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Cardiac Electrophysiology

Andrea Natale • Amin Al-Ahmad Paul J. Wang • John P. DiMarco

(Editors)

Cardiac

Electrophysiology

Clinical Case Review

Andrea Natale • Amin Al-Ahmad Paul J. Wang • John P. DiMarco (Editors) Cardiac Electrophysiology Clinical

Editors Andrea Natale Texas Cardiac Arrhythmia Institute St. David’s Medical Center 1015 East 32nd Street

Paul J. Wang School of Medicine Stanford University 300 Pasteur Drive

Suite 516,

H-2146,

Austin, TX 78705 USA

Stanford, CA 94305 USA

Amin Al-Ahmad School of Medicine Stanford University 300 Pasteur Drive

John P. DiMarco Cardiovascular Division University of Virginia Health System 1215 Lee Street

H-2146,

Charlottesville, VA 22908

Stanford, CA 94305 USA

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

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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 elec- trophysiology, there are few case-based books that comprehensively cover clinical electro- physiology, 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 impor- tant 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

Contents

Section 1

Ablation

Case 1

3

Amin Al-Ahmad

Case 2 Michel Haissaguerre

7

Case 3

11

Amin Al-Ahmad

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

x

Contents

Case 12 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

51

Case 13 Bradley P. Knight

53

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

69

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

83

Case 21 Bradley P. Knight

85

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 Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

101

Case 25 Bradley P. Knight

103

Contents

xi

 

Case 27

111

M.

Eyman Mortada, Jasbir S. Sra, and Masood Akhtar

Case 28 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

115

Case 29 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

123

Case 30 Luis C. Sáenz and Miguel A. Vacca

125

Case 31 Bradley P. Knight

133

Case 32 Luigi Di Biase, Rodney P. Horton, and Andrea Natale

135

 

Case 33

139

M.

Eyman Mortada, Jasbir S. Sra, and Masood Akhtar

Case 34 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele

143

Case 35 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

147

Case 36 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

151

Case 37 Bradley P. Knight

153

Case 38 Luigi Di Biase, Rodney P. Horton, and Andrea Natale

157

 

Case 39

159

M.

Eyman Mortada, Jasbir S. Sra, and Masood Akhtar

Case 40 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele

163

xii

Contents

Case 42 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

185

Case 43 Bradley P. Knight

189

Case 44 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele

191

Case 45 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

195

Case 46 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

199

Case 47 Bradley P. Knight

201

Case 48 Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele

203

Case 49 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

217

Case 50 Bradley P. Knight

221

Case 51 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

223

Case 52 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

229

Case 53 Bradley P. Knight

233

Case 54 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

235

Case 55 Eric Buch, Shiro Nakahara, Marmar Vaseghi, Noel G. Boyle, and Kalyanam Shivkumar

241

Contents

xiii

Case 57 Yash Y. Lokhandwala, Anoop K. Gupta, and Ranjan K. Thakur

247

Case 58 Roopinder Sandhu, Dimpi Patel, William R. Lewis, and Andrea Natale

253

Case 59 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar

263

Case 60 Matthew D. Hutchinson

267

Case 61 Ronald Lo, Henry H. Hsia, and Amin Al-Ahmad

271

Case 62 Richard H. Hongo and Andrea Natale

275

Case 63 David J. Callans

279

Case 64 J. David Burkhardt, Dimpi Patel, and Andrea Natale

283

Case 65 Matthew D. Hutchinson

287

Case 66 Matthew D. Hutchinson

291

Case 67 Matthew D. Hutchinson

295

Case 68 Matthew D. Hutchinson

299

Case 69 Matthew D. Hutchinson

303

Case 70 Matthew D. Hutchinson

307

Case 71 Matthew D. Hutchinson

311

Section 2

Devices

xiv

Contents

Case 73 Amin Al-Ahmad and Paul J. Wang

319

Case 74 Kenneth A. Ellenbogen

321

Case 75

325

Nora Goldschlager

Case 76 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager

327

Case 77 Gregory M. Marcus and Nora Goldschlager

331

Case 78 Amin Al-Ahmad and Paul J. Wang

335

Case 79 Kenneth A. Ellenbogen and Rod Bolanos

337

Case 80

341

Nora Goldschlager

Case 81 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager

343

Case 82 Amin Al-Ahmad and Paul J. Wang

345

Case 83 Kenneth A. Ellenbogen

347

Case 84

349

Nora Goldschlager

Case 85 Anurag Gupta and Amin Al-Ahmad

351

Case 86 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager

353

Case 87 Kenneth A. Ellenbogen

357

Case 88

361

Nora Goldschlager

Contents

xv

Case 90 Fred M. Kusumoto, Jennifer Crain, and Nora Goldschlager

369

 

