The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 2020934193, 9781942909415, 9781942909477

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THE ORIGINS OF

Ventricular Arrhythmias Using the ECG as a Key Tool for Localization

VOLUME 2

Frank M. Bogun, MD, FACC Professor of Internal Medicine Section of Cardiac Electrophysiology Division of Cardiovascular Medicine University of Michigan Ann Arbor, Michigan

B cardiotext. PUBLISHING

Minneapolis, Minnesota

© 2020 Frank M. Bogun Cardiotext Publishing, LLC 3405 W. 44th Street Minneapolis, Minnesota 55410 USA www.cardiotextpublishing.com Any updates to this book may be found at: www.cardiotextpublishing.com/electrophysiology-heart-rhythm-mgmt/ the-origins-of-ventricular-arrhythmias-v2 Comments, inquiries, and requests for bulk sales can be directed to the publisher at: [email protected]. All rights reserved. No part of this book may be reproduced in any form or by any means without the prior permission of the publisher. All trademarks, service marks, and trade names used herein are the property of their respective owners and are used only to identify the products or services of those owners. This book is intended for educational purposes and to further general scientific and medical knowledge, research, and understanding of the conditions and associated treatments discussed herein. This book is not intended to serve as and should not be relied upon as recommending or promoting any specific diagnosis or method of treatment for a particular condition or a particular patient. It is the reader's responsibility to determine the proper steps for diagnosis and the proper course of treatment for any condition or patient, including suitable and appropriate tests, medications or medical devices to be used for or in conjunction with any diagnosis or treatment. Due to ongoing research, discoveries, modifications to medicines, equipment and devices, and changes in government regulations, the information contained in this book may not reflect the latest standards, developments, guidelines, regulations, products or devices in the field. Readers are responsible for keeping up to date with the latest developments and are urged to review the latest instructions and warnings for any medicine, equipment or medical device. Readers should consult with a specialist or contact the vendor of any medicine or medical device where appropriate. Except for the publisher's website associated with this work, the publisher is not affiliated with and does not sponsor or endorse any websites, organizations or other sources of information referred to herein. The publisher and the author specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the contents of this book. Unless otherwise stated, all figures and tables in this book are used courtesy of the authors. Library of Congress Control Number: 2020934193 lSBN: 978-1-942909-41-5 eISBN: 978-1-942909-47-7 Printed in Canada

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25 24 23 22 21 20

To Claire, Max, and Lulu.

PREFACE

The first volume of these books highlighted the value of the 12-lead ECG for the localization of sites of origin or exit sites of ventricular arrhythmias. My intent was to make electrophysiology fellows in training aware of certain ECG patterns that may help to localize the origin of arrhythmias. For this second volume, I chose to also emphasize the anatomic relationship of arrhythmia origins. Therefore, the tracings are complemented by cardiac magnetic resonance imaging and realtime echocardiographic data, in order to help visualize the actual location of ablation target sites for each case. The value of appropriate imaging in addition to the 12-lead ECG is highlighted throughout. Many of these cases were challenging; the patients had failed ablation procedures elsewhere, and therefore the approach taken by the operator to reach a particular area may be of particular interest to the reader. I hope that this book will aid in the understanding of the localizing value of the 12-lead ECG for ventricular arrhythmias, which is key for successfully targeting these arrhythmias using catheter ablation.

This book presents the cases as a series of "unknowns." For the reader interested in reviewing a specific type of case, or the answers to the questions, please note that there is an appendix provided at the end of the book that identifies the origin of the VT or PVC.

• vii

ABBREVIATIONS

AMC Ao

ASD

AVI BBRVT CMP CMR CVS EAM EF

EGM GCV HPS

HRA IA IHD LAD

LBBB LBBBIA LM LVEF

LVOT MA MB MCV MVA NICM NSVT NYHA class PA PAP

PVC RBBB RF

RVA RVOT S-QRS

aortomitral continuity aortic atrial septa! defect anterior interventricular vein bundle branch reentry VT cardiomyopathy cardiac magnetic resonance imaging coronary venous system electroanatomic map ejection fraction electrogram great cardiac vein His-Purkinje fiber system high right atrium inferior axis ischemic heart disease left anterior descending artery left bundle branch block left bundle branch block inferior axis left main coronary artery left ventricular ejection fraction left ventricular outflow tract mitral annulus/annular moderator band middle cardiac vein mitral valve annulus nonischemic cardiomyopathy nonsustained VT New York Heart Association functional class pulmonary artery, pulmonic annulus papillary muscle premature ventricular complex right bundle branch block radiofrequency right ventricular apex right ventricular outflow tract stimulus-QRS interval

• ix

SA

sv TVA VA

supenor axis sinus ofValsalva tricuspid valve annulus ventricular arrhythmia

GLOSSARY Pace mapping: Pacing from the catheter tip of the mapping catheter aiming to replicate the morphology of a targeted ventricular arrhythmia. For reentrant VTs, a matching pace map indicates an exit site and for idiopathic VAs or focal arrhythmias, it indicates the site of origin.

x •

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

CASE

1 CLINICAL HISTORY A 58-year-old man presented with frequent premature ventricular complexes (PVCs). His PVC burden was 22% and his left ventricular ejection :fraction (LVEF) was 45%. Cardiac magnetic resonance imaging (CMR) showed an intramural scar in the anterobasal septum. His PVCs are shown in Figure 1-1. He also had easily inducible VT with the morphology shown in Figure 1-2.

Questions What is the origin of the PVCs and the VT? What should be done about the VT?

Figure 1-1

I

aVR

Vl

V4

II

aVL

V2

vs

III

a VP

V3

V6

A 12-lead ECG of PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 1

x

avtt

Vl

V4

II

aVL

V2

VS

VJ

V6

XII

II

Figure 1·2 A 12-lead ECG of induced VT.

Answer The PVCs as well as the VT were intramural in origin. The exit site of the PVC was targeted in the anterior basal LV. There was no matching pace map at the site with the earliest activation time. Characteristics suggesting a basal origin include the positive concordance in the precordial leads. There is a qR complex in V1 that suggests an origin in the aortomitral continuity (AMC). indicating that the initial vector goes away from lead V1, which is typical for this origin. However, other characteristics support a different origin: r wave in lead aVL and large R in I as well as relatively narrow QRS support an origin closer to the conduction system. The qR pattern is specific1 but not sensitive2·3 for an origin in the aortomitral continuity. The effective ablation site fur the PVC was located at the AMC and coincided with the site of earliest site of activation. The VT in comparison originates or exits from a more superior and more leftward position: inferior axis, positive R-wave concordance, R-wave amplitude in inferior leads higher, aVL more negative, R wave in lead III more positive. For the VT there were matching pace maps in the left sinus ofValsalva (LSV) (shorter S-QRS interval, but still relatively long S-QRS interval) and just below the LSV (long S-QRS interval, Figures 1-3 and 1-4). The intramural origin of the VT is based on the observation that a short

2 • The Origins of Ventricular A"hythmias: Using the ECG as a Key Tool for localization, Volume 2

matching S-QRS was not obtained, the S-QRS intervals were all relatively long: 85 ms for the LSV and 130 ms below the LSV. The exit was not identified, the matching pace maps with long S-QRS interval indicate capture of tissue remote to the exit. The intramural scar in this region extending to the aortic valve supports an intramural origin. Ablation at the sites with matching pace maps did render the VT noninducible. An ICD was implanted the following day. Patients with frequent PVCs and scar tissue should have programmed stimulation for risk stratification and in the presence of inducible VT, even in the absence of a history of VT, should undergo ICD implantation because of high VT recurrence rates in the setting of inducible VTs in the presence of scarring.4•5

Induced VT

Pacing in LSV

Pacing below LSV in LVOT

~-_........-~

Figure 1-3 Left panel: A 12-lead ECG of inducible VT. Mlddle panel: Pace mapping morphology when pacing is performed from the aortic aspect of the left sinus of Valsalva (LSV). There is matdl with the VT morphology. Note the relatively long stimulus-QRS interval of 85 ms. Right panel: Pace map performed from the ventricular aspect of the LSV. The S-QRS interval is long with 130 ms. There is a matching pace map with the inducible VT.

Case 1 • 3

Figure 1·4 Left panel: 30 reconstruction of echocardiographic contours (green) of the left ventricle from an anterior view showing the aortic (Ao) valve and the left ventricular apex. The catheter location where the PVC was eliminated is shown (arrow). Middle panel: 30 reconstruction of echocardiographic contours (green) of the left ventricle from an anterior view showing the AV and the left ventricular apex. The catheter location where pace mapping was performed (Figure 1·3) is shown. Right panel: 30 reconstl'\lction of echocardiographic contours (green) of the left ventricle from an anterior view showing the AV and the left ventricular apex. The catheter location where pace mapping was performed (Figure 1-3) is shown.

REFERENCES 1. Dixit S, Gerstenfeld EP, Lin D, et al. Identification of distinct electrocardiographic patterns from the ba.W left ventricle: Distinguishing medial and lateral sites of origin in patients with idiopathic ventricular tachycardia. Heart Rhythm. 2005;2(5):485-491. 2. Kuma.gai K, Fukuda K, Wakayama Y, et al El.e III indicates a more lateral origin, inferior leads II and aVF without r wave indicate an inferior origin; taken together: inferolateral tricuspid valve annulus (TVA). There were similar pace maps to the VT morphology (Figures 5-2 and 5-3) identified where ablation was carried out. The patient was noninducible after the ablation procedure. An echocardiographic image shows the proximity of the bioprosthetic valve and the ablation site (Figure 5-4).

I II

I II

III aVR

III

aVL aVF VI V2 V3 V4

aVR aVL aVF Vl V2 V3 V4

vs

vs

V6

V6

Figure 5·2 Left panel: A 12-lead ECG of the induced VT. Right panel: The pace map at the lateral tricuspid valve annulus.

20 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 5-3 Left panel: Electroanatomic voltage map of the right ventricle showing the tricuspid valve annulus (TVA} with the bioprosthetic tricuspid valve (BV} and the pulmonic valve annulus. The catheter location at the site with the best pace map is indicated (arrow). Right panel: 30 reconstruction of CMR contours of the right ventricle and the scar in the right ventricle (yellow}.

CASE 5 • 21

Figure 5-4 lntracardiac echo showing the bioprosthetic valve (BV) and the ablation catheter (arrow) where ablation was performed.

REFERENCES 1. Obioha-Ngwu 0, Milliez P, Richardson A, Pittuo M, Josephson ME. Ventricular tachycardia in Ebstein's anomaly.

Circulation. 2001;104(18):E92-E94. 2. Warnes CA. Adult congenital. heart disease importance of the right ventricle.] Am Colt Cardiol. 2009;54(21):1903-1910.

22 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

CASE

6 CLINICAL HISTORY An 82-year-old patient presented with frequent symptomatic PVCs (Figure 6-1) and left ventricular dilatation. The PVC burden was 16%, the ejection fraction (EF) was 60%. The patient had mitral valve prolapse.

Question Where does the PVC originate from?

Jy---

-~-.---"\...-

/!\...

_,.. -"'r·

\,-J a VP

III

-·

""-- -...r'

__ '""'-- r'-

vs

V2

aVL

II

V3

,

VJ

j

· ( ·,·~

.

