiac electrograms registered during tachycardia
shows a really broad zone of early activation (in red) suggesting a passive activation from another site.2 Moreover, the isochronal activation between the distal coronary sinus electrode and the earliest electrogram over the superior vena cava suggests that the cardiac site responsible for originating the tachycardia is activating these structures almost at the same time. In normal conditions this place would be equidistant between the distal coronary sinus and the superior vena cava. In this way, the origin of the tachyCase Discussion cardia would be in the left atrium.3 In fact, the EKG of the tachycardia (Fig. 30.1) shows a positive p wave in the preThe accuracy and reliability of a CARTO map are dependent cordial and inferior leads with negative p wave in aVL and on having an adequate number of contact points taken in iso-biphasic in DI suggesting that the origin of the tachycarorder to construct the chamber(s) of interest. The CARTO dia is from the left pulmonary veins.4 system constructs a map solely with information taken from A CARTO left atrial activation map integrating the elecsites where the tip of the roving catheter contacts cardiac tis- trical information of the right atrium, superior vena cava, and sue. The system can construct a map that provides informa- coronary sinus was performed and showed in Fig. 30.5. This tion about the site of earliest activation. When using the map showed the actual site of earliest activity to be over the CARTO system it is important to correlate the 3D color maps Carina between the left pulmonary veins as shown by the with information provided from the electrograms taken from tachycardia EKG. different cardiac places and verify and appropriate informaThe corresponding propagation CARTO map is showed tion provided by the system. in Fig. 30.6. The sequence shows a focal origin of the tachyIn Fig. 30.3, the CARTO activation map shows the ear- cardia between the left pulmonary veins (photo 1 of the liest activation zone over the posterior aspect of the supe- sequence) with spreading of the activation to the posterior rior vena cava. However, the intra-cardiac electrograms in wall and the roof of the left atrium (photo 2 and 3 of the Fig. 30.3 showed an almost isochronal activation between sequence). The activation reaches the anterior wall of the LA the distal coronary sinus electrode and the earliest electro- and the posterior aspect of the superior vena cava and almost gram over the superior vena cava. Moreover, the coronary at the same time the distal coronary sinus is depolarized from sinus electrodes show a discrete distal to proximal activa- the posterior wall of the LA (photo 4 of the sequence). tion. The bipolar electrograms registered from the posteFinally, the RA is passively activated through an isorior aspect of the superior vena cava are double potentials chronic front of waves from the posterior aspect of the supeof high amplitude and just 13 ms before the onset of the p rior vena cava and the distal coronary sinus (photo 4 of the wave. The corresponding unipolar electrograms from this sequence). place showed an r/S pattern. The analysis of the intra- The passive activation of one atrial chamber with the eleccardiac bipolar and unipolar electrograms suggests that trical activity originating in the other atrium is a phenomenon despite the CARTO showing that the earliest activation is that can cause confusion during mapping. Unnecessary radi over the posterior aspect of the superior vena cava, it would ofrequency applications maybe made targeting the passive be a passive electrical activation from another cardiac site.1 activation sites without having an effect on the tachycardia. Furthermore, the CARTO map of the superior vena cava Inter-atrial connections have been described and are By analyzing the EKG in Fig. 30.1, what is the possible origin of the tachycardia? Considering both the electrograms and CARTO maps, why does the posterior aspect of the superior vena cava and the distal coronary sinus have almost the same time of activation? What is the best next step to do in this case?
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Fig. 30.4 CARTO activation and propagation maps of the right atrium, superior vena cava, and coronary sinus shown in a posterior view
Posterior view
Fig. 30.5 The CARTO activation map integrating the electrical information of the right atrium, superior vena cava, coronary sinus, and the left atrium
Anterior view
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Fig. 30.6 CARTO propagation map integrating the electrical information of the right atrium, superior vena cava, coronary sinus, and the left atrium shown as a sequence of pictures from the superior to inferior views
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responsible for this phenomenon.5 The most recognized interatrial connection between the atrial chambers is through the Bachmann Bundle, which connects the left atrial appendage and the superior portion of the Crista Terminalis in the anterior aspect of the superior vena cava, Fig. 30.7. Another connection is between the posterior wall of the LA and the coronary sinus and between the coronary sinus and the RA, Fig. 30.7. There are other less recognized inter-atrial connec-
tions as through the fossa ovalis and between the right pulmonary veins and the superior vena cava, Fig. 30.8. Remarkably, in this particular case the earliest activation of the RA was founded over the posterior aspect of the superior vena cava. So, it seems to correspond to a passive activation through a connection between the right superior pulmonary vein and this part of the superior vena cava as showed in Fig. 30.8.
Anterior-superior view
LAO view
Bachmann CT
Fig. 30.7 Anatomical and CARTO pictures showing the inter-atrial connections
LAO view
Fig. 30.8 Drawing and CARTO pictures showing the inter-atrial connections
Posterior view
Case 30
The atrial tachycardia was slowed by radiofrequency applications over the carina between the left pulmonary veins as showed in Fig. 30.9. This site revealed atrial bipolar electrogram of low amplitude, fractionated, and earlier 52 ms than the onset of the p wave. The corresponding unipolar electrogram showed a QS pattern. See Fig. 30.3 for comparison. The EKG post ablation showed a p wave with a positive/ negative morphology in V1, positive in lead I and aVL, and was predominantly negative in the inferior leads suggesting an escape low CT rhythm, Fig. 30.10a. Retrospectively, the
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organized and 1:1 atrioventricular conduction rhythm (showed in Fig. 30.2b and magnified in Fig. 30.10a) would be the same ablated atrial tachycardia with fixed exit block of the conduction from the pulmonary vein to the LA that can be confused with a normal sinus rhythm. This case points out that although electroanatomic mapping is a useful tool, the information obtained by the system needs to be validated with electrograms and entrainment. The inter-atrial connections can muddy the interpretation of the activation map. Because of that registration of electrical activity from only one chamber can be misleading.
Fig. 30.9 CARTO and ICE showing the location of successful RF ablation
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Post ablation I II III AVR AVL AVF V1 V2 V3 V4 V5 V6
Fig. 30.10 (a and b) Comparison between the pre- and post-ablation p waves morphology
References 1. Stevenson WG, Soejima K. Recording techniques for clinical electrophysiology. J Cardiovasc Electrophysiol. 2005;16:1017-1022. 2. Markowitz SM, Lerman BB. How to interpret electroanatomic maps. Heart Rhythm. 2006;3:240-246. 3. Lemery R, Soucie L, Martin B, et al. Human study of biatrial electrical coupling. Circulation. 2004;110:2083-2089.
4. Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P-wave morphology in focal atrial tachycardia. J Am Coll Cardiol. 2006;48:1010-1017. 5. Ho SY, Sanchez-Quintana D, Cabrera JA, et al. Anatomy of the left atrium: implications for radiofrequency ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 1999;10:1525-1533.
Case 31 Bradley P. Knight
Case Summary A young woman with a permanent form of reciprocating tachycardia (PJRT) underwent an electrophysiology
procedure. The 12-lead ECG is shown in Fig. 31.1. The results of pacing maneuvers were consistent with orthodromic AV reentry using a slowly conducting accessory pathway (AP). Where is the AP most likely located?
Fig. 31.1 A 12-lead rhythm strip showing a nearly incessant, supraventricular tachycardia with a long RP interval
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_31, © Springer-Verlag London Limited 2011
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Case Discussion The most likely location for an AP with decremental conduction that participates in PJRT is the posterior septum. Therefore, efforts to map the atrial insertion during tachycardia should initially focus in this region. However, it is not uncommon for these pathways to be located elsewhere. At least two studies have found that the site of earliest retrograde atrial activation occurs at annular locations other than the posteroseptal region in approximately one fourth of cases. In this case, the earliest retrograde activation during single echo beats was along the lateral mitral annulus across from the distal coronary sinus electrode (Fig. 31.2). Radiofrequency ablation at this site eliminated AP conduction. Less than 5% of cases are found in the left lateral location.
Fig. 31.2 This tracing was recorded during catheter ablation of a supraventricular tachycardia. Shown are surface electrograms from leads I, II, III, V1, and V5, and the intracardiac electrograms from the high right atrium (HRA), the ablation catheter (Abl) positioned at the lateral mitral annulus where the earliest local activation could be recorded, and the coronary sinus (CS). The vertical line shows that the earliest local atrial activation precedes the onset of the p-wave on the surface tracing
Bibliography Gaita F, Haissaguerre M, Giustetto C, et al. Catheter ablation of PJRT with RF current. J Am Coll Cardiol. 1995;25:648-654. Meiltz A, Weber R, Halimi F, et al. PJRT in adults: Peculiar Features and Results of RF Ablation. Europace. 2006;8:21-28.
Case 32 Luigi Di Biase, Rodney P. Horton, and Andrea Natale
Case Summary A 66-year-old male with essential hypertension and a history of bilateral hernia surgery, was self-referred to our institution regarding persistent shortness of breath status post-“redo” pulmonary vein isolation performed at another institution. At admission he denied any chest discomfort, palpitations, presyncope, or syncope. The patient began experiencing symptomatic episodes of atrial fibrillation in 2003. His echocardiogram and blood screening resulted within the normal range. The arrhythmia was initially treated both with propafenone and flecainade at the appropriate dosages. These AADs were ineffective. Since his AF became more persistent, the patient underwent several cardioversions. In 2006 he finally underwent pulmonary vein isolation (PVI). The procedure had no complications and a CT scan performed 3 months after the ablation showed no pulmonary vein stenosis. Five months following the ablation, the patient went into atrial flutter which required cardioversion. In 2008 the patient underwent a repeat procedure. One month following the second ablation procedure, he started experiencing progressively worsening dyspnea on exertion with daily activities such as walking across the street. He also reported orthopnea. At admission, his blood screening and physical examination resulted normal.
L. Di Biase (*) Department of Electrophysiology, St. David’s Medical Center, 1015 32nd Street, Suite 506, Austin, TX 78705 email:
[email protected] R.P. Horton Department of Electrophysiology, Texas Cardiac Arrhythmia Institute, 1015 East 32nd Street, Austin, TX 78705 A. Natale Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32nd Street, Suite 408, Austin, TX 78705
Which should be the diagnostic and therapeutic steps for this patient? a) Perform an Echocardiogram b) Perform a Transesophageal Echocardiogram c) Perform a CT scan e/o MRI scan d) Perform a CT scan and a Transesophageal Echocardiogram e) Perform a ventilation/perfusion scan f) Perform a chest x ray g) Perform all the above
Case Discussion The patient had a CT scan and an echocardiogram 9 months after the redo procedure. The echocardiogram showed normal EF and an enlarged pulmonary artery with increased pulmonic valve velocities consistent with pulmonary hypertension. Additionally there was mild right ventricular hypertrophy, and mild tricuspid regurgitation. The TEE was technically difficult and with suboptimal echocardiographic images. No thrombus was appreciable in the left atrium and the left atrium appendage. Solely the left superior pulmonary vein was visualized. EF was estimated at 60%. Generally all the structures were poorly visualized. The Doppler echocardiogram showed increased velocities in the distal portion of the left superior pulmonary vein, consistent with a significant stenosis. The CT scan showed complete occlusion of the LIPV and severe stenosis of both left and right superior pulmonary veins. An enlarged pulmonary artery was also noted (Fig. 32.1 and 32.2). Based on the CT reports which should be the treatment stategy? a) Anticoagulation and clinical follow up b) Dilation with baloon and anticoagulation c) Dilation with balloon, anticoagulation and follow up with VQ/scan d) None of the above e) All the above
A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_32, © Springer-Verlag London Limited 2011
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There were no significant gradient across these stenosis following the dilation. Based on the good angiographic results of the balloon angiography the patient should: a) Stop anticoagulation therapy b) Continue anticoagulation therapy and repeat the CT scan at follow up c) Continue anticoagulation therapy and repeat TEE at follow up d) All the above e) None of the above
Fig. 32.1 CT scan showing complete occlusion of the LIPV and severe stenosis of both left and right superior pulmonary veins
Fig. 32.2 CT scan showing an enlarged pulmonary artery with severe stenosis of the right and left superior pulmonary veins
Because of the significant dyspnea and pulmonary hypertension related to pulmonary vein stenosis of at least three pulmonary veins, the decision was made to undergo balloon angioplasty and possible stenting. The left superior, left inferior, and right superior pulmonary veins were found severely occluded (³90%) at the angiograms and were dilated with balloon angioplasty.
The reported incidence of PV stenosis/occlusion defined as >70% narrowing or ³90% affects 3.4% of patients following catheter ablation of atrial fibrillation.1–3 The incidence has decreased in the most recent years due the utilization of different techniques for the PV isolation that limit the burnings at the antrum of the pulmonary veins which is at a considerable distance from the true PV ostia.1 The clinical presentation of these patients is variable; from totally asymptomatic or with mild dyspnea to severe dyspnea with hemoptysis, fever, or pleuritic chest pain.1,3 The pathogenesis is due to an initial ablative insult that precipitates a healing reaction culminating in an endovascular contraction and proliferation of the elastic lamina/intima. Misdiagnosis is very common in these patients (pulmonary embolism, lung cancer, pneumonia, and new onset of asthma, are the most common1,3), because symptoms may occur far from the procedural time. This is why imaging following catheter ablation is crucial also in asymptomatic patient. In fact, PV stenosis may progress insidiously. Patients can present with a variety of respiratory symptoms, but may also remain asymptomatic especially when only one vein demonstrates severe stenosis. Chest x-ray is usually not helpful in diagnosing this condition. As shown in this case, TEE does not always provide clear images of the pulmonary veins. CT scan and/or magnetic resonance imaging are the best tools for diagnosis.4,5 Many groups suggest that the assessment of PV diameter using CT scan or MRI 3 months after ablation provides the best identification of PV stenosis since the caliber remain relatively stable beyond 3 months after ablation. However, late progression from a mild to a severe PV stenosis has been described and a repeat imaging is required for any patient who develops new symptoms consistent with stenosis.1 In patients with moderate to severe stenosis, ventilation/perfusion (V/Q) scan may be useful because it provides a good measure of the lung functionality. The CSI index (cumulative stenosis index [CSI] = sum of the percent stenosis of the unilateral veins divided by the total number of ipsilateral veins) has been proposed with a cutoff value of 75% to identify patients at greatest risk of severe symptoms and lung diseases. In these patients,
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early and, when required, repeated PV intervention should be considered for restoration of pulmonary flow and prevention of associated lung disease.1 Late opening of the vessel although feasible will not be able to reduce patient’s symptoms and restore lung functionality. In the absence of symptoms, there is no consensus on the best treatment strategy and the CSI index may be useful to identify patients at higher risk. Balloon angioplasty with or without stenting has been shown to achieve satisfactory results although restenosis requiring repeat intervention is necessary in nearly 45–50% of patients.1,6 As shown in this case, after the second ablation, the patient did not undergo CT scan. As described earlier in the text, imaging is very important to detect stenosis even in asymptomatic patients. The dyspnea reported by the patient was underestimated for several months. This resulted in severe pulmonary hypertension and pulmonary artery dilatation (as demonstrated by the CT scan). In such a case, late dilatation of the occluded pulmonary veins although angiographically successful may not solve the patient’s symptoms.
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References 1. Di Biase L, Fahmy TS, Wazni OM, et al. Pulmonary vein total occlusion following catheter ablation for atrial fibrillation: clinical implications after long-term follow-up. J Am Coll Cardiol. 2006;48: 2493-2499. 2. Saad EB, Marrouche NF, Saad CP, Natale A et al. Pulmonary vein stenosis after catheter ablation of atrial fibrillation: emergence of a new clinical syndrome. Ann Intern Med. 2003 Apr 15; 138(8):634-638. 3. Saad EB, Rossillo A, Saad CP, et al. Pulmonary vein stenosis after radiofrequency ablation of atrial fibrillation: functional characterization, evolution, and influence of the ablation strategy. Circulation. 2003;108:3102-3107. 4. Packer DL, Keelan P, Munger TM, et al. Clinical presentation, investigation, and management of pulmonary vein stenosis complicating ablation for atrial fibrillation. Circulation. 2005;111: 546-554. 5. Neumann T, Sperzel J, Dill T, et al. Percutaneous pulmonary vein stenting for the treatment of severe stenosis after pulmonary vein isolation. J Cardiovasc Electrophysiol. 2005;16:1180-1188. 6. Qureshi AM, Prieto LR, Latson LA, et al. Transcatheter angioplasty for acquired pulmonary vein stenosis after radiofrequency ablation. Circulation. 2003;108:1336-1342.
Case 33 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
Case Summary A 55-year-old male presented with recurrent symptoms of dizziness and palpitations. He was found to have stable vitals and abnormal rhythm (Fig. 33.1). The 12-lead ECG at baseline during sinus rhythm is shown in Fig. 33.2. The patient underwent a complex electrophysiology study. The intracardiac tracing shown in Fig. 33.3 demonstrates the wide complex tachycardia rhythm.
What is the diagnosis? Radiofrequency ablation was performed successfully. Where was the ablation performed?
