Decoding Cardiac Electrophysiology: Understanding the Techniques and Defining the Jargon [1st ed. 2020] 978-3-030-28671-2, 978-3-030-28672-9

Table of contents :
Front Matter ....Pages i-v
Front Matter ....Pages 1-1
The Basic Language of Cardiac Electrophysiology—An Introduction to Intracardiac Electrograms and Electrophysiology Studies (Sandeep Prabhu, Afzal Sohaib)....Pages 3-19
The Kit: Access, Catheter Placement, Transeptal Puncture, Ablation Technology, 3D Mapping (Jason V. Garcia, Daniel K. Y. Wan)....Pages 21-39
Front Matter ....Pages 41-41
Atrioventricular Nodal Re-entry Tachycardia (AVNRT) & AV node Ablation (Jonathan M. Behar)....Pages 43-49
Accessory Pathways and Atrioventricular Re-entrant Tachycardia (AVRT) (Wei Yao Lim, Marco Baca)....Pages 51-57
Typical Atrial Flutter (Kevin Ming Wei Leong)....Pages 59-69
Front Matter ....Pages 71-71
Ablation of Atrial Fibrillation and Atrial Tachycardia (Vishal Luther, George Katritsis)....Pages 73-86
Ventricular Ectopic Ablation (David Duncker, Johanna L. Müller-Leisse, Christos Zormpas, Jörg Eiringhaus, Christian Veltmann)....Pages 87-98
Ventricular Tachycardia Ablation (Neil T. Srinivasan, Alex Cambridge)....Pages 99-107
Back Matter ....Pages 109-109

Citation preview

Afzal Sohaib Editor

Decoding Cardiac Electrophysiology Understanding the Techniques and Defining the Jargon

Decoding Cardiac Electrophysiology

Afzal Sohaib Editor

Decoding Cardiac Electrophysiology Understanding the Techniques and Defining the Jargon

Editor Afzal Sohaib St Bartholomew’s Hospital London, UK King George Hospital Ilford, Essex, UK

ISBN 978-3-030-28671-2 ISBN 978-3-030-28672-9  (eBook) https://doi.org/10.1007/978-3-030-28672-9 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Contents

Part I  The Tools for Understanding Cardiac Electrophysiology 1 The Basic Language of Cardiac Electrophysiology—An Introduction to Intracardiac Electrograms and Electrophysiology Studies. . . . . . . . . . . . . . . . . . . 3 Sandeep Prabhu and Afzal Sohaib 2 The Kit: Access, Catheter Placement, Transeptal Puncture, Ablation Technology, 3D Mapping . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Jason V. Garcia and Daniel K.Y. Wan Part II  Standard Ablation 3 Atrioventricular Nodal Re-entry Tachycardia (AVNRT) & AV node Ablation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Jonathan M. Behar 4 Accessory Pathways and Atrioventricular Re-entrant Tachycardia (AVRT). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Wei Yao Lim and Marco Baca 5 Typical Atrial Flutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Kevin Ming Wei Leong Part III  Complex Ablation 6 Ablation of Atrial Fibrillation and Atrial Tachycardia. . . . . . . . . . . . . . . . . . . . . . 73 Vishal Luther and George Katritsis 7 Ventricular Ectopic Ablation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 David Duncker, Johanna L. Müller-Leisse, Christos Zormpas, Jörg Eiringhaus and Christian Veltmann 8 Ventricular Tachycardia Ablation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 Neil T. Srinivasan and Alex Cambridge Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

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Part I The Tools for Understanding Cardiac Electrophysiology

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The Basic Language of Cardiac Electrophysiology— An Introduction to Intracardiac Electrograms and Electrophysiology Studies Sandeep Prabhu and Afzal Sohaib

Abstract

This chapter aims to introduce the reader to some of the core principles which underpin clinical cardiac electrophysiology and how it is applied in cardiac catheter laboratories, where ablations take place. Key language and terminology are introduced before these concepts are explored further in subsequent chapters.

Keywords

Electrograms · Electrophysiology study · Ablation · Arrhythmia mechanisms · Refractory periods · Decrementation · Re-entry · Automaticity

1.1 Cardiac Electrophysiology—Why the Mystique? To the uninitiated, there is a perceived ‘mystique’ about cardiac electrophysiology (EP) that often acts as a barrier to an even rudimentary understanding of EP procedures. Unhelpfully, this view of EP is not infrequently perpetuated by electrophysiologists themselves, with most apparently communicating in a language indecipherable, even to the seasoned general cardiologist. The purpose of this book is to simplify this jargon, and decode it into terms to allow newcomers to the field to find their way among the world of EP. A. Sohaib (*) Consultant Cardiac Electrophysiologist Department of Cardiology, Barts Heart Centre, St Bartholomew’s Hospital, London, UK e-mail: [email protected] S. Prabhu Department of Cardiology, Barts Heart Centre, St Bartholomew’s Hospital, London, UK e-mail: [email protected] S. Prabhu  The Heart Centre, Alfred Hospital, Melbourne, VIC, Australia S. Prabhu The Baker Heart and Diabetes Institute, Melbourne, VIC, Australia

Unlike other realms of cardiology such as imaging, angiography and structural intervention, which have an obvious visual element (a regurgitant valve, a narrowed artery, etc.), electrophysiology instead relies upon the interpretation of electrical signals and the manner in which they propagate throughout the cardiac tissue. Since electricity itself cannot be physically visualised in real time, its presence and course through various cardiac structures instead needs to be inferred by the detection of electrical signals at various intra-cardiac sites. The direction and pattern of electrical wavefronts through tissue is determined by the timing of electrical signals in relation to each other, the surface ECG and/or a stable reference signal. For this reason, the ‘language’ of electrograms needs to be comprehended before electrophysiological procedures can make sense. Fortunately, like any language, there are key fundamental principles and concepts which will aid the interested student in understanding and eventually becoming proficient in this language. This chapter focuses on describing these key concepts. Subsequent chapters will then apply these principles to the treatment of various commonly treated conditions. “Decoding the Jargon” and “Beyond the Basics” Electrophysiologists have a tendency to very quickly slip into using jargon. For this reason throughout the book, we have highlighted commonly used terms and described them in “decoding the jargon” boxes. Each chapter is structured so that the core concepts are the main focus and some of the more complex concepts are discussed in sections entitled “beyond the basics” towards the end of each chapter.

1.2 What Happens in the EP Lab Before exploring some of these fundamental concepts it is useful to have an overview of the range of procedures which happen in the electrophysiology laboratory and the rest of the book will deal with each of these areas in detail.

© Springer Nature Switzerland AG 2020 A. Sohaib (ed.), Decoding Cardiac Electrophysiology, https://doi.org/10.1007/978-3-030-28672-9_1

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Procedures can be divided into “standard EP” and “complex EP”. This is an oversimplification and often what is classified as standard can be very complex and vice versa, but it is a useful way to orientate oneself, and these categories are frequently used by various bodies involved in overseeing electrophysiology [1]. Standard EP usually refers to procedures which can deal with arrhythmias frequently from the right sided circulation and includes AV node ablation, AV nodal re-entry tachycardia (AVNRT), typical atrial flutter, and ablation of accessory pathways. These often can be done with a relatively simple arrangement of catheters and fluoroscopy. The risks are usually at the lower end, and procedure duration is usually at the lower end of the spectrum for electrophysiology procedures. Complex EP usually refers to procedures with deal with arrhythmias from the left sided circulation and includes ablation for atrial fibrillation, left sided atrial tachycardias,

and ventricular tachycardia (VT). Procedures tend to be slightly longer. Heparinisation is required as the left sided circulation is being instrumented. Consequently, the risks are at the higher or more serious end of the spectrum. Key elements of these procedures are described in Table 1.1. A “standard” EP procedure may become complex depending on the nature of the arrhythmia. For example, a narrow complex tachycardia may initially look like a form of accessory pathway mediated tachycardia (AVRT), however, upon further testing, may reveal itself (after appropriate diagnostic manoeuvres), to be a left sided focal atrial tachycardia. Similarly, what may appear like a complex VT or ventricular ectopic ablation, may arise from the right ventricular outflow tract, which is generally readily accessible from the right femoral vein and may require just a single catheter (ablation catheter) to treat. Therefore, the distinction between standard and complex EP is somewhat artificial.