I

Jv

-Jl

V6

~ ~J---"--1\~- J.~

Figure 6-1 A 12·1ead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 23

Answer The origin is the inferior mitral annulus. The differential is an origin of the posteromedial papillary muscle (PAP) vs. the inferior mitral annulus. Sometimes these two origins are impossible to distinguish. PAP origins usually do not have positive concordance and have an R/S transition in lead V3 or V41•2; a transition in V6 is unusual for a PAP origin but is possible if the PAP inserts into the mitral annulus or close to the mitral annulus. An origin from the posterior mitral annulus is not frequently seen and positive concordance may not universally be present as one might expect. This may be due to tilting of the mitral valve annulus, bringing the posterior part closer to the apex compared to the anterior part of the mitral annulus. In this patient we started mapping the posteromedial PAP and then went posterior to the annulus where the earliest site with -26 ms (Figures 6-2 and 6-3) was identified; radiofrequency (RF) ablation there eliminated this PVC.

I II

I II

m

m

aVR

aVR

aVL

aVL

aVF

aVF

Vl

Vl

V2

V2

V3

V3

V4

V4

V5

V5

V6

V6

Mapd

Mapd

Figure 6-2 Left panel: lntracardiac recordings from the posterior mitral valve annulus at the earliest site (Map d).Activation time is -26 ms. Right panel: The pace map at this site matched the isolated PVC morphology.

24 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 6-3 30 reconstruction of echocardiographic contours of the left ventricle from a posterior view showing the aortic valve (AV), the mitral valve annulus (MVA), and a superimposed transparent activation map. The catheter location where the earliest site of the PVC was mapped to is indicated by an arrow.

REFERENCES 1. Good E, Desjardins B,Jongna:ra.ngsin K, et al. Ventri.cular arrhythmias originating from a papillary muscle in patients without prior infarction: A comparison with &scicular arrhythmias. Heart Rhythm. 2008;5(11):1530-1507. 2. Al'Aref SJ, Ip JB, Markowitz SM, et al. Differentiation of papillary miucle &om fucicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Citt Arrhythm Blectrophysicl. 2015;8(3):616-624.

CASE 6 • 25

CASE

7 CLINICAL HISTORY The patient was a 51-year-old man with a history of ischemic cardiomyopathy with an ejection fraction (EF) of 15% and recurrent ICD therapies. The arrhythmia shown was inducible in addition to seven other inducible VTs.

Questions What is the mechanism of this arrhythmia? Where is the origin?

aVR

Vl

V4

II

aVL

V2

vs

XII

a VF

V3

V6

Figure 7-1 A 12-lead ECG of the patient's broad QRS tachycardia.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 27

Answer The origin is bundle branch reentry tachycardia (BBRVT). It shows a typical LBBB with a sharp initial component indicating involvement of the specialized conduction system (Figure 7-1). The patient had an identical QRS morphology during sinus rhythm (Figure 7-2) at that time, indicating that activation during SR and VT is identical A supraventricular tachycardia needs to be included in the differential, of course. The patient's HV at baseline was 89 ms (Figure 7-3). During BBRVT it was 103 ms (Figure 7-4). The possibility of BBRVT as well as SVT should be considered, based on the SR ECG. Figure 7-4 confirms that there is AV block, and that changes in the HH intervals precede changes in the RR intervals. The RBB was ablated, and this VT was no longer seen. For each VT ablation procedure, one needs to make sure that BBRVT is not missed. In order not to miss this important diagnosis, one will need either a good His position (this is preferable, as in this case) or a catheter placed in the apical RV location. A post-pacing interval of:!:: 30 ms is compatible with BBRVT.1 It is important to follow this practice for all VT ablations, no matter what structural heart disease is present (dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM) or any other cardiomyopathy); BBRVT has been described even in Brugada syndrome.

I

aVR

Vl

v•

II

aVL

V2

vs

III

a VP

V3

V6

Figure 7·2 A 12·1ead ECG of the patient's sinus rhythm.

28 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

I II

~

~

III

Vl V6 HRA

His 1/2 His 2/3

RVA

~~\

~ -t--

,\--.t

~~

-1

~

I __,r~r \'I

.,.

'v'11

"(1'-'\ ~

I

~~~

·~

~\

I

n '!--\~

t

Figure 7-3 Surface lead recordings and intracardiac recordings from the high right atrium (HRA), the His bundle (His 1/2 and His 213), and the right ventricular apex (RVA} during sinus rhythm; the HV interval is prolonged and measures 89 ms.

CASE 7 • 29

I II ill

Vl V6 HRA His 112 His 2/3 His 3/4

RVA Figure 7·4 Surface lead recordings and intracardiac recordings from the high right atrium (HRA), the His bundle (His 1/2, His 213, His 3/4), and the right ventricular apex (RVA) during bundle branch reentry tachycardia; the HH intervals and RR intervals are indicated.

REFERENCE 1. Merino JL, Peinado R, Fernandez-Lozano I, Sobrino N, Sobrino JA. Transient entrainment of bundle-branch reentry by atrial and ventricular stimulation: Elucidation of the tachycardia mechanism through analysis of the aurfu:e ECG. Circulation. 1999;100(17):178-490.

30 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

CASE

8 CLINICAL HISTORY A 62-year-old man presented with frequent asymptomatic PVCs and a history of aortic valve replacement seven years earlier with a bioprosthesis. His PVC burden was 22% and his ejection fraction (EF) was 45% (Figure 8-1). He denied syncope or presyncope. A cardiac MRI showed a predominantly intramural scar.

Questions Where is the origin of the VT? What would be the next step after ablation of his ventricular arrhythmias?

I

aVR

II

III

a VP

V1

V4

V2

VS

V3

V6

~~~~~ Figure 8-1

A 12-lead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 31

Answer The origin is the intramural LVOT close to the conduction system. The qR in lead Vt suggests an origin close to the aortomitral continuity. The superior axis, however, indicates that the origin is not anterior but more likely in a posterior location. The sizable R wave in lead I and the R wave in aVL together with the relatively narrow QRS complex indicate an origin closer to the conduction system. Indeed, when pacing from a site 2-3 mm posterior to the His position (Figure 8-2 and Figure 8-3). a site with a matching pace map is identified. Note the long stimulus-QRS interval indicating that this is not the exit site but a site remote from the exit, which is likely located deeper, corresponding to a predominantly intramurally located scar. The patient had frequent PVCs at the onset of the ablation procedure. Programmed ventricular stimulation was performed for risk stratification because of the presence of scarring. We were able to induce four different monomorphic VTs, the present VT being one of them. We targeted both VTs and frequent PVCs. His PVCs as well as his VTs had intramural origins, and radiofrequency (RF) energy was guided by activation mapping and pace mapping. Postablation, his VTs were no longer inducible and the predominant PVC was not seen anymore. After the ablation, the patient underwent ICD implantation. He subsequently had antitachycardia pacing for one of the VTs. His EF normalized during follow up. Programmed ventricular stimulation is important for risk stratification in patients with structural heart disease, as illustrated in this case. Patients with inducible VT do have VT recurrences, as demonstrated in several reports, even though they may have preserved left ventricular function and no history of prior VT.1•2 ICD implantation should strongly be considered.

I II

I II

m

m

aVR aVL aVF

aVR aVL aVF

Vl V2

Vl V2

V3 V4 V5 V6

V3 V4 V5 V6

Figure 8·2 Left panel: A 12-lead ECG of the targeted VT. Right panel: The pace map at this site matched the induced VT. Note that there is a long stimulus-QRS interval measuring 180 ms.

32 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 8·3 30 reconstNction of echocardiographic contours of the left ventricle from a posterior view showing the aortic valve {AV), the mitral valve annulus (MVA}, and a superimposed voltage map. The catheter location with a matching pace map to the targeted VT (Figure 8-2) is indicated by an arrow. The pulmonic valve and tricuspid valve annulus (TVA} are also shown. Orange tags indicate the location of the bundle of His.

REFERENCES 1. Glunnam M, Siontu KC, Kim MH, et al. Risk stratification in patients with frequent premature ventricular complexes in the absence ofknown heart disease. Heart Rhythm. 2019. Epub ahead of print, September 30, 2019. 2. Yokobwa M, Siontis KC, Kim HM, et al. Value of cardiac magnetic resonance imaging and programmed ventricular stimulation in patients with frequent premature ventricular comple:ia:s undergoing radiofrequency ablation. Heart Rhythm. 2017;14(11):1695-1701.

CASE 8 • 33

CASE

9 CLINICAL HISTORY A 48-year-old man presented with cardiac sarcoidosis. CMR showed a predominantly right-sided scar. He had recurrent VT refractory to medical therapy.

Question Where does this VT (Figure 9-1) originate from?

II

\.,/\J\)'v \/\)\j \/

.. .,. '-

Ill

:...

aVR

Vl

Vt

aVL

V2

vs

·Jv' \)'' ' . '

......

v

•VI'

VJ

V6

" '· \)'i

Figure 9-1 A 12-lead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 35

Answer The origin is trabeculations connecting the RV septum with the RV free wall. LBBB IA suggests some location in the RVOT. However, the level in the RVOT is about where the His is located: Q in V1. tall R wave in lead I and R in aVL; i.e., the beginning of the RVOT rather than higher up in the RVOT. The origin was literally on the same level as the His, but 3-4 cm further anterior in the RV. The origin is not from the moderator band (MB) that also connects the RV septum with the RV anterior free wall, and the MB is more inferiorly located below the infundibulum or conus. MB arrhythmias, therefore, usually have a superior rather than an inferior axis,3 and indeed the moderator band was about 1-2 cm below these trabeculations. Because the moderator band contains the right bundle branch and the specialized conduction system, arrhythmias arising from there tend to have a narrower QRS width,3 and tend to have a more rapid onset-not as slurred as here (Figure 9-2). The origin is from one of the septa! bands constituting the myocardial muscle of the septum (in contradistinction to the parietal band that forms the myocardium of the posterolateral RV). The septal band is continuous with the moderator band, and also fans out into different individual bands that form trabeculations connecting the septum with the anterior free wall (Figure 9-3). The transition is expected to be relatively late, since the origin is not from the septum per se. The arrhythmia was difficult to target because the catheter kept slipping off the trabeculation. It was located in an area close to the border zone of the scar.

I

I

II

II

III

III

aVR

aVR

aVL

aVL

a VF Vl

aVF

V2

V2

Vl I

V3

V3

V4

V4

'l i

I

1,

V5

V5

V6

V6

t

t I

J

I

'

Figure 9-2 Left p1nel: A 12-lead ECG of the targeted VT. Right panel: The pace map at this site matched the induced VT.

36 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 9-3 Top Left panel: 30 reconstruction of echocardiographic contours of right and left ventsicles from an anterior view showing the RV apex and RVOT. Scar located in the Rl/OT based on CMR is colored in yellow. Interrupted llnes indicate a septa! muscle band on the anterior surface of the RV. Top right panel shows a voltage map of the right and left ventricles with low voltage in the RVOT COITesponding to scar location in the RVOT. The septa! myocardial bundle is indicated with intenupted lines; an arrow indicates the location of the ablation catheter at a site with matching pace maps with the targeted VT (Figure 9-2). The middle bottom panel shows the septa! band (Interrupted llnes) by intracardiac echocardiography.

CASE 9 • 37

CASE

10 CLINICAL HISTORY A 22-year-old woman presented with VT and presyncope after a failed ablation procedure at an outside hospital; she was referred for a repeat ablation (Figure 10-1). The right ventricular outflow tract was targeted during the ablation.

