Josephson Clinical Cardiac Electrophysiology

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David J. Callans, MD Professor of Medicine Perelman School of Medicine at the University of Pennsylvania Associate Director of Electrophysiology University of Pennsylvania Health System Philadelphia, Pennsylvania CASE STUDIES CONTRIBUTOR Ramanan Kumareswaran, MD Assistant Professor of Clinical Medicine Department of Cardiac Electrophysiology The Hospital of the University of Pennsylvania Philadelphia, Pennsylvania

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6th edition © 2021 Wolters Kluwer; 5th edition © 2016 Wolters Kluwer; 4th edition © 2008 by Lippincott Williams & Wilkins; 3rd edition © 2002 by Lippincott Williams & Wilkins; 2nd edition © 1993 by Lea & Febiger. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permis sion, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at permissions@lww.com, or via our website at shop.lww.com (products and services). 9 8 7 6 5 4 3 2 1 Printed in the United States of America

Library of Congress Cataloging-in-Publication Data ISBN-13: 978-1-975201-16-6 ISBN-10: 1-975201-16-7 Library of Congress Control Number: 2023912836

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This book is dedicated to my beloved Melissa. Even though she knew what was going to happen because of the last edition, she again stood by me through all the work and the doubt. Her love and support and her belief in me have been so strong. There is no way that I could have done this without her. It might seem proper to dedicate this book to Mark Josephson, but it is and will always be Mark’s book and not mine. He ignited the spark that became my love for electrophysiology and he is one of the best friends I have ever had. I must also recognize Mark’s colleagues, friends, fellows—Mark’s army—following his example to fight for all that is right and good with this noble field. —D.C.

Historical Perspectives

FOREWORD

The study of the heart as an electrical organ has fascinated physiologists and physicians for over 150 years. Matteucci 1 studied electrical current in pigeon hearts, and Kölliker and Müller 2 studied discrete electrical activity in association with each cardiac contraction in the frog. Study of the human elec trocardiogram awaited the discoveries of Waller 3 and, most importantly, Einthoven, 4 whose use and development of the string galvanometer permitted the standardization and wide spread use of that instrument. Almost simultaneously, anato mists and pathologists were tracing the atrioventricular (A-V) conduction system. Many of the pathways, both normal and abnormal, still bear the names of the men who described them. This group of men included His, 5 who discovered the muscle bundle joining the atrial and ventricular septae that is known as the common A-V bundle or the bundle of His. During the first half of the 20th century, clinical electro cardiography gained widespread acceptance, and in feats of deductive reasoning, numerous electrocardiographers con tributed to the understanding of how the cardiac impulse in humans is generated and conducted. Those researchers were, however, limited to observation of atrial (P wave) and ventricular (QRS complex) depolarizations and their relation ships to one another made at a relatively slow recording speed (25 mm/sec) during spontaneous rhythms. Nevertheless, com bining those carefully made observations of the anatomists and the concepts developed in the physiology laboratory, these researchers accurately described, or at least hypothesized, many of the important concepts of modern electrophysiology. These included such concepts as slow conduction, concealed conduction, A-V block, and the general area of arrhythmo genesis, including abnormal impulse formation and reentry. Some of this history was reviewed by Langendorf. 6 Even the mechanism of preexcitation and circus movement tachycar dia were accurately described and diagrammed by Wolferth and Wood from the University of Pennsylvania in 1933. 7 The diagrams in that manuscript are as accurate today as they were hypothetical in 1933. Much of what has followed the innova tive work of investigators in the first half of the century has confirmed the brilliance of their investigations. In the 1940s and 1950s, when cardiac catheterization was emerging, it became increasingly apparent that luminal cath eters could be placed intravascularly by a variety of routes and safely passed to almost any region of the heart, where they could remain for a substantial period of time. Alanis et al 8 recorded the His bundle potential in an isolated perfused ani mal heart, and Kottmeier et al 9 recorded the His bundle poten tial in humans during open heart surgery. Giraud et al 10 were the first to record electrical activity from the His bundle by a catheter; however, it was the report of Scherlag et al, 11 detail