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 Kenneth A. Ellenbogen and Rod Bolanos

379

Case 95 Byron K. Lee

383

Case 96 Amin Al-Ahmad and Paul J. Wang

387

Case 97 Kenneth A. Ellenbogen and Rod Bolanos

389

Case 98 Kenneth A. Ellenbogen

391

Case 99 Amin Al-Ahmad and Paul J. Wang

395

Case 100 Kenneth A. Ellenbogen

399

Case 101 Amin Al-Ahmad and Paul J. Wang

403

Case 102 Kenneth A. Ellenbogen

405

Case 103 Amin Al-Ahmad and Paul J. Wang

407

Case 104 Kenneth A. Ellenbogen

411

Case 105 Kenneth A. Ellenbogen and Rod Bolanos

415

xvi

Contents

Case 107 Paul A. Friedman and Charles D. Swerdlow

423

Case 108 Paul A. Friedman and Charles D. Swerdlow

427

Case 109 Paul A. Friedman and Charles D. Swerdlow

431

Case 110 Paul A. Friedman and Charles D. Swerdlow

433

Case 111 Paul A. Friedman and Charles D. Swerdlow

439

Case 112 Paul A. Friedman and Charles D. Swerdlow

441

Case 113 Paul A. Friedman and Charles D. Swerdlow

443

Case 114 Paul A. Friedman and Charles D. Swerdlow

447

Case 115 Paul A. Friedman and Charles D. Swerdlow

451

Case 116 Paul A. Friedman and Charles D. Swerdlow

453

Case 117 Paul A. Friedman and Charles D. Swerdlow

455

Case 118 Paul A. Friedman and Charles D. Swerdlow

459

Case 119 M. Eyman Mortada, Jasbir S. Sra, and Masood Akhtar

465

Case 120 Paul A. Friedman and Charles D. Swerdlow

469

Case 121 Kenneth A. Ellenbogen

471

Case 122

473

Anurag Gupta

Contents

xvii

Case 124 Ronald Lo, Amin Al-Ahmad, and Paul J. Wang

481

Case 125 Ronald Lo, Amin Al-Ahmad, and Paul J. Wang

483

Section 3

Clinical Cases

Case 126 Mehmet K. Aktas, Abrar H. Shah, and James P. Daubert

487

Case 127 Loren P. Budge and John P. DiMarco

491

Case 128 David J. Callans

495

Case 129 Andrew E. Darby and John P. DiMarco

497

Case 130 Thomas J. Sawyer, Burr W. Hall, and James P. Daubert

501

Case 131 John P. DiMarco

505

Case 132 John P. DiMarco

509

Case 133 John P. DiMarco

511

Case 134 John P. DiMarco

513

Case 135 John P. DiMarco

517

Case 136 John P. DiMarco

521

Case 137 John P. DiMarco

523

Case 138 John P. DiMarco

527

xviii

Contents

Case 140 John P. DiMarco

531

Case 141 John P. DiMarco

535

Case 142 John P. DiMarco

539

Case 143 John P. DiMarco

545

Case 144 John P. DiMarco

551

Case 145 John P. DiMarco

555

Case 146 Brett A. Faulknier, David T. Huang, and James P. Daubert

559

Case 147 Stefan H. Hohnloser and Joachim R. Ehrlich

565

Case 148 Joachim Ehrlich and Stefan H. Hohnloser

567

Case 149 Bradley P. Knight

571

Case 150 Bradley P. Knight

575

Case 151 Bradley P. Knight

577

Case 152 Andrew D. Krahn

579

Case 153 Byron K. Lee, Melvin M. Scheinman, and Zian H. Tseng

583

Case 154

585

Srijoy Mahapatra

Case 155 Pamela K. Mason

589

Contents

xix

Case 157 Pamela K. Mason 595 Case 158 Pamela K. Mason 597 Case 159 Lisa
Case 157
Pamela K. Mason
595
Case 158
Pamela K. Mason
597
Case 159
Lisa G. Umphrey and John Paul Mounsey
599
Case 160
James A. Reiffel
603
Case 161
James A. Reiffel
607
Case 162
Jens Seiler and William G. Stevenson
611
Case 163
Jens Seiler and William G. Stevenson
617
Case 164
Jens Seiler and William G. Stevenson
625
Case 165
J. Jason West and John Paul Mounsey
631
Case 166
Darren Traub, James P. Daubert, and Spencer Rosero
635
Case 167
Vikas P. Kuriachan and George D. Veenhuyzen
639
Case 168
Vikas P. Kuriachan and George D. Veenhuyzen
643
Case 169
Jeffrey D. Booker and George D. Veenhuyzen
647
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
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655

Section

Ablation

I

Case Summary

Case 1

Amin Al-Ahmad

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 arrhyth- mia 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 tachyar- rhythmia 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

entrainment pacing at the tricuspid valve (TV) to inferior Fig. 1.1 Twelve-lead ECG showing atrial arrhythmia.