Case Discussion In defining a wide complex tachycardia, it is important to differentiate between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) (associated with aberrancy,
Fig. 33.1 At presentation, the patient was found to have stable vitals and abnormal rhythm demonstrated in this 12-lead ECG
M.E. Mortada (*), J.S. Sra, and M. Akhtar Department of Electrophysiology, Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke’s Medical Centers, University of Wisconsin School of Medicine and Public Health, 2801 W. Kinnickinnic River Parkway, #777, Milwaukee, WI 53215 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_33, © Springer-Verlag London Limited 2011
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preexcitation, preexistent wide QRS complex, or antidromic AV reentry tachycardia). All of these are possible diagnostic options in this case. The seventh complex on the wide QRS complex tachycardia is premature and results in an earlier initiation of the tachycardia after the premature beat. This response fits all of the above mentioned diagnostic possibilities. If this is a VT, the premature beat could be a premature ventricular capture (PVC) that entrained the ventricular tachycardia and accelerated the rhythm for that one beat (Fig. 33.4). If this is atrial flutter with 2:1 AV conduction or reentry atrial tachycardia associated with left bundle branch block, the premature beat could be a premature atrial capture (PAC) that entrained the reentry circuit and accelerated the rhythm for that one beat (though atrial flutter option is the least possible, due to the fast rate of the atrial flutter, 366 bpm [160 ms]) (Fig. 33.5). If this is an orthodromic AV reentry tachycardia with left bundle branch block, the premature beat could be a PAC or PVC that entrained the circuit and accelerated the rhythm for that one beat (Fig. 33.6). If this is an AV nodal reentry tachycardia with left bundle branch block, the premature beat could be a PAC that entrained the circuit and accelerated the rhythm for that one
Fig. 33.2 The patient’s 12-lead ECG at baseline during sinus rhythm
M.E. Mortada et al.
beat (Fig. 33.7). Intravenous adenosine affects the atrioventricular node; hence it affects almost all SVTs by terminating the tachycardia or producing atrioventricular dissociation. Few ventricular tachycardias are sensitive to adenosine (e.g., normal heart VT), thus response to adenosine is no help in making a diagnosis. The absence of structural heart disease is an important piece of information, increasing the likelihood that the tachycardia is SVT rather than VT in origin. The most helpful piece of information for differential diagnosis in this case was the baseline 12-lead ECG, which showed the same QRS morphology. Therefore, VT could be easily excluded. Acceleration of the tachycardia by one premature beat, as seen in the first ECG (the seventh beat), favors the diagnosis of orthodromic AV reentry tachycardia (AVRT) over AV nodal reentry tachycardia (AVNRT). Intracardiac electrocardiograms taken during the tachycardia revealed the activation of the atria to be from the distal to the proximal coronary sinus, followed by the high right atrium and His (septum). It also revealed constant VA linking. These findings confirmed the diagnosis of an orthodromic AVRT using a left lateral free-wall accessory pathway and the best location for successful radiofrequency ablation is the lateral side of the mitral valve annulus.
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Fig. 33.3 Intracardiac tracing demonstrating the wide complex tachycardia rhythm (Rhythm tracing from top to bottom: Lead I, Lead II, Lead V1, high right atrium recording “HRA,” proximal coronary sinus recording (CS 9,10) to distal coronary sinus recording (CS 1,2), and His bundle recording “proximal HSp, and distal HSd.”) HRAp: proximal high right atrium; CS: coronary sinus; HSp: proximal His; HSd: distal His
Fig. 33.4 The seventh complex on the wide QRS complex tachycardia is premature and results in an earlier initiation of the tachycardia after the premature beat. If this patient has a ventricular tachycardia (VT), the premature beat could be a premature ventricular capture that entrained the VT and accelerated the rhythm for that one beat
Fig. 33.5 If this patient has atrial flutter with 2:1 AV conduction associated with left bundle branch block, the premature beat could be a premature atrial capture that entrained the atrial flutter and accelerated the rhythm for that one beat (though this option is the least possible, due to the fast rate of the atrial flutter--366 bpm “160 ms”)
Fig. 33.6 If this patient has an orthodromic AV reentry tachycardia with left bundle branch block, the premature beat could be a PAC or PVC that entrained the circuit and accelerated the rhythm for that one beat
Fig. 33.7 If this patient has an AV nodal reentry tachycardia with left bundle branch block, the premature beat could be a PAC that entrained the circuit and accelerated the rhythm for that one beat
Case 34 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary
Case Discussion
The patient is a 28-year-old female with frequent runs of SVT. No relevant structural changes on echocardiography. Based on Figs. 34.1 and 34.2, what is the likely mechanism of the tachycardia?
This tachycardia is a long RP tachycardia, thus the differential diagnosis includes atypical AVNRT, atrial tachycardia, or AVRT that utilizes a slowly conducting AP. When a single VPC is delivered the tachycardia terminates without reaching
Fig. 34.1 12-lead ECG taken during SVT (paper speed 25 mm/s) showing a negative P wave in the inferior leads with a short PQ interval and a heart rate of 120 bpm
A. Rossillo (*), S. Themistoclakis, A. Bonso, and A. Corrado Cardiovascular Department, Ospedale dell’Angelo, Mestre, Venice, Italy A. Raviele Chief of Cardiology, Chief of Cardiovascular, Cardiovascular Department, Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_34, © Springer-Verlag London Limited 2011
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the atrium. This makes AT unlikely. Distinguishing AVRT that utilizes a slowly conducting AP versus AVNRT can be difficult, but as the tachycardia terminated during a HIS
Fig. 34.2 Intracardiac recordings taken at baseline during the electrophysiology study (paper speed 100 mm/s). Four surface ECG leads are shown (I, aVF, V1, V6), one bipolar recording from the pacing catheter (HRA), three bipolar recordings from the distal His bundle region (HIS D = distal, HIS I = medial, and HIS P = proximal), two bipolar recordings from the coronary sinus (CS1 = distal CS and CS4 prox CS), and the distal bipolar recording of the mapping catheter (MC D Bi). A single paced beat from the right ventricle with a coupling interval allows for anterograde activation of the His bundle which interrupted the tachycardia twice. (A atrium, V ventricle, and H His bundle)
Fig. 34.3 Intracardiac recordings (paper speed 200 mm/s). Same display as shown in Fig. 34.2. Ablation site: earliest activation on MC D Bi
A. Rossillo et al.
refractory VPC, the likely diagnosis is AVRT or PJRT. This tachycardia is often clinically frequent or incessant. In Fig. 34.3 and 34.4 the ablation site is shown.
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Fig. 34.4 RAO and LAO projection of mapping catheter at the ablation site
RAO
Bibliography Coumel PH, Attuel P, Leclerque JF. Permanent form of junctional reciprocating tachycardia: mechanism, clinical and therapeutic impli cation. In: Narula OS, ed. Cardiac Arrhythmias. Electrophysiology, Diagnosis and Management. Baltimore/London: Williams & Wilkins; 1979:347-363. Critelli G, Scherillo M, Monda V, D’Ascia C, Musumeci S, Antignano A. Transvenous catheter ablation of the accessory atrioventricular
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p athway in the permanent form of junctional reciprocating tachycardia. Am J Cardiol. 1985;55:1639-1641. Farré J, Ross D, Wiener I, Bär FW, Vanagt EJ, Wellens HJ. Reciprocal tachycardias using accessory pathways with long conduction times. Am J Cardiol. 1979;44:1099-1109. Smith RT, Gillette PC, Massumi A, McVey P, Garson A Jr. Transcatheter ablative techniques for treatment of the permanent form of junctional reciprocating tachycardia in young patients. J Am Coll Cardiol. 1986;8:385-390.
Case 35 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary
Case Discussion
A 47-year-old man presented with recurrent tachycardia (Fig. 35.1) which is responsive to verapamil. The patient has a normal heart. His ECG is normal in sinus rhythm. In the EP lab he is diagnosed with AVRT. Explain what occurs during RF delivery in Fig. 35.2.
Local AP conduction in the RF channel is eliminated evidenced by prolongation of the local VA interval. Yet, an eccentric atrial activation suggesting a left-sided AP persists in the CS recordings. RF delivery at a different location resulted in VA block (Fig. 35.3). There were two left-sided APs: the first was anterolateral and the second was posterolateral; they were 3–4 cm away from each other.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910 A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_35, © Springer-Verlag London Limited 2011
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Version WIN200 : EPTRACER V0.48
2008017 I II III AVR AVL AVF V1 V2 V3 V4 V5 V6 10 mm/mV 25mm/s
Fig. 35.1 The ECG suggests that this is likely AVRT, with a left-sided AP (long RP, ST elevation in aVR and ST depression in lead I)
Case 35
149 Your Hospital Name in File HEADING.TXT
I
2008017
AVF V1 V6 CS910 CS78 CS56 CS34 CS12 HISD HISP RFD RFP 10 mm/mV 100mm/s
Fig. 35.2 Intracardiac EGMs during RF energy application. What happens?
Version WIN200 : EPTRACER V0.48
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Version WIN200 : EPTRACER V0.48
2008017 I AVF V1 V6 CS910 CS78 CS56 CS34 CS12 HISD HISP RFD RFP 10 mm/mV 100mm/s Offline printed on 17-05-2008 at 14:23:17.
Fig. 35.3 VA block is achieved
Case 36 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 60-year-old female with a history of left atrial myxoma, resected 9 years ago, subsequently developed palpitations, fatigue, and tachycardia. Despite antiarrhythmic medications, including sotalol and amiodarone, and multiple
cardioversions, she continued to experience tachycardia and was referred for electrophysiology study and catheter ablation. Surface electrocardiogram showed wide-complex tachycardia with a ventricular rate of 115 beats per minute (Fig. 36.1). What is the differential diagnosis of this arrhythmia based on the electrocardiogram?
Fig. 36.1 Surface electrocardiogram shows a regular wide-complex tachycardia at approximately 115 beats per minute
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_36, © Springer-Verlag London Limited 2011
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Case Discussion Diagnostic electrophysiology catheters were placed in the high right atrium, at the His bundle, the right ventricular apical septum, and in the coronary sinus. Intracardiac electrograms were recorded during tachycardia (Fig. 36.2).
Fig. 36.2 Intracardiac recordings during tachycardia. Left atrial activation as seen in coronary sinus catheter proceeds from medial to lateral, consistent with a focus or reentrant circuit in the right atrium
E. Buch et al.
Electroanatomic mapping was used to show the right atrial activation sequence. The tachycardia circuit was around the lateral right atriotomy scar from previous cardiac surgery. Ablation was performed at the superior margin of the scar and the tachycardia terminated (Fig. 36.3). It could not be reinduced on multiple attempts.
Fig. 36.3 Left anterior oblique fluoroscopic view of intracardiac electrophysiology catheters. The tip of the ablation catheter is in the lateral right atrium at the superior margin of the atriotomy scar, at the site of tachycardia termination
Case 37 Bradley P. Knight
Case Summary A 25-year-old woman with Wolff–Parkinson–White syndrome was referred for catheter ablation. The 12-lead EKG is consistent with an anteroseptal accessory pathway (AP) (Fig. 37.1). A previous attempt at ablation of the AP was aborted due to its proximity to the His bundle. Another attempt at ablation was made. The baseline rhythm was sinus with ventricular preexcitation. Orthodromic AVRT was inducible and the AP had a short refractory period that was less than 250 ms. The earliest ventricular activation during sinus rhythm was at a site where there was also a large His bundle recording during block in the AP. How would you proceed?
Case Discussion In this case, the patient has symptomatic WPW with a high risk AP. There is a significant risk of causing irreversible AV block with RF current. Cryoenergy ablation is an
alternative to radiofrequency ablation. One advantage of cryoenergy over radiofrequency current is the ability to “cryo-map” to minimize the likelihood of inadvertent AV block.1 As the ablation electrode temperature is lowered below freezing, the tissue reaches a temperature where temporary conduction block occurs well before it reaches a temperature where permanent tissue destruction occurs. This permits the ability to monitor during ablation for undesirable results, such as AV block, before a permanent lesion is created. Fig. 37.2 shows early activation at the para-Hisian region with an activation time of -30 ms. Fig. 37.3 shows disappearance of ventricular preexcitation when the temperature is lowered during cryoablation. As an iceball forms on the tip of the electrode, the electrogram is lost. After rewarming of the electrode occurs, a large His bundle recording can be seen (Fig. 37.4). After elimination of the AP, AV conduction was intact and there was no VA conduction. The AP did not recover during long-term follow-up. Cryoablation should be considered when attempting to ablate an AP that is located in the para-Hisian or midseptal region, to minimize the risk of AV block.
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_37, © Springer-Verlag London Limited 2011
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Fig. 37.1 This 12-lead EKG shows ventricular preexcitation consistent with an anteroseptal accessory pathway
Successful cryo site
Fig. 37.2 This tracing was recorded during catheter ablation of an anteroseptal accessory pathway. Shown are surface electrograms from leads I, II, III, V1, and V5, and the intracardiac electrograms from the high right atrium (HRA), the radiofrequency ablation catheter (Abl) positioned near the His bundle region, the cryo catheter (CRYO) with the tip positioned at the earliest local ventricular activation, and the right ventricular apex (RVA). The local ventricular activation recorded from the cryo catheter is 30 msec prior to the onset of the delta wave
−30 ms
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Fig. 37.3 This figure shows disappearance of preexcitation during cryo-ablation. The format is the same as figure 37.2
During cryoablation
University of Chicago
Appearance of his bundle during rewarming after cryo
Fig. 37.4 This figure shows the reappearance of the His-bundle recording after rewarming of the cryo-ablation electrode. The format is the same as figure 37.2
University of Chicago
Reference 1. Gaita F et al. Safety and efficacy of cryoablation of accessory pathways adjacent to the normal conduction system. J Cardiovasc Electrophysiol. 2003;14:825-829.
Case 38 Luigi Di Biase, Rodney P. Horton, and Andrea Natale
Case Summary A 65-year-old male with a 15-year history of symptomatic persistent atrial fibrillation was referred to our institution. The patient had a normal left ventricular ejection fraction. The patient denied chest discomfort, presyncope, or syncope. Atrial fibrillation was initially chemically cardioverted with Quinidine and Diltiazem. A few years later the drugs were ineffective and the patient underwent three electrical cardioversions. Quinidine and Diltiazem were replaced with Tikosyn. Because Tikosyn was ineffective, the patient decided to undergo pulmonary vein isolation. Five months following the procedure, the patient experienced symptoms related to atrial flutter with rapid ventricular response. For these reasons the patient underwent a second ablation procedure. During the second procedure, the patient did not show any recovery of conduction around the pulmonary veins. The presenting arrhythmia was atrial flutter, which was terminated during ablation in the coronary sinus. Two months after the second procedure the patient developed recurrence of left atrial flutter. The CT scan after the second procedure is shown (Figs. 38.1 and 38.2). What do you propose next for management of this patient’s rhythm abnormality, would a repeat ablation be an option, if so, what is the ablation target? What do you propose next? a) Clinical follow-up with AADs for rate control b) Propose a MAZE or COX procedure
L. Di Biase (*) Department of Electrophysiology, St. David’s Medical Center, 1015 32nd Street, Suite 506, Austin, TX 78705 e-mail:
[email protected] R.P. Horton Department of Electrophysiology, Texas Cardiac Arrhythmia Institute, 1015 East 32nd Street, Austin, TX 78705 e-mail:
[email protected] A. Natale Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32nd Street, Suite 408, Austin, TX 78705
c) Repeat catheter ablation targeting non PV site d) AV node ablation and pacing e) None of the above
Case Discussion The patient was taken to the electrophysiology laboratory for a repeat ablation. During the third procedure, before ablation in the left atrium, ablation in the persistent left superior vena cava (SVC) was performed. Once isolation was achieved, the ablation catheter was moved to the left atrium. The atrial flutter was prolonged and interrupted during ablation along the mitral annulus. During and after the infusion of high-dose isoproterenol (20 mcg/min), there were no evidence of additional firing sites. After 9 months of follow-up, the patient was asymptomatic and free from arrhythmia recurrences. This case shows that in a number of patients electrical disconnection of the pulmonary veins is not sufficient to prevent arrhythmic recurrences. This is possible in patients with left atrial scar preceding the ablation procedure, non-paroxysmal AF patients, females,1 and in patients with venous anomaly including persistent left SVC.2 In these patients, isolation of the left SVC is necessary together with the isolation of the pulmonary veins to prevent recurrences. Whether isolation of the left SVC without isolation of the PVs would have been sufficient to treat these patients is not known. Persistence of the left SVC is a congenital anomaly resulting from an abnormal development of the coronary sinus. In these patients, the left cardinal vein does not obliterate during the fetal life, and on the contrary, persists draining into either the left atrium or the right atrium through an enlarged CS. The described prevalence of left SVC persistence varies between 0.3% and 2% in individuals with a normal heart.3,4 A persistence of the left SVC can be diagnosed with echocardiography based an unusual enlarged CS, but the gold standards are CT scan and MRI.
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158 Fig. 38.1 CT scan showing the left atrium, the pulmonary veins, and the persistent LSVC
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In the above-mentioned case, spontaneous ectopies originating at different levels in the left SVC were present. It is always important to look for unusual sources of AF/Aflutter especially in patients presenting for repeat procedures. Unusual sources of AF should be considered after the failure of one or more procedures for AF ablation. Isolation of the PVs is not sufficient to prevent recurrences when a left SVC is present. Thus, diagnosis and isolation of the left SVC appears critical to avoid AF recurrence in all patients with AF and with this venous anomaly.
References
Fig. 38.2 CT scan showing a persistent LSVC draining into the coronary sinus
The left SVC when present is always a source of ectopies that can initiate AF through the electrical connections with the LA and CS. Hsu et al.5 suggested that as a consequence of the abnormal embryologic development, the persistent of the left SVC may be associated with the presence of electrical tissue, responsible for arrhythmias.
1. Verma A, Wazni OM, Marrouche NF, et al. Pre-existent left atrial scarring in patients undergoing pulmonary vein antrum isolation: an independent predictor of procedural failure. J Am Coll Cardiol. 2005;45:285-292. 2. Elayi CS, Fahmy TS, Wazni OM, Patel D, Saliba W, Natale A. Left superior vena cava isolation in patients undergoing pulmonary vein antrum isolation: impact on atrial fibrillation recurrence. Heart Rhythm. 2006;3:1019-1023. 3. Gonzalez-Juanatey C, Testa A, Vidan J, et al. Persistent left superior vena cava draining into the coronary sinus: report of 10 cases and literature review. Clin Cardiol. 2004;27:515-518. 4. Fraser RS, Dvorkin J, Rossall RE, Eidem R. Left superior vena cava: a review of associated congenital heart lesions, catheterization data and roentgenologic findings. Am J Med. 1961;31:7 11-716. 5. Hsu LF, Jais P, Keane D, et al. Atrial fibrillation originating from persistent left superior vena cava. Circulation. 2004;109: 828-832.
Case 39 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
Case Summary A 38-year-old female complained of recurrent episodes of lightheadedness and palpitations over several months. She came to the emergency room with the same symptoms, at which time her 12-lead ECG was as follows (Figs. 39.1–39.4). Two ventricular extrastimuli (S1) at cycle lengths of 400 ms were administered during the tachycardia (Fig. 39.5). What is the best initial management, and what is the most likely diagnosis?