Questions Where is the site of origin of this VT? What precautions need to be taken? I

&VR

II

IU

&VF

Vl

V4

V2

vs

V3

V6

Figure 10·1 A 12-lead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 39

Answer The answer is an intramural focus between the LV epicardium and the left sinus of Valsalva (SV). The proximity to the left main (LM) coronary artery needs to be taken into consideration. The positive concordance with the inferior axis suggests an anterobasal origin. The early transition argues for a left-sided origin. There is a clear-cut pseudo-delta wave1 suggesting an epicardial focus that led us to investigate the great cardiac vein (GCV) first. This was indeed early (-25 ms) and the pace map was good but not perfect. (10/12, Figures 10-2 and Figure 10-3). Radiofrequency (RF) energy was delivered after the coronary artery was iajected and found to be at a safe distance. However, the patient experienced chest pain during RF energy delivery and the VT did not disappear. A transition in V1/V2 with a broad R wave (> 50% of the R wave, high R/S ratio in V1 or V2) is also compatible with an SV origin. 2 In the left SV, the timing was also early (-25 ms) but far-field appearing, and the pace map was worse compared to the epicardium (Figures 10-2 and 10-3). However, RF energy delivery there terminated the arrhythmia. Unfortunately, it came back a few minutes later. The LVOT was mapped next. The pseudo-delta wave as well as the initial isoelectric component of lead I argues against an endocardial origin. 3•4 Timing there was worse and the pace map did not match. RF energy delivery failed to eliminate the VT from the LV endocardium. When the catheter was moved higher in the left SV closer to the LM, early timing-but again far-field appearing-was reconfirmed (-15 ms) and a matching pace map was also observed (12/12), albeit with a long S-QRS interval (60 ms) indicating that the origin was remote to the site of mapping. RF energy delivery at this site permanently eliminated the VT. The site was at a distance of 11.9 mm from the left main coronary artery (Figure 10-4). Ablations have been reported at sites as close as 7.3 mm from the left main ostium.2 •5 The use of intracardiac echocardiography helps to determine the distance of the left main coronary artery from the ablation catheter. A coronary angiogram is often performed at the conclusion of the procedure to determine patency of the coronary arteries if ablation was performed in the SV.

40 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

VT

SV-low

MVA

GCV

SV-high

I

I

I

I

I

II

II

II

II

II

m

m

m

aVR

aVR

aVR

aVL

aVF

aVL aVF

a VF

Vl V2

Vl V2

Vl V2

V3 V4

V3 V4

V3 V4

V3 V4

V3 V4

V5 V6

V5 V6

V5 V6

V5 V6

V5 V6

m

Figure 10-2 Left panel: A 12-lead ECG of the targeted VT. Right panels: Pace maps from great cardiac vein (GCV), the mitral valve annulus (MVA), the lower left sinus of Valsalva (SV}, and the higher left SV.

Figure 10-3 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the GCV, MVA. left SV (LSV). the tricuspid valve annulus (TVA). and the pulmonary artery (PA). White arrows indicate the location of the catheter that is located in the GCV (left panel). the MVA (mlddle panel). and the LSV (right panel). An activation map of the GCV is shown,

other anatomic structures are in gray.

CASE 10 • 41

Figure 10·4 30 reconstruction of echocardiographic contours of the sinuses of Valsalva (gray} focusing on the left SV (orange). The location of the catheter generating the pace maps from the high vs. the low left SV is indicated with a white dot. The distance between the left main coronary artery (LM in purple) and the catheter ablation site is 11.8 mm. An activation map of the great cardiac vein (GCV) is shown.

REFERENCES 1. Berruezo A, Mont L, Nava S, Chueca E. Bartholomay E, BrugadaJ. Electrocardiographic recognition of the epicardial origin of ventricular tachycardias. Ciraflation. 2004;109:1842-1847. 2. Ouyang F. Fotuhi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia. originating from the aortic sinus cusp: el~trocardiographic characterization fOr guiding citheter ablation.] Am Coll Cardiol. 2002;39:500-508. 3. Valles E, Bazan V, Marc:hlinski FE. ECG criteria to identify epicardial ventricular tachycardia. in nonischemic cardiomyopathy. Circ AJTh:ythm Eledrophysiol. 2010;3:63-71. 4. Baz:m V, Gentenfcld EP, Garcia FC, et al. Site-specific twelve-lead ECG features to identify an cp:icardia.l origin fOr left ventricular tachycardia. in the absence of myocardial infarction. Hurt Rhythm. 2007;4:1403-1410. 5. Yamada T, McEldetty HT, Doppalapudi H, et al. Idiopathic ventricular arrhythmias originating from the aortic root prevalence, electrocardiographic and electrophysiologic characteristics, and results of radio&equency catheter ablation.] Am Coll Cardiol. 2008;52:139-147.

42 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

CASE

11 CLINICAL HISTORY A 68-year-old patient presented with ischemic heart disease (IHD) and frequent PVCs. PVCs were pleomorphic with one predominant PVC (Figure 11-1 and Figure 11-2). CMR showed an inferolateral scar.

Questions Where does the PVC originate? Is the PVC morphology typical for this site of origin? I

aVR

Vl

V4

II

aVL

V2

vs

III

a VP

V3

V6

Figure 11·1 A 12-lead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 43

I II ill

I II ill

aVR aVL aVF Vl V2 V3 V4 V5 V6

aVR aVL aVF Vl V2 V3 V4 V5 V6

Figure 11·2 Left panel: A 12-lead ECG of the targeted PVC. Right panel: Pace maps from the body of the anterolateral papillary muscle (AL PAP).

Answer The origin is the anterolateral papillary muscle (PAP). There is a rightward axis with a RBBB pattern, and in a patient without structural heart disease a PAP origin would be the most likely origin. However, there is scarring in the inferolateral LV, and this makes localization more challenging. Typically, an origin from the anterolateral PAP (AL PAP) has a rightward axis, and an origin from the posteromedial PAP (PM PAP) has a leftward axis.1 In the absence ofan infarct there are typically no Q waves. The insertion of the PAPs are responsible for axis and QRS morphology and typically the AL PAP inserts in the AL apical part of the left ventricle and the PM PAP in the inferoseptal apical left ventricle. In this patient with a prior inferior myocardial infarction resulting in an inferolateral scar, the Q waves in the inferior leads indicate that the activation goes away from the inferior wall, hence the PVC should originate from the inferior wall. Of note, the blood supply is dual for the AL PAP (first diagonal of left anterior descending and obtuse marginal from the circumflex artery) and therefore it is less frequently scaned after infarctions as compared to the PM PAP that has a single blood supply (either the right coronary artery or a posterolateral branch of the circumflex artery). In this particular patient as assessed with MRI, the scarring involved both PAPs, more so the PM PAP and about half of the AL PAP (Figure 11-3). The cardiac catheterization in this patient showed a small right circumflex artery and occlusion of the first. OM; the left anterior

44 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

descending artery (LAD) had no lesions. The AL PAP in part inserts into scarred tissue that extends to the lateral wall. Pacing on the part of the PAP that inserts into the AL wall generated a typical QRS-complex with a more prominent rightward axis without Q waves in the inferior leads, and pacing on the insertion of the AL PAP generated the same pace map as the PVC (Figure 11-2); pacing on the PAP inserting into the lateral wall matched with the PVC morphology with a longer S-QRS interval. Also, the PAPs do not insert like a single stalk into the ventricular free wall, but more like columns that are extensions of different trabeculations. This explains that there may be quite different morphologies which can be generated by pacing, depending on where on the PAP pacing is performed. Radiofrequency (RF) ablation at the insertion of the PAP failed to eliminate the arrhythmia; RF energy had to be delivered on the body of the PAP in order to eliminate the PVCs. We investigated the MRI pattern of post-infarction patients in whom VAs originate from the PAP muscles, and found that the PAPs of origin often had a heterogeneous pattern of delayed enhancement,2 similar to this patient. In summary, in the presence of scarring the typical morphology of a PAP arrhythmia is changed depending on the scar location. The overall axis most often still helps to determine the most likely PAP origin.

Figure 11·3 Top row: Short axis slices of cardiac MRI of the mid left ventricle. From right to left this figure shows slices from basal to an apical direction. An asterisk indicates the approximate catheter location where the pace map shown in Figure 11-2 was obtained. There is subendocardial delayed enhancement involving both AL PAP and posterolateral PAP. Bottom panel: 30 reconstruction of MRI contours of the left ventricle and the scar in the lateral wall (dense scar in orange and border zone scar in yellow}. The AL PAP is shown in white. An asterisk and an arrow indicate the approximate catheter location where the pace map shown in Figure 11·2 was obtained.

CASE 11 • 45

REFERENCES 1. Good E, Desjardins B, Jongnarangsin K, Oral H, Chugh A, Ebinger M, et al. Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: A comparison with fascicular arrhythmias. Heart Rhythm. 2008;5(11): 1530-1537. PubMed PMlD: 18984528. 2. Bogun F, Desjardins B, Crawford T, Good E, Jongnarangsin K, Oral H, et al. Post-infarction ventricular arrhythmias originating in papillary muscles.] Am Coll Cardiol. 2008;51(18):1794-802. PubMed PMID; 18452787.

46 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Too/ for localization, Volume 2

CASE

12 CLINICAL HISTORY The patient was a 62-year-old man with nonischemic cardiomyopathy and intramural scarring as well as aortic valve replacement with a bioprosthetic valve. The patient had frequent symptomatic PVCs (Figure 12-1).

Question Where does the PVC originate from? I

aVR

Vl

V4

II

aVL

V2

vs

III

a VF

V3

V6

Figure 12-1 A 12-lead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 47

Answer The origin is the intramural septa] left ventricular outflow tract (LVOT). There is a RBBB IA, indicating an outflow tract origin. This could be from the mitral annulus, the left ventricular outflow tract or the sinuses of Valsalva. Differentiation between these origins is not clear cut. Ouyang described ablation of LVOT arrhythmias using a transseptal approach.1 The majority did have a LBBB morphology. In their manuscript they identify three ECG criteria that are often present in failed LVOT arrhythmias, possibly indicating a deeper origin, or an origin from the epicardial left ventricular summit: aVL/aVR ratio > 1.4, lead III/II R-amplitude > 1.1, and PDI > 0.6 (interval of beginning QRS-to-Peak QRS/QRS width in the inferior leads).2- 4 All of these criteria are fulfilled here, and indeed the origin is intramural. This patient had replacement of the aortic valve with a porcine free style prosthesis. Mapping in the cusps showed sites with late activation timing in the right and in the left cusps, with far-field EGMs that were slightly presystolic and would not capture with pacing. Below the cusps on the septa! aspect of the LVOT, the earliest site had a farfield appearing electrogram (-15 ms) without matching pace map (Figure 12-2). The site was adjacent to the intramural scar that was located in the septa! aspect of the LVOT (Figure 12-3). Other mapping sites within the RVOT, PA as well as the CVS were late (positive intervals). R.adiofrequency (RF) ablation in the LVOT resulted in disappearance of this PVC. For intramural ventricular anhythmias, mapping the breakout sites helps to identify ablation target sites.

I

I

II

II

III

III

aVR aVL aVF Vl V2 V3 V4 V5 V6

aVR aVL aVF Vl V2 V3 V4 V5 V6

Abld Figure 12-2 Left panel: lntracardiac recordings from the septal left ventricular outflow (LVOT) tract at the earliest site (Abl d). Activation time is -15 ms. Right panel: The pace map at this site did not match with the isolated PVC morphology.

48 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 12-3 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the great cardiac vein (GCV), mitral valve annulus (MVA), aortic (Ao) valve, the tricuspid valve annulus (TVA), and the pulmonary artery (PA). White arrows indicate the location of the catheter located in the LVOT. Yellow arrows indicate the location of intramural scarring registered from the MRI.