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

3

4

A. Al-Ahmad

vena cava (IVC) isthmus. Reverse typical atrial flutter would be unlikely given the morphology of the flutter waves. Scar- related atrial flutters should also be considered. Ablation of all potential atrial flutter circuits in patients post cardiac sur- gery may reduce the likelihood of recurrence. 1

In this case, entrainment at the TV-IVC isthmus demon- strated 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.

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

ABL d

Stim 4

200ms PPI TCL 12:22:16 PM 12:22:17 PM
200ms
PPI
TCL
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

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

500ms 1:01:47 PM 1:01:48 PM 1:01:49 PM 1:01:50 PM 1:01:51 PM
500ms
1:01:47 PM
1:01:48 PM
1:01:49 PM
1:01:50 PM
1:01:51 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.

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-Plessis- Robinson, 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

circumferential I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Fig. 2.1 Twelve-lead

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

7

8

M. Haissaguerre

catheter (Lasso, Biosense Webster, Diamond Bar, CA) were

the

adjacent LA and is synchronous with the second half of

introduced through a long sheath in the left atrium (LA). The

the

P-wave (in the right PVs it should be the first part of the

circumferential catheter was placed in the left superior pul- monary vein (LSPV) and recorded venous and atrial poten-

P-wave). The second potential reflects local activity from the PV striated musculature (black star). When ectopy

tials (Fig. 2.2).

occurs in the PV (Fig. 2.2, second complex), there is a rever-

What mechanism is illustrated and what action is

sal

of the described activation sequence, with the PV poten-

required?

tial

preceding the atrial potential. This pattern of reverse

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 com- plex). The first potential (white star) represents activation of

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 connect-

ing 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

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

9

of the left PVs; however, due to the ridge between the left pulmonary veins and the left atrial appendage (LAA), cath- eter 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,

segmental or circumferential ablation with a continuous cir- cular 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 polar- ity 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.

A B C I II V1 PV 1-2 PV 2-3 PV 3-4 PV 4-5 PV
A
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 cir- cumferential 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)

10

M. Haissaguerre

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

17 18 19 20 21 22 23 24 25
17
18
19
20
21
22
23
24
25

26

Fig. 2.4 Endocardial tracings recorded during sinus rhythm from the left superior pulmonary vein (LSPV). Recording from a decapolar cir- cumferential 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, Shah DC, Jaïs P, et al. Electrophysiological break - throughs from the left atrium to the pulmonary veins. Circulation.

2000;102:2463-2465.

Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long- lasting persistent atrial fibrillation: critical structures for termina- tion. J Cardiovasc Electrophys. 2005;16(11):1125-1137.

Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources main - taining atrial fibrillation organized by prior ablation. Circulation.

2006;113(5):616-625.

Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachy - cardia 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.

Case Summary

Case 3

Amin Al-Ahmad

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 per- sistent 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 maneu- vers may help determine the best area to ablate?

Case Discussion

Atrial flutter can be common immediately after lung trans- plantation. Canine models have suggested a substrate for atrial flutter in the left atrium due to suture lines. In addition,

flutter in the left atrium due to suture lines. In addition, Fig. 3.1 Twelve-lead ECG of

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

11

12

A. Al-Ahmad

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 flut- ter 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 flut- ter and help guide ablation. In this case, entrainment on the right side clearly demon- strated 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).

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

CS 3,4

CS 1,2

HIS p

HIS m

HIS d

ABL

ABL d

Stim 3

200ms S PPI TCL C S1 S1 S1 S1 S1 9:42:27 AM 9:42:28 AM
200ms
S
PPI
TCL
C
S1
S1
S1
S1
S1
9:42:27 AM
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

I 200ms II V1 V6 RA 9,10 RA 7,8 RA 5,6 RA 3,4 RA 1,2
I
200ms
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
PPI
TCL
S1
S1
S1
Stim 4
12:55:47 PM
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

the right inferior pulmonary vein yields a near-perfect PPI Fig. 3.4 Right anterior oblique view of

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

Bibliography

Nielsen TD, Bahnson T, Davis RD, Palmer SM. Atrial fibrillation after pulmonary transplant. Chest. August 2004;126(2):496-500.

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 elec- trophysiological 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 pulmo- nary 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 pro- longation 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?