Case Discussion The P-wave occurring between the two R-waves, seen in the first 12-lead ECG of this young female with documented normal PR interval during sinus rhythm in the past, suggests a diagnosis of supraventricular tachycardia, specifically AV nodal reentry tachycardia (AVNRT) with 2:1 AV conduction. Since we were unable to exclude other possibilities, such as atrial tachycardia a complex electrophysiology study was required. When the patient’s rhythm spontaneously changed from a 460- to a 230-ms R-R cycle length (Figs 39.1 and 39.3), it revealed the presence of 2:1 AV conduction, which then
M.E. Mortada (*), J.S. Sra, and M. Akhtar Department of Electrophysiology, Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke’s Medical Centers, University of Wisconsin School of Medicine and Public Health, 2801 W. Kinnickinnic River Parkway, #777, Milwaukee, WI 53215 e-mail:
[email protected]
changed to 1:1 AV conduction. This excludes the diagnosis of accessory pathway-mediated tachycardia, as it would not occur in the presence of 2:1 AV block. The patient was symptomatic with her tachycardia, so the best next step in management is to convert her to normal rhythm and then perform further work-up to diagnose and treat her condition. She was hemodynamically was stable, therefore DC cardioversion is not indicated, but adenosine IV bolus is the best first-line approach. b-blockers or calcium channel blockers are acceptable therapies, yet, complex electrophysiology study post conversion is more appropriate to confirm the diagnosis and cure the patient’s arrhythmia by ablation therapy. The first intracardiac tracing (Fig. 39.4) showed narrow complex tachycardia with two atrial activities recorded for each incident of ventricular activity. When there ventricular activity, the VA relationship was fixed. Notice that the His was present before each atrial activity, which suggests the location of the block is in the His–Purkinje system in a 2:1 pattern due to refractoriness. The first ventricular extrastimuli penetrated the Purkinje system but not the His. Therefore, it did not engage the circuit and did not change the cycle length of the tachycardia. The second ventricular extrastimuli was given earlier in the tachycardia cycle length and it penetrated also to a level below the His. Hence, the cycle length of activation at this vulnerable location of block has shortened. The His-Purkinje system’s refractoriness is directly related to the duration of proceeding cycle length1. Therefore, the site of block’s refractory period is also shortened. That leads to the penetration of the next atrial activity into the His-Purkinje system and setting a 1:1 AV conduction. Notice the fixed VA relationship before and after the ventricular extrastimulation. This linking suggests that the tachycardia diagnosis is most likely AV nodal reentry tachycardia.
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Fig. 39.1 The patient’s 12-lead ECG upon admission to emergency room with symptoms of lightheadedness and palpitations
Fig. 39.2 The patient’s previous baseline 12-lead ECG
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Fig. 39.3 The patient spontaneously switched into the rhythm shown in this 12-lead ECG, accompanied by worsening symptoms, but she remained hemodynamically stable
Fig. 39.4 Intracardiac tracing of the same tachycardia the patient presented first to the ER. (Rhythm tracing from top to bottom: lead I, Lead II, Lead V1, high right atrium recording “HRA”, His bundle recording
“HIS”, and right ventricular apex recording “RVa”. Labels used in this figure are similar to the labels used in subsequent figures)
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Fig. 39.5 Two ventricular extrastimuli (S1) at cycle lengths of 400 ms were administered during the tachycardia. The tachycardia accelerated from 2:1 AV conduction to 1:1 AV conduction
Reference 1. Akhtar M, Mahmud R, Tchou P, Denker S, Gilbert CJ. Normal electrophysiologic responses of the human heart. Cardiol Clin 1986;4: 365–386.
Case 40 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary
Case Discussion
The patient is a 40-year-old female with a prior history of palpitations and is being medically managed for mild hypertension. The episodes became more frequent 2 months prior to the time of ablation. The ECG recordings were taken while the patient was having palpitations. The ECG revealed both orthodromic and antidromic tachycardia. Where is the likely position of the AP?
This bypass tract is likely located in the posterior septal space given the morphology of the maximally preexcited tracing (Figs. 40.1, 40.2) and it was successfully as shown in figs. 40.3–40.14.
A. Rossillo, S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele (*) Cardiovascular Department, Ospedale dell’Angelo, Mestre, Venice, Italy e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_40, © Springer-Verlag London Limited 2011
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Fig. 40.1 The 12-lead resting ECG (paper speed 25 mm/s) showing normal sinus rhythm with a ventricular rate of 109 bpm with a short PR interval (118 ms) and a QRS width of 81 ms with mild delta wave in the initial portion of the QRS
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Fig. 40.2 12-lead ECG taken during atrial pacing (paper speed 25 mm/s) showing maximum ventricular preexitation with an early transition of the R wave between leads V1 and V2 and negative wave in the inferior leads
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Fig. 40.3 Intracardiac recordings taken at baseline during the electrophysiology study (paper speed 200 mm/s). Four surface ECG leads are shown (I, aVF, V1, V6): (1) bipolar recording from the high right atrium (HRA), (2) bipolar recording from the distal His bundle region (HIS D)
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(3) five unipolar recordings from the coronary sinus (CS), (4) the unipolar (MC U-CATH) and the distal bipolar recording of the mapping catheter (MC D). (A atrium, V ventricle and H His bundle)
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Fig. 40.4 Intracardiac recordings taken during baseline while ventricular pacing (paper speed 200 mm/s). Same display as shown in Fig. 40.3 (A atrium, V ventricle)
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A Fig. 40.5 Intracardiac recordings taken during programmed atrial stimulation (paper speed 100 mm/s). Same display as shown in Fig. 40.3. Panel A: At a coupling interval of 290 ms the ventricular
preexitation was still present and in Panel B: With a coupling interval of 280 ms suddenly disappeared (ERP of bypass fiber). (A atrium, V ventricle and H His bundle)
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B Fig. 40.5 (continued)
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A Fig. 40.6 Intracardiac recordings taken during programmed ventricular stimulation (paper speed 200 mm/s). Same display as shown in Fig. 40.3. Panel A: At a coupling interval of 280 ms, the Stim-A interval
was 130 ms and suddenly increased and in Panel B to 180 ms with a coupling interval of 270 ms (retrograde ERP of a bypass fiber). (A atrium, V ventricle)
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B Fig. 40.6 (continued)
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Fig. 40.7 Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s). Same display as shown in Fig. 40.3. AVRT induction (AA 280 ms) with a single extrastimulus (drive 500 ms and S1–S2 230 ms). (A atrium, V ventricle)
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Fig. 40.8 Intracardiac recordings (paper speed 200 mm/s). Same display as shown in Fig. 40.3. Ablation site. The bipolar recording of the ablation catheter shows presence of an atrial signal and of the bypass
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fiber without ventricle activity that is present only in the unipolar recording. (A atrium, K Kent bundle, and V ventricle)
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Fig. 40.9 Intracardiac recordings (paper speed 100 mm/s). Same display as shown in Fig. 40.3. Ablation site. The bipolar recording of the ablation catheter shows presence of an atrial signal and of the bypass
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fiber without ventricle activity that is present only in the unipolar recording (A atrium, K Kent bundle, and V ventricle)
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Fig. 40.10 Intracardiac recording taken during radiofrequency delivery (paper speed 200 mm/s). Same display as shown in Fig. 40.3. The second beat disappeared during ventricular preexitation and the intrac-
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ardiac recording showed a clear separation between atrial (A) and ventricular signals (V). H His signal
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Fig. 40.11 Intracardiac recordings taken during radiofrequency delivery (paper speed 25 mm/s). Same display as in Fig. 40.3. The arrow shows the elimination of the ventricular preexcitation. The circle shows
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the ventricle signal on the ablation catheter before and after the elimination of the bypass fibers
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A Fig. 40.12 Intracardiac recordings taken during programmed ventricular stimulation (paper speed 200 mm/s). Same display as shown in Fig. 40.3. Panel A: At a coupling interval of 280 ms, the Stim-A interval
was 160 ms and Panel B: At a coupling interval of 270 a decremental VA conduction was present (A atrium, V ventricle)
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B Fig. 40.12 (continued)
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Fig. 40.13 Intracardiac recording taken at the end of the procedure (paper speed 200 mm/s). The same display as shown in Fig. 40.3 (A atrium, V ventricle, H His bundle)
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Bibliography
A
RAO
Calkins H, Langberg J, Sousa J, et al. Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients. Abbreviated therapeutic approach to Wolff-Parkinson-White syndrome. Circulation. 1992;85:1337-1346. 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. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324:1605-1611. Scheinman MM, Wang YS, Van Hare GF, Lesh MD. Electrocardio graphic and electrophysiologic characteristics of anterior, midseptal and right anterior free wall accessory pathways. J Am Coll Cardiol. 1992;20:1220-1229.
LAO
MV
H RA TT
CS MCV
B
TV
Fig. 40.14 Panel A: RAO and LAO of the mapping catheter at the ablation site in the proximal coronary sinus. Panel B: LAO picture of the mapping catheter at the ablation site in the proximal coronary sinus (RA right atrium, TT Todaro’s tendon, TV tricuspid valve, CS coronary sinus, MCV middle cardiac vein, H His bundle, MV mitral valve)
Case 41 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary
Case Discussion
A 36-year-old woman with a normal heart had this ECG in the lab (Fig. 41.1). A narrow QRS tachycardia is seen without visible P waves; sharp J point in V1; this likely represents AVNRT. Multiple APDs change or accelerate tachycardia – how?
Tachycardias, pre- and post-APDs, are AVNRT. The APDs block in the first slow pathway and conduct by another slow pathway (Fig. 41.2). RF energy delivered in slow pathway region eliminated dual AVN physiology and inducibility.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_41, © Springer-Verlag London Limited 2011
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I II III AVR AVL AVF V1 V2 V3 V4 V5 V6 10 mm/mV 25 mm/s
Fig. 41.1 SVT with change in cycle length
Case 41 2008083 I AVF V1 V6
CS78
CS34
CS12
HISD
HISP
rfD
rfP 10 mm/mV 50 mm/s
Fig. 41.2 SVT with change in antegrade limb resulting in faster cycle length
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Case 42 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 59-year-old male was referred for radiofrequency catheter ablation of atrial flutter and atrial fibrillation. He had a 3-year history of highly symptomatic paroxysmal atrial fibrillation that failed to respond to multiple medications. He underwent catheter-based radiofrequency ablation (RFA) with pulmonary vein isolation and subsequently a modified left- and right-sided surgical maze procedure after recurrence of atrial fibrillation. Following the maze procedure, patient developed incessant atrial flutter causing palpitations and fatigue. He was referred for catheter ablation. Diagnostic electrophysiology catheters were placed at the His bundle, the right ventricular apical septum, and in the coronary sinus. A multipolar halo catheter was placed in the right atrium with the distal electrodes in the coronary
sinus, middle electrodes along the lateral right atrial wall, and proximal electrodes near the roof of the right atrium. Intracardiac activation map showed atrial flutter with distal to proximal coronary sinus activation and passive counterclockwise activation of the right atrium (Fig. 42.1). After transseptal catheterization, electroanatomic mapping of the left atrium suggested that the tachycardia circuit utilized an isthmus between the mitral annulus and the left inferior pulmonary vein. Entrainment mapping confirmed that this left-sided isthmus was critical to the tachycardia circuit. During ablation in the region between the left inferior pulmonary vein and the mitral annulus (Fig. 42.2b), the intracardiac activation sequence changed abruptly, yet tachycardia persisted (Fig. 42.3). What is responsible for this change in sequence?
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_42, © Springer-Verlag London Limited 2011
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186 Fig. 42.1 Intracardiac recordings during tachycardia. Coronary sinus activation is from distal to proximal, consistent with a left atrial tachycardia circuit. Right atrial activation is earliest at the high septum (HALO 10) due to conduction through Bachman’s bundle, then conducts along the roof and down the lateral right atrial wall (HALO 9 to HALO 5). There is competing activation through the coronary sinus (HALO 1 to HALO 4), resulting in fusion of right atrial activation
E. Buch et al. I aVF V1 V6 ABL d HIS p HIS m HIS d HALO 10 HALO 9 HALO 8 HALO 7 HALO 6 HALO 5 HALO 4 HALO 3 HALO 2 HALO 1 CS 9, 10 CS 7, 8 CS 5, 6 CS 3, 4 CS 1, 2
Case Discussion Successful ablation of the mitral isthmus, which was critical for perpetuation of the left atrial macroreentrant tachycardia, resulted in termination of that rhythm. However, it unmasked an underlying typical counterclockwise right
atrial flutter with a longer tachycardia cycle length. In effect, the typical right atrial flutter had been entrained by the left atrial flutter. The patient then underwent further ablation at the cavotricuspid isthmus, resulting in termination of the atrial flutter, bidirectional isthmus block, and noninducibility of either tachycardia.
Case 42 Fig. 42.2 (a) Three-dimensional voltage map of the left atrium, left posterior oblique view. Large areas of scar are seen (in red), likely from prior catheter and surgical ablation procedures. (b) Posteroanterior view of same patient’s left atrium, showing ablation sites (red points) between left inferior pulmonary vein and mitral annulus. Pacing at these sites showed entrainment of the atrial flutter with postpacing interval near tachycardia cycle length
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a
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E. Buch et al. I aVF V1 V6 ABL d HIS p HIS m HIS d HALO 10 HALO 9 HALO 8 HALO 7 HALO 6 HALO 5 HALO 4 HALO 3 HALO 2 HALO 1 CS 9, 10 CS 7, 8 CS 5, 6 CS 3, 4 CS 1, 2
TCL 228 ms
TCL 280 ms
Case 43 Bradley P. Knight
Case Summary A patient with recurrent PSVT undergoes an electrophysiology procedure. A regular narrow QRS complex tachycardia is induced with a CL 360 ms and a 1:1 AV relationship with simultaneous atrial and ventricular activation. Figure 43.1 shows the response immediately after overdrive atrial pacing at a CL of 350 ms. Shown are the surface recordings I, II, V1, and V5 and intracardiac recordings from the high right atrium (HRA), at the His bundle region with the ablation catheter (Abl), and right ventricular apex (RV). A stimulation channel is also displayed. What is the diagnosis of the tachycardia?
Case Discussion During a regular supraventricular tachycardia with a 1:1 AV relationship, the differential diagnosis includes AV nodal reentry (AVNRT), orthodromic AV reentry (ORT), and atrial
tachycardia (AT). Atrial overdrive pacing can be used to help “rule in” or “rule out” atrial tachycardia as the mechanism.1,2 The principle is that during atrial overdrive pacing just slightly faster than the tachycardia, a 1:1 AV relationship can sometimes be maintained. In the case of an AT, the first atrial depolarization immediately after atrial pacing is stopped will occur independent of the last QRS complex that was a result of AV conduction during atrial pacing. Therefore the first VA interval would most likely differ from the VA interval during tachycardia. In contrast, in the case of an AV nodal– dependent tachycardia, such as AVNRT or ORT, the VA interval of the first return beat is usually the same as the VA interval during tachycardia because the atrial depolarization is dependent on VA conduction. However, there is always a small chance that the first VA interval will be the same or similar as that during tachycardia by chance alone. In this example, the AH interval is increasing during atrial pacing, but 1:1 AV conduction remains intact. The first VA interval after pacing is the same as that during tachycardia. Because the short VA interval excludes ORT as a mechanism,2 the diagnosis is most likely AVNRT.
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_43, © Springer-Verlag London Limited 2011
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Fig. 43.1 Example of atrial overdrive pacing during tachycardia to determine the mechanism of tachycardia. See text for format and abbreviations
References 1. Knight BP, Zivin A, Souza J, Flemming M, Pelosi F, Goyal R, Man KC, Strickberger SA, Morady F. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol 1999;33:775-81.
2. Knight BP, Ebinger M, Oral H, Kim MH, Sticherling C, Flemming M, Pelosi F, Michaud GF, Strickberger SA, Morady F. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol 2000;36:574-82.
Case 44 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary The patient is a 76-year-old male with history of AVNRT since childhood and very frequent episodes occurring in the last 2 months. Ischemic heart disease with mild reduction of LVEF was present. Coronary angiography showed a moderate stenosis in the right and circumflex coronary and no significant stenosis of LAD (Fig. 44.1). An EP study was scheduled to define the arrhythmia (Fig. 44.2). What type of tachycardia is this? What ablative strategy would you choose?
Case Discussion The tachycardia is clearly an AVNRT and the presence of a first-degree AV block suggests the absence or pathological
anterograde conduction through the fast pathway. According to this finding, a standard ablative approach targeting the slow pathway may result in complete AV block. Pace mapping Koch’s triangle to define anterograde and retrograde structures of the AV node is useful in preventing this complication. In this case, pace mapping showed an absence of an anterograde fast pathway and the presence of a retrograde fast pathway in the anteroseptal region of the Koch’s triangle. Therefore, a single RF lesion was applied in the region of the fast pathway, and Fig. 44.3 shows a junctional rhythm during the ablation. The red arrow shows when the retrograde conduction skips from the fast to the slow pathway (A = atrium, V = ventricle). A transient complete AV Block (15s) was present at the end of RF energy delivery. The EP study performed at the end of the procedure showed a normal Wenckebach point and the tachycardia was no longer inducible.
A. Rossillo (*), S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele, Cardiovascular Department, Ospedale dell’Angelo, Mestre, Venice, Italy e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_44, © Springer-Verlag London Limited 2011
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Fig. 44.1 12-lead resting ECG (paper speed 25 mm/s) showing sinus rhythm with first-degree AV block
Fig. 44.2 Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s) with the induction of the tachycardia with a cycle length of 428 ms study (A atrium, V ventricle, and H His bundle)
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Fig. 44.3 A junctional rhythm during the ablation. The red arrow shows when the retrograde conduction skips from the fast to the slow pathway (A atrium, V ventricle)
Bibliography Delise P, Gianfranchi L, Paparella N, et al. Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation. Am J Cardiol. 1997;79:1421-1423. Delise P, Sitta N, Bonso A, et al. Pace mapping of Koch’s triangle reduces risk of atrioventricular block during ablation of atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol. 2005;16:30-35. Haissaguerre 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: 2162-2175. Haïssaguerre M, Jaïs P, Shah DC, et al. Analysis of electrophysiological activity in Koch’s triangle relevant to ablation of the slow AV nodal pathway. Pacing Clin Electrophysiol. 1997;20:2470-2481. 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;327:313-318. Natale A, Greenfield RA, Geiger MJ, et al. Safety of slow pathway ablation in patients with long PR interval: further evidence of fast and slow pathway interaction. Pacing Clin Electrophysiol. 1997; 20:1698-1703.