REFERENCES 1. Ouyang F, Mathew S, Wu S, Kamioka M, Metzner A, Xue Y, et al. Ventricular atthytbmias aruing from the left ventricular outflow tr:act below the aortic sinus cusps: Mapping and catheter ablation via transseptal approach and electrocardiographic characteristics. Circ Anhythm Eluttophysiol. 2014;7(3):445-455. PubMed PMID: 24795340. 2. Yamada T, McElderry HT, Doppalapudi H, Murakami Y, Yoshida Y, Yoshida N, et al. Idiopathic ventricular arrhythmias originating from the aortic root prevalence, electrocardiographic and electrophysiologic characteristics, and results of radiofrequency catheter ablation.] Am Coll Cardiol. 2008;52(2):139-147. PubMed PMID: 18598894. 3. Ito S, Tada H, Naito S, Kurosaki K. Ueda M, Hoshizaki H, et al. Development and validation of an .ECG algorithm for identifying the optimal ab~ion site foridiopathic ventricular outflow tract tachycardia.] Cardiovasc Elemophysiol. 2003;14(12): 1280-6. PubMed PMID: 14678101. 4. Hachiya H, Hirao K, Sasaki T, Higuchi K, Hayashi T, Tanaka Y, et al. Novel ECG predictor of difficult caaes of outflow tract ventricular tachycardia: peak deflection index on an inferior lead. CircJ. 2010;74(2):256-261. PubMed PMID: 20009358.

CASE 12 • 49

CASE

13 CLINICAL HISTORY A 67-year-old man presented with ischemic cardiomyopathy and recurrent VT while on amiodarone. His ejection fraction (EF) was 42% with moderately reduced right ventricular function. The patient was status post-coronary artery bypass grafting and status post-MAZE procedure and atrial septa! defect (ASD) repair 11 years earlier. Figure 13-1 shows one of the inducible VTs in this patient.

Questions Where does the VT originate from? What is the mapping strategy? r

aVlt

rrr

a VF

Vl

V4

V2

V5

VJ

V6

~-~---~

Figure UM A 12·1ead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 51

Answer A left bundle branch block (LBBB) VT after myocardial infarction usually originates from the septum unless it is an idiopathic VT or the scar extends to the free wall of the right ventricle. In this patient, there is really no R wave in leads V1 and V2, making this a QS complex, and there are Q waves in leads II, III, and aVF, suggesting an inferoseptal origin. The question of right vs. left is important, and since it is a reentry circuit, there is a chance that some parts can be reached from either the right or the left side. Typically, in post-infarction patients, the left side is mapped first; in this patient there was a matching pace map in the basal septal LVOT about 1 cm below the bundle of His, but VT remained inducible despite multiple ablations in that area, and therefore RV mapping was performed. On the juxtaposed RV septum, matching pace maps were also found with the same S-QRS interval of 105 ms from either side of the septum (Figure 13-2). CMR revealed involvement of the inferobasal septum with transmural involvement and thinning (Figure 13-3), and radiofrequency (RF) energy was delivered from the RV side as well. It became apparent that the scar extended not just to the septum, but also the RV free wall, and that two VTs had their exit at the RV free wall (Figure 13-4). For post-MI VTs, RV mapping/ablation needs to be performed if LBBB VTs cannot be eliminated from the left ventricular septum.1 The fact of a matching pace map from both sides with relatively long and similar S-QRS intervals indicates that we are not capturing the exit but an area at a distance from the exit, and since they are almost identical pace maps from both sides of the septum, the exit is likely intramural. The scar on this level of the septum was transmural as shown in Figure 13-3. After ablation on both aspects of the septum the VT was no longer inducible. LV septum

VT

,_,,.,

RV septum

I

I

II

II

II

ill

III

III

aVR aVL aVF VI V2 V3 V4 V5 V6

aVR aVL aVF VI V2 V3 V4 V5 V6

aVR aVL aVF VI V2 V3 V4 V5 V6

I

Figure 13-2 Left panel: VT morphology. Mlddle panel: Pace map from the left interventsicular septum. Right panel: Pace map from the right interventricular septum.

52 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 13-3 CMR with short-axis view of the basal septum. White aJTows indicate the approximate location of the catheters where pacing was performed from the left and ride side of the septum.

CASE 13 • 53

Figure 13-4 30 re S complex in V6 indicates the more proximal origin in the crux (as in the patient here) vs. an R < S complex for a more apical origin. For more proximal septal epicardial VAs that can be reached via the coronary sinus (CS) and MCV, one has to be careful with respect to the coronary arteries, since their course can be dose to the veins. In this patient, the PVCs resulted in PVC-induced cardiomyopathy (CMP). An epicardial PVC origin predisposes patients to development of PVC-CMP more than any other location. After a rather long mapping procedure, eventually a site within the coronary venous system (CVS) was identified that preceded the onset of the PVC by 31 ms, and this was the effective site (Figure 19-2 and Figure 19-3). The more distal septa!, epicardial inferior wall arrhythmias need to be targeted via a subxiphoid epicardial approach. I II

I II

ill

m

aVR

aVR

I

II Ill a VR

Vl V2

aVL a VF Vl V2

V3

V3

V3

V4

V4

V5

V5 V6

aVL aVF Vl V2

V6

-

aVL

aVF

--......-'l'V'------~ 1 - - -

Figure 19-2 Left panel: A 12-lead ECG of the targeted PVC. Middle panel: Pace maps from middle cardiac vein (MCV). Right panel: A 12-lead ECG and intracardiac tracings from the mapping catheter (Map 1/2) of the site of origin within the MCV.

76 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 19-3 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the great cardiac vein (GCV), the mitral valve annulus (MVA), the aortic (Ao) valve, the tricuspid valve annulus (TVA). and the pulmonary artery (PA). A white arrow indicates the location of the catheter within the MCV.

REFERENCE 1. Kawamura. M, Gerstenfeld EP, Vedantham V, Rodrigues DM, Burkhardt JD, Kobayashi Y, et al. Idiopathic ventricular arrhythmia originating &om the cardiac crux or inferior septum: Bpicardial idiopathic ventricular arrhythmia. Cift: A,,hythm Eketrophysiol. 2014;7:1152-1158.

CASE 19 • 77

CASE

20 CLINICAL HISTORY The patient was a 69-year-old man with a history of symptomatic PVCs with a prior ablation at an outside hospital. The procedure failed to eliminate the targeted PVC (Figure 20-1), and apparently a steam pop occurred during the ablation, associated with a decrease in blood pressure and temporary elimination of PVCs; there was no pericardia} effusion present, and PVCs recurred with a lower PVC burden. Postablation, the patient remained symptomatic, his ejection fraction (EF) was 53%, and the PVC burden was 16%. His CMR showed endocardial delayed enhancement in the left basal interventricular septum.

Questions Where does the PVC originate from? What do you expect to encounter in a patient after a steam pop occurred?

III

aVR

Vl

v•

aVL

V2

vs

a VP

V3

V6

I

l

Figure 20·1 A 12·1ead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1·942909·41·5

• 79

Answer The origin was an intramural site in the basal inferoseptal area about 1 cm below the His. The proximity to the conduction system can be predicted by the relative narrow QRS complex. Other hints indicating a close proximity to the conduction system include the q in V1, large R-wave amplitude in lead V1, R wave in lead aVL, and early transition (V1). In contradistinction to a VA originating from the fascicular system, the QRS width is too broad (145 ms); furthermore, there are no small q waves in the lateral leads, and a positive concordance is usually not a characteristic of fascicular arrhythmias due to the insertion of the fascicular system closer to the apex. The superior axis points toward an inferoseptal origin. The answer for the second question can be quite variable, and depends on where the steam pop occurred and what force was generated during the steam pop. If this occurs during an ablation, it is prudent to check for an effusion since a perforation might have occurred. Often an effusion is not present, and the procedure can be continued. If the steam pop occurred during a prior procedure, imaging can help to identify the remnants of the steam pop, as in our case, and knowledge of the location can help the operator to be aware of the presence of wall thinning in order to avoid more steam pops if more radiofrequency (RF) energy needs to be delivered in this area. In this case, imaging data revealed that the steam pop most likely resulted in a relatively large area of wall thinning similar to an aneurysm (Figure 20-2). There is no definitive proof that indeed the aneurysm was caused by the steam pop, and an alternative possibility would be the presence of an idiopathic aneurysm, which is quite rare. A prior report described steam pops in computed tomography and showed a similar crater-like image after a steam pop, possibly due to an intramyocardial hematoma communicating with the ventricular cavity.1 This case further illustrates that one has to be vigilant when performing ablation procedures, even when the catheter is located at the interventricular septum where a perforation is unlikely to occur. This is further illustrated by a case report of a patient in whom a ventricular septal defect was caused after a steam pop occurred.2 Steam pops do not occur frequently, and in a series of 38 patients in whom > 4000 ablation lesions were delivered, steam pops occurred in 62 lesions (1.5%) and cardiac perforation in only 1 of these cases (2%). 3 The use of half normal saline increases the prevalence of steam pops and requires the operator to be attentive when ablation is performed with this irrigant. The activation time was equally early on the LV septum as compared to the RV septum (-55 ms, Figure 20-3), and there were no matching pace maps from either site (Figure 20-4). RF energy was delivered on the septa! aspect of the left ventricle first, and this eliminated the PVCs, which subsequently came back with a different morphology and RF energy was delivered also on the RV site, corresponding to the slow pathway location, resulting again in temporary elimination of PVCs and subsequent occurrence of yet a different morphology. This went back and forth a few more times with the breakout site getting closer and closer to the His bundle. Eventually the last RF lesion was delivered on the left a few millimeters next to the His and the PVCs did not come back thereafter (Figure 20-5). In this case, it was quite unusual that we encountered several intramural arrhythmias that were difficult to target given the close location of the conduction system; the relation to the aneurysmal transformation of the area where the steam pop occurred may have had a causal relationship.

80 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

Figure 20-2 Short-axis view of a cardiac MRI with delayed enhancement of the basal aspect of the heart showing a basal inferior aneurysm (orange •rrows}.

CASE 20 • 81

I II

II

ill

ill

aVR aVL

aVR aVL

aVF

aVF

VI V2 V3 V4 V5 V6

Vl V2 V3 V4 V5 V6

Map 1/2

Map 1/2

I

Figure 20-3 Left panel: A 12-lead ECG of the targeted PVC with intracardiac tracings (Map 1/2) from the ablation catheter located at the right ventricular septum. Right panel: A 12-lead ECG of the targeted PVC with intracardiac tracings (Map 1/2) from the ablation catheter located at the left ventricular septum.

I II ill

aVR aVL aVF Vl V2 V3 V4 V5 V6

:::J''

c:::=

~

I II

I II

ill

III

aVR aVL aVF VI V2 V3 V4 V5 V6

aVR aVL aVF VI V2 V3 V4 V5 V6

Figure 20-4 Left panel: A 12-lead ECG of the targeted PVC. Mlddle panel: Pace map at the right ventricular breakout site of the targeted PVC. Right panel: A 12-lead ECG pace map at the left ventricular breakout site of the targeted PVC.

82 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 20-5 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the mitral valve annulus (MVA}, the aortic (Ao} valve, the tricuspid valve annulus (TVA). the pulmonary artery (PA), and a superimposed biventricular activation map. A white arrow indicates the location of the catheter in the slow pathway area and a red arrow indicates the location of the ablation catheter in the left inferoseptal area.

REFERENCES 1. Cochet H, Sacher F, Chaumeil A. Ja1s P. Steam pop during radiofiequency ablation: Imaging matures on magnetic resonance imaging and multidetector computed tomography. Circ Arrbythm BlectrophyJiol. 2014;7:559-560. 2. Schonbauer R, Sommer P, Misfeld M, Dinov B. Fiedler L, Huo Y, et al. Relevant ventricular septa! defect caused by steam pop during ablation of premature ventricular contraction. Circuwtion. 2013;127:e843-844. 3. Seiler J, Robem-Thomson KC, Raymond JM, Vest], Delacretaz E, Stevenson WG. Steam pops during inigated radiofrequency ablation: Feasibility of impedance monitoring for prevention. Heart Rhythm. 2008;5:1411-1416.

CASE 20 • 83

CASE

21 CLINICAL HISTORY A 59-year-old man presented with a history of hypertension, psoriasis, and persistent atrial fibrillation status postablation. He underwent a PVC ablation for frequent pleomorphic PVCs 2 years earlier and his PVC burden decreased from 18% to 2%; however, over time his PVC burden increased back to 17% (Figure 21-1). A CMR showed an ejection fraction (EF) was 36% without scarring.

Question Where does the PVC originate? I

•Vil

Vl

V4

V2

vs

V3

V6

r

II

aVL

I

l III

a VP

r

Figure 21-1 A 12·1ead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909·41-5

• 85

Answer The origin is from the posterior aspect of the mitral valve annulus. The key features are the RBBB SA with prominent R waves in V1-V6, although there is no positive concordance which one would expect from the basal left ventricle. This, however, is not always the case, especially from the inferior annulus. The origin needs to be distinguished from the posteromedial papillary muscle (PAP). PAPs often have a q wave in V1, indicating activation going away from the septum, whereas this is usually not the case for mitral annular arrhythmias unless they come from the aortomitral continuity. That said, the QRS morphology otherwise may look similar and it might not be distinguishable from PAP origins. In this patient the transition is in lead V6; in PAP arrhythmias it is usually {but not always) earlier, i.e., in leads V4/VS. The transition depends on where the part of the PAPs generating the VAs insert into to ventricular myocardium-the closer to the mitral annulus, the later the transition-with positive concordance if they insert in the mitral annulus (infrequent). Finally, there are usually no q waves in the inferior leads in PAP arrhythmias. The Q waves in the inferior leads suggested an epicardial origin in the absence of significant scarring. Mapping in the middle cardiac vein (MCV); however, was late and when we mapped the mitral annulus, we had early timing (-29 ms) and a matching pace map (Figures 21-2, 21-3, and 21-4).

I

.., ""I"''. I 7

c=::··'

I

I" '.''"",. ·:

':;z:::::c

n ID aVR aVL

aVF VI V2 V3

V4

V5 V6 Map 1/2 Map 3/4 Figure 21·2 At the site of origin, the activation time precedes the QRS onset by 29 ms.

86 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

I

II ill

aVR aVL aVF

:::::=:71C

I

~

II ill

aVR aVL aVF

Vl V2

Vl V2

V3 V4 V5

V3 V4 V5

V6

-----1=

V6

Figure 21·3 Left panel: A 12·1ead ECG of the targeted PVC. Right panel: Pace map at the posterior mitral annulus showing a matching pace map.

Figure 21·4 30 reconstruction of echocardiographic contours of the left ventricle from a posterior view showing the mitral valve annulus (MVA) and the aortic (Ao) valve. A white anow indicates the location of the catheter at the posterior mitral annulus.

CASE 21 • 87

CASE

22 CLINICAL HISTORY A 54-year-old man presented with a history ofBrugada syndrome status post-single-chamber ICD implantation for primary prevention. He had recurrent sustained monomorphic VT resulting in ICD therapy. All the episodes were spontaneously terminated or successfully terminated with ATPs. He has never had an ICD shock, but becomes symptomatic with the VT episodes (palpitations, lightheadedness without syncope). A transthoracic echocardiogram showed normal right and left ventricular function and size. A preprocedural CMR showed inferobasal delayed enhancement.

Questions Where is the origin of the VT shown in Figure 22-1? What is the prevalence of monomorphic VTs as the clinical VT in patients with Brugada syndrome? Where do they usually originate? I

aVR

V1

V4

&VL

V2

VS

Figure 22-1 A 12-lead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 89

Answer The origin was the intramural, basolateral inferior left ventricular (LV) myocardium close to the mitral annulus. The patient has Brugada syndrome; monomorphic VTs are very rare in this patient population and account for only about 5% of their arrhythmias.1•2 In a series of patients with inducible VT, the most frequent origin were RVOT VTs, bundle branch reentry VT, or monomorphic VT after initiation oftherapy with quinidine or after extensive ablation procedures. Neither ofthose was the case here. Several family members of the patient also have a history of cardiomyopathy, suggesting a possible genetic etiology for his cardiomyopathy in addition to the SCN5A mutation. This patient had epicardial and intramural scar in the basal inferior left ventricle. Two of the four inducible monomorphic VTs originated from the scar. The other VTs originated from the RV. The origin of the VT was the intramural, basal, inferior LV close to the mitral annulus, where the intramural/epicardial scar was located. Pace maps form the coronary venous system (CVS) and the LV endocardium both equally matched with this VT, indicating an intramural origin (Figure 22-2). There was positive concordance, although the S wave in V6 is a bit deeper than the R wave in V6. The most likely origin is still the basal LV. Knowledge that there is a scar also helps to differentiate this area from sites that are located further away from the annulus. The Q waves in the inferior leads indicate an epicardial origin (in the absence of scarring) or a scar related endocardial origin (in case of a transmural scar), and based on the mapping data this turned out to be an intramural origin (Figures 22-3 and 22-4). The origin was more lateral than septa!.

I II

7"'VC7C::

LVendo

LVepi

I

I II

II

m

m

m

aVR aVL

aVR aVL

aVF VI

a VF VI

aVR aVL aVF

V2

V2

V2

V3

V3

V3

V4

V4

V4

V5

V5

V5

V6

V6

V6

VI

Figure 22·2 Left panel: A 12-lead ECG of the patient's VT. Middle panel: Pace map from the inferior basal left ventricular endocardium. Right panel: Pace map from the great cardiac vein. Both pace maps match with the targeted VT morphology.

90 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 22-3 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the mitral valve annulus (MVA), the aortic (Ao) valve, the tricuspid valve annulus (TVA), the pulmonary artery (PA), and a superimposed biventrirular voltage map. A white anow indicates the location of the ablation catheter. Left panel: Catheter located in the inferior mitral annulus. Right panel: Catheter located in the great cardiac vein.

CASE 22 • 91

Figure 22-4 30 reconstruction of the left lateral aspect of the left ventside, including coronary arteries, the phrenic nerve (green), the great cardiac vein (GCV), and the left ventricular apex with the left anterior descending artery (LAD) complemented with the CMR defined scar in the basolateral left ventricle (yellow). A white arrow indicates the approximate location of the VT origin.

REFERENCES 1. Rodriguez-Manero M, Sacher F, de Asmundis C, et al. Monomorphic ventricular tachycardia in patients with Brugada. syndrome: A multicenter retrospective study. Heart Rhythm. 2016;13:669-682. 2. Eckhardt LL. Monomorphic ventricular tachycardia in Brugada. syndrome: True-true but related? Heart Rhythm. 2016;13:683-685.

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CASE

23 CLINICAL HISTORY A 56-year-old man presented with a history of nonischem.ic cardiomyopathy (ejection fraction [EF] of 15%) and a history of hypertension, dyslipidemia, diabetes mellitus, and COPD. The patient had several failed prior VT ablation procedures. A CMR showed an intramural septa! scar. The patient presented for a repeat ablation procedure.

Questions Where does the VT shown in Figure 23-1 originate? What is a possible ablation strategy for this VT? I

Figure 23-1

Vl

V4

II

aVL

V2

VS

III

avr

V3

V6

A 12-lead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

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Answer The origin is the intramural septum. There is a left bundle branch block (LBBB) inferior axis morphology, with a transition in V5/V6 and notching in the inferior leads. The scarring located in the high intramural septum makes localization of the origin difficult. In a patient without structural heart disease, based on the above-mentioned features, the origin would be more in the lateral RVOT free wall. Although the best pace maps were located in the high septum just below the pulmonary artery (Figure 23-2), the stimulus-QRS interval was 80 ms and the pace map was only about 10/12, i.e., the exit was likely intramural where the scar was located in the CMR (Figure 23-3). It is not uncommon in patients with septal scar to have a late transition even though the exit is located on the septum.1 This is usually not seen in patients with idiopathic RVOT VTs, where the transition is earlier if the origin is on the septum. The case illustrates that in order to identify critical sites for intramural septa! VTs, the entire RV septum needs to be mapped. With respect to an ablation strategy, we could demonstrate that the success rate of ablation of intramural VTs depends on the depth of the intramural scar as it projects to the closest endocardial surface. The larger the projected scar surface (cut-off is > 16%) at a depth of> 5 mm, the less likely an ablation will be successful when using a conventional irrigated tip catheter for ablation. In case a conventional approach (targeting sites with abnormal electrograms, matching pace maps, sites with early activation or sites with concealed entrainment) fails to eliminate VT, a more extensive approach has been shown to be effective when both aspects of the intramural scar are targeted. 2

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94 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

Figure 23-3 Left panel: 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the mitral valve annulus (MVA}, the aortic (Ao) valve, the tricuspid valve annulus (TVA), the pulmonary artery (PA), and a superimposed biventricular voltage map. A white arrow indicates the location of the site of pace mapping from Figure 23-2. Right panel: Biventricular short-axis view of CMR showing intramural scarring: The top panel indicates a basal and the bottom panel a more apical view. The intramural scar is indicated with yellow arrows.

REFERENCES 1. Yokobwa M, Good E, Crawford T, et al. Value of right ventricular mapping in patients with postinfarction ventricular tachycardia. Heart Rliythm. 2012;9:938-942. 2. GhaDnam M, Siontis KC, Kim M, et al. Stepwise approach for ventricular tachycardia ablation in patients with predominantly intramural scar.JACC Clin Btearophysiol. 2020\Jan 29: [Epub ahead of print].

CASE 23 • 95

CASE

24 CLINICAL HISTORY The patient was a 57-year-old man with a history of ischemic cardiomyopathy status post-coronary artery bypass graft and an ejection fraction (EF) of 35%. He had several appropriate ICD shocks for polymorphic VT/VF. His ischemic work-up showed a chronically occluded left anterior descending artery (LAD) and right circumflex artery. His left internal mammary artery graft to the LAD was patent, also a saphenous vein graft to an obtuse marginal and the posterior descending artery were patent. A stress test showed a partially reversible defect in the LAD territory. The patient was not thought to be a candidate for opening of the chronically occluded vessels. A CMR showed transmural delayed enhancement in the mid-anterior wall and the anterior septum extending to the LV apex.

Questions The patient has frequent monomorphic PVCs that, at times, are associated with nonsustained and sustained polymorphic VT. Where does the PVC triggering polymorphic VT in Figures 24-1 and 24-2 originate from? What is the mapping strategy?

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 Cl 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 97

I II III

aVR aVL aVF

Vl V2

V3

V4 V5

V6

Figure 24·1 A 12·1ead ECG of the patient's polymorphic VT.

98 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2

I

171

II

aVL

III

a VP

V2

VS

176

Figure 24-2 A 12-lead ECG of the PVC that triggered polymorphic VT.

Answer The origin is the Purkinje fibers close to the posterior fascicle. The problem was to find the correct morphology ofV1 which is the key lead. On the 12-lead Holter monitor, lead V1 fell off (Figure 24-1). Luckily, in one of the patient's 12-lead ECGs a PVC was recorded showing the complete 12-lead morphology of his PVC (Figure 24-2). In the absence of lead V1, we would likely have misinterpreted the origin as an origin from the RV moderator band, which is an area that can also generate PVC-induced VF. One recording in this patient also existed on which there was an episode of polymorphic VT initiated by a LBBB PVC morphology; however, it turned out that lead V1 was incorrectly placed (it was placed at the typical location of V2: left parasternal fourth intercostal space). In a patient with frequent PVCs and VF, a 12-lead ECG with the triggering PVC morphologies is critical. One should always document the ECG in the presence of PVCs because they may disappear subsequently and make identification of the triggering arrhythmias difficult. The QRS width (Figure 24-1) is actually less than the paced-QRS width. indicating an origin dose to the conduction system. Based on the other leads from the 12-lead Holter, the beginning of the QRScomplex shows a rapid activation. The axis is superior, indicating proximity to the inferoseptum of the conduction system; i.e.• the posterior fascicle. In patients without apparent structural heart disease, VF is often triggered from the Purkinje fiber system; this has initially been demonstrated by Ha!ssaguerre et al.1•2 In patients with structural heart disease, Bansch et al. demonstrated the same for post-infarction patients.3 In the absence of PVCs, we would identify sites with Purkinje potentials and pace from there in order to correlate with the 12-lead morphology of documented triggering PVCs (Figure 24-3). In the absence of a CASE 24 • 99

documented 12-lead PVC, we would compare the ICD electrogram (EGM) morphology of the paced QRS complex with the ICD EGM morphology ofthe PVC triggering VT/VF episodes. This works only if the predetection electrograms are recorded (in some ICD manufacturers predetection EGMs are not recorded to save battery life). In this patient, we saw frequent PVCs only in the isoproterenol withdrawal phase, and they matched the ECG configuration from the 12-lead Holter combined with the 12-lead V1 morphology of the PVC with a RBBB configuration. This was the targeted PVC. It originated from the Purkinje fibers close to the posterior fascicle that was broadly targeted (Figure 24-4); postablation the 12-lead ECG changed to a posterior fascicular block pattern. During radiofrequency (RF) ablation, polymorphic VT/VF often occurs (Figure 24-5). and one needs to be prepared to cardiovert the patient. There was another PVC with a broader QRS and a similar overall morphology that originated from the insertion of the posteromedial PAP, which was also targeted. Subsequently, isoproterenol challenge and withdrawal did not show any further PVCs. However, if VF is triggered by different PVC morphologies, this strategy may not work. This was not the case in this patient, who had VF storm triggered by one or two morphologies. Recording of both fu and near-field ICD EGMs is beneficial to identify whether a single trigger is present, and also to target the triggering PVC based on the ICD EGMs:4

I

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aVL

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V3

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V4

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V5

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V6

V6

Figure 24-3 Left panel: A 12-lead ECG of the targeted PVC. Right panel: Pace map at the site of origin of the targeted PVC.

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Figure 24·4 Left panel: 30 reconstruction of echocardiographic contours of the left ventricle from a septa! view showing the aortic (Ao) valve. the apex. and a superimposed biventricular voltage map. A white arrow indicates the location of the catheter with the recordings displayed in Figure 24-3. Light blue dots indicate sites where Purkinje potentials were recorded. Dark red dots indicate ablation sites.

CASE 24 • 101

I II

m aVR aVL aVF Vl V2

V3 V4 V5 V6 Map 1/2

Figure 24-5 A 12-lead ECG of the polymorphic VT triggered by the patient's PVC. The intracardiac recordings were obtained at the site of origin of the PVC; a sharp Purkinje potential precedes the PVC (arrow).

REFERENCES 1. Hilssaguerre M, Shah DC, Ja!s P, Shoda M, Kautzner J, .Arentz T, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lanut. 2002;359:677-678. 2. Haissaguerre M, Shoda M, jais P, Nogami A, Shah DC, Kautzner J, et al. Mapping and ablation of idiopathic ventricular fibrillation. Cimdation. 2002;106: 962-967. 3. Bansc:h D, Oyang F, Antz M, Arentz T, Weber R, Val-Mejias JE, et al. Successful catheter ablation of electrical storm after myocardial infarction. Cinulation. 2003;108:3011-3016. 4. Lowery CM, Lewkowiez L, Sauer WH. Supraventricular tachycardia with atrioventricular block: What is the mechanism? HU11t Rhythm. 2010;7:1704-1705.

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CASE

25 CLINICAL HISTORY A 75-year-old woman presented with a history of atrial fibrillation, complete AV block status post-dual-chamber pacemaker implantation, status post-MAZE procedure in 2003, status post-biventricular-ICD upgrade for high RV pacing burden with reduced left ventricular ejection fraction (LVEF), and primary prevention for Lamin A/C mutation cardiomyopathy. She later developed recunent VT resulting in multiple ICD therapies. Her ejection fraction (EF) was 40% with global hypokinesis. A CMR was not performed because of a spinal stimulator. Figure 25-1 shows the induced clinical VT.

Questions Where is the site of origin? What is the mapping strategy? V4

Figure 25-1

II

&VL

V2

V5

III

&VP

V3

V6

A 12·1ead ECG of the patient's VT.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909·41-5

• 103

Answer The origin was (most likely) the basal left ventricular epicardium. The hints are the broad QRS complex with pseudo-delta wave and the QS pattern in lead 1.1•2 The mapping and ablation strategy was difficult because we did not have a CMR to indicate the precise location of scarring, and because the mid-distal coronary venous system (CVS) was occluded, most likely due to her prior MAZE procedure. The CVS was already occluded when the biventricular (BI-V) upgrade was performed and the left ventricular lead was placed in the middle cardiac vein proximal to the CVS occlusion. Mapping within the CVS would have been helpful to better indicate the exit of the epicardial VT. Furthermore, the basal LV endocardium showed mostly preserved bipolar voltage and there were no matching pace maps. The best pace map (Figure 25-2) was similar, but had a long stimulus-QRS interval, indicating that the exit site was at a distance from the pacing site. Unipolar voltage, however, indicated an area of decreased voltage in the anterobasal left ventricle.3 In the absence of a CMR, the use of unipolar voltage has been helpful to localize deeper-seated scaITing (Figure 25-3).4 Radiofrequency (RF) ablation was delivered in the area of the basal LV endocardium where there was low unipolar voltage, including the aortomitral continuity and basal mitral annular area, and the left aortic cusp where a similar pace map was found. Subsequently with programmed stimulation, VT was no longer inducible.

I II

I II

m

m

aVR aVL aVF Vl V2 V3 V4 V5 V6

aVR aVL aVF Vl V2 V3 V4 V5 V6 I

r

Figure 25-2 Left panel: A 12-lead ECG of the patient's VT. Right panel: Pace map from the anterior mitral annulus.

104 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

r

Figure 25-3 Left panel: 3D reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing Ute mitral valve annulus (MVA}, the aortic (Ao) valve, the tricuspid valve annulus (TVA), the pulmonary artery (PA), a superimposed biventricular voltage map (left panel), and unipolar voltage map (lfght panel). A white arrow indicates the location of the site of pace mapping from Figure 25-2.

REFERENCES 1. Berrue:io A, Mont L, Nava S, Chueca E, Bartholomay E, BrugadaJ. Electrocardiographic recognition of the epi.cudial origin of ventricular tachycardias. Circulalion. 2004;109:1842-1847. 2. Valles .B, Bazan V, Marchlinski FE. ECG criteria to identify epicardial ventricula.r tachycardia in noniscbemic cardiomyopathy. Cin Arrliythm Blectrophysiol. 2010;3:63-71. 3. Hutchinson MD, Gerstenfeld EP, Desjardins B, et al. Endocardial unipolar voltage mapping to detect cpicardial ventricular tachycardia substrate in patients with nonischemic left ventricular cardiomyopathy. Circ Arrhythm Euctrophysiol. 2011;4:49-55. 4. Desjardins B, Yokokawa M, Good E, et al. Characteristics of intramural scar in patients with nonischcmic cardiomyopathy and relation to intramural ventricular arrhythmias. Circ Arrliythm Electrophysiol. 2013;6:891-897.

CASE 25 • 105

CASE

26 CLINICAL HISTORY A 30-year-old man presented with systemic sclerosis, status post-sub-Q ICD implantation for primary prevention receiving multiple shocks for monomorophic VT. He had biventricular cardiomyopathy with a left ventricular ejection fraction (EF) of 30%. The patient had a CMR showing scarring in the RV free wall, the basal LV septum, the PAPs and the basal anterior LV free wall. The scar was subendocardial. The patient was not inducible for sustained VT. Figure 26-1 shows electrograms of the predominant clinical VTs (far-field recording from the sub-Q ICD) and a 12-lead ECG with programmed stimulation from the RV apex-inducing polymorphic nonsustained VT (NSVT). The tracing below shows the simultaneous recordings from the sub-Q ICD.

Questions Based on the available data, where would you map first given that no VT is inducible? Why?

1. RV free wall 2. LV septum 3. LV PAPs 4. Basal LV 5. Epicardium

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 Cl 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

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ICDVT-5

I II

m aVR aVL

ICDVT-7

V2

V4

V5 V6

Figure 26·1 Left insert top and bottom: Sub·Q ICD electrograms of the predominant clinical VTs (VT7 and VTS). Right panel: A 12-lead ECG with programmed stimulation from the RV apex-inducing polymorphic nonsustained VT. Bottom panel: Simultaneous recordings from the sub·Q ICD. Note that the QRS complexes during RV pacing (red arrows) are predominantly positive, whereas the triggered polymorphic VT has predominantly negative deflections (black arrow).

Answer The challenge in this case was where to start; the patient also had PVC-induced VF, but there was no single trigger, and the PVCs came from just about everywhere. Therefore, we wanted to predominantly target the VTs that were treated by the sub-Q ICD with shocks. The key observation was that RV pacing generates a positive deflection of the electrogram recorded by the sub-Q ICD. The resulting burst of polymorphic nsVT was all negative, and based on the 12-lead ECG, the NSVT originated from the left ventricle (all RBBB morphologies). Therefore, the ICD electrogram morphology generated by RV pacing looks closer to the ICD electrograms of the two predominant VTs compared to the polymorphic NSVT. Hence, starting on the right ventricular free wall would be the next step. The recording vector from the SQ-ICD was from the xiphoid part of the lead to the ICD can (B-to-can); therefore, everything originating from the right ventricle would be positive and arrhythmias originating from the left ventricle would be negative. Mapping of the right ventricle showed low voltage in the basal peri-tricuspid free wall and the area between the pulmonic valve and the tricuspid valve. Using pace mapping simultaneously with the sub-Q ICD recordings, we

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identified multiple matching areas (for three of the seven monomorphic VTs) and delivered radiofrequency (RF) energy in the matching areas (Figures 26-2 and 26-3) and sites with low voltage connecting the area between the pulmonic valve and the tricuspid valve annulus (Figure 26-4).

I II ill aVR aVL

aVF Vl V2 V3 V4 V5

V6 ICD VT-5

PM site 103

Figure 26·2 Top panel: Pace map from the posterobasal tricuspid valve annulus. Bottom panel left: sub·Q ICD tracings from clinical VTS. Bottom panel right: Tracings obtained simultaneously when pacing was performed from site 103. There is a matching pace map with the recordings of VTS.

CASE 26 • 109

I II ID aVR aVL

aVF VI V2

V3 V4

V5 V6

ICD VT-7

PM site 799

Figure 26-3 Top panel: Pace map from the inferobasal tricuspid valve annulus. Bottom panel left: Sub-Q ICD tracings from clinical VT7. Bottom panel right: Tracings obtained simultaneously when pacing was performed from site 799. There is a matching pace map with the recordings of VT7.

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Figure 26·4 Left panel: 30 reconstruction of echocardiographic contours of right and left ventricles from an oblique right anterior view showing the tricuspid valve annulus (TVA}. the pulmonary artery (PA), parts of the left ventricle (LV), and a superimposed biventricular voltage map. The middle panel shows a posterior view of the right ventricle, an arrow indicating a site with a matching pace map displayed in Figure 26·2. The right panel shows the same view as the middle panel, with an arrow indicating the catheter position of the pace mapping site shown in Figure 26·3.

CASE 26 • 111

CASE

27 CLINICAL HISTORY The patient was a 47-year-old woman with frequent, symptomatic, multiform PVCs (33%) with a predominant morphology (Figure 27-1). The patient had a prior ablation that reduced her PVC burden but did not eliminate all her PVC morphologies.

Questions Where does this PVC originate? What is the next step?

l

&VR

Vl

V4

lI

aVL

V2

vs

lll

&VF

V3

V6

Figure 27-1 A 12-lead ECG of the patient's predominant PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

• 113

Answer The origin is the intramural aspect of the anterior basal left ventricle. The QRS morphology suggests an LVOT origin: Right bundle branch block with inferior axis. The R-wave progression in the precordial leads is interesting and goes from a predominantly positive R wave to a lower R/S ratio and back to a larger R/S ratio. This is not the same as a pattern break. The description is similar, and focuses on the R/S ratio as opposed to the R wave alone. V2 obviously has a big S wave that is at least as big as the R wave. The S in V2 indicates that at V2 (located over the basal septum), the initial vector goes into the direction of V2, and the later activation goes away from lead V2. This is not really the case in any other precordial lead. The significance of this is not entirely clear, although this is often seen in epicardial or intramural origins close to the septum. In this patient we mapped the coronary venous system (CVS) first, and had a timing of-31 ms with a similar pace map (10-11/12) in the distal great cardiac vein (Figure 27-2 and 27-3). Ablation from within the CVS or adjacent structures has been effective in eliminating epicardial arrhythmias in about 70% of patients, provided the site of origin is not too close to an epicardial coronary artery.1 An epicardial ablation via subxiphoid access is not a good alternative to reach the epicardial origin for several reasons: the proximity to the coronaries is the same and the myocardium is at a further distance from the catheter located in the epicardial space due to the epicardial fat pad that is thickest in this region. 2 These data have been confirmed by others, 3 and therefore a subxiphoid procedure is usually not done to target these arrhythmias. In this case, the catheter was very close to the left anterior descending artery (LAD) (approximately 2 mm distance) and therefore we did not ablate there; rather we mapped the cusps and the mitral annulus. The use of cryoablation may be somewhat safer than radiofrequency (RF) energy, but 2 mm is too close for a safe ablation procedure even if cryoablation is used. The definition of a safe distance remains to be determined; in general distances ranging from 0.5-1.0 cm have been suggested to be safe. If the site of epicardial origin is within 1 cm of the endocardial aspect of the mitral annulus, an ablation lesion from the mitral annulus juxtaposed to the site of origin can eliminate the ventricular arrhythmia. 4 It is important to mark the site of origin in 3D space so that it can be targeted from the opposite site of the mitral annulus or an alternative site close by, in case the site is too close to the coronary arteries and ablation within the CVS cannot be performed. In this case, the timing at the mitral annulus was -25 ms, with a more far-field appearance and in the cusp the timing was -15 ms without matching a pace map at either side (Figure 27-3). RF energy was delivered at the mitral annulus and PVCs did disappear and reappeared 20 minutes later with the same morphology. Thereafter we decided to inject the CVS to better define its anatomy, and saw that there was a septa! perforator vein present (figures with arrow). We placed the catheter in that vein and paced from the orifice of the perforator vein (PVCs were too infrequent now to do activation mapping). There was a better pace map at this location (Figure 27-3). This was below the LAD (> 5 mm), and we delivered RF energy there (Figure 27-4). Subsequently, we did not see that PVC anymore. Therefore, this was an intramural PVC, and we were able to reach the site of origin with a catheter placed into a perforator vein that drained the intramural septum. This case is similar to other intramural arrhythmias we reported on previously.5

114 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

I II

m aVR

aVL aVF VI V2 V3 V4

V5

V6 Map 1/2 Figure 27-2 A 12-lead ECG of the PVC with intracardiac recording from the ablation catheter located in the distal great cardiac vein.

CASE 27 • 115

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Figure 27-3 In different panels next to the spontaneous PVC are panels from left to right indicating pace maps obtained from the coronary venous system CVS), the perforator vein, the left sinus of Valsalva (SV), and the mitral annulus.

Figure 27-4 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the mitral valve annulus (MVA), the great cardiac vein (GCV), the aortic (Ao) valve, the tricuspid valve annulus (TVA), the pulmonary artery (PA), and a superimposed activation map. A white arrow indicates the location of the ablation catheter: Left panel: Catheter in the GCV with the tip located in a perforator vein. Middle panel: Superimposed CT·derived angiogram shows the proximity of the ablation catheter to the coronary arteries. Right panel shows the catheter at the anterior mitral annulus.

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How to distinguish epicardial from intramural origins? The absence of a matching pace map at the earliest site within the CVS points to an intramural location, and if the catheter is placed through a perforator vein, there is early activation with a matching pace map. Also, temporary suppression of PVCs during irrigation with saline (via the ablation catheter-60 ccs/min for 5-10 sec) within the distal CVS suggests an intramural focus. 6 The case further illustrates one of the potential problems in patients with pleomorphic PVCs. In case of a predominant morphology in the majority of cases, even if not targeted, PVCs with a lower prevalence usually keep a low profile. However, this is not invariably the case as illustrated by this patient, and in ~15% of patients with pleomorphic PVCs, a less prevalent, nontargeted PVC can become frequent enough to be of clinical concem.7 REFERENCES 1. Haman TS, Ilg KJ, Gupta SK, Good E, Chugh A, Jongnarangsin K, et al. Mapping and ablation of epicardial idiopathic ventricular arrhythmias from within the coronary venous system. Cirr: A"hythm Electrophysiol. 2010;3{3):274-279. PubMed PMID: 20400776. 2. Carrigan T, Patel S, Yokokawa M, Schmidlin E, Swanson S, Morady F, et al. Anatomic relationships between the coronary venous system, surrounding structures, and the site of origin of epicardial ventricular arrhythmias. ] Cardiovasc Electrophysiol. 2014. PubMed PMlD: 25066476. 3. Nagashima K, Choi EK, Lin KY, Kumar S, Tedrow UB, Kaplan BA, et al. Ventricular arrhythmias near the distal great cardiac vein: challenging arrhythmia for ablation. Cirr: A"hythm Electrophysiol. 2014;7(5):906-912. PubMed PMID: 25110163. 4. Yokokawa M, Latchamsetty R, Good E, Chugh A, Pelosi F,Jr., Crawford T, et al. Ablation of epicardial ventricular arrhythmias from nonepicardial sites. Heart Rhythm. 2011;8(10):1525-1529. PubMed PMID: 21703218. 5. Yokokawa M, Good E, Chugh A, Pelosi F, Jr., Crawford T, J ongnarangsin K, et al. Intramural idiopathic ventricular arrhythmias originating in the intraventricular septum: mapping and ablation. Cirr: A"hythm Electrophysiol. 2012;5(2):258-263. PubMed PMID: 22407415. 6. Yokokawa M, Morady F, Bogun F. Injection of cold saline for diagnosis of intramural ventricular arrhythmias. Heart Rhythm. 2016;13(1):78-82. PubMed PMID: 26325530. 7. Sheldon SH, Latchamsetty R, Morady F, Bogun F. Catheter ablation in patients with pleomorphic, idiopathic, premature ventricular complexes. Heart Rhythm. 2017;14(11):1623-1638. PubMed PMlD: 28648668.

CASE 27 • 117

CASE

28 CLINICAL HISTORY The patient was a 72-year-old man with a history of hypertension, hyperlipidemia, diabetes mellitus, and frequent asymptomatic PVCs. His initial PVC burden was documented at 35% with an ejection fraction (EF) of 30%-40%. He underwent ablation at an outside hospital 6 months earlier; however, his PVC burden remained elevated. Subsequently, he was started on amiodarone. He presented for follow up with a Holter that showed a PVC burden of 14% (on amiodarone), and a normalized left ventricular EF of 60% by echocardiogram. A CTA showed nonocclusive coronary artery disease and a CMR showed a nonspecific basal septal delayed enhancement pattern.

Questions 1. What is the site of origin of the PVC (Figure 28-1)?

2. What next steps would you do in this patient? A. Perform programmed ventricular stimulation (PVS), PVC ablation, and future care depending on results of PVS and ablation. B. Continue amiodarone, the patient's PVC burden is lower and his EF has recovered. C. Target the PVC with an ablation since amiodarone has significant potential side effects and his PVC burden is still elevated. D. Discontinue amiodarone and start a trial of dofetilide.

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• 119

I

aVR

Vl.

V4

II

aVL

V2

vs

III

a VP

V3

V6

Figure 28-1 A 12-lead ECG of the patient's PVC.

Answer The origin was intramural. The ECG with the right bundle branch block inferior axis is suggestive of an origin from the anterobasal left ventricular outflow tract (LVOT). The qr complex in lead I suggests an epicardial origin. However, an intramural origin cannot be excluded. None of the prior studies where certain ECG criteria were detennined1-3 had intramural origins as a control group, so an intramural origin is always a possibility. Mapping of the great cardiac vein showed the earliest timing-at most -5 ms. Other anatomic structures were later (LV endocardium, aortic cusp, right ventricle). It was striking that the paced-QRS complex was 220 ms in the coronary venous system (CVS) at the earliest, not matching at all with the targeted PVC morphology (the targeted PVC was only 180 ms in width). That site was adjacent to the circumflex artery, and no ablation was performed there. The anterior basal area about 1 cm anterior to the mitral annulus showed a far-field electrogram preceding the QRS by -5 to -10 ms. Radiofrequency (RF) energy delivery there failed to eliminate the PVC, but temporarily suppressed it and rendered it less frequent. With respect to Question 2, Answer A is correct. Programmed ventricular stimulation was performed up-front and we induced two monomorphic, sustained VTs with a cycle length of 240 ms. The morphology ofVT2 was similar to the PVC morphology (Figure 28-2). Figure 28-3 illustrates the anatomical relationship between the CVS and the mitral annulus as well as the coronary arteries. After the ablation. this VT was no longer inducible, but the PVCs were still seen. It is not uncommon for the PVCs in patients with scarring to share the exit site with inducible VTs. Elimination ofthe PVC usually eliminates the VT, as well:~

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However, it is possible that if the exit site is out of reach of the ablation catheter, the VT can still be eliminated from critical sites of the reentry circuit other than the exit, and PVCs might persist. The patient was switched from amiodarone to sotalol and an ICD was implanted. Of note, the patient had a prior procedure elsewhere during which the PVCs were targeted, but no programmed stimulation was performed. This is not recommended, since patients with scar on CMR often have inducible VT,5 and programmed stimulation should be performed in these patients as recommended by a recent expert consensus document. 6

I

n m aVR aVL aVF Vl V2 V3 V4 V5 V6

I II

m aVR aVL aVF Vl V2 V3 V4 V5 V6

Figure 28·2 Left panel: A 12·1ead ECG of the targeted PVC. Right panel: A 12·1ead of the induced VT that has a similar morphology to the predominant PVC.

CASE 28 • 121

Figure 28-3 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the mitral valve annulus (MVA), the great cardiac vein (GCV}, the aortic (Ao) valve, the left main coronary artery (LM), the tricuspid valve annulus (TVA). and the pulmonary artery (PA). A white arrow indicates the location of the ablation catheter at the anterior mitral annulus.

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REFERENCES 1. Bazan V, Gerstenfeld EP, Garcia FC, Bala R, Rivas N, Dixit S, et al. Site-specific twelve-lead ECG features to identify an epicardial origin for left ventricular tachycardia in the absence of myocardial infarction. Heart Rhythm. 2007;4(11):1403-1410. PubMed PMID: 17954399. 2. Berruezo A, Mont L, Nava S, ChuecaE, Bartholomay E, BrugadaJ. Electrocardiographic recognition ofthe epicardial origin of ventricular tachycardias. Circulation. 2004;109(15):1842-1847. PubMed PMID: 15078793. 3. Valles E, Bazan V, Marchlinski FE. ECG criteria to identify epicardial ventricular tachycardia in nonischemic cardiomyopathy. Gire A"hythm Electrophysiol. 2010;3(1):63-71. PubMed PMlD: 20008307. 4. Begun F, Crawford T, Chalfoun N, Kuhne M, SarrazinJF, Wells D, et al. Relationship of frequent postinfarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia. Heart Rhythm. 2008;5(3):367-374. PubMed PMID: 18313593. 5. Yokokawa M, Siontis KC, Kim HM, Stojanovska J, Latchamsetty R, Crawford T, et al. Value of cardiac magnetic resonance imaging and programmed ventricular stimulation in patients with frequent premature ventricular complexes undergoing radiofrequency ablation. Heart Rhythm. 2017;14(11):1695-1701. PubMed PMCD: 28688990. 6. Cronin EM, Bogun FM, Maury P, Peichl P, Chen M, Namboodiri N, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias: Executive summary. Heart Rhythm. 2019. PubMed PMID: 31102616.

CASE 28 • 123

CASE

29 CLINICAL HISTORY A 78-year-old man presented with ischemic cardiomyopathy and status post-anterior wall myocardial infarction with an ejection fraction (EF) of25%. The patient had recurrent VT and !CD shocks while on antiarrhythmic medications.

Questions 1. Where is the exit site of the VT shown in Figure 29-1?

2. Where in the reentry circuit is the catheter located when pacing was performed in Figure 29-2?

A. Exit site

B. Common pathway

c.

Inner loop

D. Entry zone

E. Outer loop 3. What is the response when radiofrequency (RF) energy is delivered at this site?

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 Cl 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

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II

.....

...

aVL

Vl

....

Figure 29·1 A 12-lead ECG of the patient's predominant PVC.

Answer The VT exit is on the left ventricular aspect of the interventricular septum. The catheter is located at the anterior free wall Figure 29-2 shows VT termination with nonglobal capture, and therefore this is a critical part of the reentry circuit.

126 • The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for localization, Volume 2

I II

m aVR aVL

aVF Vl V2

V3 V4

V5

V6 Map 1/2

•..ff I.

/

(

Figure 29·2 Left panel: A 12-lead ECG of the predominant PVC. Right panel: A 12-lead ECG of one of the inducible VTs; this VT has a similar morphology compared to the targeted PVC.

It is actually important to notice that the VT is indeed terminated by this stimulus; this may be quite subtle, and often one has to look carefully to appreciate it. If missed, one might miss out on the only site that might eliminate a particular VT. What is the relevance of this termination? This was a critical site that resulted in elimination of the clinical VT when ablation was performed there. Nonglobal capture is highly specific for identifying critical sites for reentrant circuits.1 The specific mechanism of nonglobal capture and VT termination is unclear, but may be secondary to prolongation of local refractoriness by the pacing impulse delivered to poorly coupled tissue. The VT terminated and the resulting QRS complexes are paced and not entrained. However, they have the same QRS morphology as the VT, so pacing is from an area protected by fixed barriers, and the stimulus-QRS/VT cycle length ratio can be determined in the same way as if there was concealed entrainment. The stimulus/QRS ratio is 0.59, this therefore indicates that the catheter is located in the common pathway of the reentrant circuit. A stimulus-QRS/VT cycle length ratio~ 0.3 indicates the exit, a stimulus-QRS/VT cycle length ratio> 0.3-0.7 indicates the common pathway, and a stimulus-QRS/VT cycle length ratio > 0.7 indicates an inner loop, or the entry zone of the reentrant circuit. It is unusual to have a left bundle branch block (LBBB) IA VT originate from the anterior LV where the catheter is located (Figure 29-3). However, there is a long stimulus-QRS interval when capture occurs, indicating that the catheter is located at a site distant from the exit; the exit was CASE 29 • 127

indeed located at the anteroseptal segment as indicated by the LBBB morphology of the VT. For an RV origin, the septum needs to be part of the scar; if it is, the RV septum can be the breakout site for a septal VT. In this patient, most of the circuit (except the exit) was not in the septum despite the LBBB morphology. Furthermore, the patient &iled a prior ablation at another hospital where the RV breakout was specifically targeted from both aspects of the septum.

Figure 29-3 30 reconstruction of echocardiographic contours of the left ventricle from a septa! view showing the aortic (Ao) valve and the left ventricular apex. A white arrow indicates the location of the ablation catheter at the anterior free wall.

REFERENCE 1. Bogun F, Krishnan SC, Marine JE, Hohnloser SH, Schuger C, Oral H, et al. Catheter ablation guided by termination of post-infarction ventricular tachycardia by pacing with nongl.obal capture. Hutt Rhythm. 2004;1(4):422-426.

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CASE

30 CLINICAL HISTORY The patient was a 68-year-old man with frequent asymptomatic PVCs and a reduced ejection fraction (EF) of 40%. The patient failed a prior ablation procedure a year earlier and was started on amiodarone. Despite amiodarone, his PVC burden remained high, in the 40% range. On CMR there was an intramural scar present in the basal septum.

Questions Where is the site of origin of the PVC shown in Figure 30-1? What is the preferred approach to map/ablate at this site of origin?

II

III

&VP

V1

V4

V2

vs

VJ

V6

II

Figure 30-1 A 12-lead ECG of the patient's PVC.

The Origins of Ventricular Arrhythmias: Using the ECG as a Key Tool for Localization, Volume 2 0 2020 Frank M. Bogun. Cardiotext Publishing, ISBN: 978-1-942909-41-5

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Answer The origin was the subepicardial anterior left ventricle. The RBBB IA with positive concordance indicates an origin in the basal LV, or the aortic cusp. There is, however, no pseudo-delta wave present, and the small r wave in lead I may also be seen with an endocardial or intramural LVOT origin. The absence of a q in lead I somewhat argues against an epicardial origin. The best mapping approach is first via the coronary venous system (CVS). This proved difficult due to a valve of Vieussens, but eventually was accomplished. The earliest timing in the distal great cardiac vein was -25 ms, without a matching pace map. The distal electrodes pairs being activated first, we wanted to determine whether an earlier timing could be obtained further distally, and eventually we managed to advance the catheter further distal into the anterior interventricular vein (AVI) where the timing indeed was earlier (-35 ms), with a better pace map, although still no 12/12 lead match (Figure 30-2). Further distal, the timing was worse, and the pace maps were also worse. This case illustrates that when reporting "late timing" in the distal CVS, it is important to note how distal mapping was carried out and how the pace map correlates to the site of earliest activation mapping. Injection of the coronary arteries showed that the catheter was clear from adjacent epicardial coronary arteries. Radiofrequency (RF) energy was delivered there, and this suppressed the PVCs for some time. But it did not eliminate his PVCs, and resulted in a change in morphology as well. At an alternate site in the AVI where early timing was recorded with a matching pace map, more RF energy was delivered, the morphology changed again, and still the PVC was present, although less frequent (changing from a constant bigeminal rhythm to a PVC once per minute (Figure 30-3). More RF energy was delivered in the CVS until there was no more capture. Thereafter, we went to the opposite left ventricular endocardium where the timing from the left aortic cusp to the area just below the earliest timing of the AVI was early, but not as early as in the AVI (-25 ms). RF energy was delivered at the anterior LV juxtaposed to the site with the earliest AVI timing (Figure 30-4). PVCs became less and less frequent and eventually were no longer seen.

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II

I II

m

m

aVR aVL aVF Vl V2 V3 V4

aVR aVL aVF Vl V2 V3 V4

vs

vs

V6

V6

I

/ Figure 30-2 Left panel: A 12-lead ECG of the targeted PVC. Right panel: Pace map from a site in the anterior interventricular vein (AIV) where activation was early.

I

I II

I II

II

III

ill

III

aVR

aVR

aYR

aVL aVF Vl V2 V3 V4

aVL aVF Vl V2 V3 V4

aVL aVF Vl V2 V3 V4

vs

vs

vs

V6

V6

V6 Map 112- - - A o Map 3/4

Figure 30-3 Left panel: A 12-lead ECG with recordings from the ablation catheter (Map 1/2 and 3/4). This was the earliest mapped site in the AIV. Mlddle panel: Postablation the PVC morphology changed and there is still early timing at an alternate site in the AIV. Right panel: Postablation there was yet another change of the PVC morphology; timing remained early and more ablation was delivered in the AIV.

CASE 30 • 131

Figure 30·4 30 reconstruction of echocardiographic contours of right and left ventricles from a posterior view showing the great cardiac vein (GCV), the anterior interventricular vein (AIV), the mitral valve annulus (MVA), the aortic (Ao) valve, the tricuspid valve annulus (TVA), and the pulmonary artery (PA). An activation map of the GCV is shown; other anatomic stRJctures are in gray. White arrows indicate the location of the catheter that is located in the AIV (left panel) and the MVA (right panel).

The origin was intramural but closer to the epicardium than to the endocardium, based on the activation timing and the pace maps. Delivering RF energy in the CVS changed the exit and reduced the PVCs. Ablation from other adjacent sites was still carried out, since occasional PVCs remained. Whether this was indeed necessary is not clear.

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APPENDIX

Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case Case

1: PVC and VT with an intramural anterobasal left ventricular origin 2: PVCs originating from the intramural basal myocardium 3: PVC originating from the tricuspid annulus 4: Ventricular arrhythmias with an intramural septal origin 5: VT originating from the lateral tricuspid annulus 6: PVC originating from the inferior mitral annulus 7: VT due to bundle branch reentry 8: VT originating from the intramural LVOT 9: VT originating from the septal bands in the right ventricle 10: VT originating from the intramural myocardium between left sinus ofValsalva and the great cardiac vein 11: PVC originating from the anterolateral papillary muscle 12: PVC from the intramural septa! outflow tract 13: Post-infarction VT originating from the septum 14: PVC originating from the parahisian area 15: VTs originating from scar at the mitral valve annulus 16: VT originating from the epicardial crux of the heart 17: VT originating from the tricuspid valve annulus 18: VT originating from scar close to the inferoseptal mitral annulus 19: PVC originating from the epicardial inferobasal septum 20: PVC originating from the intramural inferoseptum 21: PVC originating from the posterior mitral annulus 22: VT originating from scar at the mitral annulus 23: VT originating from the intramural septum 24: PVC originating from the Purkinje fiber system 25: VT originating from the anterobasal left ventricular epicardium 26: VT originating from the basal right ventricular free wall 27: PVC originating from the anterobasal LVOT 28: PVC originating from the anterobasal intramural LVOT 29: VT originating from scar in the anterior left ventricular free wall 30: VT originating from the subepicardial anterior left ventricle

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