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

I II V1 LAA RAA CSd CSp
I
II
V1
LAA
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

15

16

M. Haissaguerre

7CFE Mean Map 120 mS 65 mS 0 mS
7CFE Mean Map
120 mS
65 mS
0 mS

Fig. 4.2 NavX (EnSite System, St. Jude Medical, MN, USA) fraction- ation map of the left atrium and coronary sinus after isolation of the four pulmonary veins showing ubiquitous distribution of complex frac- tionated 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 simultane- ously 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 cal- culated. The electrogram annotation is then verified manu- ally online to ensure accuracy (Fig. 4.1). The electrograms measured at the top of both append- ages 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 esti- mated 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 simultane- ously to measure the impact of ablation in both chambers. Initial AFCL has been shown to be the strongest predic- tor of success for AF ablation (AF of less than 5 years

continuous duration). AFCL of less than 140 ms is associ- ated 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 usu- ally observed (a change in AFCL greater than 6 ms is con- sidered 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 abla- tion 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 poste- rior 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

17

Case 4 17 Recording of the ablation catheter (RF) and the coronary sinus ( CS 1–2

Recording of the ablation catheter (RF) and the coronary sinus

(CS 1–2 to 9–10). Panel A: Ablation along the inferior left atrium tar- geting continuous electrical activity. Panel B: Ablation at the posterior part of the left atrial appendage targeting centrifugal activation with

Fig. 4.3

consistent distal-to-proximal fractionated electrograms. Panel C:

Ablation was then performed along the roof targeting almost continu- ous fractionated electrograms

18

M. Haissaguerre

I I II II V1 V1 RFp CS 1-2 RFd CS 3-4 CS 1-2 CS
I
I
II
II
V1
V1
RFp
CS 1-2
RFd
CS 3-4
CS 1-2
CS 5-6
CS 3-4
CS 7-8
CS 5-6
CS 7-8
CS 9-10
CS 9-10

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 break - throughs from the left atrium to the pulmonary veins. Circulation.

2000;102:2463-2465.

Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long- lasting persistent atrial fibrillation: critical structures for termina- tion. J Cardiovasc Electrophys. 2005;16(11):1125-1137.

Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources main - taining 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 tachy - cardia 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 elec- trode 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 maneu- vers 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

positive D in V1, and negative D in aVF, is suggestive Fig. 5.1 Twelve-lead ECG during

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: agupta@stanfordalumni.org; aalahmad@stanford.edu

A. Natale et al. (eds.), Cardiac Electrophysiology,

DOI: 10.1007/978-1-84996-390-9_5, © Springer-Verlag London Limited 2011

19

20

A. Gupta and A. Al-Ahmad

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

D distal electrode pair, RVA right ventricular apex Fig. 5.3 Induced SVT. Note the change in

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?

same rate. Is this evidence for another accessory pathway? of a right posterior/right posterolateral 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 spontane- ously 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 termi- nated 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 retro- grade pattern seen intermittently during the initial SVT. Para-Hisian pacing is performed (Fig. 5.4).Ventricular pac- ing next to the His bundle and proximal to the right bundle branch at high output directly captures the His bundle, thus

Case 5

21

Fig. 5.4 Para-Hisian pacing is performed. The first QRS complex obtained with high- output 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

to atrial interval and in atrial activation sequence activating the ventricles through the His–Purkinje system

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 evi- denced by left bundle branch block (LBBB) QRS morphol- ogy 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 tachy- cardia, and no further SVT was inducible.

Bibliography

Chiang CE, Chen SA, Teo WS, et al. An accurate stepwise electrocar- diographic algorithm for localization of accessory pathways in patients with Wolff–Parkinson–White syndrome from a compre- hensive 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 per- sistent 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 ante- rior 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 rela- tively 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-to- distal 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. 6.26.4). What inferences can be made from Figs. 6.16.4 with relevance to the mechanism of atrial arrhythmia?

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 activa- tion sequence for (arbitrarily) ³75% of the time over a 10-min

M. Haissaguerre

Department of Cardiology and Electrophysiology, CHU de Bordeaux, Hospital Cardiologique de Haut Leveque, Avenue de Magellan, Pessac 33604, France

time period. Mapping of such organized AF can be per- formed conventionally and allows in most cases to determi- nate 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) rep- resenting 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 cen- trifugal 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

AV R

AV L

AV F

VI

V2

V3

V4

V5

V6

distal electrode I II III AV R AV L AV F VI V2 V3 V4 V5

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

23

24

M. Haissaguerre

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)

V1

RFd

RFp

CSd

A B LAA LPV RPV CS 100 ms Septum
A
B
LAA
LPV
RPV
CS
100 ms
Septum

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 tachy- cardia. 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 main- tenance, 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 con-

verges 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 – harbor-

ing 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 local-

ized 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

25

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 B V1 RFd RFp CSd 100 ms
A
B
V1
RFd
RFp
CSd
100 ms

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 sub- strate for further arrhythmia by creating an anchoring point potentially able to maintain re-entry. Therefore the mecha- nism 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 pre- disposing 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.