Table 1.1  Procedures performed in the EP laboratories. Access and equipment required is listed Access “Standard” ablation procedures AV node ablation Femoral vein to access right atrium Atrial flutter

Femoral vein to access right atrium

AVNRT

Femoral vein to access right atrium

Accessory pathways

Femoral vein to access right atrium

Right sided atrial tachcyardia

Femoral vein to access right atrium

“Complex” ablation procedure Ventricular tachycardia

Femoral artery to access LV. Femoral vein to access LV via transeptal. Epicardial

Ventricular ectopic ablation

Femoral vein to access right ventricle or LV via transeptal. Femoral artery to access aortic root/LV

Atrial fibrillation

Femoral vein to access LA via transeptal

Left sided atrial tachycardias

Femoral vein to access LA via transeptal

Equipment required Fluoroscopy ablation catheter Fluoroscopy ablation catheters Diagnostic EP catheters Fluoroscopy ablation catheters Diagnostic EP catheters Fluoroscopy Ablation catheters Diagnostic EP catheters 3D mapping system may be useful but not a requirement Fluoroscopy Ablation catheters Diagnostic EP catheters 3D mapping system Fluoroscopy Ablation catheters Diagnostic EP catheters 3D mapping system Fluoroscopy Ablation catheters Diagnostic EP catheters 3D mapping system Fluoroscopy Ablation catheters Diagnostic EP catheters 3D mapping system Fluoroscopy ablation catheters Diagnostic EP catheter 3D mapping system

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1.3 Important Cardiac Anatomy

cava (IVC)) or superiorly (via the internal jugular and superior vena cava (SVC)). Several key structures are located in or accessible via the RA. The right ventricle (RV) is readily accessible from the RA by advancing across the tricuspid valve. The right ventricular outflow tract (not shown in this figure), the region of the RV inferior to the pulmonary valve, is often a source of arrhythmia and a frequent target for ablation in the RV [3]. Its anatomy will be described in detail in the relevant section. The left atrium (LA) can be accessed in 3 main ways: (1) via trans-septal puncture across the inter-atrial septum, (2) epicardially from the coronary sinus (see below) or (3) retrogradely through the aortic valve and mitral valve (uncommonly). Similarly, the left ventricle (LV) can be accessed in the same 3 ways as the LA, however, limited parts of the epicardial surface may be accessible via branches from the coronary sinus (such as the great cardiac or middle cardiac veins). In the case of trans-septal

A thorough understanding of cardiac anatomy is of particular importance in electrophysiology as literally any part of the heart tissue may be involved in the mechanism of an arrhythmia and/or be a target for ablation. A review of some key anatomical features specifically relevant to electrophysiology procedures are described here. More specific details for some anatomical structures may be found in the relevant chapters discussing specific procedures [2].

1.3.1 Accessing the Heart Chambers The chambers of the heart are shown in Fig. 1.1. The right atrium (RA) is most readily accessible chamber of the heart either inferiorly (via the right femoral vein and inferior vena

Aortic Valve

SVC

Mitral Valve

1

4

Right Ventricle 1. IVC - trans-tricuspid 2. Epicardial Left Atrium 1. Trans-septal 2. Coronary sinus 3. Retrograde aortic and trans-mitral 4. Epicardial

LA 3 2

3

2

RA

1

IVC

LV

Tricuspid Valve

2 3

1 RV

2

Right Atrium 1. IVC 2. SVC 3. Epicardial

1

Left Ventricle 1. Retro-grade aortic 2. Trans-septal - trans-mitrial 3. Coronary Sinus (LV branch) 4. Epicardial

4

Pericardial access to epicardium

Fig. 1.1  Accessing the chambers of the heart. The access to each chamber is described by arrows and colour coded by chamber. IVC access is the most common for right heart structures, although the Ra can be accessed via the SVC from the internal jugular vein if required. Access to the left structures is via the interatrial septum (via

trans-septal puncture), through the coronary sinus (down LV branches to access LV epicardium) or retrogradely from the aorta. Any chamber can be accessed via an epicardial approach however this is most commonly used for ventricular chambers

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access, the LV is reached by advancing across the mitral valve. Modern techniques such as epicardial access via the pericardium can also allow access to most cardiac structures epicardially. This approach is most often utilised to access the epicardium of the LV or RV in complex ventricular tachycardia ablation procedures. Currently, this is usually limited to being performed in highly specialised tertiary or quaternary centres with experienced operators.

1.3.2 Cardiac Structures with Electrophysiological Significance Figure 1.2 outlines some key anatomical structures that have specific relevance for electrophysiological procedures.

1.3.2.1 AV Node Complex This will be discussed in more detail in the section on AVNRT. In the absence of an accessory pathway, the AV node is the only electrical communication between the atria and the ventricles, and the pathway used for normal impulse conduction. The compact AV node is located in the centre of the heart. It is electrically insulated and so does not have any detectible electrical signal, however the

His bundle located just distal to the AV node, does record a small electrical signal (called a His deflection), allowing a catheter spanning across it to identify the approximate the location of the AV node. The AV node often receives inputs from extensions with differing degrees of decremental properties (often termed slow and fast pathways), which are involved in the mechanism of AVNRT (see chapter on AVNRT). The AV node complex is often described with a triangular border known as the Triangle of Koch, which delineates the slow and fast inputs into the complex. Decremental conduction is a key property of the AV node and is discussed below.

1.3.2.2 The Coronary Sinus The coronary sinus is the collection point of the venous drainage of the coronary circulation. It drains the anterior interventricular vein, the posterior interventricular vein and middle cardiac vein (along with other lateral venous branches). Crucially it runs on the epicardial surface along the atrio-ventricular groove (predominately along the atrial aspect) along the posterior/inferior surface of the left atrium, before draining into the right atrium at the inferior interatrial septum. The coronary sinus is of crucial importance in electrophysiology procedures for several reasons:

SVC Pulmonary veins Anatomy of the Triangle of Koch

Contral fibrous body His bundle CT

Great cardiac vein

SN

Tricuspid valve annulus

FO FO Tendon of Todaro

Posterior cardiac vein

CS ER

IVC

TCV

EV

Slow pathway

RA

Middle cardiac vein

AV node complex

LBB

Coronary sinus Cristae Terminalis

Fast pathway exit

LA

Small cardiac vein

Coronary sinus

MV

IVC

LV

TV

Aorta Pulmonary trunk Aortic valve

Fossa ovalis RV

CS os Inter-atrial septum

Anterior leaflet of mitral valve Antero-lateral papillary muscle

Cavo-tricuspid isthmus RBB

Left ventricle

Chord Postero-media tendonae papillary muscle

posterior leaflet of mitral valve

Papillary muscles

Fig. 1.2  Key anatomical structures for electrophysiological procedures. The listed structures have key significance in electrophysiological procedures. Details are described further in the text

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1. By positioning catheters in the coronary sinus, electrical information is obtained regarding the left atrium (LA), without the catheter having to be in the systemic circulation (unlike, for example if it were sitting inside the LA), avoiding the need for anticoagulation and minimising the risk of embolic complications. 2. Unlike catheters inside the LA, the coronary sinus provides access to the epicardial surface of the LA. 3. Branches of the coronary sinus, may allow limited access to certain epicardial aspects of the left ventricle.

1.3.2.3 The Cavo-Tricuspid Isthmus The cavo-tricuspid isthmus (CTI) is the region on the floor of the right atrium from the inferior aspect of the tricuspid valve to the anterior portion of the IVC. This area contains complex anatomy making the surface far from smooth, particularly at the septal aspect. The Eustachian ridge and the often trabeculated myocardial tissue in this area lead to slowed conduction—a kind of electrical ‘bottleneck’. This slowed conduction can allow electrical circuits to sustain by allowing an opportunity for an excitable gap to form in the circuit. See Sect. 1.4.4. Typical atrial flutter utilises the cavo-tricuspid isthmus as part of its re-entry circuit around the tricuspid annulus—often termed CTI-dependent flutter. This electrical bottleneck is the target for the ablation of this tachycardia with an ablation line from the electrically inert annulus to the inferior vena cava (blue dotted line in Fig. 1.2) effectively interrupting this circuit. 1.3.2.4 The Cristae Terminalis The cristae terminalis (CT) is a curved ridge delineating the border between the smooth and trabeculated endocardial surfaces of the RA. It runs superior-inferiorly from the

Fig. 1.3  The orientation of the interatrial septum. The interatrial septum sits in an oblique plane in the body as shown in the transverse cartoon as viewed from below (like a CT scan). The fossa ovalis is the true single membranous connection between the RA and LA, the thinnest part of the IAS and the target location for trans-septal puncture. To puncture outside this region runs the risk of extra-cardiac

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IVC to the SVC along the postero-lateral aspect of the RA. It is also an area of slowed conduction and its specific fibre orientation promotes electrical conduction superiorly and inferiorly along its edges rather than transversely across it. The superior aspect of the CT gives rise to the sinus node complex. The body of the cristae acts as an electrical channel, promoting the conduction around the tricuspid annulus in the case of atrial flutter. The atrial tissue in the cristae is a common source of focal atrial tachycardia.