Case 45 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary
Case Discussion
A 25-year-old man with normal heart presents with SVT. His tachycardia is initiated with ventricular pacing (Figs. 45.1 and 45.2). The response to ventricular pacing is shown in Fig. 45.3. What is the diagnosis?
Tachycardia is instantiated by VPDs. VA interval is long during tachycardia and the atrial pattern during tachycardia is similar to that of the retrograde A waves (in the limited leads available). V pacing at a faster rate than the tachycardia shows VA dissociation suggesting that this is atrial tachycardia.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_45, © Springer-Verlag London Limited 2011
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Case 46 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 79-year-old male with a history of hypertension, coronary artery bypass grafting, and implantable cardioverterdefibrillator for ventricular fibrillation, presented with symptomatic supraventricular tachycardia. He had failed antiarrhythmic medications and cardioversion attempts, and was referred for electrophysiology study and catheter ablation. Twelve-lead electrocardiogram showed organized
atrial activity with positive flutter waves in lead V1 and inferior leads, not suggestive of typical counterclockwise atrial flutter (Fig. 46.1). Diagnostic electrophysiology catheters were placed at the His bundle, the right ventricular apical septum, and in the coronary sinus. Intracardiac activation map obtained during tachycardia showed counterclockwise activation of the right atrium. Ablation of the cavotricuspid isthmus was performed without tachycardia termination. Why did the tachycardia persist?
Fig. 46.1 Surface electrocardiogram of clinical tachycardia. There is an organized atrial rhythm with low-amplitude flutter waves that are predominantly positive in lead V1. Variable conduction to the ventricles results in an irregular ventricular rhythm
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_46, © Springer-Verlag London Limited 2011
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Case Discussion Entrainment mapping from the septal side of the cavotricuspid isthmus and the distal coronary sinus were performed. Although the tachycardia could be entrained from both sites, the post-pacing interval was much shorter from the distal coronary sinus, suggesting a left atrial flutter circuit with passive counterclockwise activation of the right atrium. After transseptal catheterization, electroanatomic mapping of the left atrium was performed. Voltage mapping revealed an area of scar on the left atrial roof. Activation a
map shown in Fig. 46.2a demonstrates a left atrial tachycardia with centrifugal activation of the left atrium originating near a scar on the left atrial roof. Several viable sites were found adjacent to the scar, with early activation (Fig. 46.2b). Pacing from these locations resulted in entrainment with concealed fusion, and post-pacing interval near tachycardia cycle length. During ablation (Fig. 46.3) the tachycardia spontaneously terminated, and could not be reinduced. This case illustrates that typical counterclockwise activation of the right atrium does not prove that it is part of the tachycardia circuit. b
Fig. 46.2 (a) Three-dimensional electroanatomical activation map of the left atrium during tachycardia, anteroposterior view. Earliest activation of the left atrium is at the roof (red area), just lateral to a region of scar (gray
area) near the superior aspect of the left atrial septum. (b) Right posterior oblique view. Radiofrequency energy was applied at viable sites adjacent to the scar (red points within red area) with low-amplitude potentials
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Case 47 Bradley P. Knight
Case Summary A patient with recurrent PSVT undergoes an electrophysiology procedure. Fig. 47.1 shows a recording during the procedure. Shown are the surface recordings and intracardiac recordings from the His bundle electrogram (HBE) ablation catheter (Abl), coronary sinus (CS), and right ventricular apex (RV). What is the diagnosis of the tachycardia?
Case Discussion The differential diagnosis of a regular narrow QRS complex tachycardia in the EP lab includes AV nodal reentry, orthodromic AV reentry, and atrial tachycardia. The transition zones during tachycardia can be very useful when trying to make a diagnosis. In this case the tachycardia terminates. Before termination, one can see that there is simultaneous
activation of the atrium and ventricle with a septal VA interval that is close to zero. This excludes AV reentry using an accessory pathway. When attempting to measure the septal VA interval, it can be difficult at times to differentiate the atrial signal from the ventricular signal on the His bundle recording. In this example, the proximal coronary sinus recordings (CS9-10) can be used to identify the timing of septal atrial activation. The termination of the tachycardia is associated with spontaneous AV block. This observation excludes an AT which would be expected to conduct to the ventricle upon termination if there is a 1:1 conduction during the tachycardia. In this case the tachycardia actually slows slightly before termination. Therefore, it would be extremely unlikely that an atrial tachycardia that spontaneously slows just before termination would be associated with AV block on the last beat. Another observation that excludes an atrial tachycardia is that as the tachycardia cycle length increases the VA interval remains constant. This fixed relationship suggests an AV nodal–dependent tachycardia.
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL, 60611 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_47, © Springer-Verlag London Limited 2011
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Fig. 47.1 Tracing recorded during an electrophysiology procedure in a patient with recurrent paroxysmal supraventricular tachycardia. Spontaneous termination of tachycardia occurs. See text for format and abbreviations
Case 48 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele
Case Summary A 47-year-old male patient without any structural heart disease presented with a history of palpitations since childhood. All ECGs recorded while the patient experienced palpitations showed a wide QRS complex tachycardia with a left bundle branch block pattern. The arrhythmia was always
sustained and external DC shock was necessary on three occasions to restore sinus rhythm. Pharmacologic treatment (including amiodarone and propafenone) was unsuccessful and the two last episodes of tachycardia were reported to be faster than usual and poorly tolerated (Figs. 48.1–48.8). Based on the previous tracings, what is the tachycardia mechanism?
Fig. 48.1 12-lead resting ECG (paper speed 25 mm/s) showing sinus rhythm, a normal PR interval (170 ms), and a QRS width of 100 ms with slight slurring of the initial portion of the QRS
A. Rossillo (*), S. Themistoclakis, A. Bonso, A. Corrado, and A. Raviele Cardiovascular Department, Ospedale dell’Angelo, Mestre, Venice, Italy A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_48, © Springer-Verlag London Limited 2011
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Fig. 48.2 Intracardiac recordings at baseline during the electrophysiology study (paper speed 100 mm/s). Four surface ECG leads (I, aVF, V1, V6), two bipolar recordings from the His bundle region (HIS D for distal and HIS P for proximal), seven bipolar recordings from the epi-
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cardial side of the tricuspid annulus obtained by a Cardima catheter positioned in the right coronary artery (C1–C7), and one bipolar recording from the coronary sinus (SC). AH interval is 80 ms and HV interval 30 ms
Case 48
Fig. 48.3 Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s). Same display as shown in Fig. 48.2. During programmed atrial stimulation (coupling interval between S1 and S2: 375 ms) A-H interval increased from 105 to 125 ms,
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H-V interval decreased from 30 to 10 ms, and the QRS complex on the surface ECG became wider with a left bundle branch block morphology
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Fig. 48.4 Intracardiac recordings taken during programmed atrial stimulation (paper speed 200 mm/s). Same display as shown in Fig. 48.2. At the coupling interval of 300 ms, atrioventricular node duality was demonstrated with an A-H interval which increased suddenly from 111 to 192 ms
Case 48
Fig. 48.5 Intracardiac recordings taken during atrial stimulation (cycle length 410 ms; paper speed 100 mm/s). Same display as shown in Fig. 48.2. Ventricular preexcitation is present with a negative (−10 ms)
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H-V interval, a His bundle potential identified at the very beginning of the QRS complex, and a left bundle branch block morphology on the surface ECG
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Fig. 48.6 Intracardiac recordings during atrial stimulation (paper speed 100 mm/s). Same display as that shown in Fig. 48.2. When atrial pacing at a cycle length of 270 ms is abruptly interrupted, two atrioventricular node echoes appeared (slow–fast type)
Case 48
Fig. 48.7 Intracardiac recordings taken during the tachycardia induced during programmed atrial stimulation (paper speed 100 mm/s). Same display as Fig. 48.2. The tachycardia had a cycle length of 330 ms and
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a left bundle branch block morphology. Intracardiac recordings showed that the site of earliest atrial activation occurred in the His bundle region with a retrograde His deflection
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Fig. 48.8 12-lead ECG taken during the induced tachycardia (rate: 186 bpm; paper speed 25 mm/s) showing left bundle branch block morphology. In fact, the induced tachycardia on 12-lead ECG is identical to the one observed during rapid atrial stimulation (see Fig. 48.6)
Case Discussion The patient has an atriofascicular pathway or so-called Manheim. Based on Fig. 48.9 this is likely antidromic tachycardia with retrograde conduction over either the fast or slow pathway (Figs. 48.10–48.13).
Case 48
Fig. 48.9 Intracardiac recordings taken during the tachycardia (paper 200 mm/s). Same display as shown in Fig. 48.2. A spontaneous change in H-A interval was observed (from 120 to 69 ms) without any change in atrial retrograde activation pattern but with shortening of the tachy-
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cardia cycle length (from 670 to 570 ms). This figure illustrates an abrupt switch from the slow to the fast retrograde pathway excluding the slow–fast atrioventricular node reentrant tachycardia as the mechanism of the induced tachycardia
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Fig. 48.10 Intracardiac recordings taken during mapping of the tricuspid annulus during sinus rhythm. Same representation as shown in Fig. 48.2, except that a bipolar recording obtained from the tip of the
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ablation catheter (MC BIP) is now displayed. In the lateral region of the tricuspid annulus a specific potential was recorded (M potential)
Case 48
Fig. 48.11 Intracardiac recordings taken during mapping of the tricuspid annulus during sinus rhythm. Same representation as shown in Fig. 48.2. When mapping the region where the M potential was
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recorded, mechanical block occurred (normalization of the QRS complex on the surface ECG, normalization of H-V interval) (arrow). Ablation was performed at this site
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Fig. 48.12 12-lead ECG recorded after the ablation procedure (paper speed 25 mm/s). Radiofrequency current was applied on the site shown in Fig. 48.12. The 12-lead ECG is now normal without any ventricular preexcitation
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Aliot E, de Chillou C, Revault d’Allones G. Mahaim tachycardias. Eur Heart J. 1998;19(suppl E):E25-E31. Ellenbogen KA, Ramirez NM, Packer DL, et al. Accessory nodoventricular (Mahaim) fibers: a clinical review. PACE. 1986;9:868-875. Gallagher JJ, Smith WM, Kasell JH, et al. Role of Mahaim fibers in cardiac arrhythmias in man. Circulation. 1981;64:176-184. Haissaguerre M, Cauchemez B, Marcus F, et al. Characteristics of the ventricular insertion sites of accessory pathways with anterograde decremental conduction properties. Circulation. 1995;91:10771085. Josephson ME. Nodoventricular and fasciculoventricular bypass tracts. In: Josephson ME, ed. Clinical Cardiac Electrophysiology: Techniques and Interpretation. 2nd ed. Malvern: Lea & Febiger; 1993:396-416. Mounsey JP, Griffith MJ, McComb JM, et al. Radiofrequency ablation of Mahaim fiber following localization of Mahaim pathway potentials. J Cardiovasc Electrophysiol. 1994;5:432-434. Tchou P, Lehmann MH, Jazayeri M, et al. Atriofascicular connections or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit. Circulation. 1988;77:837-841.
Case 49 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary
Case Discussion
A 30-year-old female with primary pulmonary hypertension had recurrent atrial flutter despite amiodarone treatment and multiple cardioversions. Because of worsened dyspnea resulting from atrial flutter, she was referred for electrophysiology study and catheter ablation. Preprocedural surface electrocardiograms, both recorded during the month prior to ablation, showed organized atrial activity with variable flutter wave morphology (Fig. 49.1). Based on the 12-lead ECG, what is the diagnosis? Do these arrhythmias arise from multiple flutter circuits?
By definition, typical atrial flutter is a macroreentrant tachycardia bound anteriorly by the tricuspid isthmus and posteriorly by the inferior vena cava, the terminal crest, and most commonly, the superior vena cava.1 The majority of these tachycardias are counterclockwise (CCW), with activation descending the anterolateral and ascending the septal RA. Less commonly, isthmus-dependent atrial flutter is clockwise (CW), with activation descending the septal and ascending the anterolateral RA. Multiple studies have attempted to characterize the surface ECG appearance of
Fig. 49.1 Surface electrocardiogram showing flutter waves that are predominantly negative in lead V1 and biphasic in the inferior leads, not typical of cavotricuspid isthmus dependent counterclockwise atrial flutter
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_49, © Springer-Verlag London Limited 2011
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CW and CCW flutter.2 It is currently accepted that predominantly negative F wave deflections in the inferior leads and in lead V6 and positive deflection in V1 indicate CCW flutter, while CW flutter has positive F waves in the inferior leads and V6, and negative F waves in lead V1.1,2 In this
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case, negative F wave deflection in V1 and positive deflection in inferior leads (Fig. 49.1a) predicted CW flutter, which was established by intracardiac mapping (Fig. 49.2). The other surface ECG (Fig. 49.1b) was likely CCW flutter. Neither arrhythmia was inducible after ablation at the
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Fig. 49.2 (a) Left anterior oblique fluoroscopic view of intracardiac electrophysiology catheters. The duopecapolar catheter (D1–D10) is curled in the right atrium, with the proximal bipoles (D9, D10) near the right atrial roof, the middle bipoles (D4–D8) along the lateral right atrial wall, and the distal bipoles (D2, D3) near the cavotricuspid
isthmus, with the most distal bipole (D1) in the proximal coronary sinus. (b) Surface and intracardiac recordings. The activation sequence proceeds from distal to proximal, consistent with clockwise isthmusdependent atrial flutter
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Fig. 49.3 With the ablation catheter positioned as shown in Fig. 49.2 above, radiofrequency energy was applied. Intracardiac recordings during ablation, showing termination of tachycardia
cavotricuspid isthmus (Fig. 49.3). Of note, F wave morphology not adhering to the above criteria has been described in a minority of patients when the left atrium is activated by Bachmann’s bundle. In this case, CCW flutter can manifest as positive F waves in the inferior leads, and clockwise flutter can manifest as negative F waves in the inferior leads. (Figs 49.2 and 49.3).3
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: 852-866. 2. Milliez P, Richardson AW, Obioha-Ngwu O, Zimetbaum PJ, Papageorgiou P, Josephson ME. Variable electrocardiographic characteristics of isthmus-dependent atrial flutter. J Am Coll Cardiol. 2002;40:1125-1132. 3. 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; 7:215-223.
Case 50 Bradley P. Knight
Case Summary
Left-sided slow pathway ablation
An attempt was made to ablate the slow pathway in a 45-year-old woman with recurrent SVT and reproducibly inducible typical AV nodal reentry. Using a standard 4-mmtip electrode ablation catheter, a total of 55 applications of RF current were delivered using 50 W at several sites just outside and slightly within the coronary sinus ostium. Despite adequate tissue heating and the occurrence of an accelerated junctional rhythm with most lesions, the tachycardia remained inducible. What other approach could be used?
RF site
Case Discussion A very small number of patients who have what appear to be the slow–fast type of AV nodal reentry cannot be successfully ablated using a right-sided approach. It is likely that there are left-sided inputs to the AV node that require ablation to eliminate slow pathway function. Using a retrograde aortic approach the left posterior septal aspect of the mitral annulus was explored (Fig. 50.1). A site was identified that was associated with a complex, fractionated atrial electrogram (Fig. 50.2). A single application of RF current at this site resulted in an accelerated junctional rhythm and elimination of slow pathway function (Fig. 50.3).
Fig. 50.1 A fluoroscopic image in a left anterior oblique projection during ablation of a slow pathway using a left-sided approach. Three catheters can be seen in the right heart including a right ventricular, His-bundle, and coronary sinus catheter. There is also a left sided ablation catheter that has been positioned along the posteroseptal mitral annulus using a retrograde aortic approach
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_50, © Springer-Verlag London Limited 2011
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Fig. 50.2 Tracing showing the electrogram at the successful ablation site during sinus rhythm in a patient undergoing a left-sided slow AV nodal pathway ablation. Shown are surface recordings from leads I, II, V1, and V5, and the intracardiac recordings from high right atrium (HRA), His-bundle electrogram region (HBE), left ventricle (LV), and right ventricular apex (RVA)
Bibliography Katritsis DG, Becker AE, Ellenbogen KA, et al. Right and left inferior extensions of the atrioventricular node may represent the anatomic substrate of the slow pathway in humans. Heart Rhythm. 2004;1:582-586.
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Fig. 50.3 Tracing demonstrating an accelerated junctional rhythm during delivery of radiofrequency current at the successful ablation site in a patient undergoing a left-sided slow AV nodal pathway ablation. The format and abbreviations are the same as in Figure 50.2
Case 51 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary A 54-year-old woman with a normal heart presents to the EP lab with an SVT (Fig. 51.1). The tachycardia could be induced with three APCs or with ventricular premature beats (Figs. 51.2 and 51.3). Explain the mechanism of the tachycardia?
Tachycardia is initiated by a decrementally conducting PVC. VA time is long; earliest in proximal CS. With PVC placed when the His was refractory, no atrial preexcitation was observed, suggesting that the likely mechanism was atypical AVNRT. There is slow–intermediate and slow–slow AVNRT, hence ablation of the slow pathway was performed; no tachycardia was observed after this. The VA time at initiation of even typical AVNRT often shortens over the initial few complexes, more so in older patients; hence an apparently atypical AVNRT may later appear typical (Fig. 51.4).