ing the electrode catheter techniques in dogs and humans, to reproducibly record His bundle electrogram, which paved the way for the extraordinary investigations that led to modern cardiac electrophysiology. At about the same time Durrer et al in Amsterdam and Coumel and his associates in Paris independently devel oped the technique of programmed electrical stimulation of the heart in 1967. 12,13 This began the first decade of clinical cardiac electrophysiology. Although the early years of intra cardiac recording in humans were dominated by descriptive work exploring the presence and timing of His bundle activa tion (and that of a few other intracardiac sites) in a variety of spontaneously occurring physiologic and pathologic states, a quantum leap occurred when the technique of programmed stimulation was combined with intracardiac recordings by Wellens. 14 Use of these techniques furthered our understand ing of the functional component of the A-V specialized con ducting system, including the refractory periods of the atrium, A-V node, His bundle, Purkinje system, and ventricles, which enabled us to assess the effects of pharmacologic agents on these parameters, to induce and terminate a variety of tachyarrhythmias, and, in a major way, led to a greater under standing of the electrophysiology of the human heart. Shortly thereafter, enthusiasm and inquisitiveness led to placement of an increasing number of catheters for recording and stimu lation to different locations with the heart, first in the atria and thereafter in the ventricle. This led to the development of endocardial catheter mapping techniques to define the loca tion of bypass tracts and the mechanisms of supraventricular tachyarrhythmias. 15,16 Beginning in the mid-1970s, Josephson and his colleagues at the University of Pennsylvania were the first to use vigor ous, systematic, multisite programmed stimulation in the study of sustained ventricular tachycardia (VT) resulting from myocardial infarction. 17-19 Subsequent investigators sought to establish a better understanding of the methodology used in the electrophysiology study to induce arrhythmias. Several studies validated the sensitivity and specificity of programmed stimulation for induction of uniform tachycardias, and the nonspecificity of polymorphic arrhythmias induced with vig orous programmed stimulation was recognized. 19,20 In the same time period, Josephson et al 21-23 developed the technique of endocardial catheter mapping of VT, which for the first time demonstrated the safety and significance of plac ing catheters in the left ventricle. This led to the recognition of the subendocardial origin of the majority of ventricular tachyarrhythmias associated with coronary artery disease and the development of subendocardial resection as a therapeutic cure for this arrhythmia. 24

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Foreword: Historical Perspectives

For the next decade, electrophysiologic (EP) studies increased our understanding of the mechanisms of human arrhythmias by comparing the response to programmed stimulation in the response to in vitro and in vivo stud ies of abnormal automaticity, triggered activity caused by delayed and early afterdepolarizations, and anatomical functional reentry. These studies, which used programmed stimulation, endocardial catheter mapping, and response of tachycardias to stimulation and drugs, have all suggested that most sustained paroxysmal tachycardias were due to reentry. The reentrant substrate could be functional or fixed or combinations of both. In particular, entrainment and resetting during atrial flutter and VT were important techniques used to confirm the reentrant nature of these arrhythmias. 25-30 Resetting and entrainment with fusion became phenomena that were diagnostic of reentrant exci tation. Cassidy et al, 31 using left ventricular endocardial mapping during sinus rhythm, for the first time described an EP correlate of the pathophysiologic substrate of VT in coronary artery disease—a low-amplitude fragmented elec trogram of long duration and late potentials. 31,32 Fenoglio, Wit, Josephson, and their colleagues from the University of Pennsylvania documented for the first time that these arrhythmogenic areas were associated with viable muscle fibers separated by and imbedded in scar tissue from the infarction. 33 They demonstrated that the quality and quan tity of abnormal electrograms (and, hence, the pathophysi ologic substrate) differed for sustained monomorphic VT, nonsustained VT, and ventricular fibrillation in patients with prior infarction and cardiomyopathy. Experimental studies by Gardner et al 34 demonstrated that these fraction ated electrograms resulted from poorly coupled fibers that were viable and maintained normal action potential charac teristics but that exhibited salutatory conduction caused by nonuniform anisotropy. Further exploration of contributing factors (triggers), such as the influence of the autonomic nervous system or ischemia, will be necessary to enhance our understanding of arrhythmogenesis. This initial decade or so of clinical electrophysiology could be likened to an era of discovery. Subsequently, and overlapping somewhat with the era of discovery, was the development of the concept and use of programmed stimulation as a tool for developing therapy for arrhythmias. The ability to reproducibly initiate and terminate arrhythmias led to the development of serial drug testing to assess antiarrhythmic efficacy. 35 The ability of an antiarrhyth mic drug to prevent initiation of a tachycardia that we reliably initiated in the control state appeared to predict freedom from the arrhythmia in the 2- to 3-year follow-up. This was seen in many nonrandomized clinical trials from laboratories in the early 1980s. The persistent inducibility of an arrhythmia universally predicted an outcome that was worse than that in patients in whom tachycardias were made noninducible. The natural his tory of recurrences of ventricular tachyarrhythmias (or other arrhythmias for that matter) and the changing substrate for arrhythmias were recognized as potential limitations of drug