26

M. Haissaguerre

Fig. 6.4 Same graphic as Fig. 6.2. Ablation catheter positioned anterior and septal to the roofline

V1

RFd

RFp

CSd

LAA RPV LPV CS 0, 100 mV RFd 100 ms Septum
LAA
RPV
LPV
CS
0, 100 mV
RFd
100 ms
Septum

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

V1

RFd1

RFd2

RFd3

CSd

0, 100 mV RFd LAA POST RPVs LPVs CS Septum
0, 100 mV
RFd
LAA
POST
RPVs
LPVs
CS
Septum

100 ms

Case 6

27

Bibliography

Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources main - taining atrial fibrillation organized by prior ablation. Circulation.

2006;113(5):616-625.

Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological break - throughs from the left atrium to the pulmonary veins. Circulation.

2000;102:2463-2465.

Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long- lasting persistent atrial fibrillation: critical structures for termina- tion. J Cardiovasc Electrophys. 2005;16(11):1125-1137. Sanders P, Hocini M, Jais P, et al. Characterization of focal atrial tachy - cardia 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) car- dioversions was referred for ablation. The inital procedure consisted of pulmonary vein (PV) isolation, extensive abla- tion 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 dur- ing sinus rhythm. Early recurrence of AT necessitated a second ablation pro - cedure 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% irregular- ity. 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 pos- terior 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 situ- ation, 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 mid- diastolic 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 poste- riorly). 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 per-

formed in this area where a site displaying most of the CL

was found at the anterior mouth of the LAA (Fig. 7.1); how-

ever, 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 activa- tion gradient on the electrogram recording and a short PPI (10 ms) was mapped on the anterior LA (Fig. 7.3). A three- dimensional 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

29

30

M. Haissaguerre

I

II

V1

RFd

RFp

CS 1-2

CS 3-4

CS 5-6

CS 7-8

CS 9-10

55 56
55
56

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

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

PPI to assess number of segment(s) involved

≤2 segments FOCAL
≤2 segments
FOCAL

• EGM spanning all the AT cycle length in the invo lved segment(s)

• Mid diastolic potentials

>2 segments MACRO RE-ENTRY
>2 segments
MACRO RE-ENTRY

Activation compatible with :

• Perimitral macro re-entry

• Roof dependant macro re-entry

• Peritricuspid macro re-entry More complex macro re-entry

Case 7

31

I 29 30 II
I
29
30
II

V1

RFd

RFp

CS 1-2

CS 3-4

CS 5-6

CS 7-8

CS 9-10

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 frac- tionated electrograms with a gradient of activation between the proximal and distal bipoles (black arrows)

32

M. Haissaguerre

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

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

rhythm, local double potential visualized after ablation 27 28 I II 154 ms V1 RFd CS
27 28 I II 154 ms
27
28
I
II
154 ms

V1

RFd

CS 1-2

CS 3-4

CS 5-6

CS 7-8

CS 9-10

Case 7

33

Bibliography

Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological break - throughs from the left atrium to the pulmonary veins. Circulation.

2000;102:2463-2465.

Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long- lasting persistent atrial fibrillation: critical structures for termina- tion. J Cardiovasc Electrophys. 2005;16(11):1125-1137.

Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources main - taining 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 tachy - cardia 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 car- dioversions 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 isola- tion, 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

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 cath- eter was placed into the coronary sinus (CS) and demon- strated 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 activa- tion was determined by moving the ablation catheter sequen- tially in the anterior LA (Fig. 8.1, panel A, low anterior; and

A I B C D I I I II II II II V1 V1 V1
A
I
B
C
D
I
I
I
II
II
II
II
V1
V1
V1
V1
Abl
Abl
Abl
Abl
CS
CS
CS
CS
B
C
D
A

Fig. 8.1 Location of different recordings in the anterior and posterior left atrium, high and low

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

35

36

M. Haissaguerre

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 aris- ing in the context of catheter ablation of AF, the following definitions are employed: macro re-entry is defined as a cir- cuit 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 auto- maticity, 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 con - text of prior AF ablation (Fig. 8.2). After confirmation of PVI, it consists of

1. Assessment of AT cycle length variability: if >15%, sug - gestive 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)

CL Irregularity Yes No >15% Focal Focal or macroreentry Map earliest region Activation compatible with:
CL Irregularity
Yes
No
>15%
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 likeli- hood 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 evalu- ate 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 roof- dependent 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 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.