Case Discussion With application of three atrial extrastimuli, tachycardia is induced. Induction is preceded by lengthening of the AH interval; this suggests that the likely mechanism is AVNRT.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_51, © Springer-Verlag London Limited 2011
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Case 52 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 79-year-old male with a history of hypertension, diabetes, coronary artery bypass grafting, recently diagnosed with atrial flutter and referred for electrophysiology study and catheter ablation. Initial 12-lead electrocardiogram (Fig. 52.1) showed organized atrial activity with a cycle length of
approximately 220 ms with negative F waves in leads II, III, and aVF, positive F waves in V1, suggesting typical counterclockwise atrial flutter. Conduction to ventricles was predominantly 4:1. Electroanatomic mapping suggested macroreentrant arrhythmia in the right atrium. As seen in Fig. 52.2, the direction of activation was counterclockwise, and the circuit
Fig. 52.1 Surface electrocardiogram of clinical tachycardia. Atrial flutter is seen, with F waves that are predominantly negative in the inferior leads and upright in V1, consistent with typical counterclockwise atrial flutter
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_52, © Springer-Verlag London Limited 2011
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Fig. 52.2 Three-dimensional electroanatomic mapping during tachycardia. Anteroposterior view of right atrium shows the reentrant circuit, with early meeting late activation in a circuit around the tricuspid annulus. Pacing from the tip of the ablation catheter, which was positioned at the cavotricuspid isthmus, showed entrainment with concealed fusion and a postpacing interval of 10 ms longer than tachycardia cycle length
involved the cavotricuspid isthmus. What maneuvers are useful in proving that the cavotricuspid isthmus is part of the tachycardia?
Case Discussion One maneuver that can show whether a given location is close to the arrhythmia circuit is entrainment mapping.1 This is accomplished by pacing slightly faster than the tachycardia cycle length to repeatedly reset the reentrant circuit. If paced P wave morphology is identical to that observed during atrial flutter, this is termed entrainment with concealed fusion. If tachycardia continues after cessation of pacing, the first postpacing interval will be close to the tachycardia cycle length, provided that the pacing site is near the reentrant circuit.2 Postpacing interval is defined as the time from last paced stimulus to the next local electrogram during tachycardia, measured at the site of pacing.
In this case, pacing from the cavotricuspid isthmus showed entrainment with concealed fusion, with identical surface flutter wave morphology and intracardiac activation pattern as compared to tachycardia. The postpacing interval was within 10 ms of the flutter cycle length. This showed that the cavotricuspid isthmus was likely part of the tachycardia circuit, and therefore radiofrequency ablation of the isthmus was performed. The ablation catheter was advanced into the right ventricle, curved, and pulled inferiorly to seat it on the cavotricuspid isthmus, with the catheter tip at 6 o’clock in the left anterior oblique view. A series of radiofrequency applications were delivered to create a line of conduction block across the cavotricuspid isthmus. During ablation, the cycle length suddenly prolonged and the arrhythmia terminated with a long pause (Fig. 52.3). Normal sinus node function and atrioventricular conduction resumed after a few seconds, and atrial flutter was no longer inducible at the end of the ablation procedure.
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Fig. 52.3 Three-dimensional electroanatomic mapping during radiofrequency ablation, caudal left anterior oblique view. As the line of conduction block across the cavotricuspid isthmus was completed, the flutter terminated spontaneously and could not be reinduced
References 1. Cosio FG, Lopez Gil M, Arribas F, Palacios J, Goicolea A, Nunez A. Mechanisms of entrainment of human common flutter studied with multiple endocardial recordings. Circulation. 1994;89:2117-2125.
2. 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;88:1647-1670.
Case 53 Bradley P. Knight
Case Summary A patient is scheduled to undergo a catheter ablation procedure for recurrent PSVT, which appears most likely to be typical AV nodal reentry. You discover that the patient underwent insertion of an inferior vena cava filter 2 years ago after a pulmonary embolism. How would you proceed with this case?
Case Discussion When performing a slow pathway ablation procedure, it is important to monitor VA conduction during the accelerated junctional rhythm to avoid AV block. Therefore, it is usually necessary to place two catheters in the heart during the procedure. Unfortunately, some patients represent vascular access challenges. In this case, the patient has a filter in the
inferior vena cava. Although there are some risks associated with crossing the filter with a catheter, it is clear that an electrophysiology procedure can be performed safely in these patients from the femoral vein.1 It is helpful to be certain that the vena cava is patent before the procedure with a CT scan or venography. But assuming that the IVC is patent, long guiding sheaths and electrophysiology catheters can be passed safely through the filter. Figure 53.1 shows a long sheath already through the filter, and a second one being advanced over a guidewire that has been passed through the filter. There are times, however, when the vena cava is completely obstructed. In this situation, options include a superior or transhepatic central venous approach. One reasonable approach that has been shown to be successful in patients with AV nodal reentry is to place two central venous sheaths in the right internal jugular vein.2 This allows placement of a diagnostic catheter in the high right atrium and an ablation catheter along the tricuspid annulus (Fig. 53.2).
B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_53, © Springer-Verlag London Limited 2011
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Fig. 53.1 Fluoroscopic image during catheter placement from a femoral vein approach through an inferior vena cava filter. Two sheaths were advanced over a guidewire to access the heart with two electrophysiology catheters. See text for details
References 1. Sinha SK, Harnick D, Gomes JA, Mehta D. Electrophysiologic interventions in patients with inferior vena cava filters: safety and efficacy of the transfemoral approach. Heart Rhythm. 2005;2:15-18.
B.P. Knight
Fig. 53.2 Right anterior oblique fluoroscopic view after placement of an ablation catheter and diagnostic quadrapolar catheter via the internal jugular vein, during a catheter ablation procedure for typical atrioventricular nodal reentry in a patient without inferior vena cava access 2. Salem Y, Burke MC, Morady F, Knight BP. Slow pathway ablation for atrioventricular nodal reentry using a right internal jugular vein approach: a case series. Pacing Card Electrophysiol. 2006; 29:59-62.
Case 54 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary An 18-year-old young man with normal heart presents to the EP lab. His initial tracing shows AF followed by an SVT (Fig. 54.1). Figures 54.2 and 54.3 show the response to ventricular premature beats and ventricular pacing. Does this help elucidate the cause of the tachycardia?
Case Discussion Even a very early PVC from the right ventricle does not advance the “A.” This makes AVRT extremely unlikely because (1) left-sided AP is ruled out by the activation
sequence and (2) a right-sided AP should have caused atrial preexcitation. This PVC does not rule out AVNRT because to do so, the PVC must be delivered when the His is refractory. Thus, the differential diagnoses at this point include AVNRT and atrial tachycardia. Ventricular pacing is performed during tachycardia. VA dissociation is seen with continuation of tachycardia, proving a diagnosis of atrial tachycardia. The tachycardia itself does not lend itself to analysis of the P waves. The tachycardia continues in spite of bursts of PVCs, suggesting that this is atrial tachycardia. P wave morphology is revealed after the bursts; upright in I, II, III and aVF, suggesting high right atrial origin (Fig. 54.4)
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910, USA e-mail:
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Fig. 54.1 The left half shows AF which initiates a narrow complex SVT. AF termination is followed by a junctional beat and then, SVT. SVT starts with an “A”
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Fig. 54.4 P wave morphology can often be uncovered after ventricular pacing
Case 55 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar
Case Summary A 52-year-old male with history of hypertension, diabetes, and coronary artery disease status post coronary artery bypass grafting was recently seen for palpitations and dyspnea. Surface
electrocardiogram showed a regular supraventricular tachycardia at a rate of approximately 250 per minute, with 2:1 conduction to the ventricles (Fig. 55.1). He was referred for electrophysiology study and catheter ablation. Based on this ECG tracing, what is the most likely mechanism of this tachycardia?
Fig. 55.1 Surface electrocardiogram of the clinical tachycardia. Sawtooth flutter waves are predominantly negative in the inferior leads, upright in V1, and inverted in V6
E. Buch (*), S. Nakahara, M. Vaseghi, N.G. Boyle, and K. Shivkumar UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, A2-237 CHS, Los Angeles, CA 90095-1679 e-mail:
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Fig. 55.2 (a) Fluoroscopic left anterior oblique view showing catheter positions. The duodecapolar (DD) catheter is curled in the right atrium such that the proximal, mid, and distal bipoles of the catheter are near the right atrial roof, anterolateral wall, and coronary sinus os, respectively. Arrows show the direction of activation. (b) Intracardiac tracings.
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Right atrial activation is seen to proceed from septal to lateral along the superior right atrium, down the anterolateral wall to the cavotricuspid isthmus area, then up the atrial septum to complete the circuit. As seen in the CS catheter, bystander left atrial activation occurs simultaneously with right atrial septal activation
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Case Discussion Diagnostic electrophysiology catheters were placed at the right atrium, the His bundle, the right ventricular septum, and in the coronary sinus. A multipolar deflectable catheter was curled in the right atrium with its distal bipoles near the mouth of the coronary sinus, and the proximal bipoles near the roof of the right atrium (Fig. 55.2a). Intracardiac recordings from these catheters show that right atrial activation proceeds in a counterclockwise direction in the left anterior oblique view, from proximal to distal bipole on the duodecapolar catheter (Fig. 55.2b). An ablation catheter was advanced into the right ventricle, pulled back slowly to seat the tip on the cavotricuspid isthmus. Beginning at the edge of the tricuspid annulus, where the ventricular electrogram from the distal bipole of the ablation catheter was larger than the atrial electrogram, a line of
References 1. Disertori M, Inama G, Vergara G, Guarnerio M, Del Favero A, Furlanello F. Evidence of a reentry circuit in the common type of atrial flutter in man. Circulation. 1983;67:434-440. 2. Cabrera JA, Sanchez-Quintana D, Ho SY, Medina A, Anderson RH. The architecture of the atrial musculature between the orifice of the inferior caval vein and the tricuspid valve: the
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ablation was created across the isthmus, connecting the tricuspid annulus to the inferior vena cava. In the right anterior oblique projection, the ablation catheter was seen to be well separated from the His bundle catheter. In the left anterior oblique projection, the ablation catheter was near the 6 o’clock position. During ablation, the flutter terminated. After ablation, bidirectional conduction block across the isthmus was verified by pacing from either side of the isthmus. The common form of atrial flutter is a macroreentrant right atrial arrhythmia with a counterclockwise pattern of activation as seen from the left anterior oblique view.1 Critical to perpetuation of the arrhythmia is a narrow area of slow conduction bounded by the inferior vena cava and tricuspid valve, called the cavotricuspid isthmus.2 Surgical or catheterbased ablation of the isthmus can result in conduction block and effective treatment of this arrhythmia.3,4
anatomy of the isthmus. J Cardiovasc Electrophysiol. 1998;9: 1186-1195. 3. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol. 1986;57:587-591. 4. Feld GK, Fleck RP, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation. 1992;86:1233-1240.
Case 56 Bradley P. Knight
Case Summary A regular supraventricular tachycardia with a 1:1 AV relationship and a CL of 420 ms is induced in the EP lab. Activation of the high right atrium is coincident with the
QRS complex. Ventricular overdrive pacing is delivered from the right ventricular apex during tachycardia at a cycle length 30 ms less than the tachycardia CL. Figure 56.1 shows the response immediately upon cessation of ventricular pacing. What is the mechanism of tachycardia?
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Fig. 56.1 This tracing was recorded when ventricular overdrive pacing was stopped after being delivered during a regular supraventricular tachycardia with 1:1 atrioventricular conduction. Shown are surface recordings from leads I, II, V1, and V5, and the intracardiac recordings from high right atrium (HRA), His-bundle electrogram region (HBE), and right ventricular apex (RVA). Note the response after pacing can be described as a VAV response. See text for further description
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B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611, USA e-mail:
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Case Discussion During a regular supraventricular tachycardia with a 1:1 AV relationship, the differential diagnosis includes AV nodal reentry (AVNRT), orthodromic AV reentry (ORT), and atrial tachycardia (AT). The ventricular overdrive pacing can be used in the EP laboratory to help “rule in” or “rule out” atrial tachycardia as the mechanism.1,2 The principle involved is that when ventricular pacing during tachycardia often results in 1:1 retrograde conduction, the atrial rate accelerates to the ventricular pacing rate until ventricular pacing is stopped. In the case of an AT, the last atrial depolarization that is a result of retrograde VA conduction will block antegrade, because the AV node will be refractory in the antegrade direction after recent retrograde activation. After resumption of the AT, the first atrial depolarization will conduct to the ventricle. After ventricular pacing is stopped, the sequence of activation can be described as atrial–atrial–ventricular (VAAV; Figs. 56.1 and 56.2). In contrast, in the case of an AV nodal dependent tachycardia, such as AVNRT or ORT, ventricular pacing with 1:1 VA conduction entrains the tachycardia which, if it does not terminate, will conduct anterograde over the AV node as soon as the tachycardia resumes. After entraining an AV nodal dependent tachycardia, the sequence A
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Fig. 56.2 Ladder diagram showing the response to overdrive ventricular pacing during an atrial tachycardia. The response after pacing is a VAAV response. See text for more detail
B.P. Knight A
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Fig. 56.3 Ladder diagram showing the response to overdrive ventricular pacing during an atrial tachycardia. The response after pacing is a VAV response. This ladder diagram best describes the response seen in Fig. 56.1. See text for more detail
of activation can be described as atrial–ventricular (VAV; Fig. 56.3). When analyzing the response to ventricular pacing the following steps should be taken: 1. Confirm ventricular capture. 2. Confirm acceleration of atrial rate to pacing rate. 3. Identify last atrial depolarization arising from last ventricular paced beat. 4. Identify the next conducted ventricular beat. 5. Categorize the sequence as VAV or VAAV. In this case, the response immediately after ventricular pacing is VAV, which rules out AT. Because the short VA interval excludes ORT as a mechanism,2 the diagnosis must be AVNRT.
References 1. 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;33:775-781. 2. 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;36:574-582.
Case 57 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur
Case Summary A 23-year-old man with recurrent episodes of paroxysmal palpitations associated with near-syncope was referred for evaluation. Cardiac evaluation showed a normal heart.
Y.Y. Lokhandwala (*) KEM Hospital, Parel, Mumbai, India e-mail:
[email protected] A.K. Gupta Apollo Hospital, Ahmedabad, India e-mail:
[email protected] R.K. Thakur Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI 48910, USA e-mail:
[email protected]
Figure 57.1 shows the tachycardia induced during EP study. What is the interpretation?
Case Discussion The tachycardia is an orthodromic AVRT mediated by a right-sided accessory pathway because the tachycardia becomes faster with the disappearance of RBBB. This conclusion is based on the fact that if the bundle branch block is on the same side as the accessory pathway, then the tachycardia path is longer during bundle branch block, leading to a slower tachycardia rate during BBB and faster rate with its disappearance (Fig. 57.2). Parahisian pacing was also performed before and after successful ablation (Figs. 57.3 and 57.4).
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Fig. 57.4 Para-Hisian pacing after ablation. There was no VA conduction after ablation; with isoproterenol, VA conduction was seen and, therefore, para-Hisian pacing was performed. Second through sixth
complexes show His capture evidenced by narrower complexes. The VA time shortens with His bundle capture suggesting that the VA conduction is via the AV node
Case 58 Roopinder Sandhu, Dimpi Patel, William R. Lewis, and Andrea Natale
Case Presentation A 22-year-old male with no significant medical history presented with recurrent palpitations, dizziness, and chest discomfort. The patient reports having symptoms of shortness of breath and fatigue. He is currently not taking any medications. His 12-Lead ECG (Fig. 58.1) shows ventricular preexcitation. The baseline intracardiac electrograms prior to atrial pacing are shown in Fig. 58.2. The baseline intervals are: PR, 143; QRS, 104; HV, 27. Figures 58.3 and 58.4 show programmed atrial stimulation. The accessory pathway ERP is 330 ms. Figure 58.5 shows that atrial fibrillation was induced with atrial pacing. Figure 58.6 illustrates that the shortest preexcited RR interval is 298 ms or 201 BPM. These two electrograms suggest that the accessory pathway is not a high-risk pathway. Figure 58.7 shows that during ventricular pacing at 700 ms retrograde conduction is occurring over the AV node and not the accessory pathway. Figure 58.8 shows that VA block while pacing at 680 ms. Figure 58.9 reveals that a wide complex tachycardia was inducible. Figure 58.10 shows the 12-lead ECG of the wide QRS tachycardia. R. Sandhu (*) Department of Cardiology, University of Alberta, Walter Mackenzie Center, Suite 2C2, 8440 112 St, Edmonton, AB T6G 2B7, Canada e-mail:
[email protected] D. Patel St. David’s Texas Cardiac Arrhythmia Institute, 1015 E. 32nd St. #516, Austin, TX 78705, USA e-mail:
[email protected] W.R. Lewis Heart and Vascular Center, MetroHealth Medical Center, Case Western Reserve University, 2500 MetroHealth Drive, Suite H322, Cleveland, OH 44109, USA e-mail:
[email protected] A. Natale Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32nd Street, Suite 516, Austin, TX 78705 e-mail:
[email protected]
Figure 58.11 shows an atrial extrastimulus (pac) during tachycardia. What does the preceding pacing maneuver prove?
Case Discussion The differential diagnosis for patients with a preexcited tachycardia include: atrial arrhythmias, true antidromic AV reciprocating tachycardia, AV nodal reentry with a bystander pathway, or antidromic tachycardia using multiple pathways. The atrial extrastimulus at the time of the refractory His advances the ventricular activation which demonstrates the presence of an accessory pathway and its participation in the tachycardia circuit. The retrograde activation is concentric and a retrograde His prior to atrial activation is shown. The AV node is the likely retrograde conducting pathway. This is not consistent with an atrial tachycardia. We cannot exclude the presence of another pathway (ex concealed accessory pathway not participating in this reentry circuit or a slow conducting retrograde accessory pathway). The optimal ablation site is the region of earliest ventricular activation during maximal preexcitation. Presence of an accessory pathway potential can be guided by a unipolar recording. Figure 58.12 shows three sites that may eliminate the preexcitation. Site three is the most likely to eliminate preexcitation. Figure 58.13 shows application of RF at the preexcitation site and Fig. 58.14 shows that the PR, 176; QRS,100; HV, 50 after ablation. Figure 58.15 shows the post-ablation ECG. In summary, the criteria for diagnosing an antidromic AVRT includes that the QRS configuration during the tachycardia is identical to that obtained during maximal preexcitation; demonstrate the ventricles participate during the tachycardia (1:1 conduction, atrial premature depolarization advances the tachycardia with an identical morphology); the participation of the atria in the tachycardia; and to exclude atrial tachycardia, atrial flutter, or AVNRT using a bystander pathway.