testing. It was recognized very early that programmed stimu lation was not useful in selecting drugs to treat ventricular tachyarrhythmias in patients with structural heart disease other than healed infarction. 36 Despite the fact that all studies showed that patients with spontaneous VT whose arrhyth mias were rendered noninducible by antiarrhythmic agents were far better than patients with persistently inducible arrhythmias, the inability to accurately predict freedom from recurrence led to abandonment of programmed stimulation as a modality to select antiarrhythmic agents. The ESVEM study, 37 although plagued by limitations in protocol and patient selection, put the nail in the coffin for programmed stimulation as a method of selecting antiarrhythmic therapy of arrhythmias. With the known limitation of EP-guided therapy to pre dict outcomes uniformly and correctly, as well as the poten tially lethal proarrhythmic effect of antiarrhythmic agents demonstrated in the CAST study, 38 the desire for nonphar macologic approaches to therapy grew. Surgery had already become a gold standard therapy for Wolff-Parkinson-White syndrome, and innovative surgical procedures for VT had grown from our understanding of the pathophysiologic sub strate of VT and coronary disease and the mapping of VT from the Pennsylvania group. However, surgery was consid ered a rather drastic procedure for patients with a relatively benign disorder (supraventricular tachycardia and the Wolff Parkinson-White syndrome) and, although successful for VT for coronary artery disease, was associated with a high opera tive mortality. These limitations have led to two major areas of nonpharmacologic therapy that have dominated our field to this day: implantable antitachycardia/defibrillator devices and catheter ablation. These techniques were the natural evolution of our knowledge of arrhythmia mechanisms (eg, the ability to initiate and terminate the reentrant arrhythmias by pacing and electrical conversion) and the refinement of catheter map ping techniques. It was Mirowski who initially demonstrated that an implantable defibrillator could convert VT or ventricular fibrillation to sinus rhythm regardless of underlying patho physiologic substrate and prevent sudden cardiac death. 39 The initial devices that were implanted epicardially via tho racotomy have been replaced by small devices with venous leads that are implanted subcutaneously similar to a pace maker. Current devices may have single chamber, dual cham ber, and biventricular pacing capability. The antitachycardia pacing modalities that evolved from clinical EP studies are widely employed and effective in terminating monomorphic gradient from VT, particularly those with slow rates. With several major trials showing a statistical benefit of implant able cardioverter defibrillators in reducing sudden death, there has been a widespread, logarithmic increase in the use of the device. The development and the use of catheterization tech niques to manage cardiac arrhythmias have been transfor mative. The concept of using a catheter to deliver energy as a therapeutic modality came from Dr Melvin Scheinman 40 who was the first to ablate the A-V junction via a catheter

Foreword: Historical Perspectives

to control the ventricular rate in atrial fibrillation. At pres ent, focal ablation is the treatment of choice for all supraven tricular tachyarrhythmias, including A-V nodal reentry, cir cus movement tachycardias using concealed or manifested accessory pathways, incessant automatic atrial tachycardia, isthmus-dependent atrial flutter as well as other macroreen trant atrial tachycardias, and VT in both normal hearts and those associated with prior infarction. 41-55 Most exciting has been the development strategies for ablation of atrial fibril lation. While the initial studies suggested that isolating the pulmonary veins to prevent the pulmonary vein foci from initiating and maintaining atrial fibrillation 56-59 has been used successfully in paroxysmal atrial fibrillation, how best to treat persistent and chronic atrial fibrillation still remains unclear. We still do not understand the basic mechanisms of maintenance of atrial fibrillation, so it is not surprising that we don’t know how to “fix” it. Technology has grown much faster than our physiologic understanding of the atrial fibril lation disease process. One major concept I believe is critical is that we need to understand the mechanism of arrhythmias before we try to “cure” them with ablation. This was easily done for supraventricular arrhythmias. The ability to accurately define reentrant circuits causing VT and even the under lying mechanism of atrial fibrillation needs further work. Although much has been accomplished, substantial work still remains. We must not let technology lead the way. Elec trophysiologists must maintain interest in understanding the mechanisms of arrhythmias so that nonpharmacologic or even pharmacologic approaches that would be more effec tive and safe to manage these arrhythmias can be devised. New molecular approaches may be forthcoming in the near future. The world of molecular biology has seen the recog nition of ion channelopathies such as long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, and catecholaminergic polymorphic VT. Early understanding of these disorders has led to ablative therapy, particularly in Brugada syndrome, and the reintroduction of old-fashioned drugs like quinidine and programmed stimulation to treat the short QT syndrome, Brugada syndrome, and idiopathic ventricular fibrillation. 60-62 Cardiovascular genomics will play an important role in risk stratification of arrhythmias in the future and new fields of proteomics and metabolomics will be essential if we are to develop specifically targeted molecules to treat arrhythmias. The past 50 years have seen a rapid evolution of electro physiology, from one of understanding the simple mechanisms to one of developing therapeutic interventions. The future will require us to go back to the past and continue to understand more complex underlying mechanisms so that our therapeu tic modalities will be more successful and safer. Unfortunately, this quest will occur in an era of increasing clinical demands and decreasing funding for clinical investigation. Nonethe less, the increase in knowledge injected by population science, molecular biology, advanced imaging techniques, and neuro science will continue to inform clinical electrophysiology in new and exciting ways.