Case 8

37

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)

within red rectangles ) spanning the entire CL ( pink bars ) I II V1 CS
I II V1 CS
I
II
V1
CS

Post 1

Post 2

Post 3

A I II V1 0.05 mV Abl CS 18 B 19 20 21 I II
A
I
II
V1
0.05 mV
Abl
CS
18
B
19
20
21
I
II
V1
CS 1-2
CS 3-4
CS 5-6
CS 7-8
CS 9-10

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 pos- terior wall

38

M. Haissaguerre

Bibliography

Haïssaguerre M, Shah DC, Jaïs P, et al. Electrophysiological break - throughs from the left atrium to the pulmonary veins. Circulation.

2000;102:2463-2465.

Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long- lasting persistent atrial fibrillation: critical structures for termina- tion. J Cardiovasc Electrophys. 2005;16(11):1125-1137.

Haïssaguerre M, Hocini M, Sanders P, et al. Localized sources main - taining 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 tachy - cardia 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 hyperten- sion, left ventricular hypertrophy, and paroxysmal atrial fibril- lation (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 car- dioversion. 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 ejec- tion 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: adiaz@nohc.com

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

39

40

A. Diaz et al.

40 A. Diaz et al. Fig. 9.1 Lasso in the left superior pulmonary vein (LSPV) Fig.

Fig. 9.1 Lasso in the left superior pulmonary vein (LSPV)

al. Fig. 9.1 Lasso in the left superior pulmonary vein (LSPV) Fig. 9.2 Lasso in the

Fig. 9.2 Lasso in the right superior pulmonary vein (RSPV)

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. 10.110.3, 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. 10.410.8).

below the lower common pathway (see Figs. 10.4 – 10.8 ). Fig. 10.1 12-lead resting ECG

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

41

42

A. Rossillo et al.

A

42 A. Rossillo et al. A B Fig. 10.2 Panel A: 12-lead ECG taken during atrial

B

42 A. Rossillo et al. A B Fig. 10.2 Panel A: 12-lead ECG taken during atrial

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

43

Fig. 10.3 Intracardiac record- ings taken during the electro- physiology 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)

the distal bipolar recording of the mapping catheter (MC D) Fig. 10.4 The electroanatomical mapping of

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

(the red area in the LAO view). The orange tags show the area where it was

44

A. Rossillo et al.

44 A. Rossillo et al. Fig. 10.5 Electroanatomical mapping with CARTO: detailed remap of the area

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

tag shows the site of earliest activation during tachycardia, and the red tag shows where a

Case 10

45

Fig. 10.7 Intracardiac record- ings 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

appeared on the ablation catheter. Same display as that shown in Fig. 10.3. A atrium, V
appeared on the ablation catheter. Same display as that shown in Fig. 10.3. A atrium, V

46

A. Rossillo et al.

Bibliography

Chen SA, Chiang CE, Yang CJ, Cheng CC, et al. Sustained atrialtachy- cardia in adult patients. Electrophysiological characteristics, phar- macological 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 intrac- ardiac 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.

Lai LP, Lin GL, Chen TF, et al. Clinical electrophysiological character- istics 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 abla- tion of atrial tachycardias. Am Heart J. 1996;131:481-489. Tang CW, Scheinmann MM, Van Hare GF, et al. Use of P wave configu- ration 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 abla- tion 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

A 17-year-old male with a normal heart has an electrocardio-

gram (ECG) showing intermittent pre-excitation suggestive

of left free-wall accessory pathway (AP) and supraventricu-

lar tachycardia (SVT). The induced tachycardia is a narrow QRS regular tachy- cardia (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 suc- cessful ablation?

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

Case Discussion

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.

48

Y.Y. Lokhandwala et al.

I

II

III

AVR

AVL

AVF

V1

V2

V3

V4

V5

V6

2008021 10 mm/mV 25 mm/s
2008021
10 mm/mV 25 mm/s

Fig. 11.1 The electrocardiogram (ECG) shows induced tachycardia

Case 11

49

I

AVF

V1

V6

CS910

CS78

CS56

CS34

CS12

HISD

HISP

RFD

RFP

2008021 10 mm/mV 200 mm/s
2008021
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 echocar- diography. 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

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 termi- nating 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

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

A

B

C

pairs of the coronary sinus (His bundle) catheter A B C E. Buch ( * ),

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: ebuch@mednet.ucla.edu

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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E. Buch et al.

mapping of the right atrium (RA) showed large areas of low- voltage scar (colored gray in Fig. 12.2). Activation mapping revealed a macro-reentrant AT utilizing a channel in the lat - eral 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 scar- ring 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.

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

200 ms 0 ms −200 ms Conduction via Bachmann’s bundle CS catheter
200 ms
0 ms
−200 ms
Conduction via
Bachmann’s bundle
CS catheter

Reference

1. Roithinger FX, Cheng J, SippensGroenewegen A, et al. Use of elec- troanatomic mapping to delineate transseptal atrial conduction in humans. Circulation. 1999;100:1791-1797.

Case Summary

Case 13

Bradley P. Knight

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 ven- triculoatrial (VA) interval associated with the first beat of the tachycardia is nearly identical to the remaining VA intervals. Can atrial tachycardia be excluded?

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

is “VA linking.” This observation strongly suggests that the atrial depolarization is dependent on the ventricular depolar- ization, meaning that the atrial rhythm is dependent on VA conduction. This should not be present with an atrial tachy- cardia, because the first beat of the tachycardia should have no relationship to the prior QRS, which was a result of con- duction of the atrial extrastimulus to the ventricle. This observation can be useful, but it is important to rec- ognize 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.

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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B.P. Knight

I ARRHYTHMIA INDUCTION RA_d S1 = 550 S2 = 340 PRINT REVIEW FIT II 190
I
ARRHYTHMIA INDUCTION RA_d S1 = 550 S2 = 340
PRINT REVIEW FIT
II
190
360
190
550
550
420
360
350
380
360
V1
V6
HRA p
550
550
340
1520
360
ABL d
ABL m
ABL p
RVA p
540
550
550
400
370
730
360
Stim
550
550
550
340
University of Chicago

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

55

PRINT REVIEW FIT I II 610 610 610 440 410 400 410 490 V1 V6
PRINT REVIEW FIT
I
II
610
610
610
440
410
400
410
490
V1
V6
HRA p
610
610
300
790
370
360
370
ABL d
ABL m
ABL p
RVA p
620
610
600
430
420
390
400
Stim
University of Chicago

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 com- plexes 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 accel- erates 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 antero- grade activation from the next beat, causing narrow QRS morphology. 1 The narrow complex tachycardia (Fig. 14.2) has an incom- plete 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 ventricu- lar 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 inser- tion 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.

58

M.E. Mortada et al.

58 M.E. Mortada et al. Fig. 14.1 The patient’s palpitations were captured with this 12-lead ECG

Fig. 14.1 The patient’s palpitations were captured with this 12-lead ECG

patient’s palpitations were captured with this 12-lead ECG Fig. 14.2 The same tachycardia was induced in

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

59

Case 14 59 Fig. 14.3 Tracing of patient’s response to ventricular programmed stimulation with one ventricular

Fig. 14.3 Tracing of patient’s response to ventricular programmed stimulation with one ventricular extrastimuli. The recording in this fig- ure and other figures are (from top to bottom): surface ECG with leads I, II and V1, high right atrial recording, proximal coronary sinus (CS

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

middle His; HISd, distal His, RVa: apical right ventricle Fig. 14.4 Tracing demonstrating the initiation of

Fig. 14.4 Tracing demonstrating the initiation of the tachycardia with atrial programmed stimulation

60

M.E. Mortada et al.

60 M.E. Mortada et al. Fig. 14.5 Two ventricular extrastimuli during the tachycardia Fig. 14.6 Three

Fig. 14.5 Two ventricular extrastimuli during the tachycardia

14.5 Two ventricular extrastimuli during the tachycardia Fig. 14.6 Three ventricular extrastimuli during the

Fig. 14.6 Three ventricular extrastimuli during the tachycardia

Case 14

61

One extrastimuli from the high right atrium (HRA) induced tachycardia with right bundle branch block mor- phology 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 fas- cicular 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 refrac- toriness 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 tachy- cardia. 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.

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 ven- tricular 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 tachycar- dia 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 cir- cuits. Circulation 1985;71:254-265.

2. Rordorf R, Vicentini A, Petracci B, Landolina M. Intermittent rate- dependent 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 atrio- ventricular 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

A 75-year-old male with history of orthotopic heart trans-

plantation 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 evi- dence of transplant coronary artery vasculpathy or acute rejection. What is the most likely mechanism of atrial flutter

in this patient?

Case Discussion

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 occur- ring 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: ebuch@mednet.ucla.edu

A. Natale et al. (eds.), Cardiac Electrophysiology,

DOI: 10.1007/978-1-84996-390-9_15, © Springer-Verlag London Limited 2011

63

64

E. Buch et al.

A
A

B

64 E. Buch et al. A B Fig. 15.1 ( Panel A ) Activation map: this

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 lat- eral 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

The patient is a 27-year-old women with a history of palpita- tions. No heart disease was documented. Event recorder documented sustained SVT. Examine Figs. 16.116.3. What are the likely possibilities?

Case Discussion

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 dur- ing 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. 16.416.6).

AP was successfully ablated (Figs. 16.4 – 16.6 ). Fig. 16.1 Twelve-lead resting ECG (paper speed

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

65

66

A. Rossillo et al.

66 A. Rossillo et al. Fig. 16.2 Twelve-lead ECG taken during SVT (paper speed 25 mm/s)

Fig. 16.2 Twelve-lead ECG taken during SVT (paper speed 25 mm/s)

16.2 Twelve-lead ECG taken during SVT (paper speed 25 mm/s) Fig. 16.3 Intracardiac recordings taken during

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

Case 16

67

Case 16 67 Fig. 16.4 Intracardiac recordings taken during RF energy delivery (paper speed 100 mm/s).

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

of the tachycardia. A atrium, V ventricle, H His Fig. 16.5 Intracardiac recordings taken during RF

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

68

A. Rossillo et al.

68 A. Rossillo et al. Fig. 16.6 Intracardiac recordings (paper speed 100 mm/s) taken during programmed

Fig. 16.6 Intracardiac recordings (paper speed 100 mm/s) taken during programmed ventricular stimulation showing the absence of VA conduc- tion (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 syn- drome. 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 acces- sory 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, midsep- tal 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 proce-

dure for recurrent left atrial tachycardia (AT). A prior attempt

at ablation was unsuccessful. After transeptal catheteriza-

tion, an electroanatomic map of the left atrium (LA) and left atrial appendage (LAA) was created during AT. The mecha- nism 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

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 activa- tion 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 radiof- requency current was delivered. The tachycardia terminated and was noninducible. Advanced computerized three-dimensional (3D) map- ping systems have greatly improved the ability to tackle

B.P. Knight Division of Cardiology, Northwestern Medical Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611

Center, 676 N. St. Clair, Suite 600, Chicago, IL 60611 Fig. 17.1 Fluoroscopic view during ablation

Fig. 17.1 Fluoroscopic view during ablation of a left atrial appendage tachycardia. The view is left anterior oblique. A coronary sinus elec- trode 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

complex tachycardias. However, it is important to recog- nize the limitations of such systems, and to occasionally confirm the findings using conventional mapping tech- niques. In this case, the complex structure of the LAA and its trabeculations proved to be a challenge for the electro- anatomic contact mapping system to reconstruct the cham- ber accurately enough to provide a clear ablation target. The circular mapping catheter may have also distended the appendage and moved trabeculations that may have inter- fered with localization.

70

B.P. Knight

70 B.P. Knight Fig. 17.2 This tracing was recorded during ablation of a left atrial appendage

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,

20-electrode circular mapping catheter positioned in the appendage, and the octapolar electrode catheter placed in the coronary sinus. Note termi- nation of the atrial tachycardia during delivery of radiofrequency current

Case 18

Antonio Rossillo, Sakis Themistoclakis, Aldo Bonso, Andrea Corrado, and Antonio Raviele

Case Summary

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?

Case Discussion

Although the patient is elderly, the ECG shows a regular nar- row 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. 18.318.16).

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

80 bpm a short PR interval (102 ms) and a QRS width of 80 ms A.

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

71

72

A. Rossillo et al.

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, interme- diate = 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

sinus), and the distal bipolar recording of the mapping catheter (MC D). A atrium, V ventricle,
sinus), and the distal bipolar recording of the mapping catheter (MC D). A atrium, V ventricle,

Case 18

73

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

a

AVN RT Stim A2

Mestre Studio

SAP100

S: 36: 45: 408

200 mm/s 100 ms 1–1 2–avF 198 ms 3–V1 4–V6 5–hRA V 6–His D A
200 mm/s
100 ms
1–1
2–avF
198 ms
3–V1
4–V6
5–hRA
V
6–His D
A
H
7–His I
8–His P
9–CS Prox
10–CS dist
11–MC D B1
15–STIM A2
S1
S2

b

AVN RT Stim A2

Mestre Studio

jump

S: 36: 58: 779

1–1 200 mm/s 100 ms 2–avF 3–V1 307 ms 4–V6 5–hRA V 6–His D A
1–1
200
mm/s
100 ms
2–avF
3–V1
307 ms
4–V6
5–hRA
V
6–His D
A
H
7–His I
8–His P
9–CS Prox
10–CS dist
11–MC D B1
15–STIM A2
S2
S1

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A. Rossillo et al.

Fig. 18.5 Intracardiac record- ings 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

ERP with a coupling interval of 200 ms. Same display as that shown in Fig. 18.3.
ERP with a coupling interval of 200 ms. Same display as that shown in Fig. 18.3.

Case 18

75

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

induction of AVNRT (cycle length 300 ms). Same display as shown in Fig. 1.19.3. A atrium,
induction of AVNRT (cycle length 300 ms). Same display as shown in Fig. 1.19.3. A atrium,

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A. Rossillo et al.

Fig. 18.9 Intracardiac record- ings (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

region of Koch’s triangle with a stim-H interval of 81 ms. St pacing, A atrium, V
region of Koch’s triangle with a stim-H interval of 81 ms. St pacing, A atrium, V

Case 18

77

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.