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Fig 58.2 Baseline intervals: PR, 143; QRS, 104; HV, 27
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Fig. 58.3 Atrial extrastimuli
Fig. 58.4 AP ERP/AV ERP: ³600/330
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Fig. 58.6 Shortest preexcited RR
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Fig. 58.10 Antidromic AVRT
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Fig. 58.11 Atrial S2 advances tachycardia. CS distal pacing
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Fig. 58.14 Post-ablation intervals: Pr, 176msec; QRS 100 msec; HV 50 msec
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Fig. 58.15 Post-ablation ECG
Bibliography Yee R, Klein GJ, Sharma AD, et al. Tachycardia associated with accessory atrioventricular pathways. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology. Philadelphia, PA: WB Saunders; 1990:463.
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Case 59 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar
Case Summary
Case Discussion
During ventricular programmed stimulation, the following response was observed (note CS 1,2 is distal) (Fig. 59.1). What are the mechanisms of retrograde conduction seen in this tracing?
To recognize the direction of the atrial activation, it is essential to be acquainted with the normal atrial activation originating from the sinus node “high right atrium.” In this patient, the last atrial beat comes from the high right atrium “sinus node” (Fig. 59.2).
Fig. 59.1 ECG demonstrating the response of program stimulation from the right ventricle with one premature beat after pacing in a steady cycle for six beats. At the top is Lead V1 from surface ECG, followed by the intracardiac tracing. From top to bottom: tracing from the right atrial appendage “HRA,” then proximal coronary sinus to
d istal coronary sinus recording, followed by the His recording, and finally the recording from the right ventricular apex. HRA high right atrium; CS coronary sinus; HISp proximal His; HISm mid His; RVa right ventricular apex
M.E. Mortada (*), J.S. Sra , and M. Akhtar Department of Electrophysiology, Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke’s Medical Centers, University of Wisconsin School of Medicine and Public Health, 2801 W. Kinnickinnic River Parkway, #777, Milwaukee, WI 53215, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_59, © Springer-Verlag London Limited 2011
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Fig. 59.2 Response of program stimulation from the right ventricle with one premature beat after pacing in a steady cycle for 6 beats, with illustration of the activation sequence (arrows). At the top are three surface ECGs including lead I, II, and V1, followed by the intracardiac tracing. From top to bottom: tracing from the right atrial appendage “HRA,” then proximal coronary sinus to distal coronary sinus recording,
followed by the His recording, and finally the recording from the right ventricular apex. HRA high right atrium; CS coronary sinus; HISp proximal His; HISm mid His; HISd distal His; RVa right ventricular apex; H annotation of the His deflection; A annotation of the atrial deflection; V annotation of the ventricular deflection
The first atrial beat appears after a ventricular pacing rhythm, with earliest activity seen in the His, suggestive of retrograde activity over the atrioventricular node (AVN). However, the atrial activity in the second complex is clearly retrograde over the AVN, with earliest activation in the His, followed by the proximal coronary sinus, then the high right atrium. Therefore, the first atrial beat is a fusion beat between the sinus node (the activity in the high right atrium appears prior to the activity in the proximal coronary sinus) and the retrograde activation over the AVN (the activity in the His is earliest). The third atrial beat starts after premature ventricular extrastimuli. Conduction is seen from the distal to the proximal coronary sinus followed by the high right atrium and His, suggestive of retrograde activation over a left free-wall accessory pathway. The fourth atrial beat follows a left bundle QRS complex with the same VA duration and activation sequence as the third atrial complex; hence conduction is retrograde over the left free-wall accessory pathway. The fifth atrial beat has the same activation sequence as the previous two atrial complexes, but the VA duration is shorter. The rationale behind the difference in VA duration is
that the initial electrical activation for the third and fourth ventricular complexes is in the right ventricle apex, which is far from the left free-wall accessory pathway. On the other hand, the initial electrical activation of the fifth ventricular complex is over the normal conduction system to both ventricles simultaneously; thus the electrical activity reaches the accessory pathway rapidly and, subsequently, the VA duration becomes shorter. The origin of the first three ventricular complexes (left bundle branch block morphology) is right ventricular pacing. To understand the fourth ventricular complex, it is first necessary to evaluate the fifth ventricular complex. The fourth atrial complex, as explained previously, has been activated retrogradely through the left free-wall accessory pathway. After activating the atrium, it comes down through the AVN and His-Purkinje system to both ventricles. The AH duration is longer than the baseline sinus rhythm AH (compared to the sixth complex) due to the decremental property of the AVN node. The HV duration in this complex (the fifth complex) is the most accurate duration from the His to the earliest ventricular activation over the normal conduction system. The fourth ventricular complex has left bundle branch block morphology. It is preceded by a His deflection that
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comes prior to atrial activation. Therefore, this complex did not result from atrial activation. It is either a premature ventricular capture, or it is related to the previous ventricular activity (e.g. bundle branch reentry or repetitive ventricular response). The HV duration is slightly longer than the baseline HV duration when compared to the fifth complex, which is considered the most accurate HV duration over the normal conduction system, as previously mentioned. Hence, the source of this complex is probably bundle branch reentry.
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Finally, the sixth ventricular complex comes after a sinus beat, which conducts over the AV node, down to the HisPurkinje system, then to both ventricles. The possibility of a ventricular fusion beat occurring over the AV node and the left free-wall accessory pathway in the sixth ventricular complex is excluded due to the fact that the HV duration of this beat is the same as the duration of the most accurate HV duration over the AVN and His-Purkinje system (the fifth beat).
Case 60 Matthew D. Hutchinson
Case Summary A 41-year-old woman without structural heart disease presents with recurrent palpitations due to ventricular bigeminy. She had failed multiple antiarrhythmic medications, including amiodarone. She was referred to our institution for consideration of ablation. Her clinical PVC is shown in Fig. 60.1; the morphology is left bundle, inferior axis with a precordial transition at V3. Based upon the morphology of the PVCs in Fig. 60.1, what is the probable site of origin of the patient’s arrhythmia?
Case Discussion The patient presents with frequent PVCs of a left bundle, inferior axis morphology. When differentiating sites of origin for outflow tract tachycardias, it is most important to consider the precordial transition in light of the anatomical relationships between the RV and LV outflow tracts (RVOT, LVOT). The RVOT is positioned anterior to the LVOT relative to the chest wall; thus the precordial transition for RVOT sites tends to be later than LVOT sites (typically V4 or later).1 Early transitions at V1 or V2 suggest an origin more posterior than the RVOT, most commonly the aortic sinuses of Valsalva (ASOV) or the LVOT. Due to the higher prevalence of RV outflow tract tachycardias, the majority of left bundle inferior axis tachycardias with precordial transition at V3 will originate from the septal (posterior or anterior) aspect of the RV outflow tract. This is because the septal aspect is frequently crescent shaped and both extreme posterior and anterior aspects of the septal surface of the outflow region
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected]
may be recorded to the left of the midseptum. Approximately 20% of outflow tract tachycardias will originate from left sided structures such as: the ASOV, the LVOT, the coronary arterial or coronary venous musculature, or the epicardial surface. Pacemaps from the ASOV produce very different and characteristic morphologies. The non-coronary cusp sits adjacent to the inter-atrial septum, and a large atrial signal (and occasionally a His bundle defection) is recorded there. The right cusp is situated anterior and rightward to the left cusp, producing morphologies with later precordial transitions (usually at V2 or V3) and a larger R wave in lead I. Pacing more leftward within the right cusp as well as within the left cusp produces a progressively more rightward frontal plane axis, a more prominent rS complex in lead I, and an earlier precordial transition (at V1 or V2). Tachycardias originating from between the right and left cusps have a characteristic notching in the S wave in V1. The most characteristic feature of outflow-type tachycardias originating from epicardial structures is delayed initial activation in the precordial leads. Daniels and colleagues describe the maximum deflection index as the ratio of the longest time from QRS onset to maximal QRS deflection (either positive or negative) in any precordial lead to the total QRS duration.2 Ratios of ³0.55 were predictive of epicardial origin with high sensitivity and specificity. Bazan and colleagues further described the presence of Q wave in lead I and the absence of Q waves in the inferior leads as highly predictive of epicardial origin from the basal superior LV.3 Thus for our patient, the precordial transition at V3 presents a variety of possibilities for the site of origin.4 A combination of activation and pacemapping is utilized in these cases. Activation times were later than the onset of the QRS in the RVOT, and the pacemap was a poor match (Fig. 60.2). Detailed mapping of the ASOV was performed which revealed an excellent pacemap from the left cusp with an activation time 31 ms pre-QRS; however ablation at this site was unsuccessful (Fig. 60.2). We then performed mapping of the distal coronary sinus near the origin of the anterior interventricular vein (AIV); the activation time was also 31 ms pre-QRS, and the pacemap was a near perfect match
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Fig. 60.2 (a) Clinical PVC with activation time 31 ms pre-QRS as recorded from the left coronary cusp (LCC). (b) Clinical PVC with pacemaps obtained from the RV outflow tract (RVOT), the right and the left coronary cusps (RCC, LCC)
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(Fig. 60.3). Ablation in this location abolished the patient’s PVCs. In summary, the 12-lead ECG provides important information about the site of origin of outflow tract ventricular
ectopy. However, due to individual variability in the anatomical relationships between these complex structures, detailed activation and pacemapping are of critical importance when ablating outflow tract ectopy.
Case 60 Fig. 60.3 (a) Clinical PVC with activation time 31 ms pre-QRS as recorded from the proximal portion of the anterior interventricular vein (AIV). (b) Clinical PVC with pacemap obtained from the AIV. (c) Fluoroscopy obtained in the right and left anterior oblique projections demonstrating the proximity of two catheters placed in the LCC and proximal AIV
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References 1. Dixit S, Gerstenfeld EP, Callans DJ, Marchlinski FE. Electro cardiographic patterns of superior right ventricular outflow tract tachycardias: distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol. 2003;14(1):1-7. 2. Daniels DV, Lu YY, Morton JB, et al. Idiopathic epicardial left ventricular tachycardia originating remote from the sinus of Valsalva: electrophysiological characteristics, catheter ablation, and identification from the 12-lead electrocardiogram. Circulation. 2006; 113(13):1659-1666.
3. Bazan V, Gerstenfeld EP, Garcia FC, et al. Site-specific twelve-lead ECG features to identify an epicardial origin for left ventricular tachycardia in the absence of myocardial infarction. Heart Rhythm. 2007;4(11):1403-1410. 4. 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(3): 418-423.
Case 61 Ronald Lo, Henry H. Hsia, and Amin Al-Ahmad
Case Summary
Case Discussion
A 55-year-old woman with no significant past medical history has been complaining of palpitations for the past 3 years. These symptoms are associated with fatigue, activity intolerance, chest discomfort, and lightheadness. A Holter monitor was ordered which demonstrated greater than 20,000 PVCs per day. These accounted for approximately 25% of her daily heart beats. Her electrocardiogram is shown in Fig. 61.1. Her echocardiogram demonstrated an ejection fraction of approximately 45% with normal valves and cardiac chamber sizes. She was tried on beta blockers without any effect with respect to symptoms. Where is the origin of her premature ventricular contractions?
Analysis of the electrocardiogram demonstrates ventricular bigeminy with left bundle left inferior axis morphology PVCs. This suggested a possible right ventricular outflow tract origin of the PVCs; however, the early transition raises the possibility of a left ventricular outflow tract or aortic cusp site of origin. Initial mapping of the right ventricle and the right ventricular outflow tract did not locate any points of earliest activation that were earlier than ventricular activation. Mapping was then performed in the left ventricle and the aortic root along with the aortic cusps. Careful mapping using CARTO demonstrated a site between the left and right aortic cusps that was −22 ms presystolic to the earliest ventricular electrogram. The unipolar electrogram also demonstrated a QS signal as shown in Fig. 61.2. Pace mapping was also performed in the areas around the aortic cusps, with the best pace mapped site being in between the right and the left aortic cusps. Further analysis of the electrocardiogram demonstrated a qrS pattern in leads V1–V3, which appear to be due to a site of activation in between the right and left coronary cusps. The activation pattern is due to direction of the propagating wave from the right and left coronary cusps as a q wave in lead V1, and the anterior activation pattern from the RVOT to the aortic root as an r wave in V1. The remainder of the ventricular activation produced a large S wave resulting in the qrS pattern seen on the electrocardiogram. Catheter ablation in this region (Fig. 61.3) produced successful termination of the spontaneous PVCs and repeat Holter monitors afterward did not demonstrate any PVCs consistent with the ablated morphology.
R. Lo (*) Riverside Electrophysiology, 4000 14th Street, Suite 209, Riverside, CA 92501, USA e-mail:
[email protected] H.H. Hsia Department of Cardiovascular Medicine, Stanford University, 300 Pasteur Drive, H2146, Stanford, CA 94305, USA e-mail:
[email protected] A. Al-Ahmad School of Medicine, Stanford University, 300 Pasteur Drive, H-2146, Stanford, CA 94305, USA e-mail:
[email protected]
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Fig. 61.1 12-lead ECG with ventricular bigeminy with left bundle left inferior PVCs
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Bibliography Yamada T, Yoshida N, Murakami Y, et al. Electrocardiographic characteristics of ventricular arrhythmias originating from the junction of the left and right coronary sinuses of Valsalva in the aorta: the activation pattern as a rationale for the electrocardiographic characteristics. Heart Rhythm. 2008;5:184-192.
LAO
Fig. 61.3 Successful ablation site of premature ventricular contraction in between the left and right coronary cusp
Case 62 Richard H. Hongo and Andrea Natale
Case Summary The patient is a 57-year-old woman with newly diagnosed nonischemic dilated cardiomyopathy (LVEF 25–30%) and >11,000 uniform VPCs during a 24-h Holter monitor. She presented for electrophysiology study for ablation of the VPC focus (Fig. 62.1) and to assess for inducible sustained ventricular tachycardia. 3-D electroanatomic activation mapping was performed with a 4-mm Navistar RMT catheter utilizing the CARTO and Stereotaxis remote magnetic navigation systems. Earliest activation (0 ms presystolic) of the recurring VPCs within the right heart was localized to the anteroseptal RVOT, just below the pulmonary valve. Pacemapping was also performed and an 11/12-lead morphology match was achieved at the same site as the earliest activation. Ablation was performed at this site with the 4-mm RMT catheter with temperature and power limited to 52°C and 50 W, respectively. Despite multiple ablations (Fig. 62.2) achieving adequate temperature and power, there were no flurries of ventricular beats during ablations and the VPCs continued to recur. What is the most appropriate next step? Should this patient receive an ICD?
Case Discussion Prominent R waves in precordial leads V1 and V2 is most consistent with an LVOT VPC focus. Right heart electroanatomic mapping reveals earliest activation at the anteroseptal aspect of the RVOT just below the pulmonary valve. The earliest site, however, is on time with, but does not precede, the
R.H. Hongo Sutter Pacific Medical Foundation, California Pacific Medical Center, 2100 Webster Street, Suite 521, San Francisco, CA 94115, USA e-mail:
[email protected]
onset of the P wave. Pacemapping at this site is only an 11-out-of-12 leads match with the VPC morphology. Despite the less than ideal activation time and pacemapping match, attempting ablation with the 4-mm catheter is appropriate before proceeding with the higher risk left-sided mapping and ablation. Once, however, the lack of VPC flurries and the persistence of VPCs are apparent, further ablation with higher powered catheters is unlikely to be successful, and the next most appropriate step is to proceed with mapping of the LVOT; the LVOT is more approachable than the epicardium, and the VPC ECG morphology is more suggestive of an LVOT focus. Following transseptal puncture, 3-D activation mapping of the recurring VPCs was performed with remote magnetic navigation within the LVOT. A region of early activation was found just below the aortic valve, along the posteroseptal aspect of the LVOT, but was no earlier than the earliest site in the RVOT (0 ms presystolic). Within this region, however, there was a single site that demonstrated presystolic (−20 ms) activation (Fig. 62.3). The first ablation at this site resulted in a brief flurry of VPCs that was followed by complete cessation of VPCs (Fig. 62.4). Several ablations were performed adjacent to the first ablation, targeting fractioned electrogram signal. There were no recurrent VPCs observed overnight on telemetry monitoring, and the VPC focus has not recurred after 6 months. The LVEF has remained depressed (<30%), however, and she has undergone insertion of an implantable cardioverter-defibrillator for primary prevention of sudden cardiac arrest. Elimination of the VPC focus by ablation should precede insertion of an implantable cardioverter-defibrillator in this patient because there is a reasonable possibility that the newly diagnosed dilated cardiomyopathy is caused by the excessive burden of VPCs. Persistence of systolic dysfunction (LVEF of 35% or less) for over 3 months, however, prompted her to be reconsidered for implantable cardioverter-defibrillator therapy.
A. Natale (*) Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, 1015 East 32rd Street, Suite 516, Austin, TX 78705, USA e-mail:
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Fig. 62.1 12 lead ECG showing morphology of VPC
Fig. 62.2 CARTO map showing ablation lesions in the RVOT
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Case 62 Fig. 62.3 Site of earliest activation in the LVOT
Fig. 62.4 CARTO map showing site of successful ablation
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Case 63 David J. Callans
Case Summary A 46-year-old woman with a history of renal failure status post failed transplant received an ICD after an episode of ventricular fibrillation (VF). Evaluation at that time revealed normal LV function and no coronary artery disease. She was well for 6 months, but then presented with syncope and ICD shocks. Interrogation of the ICD showed 60 episodes detected in the VF zone over the previous 4 days, most of them nonsustained, but four resulting in shock delivery. Telemetry monitoring showed frequent episodes of nonsustained polymorphic VT. She was transferred to our hospital for further evaluation. 12-lead ECG monitoring at this hospital showed frequent PVCs with several different right bundle, left superior axis morphologies which frequently started episodes of
nonsustained and sustained polymorphic VT (Fig. 63.1). What is the best strategy for ablation in this patient?