■ REFERENCES 1. Matteucci C. Sur le courant électrique de la grenouille: second mémoire sur l’electricité animale, fasout suite à celui sur to torpille. Ann Chim Phys . 1842;6:301. 2. Kölliker A, Müller H. Nachweis der negativen Schuankung des Muskelstroms am náturlich sich contrahirenden Muskel. Verh Phys Med Ges . 1858;6:528-533. 3. Waller AD. A demonstration on man of electromotive changes accompa nying the heart’s beat. J Physiol . 1887;8:229-234. 4. Einthoven W. Un noveau galvanométre. Arch n se ex not . 1901;6:625-633. 5. His W. Die Thštigkeit des embryonalen Herzens and deren Bedeu-tung fÿr de Lehre yon der Herzbewegung helm Erwachsenen. Arb Med Kiln (Leipzig) . 1893;14. 6. Langendorf R. How everything started in clinical electrophysiology. In: Brugada P, Wellens HJJ, eds. Cardiac Arrhythmias: Where Do We Go From Here? Futura Publishing Company; 1987:715-722. 7. Wolferth CC, Wood FC. The mechanism of production of short PR inter vals and prolonged QRS complexes in patients with presumably undam aged hearts: hypothesis of an accessory pathway of auriculo-ventricular conduction (bundle of Kent). Am Heart J . 1933;8:297-311. 8. Alanis J, Gonzales H, Lopez E. Electrical activity of the bundle of His. J Physiol . 1958;142:127-140. 9. Kottmeier PK, Fishbone H, Stuckey JH, et al. Electrode identification of the conducting system during open-heart surgery. Surg Forum . 1959;9:202-204. 10. Giraud G, Puech P, Letour H, et al. Variations de potentiel ližes a l’activitž du system de conduction auriculoventriculaire chez l’homme (enregis trement electrocardiographique endocavitaire). Arch Mat . 1960;53: 757-776. 11. Scherlag BJ, Lau SH, Helfant RA, et al. Catheter technique for recording His bundle stimulation and recording in the intact dog. J Appl Physiol . 1968;25:425-428. 12. Durrer D, Schoo L, Schuilenburg RM, et al. The role of premature beats in the initiation and termination of supraventricular tachycardias in the WPW syndrome. Circulation . 1967;36:644-662. 13. Coumel P, Cabrol C, Fabiato A, et al. Tachycardiamente par rythme ržciproque. Arch Mat Coeur . 1967;60:1830-1864. 14. Wellens HJJ. Electrical Stimulation of the Heart in the Study and Treatment of Tachycardias . Stenfert Kroese; 1971. 15. Josephson ME, Scharf L, Kastor JA, et al. Atrial endocardial activation in man. Electrode catheter techniques for endocardial mapping. Am J Cardiol . 1977;39:972-981. 16. Josephson ME. Paroxysmal supraventricular tachycardia: an electro physiologic approach. Am J Cardiol . 1978;41:1123-1126. 17. Josephson ME, Horowitz LN, Farshidi A, et al. Recurrent sustained ven tricular tachycardia. 1. Mechanisms. Circulation . 1978;57:431-440. 18. Michelson EL, Spielman SR, Greenspan AM, et al. Electrophysiologic study of the left ventricle—indications and safety. Chest . 1979;75:592-596. 19. VandePol CJ, Farshidi A, Spielman SR, et al. Incidence and clinical sig nificance of tachycardia. Am J Cardiol . 1980;45:725-731. 20. Brugada P, Greene M, Abdollah H, et al. Significance of ventricular arrhythmias initiated by programmed ventricular stimulation: the importance of the type of ventricular arrhythmia induced and the num ber of premature stimuli required. Circulation . 1984;69:87-92. 21. Josephson ME, Horowitz LN, Farshidi A, et al. Recurrent sustained ven tricular tachycardia. 2. Endocardial mapping. Circulation . 1978;57: 440-447. 22. Josephson ME, Horowitz LN, Farshidi A, et al. Recurrent sustained ven tricular tachycardia. 4. Pleomorphism. Circulation . 1979;59:459-468. 23. Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity: a mechanism of recurrent ventricular tachycardia. Circulation . 1978;57:659-665. 25. Waldo AL, MacLean WAH, Karp RB, et al. Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery. Circulation . 1977;56:737-745. 26. Okamura K, Henthorn RW, Epstein AE, et al. Further observation of transient entrainment: importance of pacing site and properties of the components of the reentry circuit. Circulation . 1985;72:1293-1307. 27. Almendral JM, Rosenthal ME, Stamato NJ, et al. Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination. J Am Coll Cardiol . 1986;8:294-300.

Copyright © 2023 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 24. Josephson ME, Harken AH, Horowitz LN. Endocardial excision—a new surgical technique for the treatment of ventricular tachycardia. Circulation . 1979;60:1430-1439.

Foreword: Historical Perspectives

28. Almendral JM, Stamato NJ, Rosenthal ME, et al. Resetting response pat terns during sustained ventricular tachycardia: relationship to the excit able gap. Circulation . 1986;74:722-730. 29. Almendral JM, Gottlieb CD, Rosenthal ME, et al. Entrainment of ven tricular tachycardia: explanation for surface electrocardiographic phe nomena by analysis of electrograms recorded within the tachycardia cir cuit. Circulation . 1988;77:569-580. 30. Rosenthal ME, Stamato NJ, Almendral JM, et al. Resetting of ventricular tachycardia with electrocardiographic fusion: incidence and significance. Circulation . 1988;77:581-588. 31. Cassidy DM, Vassallo JA, Buxton AE, et al. Catheter mapping during sinus rhythm: relation of local electrogram duration to ventricular tachy cardia cycle length. Am J Cardiol . 1985;55:713-716. 32. Cassidy DM, Vassallo JA, Miller JM, et al. Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias. Circulation . 1986;73:645-652. 33. Fenoglio JJ, Pham TD, Harken AH, et al. Recurrent sustained ventricular tachycardia: structure and ultra-structure of subendocardial regions in which tachycardia originates. Circulation . 1983;68:518-533. 34. Gardner PI, Ursell PC, Fenoglio JJ Jr, et al. Electrophysiologic and ana tomic basis for fractionated electrograms recorded from healed myocar dial infarcts. Circulation . 1985;72:596-611. 35. Horowitz LN, Josephson ME, Farshidi A, et al. Recurrent sustained ven tricular tachycardia. 3. Role of the electrophysiologic study in selection of antiarrhythmic regimens. Circulation . 1976;58:986-997. 36. Poll DS, Marchlinski FE, Buxton AE, et al. Sustained ventricular tachy cardia in patients with idiopathic dilated cardiomyopathy: electrophysi ologic testing and lack of response to antiarrhythmic drug therapy. Circulation . 1984;70:451-456. 37. Mason JW. A comparison of seven antiarrhythmic drugs in patients with ventricular tachyarrhythmias. Electrophysiologic Study versus Electro cardiographic Monitoring Investigators. N Engl J Med . 1993;329: 452-458. 38. Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med . 1989;321:406-412. 39. Mirowski M, Reid PR, Mower MM, et al. Termination of malignant ven tricular arrhythmias with an implanted automatic defibrillator in human beings. N Engl J Med . 1980;303:322-324. 40. Scheinman MM, Laks MM, DiMarco J, et al. Current role of catheter ablative procedures in patients with cardiac arrhythmias. A report for health professionals from the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation . 1991;83: 2146-2153. 41. Haissaguerre M, Dartigues JP, Warin JP, et al. Electrogram patterns pre dictive of successful catheter ablation of accessory pathways. Value of unipolar recording mode. Circulation . 1991;84:188-202. 42. Jackman WM, Wang X, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radio frequency current. N Engl J Med . 1991;324:1605-1611. 43. Scheinman MM, Huang S. The 1998 NASPE prospective catheter abla tion registry. Pacing Clin Electrophysiol . 2000;6:1020-1028. 44. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter: relevance to catheter abla tion of the septal isthmus and a new technique for rapid identification of ablation success. Circulation . 1996;94:407-424.

45. Poty H, Saoudi N, Nair M, et al. Radiofrequency catheter ablation of atrial flutter: further insights into the various types of isthmus block: application to ablation during sinus rhythm. Circulation . 1996;94:3204 3213. 46. Schwartzman D, Callans DJ, Gottlieb CD, et al. Conduction block in the inferior vena caval-tricuspid valve isthmus: association with outcome of radiofrequency ablation of type I atrial flutter. Am Coll Cardiol . 1996;28:1519-1531. 47. Cosio FG, Arribas F, Lopez-Gil M, et al. Radiofrequency ablation of atrial flutter. J Cardiovasc Electrophysiol . 1996;7:60-70. 48. 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. 49. Morady F, Harvey M, Kalbfleisch SJ, et al. Radiofrequency catheter abla tion of ventricular tachycardia in patients with coronary artery disease. Circulation . 1993;87:363-372. 50. Stevenson WG, Friedman PL, Kocovic D, et al. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction. Circulation . 1998;98:308-314. 51. El-Shalakany A, Hadjis T, Papageorgiou P, et al. Entrainment mapping criteria for the prediction of termination of ventricular tachycardia by single radiofrequency lesion in patients with coronary artery disease. Circulation . 1999;99:2283-2289. 52. Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and non-ischemic cardiomyopathy. Circulation . 2000;101:1288-1296. 53. Callans DJ, Menz V, Schwartzman D, et al. Repetitive monomorphic tachycardia from the left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin. J Am Coll Cardiol . 1997;29:1023-1027. 54. Coggins DL, Lee RJ, Sweeney J, et al. Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol . 1994;23:1333-1341. 55. Varma N, Josephson ME. Therapy of idiopathic ventricular tachycardia. J Cardiovasc Electrophysiol . 1997;8:104-116. 56. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med . 1998;339:659-666. 57. Haissaguerre M, Jais P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol . 2000;11:2-10. 58. Haissaguerre M, Jais P, Shah DC, et al. Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation . 2000;101:1409-1417. 59. Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ecto pic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation . 1999;100:1879-1886. 60. Belhassen B, Glick A, Viskin S. Efficacy of quinidine in high-risk patients with Brugada syndrome. Circulation . 2004;110:1731-1737. 61. Belhassen B. Is quinidine the ideal drug for Brugada syndrome? Heart . 2012;9:2001-2002. 62. Belhassen B, Glick A, Viskin S. Excellent long-term reproducibility of the electrophysiologic efficacy of quinidine in patients with idiopathic ven tricular fibrillation and Brugada syndrome. Pacing Clin Electrophysiol . 2009;32:294-301.

PREFACE

This book is and will always be Mark’s book. My role is to lovingly curate and update Mark’s phenomenal experi ence and wisdom to the best of my ability. Taking on this task underscored just how much I have left to learn and, even more, how many ques tions I wish that I could dis cuss with him. All references to clini cal experience and all strong opinions are Mark’s. For

clinical practice. Unfortunately, these new therapeutic tools have captured the imagination of young electrophysiologists to such an extent that terms such as ablationist , defibrillation ist , or implanter are used to describe their practice. Their zest for the application of such therapeutic modalities has been associated with a decrease in the emphasis of understand ing the mechanisms, clinical implications, and limitations of the therapeutic interventions used to treat arrhythmias. Such behavior is often associated with a lack of, or limited, critical thought that is essential to the development of a new therapeutic concept. There should be the development of a hypothesis, questioning the rationale of the hypothesis, and testing the hypothesis prior to widespread application of the therapeutic strategy.” “The purpose of this book is to provide the budding elec trophysiologist with an electrophysiologic approach to arrhyth mias, which is predicated on the hypothesis that a better understanding of the mechanisms of arrhythmias will lead to more successful and rationally chosen therapy. As such, this book will stress the methodology required to define the mechanism and site of origin of arrhythmias so that safe and effective therapy can be chosen. The techniques suggested to address these issues and specific therapeutic interventions employed represent a personal view, one that is based on experience and, not infrequently, on intuition.”

greater emphasis, his words are marked with italic text in the present edition. I have left as many of these from the prior editions as possible. We have argued over some of these opin ions in the past; almost invariably I have been wrong. Points of view that have become less tenable in the face of advancing knowledge have been edited, but these were few. In this spirit, the unedited words from the preface of the fifth edition follow. “The past 50 years have witnessed the birth, growth, and evolution of clinical electrophysiology, from a field whose initial goals were the understanding of arrhythmia mecha nisms to one of significant therapeutic impact. The develop ment and refinement of implantable devices and, in particu lar, catheter ablation have made nonpharmacologic therapy a treatment of choice for most arrhythmias encountered in

David J. Callans, MD Philadelphia, Pennsylvania

ACKNOWLEDGMENTS

Special acknowledgments are due to two people who are responsible for major changes in this edition. Kalyanam Shiv kumar, for his incredible work on the Amara Yad project, which provided access to the McAlpine amazing heart dissec tions. Ramanan Kumareswaran for providing spectacular case studies to encourage further study of the text.

More figures of intracardiac echocardiography have been included in this edition. There is a mix of image orientations between the “traditional” way and the Penn way (with the right side representing the inferior part of the image, that is, the way that the catheter is moved). I apologize for the confu sion this may cause.

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COVER ILLUSTRATION

Solving problems, then and now. The left panel demonstrates the mechanism of subendocardial resection (adapted from Figure 11.262 ). ( A ) Bipolar recordings from a plaque elec trode positioned over the site of ventricular tachycardia origin have abnormal and fractionated electrograms. ( B ) After suben docardial resection, recordings from the same area show nor mal electrograms without fractionated or late potentials. The right panel is a three-dimensional reconstruction (courtesy

of Saman Nazarian, MD) of the left ventricle in a patient with ventricular tachycardia in the setting of nonischemic cardio myopathy and midseptal substrate (depicted by the gray shad ing in the midseptal and periaortic regions). Endocardial and epicardial (venous alcohol) ablation lesions are represented by the red areas. The substrate is much more extensive than the area of ablation, and ventricular tachycardia continued until it was successfully treated with cardiac radioablation.

CONTENTS

Foreword: Historical Perspectives vii Preface xi Acknowledgments xiii Cover Illustration xv

1 General Principles and Techniques of Electrophysiologic Investigation

2 Sinus Node Function

67 91

3 Atrioventricular Conduction

4 Intraventricular Conduction Disturbances

114 145 159 175 291 401 459 662

5 Miscellaneous Phenomena Related to Atrioventricular Conduction

6 Ectopic Rhythms and Premature Depolarizations

7 Supraventricular Tachycardias 8 Preexcitation Syndromes 9 Atrial Flutter and Fibrillation 10 Recurrent Ventricular Tachycardia

11 Catheter and Surgical Ablation in the Therapy of Arrhythmias

Appendix: Case Studies 873 Index 937

xvii

Miscellaneous Phenomena Related to Atrioventricular Conduction

CHAPTER 5

Concealed conduction, the gap phenomenon, and supernor mality are physiologic events that may be considered variants of the normal response. These phenomena are responsible for many unusual or unexpected responses of atrioventricular (A-V) conduction. This chapter addresses these separate but interrelated phenomena of cardiac conduction. CONCEALED CONDUCTION The definition of concealed conduction has been irrevocably altered by the availability of intracardiac electrophysiologic studies. The concept of concealed conduction, an explana tion for the effects of incomplete penetration of an impulse into a portion of the A-V conduction system, was introduced (and then expanded on) by Langendorf 1,2 and Katz and Pick. 3 The term was applied to unexpected phenomena observed on the surface electrocardiogram (ECG) that were compat ible with the effects of incompletely penetrating impulses that were not directly reflected on the surface ECG; hence the term concealed . Because intracardiac recordings can di rectly document the presence of these impulses during the electrophysiologic study, they are no longer truly concealed. Thus, specific consequences of incomplete penetration of impulses may be a less ambiguous term than concealed conduction of impulses to describe a variety of ECG find ings. 4 Although the A-V node is the structure with which concealed conduction has been most often associated, this phenomenon can occur in any portion of the A-V conduc tion system. The manifestations of concealed conduction (ie, the effects of incomplete penetration of an impulse) include (a) unexpected prolongation of conduction; (b) unexpected failure of propagation of an impulse; (c) unexpected facilita tion of conduction by “peeling back” refractoriness, directly altering refractoriness, and/or summation 4-6 ; and (d) unex pected pauses in the discharge of a spontaneous pacemaker. Excellent reviews of the ECG manifestations of concealed conduction are available. 7-12 Concealed conduction may result from antegrade or ret rograde penetration of an impulse into a given structure. The impulse-producing concealment may originate anywhere in the heart, including the sinus node, an ectopic atrial site, the A-V junction, the fascicles, or the ventricles. 7 The most common site manifesting the effects of concealed conduction

is the A-V node. The effects of retrograde concealment in the A-V node under different circumstances are shown in Figures 5.1 through 5.4 . Impulses from any subnodal site can produce concealed conduction. The ability of ventricu lar premature complexes (VPCs) to produce concealment in the A-V node depends on intact retrograde His-Purkinje conduction. In Figure 5.4 , similarly coupled VPCs, manifest ing different patterns of retrograde His-Purkinje conduction, have totally different effects on the A-V nodal conduction of the sinus complex that follows. The effect of His bundle, fas cicular, or ventricular extrasystoles on subsequent A-V nodal conduction is inversely related to the coupling interval of the premature depolarization. In patients with dual A-V nodal pathways, VPCs, fascicular premature complexes, and His bundle complexes can shift conduction from the fast to the slow pathway. Slow pathway conduction can be maintained by retrograde invasion into the fast pathway (see Chapter 7). Retrograde concealment at multiple levels of the A-V con duction system may also occur ( Figure 5.5 ). The levels of concealment depend on the relative timing of antegrade and retrograde impulses. The most frequent clinical circumstances in which con cealed conduction is operative are (a) atrial fibrillation dur ing which the irregular ventricular response is due to the varying depth of penetration of the numerous wavefronts bombarding the A-V node 8 ; (b) prolongation of the P-R (A-H) interval or production of A-V nodal block by a pre mature depolarization of any origin; (c) reset of a junctional (His bundle) pacemaker by atrial or subjunctional premature depolarizations; and (d) perpetuation of aberrant conduction during tachyarrhythmias. In the latter circumstance, retro grade penetration of the blocked bundle branch subsequent to transeptal conduction perpetuates aberration. 13,14 This is the most common mechanism of perpetuation of aberration during supraventricular tachycardia observed in our labora tory (~70% of cases). Wellens et al 15 have found a similar in cidence of retrograde concealment, producing perpetuation of aberration. Concealed His bundle depolarizations can produce many unusual patterns of conduction, including simulation of Type II second-degree A-V block (see Chapters 3 and 6). His bun dle depolarizations are frequently not recognized because they must conduct antegrade and/or retrograde to have any

145

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HRA

HBE

100

135

FIGURE 5.1 Retrograde concealed conduction by a fascicular extrasystole. From top to bottom, tracings represent standard leads 1 and V1 and high right atrium (HRA), coronary sinus (CS), His bundle electrogram (HBE), and time lines (T) at 10 and 100 msec. The first beat is a conducted sinus beat, with an A-H = 100 msec, H-V = 80 msec, and a right bundle branch block configuration. The second beat is a fascicular extrasystole, with an “Hr-V” = 20 msec. Note that there is no manifest conduction above the atrioventricular (A-V) junction (ie, no atrial electrogram). Note, however, in the next sinus beat that the A-H interval is prolonged to 135 msec, indicating that the retrograde wavefront from the preceding beat partially penetrated (concealed) in the A-V node, rendering it relatively refractory to the next sinus impulse. A, atrial deflection; H, His bundle deflec tion; Hr, retrograde His deflection; V, ventricular deflection.

aVF

HRA

HBE

300

Copyright © 2023 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. FIGURE 5.2 Retrograde concealed conduction by a junctional (His bundle) escape rhythm during intra-His complete heart block. Atrioventricular (A-V) dissociation is present, and there is no retrograde activation of the atria by the His bundle escape rhythm. There are three sinus depolar izations, as evidenced by early high right atrial (HRA) activation. The first sinus impulse is blocked above the proximal His bundle (ie, in the A-V node); the second conducts to the proximal His bundle with a short A-H interval, and it is then blocked; and the third conducts to the proximal His bundle with a longer A-H interval. The A-V nodal block in the first beat and the A-V nodal delay in the third beat are due to concealed retrograde conduction of the His bundle beats into the A-V node. Thus, despite antegrade intra-His block, the distal His bundle escape rhythm can conduct retrogradely and affect antegrade conduction (ie, unidirectional antegrade block is present).

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Chapter 5: Miscellaneous Phenomena Related to Atrioventricular Conduction ■

aVF

A V

HBE

RVA

LVA

FIGURE 5.3 Retrograde concealed conduction during ventricular tachycardia. The tracing is arranged from top to bottom: surface electrocardio gram (ECG) leads 1, aVF, and V1; His bundle electrogram (HBE); right ventricular apex (RVA); left ventricular apex (LVA); and time lines (T) at 10 and 100 msec. The left panel represents sinus rhythm. The right panel represents ventricular tachycardia without manifest retrograde conduction. Retrograde His bundle or atrial deflections are not seen. There are three sinus complexes, as reflected by atrial deflections (A) in the HBE trac ing. Only the second results in a propagated response with a His bundle deflection (H) and a slight alteration in the QRS complex characteristic of a fusion beat (fb). Block of the first and third sinus impulses in the atrioventricular (A-V) node and prolongation of the A-H interval during the conducted second sinus beat result from retrograde concealed conduction of the ventricular beats into the A-V node.

aVF

A H

H A A

330

HBE

HRA LRA

aVF

H V

A H V

330 V

HBE

HRA LRA

Copyright © 2023 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. FIGURE 5.4 Concealed conduction by ventricular premature complexes (VPCs). A and B. Leads 1, aVF, and V1 and electrograms from the His bundle (HBE), high right atrium (HRA), and low right atrium (LRA). Sinus rhythm is present in the first two complexes of each panel. A. A VPC is observed at a coupling interval of 330 msec with retrograde conduction through the His bundle to the atrioventricular (A-V) node. This results in concealed conduction so that the subsequent sinus complex blocks in the A-V node. B. A similarly coupled VPD fails to reach the His bundle so that no concealment in the A-V node is manifested and the sinus complex conducts with a normal H-V and normal A-H. Thus, the ability to produce concealed conduction in the A-V node by VPC depends on the ability to penetrate the A-V node via the His-Purkinje system. T, time line.

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■ Josephson’s Clinical Cardiac Electrophysiology

1 2 3 V1

HRA

A H

A V

A H

HBE

FIGURE 5.5 Multiple levels of concealed conduction during ventricular pacing. The rhythm is sinus, with ventricular pacing at a cycle length of 1,200 msec (S, arrow). Following the first stimulated ventricular complex, the spontaneously occurring sinus impulse is conducted with a long H-V interval and left bundle branch block (LBBB) aberration. This indicates asynchronous concealment into both the left and right bundle branches (long H-V and LBBB morphology). Following the second stimulated complex, the sinus impulse blocks in the atrioventricular (A-V) node, indicating concealed conduction to that structure. Following the third stimulated complex, the sinus impulse blocks below the His bundle, indicating conceal ment into the His-Purkinje system, rendering it totally refractory to the antegrade impulse.

representation on the surface ECG. Incomplete penetration (concealment) of His bundle depolarizations in either direc tion, producing unexpected abnormalities of antegrade or retrograde conduction, may present a particularly difficult di agnostic problem. 9,10 The intracardiac study may be extremely useful in assessing the causes and sites of concealed conduc tion by making all the components of the A-V conduction sys tem available for analysis. Although interference with normal antegrade con duction or with a subsidiary pacemaker by a concealed premature depolarization may be easy to conceptualize, un explained facilitation of conduction requires further expla nation. Most examples of facilitation of conduction (usually in the His-Purkinje system) can be explained by the fol lowing effects of a premature impulse: (a) allowing more time for the structure to recover excitability, which is due to peeling back the refractory period of that tissue, and/or (b) shortening the refractory period of tissues with cycle length-dependent refractoriness (ie, the atria, His-Purkinje system, and ventricles) by decreasing the cycle length pre ceding the subsequent spontaneous impulse ( Figure 5.6 ) or retrograde conduction through a site of antegrade block,

which both shortens the refractory period and allows more time for recovery. Simultaneous shortening of refractoriness and providing more time to recover excitability is the most common mechanism. Abrupt normalization of aberration by a VPC (the finding of which proves retrograde conceal ment as the mechanism for perpetuation of aberration) is based on these principles ( Figures 5.7 and 5.8 ). A-V nodal conduction time and refractoriness may be shortened by VPCs delivered simultaneously with the prior atrial depo larization ( Figure 5.9 ). In an elegant study, Shenasa et al demonstrated that VPCs shorten A-V nodal refractoriness and improve A-V nodal conduction at comparable coupling intervals at both long and short drive cycle lengths. 16 One mechanism for this is summation because VPCs without simultaneous atrial activation prolong refractoriness and slow conduction in the node. Another explanation would be for the VPC to produce earlier activation at the site of A-V nodal conduction delay or block. This allows more time for it to recover when the atrial premature contrac tion (APC) is delivered. These and other mechanisms of facilitation explain some instances of pseudo-supernormal conduction.

CL440 msec

I II

III V1

HRA

VPD A

A H

HBE

FIGURE 5.6 Facilitation of His-Purkinje conduction by a ventricular premature depolarization (VPD). During atrial pacing at a cycle length of 440 msec, 2:1 block below the His bundle occurs. A VPD (arrow) is introduced just before the fifth atrial paced complex. Following the VPD, the P wave that should block in the 2:1 sequence conducts with the same A-H and H-V intervals as other conducted complexes. Facilitation of His-Purkinje conduction results because the VPD “peeled back” His-Purkinje refractoriness, allowing the atrial impulse to propagate through the previous site of block. See text for discussion. (Reprinted from Gallagher JJ, Damato AN, Varghese PJ, et al. Alternative mechanisms of apparent supernormal atrioventricular conduction. Am J Cardiol . 1973;31:362, with permission from Elsevier.)

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