1.3.2.5 The Inter-atrial Septum Understanding the anatomy of the inter-atrial septum is crucial as trans-septal puncture has become the primary route of access to the LA in contemporary electrophysiology. Like the heart itself, the septum does not sit in the true antero-posterior plane of the heart but is angled to the left. This explains the reason during trans-septal puncture to direct the catheter tip posteriorly about 45° (4:30 position on a clock face) to ensure the septum is engaged perpendicularly to its plane (Fig. 1.3). The fossa ovalis is the thinnest part of the septum and the only true shared membrane between the RA and the LA and is therefore the target for trans-septal puncture. Puncturing outside this area runs the risk of a catheter running an extra-cardiac course prior to entering the LA resulting in cardiac tamponade. Detailed anatomy of the inter-atrial septum is described in the section explaining trans-septal puncture technique. 1.3.2.6 Papillary Muscles Papillary muscles anchor the mitral and tricuspid valve leaflets to the ventricular muscle and assist with valve functioning. The left papillary muscles (antero-lateral and postero-medial papillary muscles) in particular can be source of focal arrhythmias and the target for ablation.

passage prior to entering the LA. From the IVC approach, a catheter directed at the 4:30 pm (or 135°), should approximate a perpendicular approach to the fossa ovalis. More details can be described in the section on trans-septal technique. IAS = inter atrial septum, FO = fossa ovalis, LA = left atrium, RA = right atrium, IVC = inferior vena cava

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1.4 Basic Concepts in Electrophysiology An understanding of some core fundamental aspects of basic cardiac electrophysiology is required to understand the procedures performed in the EP lab. These include cardiac conduction and automaticity, decremental conduction, refractory periods, primary arrhythmia mechanisms and electrograms [4]. These are summarised before an outline of a standard protocol for an EP study for supraventricular tachycardia (SVT) is discussed.

1.4.1 Refractory Periods A refractory period broadly speaking reflects the fastest rate at which a cell can depolarise. This is a fundamental concept in electrophysiology but from a practical, clinical point of view, it can give clues to whether a certain tissue can sustain arrhythmia. There are a number of different types of refractory period, but the most useful of these to remember is the effective refractory period (ERP) which gives an indication for the fastest rate at which a tissue can conduct. This is particularly relevant in the case of accessory pathways, where a very short ERP (i.e. can conduct at high rates) is indicative of a more dangerous accessory pathway which could rapidly conduct atrial fibrillation. Decoding the jargon: Effective Refractory Period (ERP) This is the longest interval between two beats (i.e. slowest rate) at which a tissue can no longer conducts. Each tissue has an ERP, such as the atrium (atrial ERP), or AV node (AV nodal ERP). A short refractory period implies a tissue can conduct at a higher rate.

Why is this an important concept? This is fundamentally important for the full spectrum of arrhythmias treated. The refractory period of a tissue will determine whether it can sustain re-entrant tachycardias. For an accessory pathway, a short ERP suggests a pathway is more dangerous as it is more likely to conduct fast AF. The refractory period of a tissue will determine whether it can sustain re-entrant tachycardias. For an accessory pathway, a short ERP suggests a pathway is more dangerous as it is more likely to conduct fast AF.

1.4.2 Cardiac Conduction and Automaticity Like skeletal muscle, cardiac tissue is electrically active, capable of depolarising and contracting in response to electrical stimulation. Unlike skeletal muscle, cardiac cells are imbued with the ability to spontaneously depolarise at regular intervals, a phenomenon called ‘automaticity’. Cardiac myocytes are electrically coupled to each other so that an electrical wavefront will spread radially from any point of stimulation. Therefore, the most rapidly depolarising (or electrically discharging) part of the heart will determine the heart rate.

Each tissue in the heart has an intrinsic rate of spontaneous discharge. In the non-disease state, the most rapidly discharging structure of the heart is the sinus node and therefore this determines the heart rate (sinus rhythm). In the absence of sinus node activity, the heart rate will be determined by whichever cardiac tissue is depolarising at the fastest rate. Table 1.2 shows the intrinsic depolarisation rate of various cardiac tissues. This may be other atrial myocardium, the atrio-ventricular node, the His-Purkinje system, or the ventricular myocardium. Rhythms arising from these structures, typically called “escape rhythms”, are variably present, and may often provide a rate inadequate to provide sufficient cardiac output. Some myocardial tissue, known as conduction system tissue, are specifically designed to rapidly transmit electrical charge quickly to all parts of the heart to ensure mechanical contraction occurs rapidly to ensure efficient pumping of the heart. The conduction system consists of the sinus node, the AV node, the His bundle, the left and right bundle (the left further subdividing into anterior and posterior fascicles). Decoding the jargon: Automaticity The intrinsic rate at which cardiac conduction tissue depolarises

Why is this important concept? Features from the ECG and electrograms will give an indication for which structure is determining the heart rate. In normal individuals this will be the sinus node. Either due to damage to one of the structures of the conduction system, automaticity in another tissue will lead that to to take over and that will be reflected in the ECG and electrograms.

1.4.3 Decremental and Non-decremental Conduction Decoding the jargon: Decrementation When a tissue decrements, the faster a tissue is stimulated, the slower conduction through that tissue. This an important property of the AV node, not displayed in atrial or ventricular tissue.

Why is this important concept? A key observation in EP studies is observing such decrement. Its absence will often can give a clue to the presence of an accessory pathway. Accessory pathways (unlike the AV node) usually do not decrement, but this can be a feature of rare accessory pathways. Table 1.2  Intrinsic rhythm of cardiac tissue Structure Sinus node Atrial myocardial cells AV node His bundle Bundle branches Purkinje cells Myocardial cells

Rate (bpm) 60–100 55–60 45–50 40–45 40–45 35–40 30–35

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Fig. 1.4  Decremental versus non-decremental conduction. This figure illustrates the concept of decremental tissue. On the left panel, successive impulses arrive at decrementing tissue (such as the AV node) at progressively shorter intervals. However, due to decremental properties, the impulses emanate from the tissue with a paradoxically longer interval between the pulses. When the interval is shortened to 60 ms, conduction through the tissue is not possible as it is

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still rendered refractory from the initial impulse causing the second impulse to fail to propagate resulting in block. By contrast on the right panel, conduction through non-decremental tissue (such as an accessory pathway) is independent of the coupling interval. As such impulses are conducted through the tissue at the same rate at which they arrive. Further details are found in the text

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Decremental conduction is a description of an important concept in electrophysiology. Decremental conduction refers to a changing capacity of a myocardial tissue to conduct electricity depending upon the rate it is stimulated. In particular, in an almost paradoxical sense, decremental tissue conducts impulses more slowly, the faster the tissue is stimulated. This concept is illustrated graphically in Fig. 1.4. The hallmark tissue displaying this property is the AV node complex where its decremental properties limit the ability for the ventricular rate to match that of the atrial rate in the setting of rapid atrial arrhythmias. This protective function is the primary purpose of the AV node especially as conditions such as atrial fibrillation can cause the atria to ‘contract’ at over 600 bpm! Ventricular activation at this rate would rapidly degenerate into ventricular fibrillation. For this reason, in the normal heart, the AV node is the only electrical connection between the atria and the ventricles. Non-decremental conduction simply refers to absence of this property in tissue. Typically, accessory pathways (extra-nodal atrio-ventricular connections) do not possess decremental properties. The potential for atrial impulses to bypass the AV node and conduct to the ventricle without

decrementation via an accessory, explains the potential danger of anterogradely conducting accessory pathways.

Fig. 1.5  Cardiac conduction and arrhythmia mechanisms. Cardiac cells are electrically coupled to each other. A depolarisation wavefront in activates cells (green) which then recover their excitability. In electrically coupled cells such as in the myocardium, discharge will spread in a radial pattern from any point of stimulation which will be that tissue with the fastest rate of automaticity. In the normal heart this is the

sinus node, however an abnormal focal source of arrhythmia may also do this. Alternatively, in the disease state, an electrical circuit (re-entry circuit), can propagate continually around non-conducting tissue. A zone of slowed conduction ensures that the cells have recovered at the tail end of the wavefront, allowing the leading wavefront to continually propagate. The concept is discussed more fully in the text (Sect. 1.4.4)

1.4.4 Arrhythmia Mechanisms—Focal Versus Re-entry (Fig. 1.5) There are many descriptions of rhythm abnormalities in cardiac disease however those treatable by electrophysiological procedures generally fall into two broad mechanisms— either focal or re-entry. Table 1.3 lists the arrhythmia conditions stratified by mechanism.

1.4.4.1 Focal Mechanisms A focal mechanism of an arrhythmia refers to the situation in which some myocardial tissue is depolarising more rapidly or more frequently than it should physiologically, and overshadowing the patient’s normal rhythm. This can come from any cardiac tissue (atrial, ventricular or conduction system). Given the electrical coupling of all cardiac tissue, rapid depolarisations from any abnormal site, will spread rapidly through the myocardium and cause the surrounding

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Table 1.3  Arrhythmias stratified by mechanism Focal mechanism 1. Focal atrial tachycardia/atrial ectopy 2. Idiopathic ventricular tachycardia/ventricular ectopy

myocardium to depolarise at the same rate. Typically, electrical discharge will spread in a radial pattern away from the source. The mechanisms of rapid depolarisation have been described as either enhanced automaticity (i.e. the resting period between successive depolarisation is abnormally short resulting in rapid regular depolarisation) or triggered activity (where abnormal discharges in the later part of the action potential lead to regular repetitive discharging), however these differences have few implications for ablative therapy. Focal tachycardias can occur in isolated beats (in the case of ventricular or atrial ectopy), intermittently in short runs (such as in atrial tachycardia or nonsustained ventricular tachycardia) or may be incessant (as in the case of some atrial tachycardias). Although many focal arrhythmias can be benign or have minimal clinical impact, occasionally they can have serious implications such as triggering VF or incessant tachycardias resulting in systolic heart failure. When ablative treatment is being performed, the approach is to find the source of the rapid discharging and ablate this area. Usually, a true focal source is only a few millimetres in area and requires minimal ablation (if carefully mapped) to eliminate the source. If the source is fully eliminated, the clinical outcomes are usually excellent. A list of arrhythmias with focal mechanisms is shown in Table 1.3.

1.4.4.2 Re-entry Mechanisms Re-entry is the mechanism for many arrhythmias. Re-entry describes the situation in which an electrical circuit is present and electrical impulses can continually propagate along this electrical circuit. There are several important prerequisites for re-entry to exist. 1. There is the requirement of two separate conducting areas, separated by an area of tissue incapable of conducting—acting as an electrical barrier. This structure could be anatomical (such as valve orifice, or the atrioventricular node), pathological (such as myocardial scar) or functional (apposing tissues with such differing electrical properties that impulses cannot traverse uniformly across it). 2. During propagation of impulses around the circuit, impulses can only propagate in one direction at a time.

Re-entry mechanism 1. Atrio-ventricular nodal re-entry tachycardia (AVNRT) 2. Atrio-ventricular re-entry tachycardia (AVRT) 3. Atrial flutter (typical or atypical) 4. Ventricular tachycardia in structural heart disease (scar related) 5. Atrial tachycardias post AF ablation (micro or macro-re-entry)

This is also known as uni-directional block. If this did not occur, impulses travelling in opposing directions would collide and extinguish each other. 3. An area of slowed conduction. Slowing of conduction gives time for the tail end of the wave front to recover excitability, allowing the subsequent wavefront to effectively ‘chase the tail’. This tissue with recovered excitability behind the passing wavefront, is called the excitable gap and is essential for the circuit to exist. Given that these circuits usually exist around stable anatomical structures, they usually have a reliably consistent cycle length. When ablation is performed, the treatment relies on defining the circuit and rendering a key part of the circuit (often an electrical ‘bottle neck’) electrically inert (for example the cavo-tricuspid isthmus in the case of CTI dependent flutter, or the slow pathway in the case of AVNRT—see the relevant chapters for more details), hence removing the circuit and therefore the arrhythmia utilising it. There is no limit to the size of the electrical circuit. For example, the reentry circuit of atrio-ventricular re-entry tachycardia (AVRT) utilises the atria, the AV node, the ventricles and an accessory pathway (effectively the entire heart), whilst that of AVNRT is contained wholly within the AV node complex. Occasionally, small areas of scar or abnormal issues can create small re-entry circuits (usually defines as less than 2 cm) which are termed micro-re-entry circuits. Given their small size, their presence can mimic a focal mechanism.

1.4.5 The Signals: Electrograms Versus Electrocardiograms Interpretation of intracardiac electrograms lies at the core of electrophysiology [5]. Before any attempt is made to interpret electrograms, it is important to have an understanding of what electrograms are and how these differ from the surface ECG (Fig. 1.6). A surface ECG evaluates the net movement of electrical signal (or vector) in the direction of a given lead. A net movement of a vector towards the positive pole will result in a positive deflection and vice versa. Thus, the surface recording is the sum total of electrical vectors in the direction of a lead. In contrast, an electrogram displays

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Electrograms (EGM)

Electrocardiograms (ECG)

Lead II

Atria

1-2

AV node

2-3

Ventricle 3-4

Catheter

4

3

2

1

Fig. 1.6  Electrograms versus electrocardiograms. The figure shows the cardiac impulses progressing from the atria (green arrows) through the AV node (yellow) and the ventricles (blue arrows). The surface ECG shown on the right, lead II as an example, displays the net vector of electrical activity across the entire heart travelling in the direction of the lead (seen by the –to +arrow). In contrast, an electrogram is a measure of electrical activity on the myocardial surface at the location

that electrodes are placed on the tissue. In this example, a quad (4 electrode) catheter positioned on the RV free wall is detecting electric signals between each of the bipole pairs (1–4). The activation wave from moves across the catheter from distal to proximal (1–4) and so successive proximal bipoles are activated slightly later. Further details are in the text

the electrical information at the tissue surface which occurs between either between a set of two electrodes (bipolar signal) or by an individual electrode (unipolar). It only displays the electrical activity at the local myocardium. This displays as a sharp discreet electrogram with wavefronts moving along the bipole from distal to proximal producing a positive deflection, and vice versa. Thus, information regarding the movement of wavefronts or the direction on an electrical impulse throughout the heart, requires examining the timing relationship between electrograms from electrodes simultaneously positioned in different regions of the heart. Alternately, and often in parallel, the timings of electrograms relative to a stable reference can be recorded both in time and three-dimensional space to create a colour coded map of electrical activation (see sections on 3D mapping).

1.5 Interpretation of Electrograms

Decoding the jargon: Intracardiac electrograms These are electrical recordings taken from inside the heart using EP catheters. Catheters make recordings from specific anatomical areas within the heart: the atrium, the His bundle, the mitral annulus (via the coronary sinus), the ventricle.

Why do we need these? Intepretation of these separates a cardiologist from an electrophysiologist. They represent electrical activation of the heart at the location of the poles of the catheter.

This section details the standard positioning of catheters for an electrophysiological study, followed by some examples of how electrograms can be used to understand how electrical activity is propagating in the heart.

1.5.1 Standard Diagnostic Catheter Positions A standard EP study can consist of up to 4 catheters positioned in standardised positions in the heart to record electrograms. Catheters can have variable numbers of electrodes numbered 1, 2, 3, … etc. By convention, numbering starts from the distal end of the catheter (so 1–2 refers to the bipole between the tip and next most proximal electrode). Table 1.4 below summarises the position and the catheters for a standard EP study. Practices will vary across laboratories between the use of 2, 3 or 4 catheters for an EP study. Catheter positions and the corresponding normal appearance of electrograms in sinus rhythm are illustrated in Fig. 1.7a, b. These catheters are termed ‘diagnostic’ catheters as they can only detect electrical signals and pace the heart but cannot ablate or deliver energy. Other catheters used for specific purposes are described in the relevant sections. As shown in Fig. 1.7a the initial activation

1  The Basic Language of Cardiac Electrophysiology …

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Table 1.4  Standard diagnostic catheterlocations Catheter High right atrium (HRA) His bundle catheter

Number of electrodes 4 (2 bipoles) Quad catheter

Standard Position High lateral right atrium

Typical pattern of electrogram activationa A sharp discreet electrogram on time or just preceding P wave onset in sinus rhythm

4–6 electrodes (2–3 Spans the septal aspect of the A sharp discreet atrial electrogram followed by a small His bundle bipoles) tricuspid annulus adjacent to the potential and septal ventricular electrogram Quad or Hexpole AV node catheter Coronary 10 electrodes (5 Within the main body of the Sequential atrial activation from proximal (septal) to distal (lateral sinus catheter bipoles) coronary sinus. Usualy proximals LA). Far field ventricular electrograms may also be seen Decapole catheter poles positioned at the CS os Right ven4 electrodes (2 Distal RV septum Discreet ventricular electrogram, closely timed to the ventricular tricular apex electrodes) EGM on the his catheter Quad catheter aIn the absence of significant structural heart disease, accessory pathways or bundle branch block

is seen in the high right atrial catheter (HRA) catheter on time or ahead of P wave onset on the surface ECG. Atrial activation spreads across the atria to the AV node across the septum to the LA. The atrial deflection on the His bundle catheter (HBE) indicates the impulse reaching atrial side of the AV node complex. At a similar time, the proximal CS (CS9–10) electrodes are activated and the LA is subsequently activated from the septum laterally, as seen by the successively later electrograms as the impulse moves along CS catheter from proximal to distal. The delay between the atria and ventricle due to decrementation in the AV node can be best appreciated in the HBE catheter where a delay between atrial and ventricular activation can be appreciated. The sharp discreet electrogram labelled “H” indicates activation of the His bundle just distal to the AV node. The large ventricular electrogram on the HBE catheter indicates ventricular activation of the proximal septum adjacent to the His bundle. This is shortly followed by activation of the RVA catheter fairly rapidly after the His bundle, as the right bundle branch fascicle inserts into the RV apex. There are several standardised intervals measured in sinus rhythm which should be documented in every EP study. These are listed and described in Table 1.5. In addition to diagnostic catheters, the ablation catheter, often termed the MAP catheter, is utilised once ablation is deemed appropriate. Whilst the mechanics of the ablation catheter will be described in detail elsewhere, this catheter has 4 electrodes (2 bipoles). The distal tip also delivers ablation energy. Unlike diagnostic catheters which stay located in a defined position, this catheter has an in-built steering mechanism and is designed to be moved around the heart (also often termed a ‘roving’ catheters) to allow for mapping and/or ablation.

1.5.2 Using Electrograms to Map Mapping is the process of using electrograms to identify the source of an arrhythmia focus. How can we use the information from electrograms to help us understand what is electrically occurring inside the heart? As mentioned before, arrhythmias can be focal or re-entry in nature. In the case of focal arrhythmias, a single focus of activation must be localised to treat the arrhythmia. Figure 1.8 shows the MAP catheter at 3 different positions around a focal origin of an arrhythmia. In position A, the proximal electrodes (3–4) are closer to the focus than the distal electrodes (1–2). Therefore the proximal electrodes precede the distal suggesting that the focus is closer to where MAP3–4 is. Also, the predominantly negative deflection suggests the focus is activating the electrodes from 4–3 to 2–1—consistent with the focus being behind the catheter. In position B, MAP1–2 is now closer to the focus than MAP3–4 so MAP1–2 now leads MAP3–4. The unipolar signal from the distal tip (MAP1) has a notable R wave, suggesting that electrical signal is still traveling to the tip from another location. In position 3, the MAP1–2 is ahead of MAP3–4, and the MAP1–2 signal is much earlier than the reference electrogram. The unipolar signal from MAP1 shows a ‘Q/S’ pattern with no R wave. This means all electrical signals are moving away from the tip of the catheter suggesting that this site is the arrhythmia focus. This process of using the relationship between electrograms on the MAP catheter and a stable reference catheter, is called mapping and is a fundamental principle of electrophysiology procedures. This process is aided significantly by the use of a 3-D mapping system which allows the location and timing of a large number of points to be recorded and displayed visually.

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(a)

Standard catheter positions

Electrograms

Surface ECG II

HRA

High right atrium (HRA) catheter A

H

Coronary sinus (CS) catheter (running along posterior MV annulus)

V

HBE 1-2

CS 9-10

His bundle (HBE) catheter

CS 7-8 CS 5-6 CS 3-4 CS 1-2

Right ventricular apex (RVA) catherter

RVA

(b)

Fig. 1.7  a Standard catheter positions. This cartoon illustrates 4 standard catheter positions. CS catheter runs posteriorly along the mitral valve annulus as indicated by the dotted line. The A minimum of 2 catheters are required for an EP study, usually a HIS catheter and CS catheter. Corresponding electrograms from the catheters in normal sinus rhythm are shown on the left panel. Further details are

described in the text. b A standard set up on a screen for an EP recording system. There are 4 catheters in the standard position, high right atrium, coronary sinus, His, and right ventricular apex. The signals bipolar signals from the atrium, His bundle, and right ventricle are all highlighted. The screen runs more slowly at 100 mm/s rather than the 25 mm/s usually seen for a 12 lead ECG

1  The Basic Language of Cardiac Electrophysiology …

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Table 1.5  Baseline intervals Interval

From

Represents

PR interval

Start of P wave on surface ECG to start of QRS Overall conduction time over the atria until venon surface ECG tricular depolarisation PA interval Earliest atrial activation in any channel (EGM or Conduction from the sinus node to the AV node surface ECG) to atrial electrogram on His catheter complex AH interval Atrial EGM on his catheter to the His bundle Conduction across the AV node electrogram HV interval His bundle electrogram to earliest ventricular Conduction over the His-Purkinje conduction activation in any channel (EGM or surface ECG) system QRS duration Start of QRS to the end of the start of the ST seg- Time for ventricular depolarisation ment on the surface ECG Corrected QT intervalb Start of the QRS to the end of the T wave on Combined time of ventricular depolarisation and surface ECG repolarisation aFor adults only. Significant variation may exist. These values are a rough guide only bTypically corrected for rate using Bazett’s formula

Normal rangea (ms) 120–200 25–55 55–125 35–55 0° AS

aVF ±

aVF -

QRS axis < 0° MS

LPS

RPS

aVF +

aVF ±

+

+

±

RA RAP RAL

RL

RP RPL

channel blockers, digoxin, adenosine) is contraindicated due to the possibility of a paradoxical increase in ventricular rate and an increased risk of developing ventricular fibrillation. Presence of intermittent pre-excitation on ECG or a Holter monitor or loss of pre-excitation at higher heart rates during an exercise test suggests a “safe pathway” unlikely to cause ventricular fibrillation. Conversely, the evidence of pre-excited RR intervals shorter than 250 ms in atrial fibrillation indicates a high risk pathway (Table 4.1). The EP study remains the best way to assess pathway properties, including its safety and the ability to participate in re-entrant tachycardias. Asymptomatic manifest pre-excitation does not require treatment but it is reasonable to offer patients a diagnostic EP study to assess pathway properties and ablate the pathway if it demonstrates properties suggestive of an increased risk of ventricular fibrillation and sudden cardiac death. Wolff–Parkinson–White syndrome can be treated with anti-arrhythmic drugs or with an EP study and ablation procedure. Antiarrhythmic drugs that primarily modify conduction through the AV node include: digoxin, verapamil/diltiazem, beta blockers. Antiarrhythmic drugs that depress conduction across the accessory pathway include: class I drugs (procainamide, disopyramide, propafenone, flecainide), class III drugs, such as ibutilide, sotalol, and amiodarone. It is advisable to combine a class I/III antiarrhythmic drug and an AV node blocking drug (for example flecainide and bisoprolol).

4  Accessory Pathways and Atrioventricular … Table 4.1  Features of a “dangerous” accessory pathway

53 • A short pathway effective refractory period • Presence of multiple pathways • Symptomatic SVT • Inducibility of AVRT or atrial fibrillation during the EP study

4.4 EP Study The most pertinent features of an EP study related to accessory pathways are discussed here.

Key steps: An EP study for suspected accessory pathways This can appear very complex to a newcomer. Essentially four things are being done when assessing an accessory pathway. Once these four aims are understood, it is easier to develop an understanding of the more advanced concepts: • Observe in sinus: Is there any evidence of pre-excitation on the ECG? Is there a short HV interval? • Test in sinus: Pacing the ventricle or the atrium and observing the response of the atrium or ventricle respectively. • Observe in tachycardia: What does the 12 lead ECG show in tachycardia. What is the activation pattern of the atrium and ventricle during tachycardia. • Test in tachycardia: Pacing manoeuvres during tachycardia can give clues to the circuit involved. Such manoeuvres include entrainment, His synchronous VPBs

Core Concept: When pacing V, look at the A When pacing the ventricle during an EP study, the operator should focus on the response of the atrium. Is there 1:1 conduction? If so, this could be via the pathway or the AV node. The way the atrium is activated gives a clue to which (see “Decoding the jargon: Concentric vs. eccentric activation”). A lack of 1:1 conduction suggests no conduction via the pathway.

When VA conduction is noted, it is important to differentiate if this nodal (via the AV node) or up an accessory pathway. In nodal conduction VA time would gradually increase with during a retrograde curve. If the patient has an AP, VA tends to be fixed before a sudden loss of VA conduction. The pattern of the retrograde atrial activation also gives an indication of where the pathway is located. For example, a left sided accessory pathway would have the earliest atrial activation in the distal electrodes of the coronary sinus catheter (CS1–2) (with the CS9–10 at the CS OS) (Fig. 4.3). Pacing the ventricle and observing the retrograde A conduction can help ‘bracket’ the location of an accessory pathway. This is done by moving the CS catheter to look for the earliest atrial activation on an electrode pair with later activation on adjacent electrode pairs.

4.4.1 Baseline Surface ECG—Pre-excitation can be seen in patients with manifest pre-excitation. Pre-excitation can be seen on the His catheter with the HV interval being very short or even negative (Normal HV interval: 35–55 ms). The HV interval is measured from the His electrogram to the earliest V (usually on the surface ECG) (Fig. 4.2).

4.4.2 Ventricular Pacing The ventricle can be paced at incremental rates called Incremental Ventricular Pacing (IVP) or a retrograde curve where the ventricle is paced at a fix rate for 8 beats (known as a drive train conventionally at 600 and 400 ms) with an extra beat delivered at progressively shorter coupling intervals following each repeat of 8 stimuli.

Decoding the jargon: Eccentric versus Concentric Activation When the ventricle is paced and the beat is conducted to the atrium, the order in which the catheters demonstrate activation of the atrium gives a clue to the presence of a pathway. • Concentric activation: This suggests conduction from the ventricle to the atrium via the His-Purkinje system and AV node. The earliest atrial signals are seen closest to the AV node (the His catheter and proximal CS) and the latest ones in the distal CS and high right atrium. • Eccentric activation: This suggests conduction from the ventricle to the atrium via a pathway and not the AV node. The earliest atrial activation is seen closest to the accessory pathway. In the case of a left lateral pathway this might be the distal electrodes of the coronary sinus catheter.

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Fig. 4.2  Pre-excitation is seen on surface ECG. Earliest V in distal coronary sinus. HV interval is negative with His signal buried in V on His channel

Fig. 4.3  Pacing the ventricle. In this example conduction to the atrium is seen. The earliest signals are seen in CS 1, 2, the distal electrodes of the coronary sinus, indicating there is a left lateral accessory pathway

4  Accessory Pathways and Atrioventricular …

4.4.3 Atrial Pacing Pacing the atrium at an incremental rate or Incremental Atrial Pacing (IAP) for patients with APs helps determine two important properties of the AP. 1. Pathway Effective Refractory Period (ERP) 2. Rate that gives maximal pre-excitation A sudden loss of pre-excitation during IAP is known as the pathway ERP. This is important as pathways that cannot conduct below 250 ms are usually considered to be safe. Determining the rate of maximal pre-excitation is useful during antegrade mapping of the AP (see below). Performing an antegrade curve is an other atrial pacing manoeuvre. Similar to the retrograde curve, a series of 8 stimuli at a fixed cycle length (600 and 400 ms) is delivered with a progressively shorter coupling interval on the final extra stimulus. This can help determine pathway ERP and rate of maximal pre-excitation. AV node duality can sometimes be present when performing baseline testing (See Chap. 3).

4.4.4 Analysing the Tachycardia Tachycardia can start spontaneously, often with catheter placement or with the addition of a chronotropic agent such as isoprenaline. A key finding in AP mediated tachycardia is VA association, as both the atrium and ventricle are obligatory parts of the circuit. If there is VA dissociation, this can rule out AP mediated tachycardia and other mechanisms should be considered.

4.4.5 Diagnostic Manoeuvres During Tachycardia Several manoeuvres in tachycardia are useful in determining the diagnosis and support the findings. The first is entrainment (see Chap.  1: Decoding the jargon— Entrainment). This involves pacing the ventricle at a cycle length slightly shorter than the tachycardia. On termination of pacing it is important to look for the following: 1. Was entrainment successful? This can be done by measuring successive A–A intervals up until the last paced ventricular beat and ensuring they equal the paced rate. 2. What was the ‘response’ on termination of pacing, i.e. VAV or VAAV. A VAAV response is consistent with an atrial tachycardia where as a VAV response can be seen in both AVNRT and AVRT

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3. Post pacing interval-tachycardia cycle length (PPI-TCL) this should be shorter than V4) and left superior frontal plane axis [44, 55–57].

7  Ventricular Ectopic Ablation

Core concepts: ECG features of ventricular ectopics • Idiopathic PVCs should be recognized in surface ECG • Outflow tract PVCs: inferior axis, mostly LBBB morphology, relatively narrow QRS complexes • Left fascicular PVCs: feature of typical bifascicular block (left anterior or posterior fascicular block + RBBB) and even narrower QRS complexes • PVC morphology in structural heart disease is more variable. However, general principles are applicable • LBBB morphology indicates right ventricular or septal origin, RBBB morphology indicates left ventricular origin • Precordial positivity speaks in favor of more basal PVC exit, while negativity speaks in favor of more apical exit • Inferior axis indicates superior PVC exit, while superior axis indicates inferior exit.

7.4 Electophysiological Features and Mapping 7.4.1 Mapping Strategies 7.4.1.1 “Earliest Local Activation” and Unipolar Electrograms The most commonly used mapping method is the local bipolar electrogram derived from the ablation catheter which is moved around to potential ablation sites. This local signal is measured compared to the onset of the QRS. A local early activation of −20 to −25 ms or more before the QRS is indicative for an area close to the PVC origin (“earliest local activation”). Unipolar electrograms also play an important role with this mapping method. When a QS pattern is recorded in the unipolar electrogram, it indicates an area from which the electrical impulse originates, indicating the PVC focus. The combination of a unipolar QS pattern and bipolar earliest activation is a sign of optimal ablation region indicating the PVC origin. Catheterinduced ectopics can resemble the index PVC during mapping near the area of interest, so care should be taken to look out for these.

7.4.1.2 Pace-Mapping This mapping method provides the chance to localize and ablate PVCs when the frequency of ectopy is low. Even one PVC is enough to perform a pace-map. During pace-mapping, a paced QRS complex generated at a potential ablation site is compared with the intrinsic spontaneous PVC recorded before. However, this mapping method may be challenging. Comparing paced and intrinsic QRS complexes by hand is cumbersome and time-consuming. Automatic algorithms can help to ensure precise mapping. High matching rates should be aimed for.

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The stimulation output plays a crucial role in defining a precise area for the PVC origin. A high stimulation output risks depolarizing broad areas of myocardium, decreasing the specificity of the obtained pace-map. Jargon decoded: Mapping techniques Activation mapping: The ablation catheter is moved to potential ablation sites and if a PVC is seen, the local signal on the catheter is compared to the onset of the QRS. The earlier the local signal the better. This requires relatively frequent PVCs during mapping. Pace-mapping: The ablation catheter is moved to potential ablation sites and used to pace the tissue there. If the resulting QRS matches the PVC, this suggests this is a promising site for ablation. This strategy is more useful with infrequent PVCs.

7.4.1.3 3D Mapping Systems 3D mapping (see Chap. 2) has had a dramatic impact on PVC ablation. With the help of new algorithms, the “classic” mapping methods mentioned above are performed and evaluated automatically in combination with 3D mapping. The general strengths and weaknesses of 3D mapping apply to PVC ablation. All the current 3D mapping systems described in Chap. 2 can be used for this. Certain features of 3D mapping are particularly useful for PVC ablation. Activation mapping represents a combination of the identified timing of local activation in reference to a chosen reference with the localisation of the catheter on the 3D map. A surface ECG lead with a sharp R- or S-wave from the PVC will mostly be chosen as the reference. The areas of early and late activation are demonstrated using a colour scale, which can be adjusted according to user’s preference (red is usually early, purple late). Automated morphology criteria are available so mapping points are only acquired when PVCs match the “clinical” one causing symptoms. This is an important feature as catheter manipulation in the ventricle can generate ectopics many of which will be different to the target. It also allows multipolar catheters to quickly generate high density maps. The mapping systems also provide the option to map during pacing, enabling an automatic pace-map. A percentage is often used to quantify how closely the paced beat matches clinical ectopic and this is represented in a colour coded manner on the 3D map. Figure 7.5 shows an activation map of a PVC originating from the RVOT in a child.

7.5 Ablation Strategies for Ventricular Ectopy Strategies for ablation and success rates vary according to the site of ablation and the most common sites are covered here.

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Fig. 7.5  An activation map on the left with the corresponding IEGM on the right. The red dots represent the area of successful ablation. The corresponding point of early activation on the IEGM is highlighted with a white arrow (figure courtesy of [58])

7.5.1 Right Ventricular Outflow Tract The RVOT is the most common site for PVCs in structurally normal hearts (70–80%) [59]. In most cases, the origin is the septal RVOT inferior to the pulmonary valve, the most common origin being the anteroseptal and midseptal area. A non-irrigated 4-mm ablation catheter can be used, but irrigated contact force catheters can provide more information. Application of 20–30 W for non-irrigated and 20–40 W for irrigated catheters is usually enough to suppress PVC activity [60]. Rarely the origin is in the pulmonary sinus cusps. Due to the proximity of this area to the aorta and the aortic cusps, ventriculography, pulmonary artery angiography and/or coronary angiography can be performed before ablation [61].

7.5.2 Left Ventricular Outflow Tract The LVOT accounts for approximately 10% of idiopathic PVCs [59]. It is frequently difficult to differentiate the anatomic origin of LVOT, aorto-mitral continuity, aorta and LV summit as shown in Fig. 7.5. The anatomy of this region is

much more challenging than that of the RVOT. Achieving sufficient stability in this region can be challenging. The ablation is performed via an irrigated 3.5 mm catheter in order to allow higher RF energies and prevent the formation of thrombi [62]. In particular, contact-force catheters can be useful to control stability of the catheter and effectiveness of the lesion. Irrigated RF energy of maximal 30 W is usually applied in this region [63]. In case of insufficient PVC suppression despite optimal mapping conditions, an origin from adjacent structures should be considered. A transeptal approach should be considered providing better stability in some regions like the septal LVOT.

7.5.3 Aorta In a small number of cases (1 cm between the ablation site and ostium of the

7  Ventricular Ectopic Ablation

coronary artery is considered safe for ablation [65]. Due to its relationship with the RVOT, thorough mapping of the RVOT may be performed before deciding to ablate in the aorta.

7.5.4 Coronary Sinus and LV Summit The coronary sinus (CS) surrounds the mitral valve from posterior and continues anteriorly, and provides a route to access the LV summit. PVCs can arise from the epicardial area of the CS veins, the great cardiac vein (GCV) and the anterior inter-ventricular vein (AIV) [65, 66].

Decoding the jargon: LV summit The LV summit can be a source of ectopy. As the name implies this is the highest point of the LV. It is on the epicardial surface, and is bounded by the left anterior descending artery and left circumflex artery and great cardiac vein. This can be a particularly challenging area to ablate.

There are particular limitations in case of ablation via the CS. Low blood flow in the CS can pose an important challenge in trying to deliver sufficient RF energy and consequently an effective lesion. The cooling effect is usually low and impedance and temperature rise quickly. The wall of the veins are thin, so application of irrigated RF energy should be applied with caution in order to avoid pericardial tamponade and damage to the coronary arteries. Coronary angiography can be useful to identify the exact location of the adjacent coronary arteries. The ability to reach these epicardial regions depends very much on the anatomy of the CS as well as the history of cardiac surgery. CS angiography can be helpful to assess CS anatomy. The LV summit can rarely be the origin of idiopathic PVCs and is complex to reach via an endoardial approach [65, 66]. This triangular region is bounded by the left anterior descending, the left circumflex artery and the GCV. Although parts of the LV summit can usually be reached via the CS, CS anatomy is variable and does not always enable ablation in this region. Typically, the lateral part of the LV summit is accessible for mapping through the CS. Thus, an epicardial approach can be considered in certain cases, especially in PVC-induced cardiomyopathy.

7.5.5 Papillary Muscles The papillary muscles can, in rare cases, be the PVC origin in structurally normal hearts [35, 36]. It can be challenging to distinguish a PVC origin from a papillary muscle compared

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to PVCs involving the specific conduction system, although PVCs from the papillary muscles are broader and look less like typical bundle branch block [67]. Papillary muscle PVCs can demonstrate a variation of exits leading to shifts in QRS morphology, thus making activation mapping challenging. The same is true for pace-mapping, since even in the case of adequate catheter stability multiple QRS morphologies can be induced due to the multiple exits. Thus, ablation at a site of good pace-map may not lead to immediate PVC suppression but merely to a modulation of the exit site. Due to the thicker myocardium in these regions, higher RF energies of 30–40 W are acceptable [62]. Typically, irrigated 3.5 mm catheters are used and RF energy is applied for 1–2 min if effective. If no adequate stability can be achieved, cryoablation can be considered [54, 68]. Key points • The most common origin of PVC in structurally normal hearts is the RVOT • Ablation of idiopathic PVCs (especially of RVOT origin) is associated with a high success rate • Ablation via the CS represents a feasible approach for epicardial PVCs • Ablation of PVCs in channelopathies can be a therapeutic strategy in selected patients.

7.5.6 Success Rates and Complications Success rates of PVC ablation (with definition of acute success as an 80% reduction of the initial PVC burden) generally depend on PVC origin, PVC frequency, number of PVC morphologies and operater and centre experience [69]. Quoted rates are variable and range between 65–95%, with the highest rates from the RVOT and the lowest due to epicardial origins. In patients with PVC-induced cardiomyopathy, catheter ablation can lead to a significant reduction of PVC burden (from 27 to 5%) and increase in LVEF (from 38 to 50%) [5]. In patients with frequent PVCs and non-ischaemic cardiomyopathy, LVEF and NYHA functional class can be improved by successful PVC ablation [14]. Usually, PVC-induced cardiomyopathy resolves within 4 months after successful catheter ablation but can be delayed up to 45 months [70]. Complication rates during ablation procedures of PVCs have been reported to occur at about 5% for all complications and 2.4–3.4% for major complications [5, 33, 71]. More than half of the complications are related to vascular access [5, 33]. Cardiac perforation and pericardial tamponade were reported in less than 1% [5, 71]. Other less frequent complications include development of AV block, heart failure exacerbation, coronary artery occlusion with myocardial infarction, stroke and pulmonary embolus [5, 69, 71].

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97 49. Kamakura S, Shimizu W, Matsuo K, Taguchi A, Suyama K, Kurita T, Aihara N, Ohe T, Shimomura K. Localization of optimal ablation site of idiopathic ventricular tachycardia from right and left ventricular outflow tract by body surface ECG. Circulation. 1998;98:1525–33. 50. Betensky BP, Park RE, Marchlinski FE, et al. The V(2) transition ratio: a new electrocardiographic criterion for distinguishing left from right ventricular outflow tract tachycardia origin. J Am Coll Cardiol. 2011;57:2255–62. 51. Yoshida N, Yamada T, McElderry HT, Inden Y, Shimano M, Murohara T, Kumar V, Doppalapudi H, Plumb VJ, Kay GN. A novel electrocardiographic criterion for differentiating a left from right ventricular outflow tract tachycardia origin: the V2S/V3R index. J Cardiovasc Electrophysiol. 2014;25:747–53. 52. Zhang F, Hamon D, Fang Z, Xu Y, Yang B, Ju W, Bradfield J, Shivkumar K, Chen M, Tung R. Value of a posterior electrocardiographic lead for localization of ventricular outflow tract arrhythmias: the V4/V8 ratio. JACC: Clin Electrophysiol. 2017;3:678–86. 53. Ito S, Tada H, Naito S, Kurosaki K, Ueda M, Hoshizaki H, Miyamori I, Oshima S, Taniguchi K, Nogami A. Development and validation of an ecg algorithm for identifying the optimal ablation site for idiopathic ventricular outflow tract tachycardia. J Cardiovasc Electrophysiol. 2003;14:1280–6. 54. Yamada T, Doppalapudi H, McELDERRY HT, et al. Idiopathic ventricular arrhythmias originating from the papillary muscles in the left ventricle: prevalence, electrocardiographic and electrophysiological characteristics, and results of the radiofrequency catheter ablation. J Cardiovasc Electrophysiol. 2010;21:62–9. 55. Sadek MM, Benhayon D, Sureddi R, et al. Idiopathic ventricular arrhythmias originating from the moderator band: electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm. 2015;12:67–75. 56. Al’Aref SJ, Ip JE, Markowitz SM, Liu CF, Thomas G, Frenkel D, Panda NC, Weinsaft JW, Lerman BB, Cheung JW. Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ: Arrhythmia Electrophysiol. 2015;8:616–24. 57. Paraskevaidis S, Theofilogiannakos EK, Konstantinou DM, Mantziari L, Kefalidis C, Megarisiotou A, Sarafidou A, Styliadis I. Narrow QRS complex in idiopathic (fascicular) left ventricular tachycardia. Herz. 2015;40:147–9. 58. Akdeniz C, Gul EE, Celik N, Karacan M, Tuzcu V. Catheter ablation of idiopathic right ventricular arrhythmias in children with limited fluoroscopy. J Interv Card Electrophysiol. 2016;46:355–60. 59. Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012;59:1733–44. 60. Heeger C-H, Hayashi K, Kuck KH, Ouyang F. Catheter ablation of idiopathic ventricular arrhythmias arising from the cardiac outflow tracts–recent insights and techniques for the successful treatment of common and challenging cases. Circ J. 2016;80:1073–86. 61. Liao Z, Zhan X, Wu S, et al. Idiopathic ventricular arrhythmias originating from the pulmonary sinus cusp: prevalence, electrocardiographic/electrophysiological characteristics, and catheter ablation. J Am Coll Cardiol. 2015;66:2633–44. 62. Pathak RK, Ariyarathna N, Garcia FC, Sanders P, Marchlinski FE. Catheter ablation of idiopathic ventricular arrhythmias. Heart Lung Circ. 2019;28:102–9. 63. Hachiya H, Aonuma K, Yamauchi Y, Igawa M, Nogami A, Iesaka Y. How to diagnose, locate, and ablate coronary cusp ventricular tachycardia. J Cardiovasc Electrophysiol. 2002;13:551–6. 64. Yamada T, McElderry HT, Doppalapudi H, et al. Idiopathic ventricular arrhythmias originating from the aortic root prevalence, electrocardiographic and electrophysiologic characteristics, and results of radiofrequency catheter ablation. J Am Coll Cardiol. 2008;52:139–47.

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8

Ventricular Tachycardia Ablation Neil T. Srinivasan and Alex Cambridge

Abstract

Ventricular tachycardia (VT) ablation can in many cases be one of the most challenging areas of invasive electrophysiology. Reducing symptoms associated with VT and reducing the morbidity associated with ICD shocks remain the most common indications for VT ablation. There are three broad categories of VT: VT secondary to ischaemic heart disease, non-ischaemic heart disease, and normal heart VT. The approaches to ablation in each setting are slightly different and are outlined here.

Keywords

Monomorphic ventricular tachycardia · Polymorphic ventricular tachycardia · Ventricular fibrillation · Substrate ablation · Late potentials

8.1 Introduction Ventricular tachycardia (VT) is an important cause of morbidity and mortality. The major advance in the prevention of sudden cardiac death from ventricular arrhythmia has been the introduction of the implantable cardioverter defibrillator (ICD) [1]. However, recurrent VT occurs in roughly 20–30% of primary prevention ICD recipients and 40–60% of secondary prevention recipients. Management of VT and ICD shocks with medical therapy such as beta-blockers and amiodarone while reducing the rate of ICD therapy, can result in a significant burden of drug-related adverse effects

N. T. Srinivasan (*) · A. Cambridge  Bart’s Heart Centre, St Bartholomew’s Hospital, London, UK e-mail: [email protected]

[2]. Thus catheter ablation is an important strategy in reducing VT burden and can be life-saving in incessant VT [3]. This is supported by evidence from the VANISH trial, which showed a reduction in the composite endpoint of death, VT storm or ICD shocks in patients who underwent ablation as opposed to escalation of anti-arrhythmic therapy following recurrent VT [4].

8.2 Types of VT Clinical history and the appearance of the surface ECG provide important clues as to the aetiology of the VT (Table 8.1). Monomorphic VT occurs most commonly due to reentry over a fixed anatomical barrier, namely ventricular scar, and suggests ventricular activation using a fixed anatomical path over a fixed anatomical substrate or a focus for triggered activity that can be targeted for ablation. Polymorphic VT implies that the activation sequence is continually changing and the VT circuit follows a variable path. Numerous conditions are associated with polymorphic VT (Table 8.1) and ablation is only indicated if a clear monomorphic ectopic triggers the VT.

8.3 Ablation of Scar Related Monomorphic VT Sustained monomorphic VT in the context of structural heart disease is the most commonly seen VT in clinical practice. Myocardial scar secondary to previous myocardial infarction or cardiomyopathies contains within it regions of abnormal remodelling, with regions of dense fibrosis surrounded by surviving myocardial bundles. This results in regions of slow electrical conduction and conduction block which facilitate re-entry. Additionally, scar-related VT often utilises a region of slow conduction within the scar known as an isthmus

© Springer Nature Switzerland AG 2020 A. Sohaib (ed.), Decoding Cardiac Electrophysiology, https://doi.org/10.1007/978-3-030-28672-9_8

99

Mitral annulus Fasicular reentry (verapamil sensitive)

Outflow type

Purkinje disease

Monomorphic

Type of VT Polymorphic

Causes Myocardial infarction Ion channel disease (long-QT, short-QT, Brugada, CPVT, early repolarization syndrome) Idiopathic VF, hypertrophic cardiomyopathy and other cardiomyopathies Scar related—previous infarction, cardiomyopathies • LV—idiopathic, myocarditis, sarcoid, Chagas, idiopathic aneurysm, arrhythmogrnic cardiomyopathy • RV—ARVC, sarcoid, idiopathic congenital—surgical incision sites, tetralogy of fallot Bundle branch reentry • Normally coexistent conduction system disease Enhanced automaticity in Purkinje system Focal in origin Right • Arise from RVOT or Pulmonary Artery Left • LVOT, Aortic Sinus, Epicardial Involves the mitral annulus Idiopathic VT in structurally normal heart patient. Often young 15–40 years. RBBB with left axis devotion and QRS 70% TCL

Bystander Concealed Fusion PPI > +30ms VTCL Stim-QRS > Egm-QRS

Isthmus Exit Concealed Fusion PPI = VTCL +/- 30ms Stim-QRS = Egm-QRS Stim-QRS 30 ms, and this difference will approximate the S-QRS–EGM-QRS discrepancy (i.e. these two measurements are essentially surrogates). Based on these findings, the likelihood of ablation success can be stratified, with 3% termination at remote bystander regions, 10% termination in outer loop sites and 37% termination at exit sites (S-QRS ≤ 30% of the TCL, with concealed fusion), with similar good success at central

Fig. 8.2  An example of activation mapping. The middle panel represents a 3-dimensional map made of the heart using intracardiac catheters. Panels to the left and right represent the signals recorded within the heart and the surface ECG. The blue signal represents the ablation catheter signal recorded during mapping and this is timed against the

onset of the QRS to estimate where the location corresponding to the signal (red arrows) is in relation to the VT circuit. In the left panel the local fractionated signal is after the QRS representing a VT entrance site. In the right panel this site precedes the QRS representing a VT exit site and a good ablation target

8  Ventricular Tachycardia Ablation

103

Entrainment With Concealed Fusion

(a)

yes

no PPI = VTCL +/- 30ms

PPI = VTCL +/- 30ms or S-QRS = Egm-QRS +/- 20ms

yes

no Outer Loop yes

no Remote Bystander

Bystander

S-QRS / VTCL X 100

70%

Inner Loop

Within Critical Isthmus

(b)

Fig. 8.3  a The first step in entrainment is to look for evidence of concealed fusion (the entrained QRS morphology looks similar to the VT morphology). Subsequent to this, using post pacing interval

(PPI)-VT-cycle length (VTCL) and Stim-to-QRS (S-QRS) may be used to determine the location of the pacing site as depicted in the flow diagram. b Example of concealed entrainment with PPI = VTCL  ± 30 ms

(S-QRS 31–50% TCL, with concealed fusion) and proximal (51–70% TCL, with concealed fusion) isthmus sites (Fig. 8.2) [7]. Inner loop regions have an S-QRS >70% and

are thought to represent regions of broad isthmus activation regions less amenable to ablation, with 9% tachycardia termination in studies [7].

104

N. T. Srinivasan and A. Cambridge

Jargon decoded: Approaches to VT ablation

Late Potential Ablation

• Activation mapping: A 3D map of the VT is made with the patient in VT. This is used to identify parts of the circuit which can be ablated to terminate the VT. • Entrainment mapping: While the patient is in VT, the ventricle is paced faster than the VT (entrainment) and this is used to identify how “close” to the circuit the ablation catheter is. This can help overcome the challenges of interpreting a potetially complex activation map. • Substrate mapping: Methods are used to identify “likely” sites for the VT to originate from (“the substrate”). This is usually scar tissue but details are presented in the relevant section.

Several definitions of late potentials (LP) have been defined. The most commonly used definition is double or multiple component electrograms separated by a 50 ms isoelectric line in sinus rhythm and 150 ms in RV pacing [10]. Others have suggested that late potentials should occur after the end of the surface QRS and be separated from the higher amplitude local ventricular electrogram component by 20 ms [11]. Regions with LP electrograms are highlighted for ablation in sinus rhythm or RV pacing, and studies have suggested that elimination of these areas may result in an 80% long-term VT ablation success rate [10, 11]. Besides the differences in the definition of late potentials, this method is further limited by a lack of clarity regarding how much areas should be sampled for LPs, the lack of physiological characterization of the substrate, the potential need to re-map to look for elimination of LPs, and what pacing methodology to use if any [12].

Why different methods? Substrate mapping allows the patient to undergo ablation when they are not in VT. This is advantageous if the VT is very fast or not haemodynamically tolerated. The other methods where the clinical VT is mapped and ablated are potentially more elegant as they offer greater assurance the clinical VT is terminated and non-inducible after ablation. This requires the patient to have a reasonable blood pressure for the duration that the mapping, manoeuvres and ablation are being performed.

8.3.1.3 Substrate Mapping An alternative to mapping patients in VT is substrate mapping. Substrate mapping is advantageous where the VT is haemodynamically unstable or there are multiple VTs. In the age of primary PCI with reduced myocardial damage, we increasingly see shorter isthmuses with more rapid and unstable VT. Substrate mapping has therefore become an important tool in the management and ablation of VT. Defining The Voltage Criteria For Scar: Peak-to-peak voltage on the bipolar electrogram is used to analyse whether the underlying myocardium is healthy or diseased. Standard cutoffs used define normal myocardium as >1.5 mV and dense scar as