Case Discussion In the electrophysiology laboratory, she had multiple morphologies of both left and right bundle PVCs, all of which were preceded by an apparent Purkinje potential (Fig. 63.2). Catheter ablation was targeted at elimination of Purkinje potentials in the area around earliest onset of PVCs. Afterward, no further spontaneous PVCs were noted despite isoproterenol infusion (Fig. 63.3). The patient has been well, without recurrent syncope or ICD shocks over 6 months follow-up.
D.J. Callans (*) Department of Cardiology, University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_63, © Springer-Verlag London Limited 2011
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Fig. 63.1 Frequent PVCs, with slightly different right bundle, left superior axis morphologies, often causing runs of nonsustained and sustained polymorphic ventricular tachycardia
Case 63 Fig. 63.2 Left and right bundle PVCs with intracardiac recordings from a mapping catheter (Carto P, Carto D), and RV apical catheter. Note that PVCs were preceded by a sharp potential, presumably from the Purkinje system
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Fig. 63.3 Left ventricular voltage mapping in the RAO and LAO projections. The voltage maps are essentially normal. Although some abnormalities are suggested at the junction of the inferior wall and the septum,
the electrograms recorded in this region were normal in morphology. Red dots represent individual ablation lesions which were targeted by finding Purkinje-like potentials in sinus rhythm and before PVCs
Case 64 J. David Burkhardt, Dimpi Patel, and Andrea Natale
Case Summary A 48-year-old Hispanic male presents with a history of dyspnea on exertion that has been present for two months. He has been evaluated by an internist who discovered on monitoring that the patient had frequent PVCs and runs of monomorphic ventricular tachycardia. He had an echocardiogram that revealed an EF of 25% without segmental wall motion abnormality. A nuclear stress test revealed no scar or ischemia. A 24-h Holter monitor revealed frequent runs of ventricular tachycardia at a rate of 150 BPM up to 12 beats and 45,000 PVCs. All of the PVCs and VT are of the same morphology. An EKG is included below (Fig. 64.1). Laboratory tests including TSH were unremarkable. He denies syncope or recent illness.
What is the diagnosis? Where is the origin of the VPC? What is the best strategy for management of this patient?
Case Discussion The case is consistent with a PVC-induced cardiomyopathy. The high frequency of PVCs is the likely culprit behind the symptoms and left ventricular dysfunction. The location appears to be LVOT and specifically aortic cusp. The features include high amplitude R waves in II, III, and aVf, as well as the early transition and notched upstroke of the R wave in lead V6. With a normal stress test and typical location of “normal heart” PVCs further evaluation is not necessary. The LV
J.D. Burkhardt (*) and A. Natale Texas Cardiac Arrhythmia Institute, 1015 E. 32nd Street, Suite 505, Austin, TX 78705 e-mail:
[email protected];
[email protected] D. Patel St. David’s Texas Cardiac Arrhythmia Institute, 1015 E. 32nd St. #516, Austin, TX 78705 e-mail:
[email protected]
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dysfunction and congestive heart failure symptoms will likely resolve with elimination of the PVC. An ICD is not indicated since this is likely a reversible condition. The patient was tried on a medication; however there was no decrease in the number of VPCs. Ablation is the next reasonable step to give the patient the best chance of full
25mm/s 10mm/mV 150Hz 005E 12SL 250 CID:19
Fig. 64.1 12-lead ECG showing the VPC
Fig. 64.2 Intracardiac echo helps with the anatomy of the aortic valve region
J.D. Burkhardt et al.
recovery. ICE may be a useful aide in this endeavor (Fig. 64.2). It is difficult to appreciate the anatomy of the aortic valve using flouroscopy or electroanatomic mapping alone. Pacemapping at the aortic cusp revealed a perfect pacemap (Fig. 64.3). This location was targeted for ablation and was successful in eliminating the VPC.
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Case 65 Matthew D. Hutchinson
Case Presentation A 36-year-old woman was referred to our institution for repetitive, polymorphic ventricular tachycardia and ventricular fibrillation (PMVT, VF). A comprehensive cardiovascular evaluation revealed normal left ventricular structure and function. The baseline QT interval was normal and there was no family history of sudden cardiac death. She had an ICD placed due to recurrent presyncope with these episodes. Intracardiac electrograms and telemetric monitoring revealed recurrent PMVT episodes which were initiated with shortcoupled PVCs of uniform morphology. She had failed multiple antiarrhythmic agents, as well as a previous ablation attempt. The 12-lead morphology of her initiating PVC is given in Fig. 65.1. What are the common sites of origin for idiopathic PVCs initiating PMVT/VF? What is the likely site of origin for the patient’s inciting PVC, and what strategy is most effective in mapping such PVCs?
Case Discussion This case highlights the uncommon clinical entity of idiopathic PMVT/VF. These patients have normal corrected QT intervals and lack the characteristic findings of catecholaminergic polymorphic ventricular tachycardia on exercise testing. The largest experience of 27 patients by Haissaguerre
and colleagues found that the inciting PVC originated either in the right ventricular outflow tract (15%) or the Purkinje network (85%).1 Those beats originating in the LV Purkinje network were characterized by a relatively narrow QRS duration (115 ± 11 ms) compared to those from the RV (143 ± 10 ms). This patient’s PVC morphology is narrow (ms) and has a right bundle superior axis which is consistent with an origin from the left ventricular Purkinje network. In the aforementioned Haissaguerre series, the earliest Purkinje deflections for LV ectopy preceded the local ventricular activation by an average of 46 ± 29 ms (range 10–150 ms).The most common ablation strategy is to identify the earliest presystolic Purkinje activity; this is most easily accomplished via electroanatomical mapping of the Purkinje pre-potentials. Figure 65.2 demonstrates mapping along the LV septum in our patient. Note the dramatic prematurity seen in the conducted ectopic beats. Also shown in Fig. 65.2 is a more premature Purkinje depolarization which is not conducted to the local myocardium. Figure 65.3 depicts an episode of NSVT with early Purkinje pre-potentials driving the tachycardia. Ablation at this site abolished the clinical PVC; however a second PVC morphology was then seen. This PVC was mapped more apically and was noted to have extremely early Purkinje activation in this region (Fig. 65.4). Ablation at this site abolished the patient’s PVCs. The majority of these patients have an excellent long-term result after ablation, and 89% of patients in the Haissaguerre group were arrhythmia free off of antiarrhythmic drugs at a mean follow-up of 2 years.
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_65, © Springer-Verlag London Limited 2011
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288 Fig. 65.1 The patient’s dominant clinical PVC is shown in a trigeminal pattern in sinus rhythm. The ventricular ectopy is narrow, and has a right bundle superior axis
M.D. Hutchinson I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Fig. 65.2 Intracardiac recordings obtained during LV activation mapping of the clinical PVC. Bipolar recordings are shown from the His bundle position (His 1–5) and LV septum (LV 1–5). There are sharp early potentials (asterisks) on the ablation catheter poles (Abl) recorded after the first sinus beat which represent Purkinje potentials which do not activate the LV myocardium. After the second sinus beat, there are later-coupled Purkinje potentials which do conduct to the myocardium and produce the clinical PVC
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Fig. 65.3 (a) 12-lead ECG demonstrating a typical episode of NSVT initiated by the clinical PVC. (b) Intracardiac recordings from the episode of NSVT pictured in panel A. Note the premature Purkinje potentials (asterisks) preceding both the clinical PVC and each beat of nonsustained VT
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 LV5 LV4 LV3 LV2 LV1 Abld Ablp His5 His4 His3 His2 His1 RVa
Fig. 65.4 Intracardiac recordings of a second PVC which was seen after ablation of the clinical PVC. Note the dramatically premature Purkinje potentials noted on the ablation catheter (asterisks). This PVC was targeted at the anteroapical LV
Reference 1. Haissaguerre M, Shoda M, Jais P, et al. Mapping and ablation of idiopathic ventricular fibrillation. Circulation. 2002;106(8): 962-967.
Case 66 Matthew D. Hutchinson
Case Presentation A 73-year-old man with a longstanding nonischemic cardiomyopathy and an implantable defibrillator placed for secondary prevention of sudden death was referred for increasingly frequent ICD shocks due to rapid VT. Interrogation of his ICD revealed three distinct intracardiac morphologies. He was referred for EP study and voltage mapping, at which time he had a single VT morphology reproducibly induced with programmed stimulation (Fig. 66.1). The intracardiac electrograms of this induced tachycardia matched one of the patient’s dominant clinical arrhythmias. Biventricular voltage maps were normal with the exception of a small area of attenuated electrograms at
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the lateral mitral annulus (Fig. 66.2). Endocardial pacemaps for the clinical VT were poor and activation times late during VT; thus no ablation was performed. The patient was taken back to the EP lab on a later date for an epicardial approach. Percutaneous epicardial access was obtained using the Sosa technique. Epicardial bipolar voltage mapping was performed which revealed a large, confluent area of low voltage along the lateral LV extending from the mitral annulus to the mid-cavity (Fig. 66.3). Despite aggressive programmed stimulation with up to triple extrastimuli and isoproterenol infusion, only polymorphic VT was inducible. What features of the clinical tachycardia suggest an epicardial site of origin? Based upon the information available, describe the most effective ablation strategy for this patient.
200 ms
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Fig. 66.1 (a) Sinus rhythm QRS morphology. (b) Clinical VT morphology
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected]
Case Discussion There are several ECG criteria for predicting LV epicardial VT origin in patients with nonischemic dilated cardiomyopathy. Based upon the ECG morphology of the VT in Fig. 66.1, one would expect a mid-inferolateral exit site. Bazan and colleagues prospectively examined several criteria to differentiate basal and apical inferior epicardial tachycardias, and found the following to have significant predictive value: the presence of Q waves in the inferior leads; a pseudodelta wave ³34 ms (measured from onset of QRS to earliest rapid deflection in precordial leads); and the shortest precordial RS complex ³121 ms (measured from onset of precordial QRS to earliest nadir of S wave). All of the above criteria are met for our patient’s tachycardia (Fig. 66.4). The most effective method of localizing the site for VT ablation is entrainment mapping; however this is not possible in many patients due either to arrhythmia noninducibility or to hemodynamic compromise during VT. In this case in which no VT is inducible, an alternate strategy utilizing substrate-based ablation is necessary. The technique of substrate-based ablation was previously described by Marchlinski
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Fig. 66.2 Bipolar LV and RV endocardial voltage maps in LAO (left) and PA (right) projections. There is a limited region of low voltage present at the basal anterolateral LV
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and colleagues, and requires a detailed knowledge of the patient’s substrate.1 High-density voltage mapping to define the area of bipolar voltage attenuation is performed; bipolar signals <1.5 mV on the endocardium and <1.0 mV on the epicardium are characterized as abnormal. Sites with abnormal electrogram characteristics including fractionated, late, and split potentials are given anatomical tags; these areas represent regions of surviving myocardium within the scar which exhibit abnormal conduction properties and may participate in tachycardia circuits. When information regarding the patient’s spontaneous or induced arrhythmias is available, the approximate exit sites for these tachycardias are localized by pacing at the border zone of the bipolar voltage abnormality. Linear lesions sets are designed incorporating the individual VT exit sites identified by pacemapping and extending through the border zone into the dense scar
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Fig. 66.4 (a) The sinus rhythm QRS complex with arrows indicating the absence of Q waves in the inferior leads. (b) The patient’s VT morphology demonstrates prominent QS waves in the inferior leads. The pseudodelta wave measured in the precordial leads is 52 ms; the shortest RS complex (measured in V4) is 164 ms. These features suggest an epicardial VT exit site. See text for discussion
(defined by a bipolar voltage <0.5 mV). Whenever possible, targeting areas of markedly abnormal (late and split) electrograms is also performed. In this case, we have detailed information about the patient’s substrate from electroanatomical mapping. The gray dots in Fig. 66.3 represent abnormal bipolar electrograms within the low voltage region. We also have a 12-lead morphology of one of the patient’s clinical arrhythmias which was induced during the initial EP study. Pacemapping of this VT morphology was performed, with the best match from the inferior scar border (Fig. 66.5). Linear lesions were applied extending from the region of the best pacemap for the clinical VT into the dense scar. Additional linear lesions were given to transect regions
Case 66 Fig. 66.5 Comparison of the best pacemap morphology to the clinical VT. The pacing site is indicated by the star on the electroanatomical map
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Fig. 66.6 (a) Lesion set design which incorporates an initial linear lesion (yellow dashed line) through the VT exit region localized by pacemapping and extending into dense scar. The other linear lesions (white dashed lines) transect regions with abnormal electrogram characteristics. (b) Final electroanatomical map with ablation lesions represented as red tags
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with abnormal electrograms as shown in Fig. 66.6. The usual procedural endpoint of arrhythmia noninducibility is not applicable in this case; however when properly executed, substrate-based ablation strategies are as effective as entrainment-based strategies in achieving long-term arrhythmia suppression.
Reference 1. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000;101(11):1288-1296.
Case 67 Matthew D. Hutchinson
Case Presentation A 39-year-old man with familial hypercholesterolemia, prior coronary endarterectomy, mechanical aortic valve replacement, and mitral valve annuloplasty presented with symptomatic recurrent monomorphic ventricular tachycardia (MMVT). His sinus rhythm ECG indicated prior inferior infarction; his left ventricular ejection fraction was 50% with mild concentric hypertrophy. He was noted to have frequent monomorphic PVCs (right bundle, left superior axis) which appeared to initiate the episodes of MMVT (Fig. 67.1). He was then brought to the EP lab for mapping and ablation. The left ventricle was accessed by transseptal approach due to the mechanical aortic prosthesis. His bipolar voltage map revealed patchy endocardial low voltage regions involving the basal and mid inferior walls. The clinical VT (right bundle, left superior axis morphology; CL 280 ms) was reliably initiated by a distinct unifocal PVC (Fig. 67.2). The blood pressure was marginal during VT, and the patient was quite symptomatic. Based on the ECG morphologies, where are the sites of origin/exit for both the PVC and the sustained VT? What would be your ablation strategy for this VT; how can the frequent PVCs be incorporated into this strategy?
Case Discussion This patient likely has an ischemic substrate for ventricular tachycardia based on the history of premature coronary artery disease, ECG evidence of prior inferior infarction, and evidence of patchy endocardial scar by voltage mapping in the typical inferior regional distribution. Importantly, there may
be more endocardial scar than seen here with the typical CARTO color settings used (<1.5 mV), as underlying myocardial hypertrophy with larger baseline local potentials can mask superficial scar. Adjustment of the color range may be necessary at times to highlight endocardial scar in the setting of ventricular hypertrophy. Figures 67.1 and 67.2 demonstrate frequent monomorphic PVCs which appear to originate from the mid inferior wall (apical-septal aspect of this area) based on the ECG. Interestingly, the clinical VT which is initiated by this PVC has an overall similar morphology, but exits more basally (later precordial transition) and slightly further from the septum (wider QRS). The close relationship between single PVCs and reentrant VT arising from the area of scar in ischemic substrate has been described by Bogun and colleagues.1 When the PVC is frequent, it can serve as a target for mapping and ablating a potentially arrhythmogenic area of the ischemic scar, especially if the clinical VT is not sustained or tolerated to allow for more detailed entrainment mapping. In this case we performed activation and pacemapping of the PVC, leading us to focus on the area just basal and septal to the posteromedial papillary muscle. While mapping here, the clinical VT was initiated by a catheter-induced PVC, and large mid-diastolic potentials were seen at this site. Entrainment was quickly performed while the VT was still tolerated, and the response suggested that this was an isthmus site. RF delivered here terminated the VT. After termination, we performed pacemapping from the distal and proximal bipoles of the ablation catheter (spacing configuration 2 mm–5 mm–2 mm). Interestingly, pacing at threshold from the more apical bipole produced a pace match for the spontaneous PVC (Fig. 67.3), and pacing at threshold from the more basal bipole produced an excellent pacemap match for the clinical VT (Fig. 67.4). Several additional lesions in this area significantly raised the pacing threshold, eradicated the PVCs, and rendered the VT noninducible.
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_67, © Springer-Verlag London Limited 2011
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296 Fig. 67.1 12-lead surface ECG obtained at rest outside of the electrophysiology lab. Note baseline right bundle-branch block as well as Q waves in the inferior leads (arrows). There are frequent spontaneous monomorphic PVCs (stars), the last one initiating a run of monomorphic ventricular tachycardia
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Fig. 67.2 12-lead surface ECG obtained in the electrophysiology lab at start of the ablation procedure. Again the sinus beat is followed by the same PVC (star) which initiates the patient’s clinical VT
V3 V4 V5 V6
Case 67 Fig. 67.3 Bipolar voltage map of the left ventricle (inferior view; purple color denotes voltage > 1.5 mV, red color denotes voltage < 0.5 mV) with site (star) of threshold pacemap compared with spontaneous PVC
297 PVC
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<0.5 mV Base
Fig. 67.4 Bipolar voltage map of the left ventricle (inferior view; purple color denotes voltage > 1.5 mV, red color denotes voltage < 0.5 mV) with site (star) of threshold pacemap compared with clinical VT
Reference 1. Bogun F, Crawford T, Chalfoun N, et al. Relationship of frequent postinfarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia. Heart Rhythm. 2008; 5(3):367-374.
Apex
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Case 68 Matthew D. Hutchinson
Case Presentation A 54-year-old man with CAD and previous inferior infarction and prophylactic single chamber ICD implantation was referred for recurrent, symptomatic monomorphic ventricular tachycardia and ICD shocks despite amiodarone. He was also noted to have frequent, monomorphic PVCs with an intracardiac morphology matching his clinical tachycardia. He subsequently underwent an electrophysiology study during which the clinical VT was induced and characterized with activation mapping. Activation times for the clinical PVCs of up to 30 ms pre-QRS were recorded from the right ventricular outflow tract; however ablation in this area was acutely unsuccessful. The patient was subsequently referred to our institution for a repeat ablation procedure. The patient’s admission ECG is shown in Fig. 68.1. Based upon the morphology of the PVCs on the presenting ECG (Fig. 68.1), what is the differential diagnosis for the site of origin of the patient’s arrhythmia? What are important laboratory considerations when mapping tachycardias of this type?
Case Discussion The patient presents with frequent PVCs of a left bundle, inferior axis morphology. This combination of features most commonly represents a right ventricular outflow tract origin. As discussed previously, however, when the ectopy transition is at V3 it is important to left-sided sites of origin (the aortic sinuses of valsalva, the left ventricular outflow tract, the coronary arterial or venous musculature, or the epicardial surface).
Interestingly, the patient’s PVC recorded in the EP lab demonstrated a different precordial morphology with an earlier transition at V2 (Fig. 68.2). The difference in morphology is due to erroneous placement of the precordial leads in Fig. 68.1. Leads V1 and V2 should be placed at the fourth intercostal space along the sternal borders. In this case, the lead positioning for V1 and V2 in Fig. 68.1 was most likely at the third interspace (note the similarity between leads V3 on the initial ECG and V2 on the adjacent laboratory recording). It is critically important to check the lead placement whenever using the ECG to predict tachycardia site of origin. In this case, the large R wave in lead V2 and biphasic complex in lead I suggest a more posterior site of origin from the aortic sinuses of valsalva. During the procedure, the patient had very infrequent PVCs and was noninducible for VT with programmed stimulation. The administration of sedative medications can have important implications for arrhythmia inducibility. Moreover the administration of local anesthetic agents subcutaneously can result in measurable serum concentrations which can further suppress arrhythmias. On review it was noted that the patient had been administered intravenous benzodiazepines for sedation prior to sheath insertion. After administration of isoproterenol 0.5 mcg/min, the patient had ventricular bigeminy. Activation times of 37 ms pre-QRS were recorded in the RV outflow tract; however the pacemap did not match the spontaneous PVC (Fig. 68.3). The aortic sinuses were then mapped via a retrograde approach. The earliest activation was 45 ms pre-QRS at the junction between the right and left coronary sinuses; pacemapping this region replicated perfectly the clinical PVC morphology (Fig. 68.4). Ablation at this site abolished the patient’s ectopy.
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_68, © Springer-Verlag London Limited 2011
299
300
M.D. Hutchinson
Fig. 68.1 The presenting 12-lead ECG demonstrates frequent left bundle, right inferior axis ventricular ectopy
a
b I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Fig. 68.2 (a) The same ECG from Fig. 68.1 is reproduced; the black arrow indicates a large R wave in lead V3. (b) The 12-lead ECG taken in the EP lab for the same patient shows an earlier precordial transition
at V2 (arrow). This most likely represents erroneous placement of leads V1 and V2 in the third intercostal space
Case 68 Fig. 68.3 (a) Comparison of the clinical PVC morphology to the best pacemap obtained from the RV outflow tract. Although the frontal plane axis matches the clinical ectopy well, the precordial transition is much later from the RVOT. (b) The earliest activation time for the clinical PVC from the RVOT is 37 ms pre-QRS
301
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Fig. 68.4 (a) Comparison of the clinical PVC morphology to the best overall pacemap obtained from the junction of the right and left coronary cusps. (b) The earliest overall activation time for the clinical PVC obtained from the junction of the right and left coronary cusps with a sharp pre-potential 45 ms pre-QRS
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Case 69 Matthew D. Hutchinson
Case Summary A 57-year-old man with history of isolated septal myocardial infarction had a CRT-D device implanted several years ago for ventricular tachycardia and congestive heart failure. He presented now with repeated ICD shocks despite treatment with amiodarone. Interrogation of the ICD demonstrated two predominant VT morphologies with similar cycle lengths (520–550 ms). The patient was brought to the electrophysiology lab for mapping and ablation. Voltage mapping demonstrated a moderately large area of basal septal scar, and programmed stimulation with single extrastimuli induced two VT morphologies (Figs. 69.1 and 69.2) which matched with the ICD electrograms of the patient’s spontaneous tachycardias. Based on the ECG morphologies, where are the likely sites of origin/exit for each VT? How might these VTs be associated with the scar, and what would be your ablation strategy?
Case Discussion Despite the atypical scar location, this patient has an ischemic substrate due to known occlusion of a large septal perforator. The first VT (Fig. 69.1) has a left bundle, inferior axis morphology with a precordial transition at V3 suggesting exit from the mid superior septum. The second VT (Fig. 69.2) has a right bundle, left superior morphology with
precordial transition at V4 suggesting an exit from the mid inferior wall adjacent to the septum. Given that the VT circuits in ischemic patients are often large, multiple different VT morphologies may share components of the tachycardia circuit. The similar tachycardia cycle lengths also suggest a similar topography for the two VT morphologies. Localizing these VT exit sites on this patient’s voltage map indicates that they likely originate from opposite sides of the septal scar. In this case, detailed mapping of the septal scar during VT 2 revealed several sites with mid-diastolic potentials (Fig. 69.3) which were demonstrated by entrainment to be isthmus sites. RF lesions at these sites terminated VT 2. Upon repeat programmed stimulation, neither VT 2 nor VT 1 could be re-induced. Thus it appeared that the two VTs shared a common critical isthmus for reentry, with wavefronts travelling in opposing directions and exiting on opposing sides of the scar. It is important to remember that scar-related VT can take long and circuitous routes, especially if there are extensive areas of scarring. As is seen in this case, the VT cycle length can be extremely long on antiarrhythmic drug therapy, even when the scar is not extensive. Thus in patients with extensive scar, two or more VTs of potentially widely disparate morphologies are the rule. However, as in this case, some of the VTs may simply travel in opposing directions through a common isthmus, and ablation of this common isthmus would abolish the pathway for multiple reentry circuits. Certainly this is good reason not to be discouraged when multiple VTs are induced at the start of the procedure.
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_69, © Springer-Verlag London Limited 2011
303
304 Fig. 69.1 12-lead surface ECG of the first ventricular tachycardia (VT) morphology induced during ablation procedure. The tachycardia cycle length as denoted is 550 ms
M.D. Hutchinson 200 ms I II III aVR aVL aVF V1
550 ms
V2 V3 V4 V5 V6
200 ms I II III aVR aVL aVF V1 V2 V3 V4
Fig. 69.2 12-lead surface ECG of the second VT morphology induced. The tachycardia cycle length as denoted is 526 ms
V5 V6
526 ms
Case 69 Fig. 69.3 Bipolar voltage map of the left ventricle illustrating the site (white star) of middiastolic potentials during VT 2 (Abl recording from ablation catheter, d distal bipole, p proximal bipole). The large white arrows represent the approximate exit sites for the two VT morphologies induced
305 I II III
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aVR aVL aVF V1 V2 V3 V4 V5 V6
>1.5 mV VT2
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200 ms
Case 70 Matthew D. Hutchinson
Case Presentation A 71-year-old man with history of distant inferior myocardial infarction with subsequent coronary artery bypass graft surgery and St. Jude mechanical mitral valve prosthesis initially presented with symptomatic ventricular tachycardia which was treated with amiodarone and implantation of an ICD. Now, several years later, he presented with ICD shocks for recurrent sustained monomorphic VT despite continued amiodarone therapy. He was referred for mapping and ablation of VT. His bipolar voltage mapping revealed an extensive scar involving the basal inferior and lateral LV. The clinical VT (right bundle, right inferior axis; CL 510 ms) was easily induced with programmed stimulation and was well-tolerated hemodynamically allowing detailed entrainment mapping. Several sites with mid-diastolic potentials during VT were found in the basal inferolateral wall; Figs. 70.1 and 70.2 demonstrate responses to attempted entrainment from two of these sites. Describe the response to entrainment shown in Figs. 70.1 and 70.2. Should either site be considered a good target for ablation of the clinical VT?
Case Discussion Figure 70.1 demonstrates the entrainment response at the end of pacing at a site of mid-diastolic potentials. There is relatively long stimulus-QRS (S-QRS) interval during
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected]
pacing with concealed entrainment – suggesting that the paced beats are exiting the scar in the same fashion as the VT. However, the local return cycle length is significantly longer than the tachycardia cycle length (Fig. 70.3). This entrainment response suggests that the sharp potential on the ablation catheter does not directly participate in perpetuating the VT; it is being activated passively as the wavefront travels through the scar, thus producing mid-diastolic potentials unrelated to the critical circuit. Ablation at this location would be unlikely to disrupt the reentrant wavefront. Figure 70.2 is obtained at another site of mid-diastolic potentials. In this case, an early-coupled extrastimulus terminates the tachycardia without activating the left ventricular myocardium. The response to this so-called non-propagated extrastimulus suggests that the pacing stimulus is delivered within the protected isthmus of the reentrant circuit, thereby extinguishing the reentrant wavefront in both an orthodromic (encountering tissue still refractory after the previous reentrant beat) and an antidromic (colliding with the subsequent reentry wavefront as it travels into the isthmus) manner. Interrupting the reentrant circuit with this extrastimulus also implies that the critical isthmus traversing the pacing electrode is relatively narrow, thus susceptible to disruption. It is also noted that the subsequent pacing stimulus reproduces the clinical VT morphology perfectly, and activates the myocardium with a long stimulus-QRS interval. This suggests that the pacing stimulus is delivered proximally within the reentrant circuit and without antidromic capture. In this case, VT was repeatedly reinduced with programmed stimulation and terminated with nonpropagated extrastimuli. VT was subsequently terminated and rendered noninducible after a single RF lesion in this location. In summary, locating early diastolic activity during VT identifies regions of viable myocardium within the scar; however these potentials may or may not participate in the tachycardia circuit. The accurate interpretation of the entrainment response can easily differentiate the critical tachycardia isthmus from a passively-activated bystander loop.
A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_70, © Springer-Verlag London Limited 2011
307
308 Fig. 70.1 12-lead surface ECG and intracardiac recordings of the response to entrainment at a site of mid-diastolic potentials during ventricular tachycardia. See text for discussion. Abl ablation catheter electrogram, d distal bipole, p proximal bipole, RVa electrogram recording from the right ventricular apex
M.D. Hutchinson 200 ms I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Abld Ablp RVa
400 ms I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Fig. 70.2 ECG and intracardiac recordings from another site of mid-diastolic potentials during ventricular tachycardia
Abld Ablp RVa
Case 70 Fig. 70.3 Same snapshot as Fig. 70.1, with measured time intervals as denoted (ms)
309 200 ms I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Abld Ablp RVa
551
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Case 71 Matthew D. Hutchinson
Case Summary A 69-year-old man with ischemic cardiomyopathy and remote anterior infarction presented to the Emergency Department with palpitations. He was noted on ECG to have monomorphic ventricular tachycardia (left bundle, left superior axis; CL 420 ms). He was treated with intravenous amiodarone and lidocaine; however he had recurrent arrhythmias which uniformly responded to anti-tachycardia pacing. An example of the 12-lead rhythm strip and intracardiac recordings obtained during the pace termination of an episode of VT is included in Fig. 71.1. Coronary angiography revealed no significant disease progression since his last evaluation. He was referred for EP study and ablation.
In the EP lab, bipolar voltage mapping revealed a large area of low voltage involving the distal anterior wall and LV apex. The patient’s clinical VT was easily inducible (CL 410 ms) with single extrastimuli. As the VT was well-tolerated hemodynamically, detailed activation and entrainment mapping was performed. Figures 71.2 and 71.3 depict the response to entrainment at the sites indicated in the electroanatomical map. What information about the VT circuit is gained by examination of the 12-lead and intracardiac recordings in Fig. 71.1? Describe the response to entrainment in Figs. 71.2 and 71.3. Ablation at which of these sites would be expected to abolish the tachycardia? If neither, where would one expect
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Fig. 71.1 Panel A 12-lead ECG illustrating overdrive pacing during VT from the ICD lead. Panel B Intracardiac recording simultaneous with ECG in panel A. See text for discussion. VEGM local bipolar ventricular electrogram
V3 V4 V5 V6
M.D. Hutchinson Cardiovascular Division, Department of Medicine, University of Pennsylvania, 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_71, © Springer-Verlag London Limited 2011
311
312 Fig. 71.2 Panel A Electroanato mical map with large area of low voltage involving LV anterior wall and apex. Panel B Overdrive pacing during VT performed at the site indicated with star in panel A
M.D. Hutchinson 200 ms
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Fig. 71.3 Panel A Electroanato mical map as described in Fig. 71.2. Panel B Overdrive pac ing during VT performed at the site indicated with star in panel A
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to find the most appropriate ablation site based upon the information presented?
Case Discussion This case illustrates a common presentation of stable, MMVT occurring after healed anterior myocardial infarction. Figure 71.4 demonstrates the response to overdrive pacing from
the ICD lead (the local bipolar electrogram [B, bottom panel] and the marker channel [A, top channel] are shown). Importantly, examination of the morphology and post-pacing interval (PPI) on the local bipolar electrogram reveals intracardiac fusion and a postpacing interval (PPI) <30 ms of the tachycardia cycle length (TCL). This suggests that the RV lead pacing site represents an outer loop of the tachycardia circuit. Examination of the 12-lead ECG obtained during ATP confirms these findings. These findings can be particularly helpful when the 12-lead morphology of the clinical VT is not available.
Case 71 Fig. 71.4 Panel A 12-lead ECG from Fig. 71.1 with QRS fusion during pacing and a postpacing interval within 30 ms of the tachycardia cycle length (TCL). Thus, pacing from the RV apex is an outer loop site for the clinical VT. Panel B Intracardiac recording confirming the observations in panel A. VEGM local bipolar ventricular electrogram
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Fig. 71.5 Panel A Electroanato mical map as described in Fig. 71.2. Panel B Overdrive pacing during VT performed at the site indicated with star in panel A. This represents an entrance site for the clinical VT. See text for discussion
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Pacing within a protected part of the VT circuit produces a paced morphology identical to the spontaneous VT morphology. The degree of prematurity of the bipolar electrogram (EGM) recorded within the protected circuit relative to the onset of the surface QRS complex correlates to the degree of proximity within the circuit.1–3 Figure 71.2 demonstrates concealed entrainment with a PPI-TCL < 30 ms. The stimulus-QRS (S-QRS) interval equals the electrogram-QRS (EGM-QRS) interval and is quite long (300 ms, 73% TCL; Fig. 71.5). This
represents an entrance site for the VT which is oriented at the lateral border of the low voltage region. Figure 71.3 also shows concealed entrainment with a PPI-TCL < 30 ms. Here the stimulus-QRS interval (equal to the EGM-QRS) is 30 ms (8% TCL; Fig. 71.6); this represents an exit site which is located at the septal side of the low voltage region. Focal ablation of VT can be performed by careful mapping and targeting of the critical tachycardia isthmus. The broad nature and potential redundancy of entrance and exit
314 Fig. 71.6 Panel A Electroanato mical map as described in Fig. 71.2. Panel B Overdrive pacing during VT performed at the site indicated with star in panel A. This represents an exit site for the clinical VT. See text for discussion
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Fig. 71.7 Panel A Electroanatomical map as described in Fig. 71.2. Panel B Overdrive pacing during VT performed at the site indicated with star in panel A. This represents an isthmus site for the clinical VT. See <0.5 mV text for discussion
sites for a given tachycardia limits the efficacy of focal ablation at these sites. Detailed mapping and targeting of the critical isthmus is more effective in eliminating the tachycardia with focal ablation. In this case, mapping earlier diastolic activity within the dense scar more proximal to the exit site identified an isthmus site (StimulusQRS = EGM-QRS = 173 ms; 42% TCL; Fig. 71.7). Ablation at this isthmus site terminated the tachycardia and rendered it noninducible. In summary, a combination of detailed activation and entrainment mapping remains the most efficient method of ablating tolerated VT.
V6 Abld Ablp
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173 414
References 1. Josephson ME. Clinical Cardiac Electrophysiology: Techniques and Interpretations, vol. 3. 3rd ed. Philadelphia, PA: Lippincott, Williams, & Wilkins; 2002. 2. Almendral JM, Gottlieb CD, Rosenthal ME, et al. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. Circulation. 1988;77(3):569-580. 3. 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(4 Pt 1):1647-1670.
Section Devices
II
Case 72 Amin Al-Ahmad and Paul J. Wang
Case Summary
Case Discussion
A 19-year-old woman with a history of cardiac transplantation 5 years prior is admitted with acute rejection. She has a dual chamber PPM, Medtronic Kappa 401. Telemetry strip revealed pacemaker artifact after the QRS. A 12-lead ECG is shown in Fig. 72.1. Her pacemaker settings are as follows:
This ECG shows normal sinus rhythm with low voltage and poor R wave progression, in addition to a rightward axis. There are pacemaker artifacts after each QRS. This indicates clear undersensing on the ventricular channel. In this tracing, the pacemaker detects the intrinsic atrial activation and because of ventricular undersensing delivers a pacemaker stimulus after the AV delay interval ends. Could this pacing artifact be an atrial stimulus? With ventricular undersensing the pacemaker may deliver an atrial stimulus, but would follow this with a ventricular stimulus. As there is only one stimulus regularly seen in this ECG, the pacemaker is adequately sensing the intrinsic atrial activation and tracking appropriately.
Mode
DDD
LRL/URL
50/150 bpm
Sensing, ventricular channel
2.8 mV
AV delay
Is the pacemaker function appropriate? Should any programming changes be made in this case?
A. Al-Ahmad and P.J. Wang (*) School of Medicine, Stanford University, 300 Pasteur Drive, H-2146, Stanford, CA 94305, USA e-mail:
[email protected] A. Natale et al. (eds.), Cardiac Electrophysiology, DOI: 10.1007/978-1-84996-390-9_72, © Springer-Verlag London Limited 2011
317
318
Fig. 72.1 12-lead ECG showing pacing artifact
A. Al-Ahmad and P.J. Wang
Case 73 Amin Al-Ahmad and Paul J. Wang
Case Summary A 32-year-old woman with a history of corrected transposition of the great vessels and a pacemaker placed for sinus node dysfunction is seen for a routine pacemaker check. She has a Medtronic Kappa Model KDR401/403. Atrial sensing was 2.0 mV, the threshold was 0.5 V @ 0.25 ms. Ventricular sensing was 4 mV and the threshold was 1.5 V @ 0.6 ms. Lead impedance on both leads was stable. Device settings are as follows:
