Anatomy for cardiac electrophysiologists : a practical handbook 9781935395676, 193539567X

Table of contents :
Cover
Title Page
Copyright Page
Table of Contents
Foreword
Preface
Abbreviations
About the Authors
Overview of Anatomy and Imaging
Chapter 1: General Anatomy of the Heart
Chapter 2: The Neighborhood and Collateral Damage
Chapter 3: Overview of Imaging Modalities: Pros and Cons
Chapter 4: Positioning of Standard Catheters: Electrophysiology and Anatomy
Atria
Chapter 5: Electrical Anatomy and Accessory Pathways
Chapter 6: The Right Atrium Relevant to Supraventricular Tachycardia
Chapter 7: The Atrial Septum and Transseptal Access
Chapter 8: The Left Atrium and Pulmonary Veins Relevant to AF Ablation
Ventricles and Malformations
Chapter 9: The Right Ventricle
Chapter 10: The Left Ventricle
Chapter 11: Congenital Heart Malformations
Pitfalls
Chapter 12: Pitfalls and Troubleshooting
Index
Back Cover

Citation preview

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Anatomy

Cardiac Electrophysiologists for

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S. Yen Ho Sabine Ernst

Anatomy

Cardiac Electrophysiologists for

A Practical Handbook

Minneapolis, Minnesota

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© 2012 S. Yen Ho, Sabine Ernst 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/titles/detail/9780979016448 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:  2012937891 ISBN: 978-0-9790164-4-8 Printed in Canada.

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Contents Foreword  vii Preface  ix Abbreviations  xi About the Authors   xiii

OVERVIEW OF ANATOMY AND IMAGING   3 Chapte r 1  General Anatomy of the Heart   5 Chapte r 2  The Neighborhood and Collateral Damage   27 Chapte r 3  Overview of Imaging Modalities: Pros and Cons   39 Chapte r 4 Positioning of Standard Catheters: Electrophysiology and Anatomy   51

ATRIA  65 Chapte r 5  Electrical Anatomy and Accessory Pathways   67 Chapte r 6  The Right Atrium Relevant to Supraventricular Tachycardia   97 Chapte r 7  The Atrial Septum and Transseptal Access   129 Chapte r 8 The Left Atrium and Pulmonary Veins Relevant to AF Ablation   153 v

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VENTRICLES AND MALFORMATIONS   179 Chapte r   9 The Right Ventricle  181 Chapte r 10 The Left Ventricle  195 Chapte r 11 Congenital Heart Malformations  213

PITFALLS  231 Chapte r 12 Pitfalls and Troubleshooting  233

I n dex  243

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Contents

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Foreword It is my great pleasure to contribute a foreword to this excellent essay, which the authors modestly call a handbook for trainees in clinical cardiac electrophysiology. In fact, this book can be put to good use by even much more experienced cardiac electrophysiologists. As the frontiers of catheter ablation are being extended to more and more complex cases, including atrial fibrillation and complex flutter ablation and for patients with unstable ventricular tachycardia, it has indeed become crucial for the clinician to be comfortable with both normal anatomy and that associated with complex congenital heart disease. The authors, for example, have nicely correlated the need for understanding the relationship between the left atrium and the esophagus as well as the respective phrenic nerves so as to avoid collateral damage in the process of pulmonary vein isolation. A proper understanding of these and related relationships is critical for achieving excellent results with minimal harm to the patient. We are indeed fortunate to have an ideal partnership between an experienced and renowned clinician (Sabine Ernst) and an outstanding cardiac morphologist (Yen Ho) who are not only expert in their crafts but are also master teachers. This gem of a book stands alone as a brilliant starting point to meld interventional techniques such as ablation with the intricacies of cardiac anatomy.

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The authors are indeed to be congratulated for putting together the critical elements required by a clinician for proper ablation. The anatomical figures that are provided are spectacular. Moreover, the authors have greatly helped us by a sound integration of cardiac anatomy with current state-of-the-art imaging techniques, including intracardiac echocardiography, radiography, and 3D mapping, as well as simplified schematics where necessary. In summary, I can highly recommend this eminently readable and superb contribution not only to the beginning trainee in cardiac electrophysiology but also to my more experienced colleagues. The authors are to be congratulated for a superb effort, and I look forward to further educational contributions in the future. Melvin M. Scheinman, MD Professor of Medicine and Shorenstein Chair in Cardiology University of California, San Francisco

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Foreword

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Preface More and more complex electrophysiological procedures are carried out nowadays by invasive cardiologists who are guided mainly by 2D fluoroscopic imaging. Although performing simple procedures such as single- or dual-lead device implantation or supraventricular tachycardia ablation does not specifically require 3D visualization beyond standard C-arm angulations, the more complex procedures can benefit from detailed 3D display of the cardiac structures. For the trainee entering the world of electrophysiology (EP), the initial phase of getting the heart structure oriented is daunting, and for many, it is a major hurdle to overcome. Although the more experienced operators have learned to identify typical sites in the heart and are able to manipulate catheters to reach the targets, there remain details and variations of normal structures that can provide a challenge even for experts. This handbook is aimed primarily to facilitate the understanding of the normally structured heart and to link it to typical situations in the catheter laboratory. Whenever possible, standard projections are used to illustrate how to identify key features and help in orienting them in the “invisible,” nonradiopaque heart. Conventional imaging by fluoroscopy provides the majority of figures, but novel 3D imaging such as computed tomography, magnetic resonance imaging, and (intracardiac) ultrasound, as well as images provided by 3D mapping systems, is included to help with orientations.

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Starting with a general description of the heart and its neighborhood, the reader is invited to take a journey through the heart. By a combination of descriptions of anatomical features relevant to arrhythmias and EP perspectives in each chapter, beginning with supraventricular tachycardias, moving on to atrial fibrillation, and leading finally to ventricular arrhythmias, this handbook aims to provide a foundation and quick reference for trainees in their preparations for the realities of the catheter laboratory as well as a refresher for the more experienced operator. To this end, we have included a short chapter on the most frequently encountered congenital cardiac malformations as well as a chapter on troubleshooting issues. The latter is not meant to be exhaustive but is to provide some tips that may be useful at some time during one’s EP practice. Although EP remains one of the most challenging (and interesting!) subjects that invasive cardiology has to offer, it never becomes a routine. The “understand it before you (try to) treat it” concept is paramount. Cardiac anatomy plays a major role in this understanding, and even simple arrhythmias can present as a difficult task, when anatomy is “adverse” or deviates from the norm expected. Because learning is a two-way process, we are indebted to our students/trainees and colleagues for their discussions and contributions that have helped us prepare this handbook. We sincerely hope that in some way or another, however infinitesimal, this handbook adds to promoting safe practice in EP. We certainly hope it serves to help the operators find their way around the heart and enjoy invasive electrophysiology! Siew Yen Ho   Sabine Ernst Royal Brompton and Harefield NHS Foundation Trust January 2012, London, UK

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Preface

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Abbreviations 2D 3D 4D

two-dimensional three-dimensional four-dimensional

DAo DICOM

descending (thoracic) aorta Digital Imaging and Communications   in Medicine

AMRT

EP ER Es, Eso

electrophysiological/   electrophysiology Eustachian ridge esophagus

FAM FAT FP

fast anatomical mapping focal atrial tachycardia fast pathway of AVNRT

GCV

great cardiac vein

AVSD

atrial macroreentrant   tachycardia aorta accessory pathway/connection;   anteroposterior atrial septal defect atrioventricular atrioventricular node artery to the atrioventricular node atrioventricular nodal reentrant   tachycardia atrioventricular septal defect

HIS

c atheter recording the penetrating    bundle (bundle of His)

BB

Bachmann’s bundle ICD ICE ICV/IVC

implantable cardioverter-defibrillator intracardiac echocardiography inferior caval vein/inferior vena cava

LA LAA LAD

left atrium left atrial appendage left anterior descending coronary      artery

Ao AP ASD AV AVN AVNA AVNRT

CE CMR CRT CS CT CX

concealed entrainment cardiac magnetic resonance   (imaging) cardiac resynchronization therapy coronary sinus computed tomography circumflex artery

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LAO LAT LBB LCA LGE-MRI LI LM LS LSPV LSVC LV LVOT MA MAP MB MCV MP MV

mitral annulus mapping catheter moderator band middle cardiac vein multipurpose catheter mitral valve

SCV/SVC s uperior caval vein/    superior vena cava SMT septomarginal trabeculation SN sinus node SP slow pathway of AVNRT SR sinus rhythm SVT supraventricular tachycardia

OL OMV OT

outer loop obtuse marginal vein outflow tract

TC TCPC TEE/TOE

PA PB PCI

posteroanterior; pulmonary artery penetrating bundle (of His) percutaneous coronary   intervention patent/persistent foramen ovale phrenic nerve pulmonary trunk (main pulmonary   artery) pulmonary vein

Tr TS TV

terminal crest total cavopulmonary connection transesophageal echocardiography   (probe) trachea transseptal sheath tricuspid valve

VA VSD VT

ventriculoatrial ventricular septal defect ventricular tachycardia

WPW

Wolff-Parkinson-White (syndrome)

PFO PN PT PV

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RA RAA RAO RBB RCA RI RS RSPV

left anterior oblique local activation time left bundle branch left coronary artery late gadolinium enhancement    magnetic resonance imaging left inferior left main stem of LCA left superior left (lateral) superior pulmonary vein persistent left superior caval vein left ventricle left ventricular outflow tract

RV RVA RVOT

right atrium right atrial appendage right anterior oblique right bundle branch right coronary artery right inferior right superior right (septal) superior   pulmonary vein right ventricle right ventricular apex right ventricular outflow tract

Abbreviations

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About the Authors S. YEN HO, PhD, FRCPath, FESC, is Professor of Cardiac Morphology and Consultant Cardiac Morphologist at Royal Brompton Hospital, London, UK. Professor Ho is an expert in the postmortem examination of normally structured hearts, hearts with conduction disturbance, and hearts with congenital malformations. An internationally renowned speaker and lecturer, she has authored nearly 400 peer-reviewed articles, 100 textbook chapters, and 8 books. She serves on the Editorial Boards of Asian Cardiovascular and Thoracic Surgery Annals and the Journal of Cardiovascular Electrophysiology and is the current chairperson of the ESC Working Group on Development, Anatomy and Pathology. Sabine Ernst, MD, PhD, FESC, is Research Lead Electrophysiology and Consultant Cardiologist at Royal Brompton Hospital, London, UK. A pioneer in developing the technique of magnetic catheter ablation, Dr. Ernst’s clinical expertise is focused largely on ablation of complex arrhythmias with a special emphasis on atrial fibrillation, ventricular tachycardia, and ablations in patients with complex congenital heart disease. She serves on the Editorial Boards of the Journal of Interventional Cardiovascular Electrophysiology and Europace and has coauthored several chapters in cardiology and electrophysiology textbooks.

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Anatomy

Cardiac Electrophysiologists for

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overview of Anatomy and Imaging

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1

General Anatomy of the Heart

IN RECENT DECADES, DEVELoPMENTS of catheter interventional techniques for arrhythmias have made it necessary to have a sound understanding of cardiac anatomy primarily to avoid or minimize complications during interventional procedures. This knowledge is also relevant in providing the anatomical background for some of the substrates of certain arrhythmias and to finetuning interventional strategies and equipment.

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OVERVIEW OF ANATOMY AND IMAGING This chapter is an overview of the normally structured heart with particular focus on the spatial relationships of the cardiac chambers and neighboring structures relevant to cardiac interventions rather than to provide detailed anatomy of each cardiac chamber. The chambers, cardiac septum, and conduction system will be reviewed more explicitly in later chapters concerning the approaches to specific arrhythmias. We include in this chapter the coronary veins, interatrial connections, and fat pads because these are not covered elsewhere in the handbook, although they are relevant to interventions for arrhythmias.

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Chapte r 1  |   General Anatomy of the Heart

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The Heart and Structures in Its Neighborhood The heart must be viewed in the context of its location and relationship to surrounding structures. Although the position of the heart varies among people according to their build, in general terms the heart is a mediastinal organ positioned approximately two-thirds to the left and one-third to the right of the midline of the sternum (Figure 1.1). Lying between the lungs, the heart is nearer to the front of the thorax than the back. Its anterior surface, the right ventricle through the fibrous pericardium, lies immediately behind the sternum.

R eE 1.1 F IG U r (a) Anteroposterior (AP) projection of a 3D reconstruction of a computed tomography (CT) scan of the thorax. (b) and (c) Diagrams depicting the location of the heart in AP and left lateral views, respectively.

The Heart and Structures in its Neighborhood

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OVERVIEW OF ANATOMY AND IMAGING

R eE 1.2 F IG U r (a) The fibrous pericardium encloses the heart and the oblique and transverse sinuses. (b) This view from the front after removal of the heart shows the sinuses and recesses between veins (small arrows). Ao = aorta; ICV = inferior caval vein; LI, LS, RI, and RS = left inferior, left superior, right inferior, and right superior pulmonary veins, respectively; SCV = superior caval vein. Photograph courtesy of Professor Damian Sanchez-Quintana, Spain.

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Chapte r 1  |   General Anatomy of the Heart

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The base of the heart lies anterior to the spine from the fifth to eighth thoracic vertebrae. Anteriorly and laterally, the heart is separated from the thoracic wall by the pleura and the thin anterior parts of the lungs. It is enclosed by the fibrous pericardium that separates it from neighboring structures (Figure 1.2).

R eE 1.3 F IG U r The phrenic nerves descend bilaterally onto the fibrous pericardium. LI, LS, RI, and RS = left inferior, left superior, right inferior, and right superior pulmonary veins, respectively; SCV = superior caval vein.

The Heart and Structures in its Neighborhood

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A fibrous sac, the pericardium, encloses and separates the surface of the heart from adjacent structures. On the outer surface of the pericardial sac descend the right and left phrenic nerves and their accompanying pericardiophrenic vessels, which are branches from the internal mammary vessels (Figure 1.3). There is a variable thickness of fat around each pericardiophrenic neurovascular bundle. The nerves descend into the diaphragm behind the cardiac apex. Along the way, the right phrenic nerve has a close relationship to the superior caval vein and the right upper pulmonary vein, whereas the left phrenic nerve is in the proximity of the left atrial appendage and left ventricle (see Chapter 2 for more details).

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OVERVIEW OF ANATOMY AND IMAGING The individual course of the phrenic nerves can be located by high-output stimulation capturing the diaphragm (“hiccup”) during an invasive electrophysiology (EP) study. Using colored tags of 3D mapping systems, the 3D relationship, for example with regard to the ostium of the septal (right) pulmonary veins, can be easily depicted (Figure 1.4). When viewed in situ, the proximity of the esophagus to the posterior and posteroinferior wall of the left atrium is clear (Figure 1.5). Echocardiographers take advantage of this to measure flow and velocities in the left atrial appendage and the pulmonary veins. The esophagus can be located close to the orifices of the right or left pulmonary veins or between the venous orifices. Between the fibrous pericardium and the esophageal wall lie fibrofatty tissues that contain the esophageal arteries, the periesophageal plexus of the vagus nerve, and the lymph nodes.

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R eE 1.4 F IG U r Position of the phrenic nerve (PN) depicted as red tags on a 3D reconstruction of the right atrium (RA) using high-output stimulations. Green tags mark sites without PN capture. Note the relationship of the PN to the superior vena cava (SVC) and septal (right) superior pulmonary vein (RSPV), which can be variable. HIS = catheter recording the penetrating bundle (bundle of His); LA = left atrium.

Chapte r 1  |   General Anatomy of the Heart

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R eE 1.5 F IG U r (a) The transverse cut through a heart specimen shows the relationship of the esophagus (Es) and the descending thoracic aorta (DAo) to the posterior wall of the left atrium (LA). Note the plane of the atrial septum (between arrows) and the central location of

the aortic valve (Ao). (b) Position of the transesophageal echo probe (TOE) in relation to the LA depicted by contrast injection into the left superior pulmonary vein (LSPV) in right anterior oblique (RAO) projection. Note the displaced position of the transseptal sheaths

The Heart and Structures in its Neighborhood

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(TS) in this patient with marked scoliosis, mitral valve (MV) repair, and DDD pacemaker. (c) TOE of MV and left atrial appendage (LAA). IVC = inferior vena cava; Lat PV = lateral pulmonary vein; LV = left ventricle; RA = right atrium; RI = right inferior pulmonary vein.

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OVERVIEW OF ANATOMY AND IMAGING Understanding the spatial relationship of the esophagus to the left atrium is crucial to reduce the risk of atrioesophageal fistula and gastric hypomotility after ablation for atrial fibrillation (Figures 1.6 and 1.7). The descending aorta usually runs more posteriorly so it is some distance away from the left atrium, but in some patients it may pass close to the orifice of the left inferior pulmonary vein. The inferior wall of the fibrous pericardial sac is attached to the diaphragmatic pleura, and twothirds of this wall is to the left of the median plane, corresponding to the location of the heart in the chest. Thus, the part of the diaphragm underneath the heart is mainly related to the left lobe of the liver and the abdominal esophagus, whereas that beneath the cardiac apex overlies the fundus of the stomach. The diaphragm is pierced by the inferior caval vein to the right of the midline of the body, the esophagus to the left of the midline, and the aorta almost at the midline. Accompanying the esophagus through the opening in the diaphragm are the vagal trunks and branches of the left gastric vessels (Figure 1.7).

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R eE 1.6 F IG U r These two halves of a heart cut longitudinally show the esophagus (Es) curling around the posterior and inferior walls of the left atrium (LA). The right panel shows the descending aorta (DAo) adjacent to the left posterior part of the left atrium. Ao = aortic valve; LI and LS = left inferior and left superior pulmonary veins, respectively; Tr = trachea.

Chapte r 1  |   General Anatomy of the Heart

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Anterior view, heart removed

Posterior view

R eE 1.7 F IG U r (a) This anteroposterior (AP) view of the pericardial sac after removal of the heart and the posterior fibrous pericardium shows the course of the left vagus nerve continuing to the periesophageal plexus at the anterior aspect of the esophagus (Es). Ao = aortic valve; DAo = descending aorta; ICV and SCV = inferior and superior caval veins, respectively; PT = pulmonary trunk. (b) This posteroanterior (PA) view of a cadaver shows the esophagus in situ and its relationship with the vagus nerves (small arrows). Dissection and photograph courtesy of Professor Damian Sanchez-Quintana, Spain.

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OVERVIEW OF ANATOMY AND IMAGING Relationships of the Cardiac Chambers, Valves, and Septum Viewing the heart from the front after removal of the fibrous pericardium, it is apparent that the cardiac chambers commonly dubbed the right heart chambers are situated anteriorly relative to the left heart chambers. The frontal silhouette of the heart is nearly trapezoidal, with the upper border being much shorter than the lower. A line joining the upper left and lower right borders of the trapezoid marks the base of the ventricular mass with the silhouettes of the four cardiac valves in the order, from upper left downward, of pulmonary, aortic, mitral, and tricuspid (Figure 1.8). Indeed, the key to understanding the anatomy of the normally structured heart is to appreciate the central location of the aortic valve and hence its close relationship to all four chambers of the heart. The pulmonary valve is the most superiorly sited of the four cardiac valves, and it lies almost horizontally behind the second and third costal cartilages. The orifice of the aortic valve is tilted inferiorly at an angle posterior and to the right of the pulmonary valve. The orifice of the tricuspid valve is separated from that of the pulmonary valve, whereas the orifices

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of the aortic and mitral valves are adjacent to each other. The orifices of the tricuspid and mitral valves are offset such that, at their septal insertions, the tricuspid annulus is nearer to the cardiac apex than the annulus of the mitral valve. Thus, the basal portion of the muscular ventricular septum between these two valves has an atrioventricular location being sandwiched between the right atrium and the left ventricle. The right border of the heart is a more or less vertical line just to the right of the sternum, and it is formed exclusively by the right atrium, with the superior and inferior caval veins joining at its upper and lower margins. The inferior border lying nearly horizontally on the diaphragm is marked by the right ventricle. The left border is made up of the left ventricle, and as it merges with the upper border, the silhouette is formed by the pulmonary trunk. The upper border of the silhouette is made by the arterial trunks with the pulmonary trunk passing to the left of the aorta. Because the left atrium is the most posteriorly situated cardiac chamber, it is barely visible on the frontal silhouette. Only its appendage curling around the edge of the pulmonary trunk forms part of the left heart border.

Chapte r 1  |   General Anatomy of the Heart

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R eE 1.8 F IG U r (a) The diagram shows the location and planes of the four cardiac valves as seen in anteroposterior (AP) projection. The trapezoidal shape of the heart is superimposed. (b) Chest X-ray in AP projection. A, M, P, and T = aortic, mitral, pulmonary, and tricuspid valves, respectively.

Relationships of the Cardiac Chambers, Valves, and Septum

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OVERVIEW OF ANATOMY AND IMAGING Both the right and left atrial chambers are to the right of their respective ventricles. Viewed from the front, the right atrium is right and anterior, whereas the left atrium is situated to the left and mainly posteriorly (Figure 1.9). Consequently, the plane of the atrial septum lies at an angle to the sagittal plane of the body. The front of the left atrium and the medial wall of the right atrium lie just behind the aortic root separated only by the transverse pericardial sinus (see Figure 1.5). The posterior wall of the left atrium is just in front of the tracheal bifurcation and the esophagus with the fibrous pericardium separating the heart from these structures. The bifurcating right and left pulmonary arteries are related to the anterosuperior part of the left atrium. From the atrial chambers, the ventricles project anteriorly and leftward with the tip of the left ventricle forming the cardiac apex. The atrioventricular junctions are marked by the atrioventricular grooves that are filled with fibrofatty tissue and contain the major coronary arteries (Figure 1.10). Positioned just behind the sternum, the right ventricular chamber lies anterior to the left ventricular chamber. Traced from the inferior cardiac border, the right ventricular cavity can be seen to curve and pass superiorly over the left ventricular cavity. This is reflected in the curvature of the ventricular septum. This arrangement results in the right ventricular outflow tract overlapping and crossing the outflow tract from

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R eE 1.9 F IG U r (a) The different levels and angulations of the planes of the aortic (Ao) and pulmonary valves (PT, or pulmonary trunk) are shown as dotted ovals on the endocast, which is displayed at an approximately anteroposterior (AP) view. The right ventricular (RV) outflow tract (solid arrow) crosses anteriorly and superiorly relative to the left ventricular (LV) outflow tract (broken line). The aortic root is in the center of the heart. LAA = left atrial appendage; R = origin of right coronary artery; RA = right atrium. (b) An RV angiogram in left anterior oblique (LAO) projection in a patient with an implantable cardioverter-defibrillator (ICD). The red line marks the pulmonary valve.

Chapte r 1  |   General Anatomy of the Heart

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the left ventricle when the heart is viewed from the front, an important feature to note when ablating in the ventricular outlets (see Figure 1.9). Detailed description of the outflow tracts follows in Chapters 9 and 10. The pulmonary trunk passes cephalad and to the left of the ascending aorta before branching into the right and left pulmonary arteries. The right pulmonary artery courses rightward over the anterosuperior wall of the left atrium to pass behind the ascending aorta and inferior to the aortic arch.

R eE 1.10 F IG U r This section through the four cardiac chambers includes the aortic root. Atrial myocardium is separated from ventricular myocardium by the tissues of the atrioventricular groove (asterisks). The enlargement shows the membranous septum (arrow) lying between the aortic valve (Ao) and the crest of the muscular ventricular septum. The circle represents the location of the atrioventricular conduction bundle. LA and RA = left and right atrium, respectively; MV and TV = mitral and tricuspid valve, respectively.

Relationships of the Cardiac Chambers, Valves, and Septum

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Although the cardiac septum is mainly muscular, it has a small part that is thin and composed of fibrous tissue. This is the membranous septum of the heart (see Figure 1.10). On the right septal aspect, it is crossed by the hinge line (annulus) of the tricuspid valve, which divides it into atrioventricular and interventricular components. The membranous septum adjoins the right fibrous trigone to form the central fibrous body of the heart, which marks the apex of the nodal triangle of Koch. The membranous septum is a useful guide to the location of the atrioventricular conduction bundle (see Chapter 5). Because the aortic valve borders on the membranous septum, its commissure between the right coronary and noncoronary (posterior) leaflets can help in locating the membranous septum. On the right side of the septum, the commissure between the septal and anterosuperior leaflets of the tricuspid valve can also be used as a guide.

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OVERVIEW OF ANATOMY AND IMAGING Interatrial Connections In addition to the atrial septum, muscular continuity between atriums can be found peripheral to the septum frequently as bridges in the subepicardium. The most prominent interatrial bridge is Bachmann’s bundle (Figure 1.11). This is a broad muscular band that connects the anterior wall of the right atrium with that of the left atrium. It passes in front of the interatrial groove, bifurcating at its rightward and leftward extremities. The bundle is not insulated by a fibrous sheath. Instead, it blends indiscernibly into the atrial walls. The right superior branch passes toward the area of the sinus node at the superior cavoatrial junction, whereas its right inferior branch blends in with the anteroinferior wall of the right atrium. The leftward part of Bachmann’s bundle branches to pass around the neck region of the left atrial appendage. The myocardial strands representing the general longitudinal orientation of the myocytes in Bachmann’s bundle, as in the terminal crest, are well aligned. Multiple smaller interatrial bridges are frequently present, giving the potential for macro reentry. Some connect the muscular sleeves of the right pulmonary veins and the superior caval vein to the left atrium. In some hearts, there are broad posterior and inferior bridges joining the left atrium to the intercaval area on the right. These could provide the potential for posterior breakthrough of sinus impulse (Figure 1.12).

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R eE 1.11 F IG U r This anterior view of the heart with the aortic valve (Ao) pulled forward shows the anterior wall of the atria dissected to reveal Bachmann’s bundle (BB, thin arrows) crossing the interatrial groove (open arrow). The location of the sinus node is represented by the dotted line. LAA and RAA = left and right atrial appendages, respectively; LS and RS = left and right superior pulmonary veins, respectively; SCV = superior caval vein.

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R eE 1.12 F IG U r Bachmann’s bundle is not the only interatrial muscular connection. Further connections of varying sizes can exist elsewhere. The diagrams represent anterior and posterior views of the atrial chambers. The percentages refer to the frequency found in a series of 15 heart specimens (Ho SY, Sanchez-Quintana D, Cabrera JA.

Interatrial Connections

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J Cardiovasc Electrophysiol. 1999;10:1525-1533). The heart specimens are dissected to show the subepicardial musculature of the atria. The left panel shows an interatrial muscle bundle (asterisk) between the anterior wall of the left atrium (LA) and the intercaval area of the right atrium (RA). The right panel shows a

broad interatrial muscle band (two asterisks) between the inferior wall of the LA and the RA close to the orifice of the inferior caval vein (ICV). CS = coronary sinus; LI and RI = left and right inferior pulmonary veins, respectively; LS and RS = left and right superior pulmonary veins, respectively; SCV = superior caval vein.

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OVERVIEW OF ANATOMY AND IMAGING Inferiorly, further muscular bridges from the left atrial wall often overlie and run into the wall of the coronary sinus (Figure 1.13). The coronary sinus itself is invested in a muscular sleeve of varying extent, fading out toward its continuation with the great cardiac vein. There are also fine bridges connecting the remnant of the vein of Marshall to the left atrium.

running in the pericardium may pass in the vicinity (Figure 1.14). Although coronary veins are usually superficial to arteries, crossovers between arteries and veins are not uncommon. When deploying catheters or wires in superficial veins, the operator should be aware that the side of the venous wall farthest from the ventricular wall is thin and unprotected by muscle.

The Coronary Veins

The juncture between the great cardiac vein and the

The venous return from the myocardium either is channeled via small Thebesian veins that open directly into the cardiac chambers or, more significantly, is collected by the greater coronary venous system that drains 85% of the venous flow. The main coronary veins in the greater system are the great, middle, and small cardiac veins (see Figure 1.13). The great and middle veins run alongside the anterior descending and posterior descending coronary arteries, respectively, and drain into the coronary sinus. As the great cardiac vein ascends into the left atrioventricular groove, it passes close to the circumflex artery and under the cover of the left atrial appendage. As it approaches the coronary sinus, the great vein is joined by tributaries from the left ventricular obtuse margin and the inferior wall, as well as veins from the left atrium (see Figure 1.13). The distribution, course, and caliber of the left ventricular veins vary from individual to individual. When utilizing the left ventricular veins for pacing lead implants or for ablating ventricular tachycardia from a source close to the epicardium, it is worth noting that the left phrenic nerve

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coronary sinus is marked by the entrance of the vein of Marshall, also known as the oblique left atrial vein. When this vein is persistent, it becomes the persistent left superior caval vein opening into the right atrium via the coronary sinus (see Chapter 11). It descends along the epicardium between the left atrial appendage and the left superior pulmonary vein (see Figure 1.13). In the absence of the vein of Marshall or its remnant, the valve of Vieussens is taken as the anatomic landmark for the junction between the coronary sinus and the great cardiac vein. Found in 80% to 90% of hearts, this valve has very flimsy leaflets that can provide some resistance to the catheter (see Figure 1.13). Once past the valve of Vieussens, a sharp bend in the great cardiac vein can cause further obstruction in 20% of cases. Another marker for the junction between vein and coronary sinus is the end of the muscular sleeve around the sinus. In some cases, the sleeve may extend to 1 cm or more over the vein. Muscular bundles and strands from the sleeve can continue onto the left atrial wall and also cover the outer walls of adjacent coronary arteries (see Figure 1.13).

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R eE 1.13 F IG U r (a) The coronary venous system in anteroposterior (AP) and tilted posteroinferior (PA) views. (b) This close-up view of a heart specimen approximating to the tilted PA view shows the junction of the coronary sinus (CS) with the great cardiac vein (gcv) guarded Interatrial Connections

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by a flimsy valve of Vieussens (asterisks) close to the entrance of the vein of Marshall (arrow). (c) This dissection in similar orientation shows the middle cardiac vein (mcv) and inferior left ventricular vein (Inf LV v). The arrow indicates a band of muscular

continuity between the CS and the left atrial wall. ICV = inferior caval vein; LA and RA = left and right atrium, respectively; LAA = left atrial appendage; LV and RV = left and right ventricle, respectively; MV and TV = mitral and tricuspid valve, respectively.

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OVERVIEW OF ANATOMY AND IMAGING The middle cardiac vein drains into the coronary sinus just within the coronary sinus orifice. Occasionally the middle vein enters the right atrium directly and opens adjacent to the orifice of the coronary sinus, allowing the coronary sinus catheter to drop into it inadvertently. The middle vein passes just superficial to the right coronary artery at the cardiac crux. It is a useful portal for ablating accessory atrioventricular pathways located in the inferior pyramidal space. Very rarely, the entrance of the middle vein is dilated, giving the impression of a diverticulum of the coronary sinus (see Chapters 5 and 6). The venous wall is then surrounded by a cuff of muscle giving the potential for accessory atrioventricular connections. The small or right cardiac vein receives tributaries from the right atrium and the inferior wall of the right ventricle before coursing in the right atrioventricular junction to open to the right of the coronary sinus orifice, or into the middle cardiac vein. When joined by the acute marginal vein, or vein of Galen, the small vein becomes larger in size. Several other veins, from the anterior surface of the right ventricle and from the acute margin, drain directly into the right atrium. In some hearts, the anterior veins merge into a venous lake in the right atrial wall. Again, these may be surrounded by a cuff of myocardium that gives the potential for accessory atrioventricular connection as the vein passes through the atrioventricular groove.

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R eE 1.14 F IG U r The relationship of the left phrenic nerve (small arrows) to the great cardiac vein and to the obtuse marginal vein is shown in these two hearts. LAA = left atrial appendage. Photographs courtesy of Professor Damian Sanchez-Quintana, Spain.

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The Coronary Arteries

R eE 1.15 F IG U r Dissection and diagram viewing the heart from the front show the main coronary arteries. Ao = aortic valve; LAD = left anterior descending artery; LC, NC, and RC = left coronary, noncoronary, and right coronary aortic sinuses, respectively; LCA and RCA = left coronary and right coronary arteries, respectively; PDA = posterior descending artery; PT = pulmonary trunk.

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The two major coronary arteries arise from the aortic sinuses of Valsalva. The course and distribution of these two arteries allow the aortic sinuses to be named right and left coronary, with the third sinus being noncoronary (Figure 1.15). The noncoronary aortic sinus is posteriorly situated, lying anterior to the atria. The arterial orifices are usually located close to or immediately above the sinutubular junction. Emerging from the right coronary aortic sinus almost perpendicularly, the right coronary artery is directly related to the supraventricular crest, the muscular structure forming the roof of the right ventricle. In this region, it gives rise to a prominent infundibular branch to the right ventricle. In 55% to 60% of individuals, it also gives rise to an atrial branch that supplies the sinus node. Passing within the fatty tissues of the right atrioventricular groove, the right coronary artery gives off the acute marginal branch before turning posteriorly to the cardiac crux to give rise to the posterior descending coronary artery that runs in the inferior interventricular groove. In approximately 90% of individuals, the right coronary can also be traced into the left atrioventricular groove to supply the inferior wall of the left ventricle. In this arrangement known as right coronary arterial dominance, the right coronary also gives origin to the artery supplying the atrioventricular node in most cases.

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OVERVIEW OF ANATOMY AND IMAGING Upon emerging from its aortic sinus, the left coronary artery dips sharply to enter the space between the left atrial appendage and the pulmonary trunk. Usually, the main stem divides into the anterior descending and circumflex arteries within 1 cm of its origin. It is worth noting that the terms anterior and posterior descending reflect previous anatomical practice of standing the heart on its apex and rotating it so that the anterior and posterior interventricular grooves are in the midline. With the heart in situ, the anterior artery runs in the superior interventricular groove, and the posterior artery runs in the inferior groove. Be that as it may, the major branches of the anterior interventricular artery are the diagonal, septal perforating, and infundibular branches. Diagonal branches supply the anterior wall of the left ventricle, whereas the infundibular branches pass to the right ventricular outlet. The septal perforators pass into the ventricular septum. When the sinus node artery arises from the circumflex artery, it runs along the anterior or superior wall of the left atrium or, rarely, the posterior wall to reach the node. In the majority of individuals, the extent of the circumflex artery around the left atrioventricular junction reaches to the obtuse margin of the left ventricle.

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Only in nearly 10% of individuals does it reach the cardiac crux to give rise to the posterior descending artery, and a branch to the atrioventricular node.

Fat Pads and Innervation Extracardiac nerves from the mediastinum reach the heart through the areas bounded by the serous pericardium around the great veins at the cardiac base and around the pulmonary trunk and aorta. Nerves from the arterial pole extend predominantly to the ventricles, whereas those from the venous pole reach the atria and the ventricles, and there are also multiple interconnections. Several branches of mediastinal nerves between the aorta and the pulmonary trunk connect with the aortic root and the superior region of the left atrium (see Figure 1.7). Between 6 and 10 collections of ganglia, ganglionated subplexuses of the epicardiac neural plexus, have been described in the human heart. Half of the subplexuses are located on the atria and the other half on the ventricles. Occasional ganglia are located in other atrial and ventricular regions of the epicardium. The ganglionated subplexuses are generally associated with adipose tissue referred to as fat pads that are visible on the epicardial surface.

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The atrial fat pads are located in the interatrial groove, at the cavoatrial junctions, and on the left atrial wall in the vicinity of the venoatrial junctions and the pulmonary veins (Figure 1.16). Adrenergic and cholinergic nerves are distributed in the junctional areas between the pulmonary veins and the left atrium. The ganglia in each subplexus are interconnected by thin nerves, and the ganglia of adjacent subplexuses are also interconnected, forming the meshwork of epicardiac neural plexus. Further nerves that penetrate the myocardium become thinner and thinner and are without ganglia. Transmurally, there are more nerves on the epicardial half than the endocardial half.  

R eE 1.16 F IG U r Five atrial fat pads are recognized as containing ganglionated plexi, and the location of each is described in two alternative terms. (a) The heart is viewed from the right posterior perspective. The dotted lines attempt to highlight the pads, but adjacent pads can merge with one another. (b) This is a view of the heart from the left inferior aspect. Ao = aortic valve; CS = coronary sinus; ICV and SCV = inferior and superior caval vein, respectively; LA and RA = left and right atrium, respectively; LC = left coronary aortic sinus; LI, LS, RI, and RS = left inferior, left superior, right inferior, and right superior pulmonary veins, respectively; LV and RV = left and right ventricle, respectively.

Interatrial Connections

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the neighborhood and Collateral Damage

ELeCTRoPHYSIoLogISTS SHoULD Be AWARe of adjacent structures to the heart itself to avoid collateral damage during their procedures. Knowledge of the presence of these structures and their typical locations will guide individual identification in a given procedural setting.

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OVERVIEW OF ANATOMY AND IMAGING The Esophagus Atrioesophageal fistula is a complication most dreaded by operators carrying out ablation procedures for atrial fibrillation, as it can be fatal. The perforation may appear several days or weeks after the procedure, suggesting an initial subacute lesion of the esophageal wall or its arterial supply (Figure 2.1), resulting in an inflammatory response. The course of the esophagus begins in the neck, descending anterior to the vertebral column through the superior and posterior mediastinum. In its upper course, the esophagus is situated slightly to the left, between the trachea and the vertebral column. It then passes behind and to the right of the aortic arch to descend in the posterior mediastinum along the right side of the descending thoracic aorta. Its retrocardiac course is related to the fibrous pericardium behind the posterior and inferior walls of the left atrium and the junctional areas of the atrium with the pulmonary veins. Lower down, it curves leftward and anteriorly to be related to the posteroinferior wall of the left atrium (see Figure 1.6) before penetrating the diaphragm at the level of the tenth vertebra. In the nonextended state, its muscular wall is contracted and collapses substantially. During the swallowing act, there is variable sideways movement resulting in variable proximity to the middle of the posterior

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R eE 2.1 F IG U r Longitudinal cuts through the left atrium (LA) and the esophagus (Eso) on the gross specimen (a) and histology of the boxed area (b). Esophageal arteries are seen between the fibrous pericardium and the anterior wall of the esophagus.

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left atrial wall or to the pulmonary venoatrial junctions on either side (Figure 2.2). Sandwiched between the fibrous pericardium behind the left atrial wall and the anterior surface of the esophagus is a pad of fibrofatty tissues containing lymph nodes, branches of the vagus nerve, and esophageal arteries. The latter arise from the anterior aspect of the thoracic aorta to form arterial chains around the outside of the esophagus.

The Phrenic Nerves One of the underrecognized but greatly important epicardial structures comprises the phrenic nerves. Although the damage of the right phrenic nerve has been described as a frequent complication of balloon pulmonary vein (PV) isolation, the left phrenic nerve is frequently encountered during left ventricular lead placement in cardiac resynchronization therapy (CRT). High-output stimulation from the tip of the mapping catheter can readily identify the location of the phrenic nerve on the corresponding side. R eE 2.2 F IG U r Left panels are diagrams showing the typical structures imaged on transesophageal echocardiography using either a 0° angulation (top) or a 60° angulation (bottom). The right lower image shows an example of a patient prior to atrial fibrillation ablation in the same 60° angulation. The arrow indicates the

The Phrenic Nerves

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Coumadin ridge between the left atrial appendage (LAA) and the lateral pulmonary veins (PV). The top right panel depicts a patient undergoing transesophageal echo (TOE)–guided transseptal puncture with the probe superimposed on the transseptal sheath in left anterior oblique (LAO)

projection. Contrast is injected in the lateral superior pulmonary vein (LSPV). Also refer to Figure 1.5 on page 11. CS = coronary sinus; His = His catheter; LA = left atrium; Lat PV = lateral pulmonary vein; LV = left ventricle.

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OVERVIEW OF ANATOMY AND IMAGING

R eE 2.3 F IG U r (a) This right lateral view is shown with the right phrenic nerve (red dots) descending along the fibrous pericardium. The area of the sinus node is indicated by the irregular shape. The blue arrow marks the plane of the histological section (b) and enlargement (c) and the distance between the right superior pulmonary vein (RS) and the phrenic nerve (black arrow). LA and RA = left and right atrium, respectively; ICV and SCV = inferior and superior caval vein, respectively; RI = right inferior pulmonary vein.

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Slow pacing in close proximity to the nerve results in involuntary diaphragmatic contractions (“hiccups”). Using colored tags, these sites can then be marked on the 3D mapping system as well (see Figure 1.4).

R eE 2.4 F IG U r Example of a 3D reconstruction of a right atrium acquired using the fast anatomical mapping (FAM) feature of the CARTO system (Biosense Webster) during atrial reentrant tachycardia in a patient after right atrial atriotomy (blue lines depict double potentials along the crista terminalis or the atriotomy scar). Sites of maximal output stimulation that captured the phrenic nerve are marked in light red. Fortunately, no capture of the phrenic nerve could be achieved in the area marked with the box, allowing for a safe ablation within the critical isthmus of the reentrant circuit. The Phrenic Nerves

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The right phrenic nerve descends vertically first along the right brachiocephalic vein and then along the right anterolateral surface of the superior caval vein to be related to the right aspect of the right atrial wall (Figure 2.3). It passes in front of the root of the lung to reach the diaphragm adjacent to the lateral border of the entrance of the inferior caval vein. Its adjacency to the superior cavatrial junction and the anterior wall of the right superior pulmonary vein (Figure 2.4) renders it vulnerable to damage when ablations are carried out to isolate right pulmonary veins in atrial fibrillation or for inappropriate or reentrant sinus tachycardia. Measurements made in cadavers show that the right phrenic nerve has a close relationship with the superior caval vein (0.3 ± 0.5 mm) and the right superior pulmonary vein (2.1 ± 0.4 mm) in its descent (see Figure 2.3). The inferior course of the right phrenic nerve is related to the lateral border of the entrance of the inferior caval vein and therefore close to the so-called lateral isthmus that may be ablated for typical atrial flutter.

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OVERVIEW OF ANATOMY AND IMAGING The left phrenic nerve descends on the left side close to the aortic arch and passes onto the pericardium overlying the left atrial appendage and the left ventricle. It can take one of three courses on the fibrous pericardium. In nearly two-thirds of cadavers studied, it passes over the left lateral or obtuse margin of the left ventricle to overlie the marginal artery and vein (see Figure 1.14). In approximately one-fourth, it passes over the neck or roof of the left atrial appendage with implications for ablations of focal atrial tachycardia within the appendage. Running this course, it continues posterolaterally and inferiorly over the left ventricle and may also be vulnerable when ablating left posterolateral accessory pathways. Less commonly, the left phrenic nerve takes a more anterior course over the left ventricle. In this course, its initial descent over the heart is related to the lateral margin of the high right ventricular outflow tract, and then its descent over the anterior cardiac surface is related to the anterior descending coronary artery and the interventricular vein (see Figure 1.14).

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R eE 2.5 F IG U r (a) This cross section through a cadaver shows the relationship between the esophagus (Eso) and the left atrium (LA). The yellow arrow indicates the right phrenic nerve. The enlarged area (b) shows bundles of the periesophageal vagal plexus (within dotted lines). RI and RS = right inferior and right superior pulmonary vein, respectively.

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Periesophageal Gastric and Vagal Nerves

R eE 2.6 F IG U r Slightly rotated posterior projection of both right ventricular (RA) and left ventricular (LA) electroanatomical 3D reconstructions using the CARTO system. The left panel depicts the endocardial maps using only the “anatomical” feature. The right panel shows the epicardial map superimposed using the local activation time (LAT) information. Courtesy of Dr. Feifan Ouyang, St. Georg General Hospital, Hamburg, Germany.

Even lesser known of the large nerve structures are the periesophageal gastric and vagal nerves. These are of particular importance because damage of these nerves results in new gastric symptoms like bloating and prolonged emptying times. The vagus nerves pass behind the root of the lungs and form right and left posterior pulmonary plexuses (see Figure 1.7b). From the caudal part of the left pulmonary plexus, two branches descend on the anterior surface of the esophagus forming, with a branch from the right pulmonary plexus, the anterior esophageal plexus (Figure 2.5). The posterior and anterior esophageal plexuses reunite beneath the diaphragm to become the posterior and anterior vagal trunks that innervate the stomach and pyloric canal and the digestive tract as far as the proximal part of the colon.

Left Recurrent Laryngeal Nerve Clinically, recurrent laryngeal nerve palsy can be a significant risk for aspiration. A form of Ortner syndrome, transient hoarseness and dysphagia, following left atrial ablation has been reported. The left recurrent laryngeal nerve descends from the left vagus nerve on the left side of the aortic arch (see Figure 1.3). It then turns to pass beneath the aortic arch, near the arterial ligament, before

Left Recurrent Laryngeal Nerve

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OVERVIEW OF ANATOMY AND IMAGING ascending in the groove between the trachea and esophagus. It is in this region that it could be vulnerable to being compressed when the roof of the left atrium is pushed superiorly, for example with a stiff catheter.

Pericardial Space and Epicardial Access The heart and its adjoining great vessels are enclosed in a sac, the parietal (fibrous) pericardium. Adherent to the inside of the fibrous pericardium is the parietal layer of the serous pericardium, which reflects to cover the surfaces of the heart and proximal portions of the great vessels as the epicardium and visceral pericardium (the visceral layer), thus enclosing the pericardial cavity between the parietal and visceral layers of the serous pericardium. “Sandwich” mapping can portray this space for the epicardial approach (Figure 2.6). Superiorly, the fibrous pericardium is continuous with the adventitia of the great vessels attaching to the ascending aorta and pulmonary trunk, and to the superior caval vein several centimeters above the site of the sinus node (see Figure 2.3). Anteriorly, it is attached to the posterior surface of the sternum by superior and inferior sternopericardial ligaments that are variably developed. Laterally are the pleural coverings of the mediastinal surface of the lungs. The esophagus, descending thoracic

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aorta, and posterior parts of the mediastinal surface of both lungs are related posteriorly. Inferiorly, the fibrous pericardium is attached to the central tendon of the diaphragm and a small muscular area to the left. The pericardium rests on an almost flat area of the diaphragm known as the cardiac plateau, which extends more to the left than to the right. The profile of the diaphragm rises on either side of the cardiac plateau to a smooth convex dome, which is higher and slightly broader on the right than on the left. The right side is molded over the right lobe of the liver, the right kidney, and the right suprarenal gland, whereas the left side conforms to the left lobe of the liver, the fundus of the stomach, the spleen, the left kidney, and the left suprarenal gland. Importantly, there is a small area behind the lower left half of the body of the sternum and the sternal ends of the left fourth and fifth costal cartilages where the fibrous pericardium is in direct contact with the thoracic wall. This area does allow the pericardial space to be accessed, but the operator should take care not to enter the right ventricle, which lies behind the space. Instead, most operators use a subxiphoid approach for the puncture (see below). Under normal conditions, the pericardial cavity contains approximately 20 mL of fluid. The cavity has two sinuses and several recesses that are not complete compartments but represent extensions of the cavity.

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The first sinus, known as the transverse sinus, lies between the back of the ascending aorta and pulmonary trunk bifurcation and the front of the atrial chambers (see Figure 1.2). The inferior and superior aortic recesses are extensions from the transverse sinus. The superior recess lies between the ascending aorta and the right atrium, whereas the inferior recess between the aorta and the left atrium extends to the level of the aortic valve. The second sinus, the oblique sinus, is formed by continuity between the reflections along the pulmonary veins and caval veins. It is a large culde-sac behind the left atrium. The right and left pulmonary venous recesses are at the back of the left atrium between the upper and lower pulmonary veins on each side, indenting the side walls of the oblique sinus to greater or lesser extents. The pericardial reflections at the veins, particularly the pulmonary veins, are varied, and they can restrict manipulation of catheters around the veins. By contrast, catheters can freely access the epicardial surfaces of the ventricles except in cases with pericardial adhesions (eg, postcardiac surgery).

R eE 2.7 F IG U r (a) Anteroposterior image of a 3D reconstruction from a computed tomography (CT) scan displaying also the bony structures to illustrate landmarks for epicardial puncture site (yellow circle). (b) Same projection as in (a) with sternum and ribs removed to illustrate the proximity of the right ventricular apex. (c) Left lateral projection to display the necessary angle to reach the pericardial space (yellow line). Pericardial Space and Epicardial Access

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The most commonly used practice of access to the pericardial cavity is carried out from the subxiphoid space (Figure 2.7). This can be done by aiming a long needle toward the left mid-clavicle

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OVERVIEW OF ANATOMY AND IMAGING at an angle of 20° to 30° and advancing it under fluoroscopic guidance to heart shadow. When entering the epicardial space, a small volume (2–3 mL) of clear yellowish fluid, the pericardial fluid, can be aspirated. Subsequently, introduced under fluoroscopy is a long J-tipped wire, which should wrap itself around the heart (Figure 2.8). In some patients, especially after previous cardiac surgery (eg, for bypass grafting), the desired epicardial region might not be reachable by conventional epicardial access. In these special cases, a surgically created minimal access to the epicardium has been reported.

R eE 2.8 F IG U r Right anterior oblique (RAO, left panel) and left anterior oblique (LAO, right panel) images during epicardial puncture in a patient with ischemic ventricular tachycardia undergoing catheter ablation. Note the contrast depot that was used during the puncture (arrow) that marks the diaphragm and subsequently the entry into the pericardial space. A long wire (asterisk) is advanced through the puncture needle and wrapped around the heart to exclude inadvertent entry into the right ventricular cavity. Also visible are a right ventricular catheter (RV) and the leads of a dual-chamber implantable cardioverter-defibrillator (ICD). Photographs courtesy of Dr. Tom Wong, Royal Brompton Hospital, London, UK.

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Chapte r 2  |   The Neighborhood and Collateral Damage

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Coronary Arteries

R eE 2.9 F IG U r 3D reconstruction of computed tomography (CT) scan of a heart with corresponding locations of the major coronary vessels marked in a left anterior oblique (LAO) projection. Note that the pulmonary artery on the left-hand panel crosses the location of the aorta (depicted in the right panel). CX = circumflex artery; LAD = left anterior descending artery; RCA = right coronary artery.

Coronary Arteries

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Detailed knowledge of the individual distribution of the coronary vessels is an obvious prerequisite of any epicardial mapping and ablation attempt. However, using only the standard interventional fluoroscopic projections might make it difficult to understand the 3D anatomy. Because nowadays most of these complex EP procedures are carried out using 3D mapping systems, allowing for merging of the endocardial volume reconstructions, a 3D registered image of the coronary arteries can be used as well (Figure 2.9). Nevertheless, if the final ablation site is close to any coronary artery, then a selective angiogram needs to be performed in at least two projections to establish the distance between the target site and the nearest vessel.  

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3

overview of Imaging modalities: Pros and Cons

Fluoroscopy is the general standard to perform any interventional procedure and is available all over the world. Despite the fact that soft tissue like the myocardium is not imaged at all, the ready accessibility of fluoroscopy at low cost makes it the standard imaging technique for electrophysiology (EP) procedures. Seeing the heart in standard 2D projections like anteroposterior, left anterior oblique, and right anterior oblique allows

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OVERVIEW OF ANATOMY AND IMAGING the investigators to compute a 3D image in their heads, enabling them to be guided safely through the heart. Every novice, however, is awed by the orientation and detail that an experienced interventionist is able to obtain from looking at only a single 2D picture, whereas 3D reconstructions make the orientation simpler and understandable, even for laypeople. Fluoroscopy can cause serious side effects for both investigators and patients. Being in the direct ionizing beam, the patient is exposed at maximum levels but, hopefully, will be exposed only once in a lifetime. Depending on the direction of the imaging beam, the duration of exposure, and the volume of the radiated area, the first sign of adversity is skin reddening occurring weeks after the procedure. The potential to induce malignancies by fluoroscopic exposure in interventional procedures is relatively low, although with repeat exposures, this might become an issue for the individual patient. Fundamental to the application of fluoroscopy is the ALARA (as low as reasonably achievable) principle. Because the operator is the person with the highest exposure to scattered radiation, closest adherence to this principle is the best protection against radiation injury.

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Chapte r 3  |   Overview of Imaging Modalities

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3D Imaging In recent years, several imaging techniques have been introduced into clinical practices that allow for 3D reconstruction of the heart. These imaging studies are carried out ahead of the EP study in dedicated scanners. Information transfer is then necessary to integrate the information that was acquired elsewhere into the EP study setup.

Computed Tomography (CT)

R eE 3.1 F IG U r 3D reconstruction of a CT scan of the thorax with (upper panels) and without (lower panels) removal of bony thoracic structures in right anterior oblique (RAO; left), anteroposterior (AP; middle), and left anterior oblique (LAO; right) projections.

3D IMAGING

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Dedicated computer systems can generate a 3D image of the heart from a large series of 2D fluoroscopic images. Nowadays, using multislice techniques, high resolution and ultrafast speed allow for procedure times of about 5 minutes. Application of 50-mL to 100-mL contrast in a timely fashion allows for delineation of the cardiac anatomy in diastole, but the highresolution image comes at a cost of up to 12 mSv (equivalent to 100–600 chest X-rays). Another potential limitation is that imaging by CT angiography can only be obtained in areas where contrast has actually arrived, a problem that is especially apparent in patients with arrhythmia or congenital heart disease for whom contrast transit times can vary substantially (Figure 3.1).

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OVERVIEW OF ANATOMY AND IMAGING Cardiac Magnetic Resonance (CMR) Imaging In contrast to CT imaging, CMR imaging uses no ionizing radiation but utilizes magnetic fields to align the nuclear magnetization of (mostly) hydrogen atoms in the water content of the body. Although contrast agents might need to be used, specific imaging sequences can be performed that allow the blood to act as the contrast agent, such that contrast transit times no longer matter. A clear limitation of the CMR technology is the exclusion of patients with implanted ferromagnetic material such as pacemakers/implantable cardioverter-defibrillators (ICDs), cochlear implants, or aneurysm clips. Vascular stents give typically black holes, but both titanium and stainless steel stents can be safely imaged (Figure 3.2).

R eE 3.2 F IG U r 2D reconstructions of a noncontrast cardiac magnetic resonance acquisition of a normal heart in anteroposterior (AP) and transversal (trans.) projection, as well as in left lateral (LL) view showing left ventricular (LV) systolic and diastolic filling. The right panels show a 3D reconstruction of the same data set on the Polaris software for 3D reconstruction in right anterior oblique (RAO) and left anterior oblique (LAO) projection. Ao = aorta; LA and RA = left and right atrium, respectively; PA = pulmonary artery; PT = pulmonary trunk; RV = right ventricle.

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Rotational Angiography A very recent development in performing 3D imaging in the same procedure as the invasive EP study has been introduced by means of rotational angiography. Using a timed injection to contrast fill the target chamber (eg, the left atrium), the X-arm is rotated around the patient to acquire multiple 2D pictures (Figure 3.3). Using dedicated software, these 2D pictures are reconstructed to provide 3D images of the given area of interest. Superimposition onto the live 2D fluoroscopy monitors allows the operator to visualize the contrasted chamber.

R eE 3.3 F IG U r Various projections of a rotational fluoroscopy acquisition of the left atrium during timed contrast injection via a pigtail catheter positioned in the main pulmonary artery (PA). The pink dotted line depicts the mitral annulus. Ao = aorta; AP = anteroposterior; LA = left atrium; LAO and RAO = left and right anterior oblique, respectively; LL and RL = left and right lateral, respectively; LV = left ventricle.

3D IMAGING

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OVERVIEW OF ANATOMY AND IMAGING 3D EP Mapping Systems A major step forward in clinical electrophysiology has been the introduction of 3D mapping systems, allowing for a detailed reconstruction of the activation sequence in a 4D way. In addition to a virtual geometry, constructed on sequential locations acquired by a mapping catheter, the timing of the cardiac activation is displayed, facilitating the understanding of the tachycardia mechanism and subsequent delivery of the most effective ablation strategy (Figure 3.4).

R eE 3.4 F IG U r Examples of virtual 3D reconstructions of a left atrium as acquired using either the fast anatomical mapping (FAM) feature of the CARTO system (Biosense Webster, left panels), or the EnSiteNavX system (St. Jude Medical, right panels). The colored tags mark the sites of radiofrequency applications during pulmonary vein isolation. Both systems are also displaying the location of diagnostic catheters within the patient’s heart [note the coronary sinus (CS) catheter or the circumferential mapping catheter (yellow star). All maps are rotatable in all degrees of freedom allowing the investigators to obtain optimal orientation outside the conventional C-arm projections. LAA = left atrial appendage; LSPV = left superior pulmonary vein; RIPV and RSPV = right inferior and right superior pulmonary vein, respectively.

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Image Integration

R eE 3.5 F IG U r Superimposition of the preacquired 3D image (eg, from CMR or CT scans) with the 3D electroanatomical map (using the CARTO system). Note the relationship between the aorta (Ao) and the atria. LA and RA = left and right atrium, respectively; LAO = left anterior oblique; LV and RV = left and right ventricle, respectively; PA = posteroanterior.

3D IMAGING

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Computing a 3D image from 2D Digital Imaging and Communications in Medicine (DICOM) tomographic information generated by either CT or CMR imaging allows for instant visualization of the cardiac chambers. Various software programs are available that allow, as the next step, for those 3D images to be combined with the 3D mapping information (image merging). Registration of the optimal alignment is of key importance because malalignment could lead to significant misinterpretation of the imaging information. Image integration is especially valuable when complex anatomy or unusual presentations can easily confuse the operator. One of the most obvious limitations is that only the endocardial surface of a given cardiac chamber is imaged with no information of the adjacent wall (eg, scar/fibrosis) or inner structures (eg, papillary muscles) (Figure 3.5).

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OVERVIEW OF ANATOMY AND IMAGING Image Integration on the Fluoroscopy System Image merge information can be displayed onto the fluoroscopic imaging systems or on fluoroscopic reference images to simulate a biplane fluoroscopy image. Real-time imaging of the mapping electrode (and possibly the other diagnostic catheters in the future) allows for significant reduction of the overall fluoroscopy exposure for both patient and investigators (Figure 3.6).

R eE 3.6 F IG U r Superimposition of a 3D electroanatomical map (using CARTO RMT) of the right atrium (RA) and left atrium (LA) on fluoroscopic reference images [left panel: right anterior oblique (RAO); right panel: left anterior oblique (LAO)] using NAVIGANT software (Stereotaxis). The gray dots mark the atrioventricular (AV) annuli, the colored tubes the pulmonary veins (PVs), and the yellow dot the His recording site. The bottom images are more transparent to illustrate the position of the catheters in relation to the 3D maps. Note the relationship, for example, between the coronary sinus (CS) catheter and the LA and the site of the His recording and the position of the diagnostic His catheter.

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Echocardiography in the EP Laboratory

LAA

Standard 2D echocardiogram is the state-of-theart imaging modality when assessments of valve function, blood flow, and cardiac dimensions are performed. To exclude the presence of a left atrial appendage thrombus, transesophageal echocardiography (TOE or TEE) is recommended in all patients undergoing a catheter ablation procedure for atrial fibrillation (Figure 3.7). In addition, TOE may facilitate the transseptal puncture and is especially helpful in distorted anatomy (see Figure 1.5b). Novel 3D echocardiographic techniques allow for display of the individual anatomy with great accuracy.

R eE 3.7 F IG U r Left panels: 2D transesophageal images of the left atrium (LA) and the left atrial appendage (LAA) (yellow arrows). The bottom panel depicts a typical round thrombus in a patient with persistent atrial fibrillation. The right panel shows the interatrial septum, which is bulging toward the right atrium (RA) (note pink arrows). Caused by the higher left atrial pressure, a floppy septum initially leans to the right but during transseptal puncture can be pushed far into the left atrium during the “tenting” process. Ao = aorta; LV = left ventricle.

3D IMAGING

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OVERVIEW OF ANATOMY AND IMAGING Direct implementation of these images into 3D mapping systems, however, is largely missing at this point in time (Figure 3.8).

Echo orientation

Invasive intracardiac echocardiography (ICE) is the only online imaging tool that has been combined with 3D mapping so far. By combining several 2D slices, a 3D reconstruction of any given cardiac chamber can be achieved (Figure 3.9). Choosing the corresponding imaging plane during ablation could potentially allow for visualizing lesion formation in real time. However, no reports on accuracy of myocardial wall imaging and lesion visualization have been published yet.  

“True orientation”

PFO

PFO

R eE 3.8 F IG U r 3D reconstruction using transesophageal echocardiography with typical projection used by the echocardiographers (left panel ) and anatomically correct projection (right panel ). Note the defined limbus of the fossa ovale and the superior-posteriorly pointing patent foramen ovale (PFO) (yellow arrows). RIPV = right inferior pulmonary vein.

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Merge of ICE with 3D mapping

R eE 3.9 F IG U r 3D reconstruction of a left atrium using sequential 2D “slices” from an intracardiac echo probe (ICE) on the CARTOSOUND system. Because the ICE catheter is equipped with a similar location sensor as the mapping and ablation catheter, this facilitates the 3D orientation of the 2D echo “fans,” which are also depicted in both panels. Alignment with the ablation catheter during ablation could potentially allow for imaging of the ablation lesion during radiofrequency delivery. LAO = left anterior oblique; MA = mitral annulus; PV = pulmonary vein; RIPV and RSPV = right inferior and right superior pulmonary vein, respectively; RL = right lateral.

3D IMAGING

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4

Positioning of Standard Catheters: Electrophysiology and Anatomy

aFter gaining Vascular access, the next challenge in an invasive electrophysiology study is to position diagnostic catheters at key sites inside the cardiac chambers to allow the performance of pacing maneuvers to understand the arrhythmia mechanism. 

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OVERVIEW OF ANATOMY AND IMAGING General Aspects At the beginning of an invasive electrophysiological (EP) study, electrophysiologists need to identify the individual patient’s anatomy by evaluating standard fluoroscopy images. The heart and the spatial relationships of its chambers, however, are not easy to see, because cardiac tissue can only be displayed as a shadow. In the upper panels of Figure 4.1, the heart is depicted in right anterior oblique (RAO) 30°, anteroposterior (AP), and left anterior oblique (LAO) 40° projections, with an endocast of a human heart in the corresponding position in the lower panels. When only the outline of the heart can be seen, the exact locations of specific sites within the heart are very difficult to ascertain.

R eE 4.1 F IG U r Upper panels show a “plain” heart in right anterior oblique (RAO) 30°, anteroposterior (AP), and left anterior oblique (LAO) 40° projection without any catheters (“naked” heart). Lower panels depict endocasts of a human heart in corresponding projections. Ao = aorta; LV and RV = left and right ventricle, respectively; PA = pulmonary artery; RA = right atrium.

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In conventional EP studies, catheters are positioned in locations that allow for recording of intracardiac electrograms and stimulation from strategic areas inside the heart. Typical examples are catheters at the right ventricular apex (RVA), at the His bundle (HIS), or inside the coronary sinus (CS). Simultaneous to the recording of the electrical signals from these catheters, the locations of the catheters and their shafts allow for a more detailed depiction of the heart by using these structures as landmarks (Figure 4.2).

R eE 4.2 F IG U r Same projections as in upper panel of Figure 4.1 but with CS and His catheters in place. Ao = aorta; AP = anteroposterior; LA and RA = left and right atrium, respectively; LAO and RAO = left anterior and right anterior oblique, respectively; LV and RV = left and right ventricle, respectively; PA = pulmonary artery.

General Aspects

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OVERVIEW OF ANATOMY AND IMAGING When using bidirectional imaging (irrespective of the images being simultaneously or sequentially acquired), important 3D information can be gained (Figure 4.3).

CS as a Marker for the AV Groove The venous return of the heart is largely organized in the coronary venous system, running in parallel to the coronary artery system. In an inverse arborization, the great cardiac vein (GCV) ascends alongside the anterior descending coronary artery to merge into the CS and finally enters the right atrium at the CS orifice (Figures 4.4 and 4.5). R eE 4.3 F IG U r (a) Right anterior oblique (RAO) and (b) left anterior oblique (LAO) fluoroscopic images with CS and His catheters positioned, dividing the atrioventricular (AV) parts and the right-sided and left-sided structures of the heart.

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The GCV-CS channel more or less follows the parietal margin of the mitral valve (MV) annulus although it tends to run along the epicardial aspect of the left atrial wall, proximal to the annulus. Nevertheless, it is perfectly depicted in an LAO projection (see Figure 4.3b), enabling the MV to become visible. Using an approximation in assuming that the MV and tricuspid valve (TV) orifices are at the same level, the RAO projection becomes a good marker for the plane of the atrioventricular (AV) junction. Using this view, atrial myocardium is left (or posterior) of the foreshortened CS catheter, whereas the ventricles are to the right (or anterior) (see Figure 4.3). A more exact delineation is possible by using the local electrogram to distinguish between a relatively more atrial location (larger A than V potential) and a relatively more ventricular location (larger V than A potential) in an annular position (see Chapter 5).

R eE 4.4 F IG U r Arborization of the coronary venous system with all side branches marked, using direct contrast injection prior to left ventricular lead upgrade in a patient with dual-chamber implantable cardioverterdefibrillator (ICD). Different projections are displayed. AP = anteroposterior; CS = coronary sinus; LAO and RAO = left and right anterior oblique, respectively; MCV = middle cardiac vein; OMV = obtuse marginal vein.

CS AS A MARKER FOR THE AV GROOVE

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OVERVIEW OF ANATOMY AND IMAGING Positioning of the CS Catheter Generally speaking, a CS catheter can be positioned using a femoral approach. However, in some instances, the operator can encounter a valvular structure that acts like a gatekeeper, making access trickier (Figure 4.6).

Relationship between left coronary artery and coronary venous system

R eE 4.5 F IG U r Left panel shows contrast injection into the left coronary artery to display the relationship with the coronary sinus (marked by the CS catheter advanced distally). Right panels display contrast injections in right anterior oblique (RAO, top) and left anterior oblique (LAO, bottom) using a specialized catheter with 1-cm markers to illustrate size and diameter.

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R eE 4.6 F IG U r Varied morphology of the Thebesian valve in front of the CS ostium. The lower panels are of a heart with a large valve that completely covers the CS ostium (dotted oval). The free margin of the valve (arrow) is directed upward with the blue lines in the diagram representing superior and inferior approaches. This heart also has a prominent Eustachian ridge (ER). ICV and SCV = inferior and superior caval vein, respectively.

POSITIONING OF THE CS CATHETER

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OVERVIEW OF ANATOMY AND IMAGING Advancing the catheter via a superior approach allows, in almost all cases, for straightforward access to the CS (Figure 4.7). Starting at the annular position (with a large V potential) with a septal rotation (clockwise for the femoral approach, counterclockwise for the superior approach), the catheter is carefully pulled back until it jumps into the CS orifice (depicting an equally large A and V potential) (Figure 4.8; see Figure 4.7). From the orifice, the CS catheter can be advanced safely, without any resistance, and navigated around as it follows the parietal annulus of the MV (see Figure 4.5).

R eE 4.7 F IG U r Stepwise approach with indication of direction of rotation for safe positioning of CS catheter using a superior approach. CCW = counterclockwise; LAO = left anterior oblique.

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R eE 4.8 F IG U r Stepwise approach for positioning of the CS catheter using a femoral approach. CW = clockwise; LAO = left anterior oblique; TA = tricuspid annulus.

Positioning of the CS Catheter

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OVERVIEW OF ANATOMY AND IMAGING

R eE 4.9 F IG U r (a) Right anterior oblique (RAO) projection of a diagnostic catheter positioned across the tricuspid valve (TV). The distal two electrodes are located in the right ventricle while the paired six proximal electrodes are located in the His region recording the characteristic local signal. (b) This corresponding anatomical picture shows the AV node and His bundle (green dotted shape) and the commissure (arrow) between the anterosuperior and septal leaflets of the TV. CS = coronary sinus.

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LAO angulations

R eE 4.10 F IG U r

HIS as a Marker of the Septum The compact AV node is often referred to as the soul of the heart. The location of the His bundle is facilitated by the typical sequence of the local electrogram: small A, sharp H, and large V potential. Using an RAO projection, the catheter is advanced across the TV and stabilized with a septal rotation (clockwise) to anchor in the fold of the TV (Figure 4.9). When adjusting the LAO projection to a projection that allows for direct view of the fully foreshortened catheter, the individual cardiac axis and the ventricular septum are best depicted (Figure 4.10).

Various C-arm angulations of left anterior oblique (LAO) from 40º to 60º to individualize the standard LAO projection to the patient-specific position of the interatrial septum illustrated by the parallel depiction of the His catheter to adjust for individual cardiac axis.

HIS as a Marker of the Septum

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OVERVIEW OF ANATOMY AND IMAGING Interestingly, the compact AV node is also an ideal marker of the atrial septum (Figure 4.11), allowing for a rough orientation in the individualized LAO projection for right-sided and left-sided locations. Further catheters might be positioned to understand better a particular activation sequence, for example, counterclockwise activation around the TV in common-type atrial flutter by recording a craniocaudal activation along a multipolar catheter positioned at the right atrial free wall (so-called Halo) or a circumferential mapping catheter inside a pulmonary vein ostium. Whenever necessary, positioning of classic catheters will be described in the subsequent chapters on the specific arrhythmias.  

R eE 4.11 F IG U r Anatomical cut through a whole heart simulating left anterior oblique (LAO) projection to show the anticipated position of the AV node and His bundle (green dotted shape). Note the coronary sinus (CS) skirting the left atrial (LA) mitral valve (MV) junction. L, N, and R = left coronary, noncoronary, and right coronary aortic sinus, respectively; RA (TV) = right atrial tricuspid valve; RCA = right coronary artery.

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Atria

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5

Electrical Anatomy and Accessory Pathways

IN THiS CHAPTER, WE BEgiN BY REViEWiNg the structure of the normal conduction system and the configuration of the atrioventricular junctions. Building on the fundamentals, we discuss the anatomy and electrophysiological properties of accessory pathways, including unusual types, and the access routes to reach them.

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ATRIA The Cardiac Conduction System Although much has been written about specialized internodal tracts connecting the sinus node to the atrioventricular node, the myocardium between the nodes bears no histological characteristics that resemble insulated conduction bundles. Mainly, the internodal myocardium is arranged in broad bands that surround the orifices of the large veins, the tricuspid valve, and the oval fossa. Bands like the rim of the oval fossa and the terminal crest are raised ridges on the endocardial aspect and tend to have an orderly alignment of the myocytes approximating to myocardial strands visible on gross dissection. Bachmann’s bundle and other interatrial bundles, small as well as large, are not insulated by fibrous sheaths, nor do they have well-defined origins and terminations. In these, the myocardial strands also tend to be aligned along the length of the bundles (Figure 5.1). R eE 5.1 F IG U r The endocardium lining the right atrium has been dissected away and the atrial wall displayed to show the gross arrangement of the myocardial strands in the internodal region. Muscle bundles such as the terminal crest and pectinate muscles show strands that are better aligned longitudinally. The sinus node (colored ovals) is depicted as having been bisected by the cut through the superior caval vein (SCV). The location of the compact atrioventricular node and His bundle at the apex of the triangle of Koch is shown as an irregular shape with the fine broken lines representing the transitional cell zone. The bold broken line represents the continuation of the atrioventricular conduction bundle. cs = coronary sinus; RAO = right anterior oblique; TV = tricuspid valve.

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The Sinus Node The sinus node is shaped rather like a tadpole having a head, body, and long tapering tail. It has a mean length of 13.5 mm in the adult heart. It is located at the junction between the superior caval vein and the right atrium (Figure 5.2). Usually, the node lies in the terminal groove at the anterolateral margin of the junction. The head portion is subepicardial, close to the superior margin of the terminal groove, while the tail penetrates inferiorly into the myocardium of the terminal crest to lie closer to the subendocardium. The distal portion of the tail tends to lose its compactness and fragment into clusters of specialized cells. The node is richly supplied with nerves from both the sympathetic chains and the vagus nerve. A prominent nodal artery usually penetrates the node. The specialized myocytes of the nodal cells are set in a fibrous matrix, but the node is not encased in a fibrous sheath. R eE 5.2 F IG U r The two pictures of a heart specimen show the epicardial (upper panel) and endocardial aspects of the right atrium with the locations of the sinus node superimposed (dotted shape). The short broken lines in the upper panel represent nodal extensions into atrial myocardium. The blue lines indicate the planes of the histologic sections. The asterisk on the lower panel marks the orifice of the superior caval vein (SCV). (a) to (d) are cross sections through the sinus node and the terminal crest (TC) with the The Cardiac Conduction System

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epicardial (epi) surface to the left and the endocardial (endo) surface to the right of each panel. Staining with Masson’s trichrome stain shows the node as areas with combined red and green while ordinary atrial myocardium appears as a darker red. (a) This section through the head portion of the sinus node shows extensions of nodal cells (arrows) into the myocardial sleeve of the SCV. (b) and (c). The nodal body and tail taper and penetrate into the TC. (d) At its distal portion, the node separates into

small islands of nodal cells (arrows). (e) and (f) are high magnifications of the sinus node showing increase in fibrous tissue (green) among the nodal cells of the adult heart. (g) This closeup view of the border zone shows prongs of nodal cells (arrows) extending into ordinary atrial myocardium as well as a discrete border (broken line). CS = coronary sinus; ICV = inferior caval vein; OF = oval fossa; NA = nodal artery; RA = right atrium.

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ATRIA Mostly, the borders of the node are irregular with frequent interdigitations between nodal and ordinary atrial myocytes, facilitating communication between node and right atrial myocardium.

The Atrioventricular Conduction System Normally, the only pathway of muscular continuity between atrial and ventricular myocardium is provided by the penetrating atrioventricular bundle of His. The atrioventricular conduction system comprises the atrioventricular node, penetrating bundle, common atrioventricular bundle, branching bundle, and right and left bundle branches that branch distally into the finer and finer branches of the Purkinje fiber network (Figure 5.3). Fibrous tissue sheaths insulate the conduction system from the His bundle and into the bundle branches (Figure 5.4). The anatomic landmark for the atrioventricular node is recognized as the triangle of Koch in the right atrium.

R eE 5.3 F IG U r (a) The arrangement of the cardiac conduction system. Atrial myocardium is separated from ventricular myocardium by a fibrofatty tissue plane at the atrioventricular junction. (b) The compact atrioventricular node (AVN) with its two inferior extensions is capped by the transitional cell zone (broken lines). The node continues into the penetrating bundle of His (PB). More distally, the common atrioventricular bundle divides into the left and right bundle branches (LBB and RBB, respectively). CS = coronary sinus; LA and RA = left and right atrium, respectively.

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R eE 5.4 F IG U r This series of histological sections in comparable orientation to the diagram are taken through the His bundle, the atrioventricular (AV) conduction bundle (asterisks), and the bundle branches to show the fibrous tissue (green) surrounding the conduction tissues. AVN = atrioventricular node; CS = coronary sinus; LBB and RBB = left and right bundle branch, respectively; PB = penetrating bundle. The Cardiac Conduction System

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ATRIA The anterior border of the triangle is the hinge line (annulus) of the septal leaflet of the tricuspid valve (see Figure 5.1). Its inferior border is the orifice of the coronary sinus and the right atrial vestibule leading to the tricuspid valve. The posterior border is marked by a thin fibrous strand known as the tendon of Todaro. It is buried in the subendocardium of the sinus septum (Eustachian ridge) but can appear as a line when tension is placed on the edge of the Eustachian valve, which guards the orifice of the inferior caval vein. The tendon inserts into the central fibrous body, which is at the apex of Koch’s triangle. The atrioventricular node is located immediately inferior to the central fibrous body, and its anterosuperior extension, the His bundle, penetrates into the fibrous body to become surrounded by fibrous tissue. Part of the central fibrous body extending anterosuperiorly is the membranous septum. This is crossed by the annular insertion of the tricuspid leaflet dividing it into atrioventricular and interventricular portions. In some hearts, there is a gap in the septal leaflet at the site of the membranous septum. The valvar commissure between septal and anterosuperior leaflets is located approximately 5 mm superiorly and away from the septum. It is worth noting that the height of the triangle may be reduced in cases with an enlarged coronary sinus, for example associated with a persistent left superior caval vein.

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The compact atrioventricular node is shaped rather like a knob but with rightward and leftward inferior extensions (see Figure 5.3b). The nodal body adjoins the atrial aspect of the central fibrous body, making it an interatrial structure. In the adult heart, it is approximately 5 mm long and wide, and nearly 1 mm thick. The minimal distance of the compact node from the endocardial surface of the right atrium is approximately 0.5 to 1.5 mm. On histology, the compact node in cross section often appears to have two zones or strata. Frequently, especially in hearts from infants and children, short prongs of the small interweaving and histologically specialized myocytes of the deep stratum extend into the central fibrous body. The superficial stratum appears like a cap of specialized myocytes over the deep stratum. At the nodal interface with ordinary atrial myocardium, there is a zone of transitional cells (Figure 5.5). These cells are arranged to provide anterior, inferior, and deep inputs to the node (Figure 5.6). The anterior input sweeps from the anterior margin of the oval fossa deep to the ordinary myocardium of the tricuspid vestibule. The inferior input approaches the compact node from the musculature in the floor of the coronary sinus and from the Eustachian ridge. The deep input bridges the compact node with the left atrial vestibule and inferior rim of the oval fossa.

Chapte r 5  |   Electrical Anatomy and Accessory Pathways

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R eE 5.5 F IG U r This section through the compact node at the level indicated on the diagram (arrow and broken line) shows its proximity to the endocardial surface of the right atrium (RA) despite its interatrial location. The panels show magnifications of the cellular composition of this region. AVN = atrioventricular node; CS = coronary sinus; LBB and RBB = left and right bundle branch, respectively; PB = penetrating bundle.

The Cardiac Conduction System

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ATRIA

R eE 5.6 F IG U r These sections through three levels of the compact atrioventricular node (AVN) (within broken lines) show the inputs of the transitional cells and the ingress of the node into the central fibrous body to become the penetrating bundle (PB) of His (c). CS = coronary sinus; LBB and RBB = left and right bundle branch, respectively.

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In the majority of hearts, inferior nodal extensions diverge to pass to the right and left sides of the artery that penetrates the compact node (Figure 5.7). The right extension courses parallel and adjacent to the hinge of the tricuspid valve while the left extension projects toward the mitral vestibule to the mitral ring. The right extension lies approximately 1 to 5 mm beneath the endocardial surface and reaches inferiorly to the midlevel of the anterior border of the triangle of Koch. It may even reach the vicinity of the coronary sinus orifice in hearts with a small triangle, eg, enlarged coronary sinus associated with persistence of the left superior caval vein.

R eE 5.7 F IG U r The inferior nodal extensions are shown as red spots on the heart specimen and ovals on the histologic section. The open arrows mark the hinge lines of the mitral and tricuspid valves. AVN = atrioventricular node; CS = coronary sinus; ICV = inferior caval vein; LA and RA = left and right atrium, respectively; LBB and RBB = left and right bundle branch, respectively; LV and RV = left and right ventricle, respectively; PB = penetrating bundle.

The Cardiac Conduction System

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ATRIA Superiorly, at the apex of Koch’s triangle, the penetrating atrioventricular conduction bundle of His passes leftward through the central fibrous body. This short bundle of specialized myocardium is approximately 1 to 3 mm long and varies from almost circular to triangular shape in cross section. The emergence of the bundle in the ventricles is directly related to the membranous septum and the aortic outflow tract. The atrioventricular bundle is sandwiched between the membranous septum and the muscular crest of the ventricular septum, related closer to the left than the right side. The conduction bundle, still invested in its fibrous sheath, bifurcates into the left and right bundle branches after a short distance (see Figure 5.4). The left bundle branch fans out as it descends in the subepicardium of the septal surface of the left ventricle into three interconnecting fascicles.

R eE 5.8 F IG U r (a) This view of the right ventricle (RV) shows the atrioventricular conduction bundle and right bundle branch superimposed (spots). The right bundle branch (RBB) is cord-like and emerges from the septal musculature onto the subendocardium at the base of the medial papillary muscle (blue triangle). The arrow indicates the moderator band. (b) The left ventricle (LV) is shown with

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the membranous septum transilluminated. The left bundle branch (LBB) cascades down the subendocardium like a sheet on the septum and branches into three fascicles. The histologic section at the level of the membranous septum shows the bifurcation of the branching atrioventricular bundle immediately to the left of the septal crest. The magnified panels show the bundle branches retaining their fibrous

sheaths (green) in the subendocardium of the septum. AVN = atrioventricular node; CS = coronary sinus; L, N, and R = left coronary, noncoronary, and right coronary aortic sinus, respectively; MV and TV = mitral and tricuspid valve, respectively; PB = penetrating bundle.

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CALF

SHEEP

R eE 5.9 F IG U r These preparations show up in the Purkinje fiber network as black lines in the right ventricle of the calf and the left ventricle of the sheep. The moderator band (red arrow) carries within it a branch of the right bundle branch. False tendons (blue arrows) carry peripheral branches across to the papillary muscles (white arrows). The dark blotches are preparation artifacts. The inset is a magnification of the left ventricular septal surface showing the lace-like arrangement of the network. The histologic section in van Gieson stain shows the large vacuolated Purkinje cells.

The fascicles are ensheathed in fibrous tissue until the distal ramifications. By contrast, the right bundle branch is like a cord of specialized cells (see Figure 5.4). It is surrounded by fibrous tissue and descends through the musculature of the ventricular septum to emerge in the subendocardium at the base of the medial papillary muscle, where it continues superficially in the subendocardium of the septomarginal trabeculation. Along its descent, a prominent branch carried within the moderator band crosses to the parietal wall (Figure 5.8). As they descend toward the apical parts of the ventricles, both the right and left bundle branches begin to lose their fibrous sheaths and ramify into the peripheral conduction network. Commonly referred to as the Purkinje fibers, large and vacuolated Purkinje cells are more commonly found in ungulate hearts (Figure 5.9) than in human hearts. Branches of the peripheral network sometimes cross the ventricular cavities in “false tendons” to reach the parietal wall and papillary muscles.

Photograph of calf preparation courtesy of Professor Damian Sanchez-Quintana, Spain.

The Cardiac Conduction System

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ATRIA In the majority of hearts, the direct extension of the nodal bundle axis is the right bundle branch. In some hearts, however, the atrioventricular bundle itself continues beyond the bifurcation as a third bundle (or dead-end tract) that terminates in the central fibrous body or passes from the septal crest toward the aortic valve annulus before disappearing (Figure 5.10).

The Atrioventricular Junctions At the atrioventricular junctions, the walls of the atria and ventricles are contiguous and without myocardial continuity except at the site of the penetrating bundle of the atrioventricular conduction tissues. Anomalous muscular atrioventricular connections at the atrioventricular junctions allow for electrical shortcutting, which in the case of antegrade (atrial to ventricular) conduction (competing with normal atrioventricular nodal conduction) may produce the Wolff-ParkinsonWhite (WPW) variant of ventricular preexcitation.

R eE 5.10 F IG U r (a) The dead-end tract is the continuation of the branching atrioventricular conduction bundle. (b) The tract is superimposed on this longitudinal cut through the septum to show its relationship to the aortic valve. (c) and (d) are histological sections in the same orientation through two hearts that contained remnants of this tract (arrows). AVN = atrioventricular node; CS = coronary sinus; LA = left atrium; LBB and RBB = left and right bundle branch, respectively; MV = mitral valve; PB = penetrating bundle; N and R = noncoronary and right coronary aortic sinus, respectively.

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In describing the location of the accessory bundles, attitudinal terminology is desirable. The true septal component is limited to the area of the central fibrous body and immediate environs. The so-called anterior septum is contiguous with part of the supraventricular crest of the right ventricle, while the posterior septum is formed by the muscular floor of the coronary sinus overlying the diverging posterior walls of the ventricular mass and the vestibule of the right atrium overlapping ventricular myocardium. Anatomically, the atrioventricular junction can be described as comprising extensive right and left parietal junctions that meet with a small septal component (Figure 5.11).

R eE 5.11 F IG U r (a) The attitudinal orientation is depicted on this diagram. (b) Diagrams of the atrioventricular junctions displayed in left anterior oblique (LAO) projection. The old nomenclature (upper panel) should be replaced with terminology that is more accurate attitudinally (lower panel) when describing the locations of accessory pathways. Of note, the septal component is much smaller than previously portrayed. P1, P2, and P3 are designations used by cardiac surgeons to describe portions of the posterior leaflet affected by prolapse.

The Atrioventricular Junctions

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ATRIA The right parietal junction is relatively circular and occupies a near-vertical plane in the heart marked by the course of the right coronary artery in the atrioventricular groove. On the endocardial surface, the tricuspid vestibule overlies (overlaps) the ventricular wall. Thus, on pullback from the annulus, the big ventricular signals will give way to increasing atrial signals (Figure 5.12). The atrioventricular groove is deeper on the right parietal junction than on the left junction. The superior and most medial part of the junction abuts directly on the membranous septum.

R eE 5.12 F IG U r The right atrium and right ventricle are opened to simulate a right anterior oblique view. The catheter inserted through the inferior caval vein has crossed the tricuspid annulus (dotted line) and landed (a) in the ventricle. On pullback, the catheter is (b) at the atrioventricular junction and (c) in the right atrium. cs = coronary sinus.

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The left parietal junction surrounds the orifice of the mitral valve, and part of it is the area of fibrous continuity between the mitral and aortic valves (Figure 5.13). On the atrial side, the fibrous region is overlapped by left atrial myocardium reaching to the area of the mitral annulus. On the ventricular aspect, it is rare in humans to find ventricular myocardium interposing between the aortic and mitral leaflets. Thus, the potential for accessory atrioventricular connections is mainly limited to the junction supporting the hinge line of the mural leaflet of the mitral valve. This runs from anterosuperior to posterior and inferior when the heart is viewed in left-anterior oblique projection. R eE 5.13 F IG U r (a) This view of a cut through the short axis of a heart with a dilated left ventricle shows the area of fibrous continuity between the aortic and mitral valves (between open arrows). (b) and (c) are two halves of the same heart cut longitudinally to show the fibrous continuity between the anterior leaflet of the mitral valve (MV) and the aortic valve (arrows). Ao = aorta.

The Atrioventricular Junctions

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ATRIA The inferior area harbors the coronary sinus and its tributary, the great cardiac vein. The inferior paraseptal region, the so-called posterior septum, is the inferior pyramidal space that contains epicardial fibrofatty tissues together with the artery supplying the atrioventricular node (Figure 5.14).

R eE 5.14 F IG U r (a) and (b) are cuts through the long axis of the heart displayed in similar orientations approximating to the right anterior oblique (RAO) to demonstrate the inferior paraseptal region. (a) and (b) show the leftward and rightward extents, respectively, of the inferior pyramidal space (within broken lines) containing the right coronary artery (RCA), the coronary sinus (CS), and the artery to the atrioventricular node (AVNA). (c) By dissecting away the atrial walls at the inferior paraseptal region, this basal view shows the limited extent of the septum at the atrioventricular junction. The inferior pyramidal space (within broken lines) extends deep into the heart. The heart has a dominant left coronary pattern with the circumflex artery (Cx) supplying the posterior descending artery (PDA) and AVNA. Ao = aorta; ICV = inferior caval vein; LA and RA = left and right atrium, respectively; MV and TV = mitral and tricuspid valve, respectively.

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Accessory Pathways Accessory pathways (APs) are bridges of cardiac muscle that breach the insulating properties of the atrioventricular groove and insertions (annuli) of the valves outside the regular atrioventricular conduction tissues (Figure 5.15). Often, they are capable of rapid conduction. Accessory atrioventricular pathways most often are found in the parietal atrioventricular junctional areas including the paraseptal areas. They are rarely found in the area of fibrous continuity between the aortic and mitral valves because in this area there is usually a wide gap between atrial myocardium and ventricular myocardium to accommodate the aortic outflow tract. Usually, the accessory pathways are thread-like up to 3 mm wide, are thicker at the atrial insertions, and branch into finer strands at the ventricular insertions. Occasionally they may be like a band of muscle 10 mm or more wide.

R eE 5.15 F IG U r Accessory pathways (orange bands) traverse the fibrofatty tissues (blue and green) of the atrioventricular (AV) junction to connect atrial myocardium with ventricular myocardium, bypassing the specialized atrioventricular conduction system (red). The inset is a histologic section showing a left-sided accessory pathway (arrows) skirting the mitral annulus (green).

Accessory Pathways

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ATRIA Most APs consist of ordinary working myocardium, although a few comprising histologically specialized myocytes have been reported. Pathways may occur singly, or there may be several of them. On the left parietal side, the APs tend to be close to the annulus of the mitral valve. Because the right atrioventricular groove is much deeper than on the left side, right parietal accessory muscle bundles can cross at any distance from the tricuspid annulus (Figure 5.16).

R eE 5.16 F IG U r The four-chamber section though the heart (right panel) shows the deeper ingress of atrioventricular (AV) groove on the right atrioventricular junction compared to the left side. The diagram illustrates two accessory pathways (orange bands); the pathway can be close to the insertion of the tricuspid valve (TV) or nearer to the epicardium.

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Preferential Locations of APs For an accurate description of the location of APs, it is necessary to distinguish between parietal and septal components of the atrioventricular junctions in anatomical terms. While most APs are located along the mitral annulus, the distribution of the insertion sites varies substantially. Figure 5.17 gives an overview from a single center experience over the last 20 years.

R eE 5.17 F IG U r Schematic of the respective aspects around the tricuspid and mitral annulus with the anatomically correct terminology as seen from a left anterior oblique (LAO) projection and percentages of ablated pathways within a nearly 20-year period at a single center (St. Georg General Hospital, Hamburg, Germany).

Accessory Pathways

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ATRIA Electrophysiological Properties of AP and Resulting Arrhythmias While the term WPW syndrome is often used as a surrogate for arrhythmias arising from an AP, it correctly describes a patient with an AP with antegrade conduction properties (atrial to ventricular activation) and paroxysmal tachycardia. The morphology of the resulting delta wave depends on the site of the AP insertion and the amount of ventricular preexcitation (Figure 5.18).

R eE 5.18 F IG U r Schematic of the resulting preexcitation depending on the corresponding conduction properties of the atrioventricular (AV) node and an accessory pathway (AP). A broken line depicts slow conduction, while a solid line depicts faster conduction properties. The right panel demonstrates the effect of any AV nodal blocking agent in the presence of an antegradely conducting AP. Because these agents have no effect on the pathway conduction, conduction is exclusively across the AP resulting in maximal preexcitation with very broad QRS complexes on surface ECG.

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R eE 5.19 F IG U r Schematic of the three different arrhythmias that are possible in the presence of an accessory pathway. The left panel depicts the basis of an orthodromic atrioventricular (AV) reentrant tachycardia with antegrade conduction across the AV node and retrograde conduction across the pathway. The middle panel shows the concept of an antidromic AV reentrant tachycardia with antegrade conduction across the pathway and retrograde conduction across the AV node. Note the resulting broad QRS tachycardia. The right panel depicts conduction of atrial fibrillation across both the AV node and an antegradely conducting accessory pathway resulting in irregular broad QRS complexes and the risk of sudden cardiac death.

Accessory Pathways

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These patients can present with wide-complex QRS antidromic atrioventricular reentrant tachycardia or even more dangerously with preexcited atrial fibrillation (Figure 5.19). However, most APs actually conduct only in the retrograde direction (ventricular to atrial activation) with no evidence of the AP in a baseline 12-lead electrocardiogram (ECG) (therefore called concealed pathways). Logically, the resulting supraventricular tachycardia can only be a narrow QRS complex orthodromic atrioventricular reentrant tachycardia with antegrade conduction across the atrioventricular node. Some APs can conduct in both directions, giving rise to both orthodromic and antidromic atrioventricular reentrant tachycardia.

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ATRIA Diagnosis of the Insertion Site of APs While the baseline 12-lead ECG provides sufficient clues to the AP insertion site in an antegradely conducting AP, retrograde-only conducting APs can be diagnosed only by an invasive electrophysiological study. Typically, diagnostic catheters positioned along the atrioventricular annuli can easily provide a guide to the AP insertion site. While the coronary sinus (CS) is covering the mitral annulus, a Halo catheter can be positioned close to the tricuspid annulus. Using very thin (2–3 Fr) catheters, mapping from inside the coronary arteries (right coronary or circumflex artery) allows for identification of the site where the atrial and ventricular potentials fuse during sinus rhythm (Figure 5.20). In retrograde-only conducting APs, ventricular pacing (not too far from the suspected AP insertion) will unmask the earliest atrial activation site in the same fashion. Simultaneous recording of the activation of the His bundle region allows for differentiation of atrioventricular nodal conduction and serves as a marker of the septum in left anterior oblique view.

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R eE 5.20 F IG U r Depiction of the right coronary artery (RCA) in relation to the His recording catheter in right anterior oblique (RAO) and left anterior oblique (LAO) projections. The proximal part of the RCA is located inside the right-sided AV groove. Note that a very thin recording catheter (2–3 Fr) can be positioned inside the RCA to locate epicardial accessory pathways. RV = right ventricle.

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Using both mapping and ablation catheters, finetuned or high-resolution mapping is subsequently performed to pinpoint the AP insertion, for example around the tricuspid annulus (TA). On the exact AP insertion site, a characteristic AP potential can be mapped that, in addition to earliest ventricular/ atrial activation, serves as the target site for catheter ablation. Stable positioning with very little beat-to-beat variance of the local signal is key to mapping and ablation success.

Access to Right-Sided APs

R eE 5.21 F IG U r Example of mapping around the tricuspid annulus (yellow circle) for the insertion of a right-sided accessory pathway using a femoral approach. Especially the positions from about 10 o’clock to 2 o’clock are difficult to stabilize. Note that the difference between the ostium and an inside position in the coronary sinus (CS) is marked by the large atrial electrical signal (right top and bottom panel). LAO = left anterior oblique.

Accessory Pathways

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While most AP insertion sites along the TA can be accessed easily from an inferior approach, via a femoral vein (Figure 5.21), the upper free wall quadrant of the TA (anterior to the superoparaseptal part of the atrioventricular junction, otherwise known as the free wall to para-Hisian) can pose a significant obstacle for stable catheter positioning. An excellent alternative that allows for stable mapping is via a superior approach, using either a jugular vein or a subclavian venous access (Figure 5.22). The catheter is first positioned in the ventricle and then slowly withdrawn into the atrium, where it is stable, with little risk of dislodgment.

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ATRIA Access to Left-Sided APs Left-sided APs can be approached via two general routes. While the retrograde approach was favored by most electrophysiologists in the past (Figure 5.23), nowadays (parallel to the growing experience with transseptal punctures) more and more physicians prefer the transseptal route.

R eE 5.22 F IG U r Example of using a superior approach (eg, via subclavian vein or internal jugular vein) to reach the superior aspect of the tricuspid annulus, which improves catheter stability. CS = coronary sinus; His = His catheter; LAO = left anterior oblique.

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Crossing the aortic valve in an atraumatic fashion (sequence of catheter movements)

Retrograde Access  |  After gaining access to the femoral artery, the ablation catheter is advanced retrogradely through the aorta. Arriving in the aortic route, the catheter is flexed to cross the aortic valve in an atraumatic fashion (see Figure 5.23). This is necessary to avoid damage to the valve itself, but also to avoid blocking/rupture of the coronary arteries.

R eE 5.23 F IG U r Retrograde crossing of the aortic valve. With a completely inverted catheter, the aortic valve can be crossed without damaging the semilunar cusps. The dotted yellow line depicts the approximate location of the valve itself. Care needs to be taken that the tip of the ablation catheter is not entering into any coronary ostium, and close observation of the surface ECG ST segments is advisable. RAO = right anterior oblique; RV = right ventricle.

Accessory Pathways

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ATRIA Once the aortic valve is crossed, the catheter is positioned in a “turning and advancing” movement under the mitral valve leaflets. In order to map several sites along the mitral annulus, withdrawal and readvancing are mandatory because the mitral valve apparatus does not allow for a lateral or rotational mapping approach (Figure 5.24). Transseptal Mapping of Mitral Annulus  |  For a review of transseptal puncture techniques, please refer to Chapter 7. Since the left atrial endocardium is relatively smoother than the right, the transseptal mapping of the mitral annulus is less challenging technically, and it allows for contiguous mapping along the annulus (Figure 5.25). While the CS catheter serves as a guide to the area of the AP insertion, its location is a very useful guide in both right and left anterior oblique projections when aiming to achieve a stable catheter position at the mitral annulus. Parallel and simultaneous movement in concert with the CS catheter with little beat-to-beat variance in the local signal ascertains stable catheter-tissue contact. While mapping in itself is facilitated using this approach, its major disadvantage is apparent when dealing with an epicardially located AP that is distant from the annulus. The retrograde approach allows the ablation catheter to be much closer to the AP insertion site.

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R eE 5.24 F IG U r (a) This longitudinal section though a heart displayed in approximately anteroposterior (AP) orientation shows that the retrograde approach (broken line) to reach the inferior paraseptal area traverses through the mitral apparatus. (b) This view of the cardiac short axis looking toward the aortic outflow tract (asterisk) shows that the anterolateral (ALpm) and posteromedial (PMpm) groups of papillary muscles are located quite close to each other. Ao = aorta; CS = coronary sinus; LA = left atrium.

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Paraseptal Accessory Pathways The paraseptal location is one of the more challenging sites for catheter ablation because the conventional access might not allow for stable positioning of the ablation catheter. There is also the potential risk of complications arising from damage to the artery to the atrioventricular node in the inferoparaseptal region and the main coronary arteries in the superoparaseptal region. In addition, anatomical variations like valves at the CS may complicate the procedure (see Chapter 1). Mapping of paraseptal AP is facilitated by a proximally positioned CS catheter with close interelectrode spacing. Use of an irrigated tip catheter when ablating within the proximal part of the CS is recommended to avoid high impedances, but must be limited to low energy levels to avoid coronary artery damage and rupture.

R eE 5.25 F IG U r Example of a transseptally advanced mapping catheter (TS) in corresponding locations along the mitral annulus (marked by the coronary sinus [CS] catheter) in both left anterior oblique (LAO, upper panels) and right anterior oblique (RAO, lower panels) projections. Note that due to the individual heart axis, the exact location (more atrial versus more ventricular) can be seen easily by the locally recorded signal from the catheter tip, but the RAO view also gives a clue in this regard. The LAO projection is optimal to ascertain the location with regard to the orientation along the mitral annulus. Also note the additional guidance from the best recording electrodes of the coronary sinus catheter that can serve as an additional guide for fast identification of the pathway insertion site. His = His catheter; RV = right ventricle. Accessory Pathways

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ATRIA Unusual APs Although the majority of APs cross the regular atrioventricular junctional areas directly, some take an oblique course, or there may be multiple APs in close vicinity. The operator should also be aware of unusual variants such as those associated with the coronary venous system and those involving the specialized conduction tissues.

R eE 5.26 F IG U r Left panels depict contrast injection into the coronary sinus (CS) using a coronary “AL2” catheter to delineate the size and exact location of a CS diverticulum in a patient with a posteroseptal accessory pathway [right anterior oblique (RAO, upper panel); left anterior oblique (LAO, lower panel)]. Importantly, the neck of the diverticulum needs to be imaged optimally, since most of the accessory pathways are located exactly there. Note that the

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distal part of the CS catheter must have entered a small side branch and indeed showed large ventricular signals but only far-field atrial signals. (a) and (b) show a heart with an aneurysm (an) of the middle cardiac vein seen from the epicardial aspect (a), and its muscular wall is revealed when incised into (b). The heart shown in (c) and (d) has atrioventricular continuity due to an aneurismal coronary vein at the acute margin. The muscular venous wall is superficial

to the atrioventricular groove (triangle), and the vein opens directly into the right atrium (open arrow) in between the pectinate muscles. The histologic section from another heart shows a cuff of muscle (asterisk) around an anterior coronary vein (arrow) that opened directly into the right atrial appendage (RAA). His = His catheter; ICV and SCV = inferior and superior caval vein, respectively; RV = right ventricle; TV = tricuspid valve.

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R eE 5.27 F IG U r (a) Illustration of how to reach the proximal part of the coronary sinus (CS) using either superior or femoral access. Especially when a Thebesian valve is present, the superior approach is very helpful and even works in enlarged atria or Ebstein anomaly. (b) This extensive Thebesian valve could hinder an inferior approach to the CS, whereas a superior approach could be more direct. His = His catheter; ICV and SCV = inferior and superior caval vein, respectively; TV = tricuspid valve.

Accessory Pathways

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APs Associated With CS/Veins  |  The CS diverticulum is well recognized as a potential substrate for APs. In other cases, individual coronary veins are involved, and these appear as enlarged venous orifices in the atria. Some are related to atrial appendages overlying the ventricular mass. The few cases we have seen of this variant are mediated through coronary venous channels. The anatomical substrate is usually in the form of extensive myocardial cuffs around the vein as it crosses the atrioventricular junction or the muscular walls of the venous diverticulum extending into the ventricular mass (Figure 5.26). These APs are ablated at the neck from the atrial aspect. Access to the neck of a CS diverticulum is facilitated by a superior access (Figure 5.27). Multiple APs   |  For careful assessment of all electrical signals after ablation, especially proof of atrioventricular node conduction in the absence of ventriculoatrial dissociation, it is important to avoid overlooking dormant APs. There is ample evidence that there is a high incidence of multiple pathways in patients with Ebstein anomaly. In these patients, the hinge line of the septal and posteroinferior leaflets of the tricuspid valve is displaced toward the ventricular apex, resulting in a variable extent of so-called atrialized right ventricle. For more discussion on Ebstein, see Chapter 11.

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ATRIA Rare Accessory Pathways  |  These APs involve muscular connections to the regular atrioventricular conduction system. They are named according to the level at which they connect to the specialized conduction tissues, viz atriofascicular, nodofascicular, nodoventricular, and so on (Figure 5.28). The term atriofascicular pathway has been used to describe two different situations. Earlier, it was used to explain bundles that pierce through the central fibrous body to connect atrial myocardium with the His bundle or common atrioventricular conduction bundle. These are also known as atrio-Hisian APs. In recent decades, atriofascicular pathway is commonly used to describe those that connect atrial myocardium to the right bundle branch. Characteristically, these APs are long. They arise from the right atrium at the acute margin, where there may or may not be a rudimentary node of specialized conduction tissues, pass through the parietal atrioventricular junction, and insert into the parietal ventricular wall to descend toward the apical part, where it is thought to link with the right bundle branch passing through the moderator band.  

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R eE 5.28 F IG U r Schematic of variants of accessory pathways (orange bands) that involve the atrioventricular (AV) conduction tissues. The insets are from a case with histiocytoid cardiomyopathy. (a) and (b) show a nodal remnant (small arrow) near the acute margin of the tricuspid annulus that connects to a broad band of accessory pathway (open arrow), whereas (c) shows an accessory nodoventricular connection (asterisk) allowing the AV node to reach the crest of the ventricular septum, bypassing the His bundle. RA = right atrium; RV = right ventricle; TV = tricuspid valve.

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6

the Right Atrium Relevant to Supraventricular tachycardia

THE RIgHt AtRIUM IS tHE FIRSt PoINt of entry in the vast majority of patients who undergo an invasive electrophysiology study. This chapter gives an overview of key sites such as the atrioventricular junction, Koch’s triangle, and the isthmus between the tricuspid annulus and the inferior caval vein.

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ATRIA

R eE 6.1 F IG U r Right lateral views of the epicardial aspect of the right atrium (a) and the endocast (b) show a triangular atrial appendage. The terminal groove (broken line) and its corresponding terminal crest (crista terminalis) demarcate the border between appendage and venous components of the right atrium. Note the smooth endocardial surface of the vestibule on the endocast, which is covered by fat on the epicardial side. ICV and SCV = inferior and superior caval vein, respectively.

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Chapte r 6  |   The Right Atrium Relevant to Supraventricular Tachycardia

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Anatomy

R eE 6.2 F IG U r This anterior view of the venoatrial junction shows a myocardial sleeve covering the superior caval vein (SCV) and extending to varying lengths (red broken line). The sinus node is located in the area surrounded by the dotted line. Nodal extensions are represented by short broken lines. RA = right atrium.

Anatomy

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Anatomically, the right atrium (RA) is best considered in terms of three components— the appendage, the venous part, and the vestibule. A fourth component, the septum, is shared by the two atria. Viewed from the outside, the RA is dominated by its large, triangular appendage, which points anterosuperiorly and extends laterally. Usually, a fat-filled groove (sulcus terminalis) corresponding internally to the terminal crest (crista terminalis) can be seen on the endocardial surface demarcating the junction between appendage and venous components (Figure 6.1). The terminal crest can be likened to a C-shaped ridge that springs from the precaval bundle on the septal aspect to pass in front of the entrance of the superior caval vein to pass from anteriorly to posteriorly along the lateral wall of the atrium. The sinus node is located subepicardially in this groove, in the anterolateral part of the superior cavoatrial junction. Frequently, RA musculature extends onto the adventitial/epicardial side of the wall of the superior caval vein, sometimes over a few centimeters (Figure 6.2), whereas muscular extension around the inferior caval vein is uncommon.

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ATRIA Distinctive of the RA is its large appendage. Internally, there is a prominent muscle bundle termed the sagittal bundle that extends superiorly from the precaval bundle and sends multiple branches to line the apical part of the triangular appendage (Figure 6.3). Laterally, the precaval bundle turns into the terminal crest, and arising nearly perpendicularly from the crest is a vast array of pectinate muscles that spread throughout the entire wall of the appendage, making up the lateral wall of the RA. Commonly, short pectinate muscles extend even to the inferior walls of the atrium. Although extensively arranged, the pectinate muscles never reach the annulus of the tricuspid valve because there is always a smooth muscular rim, the vestibule, that surrounds the valvar orifice and its musculature inserting into the valvar leaflets. The pectinate muscles run on the endocardial surface, but the atrial wall between the muscular ridges is very thin and almost parchmentlike in places (see Figure 6.3). Inside the atrium, the branching and overlapping arrangement of the pectinate muscles is clearly visible. This arrangement may play a role in initiating intra-atrial reentry.

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R eE 6.3 F IG U r (a) The right atrial appendage and the orifice of the inferior caval vein (ICV) have been incised and the appendage wall flipped posteriorly to show the internal aspects. (b) Transillumination reveals the paper-thin parts of the wall between the pectinate muscles. Note the smooth vestibule proximal to the tricuspid orifice. CS = coronary sinus; OF = oval fossa; SCV = superior caval vein; TV = tricuspid valve.

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The venous component lying between the orifices of the caval veins forms the posterior wall of the atrium. It is characterized by having a smooth wall that blends into the septal aspect. The division between venous and rough pectinated zones is marked by the terminal crest, which is usually recognizable as a raised ridge. The terminal portion of the crest is indistinct, as it divides into a variable number of smaller bundles that continue toward the vestibule and the orifice of the inferior caval vein, feeding into the area of the “flutter” (cavotricuspid) or inferior isthmus (see below). The Eustachian valve, which guards the entrance of the inferior caval vein, is also variably developed (Figure 6.4). Usually it is a triangular flap of fibrous or fibromuscular tissue that inserts medially to the Eustachian ridge, or sinus septum, which is the border between the oval fossa and the coronary sinus (CS). R eE 6.4 F IG U r Examples of large Eustachian valves (EV) with the blue lines representing catheters via the inferior caval vein. (a) The valve has considerable height, and the Eustachian ridge (ER) is pronounced. There is no Thebesian valve at the coronary sinus (CS). (b) The valve extends into an aneurysm that herniates into the tricuspid orifice. The CS is on the “wrong” side of the valve. FO = fossa ovalis; TV = tricuspid valve.

Anatomy

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ATRIA The free border of the Eustachian valve continues as a tendon (of Todaro) that runs in the musculature of the Eustachian ridge. It is one of the borders of the triangle of Koch that delineates the location of the atrioventricular node (Figure 6.5). The anterior border is marked by the hinge (annulus) of the septal leaflet of the tricuspid valve. Superiorly, the central fibrous body is the landmark for the penetrating bundle of His. The inferior border of the triangle is the orifice of the CS together with the vestibule immediately anterior to it.

R eE 6.5 F IG U r (a) This approximately right anterior oblique (RAO) view of the right atrium shows the borders of the triangle of Koch (broken lines). (b) Dissection of the subendocardial myocardial strands shows a varied arrangement in the area of the triangle of Koch (between broken lines). CS = coronary sinus; EV = Eustachian valve; FO = fossa ovalis; ICV and SCV = inferior and superior caval vein, respectively; TV = tricuspid valve.

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The vestibular portion is the area often targeted for ablation of the slow pathway in atrioventricular nodal reentrant tachycardia (AVNRT). The so-called fast pathway corresponds to the area of musculature close to the apex of the triangle of Koch (Figure 6.6). A small crescentic flap, the Thebesian valve, usually guards the orifice of the CS (Figure 6.7). Frequently, the valve is fenestrated. An imperforate valve completely covering the orifice is very rare.

R eE 6.6 F IG U r (a) This window dissection into the right heart displays the right atrium (RA) in approximate right anterior oblique view. (b) The magnified view depicts the putative fast and slow pathways toward the compact atrioventricular node (dotted shape). CS = coronary sinus; ER and EV = Eustachian ridge and valve, respectively; FO = fossa ovalis; ICV and SCV = inferior and superior caval vein, respectively; RAA = right atrial appendage; RV = right ventricle; RVOT = right ventricular outflow tract; TV = tricuspid valve.

Anatomy

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ATRIA Electrophysiological Perspectives RA and AVNRT Typical AV nodal reentrant tachycardia is the most common cause of narrow QRS complex tachycardia. It mostly presents with paroxysmal episodes of palpitations, and patients often describe an “on-off ” phenomenon to characterize the sudden beginning and end of the arrhythmia. CS Size as a Marker for AVNRT  |  Some reports have emphasized the size of the CS ostium as a risk factor for AVNRT. Because different conduction properties of the two (or more) AV pathways are key to tachycardia induction, increased distance could result in significantly different conduction properties. Although direct-contrast injection, for example using a left Amplatzer diagnostic catheter (AL2), can easily delineate the size of the CS ostium, this is rarely performed during the electrophysiological study. Probing the CS ostium with the ablation catheter, however, is a practical approach demonstrating both large atrial and ventricular local signals. Although the exact reentrant circuit of AVNRT is still unknown, several hypotheses about potential inputs and courses of the activation wavefront are under discussion (Figure 6.8). The lowest rate of complete AV nodal block is reported for the ablation attempt of the so-called slow pathway (SP), whereas fast pathway (FP) modification has been abandoned because it carries a high risk of complete AV block.

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R eE 6.7 F IG U r Variations in morphology of the Thebesian valve guarding the coronary sinus orifice. The valve is a crescentic flap (a) that may have fenestrations (b) and (c), is strand-like (d), is absent (e), is extensive with fenestrations (f), or is so extensive as to allow the coronary sinus orifice to be approached via a slit from superiorly (g).

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R eE 6.8 F IG U r Different types of atrioventricular nodal reentrant tachycardia (AVNRT) and potential reentrant circuits (adapted from Nakagawa, H, Jackman, WM, Circulation, 2007). Schematics illustrate in right

Electrophysiological Perspectives

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anterior oblique (RAO; left panels) and left anterior oblique (LAO; right panels) the activation sequence marked with arrows (broken or zigzag to demonstrate slow conduction). CS = coronary sinus; FP and SP =

fast and slow pathway, respectively; ICV = inferior caval vein; LA and RA = left and right atrium, respectively; LCP = lower common pathway.

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ATRIA The key guidance to identify the SP area is the base of the so-called triangle of Koch (Figure 6.9). The body of the compact AV node is contained near the apical portion of the triangle, and the His bundle penetrates the central fibrous body at the apex. Toward the inferior portion of the triangle, there are prongs of nodal tissues that extend inferiorly rightward and leftward toward the tricuspid and mitral valves, respectively. These nodal extensions have been implicated in SP conduction. Because this area also contains the zone of transitional cells that feeds into the compact node, this too may have a role in SP conduction.

Koch’s triangle in fluoro

R eE 6.9 F IG U r Depiction of the fluoroscopy markers for Koch’s triangle in right anterior oblique (RAO) and left anterior oblique (LAO) projection. The red line marks the tricuspid annulus, depicted by the coronary sinus (CS) catheter in RAO, and starts at the His recording region, marked by the His catheter. The tendon of Todaro is a very thin structure, and its location is approximated by the proximal part of the His recording catheter. His = His catheter; RV = right ventricle.

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Using the shafts of the diagnostic catheters typically used inside the CS and in the His bundle region, Koch’s triangle can be depicted on the fluoroscopic pictures accordingly. Despite the fact that angulations need to accommodate the individual heart axis (most importantly in left anterior oblique, or LAO, to see the His catheter depicted orthogonally) (see Figure 6.9), this allows the target area to be identified for the mapping of the SP potential using the ablation catheter.

R eE 6.10 F IG U r Depiction of the mapping motion of the slow pathway in left anterior oblique (LAO) projection. Starting from a very ventricular position, the catheter is rotated clockwise. On the level of the coronary sinus (CS) catheter, the local atrial signal should be carefully analyzed. Slightly pulling the catheter back will increase the atrial voltage amplitude. His = His catheter.

Electrophysiological Perspectives

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Mapping of the SP area to depict SP potential can be made by starting with large V potential above and anterior to the CS, followed by slow withdrawal of the catheter and clockwise rotation toward the CS ostium (Figure 6.10). Because the SP is located in the endocardial region, there is no necessity to use high energy for ablation (Figure 6.11), thereby reducing the risk of penetrative collateral damage and inadvertent AV block.

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ATRIA “Displaced” AV Node  |  In some circumstances, the AV node components can be displaced, increasing the risk of total AV block when attempting SP modulation/ablation. A typical scenario would be a persistent left superior vena cava with a grossly enlarged CS ostium (Figure 6.12). The size of the triangle of Koch is reduced, resulting in the distance between the compact AV node and the CS ostium being shorter than usual.

R eE 6.11 F IG U r (a) The paraseptal isthmus (arrow) for slow pathway ablation is the portion of the vestibule between the coronary sinus (CS) orifice and the tricuspid annulus. The histologic section taken close to this level shows the atrial overlay and transitional cell zone covering the right inferior extension of the atrioventricular node (AVN). LA and RA = left and right atrium, respectively; MV and TV = mitral and tricuspid valve, respectively.

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R eE 6.12 F IG U r Example of a displacement of the slow pathway (SP) area by the presence of a persistent left superior vena cava (LSVC), which results in a massively enlarged coronary sinus (CS) as depicted by the contrast injections in right anterior oblique (RAO; left panel) and left anterior oblique (LAO; middle panel). The right panel shows the site depicting typical SP potentials with radiofrequency delivery resulting in slow junctional rhythm. His = His catheter; RV = right ventricle.

Electrophysiological Perspectives

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ATRIA

R eE 6.13 F IG U r Step-by-step approach of safely positioning a multipolar catheter at the free wall of the right atrium. Importantly, the position needs to be ventral to the crista terminalis close to the tricuspid annulus

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(sometimes a far-field ventricular signal can be seen on the distal electrodes). The right anterior oblique (RAO) projection allows for the assessment of the length of the inferior isthmus (yellow dotted line)

and helps to decide the best curve radius for the ablation catheter. CS = coronary sinus; CW = clockwise; LAO = left anterior oblique.

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RA Isthmus Dependent Atrial Flutter Common-type atrial flutter is one of the bestunderstood atrial reentrant tachycardias. It is a stable macro-reentrant circuit that has as its basis the anatomical structure of the RA, which produces anatomical barriers and functional blocks to conduction. The activation travels around the tricuspid annulus in a counterclockwise fashion, resulting in the typical sawtooth-like P-wave morphology. The target for ablation is anatomical—the isthmus of RA wall between the orifices of the inferior vena cava and the tricuspid valve (Figure 6.13). A transmural and contiguous ablation line through the isthmus has been established as the necessary curative procedure for typical atrial flutter. R eE 6.14 F IG U r Two hearts with fairly extensive Chiari networks. CS = coronary sinus; ICV and SCV = inferior and superior caval vein, respectively; TV = tricuspid valve.

Electrophysiological Perspectives

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For the electrophysiologist entering the RA via the inferior route, the first structure encountered is the Eustachian valve guarding the orifice of the inferior vena cava. Typically, it is a thin, insignificant, crescentic flap. Occasionally, the flap is larger and may impede access to the most posterior part of the isthmus. In approximately 2% of the population, the Eustachian valve has a fishnet appearance of varying size. This is known as a Chiari network (Figure 6.14); the most extensive may prolapse in and out of the tricuspid valve orifice. When electrophysiologists encounter a Chiari network, they should be aware of the potential risk of the catheter being caught or entangled by the network.

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ATRIA

R eE 6.15 F IG U r (a) This right atrial view shows the septum en face and parietal wall pulled inferiorly to display the cavotricuspid isthmus. The oval marks the orifice of the inferior caval vein (ICV). The broken lines mark (1) the paraseptal isthmus, (2) the inferior (flutter)

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isthmus, and (3) the inferolateral isthmus. Note the smooth vestibule immediately proximal to the tricuspid annulus and the variability in muscle bundles in the posterior regions. (b) A histologic section taken through the inferior isthmus shows a pouch of the

sub-Eustachian sinus. Note the lesser transmural thickness in this area. The right coronary artery (RCA) is in the epicardial fat related to the smooth vestibule. CS = coronary sinus; RV = right ventricle; TV = tricuspid valve.

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R eE 6.16 F IG U r The region of the cavotricuspid isthmus is viewed en face in this 4-chamber cut (a) and with transillumination (b). The paraseptal, inferior, and inferolateral isthmuses are marked 1, 2, and 3, respectively. The arrow indicates the sub-Eustachian pouch. CS = coronary sinus; ER = Eustachian ridge; ICV and SCV = inferior and superior caval vein, respectively; LA = left atrium.

Electrophysiological Perspectives

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The flutter isthmus, also known as the cavotricuspid isthmus, is bordered anteriorly by the hinge line (annulus) of the tricuspid valve and posteriorly by the Eustachian valve (Figure 6.15). This is a relatively large expanse of atrial wall extending medially, from the so-called septal isthmus, to inferolaterally, thus covering the sites of the three commonly deployed ablation lines: paraseptal isthmus, inferior isthmus, and inferolateral isthmus. Most commonly, the ablation line is made along the inferior wall (inferior isthmus). Hence it is also referred to as the central isthmus (6 o’clock on LAO projection). All three isthmuses have in common a smooth anterior zone being the RA vestibule that overlies to varying extents the right AV groove with the right coronary artery, and the musculature of the right ventricular wall (see Figure 6.15). In cadaver hearts, the distance between the right coronary artery and the endocardial surface of the isthmus ranges from 2 to 11 mm. By contrast, the posterior zone is composed of mainly fibrous and fatty tissue as it joins with the Eustachian valve. Between the anterior and posterior zones, the morphology and thickness of the isthmus is highly variable. In the inferior isthmus, the middle zone comprises muscle bundles that represent the terminal ramifications of the terminal crest and thin areas of fibrous tissue containing strands of muscle (Figure 6.16; see also Figure 6.15).

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ATRIA Approximately 20% of patients have a pouch-like recess known as the sub-Eustachian sinus in this zone (see Figure 6.15). The presence of this recess can cause considerable difficulty in achieving a complete line of block in this isthmus and is the reason for the preference of some operators to ablate an alternative RA isthmus line instead. Compared to the inferior isthmus, the wall of the inferolateral isthmus is longer (Figure 6.17; see also Figure 6.16), usually with thick pectinate muscles in the middle zone. Instead of the inferior or inferolateral isthmus, some ablationists use the portion of the isthmus that is more medial (nearer to the septum) in LAO projection. This is commonly referred to as the septal isthmus, although anatomically speaking it is paraseptal in location rather than truly septal. It is the smooth vestibule lying between the orifice of the CS and the annulus of the tricuspid valve. This is the shortest of the three RA isthmuses but has the thickest wall, ranging from 2 to 7 mm on heart specimens. More significantly, it is closest to the AV node, particularly the inferior nodal extensions (see Figure 6.17).

R eE 6.17 F IG U r (a) This section through the membranous septum with the atrioventricular node and bundle (dotted shape) superimposed shows the proximity of the paraseptal isthmus to the nodal region and the relative lengths of the 3 isthmuses. (b) This heart has a sub-Eustachian pouch (triangle) and a prominent Eustachian ridge (ER). CS = coronary sinus; EV = Eustachian valve; FO = fossa ovalis; ICV = inferior caval vein; RA = right atrium; TV = tricuspid valve.

Visualizing the Activation Sequence During Atrial Flutter by Conventional Catheters  |  Using the techniques described in Chapter 4, a CS catheter should be positioned at the proximal aspect of the CS. When describing the CS, we use the convention used by cardiac interventionists instead of following

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R eE 6.18 F IG U r Depiction of the catheter orientation in various left anterior oblique (LAO) angulations from 40° to 60°, allowing the operator to individualize the projection in correspondence to the cardiac axis along the atrial and ventricular septum. CS = coronary sinus; Halo and His = Halo and His catheter, respectively.

Electrophysiological Perspectives

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ATRIA direction of blood flow. Thus, proximal CS is nearest the orifice, whereas distal CS is away from the RA. In counterclockwise typical atrial flutter, the CS is activated from proximal to distal. To visualize the activation of the free wall of the RA, a multipolar catheter should be positioned in a “hockey stick” fashion, such that the most distal electrode is close to the intended ablation line (Figure 6.18; see also Figure 6.13). A catheter combining the two is available, but it crosses the ablation area limiting the maneuverability of the ablation catheter. Positioning the Halo catheter along the free wall of the RA demonstrates the direction of the activation front, for example craniocaudal in typical counterclockwise atrial flutter (Figure 6.19). If deemed necessary, a HIS/right ventricular apex catheter can be positioned to allow for monitoring of AV node conduction and instant ventricular pacing if required (especially if AV node conduction is unclear or prolonged).

R eE 6.19 F IG U r Superimposed on the left anterior oblique (LAO) projection, the activation sequence for counterclockwise (upper left panel) and clockwise (lower left panel) is indicated by colored arrows. The right panels show the typical recordings from the multipolar catheters. CS = coronary sinus; Halo = Halo catheter.

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The ablation catheter allows for confirmation of the activation wavefront running through the inferior isthmus depicting the local activation between the distal Halo and proximal CS catheters (Figure 6.20).

R eE 6.20 F IG U r Mapping of the inferior isthmus in left anterior oblique (LAO) projection. More lateral positions are reached by counterclockwise (CCW) rotation of the catheter, while more septal positions are reached by clockwise (CW) rotation. The distance toward the tricuspid annulus can be judged by the ventricular far-field potential. If the proximal electrode shows no longer an atrial potential, then the two proximal ring electrodes are no longer in contact (eg, are already in the inferior vena cava). CS = coronary sinus; Halo = Halo catheter.

Electrophysiological Perspectives

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Visualizing the Activation Sequence Using Advanced Mapping Systems  |  Sequential mapping techniques allow for complete reconstruction of the reentrant activation in the RA, helping to identify important barriers of conduction. Besides these so-called local activation time or propagation maps, further display of the local signal amplitude can be accessed (Figure 6.21). This information is helpful in understanding the precise anatomy in the ablation area of the inferior isthmus and can identify obstacles like pouches, big muscular bundles, and so on. The Ablation Target  |  Using entrainment maneuvers, the correct identification of the critical role of the inferior isthmus between the tricuspid annulus and the inferior caval vein can be easily confirmed. Mapping of the target zone by moving the ablation catheter helps to identify the barriers for the ablation line that needs to be gap-free in order to be effective over the long term.

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ATRIA

R eE 6.21 F IG U r Examples of two different right atrial activation time maps using the 3D electroanatomical mapping system CARTO. There is a difference in the coloring of the activation time results from the different “windows of interest,” but both demonstrate counterclockwise atrial flutter. LAO = left anterior oblique.

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Scanning the Target Zone  |  Starting on the ventricular aspect with a large ventricular, but small atrial, signal is the first mapping step. To reach the annulus, a right anterior oblique projection might be helpful, and the distance between the shafts of the femorally advanced diagnostic catheters in conjunction with the CS catheter can facilitate the right catheter choice (Figure 6.22).

RAO

RAO

RAO

RAO

R eE 6.22 F IG U r Examples of the lengths of the inferior isthmus from four different patients in right anterior oblique (RAO) 30º projection. The yellow dotted line depicts the approximated length assessed from the tricuspid annulus (TA) to the inferior caval vein (IVC) marked by the entrance of all catheters in the right atrium (all in right anterior oblique projection). CS = coronary sinus; Halo = Halo catheter; RV = right ventricle.

Electrophysiological Perspectives

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Once the annular position is reached, the LAO projection is a good projection to navigate from a more inferoseptal to a more posterolateral position. In order to move more septally, the ablation catheter needs to be rotated in a clockwise fashion (see Figure 6.20). Simultaneously, the local signal will move closer to the proximal CS signal. Turning the catheter handle counterclockwise will lead to a more lateral position, with the signal being closer to the distal Halo catheter (see Figure 6.20). Depending on the desired ablation line, the catheter is then slowly pulled back until the atrial signal completely vanishes and the catheter drops into the inferior vena cava. Care should be taken not to damage the AV node or its inferior inputs when deploying a more septally located line (please also compare to Figure 6.17).

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ATRIA Finding a Gap in the Ablation Line  |  Initially, termination of ongoing atrial flutter was thought to be the only endpoint necessary to achieve success. Subsequently, it became clear that success was only about 75% with a substantial number of patients re-presenting over the longer term with the same arrhythmia. Nowadays, we know that deployment of a complete line is the key endpoint, and persistent gaps along the line are responsible for recurrences. Stimulating from either side of the ablation line via a closely located electrode (Halo distal or proximal CS) will demonstrate if conduction has been blocked completely by the ablation line (Figure 6.23). Mapping along the deployed ablation line will show the signal split into double potentials (two wavefronts that arrive from opposite sites of the line) if the line is blocked. At the site of a conduction gap, the signal is single, identifying the hiatus where the wavefront is able to cross from one side of the line to the other (Figure 6.24). Mapping carefully along the ablation line will reveal double potentials that come closer and closer together, leading the way to finding the gap.

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R eE 6.23 F IG U r Schematic depictions of the findings along multipolar catheters on the opposite site of a complete line of block with pacing close to the ablation line between two areas of nonconduction.

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The same catheter movements are applied to scan the inferior isthmus for gaps as described above. The change of the activation sequence along the Halo might have occurred much earlier, but does not exclude slow conduction across the ablation line and could result in the erroneous illusion of complete line block. Potential Complications  |  The thickness of the ablation target in the inferior isthmus is variable, so careful attention has to be taken to avoid applying excessive energy. The greatest risk is to damage the right coronary artery that runs in the AV groove. Acute ST elevations are the initial marker, which should prompt direct-contrast injection into the right coronary artery, followed by percutaneous coronary intervention (PCI) if needed.

R eE 6.24 F IG U r

The AV node might be harmed when the ablation line is constructed too near toward the septum. In the past, the risk was especially high in patients who underwent FP modulation to control rapid atrial fibrillation and underwent subsequent septal RA isthmus blockade.

Schematic of findings along incomplete ablation lines. The small arrows depict the local activation through the gap: (a) A single potential or fractionated potential can be located at the site of the gap, while (b) farther away from the gap along the line, more and more split double potentials (DP) can be found.

Electrophysiological Perspectives

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ATRIA Atrial Tachycardia Atrial tachycardias are electrophysiologically confined to the atrial myocardium. They are identified easily by continuity even in the presence of a higher degree of AV nodal block (a diagnostic trick that can be achieved by, for example, vagal maneuvers or pharmacologic challenge with adenosine). Generally speaking, two mechanisms can be discriminated, the first being a focal mechanism with radial spread of the activation wavefront in all directions from a singular source, the second being a reentrant circuit with the activation wavefront traveling around a central barrier in a unidirectional activation sequence through a critical isthmus (Figure 6.25).

REENTRY

FOCAL

R eE 6.25 F IG U r Schematic of two different substrates of tachycardias. Left panel: Reentrant circuit around a central obstacle (eg, AV valve or scar area, in light blue) with a critical isthmus toward a second non-conducting barrier (eg, the inferior caval vein, in pink). The red arrow depicts the so-called critical isthmus that presents the shortest connection which can, but doesn’t necessarily, show slow conduction properties. Right panel: Focal source (orange star) with radial spread of the activation wavefront.

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RAO

LAO Crista 32/68 (47%) TA 25/68 (37%)

CS Successful ablation site

No permanent effect

R eE 6.26 F IG U r Preferential sites for origins of focal atrial tachycardia in the right atrium along the tricuspid annulus (TA), the crista terminalis (Crista), the coronary sinus (CS) ostium, and the appendage. ICV = inferior caval vein; LAO and RAO = left and right anterior oblique, respectively; RAA = right atrial appendage.

ElectrophysiologICAL Perspectives

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Concept of Focal Atrial Tachycardia  |  Since the activation wavefront spreads in all directions from the origin, the identification of the earliest site can be achieved by moving the ablation catheter and simultaneously comparing the timing of the bipolar tip signal to a stable timing reference from an intracardiac catheter, or the surface P wave. The morphology of the surface P wave can serve as a guide to identify the region that warrants high-resolution mapping. Unipolar mapping depicts a so-called QS signal at the site of origin, while a small r wave is visible when the mapping catheter is farther away from the site of origin. Because the abnormally acting myocardium is small and mostly endocardially located, only a few (ideally a single) ablation lesions are necessary to abolish the arrhythmia. Focal tachycardias are more likely to be paroxysmal in nature, but persistent focal arrhythmias have been described and are more likely to be multifocal. Predilection Sites for FAT in RA   |  Several preferential sites of origin for focal atrial tachycardia (FAT) exist in the RA (Figure 6.26), notably along the tricuspid annulus, along the terminal crest, at the fossa ovalis, and, rarely, inside the RA appendage.

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ATRIA PV Ostia MV Annulus

Predilection Sites for FAT in LA   |  Similarly, there is also evidence of predilection sites in the left atrium (LA) (Figure 6.27). Typical locations for LA focal arrhythmias include the area along the mitral annulus, along the pulmonary vein ostia, and inside the LA appendage. Important to note are the structures neighboring the RA. For example, FAT in the right pulmonary veins can mimic RA posterior origin because the veins pass immediately behind the RA. Epicardial Origin of FAT   |  Whenever application of a few ablative lesions cannot alter the focal tachycardia, or only does so transiently, an epicardial origin should be suspected (Figure 6.28). When using 3D mapping systems, a relatively large area (several square centimeters) revealed on endocardial mapping will be a typical hint. Knowledge of the adjacent structures, for example tributaries to the CS, allow the operator to choose the best epicardial approach. Thinking “outside the box” will allow mapping of extra-atrial structures like the noncoronary (posterior) aortic sinus that faces the anterior area of both atria to reveal, for example, FAT close to the His bundle.

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17/40 (43%) 16/40 (40%)

MV

Successful ablation

No permanent effect

R eE 6.27 F IG U r Preferential sites for origins of focal atrial tachycardia in the left atrium along the mitral valve (MV) annulus, the ostia of the pulmonary veins (PV), the fossa ovalis, and the appendage. CS = coronary sinus; LAA = left atrial appendage; LIPV, LSPV, RIPV, and RSPV = left inferior, left superior, right inferior, and right superior pulmonary vein, respectively.

Chapte r 6  |   The Right Atrium Relevant to Supraventricular Tachycardia

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R eE 6.28 F IG U r (a) The anterior wall of the right atrium (small arrows) is adjacent to the noncoronary sinus (N) of the aortic valve. The red arrow is nearest to the His bundle, which cannot be shown because it is located in a deeper plane than the picture. The yellow star depicts the close proximity of the distal coronary sinus (CS)

ElectrophysiologICAL Perspectives

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and the ostium of the left atrial appendage (LAA). The top right panel shows the local activation time during focal atrial tachycardia in left lateral projection. The lower right panel shows the same information in the propagation map feature, depicting the site of earliest activation in red on the blue surface

in anteroposterior (AP) projection. L and R = left and right coronary artery, respectively; LA and RA = left and right atrium, respectively; MV and TV = mitral and tricuspid valve, respectively; RIPV = right inferior pulmonary vein; SVC = superior vena cava.

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ATRIA

R eE 6.29 F IG U r Example of the typical surgical access (blue arrow) to the left atrium (LA), for example for mitral valve surgery. The upper right panel depicts a 3D electroanatomical map with a large scar in typical location. The example shows a reentrant tachycardia with a critical isthmus between the scan and the mitral annulus. The lower right panel shows the left anterior oblique (LAO) projection, clearly marking a tricuspid reconstruction (TR) ring while the mitral annulus was only reconstructed. PVs = pulmonary veins.

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R eE 6.30 F IG U r Left panel: View of the right atrium after removal of the pericardium. The red dotted line marks the typical insertion site for the bypass cannula, while the blue line marks the location for a right atriotomy, for example, shows atrial septal defect repair. Right panel: Shows the “figure of 8” with the waist of the 8 being limited by the atriotomy scar on one side and the crista terminalis on the other side. The yellow arrows illustrate the activation sequence during the tachycardia.

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Concept of Atrial Macroreentrant Tachycardia   |  The other option for atrial tachycardia mechanisms is conceived as an activation wavefront that runs in a circuit around a central barrier. A narrow isthmus sited between the central barrier (eg, atriotomy scar) and second barrier (eg, AV valve annulus) preferentially allows for unidirectional impulse propagation, which is a prerequisite for tachycardia induction. Once induced, these arrhythmias are typically persistent and, depending on the AV node conduction, can be tolerated quite well. Whenever scar tissue is present, for example as a consequence of surgery or as a result of structural heart disease, potential reentrant circuits can arise. Typical examples are LA reentry after Waterston’s groove access for mitral valve surgery (left atrial macroreentrant tachycardia, or LAMRT) (Figure 6.29) and RA reentry after atriotomy, for example for atrial septal defect (ASD) closure or after cardiopulmonary bypass (Figure 6.30).  

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7

the Atrial Septum and transseptal Access

WITH ATRIAL FIBRILLATIoN ABLATIoN procedures becoming more frequent, safe and reproducible access to the left atrium is the key for any ablation strategy on the endocardial surface. Increasingly, ablations of accessory pathways and left ventricular mapping also are carried out via transseptal access rather than a retrograde approach.

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ATRIA Anatomy THE AtRIaL SEPtUM The fact that the body of the left atrium (LA) is posterior and relatively superior to the right atrium (RA) determines the orientation of the atrial septum with respect to the bodily planes (Figure 7.1). Generally, the septal plane is at an angle to the median sagittal plane when viewed from the front of the chest, and a right anterior oblique (RAO) projection will view the septal plane more or less en face. Accessing the LA from the right requires an appreciation of the extent of the true atrial septum. R eE 7.1 F IG U r Position of left atrium (LA) slightly behind and above the right atrium (RA) in right anterior oblique (RAO; left panel) and left anterior oblique (LAO; right panel). Please note the relationship of the coronary sinus (CS) catheter toward the LA and the septal (right) pulmonary veins in relationship to the superior vena cava (SVC)/posterior wall of the RA. IVC = inferior vena cava; LAA and RAA = left and right atrial appendage, respectively; LIPV, LSPV, RIPV, and RSPV = left inferior, left superior, right inferior, and right superior pulmonary vein, respectively.

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R eE 7.2 F IG U r

The true septum that interventionists can cross without exiting the heart, or traversing through epicardial tissues, is limited to the flap valve of the oval fossa and the margin of the muscular rim that surrounds it on the right atrial aspect (Figure 7.2). Increased size of the atrial chambers, for example with age or with body mass, can affect the location of the septal plane and the oval fossa. Other considerations are previous surgical repair with patches or devices implanted to close atrial septal defects or patent foramen ovale (PFO). These may distort the anatomy of the septal aspect, or the materials used may be very tough and resistant to puncturing. Moreover, in redo cases, the fossa valve may become much thickened following previous transseptal procedures. The risk of perforating the heart is higher in such cases when attempting to circumvent the barrier by puncturing peripheral to the area of the true septum.

(a) This cross section shows the oblique plane of the atrial septum (open arrow) and the proximity of the right pulmonary vein to this plane. Note the anterior relationship of the aortic root to the atrial septum. (b) This view onto the septal surface of the right atrium (RA) shows the valve of the oval fossa (asterisk) surrounded by a muscular rim. Ao = aorta; CS = coronary sinus; Eso = esophagus; IVC and SVC = inferior and superior vena cava, respectively; LA = left atrium; LIPV and RIPV = left and right inferior pulmonary vein, respectively; RAO = right anterior oblique; RV = right ventricle; TV = tricuspid valve.

Anatomy

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ATRIA On heart specimens, the septal aspect of the RA gives an erroneous impression of there being an extensive atrial septum. The true septum, as defined by the area that can be excised without exiting the heart, is limited to the area marked by the valve of the oval fossa (the embryonic septum primum) and a raised rim of muscle immediately around it (the embryonic septum secundum) (Figure 7.3; see also Figure 7.2). After birth, the embryonic shunt is eliminated when the valve of the fossa closes against the muscular rim, like a door shutting against its frame. The rim is an infolding of the atrial wall (Figures 7.4 and 7.5).

Superior Posterior Anterior Inferior

R eE 7.3 F IG U r (a) This right atrial view shows an aneurysmal valve of the oval fossa. There is a probe patent foramen ovale (open arrow) at the anterocephalad margin. The broken line marks the tendon of Todaro traveling in the Eustachian ridge. The dotted shape indicates the location of the compact atrioventricular node and the His bundle. (b) Sectioning the heart in this longitudinal plane shows the relationship of the atrioventricular node and bundle to the membranous septum (arrow). Superior to this is the aortic root that makes a convexity into the right atrium creating the aortic mound seen in panel (a). The dotted oval marks the site of the oval fossa. aAP = anatomical anteroposterior view; Ao = aorta; aRAO = anatomical right anterior oblique view; CS = coronary sinus; EV = Eustachian valve; IVC and SVC = inferior and superior vena cava, respectively; LV and RV = left and right ventricle, respectively; MV and TV = mitral and tricuspid valve, respectively.

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Forming the interatrial groove, it is filled with epicardial fat, and the anterior part often contains the artery to the sinus node. The superior and posterior parts of the rim represent the infolding between the superior caval vein and the right pulmonary veins (see Figure 7.5). The musculature on the septal aspect that gives the impression of an extensive atrial septum is the anteromedial wall of the RA, also known as the aortic mound (see Figure 7.3). It lies behind the transverse pericardial sinus and the aortic root. Small venous orifices and pits and dents on this wall may allow the tips of catheters to become lodged, tricking the operator. R eE 7.4 F IG U r Diagrams depicting embryonic septation of the atrial portion of the heart tube. The septum primum breaks down at its upper margin as it grows toward the atrioventricular junction. The septum secundum forms as an infolding of the atrial wall.

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ATRIA

R eE 7.5 F IG U r Diagrams depicting embryonic septation of the atrial portion of the heart tube. Farther downward, growth of the septum primum obliterates the ostium primum but leaves an ostium secundum superiorly, which becomes partially covered over by the ingrowing septum secundum. Ultimately, the septum primum acts like a door that closes against the muscular rim formed by the septum secundum. Lack of adhesion between the two structures at the anterocephalad border allows the septum to be probe patent at the foramen ovale. EV = Eustachian valve; SVC = superior vena cava.

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By contrast, the left atrial aspect of the atrial septum lacks the crater-like feature of the right side because it is the fossa valve that overlaps the fossa rim, which is on the right side (Figure 7.6; see also Figure 7.5). The valve itself is usually thin (1 to 3 mm), is fibromuscular, and comprises a bilaminar arrangement of myocardial strands aligned in different directions (Figure 7.7). When the valve is aneurismal, it tends to be thinner and stretchier, posing a risk of being pushed too far toward the lateral wall of the LA during transseptal puncture.

R eE 7.6 F IG U r Transillumination of the oval fossa in the same heart shows the right atrial and left atrial views of the extent of the true atrial septum that can be punctured without going outside the heart. The Eustachian valve (EV) in this heart is particularly large. The left atrial view shows the crescentic margin of the fossa (arrows) and lack of a limbus. Ao = aorta; CS = coronary sinus; LAA = left atrial appendage; MV = mitral valve; RIPV and RSPV = right inferior and right superior pulmonary vein, respectively; SVC = superior vena cava.

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ATRIA

R eE 7.7 F IG U r (a), (b), and (c) show variations in thickness of the valve of the fossa. (d) to (h) show variations in the morphology and location of the fossa valve (asterisk), which is the true atrial septum. (d) The fossa is small, and its muscular rim is not well defined. By contrast, the fossa in (g) is large, and its rim is prominent. (f) shows a low location, and (h) shows an aneurismal fossa valve. Small pits and dents (open arrows) may be present in the atrial wall. The white arrows indicate the entrance of the superior caval vein. aRAO = anatomical right anterior oblique view; CS = coronary sinus.

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Left

Right

In practice, most hearts have a well-defined muscular rim on the right atrial aspect that allows the operator to feel the jump from firm muscular rim to tenting of the thin valve with the catheter for safe transseptal puncture. Importantly, in nearly one-fifth of hearts the rim is very flat, making it difficult to identify the fossa by feel, especially when the valve is small and thicker than usual (see Figure 7.7). Furthermore, the location of the fossa can vary to be more anterior, superior, posterior, or inferior than anticipated.

The Probe Patent Oval Fossa

R eE 7.8 F IG U r (a) Depending on the extent of overlap between the fossa valve and the rim, a patent foramen ovale (open arrow) is a tunnel lesion of varying lengths. (b) This section shows a long length of overlap between the rim (asterisk) and the valve. The inset is the same picture flipped to simulate left anterior oblique (LAO) orientation. Ao = aorta; aRAO = anatomical right anterior oblique view; CS = coronary sinus; EV = Eustachian valve; ICV and SCV = inferior and superior caval vein, respectively; LA and RA = left and right atrium, respectively; LAA = left atrial appendage; MV and TV = mitral and tricuspid valve, respectively.

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In about one-fourth to one-third of the normal population, there is probe patency of the oval fossa (PFO), even though on the left atrial side the valve is large enough to overlap the rim (Figure 7.8). This is because the adhesion of the valve to the rim is incomplete, leaving a gap usually in the anterosuperior margin corresponding to a C-shaped mark in the left atrial side. The gap can allow a catheter to be slipped between the rim and the valve to enter the LA.

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ATRIA Once inside the LA, the maneuverability of the catheter will depend on the amount and pliability of valve tissue overlapping the rim and the width of the gap. When utilizing this portal, it is important to note that owing to the location of the entry point, the catheter is directed toward the anterior and superior walls of the LA (Figure 7.9). On the other hand, restricted movement of a superiorly angulated catheter may make it more difficult to navigate to the right pulmonary venous orifices, especially the inferior orifice. Inadvertent perforation of the left atrial roof is a recognized hazard when taking advantage of this interatrial communication for left atrial access. R eE 7.9 F IG U r Orientation on fluoroscopy in left anterior oblique (LAO) with His and coronary sinus (CS) catheters and the transseptal sheath entering the left atrium (LA) via a patent foramen ovale (PFO). Note the superior position of the sheath and catheter close to the roof of the LA. aLAO = anatomical left anterior oblique view flipped; Ao = aorta; His = His catheter; FO = fossa ovale; MV and TV = mitral and tricuspid valve, respectively; RA = right atrium; RVA = right ventricular apex; SCV = superior caval vein.

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Atrial Septal Defects Congenital defects at the septal aspect can provide natural portals of access without requiring septal puncture. There are various types and locations of interatrial communications, but not all are sited at the true septum (see Chapter 11). The most common, occurring in 10% to 17% of patients with congenital heart disease, is the secundum defect, which is due to inadequacy of the flap valve to cover the oval fossa (Figure 7.10). The defect varies considerably in size, and the remnant of the valve, the embryonic septum primum, may be aneurismal. The defect may present with morphologies ranging from a single oval-shaped opening in the valve to multiple fenestrations giving the valve a fishnet appearance.

R eE 7.10 F IG U r Variations in morphology of so-called secundum atrial septal defects.

Anatomy

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ATRIA More rarely, the interatrial communication is located immediately inferior to the orifice of the superior caval vein and is described as a superior sinus venosus defect (Figure 7.11). In these cases, the upper border of the defect is the superior caval vein, and the right upper pulmonary vein usually enters the back wall of the caval vein anomalously. Rarer still is an interatrial communication at the orifice of the coronary sinus itself known as a coronary sinus defect (Figure 7.12). This is part of a spectrum of defects due to so-called unroofing of the coronary sinus. When there is persistent patency of the superior caval vein, most often the caval vein drains into an enlarged coronary sinus to enter the RA, without communicating with the LA. Rarely, defects occur between the sinus wall and the left atrial wall. These may be small perforations that allow for left atrial communication, or the deficiency may be so extensive that the communication is at the orifice of the coronary sinus (see Figure 7.12). Deficiency of the roof of the coronary sinus and the corresponding part of the left atrial wall allows for direct communication between the atrial chambers. The inferior sinus venosus defect is extremely rare. It is the counterpart of the superior defect, with the orifice of the inferior caval vein opening to both atrial chambers, and is associated with anomalous insertion of the right inferior pulmonary vein.

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R eE 7.11 F IG U r The superior sinus venosus defect (double-headed arrows) is located superior to the confines of the true atrial septum. The orifice of the superior caval vein overrides the septum, and the right superior pulmonary vein connects anomalously to the superior caval vein. CS = coronary sinus; LA and RA = left and right atrium, respectively.

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R eE 7.12 F IG U r (a) The coronary sinus (CS) is usually enlarged when it receives drainage from a persistent left superior caval vein (LSCV). (b) Deficiencies in the

Anatomy

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walls separating the CS from the left atrium (LA) as indicated by the red arrows allow for interatrial communication. (c) When the walls are not formed,

the CS is said to be unroofed, allowing for direct interatrial communication at the site of the CS. The LSCV may or may not be persistent. RA = right atrium.

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ATRIA Electrophysiological Perspectives Landmarks for Transseptal Puncture To mark the atrioventricular valve plane, a diagnostic catheter inside the coronary sinus (CS), advanced as distally as possible, can be used easily. When advanced via superior access, for example the subclavian or jugular vein, the shaft of the CS catheter marks the posterior wall of the RA in RAO projection (typically 30°). The second major landmark is the aorta. It can be depicted by a pigtail catheter in the noncoronary cusp (confirmation can be achieved by a small injection of contrast), but this approach requires arterial puncture (Figure 7.13).

(a) R eE 7.13a F IG U r (a) Schematic of the right atrium (RA) with adjacent structures such as aortic root: His catheter (His) as marker of the compact atrioventricular (AV) node marks the aorta position while the coronary sinus (CS) catheter depicts the AV junction. The posterior wall of the RA can be identified by the contour of the cardiac silhouette. RAO = right anterior oblique.

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Because the location of the His bundle is related to the commissure between the noncoronary and right coronary sinuses, a diagnostic catheter with His bundle electrocardiogram depicts the aorta in RAO projection. Because the shaft of the His catheter is leaning against the septal wall of the RA, the direction of the His depicted in left anterior oblique (LAO) marks the septum. Accurate angulation of the C-arm such that the catheter is displayed orthogonally allows for proper alignment with the individual cardiac axis (see Figure 7.13).

(b) R eE 7.13b F IG U r (b) Right anterior oblique (RAO) and left anterior oblique (LAO) projection of contrast injection via pigtail catheter in the noncoronary cusp (NCC) and its relationship to the His recording catheter (His). CS = coronary sinus; RV = right ventricle.

Electrophysiological Perspectives

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ATRIA Transseptal Puncture A whole range of different puncture kits, most of them using a modified Brockenbrough approach, consisting of a preshaped hollow steel needle and a transseptal sheath with a dilator, is available. Using an over-the-wire technique, the sheath/dilator system is advanced in the superior vena cava (SVC) (Figure 7.14). The guidewire is then withdrawn, and blood is aspirated through the lumen of the dilator followed by saline flushing to avoid air embolism.

R eE 7.14 F IG U r Transseptal puncture step-by-step 1: Guidewire in superior vena cava (SVC) and transseptal sheath (TS) and dilator (D) advanced. AP = anteroposterior; CS = coronary sinus; His = catheter positioned at His bundle region.

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Using the stylet to protect the sharp needle tip, the needle is advanced until the last 3 cm such that the needle tip is still protected inside the dilator of the sheath (Figure 7.15). When advancing the needle, the operator should be careful not to push the sheath/dilator farther into the SVC, which could lead to extracardiac perforation.

R eE 7.15 F IG U r Transseptal puncture step-by-step 2: Advance needle with stylet until ~3 cm (red line) to avoid scrapping plastic from dilator (D)! AP = anteroposterior; CS = coronary sinus; His = His catheter; SVC = superior vena cava; TS = transseptal sheath.

Electrophysiological Perspectives

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ATRIA After removal of the stylet, the needle is aspirated and flushed accordingly. Some operators prefer to connect a small contrast syringe; another technique operates with an intracardiac pressure. Pointing toward the fossa ovalis (about a 4 o’clock position on the needle clock face), the complete system is withdrawn into the RA. A first jump might be observed when entering the RA, and a second when the distal tip moves over the upper limbus of the fossa ovalis (Figure 7.16).

R eE 7.16 F IG U r Transseptal puncture step-by-step 3: Pullback of transseptal puncture kit from superior vena cava (SVC) into right atrium. AP = anteroposterior; CS = coronary sinus; D = dilator; His = His catheter; SVC = superior vena cava; TS = transseptal sheath.

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Careful assessment of the puncture site in two planes is recommended before the actual puncture is performed. In RAO projection, the position can be assessed in the anteroposterior dimension (anterior toward the His catheter/aorta, posterior toward the shadow of the RA posterior wall/shaft of the CS catheter) (Figure 7.17). In LAO projection, the height of the puncture site and the elasticity of the septum can be monitored.

R eE 7.17 F IG U r Transseptal puncture step-by-step 4: Check right anterior oblique (RAO 30°) for anteroposterior position with rotation of needle if necessary (turning toward 3 o’clock results in anterior movement, while turning toward 7 o’clock results in a more posterior position). Target zone in the middle third between posterior wall of the left atrium and His recording site (aorta). CS = coronary sinus; D = dilator; RA = right atrium; TS = transseptal sheath.

Electrophysiological Perspectives

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ATRIA Puncturing across the membrane of the fossa ovalis is performed using a rapid pushing of the needle out of the tenting sheath (Figure 7.18). When advanced maximally inside the dilator, most needles extend about 5 mm outside the tip of the dilator. Especially in obese patients, the needle tip might not be visualized adequately using normal fluoroscopy to judge its position. When using intracardiac pressure recordings, a slight increase of the recorded pressure is observed showing a characteristic LA waveform. Using the contrast method, dye injection results in immediate dispersion of the contrast but might be difficult to see using fluoroscopy only. Recording of high pressure is highly indicative of having punctured the aorta. Likewise, contrast moving in a superior direction confirms a puncture that is too anterior. Withdrawal of the steel needle and reattempting will be without hemodynamic consequences because the hole created by the needle alone is very small. Once the successful entry into the LA is confirmed, the dilator is carefully advanced over the steel needle (see Figure 7.18). Care should be applied not to push the dilator too far into the LA, since it may perforate the opposite wall (mostly the atrial roof or base of the left atrial appendage). Using intracardiac pressure monitoring, the intracavitary position can be confirmed by

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the clean pressure recordings. Touching the opposite wall would lead to flattening of the curve or rise of the pressure. Once the dilator has entered the LA, the sheath needs to be slid gently over the dilator, again avoiding pushing the whole unit farther upward. In very rigid membranes, a wiggling maneuver can facilitate the advancement of the sheath. Finally, after the sheath is safely positioned inside the LA, the dilator and needle are withdrawn. During this movement, the sheath makes a characteristic motion of straightening up because it is no longer forced into shape by the steel needle. Lack of this motion means that the tip of the sheath is fixed (mostly by perforation of the LA posterior wall or roof), and careful monitoring for signs of tamponade should be initiated immediately. To avoid air embolism, the lumen of the sheath should be aspirated and flushed immediately with heparinized saline. Subsequently, the sheath should be connected to a constant flush (eg, 15 mL of saline per hour) to keep a slightly positive pressure inside the sheath, thereby avoiding thrombus formation and air embolism with catheter exchanges. While the shape of the available sheath differs significantly, fixed curved sheaths are the standards for most operators. Steerable sheaths may allow for a wider range of motion and more stability.

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Second Transseptal Puncture

R eE 7.18 F IG U r Transseptal puncture step-by-step 5: Puncture in left anterior oblique (LAO): sequential movement as indicated in text and by arrows. CS = coronary sinus; His = His catheter; LA = left atrium.

If the operator chooses to access the LA with a second long sheath, two options to achieve this are available: conventional second puncture, either slightly anterior or posterior to the first site (check in RAO!), and attempting to cross through the same puncture hole. If the later approach is chosen, the second sheath is positioned inside the middle of the RA in the previously described over-the-wire technique. Wire and dilator of this second sheath are then positioned through the first sheath in the LA such that the wire is positioned in the left superior pulmonary vein (LSPV) (Figure 7.19). Locking the dilator to the sheath allows for forming a unit, which is subsequently moved across the puncture site to dilate the hole itself. After careful aspiration of any air, a steerable catheter is advanced through the second RA sheath to pass through the septum close to where the wire is perforating. Display in both projections and analysis of the intracardiac signals from the tip electrode of this catheter facilitate this maneuver (Figure 7.20). Once the catheter has entered the LA, it can be navigated carefully in the lateral (left) PVs (no more atrial signal on the tip electrode), and the sheath can subsequently be advanced over the shaft of the catheter. Double wiring of a transseptal sheath should be avoided at any costs, because the necessary anticoagulation measures during a left-sided ablation procedure risk excessive bleeding from the puncture site.  

Electrophysiological Perspectives

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ATRIA

R eE 7.19 F IG U r Transseptal puncture step-by-step 6: Second sheath in right atrium and dilation of puncture hole displayed in left anterior oblique (LAO) projection. Passage of same hole using a steerable recording catheter. CS = coronary sinus; FO = fossa ovalis; His = His catheter; IVC = inferior vena cava; LSPV = left superior pulmonary vein; PV = pulmonary vein; RAO = right anterior oblique.

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R eE 7.20 F IG U r Transseptal puncture step-by-step 7: Passage into left atrium (LA) using second puncture; same steps as in first puncture. AP = anteroposterior; CS = coronary sinus; FO = fossa ovalis; His = His catheter; LAO = left anterior oblique; RAO = right anterior oblique..

Electrophysiological Perspectives

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8

the Left Atrium and Pulmonary Veins Relevant to AF Ablation

IN THE RECENT DECADE, ATRiAL fibrillation ablation became routine in electrophysiology laboratories worldwide. Understanding the individual anatomy of pulmonary veins (as major target sites) and collateral structures (eg, phrenic nerves, the esophagus) is key to successful and, more importantly, safe ablation. 

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ATRIA The Left Atrium The left atrium has a body into which the appendage and the venous component receiving the pulmonary veins open. The outlet of the atrial body is surrounded by the vestibule lying immediately proximal to the mitral annulus (Figure 8.1). The septum, shared with the right atrium, forms the medial extent of the body. The epicardial aspect of the left atrium is covered to varying extents by epicardial fat pads that contain ganglionated plexi of the intrinsic cardiac nerves. The pads are located near the entrances of the pulmonary veins, near the course of the coronary sinus, and in the interatrial region (see Figure 8.1).

R eE 8.1 F IG U r (a) This view of the endocast from the back shows the posterior location of the left atrium and its relationships to the aorta (Ao), pulmonary arteries (LPA, RPA), and coronary sinus (CS). The right superior pulmonary vein (RS) passes rightward behind the junction of the superior caval vein (SCV) and the right atrium, whereas the right inferior pulmonary vein (RI) is related to the intercaval area. (b) This posterior view of a heart specimen shows the distribution of the epicardial fat pads (yellowish areas indicated by arrows) on the left atrium. (c) Another heart viewed from the diaphragmatic aspect shows large fat pads on the inferior walls of the left atrium. The ganglionated plexi are located deep in the pads. ICV = inferior caval vein; LI and LS = left inferior and left superior pulmonary veins.

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Location and Walls

R eE 8.2 F IG U r

Viewed from the frontal aspect of the chest, the left atrium is the most posteriorly situated of the cardiac chambers. Owing to the obliquity of the plane of the atrial septum and the different levels of the orifices of the mitral and tricuspid valves, the left atrial chamber is more posteriorly and superiorly situated relative to the right atrial chamber. The pulmonary veins enter the posterior part of the left atrium with the left veins located more superiorly than the right veins (Figure 8.2; see also Figure 8.1). The anterior wall of the left atrium is situated behind the transverse pericardial sinus, which separates the atrium from the root of the aorta (see Figure 8.2). Its transmural myocardial thickness measured on formalin-fixed hearts ranges from 1.5 to 4.8 mm. The tracheal bifurcation, esophagus, and descending thoracic aorta are immediately behind the pericardium overlying the posterior wall of the left atrium (Figure 8.3).

(a) This tilted anterior view shows the anterior atrial walls facing the transverse pericardial sinus (blue line) and the back of the aortic root. The right and left atrial appendages (RAA, LAA) embrace the great arteries. (b) The left atrial components and the body of the left atrium are displayed in this heart section. LS, LSPV = left superior pulmonary vein; RIPV = right inferior pulmonary vein; RS, RSPV = right superior pulmonary vein; SCV = superior caval vein.

The Left Atrium

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ATRIA The mean thickness of this wall is 4.1 ± 0.7 mm (range 2.5–5.3 mm). It tends to become thinner toward the orifices of the pulmonary veins, and measurements made on postmortem specimens showed the area between the superior veins to be thinner than between the inferior veins. The superior wall, or roof, ranges from 3.5 to 6.5 mm in myocardial thickness and is related to the bifurcation of the pulmonary trunk and right pulmonary artery (see Figure 8.3). The coronary sinus with its continuation, the great cardiac vein, tracks along the outside of the posteroinferior wall, which includes the vestibule. In left anterior oblique (LAO) projection, the course of the vein is a useful landmark for the heart border (see Figure 8.3). The coronary sinus is wrapped by its own muscle sleeve, which is thicker adjacent to the atrial wall than along the free wall. The sleeve covers a length of approximately 2.5 to 5 cm with increasing thickness toward the coronary sinus orifice. Often, there is continuity between musculature of the venous sleeve and atrial wall (see Figure 8.3).

R eE 8.3 F IG U r (a) The roof, anterior (ant), and posterior (post) regions of the left atrial (LA) wall are shown in this longitudinal cut. The proximity of structures like the transverse sinus (Tr), right pulmonary artery (RPA), and esophagus (Es) is evident. (b) The catheter in the coronary sinus (CS) and passed into the great cardiac vein marks the heart border in this view of the LA. The circle indicates the location of the aorta (Ao). (c) The diaphragmatic surface of the heart is displayed to show the CS and its muscular continuity with the LA wall (arrows). ICV = inferior caval vein; LI = left inferior pulmonary vein; RA = right atrium; RI = right inferior pulmonary vein.

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R eE 8.4 F IG U r (a) This dissection shows the alignment of the myocardial strands that make up Bachmann’s bundle (BB). The bundle (highlighted with broken lines) branches in its rightward and leftward extents. (b) An area of thin atrial wall (arrow) is seen inferior to BB. (c) The endocardial aspect shows gradual change in alignment of the subendocardial myocardial strands (blue arrows) and a thin area (triangle). (d) The left atrium is everted to show the endocardial surface with an abrupt change in alignment of the myocardial strands (blue arrows) in this heart. Ao = aorta; AP = anteroposterior; LAA and RAA = left and right atrial appendage, respectively; LI = left inferior pulmonary vein; LM = left middle pulmonary vein; LS, LSPV = left superior pulmonary vein; PA = posteroanterior; RI, RIPV = right inferior pulmonary vein; RS, RSPV = right superior pulmonary vein; SCV = superior caval vein.

The Left Atrium

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Although the walls of the left atrial body appear fairly smooth on the endocardial aspect, they are composed of several overlapping layers of differently aligned myocardial strands, and there are marked regional variations in muscular thickness. The leftward extension of Bachmann’s bundle is the most superficial of the myocardial layers in the anterosuperior wall. Bachmann’s bundle, also known as the interauricular band, is composed of nearly parallel alignment of myocardial strands (Figure 8.4), which accounts for its role as the prevalent interatrial conduction pathway for propagation of the sinus impulse to the anterior left atrial wall. Rightward, after crossing the interatrial groove, it bifurcates to embrace the right atrial appendage. Its superior arm can be traced toward the location of the sinus node, terminal crest, and sagittal bundle. Leftward, it branches to pass around the neck of the left appendage, reuniting to continue into the musculature of the lateral and posteroinferior atrial walls. Since Bachmann’s bundle can be up to approximately 1 cm thick at Waterston’s groove, it adds to the myocardial thickness of the anterosuperior atrial wall, making this area the thickest part transmurally. By contrast, a small area of the anterior wall immediately inferior to Bachmann’s bundle can be exceptionally thin and is at risk of perforating into the transverse pericardial sinus (see Chapter 7).

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ATRIA Under this most superficial layer of almost circumferentially aligned myocardial strands run obliquely and longitudinally aligned branches from the septopulmonary bundle, and the deeper septoatrial bundle (Figure 8.5). In the subendocardium, the myocardial strands of the septoatrial bundle encircle the os of the atrial appendage. The subendocardial strands at the venoatrial junctions are mainly loop-like extensions of the longitudinal and oblique strands from the atrial wall (see Figure 8.5). The interpulmonary area may show abrupt changes in alignment of the myocardial strands. Aside from Bachmann’s bundle, there are other interatrial muscular connections of varying thicknesses and widths that cross the interatrial groove and connect the muscular sleeves of the right pulmonary veins to the right atrium, the superior caval vein to the left atrium, or the coronary sinus and remnant of the vein of Marshall to the left atrium (Figure 8.6). Occasionally, hearts may demonstrate a particularly broad bridge across the posteroinferior interatrial groove joining the intercaval area of the right atrium to the left atrium, providing the potential for inferior breakthrough of the sinus impulse.

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R eE 8.5 F IG U r (a) The posterior wall of the left atrium has been incised to display the arrangement of the myocardial strands in the subendocardium. Note the loop-like arrangement of the strands around the orifices of the pulmonary veins (LI, LS, RI, RS). (b) The myocardial strands from the septopulmonary (SP) and septoatrial (SA) bundles contribute to the myocardial sleeves around the pulmonary veins (broken arrows). LAA = left atrial appendage. Photographs courtesy of Professor Damian Sanchez-Quintana, Badajoz, Spain.

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Left Atrial Appendage Characteristically, the atrial appendage is a small finger-like cul-de-sac in human hearts where thrombi may form. Owing to its tubular shape, its junction with the left atrium is narrow and fairly well defined. Even so, there is considerable variability in the shape and size of the appendage due to its lobes and branches (Figure 8.7). A study of postmortem specimens reported the appendages to be larger and associated with more endocardial fibroelastosis in patients with atrial fibrillation than those without arrhythmia. Unlike the right atrium, the left atrium lacks a terminal crest. The border between appendage and body of the left atrium is the oval-shaped os with a mean long diameter of 17.4 ± 4 mm and a mean short diameter of 10.9 ± 4.2 mm measured on heart specimens. In some hearts, the endocardial aspect of the atrial body around the os can be associated with small pits and troughs where the wall becomes paper-thin.

R eE 8.6 F IG U r (a) Interatrial muscle bundles vary in number and size. (b) In addition to Bachmann’s bundle (BB), this heart has an exceptionally broad interatrial bundle situated inferiorly (red arrow). (c) This view of the interatrial

The Left Atrium

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groove from above shows BB and small muscle bundles (red arrows) connecting the posterior wall of the right atrium to the left atrium and to the muscle sleeve of the right superior

pulmonary vein (RS). CS = coronary sinus; ICV and SCV = inferior and superior caval vein, respectively; LI, LS, and RI = left inferior, left superior, and right inferior pulmonary vein, respectively.

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ATRIA

R eE 8.7 F IG U r (a) Fluoroscopic views of the left atrial appendage (LAA; top) and left superior pulmonary vein (PV; middle) in left anterior oblique (LAO) and right anterior oblique (RAO; bottom) projection using direct contrast injection via one of the 2 transseptal sheaths. (b) and (c) are left lateral views showing the narrow os and finger-like shape of the appendage. (d) Examples of endocasts to show variability in shape of the appendage. CS = coronary sinus; Halo = multipolar catheter positioned at the free wall of the right atrium; PT = pulmonary trunk; RIPV = right inferior pulmonary vein.

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The inner aspect of the appendage is lined by a complicated network of muscular ridges and intervening membranes that form its wall. Its tip can be directed anteriorly overlying the pulmonary trunk, superiorly behind the arterial pedicle, or posteriorly. When its tip is directed anteriorly, the body of the appendage usually also overlies the main stem of the left coronary artery and the great cardiac vein (see Figure 8.7).

The Venous Component, Vestibule, and Pulmonary Veins

R eE 8.8 F IG U r (a) and (b) display the mitral isthmus. The endocardial surface is smooth but may contain pits and crevices. Myocardium is stained red on the histologic section in (b). (c) The opened left atrium and left ventricle (LV) viewed from behind shows the commissures of the mitral valve and the area of the atrioventicular node (irregular shape). CS = coronary sinus; LAA = left atrial appendage; LIPV = left inferior pulmonary vein; LPV = left pulmonary vein; LUPV = left upper pulmonary vein.

The Left Atrium

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The venous component receives the pulmonary veins, whereas the vestibular component surrounds the opening to the mitral valve. There are no endocardial landmarks to separate the vestibule from the pulmonary venous component (see Figure 8.1), although frequently a few pits or crevices are seen in the inferior wall as a surrogate for the border zone. These may be encountered when constructing ablation lines along the so-called left atrial isthmus to link the orifice of the left inferior pulmonary vein to the mitral annulus (Figure 8.8).

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ATRIA The average myocardial thickness of the mitral isthmus is approximately 4 mm at the midportion, tapering to approximately 2 mm toward the mitral annulus. The myocardium of the distal part of the vestibule overlaps the atrial surface of the mitral leaflets for a millimeter or so. The left atrial aspect of the atrioventricular node and bundle is related to the vestibular portion that overlies the right fibrous trigonal area of aortic-mitral valvar continuity, in close proximity to the posteromedial commissure of the mitral valve (see Figure 8.8). Running along the outside of the vestibule is the course of the coronary sinus and circumflex artery. In most adult hearts, the coronary sinus courses some 6 to 10 mm proximal to the level of the mitral annulus (Figure 8.9).

R eE 8.9 F IG U r These samples of sections though the mitral valve (arrows) at the posteroinferior atrioventricular junction show the variability in relationship to the coronary artery and vein (a and v, respectively).

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The pulmonary veins enter the posterior part of the left atrium with the orifices of the left (lateral) pulmonary veins located more superiorly than those of the right (septal) pulmonary veins. In humans, it is most common to find two orifices on each side, but there are many variables (Figure 8.10). Sometimes two veins of one, or both, sides unite prior to their entry to the atrium. At other times, an additional vein is found, more frequently on the right side. From the endocardial aspect, ridges described as interpulmonary carinas separate ipsilateral superior and inferior venous orifices. The transmural myocardial thickness is up to 3.2 mm, and intervenous muscular connections are commonly located toward the epicardal side (Figure 8.11).

R eE 8.10 F IG U r Examples of 3D reconstructions from computed tomography or cardiac magnetic resonance imaging of the left (upper panels) and right (lower panels) pulmonary veins (PVs). Note the variable shape and distance of the left atrial appendage (LAA) to the PV antrum and the fossa ovalis (FO) to the right PVs, respectively. LIPV, LSPV, RMPV, and RSPV = left inferior, left superior, right middle, and right superior pulmonary vein, respectively; MA = mitral annulus.

The Left Atrium

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ATRIA Viewed from the endocardial aspect, there is a ridge known to electrophysiologists as the left atrial ridge or left lateral ridge, although it is actually a fold of the left atrial wall between the os of the left atrial appendage and the left pulmonary veins (Figure 8.12). It is described as the Q-tip sign on echocardiographic imaging. The thickness of the musculature ranges from approximately 0.5 to 5 mm. It is variable in width from 2 to 12.5 mm when measured on cadaver hearts. Stability and contact of the ablation catheter may become challenging when constructing pulmonary vein isolation lines in cases with narrow ridges. The epicardial side of the fold contains the Marshall structure with its accompanying autonomic nerves and muscle strands that connect with the atrial wall. Occasionally, the artery supplying the sinus node also runs in the fold.

R eE 8.11 F IG U r (a) and (b) are histological step sections through a pair of right pulmonary veins. The myocardial sleeve (red) is circumferential around the superior vein. Section (b) is closer to the left atrium and shows myocardial strands linking superior and inferior veins (broken arrows).

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R eE 8.12 F IG U r (a) shows a broad left lateral ridge (R), and the cut section (b) displays the wide fold in the atrial wall (arrow). (b) The ridge is narrow with a tight fold (white arrow), and there are several pits (arrows) in the vicinity of the os to the appendage. (d) The vein of Marshall and its ligament run on the epicardial side of the fold. LAA = left atrial appendage; LI, LIPV = left inferior pulmonary vein; LS, LSPV = left superior pulmonary vein; MV = mitral valve.

The Left Atrium

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ATRIA The oblique vein (of Marshall) passes from superiorly to descend along the infolded left lateral atrial wall coursing posteroinferiorly to join the coronary sinus. This vein is obliterated in the majority of individuals to become the ligament of Marshall. Even when a lumen is present, it is narrow, rarely exceeding 2 cm in length before tapering to a blind end (see Figure 8.12). If adequately wide, this channel may be utilized for ablating the left atrial wall. By contrast, in 0.3% of the normal population the vein remains fully patent as the persistent left superior caval vein usually draining into the coronary sinus, which has an enlarged orifice. Notably, the orifices of the right pulmonary veins are directly adjacent to the plane of the atrial septum. Rather than round in shape, the venous orifices are oval shaped with a longer superoinferior diameter than anteroposterior diameter. On the endocardial surface, the transition between atrium and vein is smooth. The venoatrial junction is more recognizable when the shape of the vein entering the atrium is cylindrical, but it is less clear when the vein enters like a funnel. Musculature of the left atrial wall extends to varying lengths over the outer surface of the venous wall, with the longest sleeves along

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the upper veins (Figure 8.13; see also Figure 8.5). The sleeves are thicker and surround the veins at the venoatrial junction, whereas the musculature is usually thinner and tapers irregularly as the veins are traced toward the lung hilum. The peripheral margins of the sleeves are associated with increasing fibrosis and degenerative changes of the myocytes. Mainly, the myocardial strands of the sleeves are oriented circularly around the veins and are pierced with longitudinally and obliquely oriented strands. Experimental studies have shown that this complex architecture may facilitate microentry and arrhythmias associated with ectopic activity. Other candidates for substrates of automaticity have been suggested also. These include histologically specialized conduction cells and interstitial Cajal cells. The areas of the venoatrial junctions and adjoining pulmonary veins are also highly innervated by ganglionated nerves originating from the cardiac neural plexus. The epicardial subplexuses located in the atrial fat pads send abundant intrinsic nerve extensions onto these areas and penetrate into the atrial and venous walls.

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R eE 8.13 F IG U r (a) and (b) are longitudinal sections through the veins and myocardial sleeves. Myocardium is stained red while fibrous tissue is stained green. There are circumferential (circ) and longitudinal (long) arrangements of the myocardial strands and abundant nerve The Left Atrium

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bundles (arrows) in the adventitia. (c) is drawn from a reconstruction of a vein with the circumferential strands colored in pink and longitudinal and oblique strands in orange. (d) Its enlarged boxed area shows fibrotic changes in the distal parts of the sleeve.

(e) The extent of the myocardial sleeve is irregular and incomplete. LA = left atrium; LSPV = left superior pulmonary vein; RIPV and RSPV = right inferior and right superior pulmonary vein, respectively.

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ATRIA Electrophysiological Perspectives Atrial fibrillation (AF) is the most common arrhythmia, and over the last decade catheter ablation procedures increasingly are carried out in all electrophysiology laboratories. While nowadays there is consensus on the need for electrical pulmonary vein isolation as the mainstay of any ablation approach, additional substrate modification, for example by linear lesions, may be needed to treat patients with longstanding AF.

Pulmonary Veins as Sites of Origin of “Firing” Triggers for AF Initiation The observation of frequent ectopy from within the pulmonary veins (PVs) acting as initiators (“triggers”) of paroxysms of atrial fibrillation formed the early basis of developing a curative ablation strategy by targeting the ectopic foci directly or by isolating the culprit PV (Figure 8.14).

PVs as Sites of Maintenance of AF Beside the role of the PVs for initiation of the triggering event, the architecture of the musculature at the PV ostium supports the maintenance of atrial fibrillation and is therefore equally important.

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This observation was made when the ablation lesions were placed away from the PVs themselves so as to avoid narrowing or occlusion of the PVs. Encircling of the superior and inferior PV by one long linear lesion created an area large enough to sustain atrial fibrillation or fast PV tachycardia while the rest of the heart was in sinus rhythm. The crisscrossing arrangement of the muscle fibers with predominant circumferential orientation seems to be the underlying substrate to support reentry (see Figure 8.13). There is a wide variety of PV ostial morphologies including additional PVs, early side branching, and common ostium (see Figure 8.10). Although the available circumferential mapping catheters are all truly round in shape, the shape of the PV orifice is most commonly not round but rather oval shaped. A circumferential mapping catheter, therefore, most likely will distort the PV shape to some degree or flatten it sideways with various degrees of angulation, for example the inferior part more inside and the superior part more ostially positioned. While adjustable mapping catheters can accommodate for the different sizes, they still cannot adjust to the exact shape, a point that needs to be taken into account when trying to isolate the PVs electrically (see Figure 8.14).

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A 3D depiction of PVs on fluoroscopy can only be achieved by bidirectional PV angiography but need not necessarily be done simultaneously (right anterior oblique [RAO] and LAO). The shaft of the coronary sinus (CS), introduced via a superior venous access, serves as a convenient marker for the septal (right) PVs in RAO projection. In LAO, the CS marks the mitral annulus and is a good reference when positioned in an anterolateral position (distal CS) (see Figure 8.14). Besides marking the PV ostia anatomically, circumferential mapping catheters guide the ablationist to the site of earliest activation on the respective bipolar electrograms (Figures 8.15, 8.16, and 8.17).

R eE 8.14 F IG U r Simultaneous contrast injection of both right (left panels) and left (right panels) pulmonary veins (PVs) depicted in right anterior oblique (RAO; top) and left anterior oblique (LAO; bottom). The yellow dotted lines mark the area of the PV ostium. Note the shape of the ostia in the two projections, for example,

Electrophysiological Perspectives

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the round projection of the right inferior pulmonary vein (RIPV) in LAO. A circumferential mapping catheter would need to be positioned just inside the veins. A good visual reference for the level of the ostia for the right PVs is the shaft of the coronary sinus (CS) catheter, which also marks the location of the mitral

annulus. LIPV, LSPV, and RSPV = left inferior, left superior, and right superior pulmonary vein, respectively. Figures courtesy of Dr Feifan Ouyang, Hamburg, Germany.

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ATRIA

R eE 8.15 F IG U r Left panel: Schematic of the location of the circumferential mapping catheters in the left pulmonary veins (PVs) in normal catheter position. The numbers indicate the positions of the electrodes. Examples 1 through 4 face toward the left atrial appendage (LAA). Right panels: Right anterior oblique (RAO) and left anterior oblique (LAO) projections with circumferential mapping catheters in the left PVs. Using a third transseptal puncture, a mapping catheter is positioned at the posterior aspect of the left PVs (which only can be appreciated in the RAO projection). LIPV and LSPV = left inferior and left superior pulmonary vein, respectively.

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R eE 8.16 F IG U r Left panel: Schematic of a circumferential mapping catheter in an upside-down, backhand, or inverted position. Note that electrodes 1 through 4 are now facing the posterior aspect of the pulmonary veins (PVs). Right panels: Direct contrast injection in the upper left PV with corresponding catheter positions in right anterior oblique (RAO) and left anterior oblique (LAO) projections.

Electrophysiological Perspectives

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ATRIA

CS His

R eE 8.17 F IG U r Example of various positions of the ablation catheter along a linear lesion encircling both upper and lower right pulmonary veins (PVs) in right anterior oblique (RAO) and left anterior oblique (LAO) projections. The PV mapping catheter is moved to the corresponding PV in order to provide anatomical and electrical reference during energy delivery. Note the size of the left atrium, which can be assessed by the position of the coronary sinus (CS) catheter in LAO but is even more impressive in RAO projections. His = His catheter.

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Left Atrium Entering the left atrium (LA) via one or more transseptal punctures, the body of the LA varies in shape significantly. While the transverse diameter is mostly the largest (assess His catheter to distal CS in LAO projection), the cranial-to-caudal dimension can be judged only indirectly. The roof is invisible, risking perforation especially during the transseptal puncture itself. Subtle clues can be used, for example calcification in the proximal left coronary artery, while the bottom is identified by the shaft of the CS catheter (see Figure 8.14).

The Neighborhood

R eE 8.18 F IG U r

The LA is positioned posteriorly behind the right atrium (RA) with the right PVs adjacent to the intercaval area of the RA (Figure 8.18). Frequently, far-field electrical signals from the superior vena cava can be recorded inside the right superior pulmonary vein and might easily be confused with persisting PV potentials.

The specimen shows the right side of the atrial septum with the orifices of the right (septal) pulmonary veins (dotted ovals) behind. The asterisk denotes the projected location of the His bundle. The fluoroscopic images depict the right pulmonary veins (RIPV, RSPV), including a middle one (RMPV), and the relationship toward the superior caval vein (SCV), which is marked by the proximal part of the coronary sinus (CS) catheter. ICV = inferior caval vein; LIPV and LSPV = left inferior and left superior pulmonary vein, respectively; RAO = right anterior oblique.

Electrophysiological Perspectives

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ATRIA The right phrenic nerve is mostly localized between the anterior surface of the right PVs and the posterolateral wall of the RA. The distance between the right phrenic nerve and the right superior pulmonary vein usually is less than that for the right inferior pulmonary vein (see Chapter 2). Where the distance is very short (2 mm on some cadaver hearts), it is conceivable that inflating a stiff balloon or inserting a circular catheter into the right PV will push the venous/atrial wall even closer to the phrenic nerve. To lessen the risk of damaging the phrenic nerve, high-output pacing causing diaphragmatic contractions can be used to mark precisely the course of the right phrenic nerve. The left phrenic nerve is located farther from the left pulmonary veins. Mostly, it is related more on the lateral left ventricle (LV) and may be captured during LV lead placement. Again, high-output pacing allows marking the course of the nerve to avoid intolerable contractions in the post-implant period.

Specific LA Areas When making linear lesions in specific areas in an attempt to compartmentalize the LA, identification of the corresponding landmarks or boundaries is key. It is crucial to avoid ablating inside the PVs by marking the venous orifices with fluoroscopy. The so-called roofline connects the right and left PVs and is easily reached using a “big loop” approach (Figure 8.19).

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The ablation catheter is navigated in LAO projection with maximal deflection and careful advancement until it has looped around in a 180° fashion. Care should be taken to not dislodge into the ventricle. Straightening of the curve will allow for an extremely stable catheter-tissue contact with parallel aligned ablation catheter. Slow pullback of the catheter from the margin of the left PV orifice to the right PV orifice allows for complete deployment of the linear lesion, resulting in wide double potentials. The so-called lateral isthmus, or LA isthmus, line connects the left inferior PV orifice toward the inferolateral aspect of the mitral annulus. The length of the line varies, but can be judged easily in the RAO projection as the distance between a circumferential catheter inside the left inferior pulmonary vein and the CS catheter. Since the CS is displaced toward the atrium rather than at the level of the mitral orifice, identification of the annulus (small A, big V) is important to avoid leaving a conduction gap close to the annulus. Since the LA myocardium can be of significant thickness, epicardial ablation performed from inside the CS is necessary in more than half of the patients. In these, the tubular shape of the distal CS with its side branching might make it difficult to position the catheter to match exactly the endocardially deployed line, and the close proximity to the circumflex artery also needs to be taken into consideration.

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R eE 8.19 F IG U r Example of how to reach the left superior pulmonary vein (LSPV) in a big loop: starting with the sheath pointing toward the left PVs, the catheter is halfway deflected. With a far-field V signal, the catheter is then advanced and further deflected. By doing so, the stiffer portion of the catheter gets exposed from the sheath and is used to lean against the free wall of the left Electrophysiological Perspectives

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atrium (LA). Careful advancement allows the catheter to follow the contour of the LA floor. Using this technique the right inferior PV, the right superior PV, and the roof area until the LSPV can be mapped with a very stable catheter tissue contact. This is especially helpful when attempting the deployment of a roofline although care must be taken not to dislodge into any

PV ostium. Halo = multipolar catheter positioned at the free wall of the right atrium; His = His bundle recording catheter; ICV and SCV = inferior and superior caval vein, respectively; LAO = left anterior oblique; LIPV and RIPV = left inferior and right inferior pulmonary vein, respectively; MA = mitral annulus.

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ATRIA Extracardiac and Other Epicardially Located Structures Due to the fatal complication of post-ablation fistula formation between the LA and the esophagus, the knowledge of the exact location of the esophagus (see Figure 8.3) and the local temperature during LA ablation has been the target of many reports. While static imaging (computed tomography or magnetic resonance imaging scans, tubes on 3D mapping systems) just depicts the presence of the esophagus in close proximity to the LA (several millimeters), the exact location that varies with every swallowing act might be underestimated. Similarly, temperature probes might not necessarily be in the closest position toward the ablation catheter, but might be buried inside the folding mucosa of the esophagus or along its posterior wall. Low readings may therefore give a wrong sense of security. Low ablation energy (eg, 30 W) and as few ablations as necessary at the posterior wall seem to be the most careful way to avoid collateral damage.

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Ganglionated Plexus The heart is equipped with an intrinsic nervous system. The neural cell bodies of this system are located in so-called ganglionated plexi found in specific sites mostly around the atria (see Figure 8.1). Their role for triggering and sustaining arrhythmia is currently under evaluation. Endocardial ablation strategies that target those epicardial structures risk collateral damage, while epicardial ablation, for example by minimally invasive techniques, at least allow for a more targeted approach.

Transverse and Oblique Pericardial Sinuses The pericardial access to the LA and PVs is limited by the fact that the pericardial sac folds around the heart. Access between the PVs is via the oblique sinus, while the anterior part of the LA can be reached via the transverse sinus, behind the aorta/pulmonary trunk (Figure 8.20; see also Figure 1.2).  

Chapte r 8  |   The Left Atrium and Pulmonary Veins Relevant to AF Ablation

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R eE 8.20 F IG U r (a) and (b) are two halves of the same heart cut longitudinally to show the close relationship between the esophagus (Eso) and the left atrium (LA). The transverse sinus (asterisk) is anterior to the atrial wall. The small arrows indicate the cut edge of the remnant of the fibrous pericardium overlying the oblique pericardial sinus. Desc Ao = descending aorta; MV = mitral valve; PT = pulmonary trunk.

Electrophysiological Perspectives

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Ventricles and malformations

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9

The Right Ventricle

THE RIgHt VENtRICLE IS tHE MoRE familiar of the two ventricular chambers because it is directly accessible via the more commonly used venous access. However, because it is heavily trabeculated with a complex valve, detailed knowledge is valuable not only for invasive electrophysiology procedures but also for device implantations. 

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VENTRICLES AnD MALFORMATIONS Anatomy The right ventricle in the normal heart is the most anteriorly situated cardiac chamber because it is located immediately behind the sternum. It also marks the inferior border of the cardiac silhouette. The right ventricle is triangular in shape when viewed from the front (Figure 9.1). When seen from the apex, the right edge of the right ventricle is sharp, forming the acute margin of the heart. In cross section, the cavity appears like a crescent against the curvature of the ventricular septum (see Figure 9.1).

R eE 9.1 F IG U r (a) This anterior view of a window dissection shows the right ventricle (RV) extending from the tricuspid orifice (oval) to the pulmonary valve. The aortic root is above the roof of the RV. (b) The RV is crescent shaped in cross section. LV = left ventricle; RA = right atrium; RCA = right coronary artery.

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Chapte r 9╇ | ╇ The Right Ventricle

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and MALFORMATIONS

The right ventricular chamber is delimited by the hinge line (annulus) of the tricuspid valve at its inlet and the attachments of the pulmonary valve leaflets at its outlet. Anatomically, it is described as having three portions—inlet, apical, and outlet— but there are no discrete borders between adjacent portions (Figure 9.2). The inlet portion extends from the tricuspid annulus to the papillary muscles that anchor the tendinous cords and leaflets to the ventricular wall. The leaflets of the tricuspid valve can be distinguished as septal, anterosuperior, and inferior (mural or posterior). The septal leaflet with its cords inserting directly into the ventricular septum is characteristic of the tricuspid valve.

R eE 9.2 F IG U r These right lateral views show the three portions of the right ventricle and the characteristic muscle bundles. The open arrows represent the anterior and posterior limbs of the Y-shaped septomarginal trabeculation (SMT). Note the very thin wall at the apex.

Anatomy

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VENTRICLES and MALFORMATIONS The medial papillary muscle, a small outbudding from the septum, supports the junction (commissure) between the septal and anterosuperior leaflets (see Figure 9.2). The septal component adjacent to this commissure is the membranous septum that serves as a landmark for the atrioventricular conduction bundle (Figure 9.3). The tricuspid annulus crosses the membranous septum, dividing the septum into interatrial and interventricular components, but occasionally, this area may be devoid of valvar tissue with the septal leaflet showing a cleft. The septal insertion of the medial papillary muscle marks the site where the right bundle branch emerges from the septum to descend subendocardially on the septomarginal trabeculation (see Chapter 5). A larger papillary muscle, the anterior papillary muscle, supports the extensive anterosuperior leaflet and its junction with the inferior leaflet. The junction between anterosuperior and inferior leaflets is supported by a group of small papillary muscles, the inferior papillary muscles. Coarse muscular trabeculations crisscross the apical portion, which is also known as the trabecular portion. Although the overall thickness of the muscle making up the parietal wall of

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R eE 9.3 F IG U r (a) The right atrial aspect of the membranous septum shows the tricuspid annulus (broken line) crossing the membranous septum (transilluminated). This heart lacks leaflet tissue at the membranous septum. (b) The thin membranous septum and its relationship to the aortic valve are displayed in this longitudinal cut.

Chapte r 9  |   The Right Ventricle

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the ventricular body is 3 to 5 mm, excluding the trabeculations, the most apical part can thin to approximately 1.5 mm. One of the trabeculations, the moderator band, is characteristic of the right ventricle (see Figures 9.1 and 9.2). It bridges the ventricular cavity between the body of the septomarginal trabeculation and the parietal wall, giving rise to the anterior papillary muscle along the way. The moderator band carries within it a major fascicle of the right bundle branch. The septomarginal trabeculation itself is a Y-shaped muscular band that is adherent to the septal surface. Between its limbs lies the infolding of the heart wall forming the ventricular roof, an area also known as the supraventricular crest (see Figure 9.2). This crest separates the two right heart valves and is an integral part of the outlet.

R eE 9.4 F IG U r (a) In this anterior view of the right ventricular outflow tract, the muscular subpulmonary infundibulum continues imperceptibly from the supraventricular crest. (b) and (c) The semilunar attachments of the pulmonary leaflets cross the junction between the arterial trunk and the musculature of the right ventricle.

Anatomy

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The right ventricular outflow tract (RVOT) passes superiorly and cephalad over the left ventricular outflow tract, which is directed rightward, resulting in a crossover relationship between the two tracts. The supraventricular crest in the right ventricle continues into the freestanding tube-like and smoothwalled muscular subpulmonary infundibulum that supports the pulmonary valve (Figure 9.4).

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VENTRICLES and MALFORMATIONS Its wall tapers from the regular ventricular wall thickness of 3 to 5 mm to nearly 1 to 2 mm distally at the junction with the pulmonary valve. Although ablationists refer to septal and free wall portions of the RVOT, it should be noted that the infundibulum does not have a true septal component in the sense that exiting the septum leads to the extracardiac tissue plane directly related to the outer aspect of the aortic sinuses (Figure 9.5). Any perforation in the septal part is more likely to go outside the heart than into the left ventricle. Thus, anatomically, paraseptal is a more accurate description for this part of the infundibulum, distinguishing it from the free wall or parietal part (see Figure 9.5). The paraseptal component overlies the proximal courses of the left anterior descending and right coronary arteries (Figure 9.6).

R eE 9.5 F IG U r The impressions of the semilunar leaflets on the endocast demonstrate the offset relationship between aortic and pulmonary valves. The left (L) and right (R) coronary aortic sinuses are close to the paraseptal (PS) part of the infundibulum. The free wall (FW) is on the opposite of the infundibulum. The diagram depicts paraseptal versus free wall of the right ventricular outflow tract (RVOT). Ao = aorta; RA = right atrium; RV = right ventricle; SCV = superior caval vein.

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Chapte r 9  |   The Right Ventricle

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R eE 9.6 F IG U r These dissections show the central location of the aortic valve in the heart and the relationships of the three aortic sinuses (L, R, N) to adjacent structures—the infundibulum anteriorly and the atria posteriorly. (a) The His bundle is related to the juncture between right and noncoronary aortic sinuses. (b) The infundibulum has been dissected free and pulled anteriorly to reveal its proximity to the right (RCA) and left (LCA) coronary arteries. Its paraseptal (PS) component overlaps the aortic sinuses. His = His bundle location; LAD = left anterior descending artery.

Anatomy

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The configuration of the semilunar leaflets of the pulmonary valve results in the crescentic hinge lines crossing the anatomic junction between ventricular musculature and arterial wall, enclosing within the nadirs of the valvar sinuses small areas of myocardium (see Figure 9.4). The plane of the pulmonary valve is higher and nearly horizontal, whereas that of the aortic valve is tilted lower and at an angle of at least 45° from the median plane (see Figure 9.5). The difference in levels between the two sets of arterial valves may be exaggerated by the length of the infundibulum. The posteroinferior wall of the subpulmonary infundibulum overlies the anterior walls of the left and right coronary sinuses to a greater or lesser extent and may give the impression of myocardial sleeves covering the aortic sinuses. Two of the pulmonary sinuses are adjacent to the two aortic sinuses that give origin to the right coronary and left main coronary arteries (see Figure 9.6). As the coronary arteries descend toward their respective atrioventricular grooves, they pass within millimeters of the epicardial aspect of the infundibulum.

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VENTRICLES and MALFORMATIONS Fluoroscopic RV Anatomy The right ventricle (RV) forms the shadows on the right free wall when looking at a left anterior oblique (LAO) projection. Using a multipolar catheter to mark the compact atrioventricular (AV) node, the direction or axis can be depicted because the catheter will cross the triscupid annulus through the anteroseptal commissure, stabilizing itself with the distal shaft at the ventricular septum. In a right anterior oblique (RAO) projection, a His catheter can serve as a marker for the AV valve or aorta, respectively (Figure 9.7). Using contrast injection, the body of the RV can be visualized, allowing also for a clear depiction of the pulmonary valve (Figure 9.8). Equally effective is sequential mapping (either conventional or using a 3D mapping system) to delineate the valve by losing the local electrogram just at the level of the valve. In order to map the RVOT, the easiest access is by advancing the mapping catheter first toward the RV apex.

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R eE 9.7 F IG U r Illustration of the position of the aortic root (by pigtail contrast injection) and the His recording site marked by a multipolar catheter depicting the typical His signals in both right anterior oblique (RAO) and left anterior oblique (LAO) projection. Note that the pigtail catheter is located in the right coronary cusp (RCC). CS = coronary sinus; RV = right ventricle.

Chapte r 9  |   The Right Ventricle

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At about a third to midway toward the shadow of the RV apex in RAO, the catheter is rotated 180° in a clockwise fashion in order to face the slightly curved tip up toward the outflow tract. In the shadow of the heart in RAO, the catheter is then advanced carefully. Further deflection will lead to the posterior part of the RVOT (which is adjacent to the right coronary cusp). Further clockwise rotation will lead toward the free wall of the RVOT, while counterclockwise rotation will lead toward the interventricular septum. The anterior part (most ventrally located) can be mapped with the catheter completely straightened. The easiest and safest way to map the RVOT is to come from more distal locations, close to the pulmonary valve, and move slowly down toward the body of the RV. It is not advisable to advance a straightened catheter upward into the RVOT because the myocardium is very thin, especially in the anterior part, and perforations can result easily.

R eE 9.8 F IG U r Right ventricular (RV) contrast injections in left anterior oblique (LAO) and right anterior oblique (RAO) projections using an injection pump. Note the trabeculated area (asterisk) and the dip (arrow) marking the pulmonary valve. In the top panels (LAO projection), the implantable cardioverter-defibrillator (ICD) is visible, which is connected to the intracardiac permanent leads. Note the ICD coil at the very tip of the RV. RVA = right ventricular apex.

Fluoroscopic RV Anatomy

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VENTRICLES and MALFORMATIONS When mapping the body of the RV, a first landmark can be the tricuspid annulus, including the site of the His bundle recording (about 1 o’clock in LAO projection). Using the technique described above, the RVOT can be mapped accordingly. The RV apex can be best visualized in RAO, where it mostly forms the shadow on the fluoroscopic projection. However, the left ventricular apex can be superimposed, and careful attention should be given to the very thin apical part of the RV to avoid perforation (Figure 9.9). Equally, perforations can occur when positioning a permanent lead for pacing or defibrillation.

R eE 9.9 F IG U r Example of a 3D map of a patient with enlarged right ventricle (RV). The upper panels depict a 3D reconstruction of a cardiac magnetic resonance scan superimposed on the fluoroscopy pictures in corresponding projections. The lower panels show

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the 3D electroanatomical RV map using the CARTO system on the same fluoroscopy background. Note that the mapping catheter at the apex of the RV appears to be outside the 3D contour. Due to the enlargement of the RV, the catheter had actually

left the 3D space where the mapping system could still locate it appropriately, despite the fact that the catheter had not perforated the cardiac wall. LAO and RAO = left and right anterior oblique, respectively.

Chapte r 9  |   The Right Ventricle

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and MALFORMATIONS

The ventricular septum can be mapped mostly without any problems. High-frequency potentials preceding the onset of the local ventricular signal allow for the delineation of the physiologic conduction system. A substantial moderator band or abundant trabeculations might reduce the ease of catheter rotation. In the event of any resistance, the operator should retract the catheter slightly and retarget from a higher (or lower) starting point. The lateral free wall can be reached with counterclockwise rotating coming from the RV apex, or coming from the RVOT using a clockwise rotation. Ultimately, a contrast injection into the right coronary artery allows for delineation of the tricuspid annulus from its epicardial aspect. A thin catheter inside the right coronary artery can serve as an anatomical guide, for example, to epicardially located accessory connections.

Ventricular Arrhythmias Idiopathic RV Tachycardia In the absence of overt structural heart disease, ventricular tachycardia arising from the RVOT is most

Ventricular Arrhythmias

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common. Description of the locations of the foci is confounded by reference to septal and free wall parts of the subpulmonary infundibulum (see above), as well as anterior and posterior as depicted in RAO projection, but which are actually leftward (toward the patient’s left) and rightward, respectively. The majority of RVOT foci have been mapped to the distal parts of the infundibulum, near to the pulmonary valve (Figure 9.10).

Ischemic Heart Disease Ventricular tachycardia in this setting is mostly due to reentry around regions of infarction or ventricular scar. Infarction sites often show tissue heterogeneity, especially at the border zones with areas of necrosis interspersed with bundles of viable myocytes. Changes in gap junction density or distribution, separation of viable bundles by varying amounts of fibrous tissue, and initial destruction followed by regeneration of sympathetic nerves may all contribute to arrhythmogenicity. Adaptive changes of increased interstitial fibrosis and distribution of gap junctions also occur in the hypertrophied or dilated myocardium remote from the infarcted areas.

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VENTRICLES and MALFORMATIONS

R eE 9.10 F IG U r Example of the 3D electroanatomical map of the right ventricular outflow tract (RVOT) area in comparison to the 3D reconstruction of the coronary sinus (CS) and the aortic root (Ao) in both left anterior oblique (LAO; upper panels) and right anterior oblique (RAO; lower panels) projections. The yellow arrow depicts the direction of the magnetic vector used during the remote controlled ablation of an aortic cusp ventricular ectopy.

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Chapte r 9  |   The Right Ventricle

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RV Cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease of the desmosomes (Figure 9.11). Although the left ventricle can also be involved, the structural abnormalities are more prominent in the RV. The abnormalities are typically located in three regions, the inferior, apical, and infundibular, and dubbed the triangle of dysplasia. Ventricular myocardium is replaced progressively by fibrofatty tissue leaving islands of surviving myocytes interspersed with fibrous and fatty tissues. The changes begin in the epicardium or mesocardium in the RV to become transmural. Owing to its thin wall compared to the wall of the left ventricle, the affected regions may become aneurismal.  

R eE 9.11 F IG U r (a) and (b) A heart with arrhythmogenic right ventricular cardiomyopathy displayed to show the areas where myocardium is not visible grossly (arrows). On microscopy, the myocytes (yellow) are replaced with fibrous tissue (red) and fat. (c) This heart shows extensive fibrofatty replacement on cross section. Photographs of histology and cross section courtesy of Dr. Margaret Burke, London, UK.

Ventricular Arrhythmias

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10

the Left Ventricle

ForMerly a freQuent transit route for mapping the mitral annulus in a retrograde fashion in left-sided accessory pathway ablation, the left ventricle is now mapped and ablated to treat ventricular tachycardias that may arise from acquired scars or from the conduction system itself.

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VENTRICLES/MALFORMATIONS Anatomy Unlike those of the right ventricle (RV), the inflow and outflow tracts of the left ventricle (LV) are at an acute angle to one another, giving the ventricle an approximately conical shape. When the heart is viewed from the front, most of the LV is behind the RV with its outlet overlapping its inlet (Figure 10.1). This is because the central location of the aortic valve places the outflow tract in between the mitral valve and the ventricular septum. Its inferior wall is in contact with the diaphragm.

R eE 10.1 F IG U r (a) Much of the left ventricle (LV) lies behind the right ventricle (RV). The LV outflow tract is behind the outflow tract of the RV (arrows). (b) The septal surface (asterisk) below the aortic valve is smooth. (c) The three portions of the LV; the outlet lies between the septum and the inlet. (d) The LV wall (yellow arrows) tapers to become very thin at the apex (red arrows). PT = pulmonary trunk; RA = right atrium.

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Chapte r 10  |   The Left Ventricle

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The hinge (annulus) of the mitral leaflets at the entrance to the inlet has a very limited attachment to septal structures (Figure 10.2). Compared to that of the tricuspid valve, the septal hinge line of the mitral valve is farther away from the apex, and it does not have a septal leaflet. Its two leaflets are referred to as anterior and posterior, but the designations do not truly reflect their locations. Alternative terms are aortic and mural, respectively. Two-thirds of the valve annulus is at the parietal atrioventricular junction, whereas one-third is the span of fibrous continuity between the anterior leaflet and the aortic valve (see Figure 10.2).

/MALFORMATIONS

R eE 10.2 F IG U r (a) The anterior (AL) and posterior (PL) leaflets of the mitral valve viewed from the atrial aspect. The aortic valve is immediately adjacent to the mitral valve. (b) This apical view of a heart with dilated left ventricle and previous infarction shows the area of fibrous continuity (asterisks) between the aortic and mitral valves. (c) This longitudinal section shows the area of fibrous continuity from the front. At either end are the fibrous trigones (triangles) with the right trigone colored blue. PM = papillary muscle.

Anatomy

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VENTRICLES/MALFORMATIONS The extremities of the fibrous continuity are the left and right fibrous trigones, the right trigone forming the central fibrous body. The anterior leaflet in continuity with the aortic valve is deep, whereas the mural (or posterior) leaflet is shallow. The mitral leaflets are attached via tendinous cords exclusively to two groups of papillary muscles (Figure 10.3). The insertions of the papillary muscles continue into trabeculations. The papillary muscles, sited quite close to each other, can cause difficulties in manipulating the catheter in this region. The apical component of the LV extends out from the level of the insertions of the papillary muscles to the ventricular apex. The muscular wall of the LV normally is 12 to 15 mm thick, excluding trabeculations. At the apex, however, the muscular wall tapers sharply to only 1 to 2 mm thick (see Figure 10.1). The trabeculations are finer than those found in the RV (see Figure 10.3). Occasionally, fine muscular strands or false tendons extend between the septum and the papillary muscles or the parietal wall. Often, they carry the distal ramifications of the left bundle branch.

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R eE 10.3 F IG U r (a) and (b) show the outflow and inflow tracts, respectively, and the papillary muscles (PMs) of the mitral valve. (a) The atrioventricular conduction bundle enters the left ventricle through the central fibrous body (blue triangle). The upper part of the septal surface (asterisk) is smooth. (b) The oval indicates the anticipated site of the atrioventricular node. (c) This section shows a PM formed from trabeculations. False tendons are indicated (arrows). AL and PL = anterior and posterior leaflet, respectively.

Chapte r 10  |   The Left Ventricle

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R eE 10.4 F IG U r These two halves of a heart are bisected longitudinally to show the three aortic sinuses (R, L, N). The right (small arrow) and left coronary orifices are located below the sinutubular junction. The muscular subpulmonary infundibulum of the right ventricular outflow tract (RVOT) abuts the right and left coronary sinuses. LVOT = left ventricular outflow tract; MV = mitral valve; P = pulmonary valve.

Anatomy

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The left ventricular outlet is directed rightward, superiorly and anteriorly (ventral). It is bordered by the muscular ventricular septum anterosuperiorly and the aortic (anterior) leaflet of the mitral valve posteroinferiorly. The aortic wall adjoining ventricular tissues begins with three bulging sinuses (of Valsalva) before continuing into the tubular ascending aorta. In similar fashion to the pulmonary valve, the semilunar hinge lines of the aortic leaflets enclose a segment of ventricular myocardium in the nadirs but only in the right coronary aortic sinus and half of the left coronary aortic sinus (Figure 10.4). These sinuses are adjacent to the pulmonary infundibulum. The coronary orifices are usually located in the sinuses immediately below the level of the sinutubular junction rather than toward the nadirs. The musculature in the aortic sinuses may be a source of repetitive monomorphic ventricular tachycardia (VT). Because the right coronary aortic sinus abuts the crest of the ventricular septum, separated from the RV cavity by the ventriculoinfundibular fold, it is easy to mistake musculature of the fold as myocardial extensions on the adventitia aspect of the aortic root (see Figure 10.4).

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VENTRICLES/MALFORMATIONS Owing to the spatial relationship of the subpulmonary infundibulum and the left ventricular outlet (see Chapter 9), the foci may be ablated from within the part of the RV outlet that overlies the adjacent aortic sinuses, and vice versa. The noncoronary aortic sinus, immediately adjacent to the paraseptal region of the left and right atria and close to the superior atrioventricular junction, may be used to map and ablate focal atrial tachycardia in the vicinity of the His bundle (see Figure 6.28 and Figure 9.6).

R eE 10.5 F IG U r The atrioventricular conduction bundle (AVB) appears on the left side of the ventricular septum. The left bundle branch (LBB) descends the septum superficially in the subendocardium. (b) False tendons (arrows) may carry the distal ramifications of the LBB to the papillary muscles and parietal wall. ms = membranous septum; N and R = noncoronary and right coronary aortic sinus, respectively.

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Chapte r 10  |   The Left Ventricle

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Conduction Tissues The upper part of the ventricular septum leading to the aortic valve is smooth. It is here that the common atrioventricular conduction bundle emerges from the central fibrous body to pass between the membranous septum and the crest of the muscular ventricular septum (Figure 10.5). The landmark for the site of the atrioventricular conduction bundle is the fibrous body that adjoins the crescentic hinge lines of the right and noncoronary leaflets of the aortic valve. From here, the left bundle branch descends in the subendocardium and usually branches into three main fascicles that interconnect and further divide into finer and finer branches as the Purkinje network (Figure 10.6).

R eE 10.6 F IG U r These are displays of the left bundle branch and Purkinje network in ungulate hearts. The pale coloration is the fibrous sheath around the conduction tissues in this fresh preparation (a). The remaining are ink injections. (e) This histologic section and its enlargement show a nerve bundle near the conduction tissues. (f) The transition of pale staining Purkinje cells to ventricular myocardium (arrow). L, N, and R = left coronary, noncoronary, and right coronary aortic sinus, respectively.

Anatomy

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VENTRICLES/MALFORMATIONS Coronary Veins of the LV The LV veins are important channels for LV lead placement and for epicardial approaches to VT foci (see also Chapter 2). Coronary veins have thin walls; the unprotected epicardial side is at risk of perforation into the pericardial space. The great cardiac vein commences as the anterior interventricular vein close to the apex of the heart. Sometimes two or more small veins are seen near the apex, and these come together as one larger vein as they ascend to the side or superficial to the anterior descending coronary artery. As the anterior interventricular vein reaches close to the first division of the left coronary arteries, it turns into the left atrioventricular groove under the cover of the left atrial appendage and follows the groove leftward. In the first part of its course, the great vein is joined by numerous branches from the ventricular septum and the anterior aspects of both ventricles. As it passes backward and inferiorly, it is joined by veins from the left atrium, including the vein/ligament of Marshall. From the ventricular surface, the left obtuse marginal vein and the left inferior veins join the great cardiac vein, and the latter then continue into the coronary sinus. As its name suggests, the obtuse marginal vein ascends along the obtuse margin of the heart. The proximal portions of the great cardiac vein, the obtuse marginal vein, and the inferior left ventricular veins are large

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enough for inserting pacing leads in adult hearts (see Figure 1.13 and Figure 4.4). However, there is great variability in the number and distribution of these veins. The absence of a left inferior vein limits the specific areas that can be targeted for therapy. When present, the diameter of the vein, its angulation, or its tortuosity can preclude access to target areas or implantation of leads for ventricular pacing. Whether utilizing the veins for pacing or for ablation, it is worth bearing in mind the potential hazard of causing trauma to the left phrenic nerve, which may be close to the obtuse marginal vein or the great cardiac vein, depending on the course it takes on its descent (see Chapter 2). Furthermore, the relationship between vein and artery is variable; the vein may cross over an artery and vice versa.

Coronary Artery Supply of the LV The left coronary artery usually divides into two major vessels: the left anterior descending artery (LAD) and the circumflex artery (CX). Occasionally there is a third branch known as the intermediate branch. While the LAD supplies the anterolateral myocardium including the ventricular septum down toward the apex, the CX first follows the left part of the coronary sulcus and supplies the posterolateral part of the LV (see also Chapter 1).

Chapte r 10  |   The Left Ventricle

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Electrophysiological Aspects Identification of the LV by Diagnostic Catheters

R eE 10.7 F IG U r

Using two diagnostic catheters, the borders of the LV can be easily determined, although inner structures are more difficult to anticipate. A diagnostic catheter positioned in the distal coronary sinus (CS) will be a guide to the mitral valve (MV) plane and thereby the LV inlet part. The shaft of this catheter is usually projected to the shadow of the free wall when using a left anterior oblique (LAO) projection. In a right anterior oblique (RAO) projection, the CS catheter shaft marks the MV level, while the shadow of the heart apex allows for display of the LV dimension (Figure 10.7).

Left ventricular (LV) angiogram using a pump injector and a large lumen pigtail catheter positioned retrogradely across the aortic valve (purple dotted line). For both right anterior oblique (RAO; upper panels) and left anterior oblique (LAO; lower panels) projections, several snapshots from the cine acquisition are displayed to show several time points during diastole and systole and the different filling status of the LV chamber. CS = coronary sinus, which is an additional marker for the mitral annulus (green dotted line); His = His recording catheter that co-locates with the aortic valve (purple dotted line).

Electrophysiological Aspects

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VENTRICLES/MALFORMATIONS If advanced distally enough (just until the interventricular vein takes off), the CS catheter can mark the left coronary cusp and thereby depicts also the aorta (Figure 10.8). A His recording catheter usually displays the commissure between the noncoronary cusp and the right coronary cusp. In LAO projection, this catheter allows for marking the septum, while the RAO projection again displays the level of the central fibrous body. Parallel to the CS runs the CX, a neighboring structure that could be harmed during high-energy delivery from within the CS (see Figure 10.8).

R eE 10.8 F IG U r Example of a left coronary cusp (LCC) origin of a monomorphic ventricular ectopy. The selective injection in the left coronary artery in both projections marks the distance to the coronary ostium. The very distally advanced coronary sinus (CS) catheter served as a further guide during the mapping process and was an early indicator that arterial puncture and retrograde mapping were indicated in this patient. Note the location of the His recording catheter that marks the location of the right coronary cusp. Simple comparison of the local activation of the V signal on the His and CS catheter, respectively, allows for differentiation between right and left coronary cusp origin using venous catheters only. RV = right ventricle.

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LV Mapping Generally speaking, the LV can be mapped via two accesses: the traditional retrograde approach across the aortic valve and a second transmitral approach that requires transseptal puncture (Figure 10.9). While the retrograde access is easily done (see Chapter 7), positioning and mapping can be difficult sometimes, requiring the operator to invert the catheter so as to reach the anterior wall of the LV. Using a steerable sheath, the transseptal access allows for a greater freedom of movement and gives good stability. Independent of the first choice of access, operators should always consider the alternative option once they experience difficulties to reach certain areas in a given patient.

R eE 10.9 F IG U r Transseptal versus retrograde approach to left ventricular (LV) mapping and ablation. Upper panels depict the transseptal approach using a steerable sheath (Agilis) to reach the free wall of the LV. The lower panels show a retrograde approach across the aortic valve with the mapping catheter positioned along the septum toward the apex. LAO and RAO = left and right anterior oblique, respectively.

Electrophysiological Aspects

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VENTRICLES/MALFORMATIONS Ventricular Arrhythmias Ischemic Heart Disease With coronary artery disease being such a prevalent feature in Western countries, resulting cardiac ischemia of the LV is the underlying cause in most LV ventricular tachycardias (see also Chapter 9). The highest risk of ischemia-related arrhythmic death occurs around the time of an acute myocardial infarction. In the acute phase of infarction, myocytes lose contractility, myofibrils are stretched, and increases in intracellular and extracellular edema disturb intercellular connections. With persistent ischemia, the infarcted tissues extend from the subendocardial toward the pericardial of the wall segment at risk. The central zone of injured myocytes turns into coagulative necrosis while the zones bordering healthy tissue can show contraction band necrosis relating to ischemia and reperfusion. Inflammatory responses followed by macrophage infiltration, fibrovascular proliferative response, and scar tissue formation ensue, evolving to dense fibrous scar (Figure 10.10).

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R eE 10.10 F IG U r (a) This cross section shows a thin wall at the old scars anteriorly and posteroinferiorly. (a1) Dense white scar tissue interspersed with myocytes. (a2) Vacuolated myocytes due to loss of myofibrils. (a3) Contraction band necrosis. (b) Subacute haemorrhagic infarction (solid arrows) after coronary stent placement (open arrow). (b1) Histology shows extravasation of red blood cells into the interstitial spaces in an area of dead myocardium alongside nonaffected paler area. (b2) Magnified view of the haemorrhagic infarction. Pictures courtesy of Dr. Margaret Burke, Harefield Hospital, London, UK.

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Infarcts often show marked heterogeneity with necrotic areas interspersed with bundles of viable myocytes, especially at the border zones. Large transmural infarcts produce fibrous walls that may become aneurismal and contain islands of surviving myocytes in the rims. While 3D mapping systems can depict areas of low voltage nicely, this virtual reconstruction may be hampered by insufficient catheter-tissue contact and thereby overestimation of the overall scarred area (Figure 10.11).

R eE 10.11 F IG U r Example of a substrate map of the left ventricle (LV) of a patient with an inferior-basal scar after myocardial infarction using the voltage amplitude display of the local V signal amplitude. The color code is purple for a signal above 1.5 mV of the bipolar signal from the 3.5-mm-tip ablation catheter. In addition, colored tags mark specific sites such as double (blue) or fractionated (pink) potentials. The sites of best pace mapping in the isthmus between the scar and the mitral annulus are marked in purple. Ao = aorta; LAO = left anterior oblique; MV = mitral valve.

Ventricular Arrhythmias

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VENTRICLES/MALFORMATIONS Other imaging modalities, for example late gadolinium enhancement magnetic resonance imaging, can give a more detailed picture, allowing for differentiation between fully transmural and endocardial-only or epicardial-only scar tissue (Figure 10.12).

R eE 10.12 F IG U r Examples of late gadolinium enhancements of myocardial scars (arrows) in various locations using cardiac magnetic resonance imaging in various projections. Ao = aorta; LA = left atrium; LV and RV = left and right ventricle, respectively. Images courtesy of Dr. S. Prasad, Royal Brompton Hospital, London, UK.

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Idiopathic VT Approximately 10% to 20% of sustained monomorphic VT occurs in apparently structurally normal hearts. Often they are focal in origin, relating to the Purkinje fiber network. Some data suggest origin from a false tendon or fibromuscular band. Other sources have been mapped to the fascicles of the left bundle branch, the inferior and paraseptal region of the mitral annulus, and the left ventricular outflow tract, which may require the nadirs of the aortic sinuses to be targeted. Careful 3D mapping allows the operator to follow the fascicles by typical recordings of high-frequency signals that allow for identification of the junction toward the Purkinje network by delayed signals in sinus rhythm (Figure 10.13). R eE 10.13 F IG U r A 3D reconstruction of the left ventricle using the electroanatomical mapping system CARTO. Using yellow tags, sites with high-frequency sharp Purkinje-like potentials are marked, and the local activation is adjusted accordingly. The electrograms along the posterior fascicle of the conduction systems are displayed for the corresponding locations. Ao = aorta; RAO = right anterior oblique.

Ventricular Arrhythmias

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VENTRICLES/MALFORMATIONS Dilated Cardiomyopathy Dilated cardiomyopathy (DCM) is the most common form of nonischemic cardiomyopathy, with congestive heart failure being the most important clinical feature, but syncope and ventricular arrhythmia are frequently observed. It is an abnormality of ventricular structure of heterogeneous pathogenesis (genetic, postviral, autoimmune, toxic, peripartum, idiopathic) characterized by a clear history of LV dysfunction and chronic cardiac failure. The ventricular chamber is dilated, appearing globular, with eccentric hypertrophy and increase in myocardial mass (Figure 10.14). Frequently, there is diffuse endocardial thickening and atrial enlargement. The histological changes, mostly nonspecific, may have a combination of myocyte attenuation, myofibrillary loss, interstitial fibrosis, and increased T-lymphocytes. Approximately one-third of cases have areas of replacement fibrosis thought to provide substrates for sustained VT in DCM. The scars tend to be in the basal LV adjacent to the mitral annulus in the inferior and lateral walls; they have a larger surface area on the epicardium than the endocardium.

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R eE 10.14 F IG U r Dilated cardiomyopathy: (a) Dilatation of the left ventricle (LV) with eccentric hypertrophy mainly in lateral and inferior wall (arrow). (b) Two slices from a heart with LV dilatation associated with spongy myocardium. (c) LV dilatation following viral myocarditis shows scarred areas (pale color on cut surface). (d) Honeycomb pattern of interstitial fibrosis stained with Sirius Red extends into denser scars. RV = right ventricle. Pictures courtesy of Dr. Margaret Burke, Harefield Hospital, London, UK.

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Hypertrophic Cardiomyopathy

R eE 10.15 F IG U r Hypertrophic cardiomyopathy: (a) Symmetrical hypertrophy with small cavity. (b) Hypertrophy is associated with fibrosis. (c) This longitudinal cut shows the septum bulging into the left ventricular outflow tract. (d) The anterior leaflet of the mitral valve has been cut and parted to reveal the impact lesion (arrows) of endocardial thickening on the septum. Early histologic changes showing some disarray (e) and increase in fibrosis (f), which become more evident later with disarray around foci of fibrosis (g). LV = left ventricle; RV = right ventricle. Pictures, except (c), are courtesy of Dr. Margaret Burke,

Hypertrophic cardiomyopathy (HCM) is commonly characterized by an increase in LV mass with a thick wall and a normal or reduced LV cavity (Figure 10.15). Hypertrophy may be symmetrical, producing an evenly thick-walled ventricle with a small cavity. In cases with asymmetrical hypertrophy, the ventricular septum is hypertrophied, whereas the LV free wall may appear normal. These cases are characterized by bulging of the basal part of the septum into the left ventricular outflow tract, and an impact lesion of the mitral leaflet upon the septum may be seen (see Figure 10.15). Histology demonstrates myocyte hypertrophy, disarray, and interstitial fibrosis. In hypertrophied areas, replacement fibrosis and signs of acute ischemia are common. In some cases, HCM may progress to ventricular dilation, wall thinning with replacement fibrosis, mimicking dilated cardiomyopathy. Catheter navigation inside the reduced LV cavity is sometimes greatly impaired. Judging by the sheer thickness of the LV wall, conventional or even irrigated-tip radiofrequency ablation seems to be very challenging if not in vain.

Harefield Hospital, London, UK.

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VENTRICLES/MALFORMATIONS Amyloid heart disease may mimic HCM on echocardiography, showing marked thickening of the left ventricular wall and septum. In ventricular myocardium, amyloid deposits surround the myocytes, giving a lattice appearance. Following myocyte death, the amyloid deposits coalesce into nodules. Considerable fibrosis develops, leading to stiffening of the myocardium.

Giant cell myocarditis

Inflammatory Cardiomyopathy (or Myocarditis) Classed as acquired cardiomyopathy, myocarditis is at risk of ventricular arrhythmias including VT and ventricular fibrillation. Whether of infective or immune origin, usually there is ventricular dilation and pump failure, but some cases may show normal-sized chambers. Histology shows focal, multifocal, or diffuse changes of interstitial edema, inflammatory infiltrate, myocardial necrosis, and fibrosis, with replacement fibrosis appearing in chronic cases (Figure 10.16). 

Sarcoid heart disease

R eE 10.16 F IG U r (a) A case of giant cell myocarditis. (b) Typical area of histology showing giant cells (arrows), widespread myocyte death with dense pleomorphic inflammatory cell infiltrate containing numerous eosinophils, shown more strikingly in (c). (d) and (e) are cases of sarcoid heart disease, which may involve the septum, right ventricle, and inferior left ventricle (LV) preferentially. The myocardium shows white fibrous tissue. Histology shows round-shaped granulomas and surrounding myocardium (f) and scar areas (g). Pictures are courtesy of Dr. Margaret Burke, Harefield Hospital, London, UK.

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11

Congenital Heart malformations

congenital heart disease has an incidence of approximately 1% in newborn infants. Owing to advances in diagnosis and interventions over the past several decades, most patients can expect to reach adulthood. There is now a growing population of adolescent and adult patients with congenital heart malformations. However, the reparative rather than curative nature of most of the early interventions (both catheter-based and surgical) could lead to further medical issues

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VENTRICLES AnD MALFORMATIONS over the longer term. Besides hemodynamic targets, preponderance of arrhythmia is a paramount problem that poses a multifaceted challenge for interventional electrophysiologists due to the underlying anatomy and the corresponding surgical correction; the 3D morphology is altered dramatically. When faced with these patients, one needs to consider three aspects. First, proper understanding of the altered morphology in the individual patient is the key to choosing the appropriate technologies, for example preprocedural imaging, 3D mapping systems, remote navigation, and so on. Whenever possible, the surgical notes should be scrutinized to determine the incision and cannulation sites as well as the surgical techniques used. Second, appropriate measures must be taken to understand the arrhythmia mechanism although most tachycardias seem to be scar-related reentrant tachycardias. Third, only the correct choice of catheters and access routes will ensure successful abolition of the arrhythmia, and techniques such as transbaffle puncture may need to be considered versus a retrograde approach. In this chapter, we discuss some of the more common malformations that electrophysiologists may encounter in their practice. To consider the many variations of congenital heart malformations and their surgical interventions to an adequate level is beyond the realms of a handbook.

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Tetralogy of Fallot

and MALFORMATIONS

Tetralogy of Fallot

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Tetralogy of Fallot consists of four anatomical features with variable expression: subpulmonary infundibular stenosis, ventricular septal defect (VSD), aortic overriding, and right ventricular hypertrophy. The anatomical hallmark is anterocephalad deviation of the outlet septum, which is the main substrate of subpulmonary muscular stenosis (Figure 11.1). Additionally, hypertrophy of the septoparietal trabeculations along the anterosuperior wall of the right ventricular outflow tract (RVOT) exacerbates the stenosis. The ventricular septal defect is usually large, allowing the aortic valve to be connected to both ventricles across the ventricular septum (described as overriding). In approximately 75% of these hearts, the posteroinferior margin of the VSD is the area of fibrous continuity between aortic-mitral and tricuspid valves (perimembranous VSD) harboring the atrioventricular conduction bundle. Less commonly, the posteroinferior border is muscular, distancing the conduction bundle from the immediate margin (see Figure 11.1). In both forms of VSD, the branching atrioventricular conduction bundle usually runs to the left, off the septal crest, but in a small percentage of cases, it can be directly on the septal crest.

All patients with tetralogy of Fallot invariably present with cyanosis, which is due to the right-to-left shunt at the ventricular level. The amount of cyanosis corresponds to the degree of RVOT obstruction. Palliative procedures, for example Blalock-Taussig shunt and its modifications, are all aimed at augmenting the pulmonary blood flow, but nowadays early repair, in infancy, is standard. It involves relieving the RVOT obstruction and closure of the VSD. Depending on the condition of the original pulmonary valve (dysplastic or bicuspid valves are common), the pulmonary valve needs to be repaired or even replaced; valve replacement is common in late repair. Generally, the RVOT obstruction is relieved by liberating infundibular musculature. Most surgeons resect the hypertrophied septoparietal trabeculations including surrounding musculature, whereas some surgeons incise into the muscle without resection, and a patch is placed to enlarge the RVOT. In the case of a restrictive pulmonary valve annulus, a transannular patch is used (Figure 11.2). Both the outflow patch and the VSD patch can be bordered by a narrow isthmus of myocardium that becomes the critical zone for macroreentry.

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VENTRICLES and MALFORMATIONS

R eE 11.1 F IG U r (a) The four structural features of Fallot’s tetralogy. (b) and (c) are views of the right ventricular outflow tract showing the anterocephalad deviation of the outlet septum (OS) that is the anatomical hallmark

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for subpulmonary muscular stenosis. Hypertrophy of septoparietal trabeculations contribute to narrowing the outflow. The aortic valve (Ao) is at the roof of the ventricular septal defect (VSD). The red dotted lines

represent the course of the atrioventricular bundle and its continuation into the right bundle branch. RV = right ventricle.

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and MALFORMATIONS

R eE 11.2 F IG U r (a) A transannular patch has been used in this surgical repair for Fallot. (b) Example of a patient with transannular patch for tetralogy of Fallot’s repair. A 3D map of the right ventricle displaying the voltage amplitude information (red = low voltage, purple = normal voltage, top right panel). Note that the area

Tetralogy of Fallot

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of low voltage is fusing with the pulmonary valve making a reentry circuit around the patch impossible. (c) Same patient with local activation time information displayed: red color marks early activation along the superior and lower right ventricular septum as an expression of the typical right bundle branch

morphology of the QRS complex. In addition, the scar resulting from the ventricular septal defect (VSD) repair is marked in gray. LAO = left anterior oblique; PA = posteroanterior; PT = pulmonary trunk; SCV = superior caval vein; TA = tricuspid annulus.

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VENTRICLES and MALFORMATIONS Complete Transposition of the Great Arteries In hearts with complete transposition of the great arteries (also known as d-TGA), the atrial and ventricular chambers are connected in normal fashion, but the aorta arises from the right ventricle and the pulmonary trunk from the left ventricle (Figure 11.3). Frequently associated defects such as VSD (40%–45%), left ventricular outflow tract obstruction (25%), and coarctation of the aorta (5%) may be encountered. Early management is crucial in cases with intact cardiac septum so as to have adequate mixing of the venous and arterial circulations, which otherwise would be separated soon after birth following closure of the fossa ovalis and the arterial duct. Frequently, a balloon atrial septostomy is performed to allow for mixing at the atrial level.

R eE 11.3 F IG U r (a) Complete transposition with intact ventricular septum. The outflow tracts are in parallel instead of the crossover seen in normal hearts. (b) Complete transposition with malalignment of the outlet septum (OS) into the right ventricle (RV) and a ventricular septal defect. (c) and (d) show an adult heart with complete transposition. Surgical repair (Mustard’s procedure) in childhood switched the venous flows at atrial level. The systemic RV is hypertrophied while the left ventricle (LV) is dilated and thin walled. (e) and (f) are two halves of a 4-chamber cut through a heart with Mustard’s baffle. The curved arrows represent the pulmonary (red) and systemic (blue) venous flow paths. Ao = aorta; PT = pulmonary trunk; VSD = ventricular septal defect.

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In the earlier era of surgical repair for complete transposition, the focus was on rearranging the pathways of pulmonary and systemic venous flow at the atrial level. By constructing a baffle consisting of either atrial tissue (Senning) or pericardium or artificial material (Mustard) across the atrial septum, pulmonary venous return is directed to the tricuspid valve orifice, whereas systemic venous return is directed to the mitral orifice. This switching of flow at the atrial level allows the circulation to be normalized but with the right ventricle carrying the systemic load whereas the left ventricle supports the pulmonary load (see Figure 11.3). Over the long term, some patients succumb to right ventricular failure. Incisional atrial reentrant tachycardia, or atypical atrial flutter, reportedly occurs in up to half of patients with atrial switch (Figures 11.4 and 11.5). Nearly as common is bradyarrhythmia, likely the consequence of injury to the sinus node and surrounding tissues and/or arterial supply. R eE 11.4 F IG U r Superimposition of a cardiovascular magnetic resonance (CMR)–acquired 3D reconstruction of the cardiac anatomy of a patient after Mustard repair for d-TGA on both right anterior oblique (RAO) and left anterior oblique (LAO) fluoroscopic images during a catheter ablation procedure for atrial reentrant tachycardia. The upper panels (RAO and LAO)

show the systemic venous side with the systemic venous atrium (SVA) in light blue, the left ventricle (LV) in purple, and the pulmonary artery (PA) in orange. Note the trouser-shaped outline of the SVA (superior [SVC] and inferior [IVC] vena cava form the legs, while the mitral annulus forms the waist) and the slim shape of the LV. The lower panels show

Complete Transposition of the Great Arteries

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the pulmonary venous side with the pulmonary venous atrium (PVA) in sand color, the right ventricle (RV) in light purple, and the aorta (Ao) in red. Note the shape of the PVA, which consists of the RA and the PV compartments joined by the baffle and the hypertrophy of the RV.

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VENTRICLES and MALFORMATIONS

R eE 11.5 F IG U r The group of four left panels shows contrast injections into the pulmonary venous atrium (PVA) of a Mustard patient after transesophageal echocardiography– guided transbaffle puncture in both right anterior oblique (RAO) and left anterior oblique (LAO) projections. The upper panels show the contrast in the PV compartment, while the lower panels depict the right atrial compartment (red broken line to emphasize

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the contrast). All four pictures courtesy of Dr. Tom Wong, Royal Brompton Hospital, London.

The right picture shows a retrogradely advanced magnetic catheter positioned inside the left inferior pulmonary vein of the same patient as in Figure 11.4. The 3D reconstruction is more transparent than in Figure 11.4 to illustrate the course of this soft catheter crossing the aortic valve and subsequently the

tricuspid annulus to pass through the former right atrium and the baffle into the PV compartment. Since the magnetic catheter is steered from the distal tip rather than from the proximal end, these mapping maneuvers are very easy to achieve without any limitation to reach specific sites even after multiple deflections. AA = atrial appendage; LV = left ventricle; SVA = systemic venous atrium.

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Over the last two decades, anatomical correction by switching at arterial level with coronary transfer (Jatene procedure) has overtaken the practice of atrial switch. This procedure allows the left ventricle to carry the systemic load. In cases without associated intracardiac anomalies, extensive atrial scars and ventricular scars can be avoided. The incidence of arrhythmia is relatively low. For hearts with associated left ventricular outflow obstruction and VSD, the Rastelli procedure is commonly used. The patch closing the VSD is positioned in such a way as to redirect the left ventricular outflow into the aorta. The pulmonary trunk is ligated just above the valve, and a conduit is used to connect the right ventricle to the distal pulmonary trunk/ pulmonary bifurcation. Right bundle branch block, or heart block postoperatively, and development of ventricular and supraventricular tachycardia on long-term follow-up have been reported.

Hearts with Functionally Single Ventricle: The Fontan Procedure

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Hearts With Functionally Single Ventricle: The Fontan Procedure Originally intended as a physiologic correction for tricuspid atresia, the Fontan procedure now also addresses patients with hypoplastic left heart syndrome, pulmonary atresia, and other types of functionally univentricular circulations (Figure 11.6). Following on from the first Fontan case performed in 1968, extensive modifications to the original operations have been made to improve flow dynamics and reduce the risk of thromboembolism and arrhythmia (Figure 11.7). Patients who had previous atriopulmonary Fontan repair are presenting in older age with enlarged right atrium and atrial arrhythmias. Many centers have begun to convert the atriopulmonary connection to an extracardiac or intra-atrial cavopulmonary conduit in the hope of reducing the arrhythmias. Some centers carry out the conversion together with arrhythmia surgery.

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VENTRICLES and MALFORMATIONS

R eE 11.6 F IG U r Examples of hearts with single-ventricle physiology. (a) Both atrial chambers open into one large ventricle, which has left ventricular (LV) morphology. The small right ventricle (RV), not connected to the atria, receives flow from the LV via a small ventricular septal defect (VSD). (b) and (c) show tricuspid atresia where there is no evidence of a tricuspid

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valve. All the venous return into the right-sided atrium has to cross the atrial septum to enter the left-sided atrium, which then opens to a large ventricle. (d) This rarer form of tricuspid atresia has an imperforate tricuspid valve although the circulation is similar to the commoner form. (e) This case of pulmonary atresia with intact ventricular septum

shows myocardial hypertrophy that has severely reduced the RV cavity. (f) and (g) are two examples of hypoplasia of the LV. In (f) the cavity of the LV is spherical and lined with endocardial fibroelastosis. CS = coronary sinus; LA and RA = left and right atrium, respectively.

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R eE 11.7 F IG U r Schematics of Fontan modifications, Glenn, and total cavopulmonary connection (TCPC). PT = pulmonary trunk; RA = right atrium; RPA = right pulmonary artery; SCV = superior caval vein.

Hearts with Functionally Single Ventricle: The Fontan Procedure

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VENTRICLES and MALFORMATIONS Some of the different types of Fontan and its modifications, total cavopulmonary connection (TCPC) with extracardiac or lateral tunnel techniques, bidirectional Glenn, or 1½ ventricular repair, are shown in Figure 11.7. While arrhythmias in the original Fontan operation are usually located in the enlarged right atrium, the atrial target chamber in a TCPC patient may require retrograde or transbaffle access. In patients with a patch located across the tricuspid annulus, a rim of atrial tissue that can only be reached retrogradely may serve as the critical isthmus in peritricuspid atrial reentry (Figure 11.8).

R eE 11.8 F IG U r Left panels: Examples of 3D images from cardiovascular magnetic resonance (CMR) for a patient with tricuspid atresia and Fontan palliation. The right panels depict a patient with double-inlet left ventricle in whom a patch was placed across the tricuspid valve.

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The echocardiographic image shows a rim of atrial tissue behind the patch that can no longer be reached via a transvenous approach. The upper right panel shows a retrogradely advanced soft magnetic catheter (via the aortic valve and ventricular septal defect) that

crosses the tricuspid annulus reaching behind the patch. Note the closure devices that were implanted earlier to block a patch leak. CS = coronary sinus; PM = pacemaker; RA = right atrium; RV = right ventricle.

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Ebstein Anomaly In Ebstein anomaly, the attachments of the septal and inferior (posterior) leaflets of the tricuspid valve are displaced apically away from the atrioventricular junction into the right ventricular cavity (Figure 11.9). The effective valvular orifice is also displaced and, depending on leaflet morphology, may be stenotic. In most cases, varying degrees of tricuspid regurgitation result from the malformed leaflets, which in turn causes further right atrial enlargement. In a large proportion, additional malformations such as atrial septal defects (ASDs) or patent foramen ovale (PFO) are present, but also right ventricular outflow tract obstructions or pulmonary valve atresia.

R eE 11.9 F IG U r (a) A 3D reconstruction from a cardiovascular magnetic resonance (CMR) scan of a patient with Ebstein anomaly. Note the displacement of the septal leaflet of the tricuspid annulus indicated by the dotted line. (b) A 4-chamber transthoracic echocardiogram depicting the displacement of the valvar structures in another patient. Importantly, the electrical location of the tricuspid annulus is not influenced by the valvar displacement. However, Ebstein Anomaly

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the fractionated ventricular electrograms can be very difficult to interpret, and differential pacing maneuvers to differentiate between atrial and ventricular components of a given local signal are the key to identifying the exact pathway insertion site. (c) This example of Ebstein malformation has severe displacement of the hinge line attachments of the septal and inferior leaflets of the tricuspid valve (TV) deep into the right ventricle (RV). The broken line traces the level of the

atrioventricular (AV) junction, which is marked by the course of the right coronary artery and the AV groove. Owing to the apical displacement of the valvar orifice, this heart has a large atrialized portion of the RV, which functionally is part of the atrial circulation, but it has ventricular myocardium. ASD = atrial septal defect; CS = coronary sinus; ICV = inferior caval vein; LA and RA = left and right atrium, respectively; LV = left ventricle.

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VENTRICLES and MALFORMATIONS It has been thought that poor formation of the atrioventricular junction in Ebstein explains the high incidence (reportedly 6%–30%) of ventricular preexcitation in these patients, although anatomical studies found no defects in junctional formation. Clinically, right-sided and multiple accessory atrioventricular connections are commonly reported, but accessory nodoventricular connections and fasciculoventricular or atriofascicular connections (so-called Mahaim fibers) are also more common than in the general population. The latter substrate is depicted as having a bundle of specialized myocardium linking a rudimentary node in the anterolateral (acute) margin of the tricuspid annulus to the right bundle branch. Apart from arrhythmia based on accessory pathways, various other types of tachycardia such as atrial ectopic tachycardia, atrial flutter, atrial reentrant tachycardia, atrial fibrillation (especially in an enlarged right atrium), and ventricular tachycardia can occur.

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Atrial Septal Defects and Patent Foramen Ovale These common congenital defects are often associated with other cardiac malformations. They are characterized by various degrees of interatrial shunts. When occurring in isolation, the defects may only become clinically apparent when the shunt volume is large. Even so, an isolated interatrial shunt may be well tolerated for many years. Morphologically, there are various types of interatrial communications, but strictly speaking, only defects within the confines of the oval fossa are truly in the atrial septum (Figure 11.10). The most common ASD is deficiency of the fossa ovale valve, also known as secundum ASD. The latter term refers to the defect at the site of the embryonic ostium secundum, rather than a deficiency of the septum primum (see Chapter 7). The ASD is usually large when the valve (the embryonic septum primum) is totally absent.

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R eE 11.10 F IG U r A diagram and examples of atrial septal defect (ASD) and interatrial communications. The patent foramen ovale (PFO) is usually slit-like at the anterocephalad margin (arrow) of the oval fossa. Deficiencies of the oval fossa valve (ASD) vary from a small hole to multiple fenestrations. The superior sinus venosus defect (Sup SV) is an atrial communication at the

orifice of the superior caval vein (SCV). The oval fossa can be intact. Similarly, the inferior sinus venosus defect (Inf SV) is at the entrance of the inferior caval vein (ICV). The coronary sinus (CS) defect is at the orifice of the CS, allowing for interatrial communication in so-called unroofing of the coronary sinus. The atrioventricular septal defect (AVSD) is often a large

Atrial Septal Defects and Patent Foramen Ovale

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communication at the atrioventricular level, and this example shows the type with atrial and ventricular components. The atrioventricular node and bundle are displaced posteroinferiorly (dotted shape) to where the ventricular septum rises to meet the atrioventricular junction. RAO = right anterior oblique.

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VENTRICLES and MALFORMATIONS The deficiency can take various sizes and shapes; the valve can have single or multiple fenestrations, appearing like a fishnet, and can be aneurysmal. In approximately one-fifth of the normal population, the fossa valve is well formed and adequately large to overlap the muscular rim around the fossa, but a slit-like gap exists at the superoanterior quadrant, allowing a probe (or catheter) to pass obliquely from the right atrium into the left atrium (see Figure 11.10). This slit is known as the probe PFO, and it represents the fetal channel allowing blood from the right atrium to enter the left atrium. During fetal life, flow from the inferior caval vein is directed preferentially by the Eustachian valve toward this channel. The valve shuts against the muscular rim after birth and obliterates the slit and any potential for shunts. Should the atrial walls become stretched as the atria dilate, the valve may then become inadequate. For many decades, repair of oval fossa defects and PFO has required direct suture or patch closure at surgery. In the current era of minimally invasive techniques, most of these defects are closed with transcatheter devices, thereby avoiding any suture lines and cannulation sites on the right atrium.

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Much less common is a superior sinus venosus defect (see Figure 11.10). This type represents approximately 5% to 15% of ASDs but is outside of the true septum because it lies in the mouth of the superior caval vein. The superior caval vein is committed to both atrial chambers because the venous orifice forms the roof of the defect. Most frequently, the upper pulmonary veins from the right lung connect anomalously to the superior caval vein near to its junction with the atria. A comparable defect is the inferior sinus venosus defect that occurs at the mouth of the inferior caval vein, but this type is much more rare. Both superior and inferior sinus venous defects are repaired surgically with a patch rather than by device closure owing to the configuration of its margins, although this could change in the future when devices become available for this specific type of defect. The so-called ostium primum ASD is a type of defect belonging to the spectrum of atrioventricular septal defect (AVSD). Characteristically, the heart has a common atrioventricular junction, and the defect is roofed by the free margin of the atrial septum (the oval fossa often is intact), and the remainder is conjoined

Chapte r 11  |   Congenital Heart Malformations

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tissues of the superior and inferior bridging leaflets that overlie the crest of the muscular ventricular septum. When the conjoined leaflets are adherent to the muscular crest, the shunt is at the atrial level, giving the impression of an ASD. However, the AVSD spectrum includes hearts in which the bridging leaflets are not fused, the so-called complete or canal form of AVSD, where the shunt occurs at both atrial and ventricular levels. As a consequence of the common atrioventricular junction in all variants, the atrioventricular node is displaced to lie in the vicinity of the junction between the posteroinferior insertion of the ventricular septum and the atria; the penetrating atrioventricular conduction bundle passes through the valvar annulus (see Figure 11.10). The septal defect is closed surgically with one or two patches. The proximity of the coronary sinus orifice to the anticipated location of the displaced node determines where the suture line needs to be placed without traumatizing the conduction tissues. After repair, some patients will have the coronary sinus draining to the right atrium, and in other patients, the orifice is behind the patch, allowing the vein to drain into the left atrium.

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Unrepaired, patients with ASDs or interatrial communications have a higher risk of developing atrial fibrillation or flutter from the fourth decade whereas it is rare to have late arrhythmia when the defect is repaired before the age of 20 years. For patients with previous repair, the patch/device can make transseptal procedures more challenging. Whether by surgical patch or device closure, the barrier placed could serve as the central obstacle in reentrant tachycardia. More often, however, the right atrial atriotomy scar is the cause of atrial reentrant tachycardia circuits. In particular, when cannulation scars are positioned within the right atrium itself (rather than in the superior or inferior vena cava), the perfect condition for a “figure of 8” tachycardia is formed. 

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Pitfalls

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12

Pitfalls and Troubleshooting

SoMETIMEs EVEN RELATIVELY EAsY tasks are difficult to achieve during an electrophysiological (EP) study. Most of the time, alternative access ways can save the day whenever the standard way does not work. Sometimes just a small hint can make all the difference.

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PITFALLS difficulty Reaching Tricuspid Annulus Especially when there is a very long inferior isthmus, a very annular position for the catheter can be difficult to achieve. When looking in a right anterior oblique (RAO) projection the distance from the coronary sinus (CS) ostium, judged by the turning point of the CS catheter, to the inferior vena cava (IVC), where all the catheter shafts gather together, the accurate choice of reach for the ablation catheter can be made. In case of failure, a large loop along the free wall of the right atrium (RA) allows the catheter to reach the tricuspid annulus in an inverted fashion (Figure 12.1). By extending the curve when the inversion is complete, firm contact can be made. An alternative is to use long, preformed, or steerable sheaths that stabilize the catheter and ensure stable catheter-tissue contact. R eE 12.1 F IG U r Example of alternative approaches to the right atrial inferior isthmus region for ablation of atrial flutter. These approaches allow for a different tip-tissue orientation and should be considered when the conventional direct approach does not succeed to achieve bidirectional block. Upper panels depict a large lateral loop along the free wall of the right atrium in right anterior oblique (RAO; left panels) and left anterior oblique (lAO; right panels) projection. Lower panels show a transannular approach with the ablation catheter looping in the right ventricle. This is a valuable option, especially when a conduction gap at the ventricular aspect of the line is suspected. CS and halo = catheters; map = ablation catheter.

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Anterolateral Aspect of the Tricuspid Annulus Stable contact around all aspects of the tricuspid annulus is occasionally difficult to achieve. A superior access via either a jugular or subclavian approach can be advantageous in this situation (Figure 12.2).

R eE 12.2 F IG U r Stability of an ablation catheter along the tricuspid annulus can be sometimes challenging. Especially when targeting para-Hisian or anterolateral aspects a superior access via a jugular or subclavian sheath improves catheter tip-tissue contact and avoids easy dislodgement during ablation (upper left panels). The lower left panels show an example of an enlarged right atrium after tricuspid valve replacement where a conduction gap along the inferior isthmus is successfully closed via the superior approach (after all femoral attempts including a long guiding sheath has failed). The specimen opened through the parietal right atrioventricular junction and the parietal wall pulled away displays the septum in right anterior oblique (RAO) fashion. The broken line indicates a superior approach, and the dotted line traces an inferior approach to the anterolateral tricuspid annulus. CS = coronary sinus catheter; His = His recording catheter; LAO = left anterior oblique.

Anterolateral Aspect of the Tricuspid Annulus

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Pitfalls Coronary Sinus The proximal parts of the CS, especially with its most proximal branch, the middle cardiac vein, can be difficult to reach from a femoral approach. While direct contrast injection, for example using an AL2 curved injection catheter, allows for visualization of any malformation such as diverticula of various sizes, stable catheter positioning at the neck of the diverticulum is an even more challenging task. Again, a superior access can allow the ablation catheter to be positioned relatively easily at the proximal end of the CS, even when the entrance is guarded by a large Thebesian valve (Figure 12.3).

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R eE 12.3 F IG U r When struggling with a posteroseptal location close to or inside the coronary sinus (CS) ostium, consider a superior approach. The pink arrow illustrates the counterclockwise rotation to enter into the CS ostium from a more ventricular location (with a large V signal). The CS orifice in the specimen is hidden behind a large Thebesian valve, which has a slit-like opening directed upward. ICV and SCV = inferior and superior caval vein, respectively.

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Persistent Left Superior Caval Vein In approximately 0.3% of the population, there is a persistent left superior caval vein that opens via the CS into the RA (Figure 12.4). This represents complete patency of the oblique left atrial vein (vein of Marshall). Its cardiac course from superior to inferior is along the lateral left atrial wall between the left atrial appendage and the left pulmonary veins, and then along the posterior and inferior wall to join with the CS. Usually, the CS is enlarged in these cases. Owing to its dilatation, the CS wall may appear thin, but in some cases it can be well endowed with a muscular sleeve. The enlarged CS may be mistaken for an atrial septal defect. When suspected, direct contrast injection should be performed to visualize the enlarged vessel (see Figure 12.4).

R eE 12.4 F IG U r Left panels: Example of the coronary sinus (CS) ostium of a patient with a persistent left superior caval vein (LSCV). Please note the dislocation of the atrioventricular node conduction tissue and the massive dilation of the CS. Right panels: This heart with a persistent LSCV is viewed from the left side. Note the course of the vein running between the left atrial appendage (LAA) and the left pulmonary veins (LSPV, LIPV). The LSCV is cut across (small arrows) and the left atrium opened to reveal the lumen of the vein (asterisks) and its muscular wall. His = His recording catheter; LAO and RAO = left and right anterior oblique, respectively; RV = right ventricle. Persistent Left Superior Caval Vein

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Pitfalls Pulmonary Vein Angiography Some pulmonary vein (PV) ostia are more difficult to gain access to than others. The right inferior PV (RIPV) poses the biggest hurdle for many investigators, most likely due to its short distance to the fossa ovalis. Risking to lose the transseptal sheath using a direct approach, a step-wise approach using a multipurpose angiography catheter is very helpful (Figure 12.5). An alternative is to loop the catheter in left anterior oblique (LAO) and then turn it via the posterior wall of the left atrium (LA) while injecting dye. The technique is similar to positioning a steerable catheter in a big loop (Figure 12.6).

R eE 12.5 F IG U r Occasionally direct contrast injection in the right inferior pulmonary vein (RIPV) is difficult and risks dislodging the transseptal sheath in the right atrium. Using a large-diameter multipurpose catheter (MP, ideally with a marker at the tip and side holes), one can safely perform this injection. Starting from the right superior pulmonary vein (RSPV), the MP is advanced so far out of the transseptal sheath that the kink is fully exposed. When the transseptal sheath is subsequently advanced, the soft MP catheter automatically bends, and the tip of the MP exits the superior PV. By injecting some contrast and carefully advancing the MP, the ostium of the RIPV can be found easily. Once the tip of the MP is inside the ostium, the transseptal sheath can be pulled back, which allows the MP to move farther into the vein. Cine injection in both right anterior oblique (RAO) and left anterior oblique injection follows subsequently. When removing the MP from the sheath, care should be taken to first rotate counterclockwise to remove the MP from the vein and into the body of the left atrium. The transseptal sheath is then carefully advanced over the MP. CS = coronary sinus.

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R eE 12.6 F IG U r In order to reach the septal pulmonary veins (PVs), one can use the “big loop” approach. All pictures are displayed in left anterior oblique (LAO). With an initial half-deflection, the catheter is advanced until the stiffer part of the catheter has exited the sheath. Then the catheter is fully deflected and carefully advanced along the floor of the left atrium. By straightening the catheter, contact with the roof or septal PVs can be reached. CS = coronary sinus; His = His catheter.

Pulmonary Vein Angiography

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Pitfalls Catheter Maneuvering Especially when using nonlinear catheters such as circumferential catheters, careful manipulation is key to avoid entrapment in pectinate muscles or the mitral valve apparatus (Figure 12.7). A second key trick is to have the cable connected at any time to be guided by the signals: A large ventricular signal on any of the intracardiac signals is a clear warning that the catheter is positioned very close to the mitral annulus. Loss of the atrial potential should lead immediately to fluoroscopy in two perpendicular projections in order to exclude an inadvertent transannular position.

R eE 12.7 F IG U r One of the potential complications when moving a circumferential catheter is the displacement across the mitral valve annulus (which can be noted by the very large V signals when approaching the annulus!). Once the catheter is located inside the left ventricle, the catheter can easily become caught in the chordae tendinae or the tips of the papillary muscles (PMs) of the mitral valve apparatus. Very careful clockwise unscrewing of the catheter can be tried to free the catheter. If this fails, the only option is to call the cardiac surgeon to avoid destruction to the mitral valve. AL = anterior leaflet.

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Typical LA Perforation Sites One of the most common perforation sites in the LA is exactly opposite the entry site into the LA along the roof. While the dilator of the transseptal needle kit is relatively soft on its own, it is sharpened by the steel needle inside (even when the needle is no longer extending from its tip). The roof close to the ostium of the left superior PV is easily perforated, a complication that might even escape the notice of the investigator in the first instance but will lead to a cardiac tamponade within a short time. Due to the perforation being a mechanical tear rather than a puncture, a surgical repair is required in most of these cases (Figure 12.8). Using a persistent foramen ovale results in a much higher position of the entry point of the sheath as compared with the actively punctured access site, again risking perforation of the roof.

R eE 12.8 F IG U r One of the potential risks of transseptal (TS) access through a persistent foramen ovale (PFO) is the fact that the catheter (or dilator or other instrument) ends up in a very high position, which is close to the roof of the left atrium (LA; upper left panel). Compare the position of the guiding sheath to the “normal” transseptal puncture position displayed in the lower left panel. Right panel: This access to the LA via the PFO points directly to the anterior wall/roof, where small pits with thin walls may be present. CS = coronary sinus; His = His recording catheter; ICV = inferior caval vein; LAO = left anterior oblique; LSPV, RIPV, and RSPV = left superior, right inferior, and right superior pulmonary vein, respectively.

Typical LA Perforation Sites

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Pitfalls Perforation During Transseptal Puncture When the transseptal puncture is carried out too far beyond the confines of the fossa ovalis, the transseptal sheath may exit the heart and end up in the great arteries. It is the aorta that is relatively close to the anterior margin of the fossa ovalis, whereas the pulmonary trunk is too far anterior to be encountered if the puncture is too anterior (Figure 12.9). Checking the position of the transseptal needle in RAO and careful marking of the aorta, for example by a His bundle recording catheter or a pigtail in the noncoronary cusp, excludes this risk. A transseptal puncture carried out too superiorly may perforate the atrial roof and reach the pulmonary artery bifurcation or left pulmonary artery. Using an intracardiac pressure recording from the tip of the transseptal needle allows for identifying when access into the LA cavity is gained by a typical LA pressure wave. When pushing against the LA wall/roof the pressure curve is flattened (or risen!) again, this should caution the operator that perforation may be imminent.  

LSPV LIPV

R eE 12.9 F IG U r Inadvertent puncture of neighboring structures such as the pulmonary artery (PA; left panels) is a rare complication of transseptal access. The upper panel depicts contrast injection in the left PA, while the lower panel shows the injection in the left superior pulmonary vein (LSPV). The colored arrows and asterisks depict the location of the other anatomical structure, respectively (also note the surface electrocardiogram markers as a reference!). Examples courtesy of Dr. T. Wong, Royal Brompton Hospital, London, UK. Right panel: Longitudinal cut of an anatomical specimen displays part of the left atrial chamber behind the atrial septum and relationship of the atrium to the left pulmonary artery (LPA) and pulmonary trunk. Eso = esophagus; LB = left bronchus; LIPV = left inferior pulmonary vein; MV = mitral valve; RV = right ventricle.

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Index page numbers followed by c indicate captions a ablation atrial flutter, 117–121, 234c fistula formation after, 176 left atrium, 174, 176 left ventricle, 195 slow pathway, 108c accessory pathways anatomy of, 83c, 84, 84c, 96, 96c atrio-hisian, 96, 96c conduction directions for, 87 coronary sinus diverticulum associated with, 95 coronary sinus veins associated with, 95 definition of, 83 distribution of, 83, 85 electrophysiological properties of, 86c–87c, 86–87 epicardially located, 92 fasciculoventricular, 96c, 226 insertion site of, 88–89 left-sided retrograde approach to, 90–92, 91c–92c transseptal approach to, 92, 92c–93c locations of, 83, 85 multiple, 95 nodofascicular, 96c nodoventricular, 96c paraseptal, 93 posteroseptal, 94c

rare types of, 96, 96c retrograde-only conducting, 88 right-sided, 89, 89c unusual types of, 94–96 acute marginal vein, 23c adrenergic nerves, 25 amyloid heart disease, 212 angiography computed tomographic, 41 pulmonary veins, 169, 238c–239c rotational, 43 anterior descending coronary artery, 20, 24 anterior esophageal plexus, 33 anterior mediastinum, 7c anterior papillary muscles, 184–185 anterior septum, 79 anteroposterior projection (ap) of aortic valve, 15c of heart, 52, 52c of mitral valve, 15c of pericardial sac, 13c of pulmonary valve, 15c of thorax, 7c of tricuspid valve, 15c antidromic atrioventricular reentrant tachycardia, 87, 87c aorta (ao) anatomy of, 7c, 8c, 28c, 52c, 53c, 60c, 82c, 92c, 131c, 135c, 198c ascending, 17 cardiac magnetic resonance imaging of, 42c, 208c descending thoracic, 11c–13c, 242c

rotational angiography of, 43c as transseptal puncture landmark, 142 aortic arch, 17 aortic commissure, 17 aortic mound, 133 aortic recesses, 35 aortic root anatomy of, 16c–17c, 24, 133, 142c, 188c atrial septum and, 131c ventricular septal defects, 216c aortic sinuses anatomy of, 187c, 199c noncoronary, 200, 200c of Valsalva, 23, 199 aortic valve anatomy of, 11c–13c, 18c, 25c, 78c, 156c, 184c annulus of, 78 location of, 14, 15c, 187c membranous septum and, 17 mitral valve and, fibrous continuity between, 81c, 197c orifice of, 14 plane of, 16c, 187 retrograde crossing of, 91c, 91–92 apical trabeculations, 198c arrhythmogenic right ventricular cardiomyopathy, 193, 193c as low as reasonably achievable principle, 40 ascending aorta, 17 atria, 19c connections between, 18–20 ganglionated plexi in, 176

left. See left atrium right. See right atrium subepicardial musculature of, 19c atrial fat pads, 25c atrial fibrillation ablation for, 12, 29c description of, 168 firing triggers for, 168, 169c pulmonary veins’ role in as firing triggers, 168, 169c as maintenance sites, 168–172 atrial flutter ablation line for, 113, 119–120, 120c ablation of, 117–121, 234c activation sequence of catheters used to visualize, 114–117, 115c–116c sequential mapping systems used to visualize, 117, 118c atypical, 219 cavotricuspid isthmus, 112c–113c, 113 counterclockwise, 116, 116c, 118c description of, 62 inferior isthmus in, 113–114, 117, 119c isthmus, 112c, 113–114, 117, 119c right atrial isthmus-dependent, 111–121 atrial myocardium anatomy of, 17c, 70c atrioventricular node interface with, 72 left, 81 atrial reentrant tachycardia, 219, 229 atrial septal defects (asd), 139–141, 225c, 226–228

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atrial septum anatomy of, 11c, 18, 83c, 130–137 aortic root and, 131c bundle of His as marker of, 61c–62c, 61–62 conditions that affect, 131 left atrial aspect of, 135 oblique plane of, 131c plane of, 16 right anterior oblique projection of, 130c true, 132, 132c, 139 atrial tachycardia description of, 122 focal ablation of, 200 description of, 123 epicardial origin of, 124, 125c in left atrium, 124, 124c preferential sites for, 123, 123c–124c in right atrium, 123 macroreentrant (AMRT), 127, 127c mechanisms of, 122, 122c substrates of, 122c atrioesophageal fistula, 12, 28 atriofascicular pathway, 96, 96c atrio-Hisian accessory pathways, 96, 96c atrioventricular conduction bundle anatomy of, 198c, 200c location of, 17c, 76 membranous septum and, 17 site of, 201 atrioventricular conduction system, 70–78 atrioventricular groove anatomy of, 94c coronary sinus as marker for, 54–55 description of, 16, 80 left, 23, 88c, 202 right, 23, 84 atrioventricular junctions, 16 accessory bundles, 79, 83 anatomy of, 225c anomalous muscular connections at, 78 attitudinal orientation of, 79, 79c in Ebstein anomaly, 226

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inferior area of, 82 inferior paraseptal region of, 82, 82c left, 83c–84c left anterior oblique projection of, 79c parietal junctions, 79–81 posteroinferior, 162c right, 83c–84c atrioventricular nodal block illustration of, 86c rate of, 104 atrioventricular nodal reentrant tachycardia (AVNRT) coronary sinus size as marker for, 104 description of, 87, 87c narrow QRS complex tachycardia caused by, 104 right atrium and, 103–111 slow/fast, 105c slow/slow, 105c types of, 105c atrioventricular node (AVN) anatomy of, 60c, 62c, 70c, 72, 73c–75c, 78c, 227c artery to (AVNA), 82c atrial myocardium interface with, 72 block of. See atrioventricular nodal block compact, 72, 73c–74c, 106, 188 description of, 61 displaced, 108, 109c histology of, 72 inferior extensions of, 75, 75c, 108c location of, 72 morphology of, 72 right inferior extension of, 108c transitional cells, 72, 73c–74c atrioventricular septal defect, 227c, 228–229 B Bachmann’s bundle (BB), 18, 18c–19c, 68, 157, 159c balloon atrial septostomy, 218 balloon pulmonary vein isolation, 29 bidirectional Glenn repair, 223c, 224 Blalock-Taussig shunt, 215

bradyarrhythmia, 219 bundle branches, 70c–71c, 73c–74c, 76c. See also left bundle branch; right bundle branch bundle of His (HIS) anatomy of, 10c, 60c, 62c, 70c, 187c atrial septum and, 61c–62c, 61–62 catheter positioning in, 53, 53c–54c, 90c, 93c, 109c, 142c, 203c, 237c, 239c location of, 61, 143 penetrating, 70c–71c, 73c–74c, 76, 102 C Cajal cells, 166 cardiac apex, 12, 14, 16 cardiac chambers atria. See atria; left atrium; right atrium description of, 14 ventricles. See left ventricle; right ventricle cardiac conduction system. See conduction system cardiac crux, 24 cardiac magnetic resonance imaging (CMR) description of, 42 of Ebstein anomaly, 225c of left atrium, 208c of tricuspid atresia, 224c cardiac plateau, 34 cardiac resynchronization therapy (CRT), 29 cardiac silhouette, 182 cardiac valves, 14, 15c. See also specific valve cardiac veins anatomy of, 20, 21c great. See great cardiac vein middle, 20, 21c, 22, 55c right, 21c, 22 cardiomyopathy dilated, 210, 210c hypertrophic, 211c, 211–212 inflammatory, 212, 212c right ventricular, 193, 193c catheter(s) accessory pathway insertion site diagnosed using, 88, 88c

atrial flutter activation sequence visualized using, 114–117, 115c–116c in bundle of His, 53, 53c–54c, 90c, 93c, 109c, 203c, 237c, 239c circumferential mapping, 168, 169c–172c, 240 in coronary sinus atrial flutter activation sequence visualized using, 114–117, 115c–116c femoral positioning approach, 58, 59c, 236 fluoroscopy of, 138c imaging of, 53, 53c–54c left atrium size assessments using, 172c left coronary cusp identified using, 204, 204c mitral annulus transseptal mapping, 92 paraseptal accessory pathway mapping, 93 positioning technique for, 56–60 superior positioning approach to, 58, 58c technique for, 56–60 troubleshooting of, 236, 236c in electrophysiological studies, 53, 53c Halo, 88, 115c, 116 left ventricle identification using, 203–204 maneuvering of, 240, 240c pigtail, 188c in right atrium, 110c in tricuspid valve, 60c, 234c troubleshooting of, 240, 240c cavoatrial junctions, 25 cavotricuspid isthmus, 112c–113c, 113 central fibrous body, 72, 73c, 76, 79, 106, 198c central isthmus, 113 Chiari network, 111, 111c cholinergic nerves, 25 circumferential mapping catheters, 168, 169c–172c, 240 circumflex artery (CX), 20, 23c, 24, 37c, 82c, 202, 204 coarctation of the aorta, 218

Index

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complete transposition of the great arteries, 218–221 computed tomography (CT), 7c, 41 conduction system accessory pathways. See accessory pathways arrangement of, 70c atrioventricular, 70–78 atrioventricular junctions. See atrioventricular junctions description of, 68 internodal myocardium of, 68, 68c sinus node. See sinus node congenital heart disease atrial septal defects, 139–141, 225c, 226–228 coarctation of the aorta, 218 complete transposition of the great arteries, 218–221 considerations for, 214 Ebstein anomaly, 225–226 incidence of, 213 patent foramen ovale, 131, 138c, 226– 228, 241c single ventricle, 221–224 tetralogy of Fallot, 215, 216c–217c contraction band necrosis, 206c coronary arteries. See also specific coronary artery anatomy of, 23c, 23–24 left. See left coronary artery left ventricle supply from, 202 right. See right coronary artery selective angiogram of, 37 3D mapping of, 37 coronary artery disease, 206 coronary sinus (CS) anatomy of, 19c, 20, 25c, 55c, 62c, 68c, 71c, 75c, 80c, 82c, 131c–132c, 159c, 161c–162c, 165c, 184c as atrioventricular groove marker, 54–55 catheter in atrial flutter activation sequence visualized using, 114–117, 115c–116c

Index

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femoral positioning approach, 58, 59c, 236c fluoroscopy of, 138c imaging of, 53, 53c–54c left atrium size assessments using, 172c left coronary cusp identified using, 204, 204c mitral annulus transseptal mapping, 92 paraseptal accessory pathway mapping, 93 positioning technique for, 56–60 superior positioning approach to, 58, 58c troubleshooting of, 236, 236c defects in, 140, 140c, 227c distal, 116 diverticulum of, 22, 95, 95c enlargement of, 109c, 141c great cardiac vein and, 20, 156c middle cardiac vein and, 22 muscular floor of, 79 orifice of, 22, 72, 102–103, 141c ostium of, 57c, 104, 107, 108c, 123c, 236c–237c oval fossa and, 101 proximal, 95c, 116 size of, as atrioventricular nodal reentrant tachycardia marker, 104 Thebesian valve in front of, 57c, 101c, 104c 3D mapping of, 44c unroofing of, 140 coronary veins anatomy of, 20, 21c anteroposterior view of, 21c left ventricle, 202 posteroinferior view of, 21c coronary venous system arborization of, 55c description of, 54 left coronary artery and, 56c Coumadin ridge, 29c crista terminalis, 31c, 68c, 98c, 99, 127c cyanosis, in tetralogy of Fallot, 215

D

F

dead-end tract, 78, 78c descending thoracic aorta (DAo), 11c–13c, 242c diaphragm anatomy of, 7c, 8c inferior caval vein and, 12 profile of, 34 diaphragmatic pleura, 12 dilated cardiomyopathy, 210, 210c double inlet ventricle, 222c, 224c

“false tendons,” 77, 77c, 198, 198c, 200c, 209 fasciculoventricular accessory pathways, 96c, 226 fast pathways, of right atrium, 103c, 103–104 fat pads, 24, 25c, 154c fibrous pericardial sac, 12 fibrous pericardium anatomy of, 8c, 9, 28c, 30c, 34 anterior anatomy of, 34 inferior anatomy of, 34 posterior, 13c remnant of, 177c superior anatomy of, 34 fluoroscopy coronary sinus catheter, 138c image integration, 46 left atrial appendage, 160c malignancies caused by, 40 overview of, 39–40 pulmonary veins, 169c right ventricle anatomy on, 188–191 side effects of, 40 triangle of Koch, 106c focal atrial tachycardia (FAT) ablation of, 200 description of, 123 epicardial origin of, 124, 125c in left atrium, 124, 124c preferential sites for, 123, 123c–124c in right atrium, 123 fossa ovale, 48c, 57c, 101c. See also oval fossa fossa ovalis, 218, 242 fossa rim, 135, 137c fossa valve, 135, 136c–137c free wall, of right ventricular outflow tract, 186, 186f

E Ebstein anomaly, 95c, 225–226 echocardiography invasive intracardiac, 48, 48c 2D, 47c electrophysiological (EP) studies anatomy, 52, 52c catheter positioning in, 53, 53c endocardial cushion, 134c endocardial fibroelastosis, 159 epicardial access, 34–36, 35c–36c esophageal plexus, 33 esophagus (ES, ESo) abdominal, 12 anatomy of, 7c, 13c, 28c–29c, 28–29, 131c, 156c anterior wall of, 28c arteries of, 10, 28c course of, 28–29 injury to, 28–29 left atrium and, spatial relationship between, 10, 11c–12c, 28c, 32c, 176, 177c posteroanterior view of, 13c in swallowing, 28 transesophageal echocardiography of, 29c vagus nerves and, 13c Eustachian ridge (ER), 68c, 72, 101c, 103c, 132c, 184c Eustachian valve, 68c, 101c, 101–102, 103c, 111, 113, 132c, 134c–135c

G gadolinium-enhanced magnetic resonance imaging, 208, 208c ganglia, 24 ganglionated plexus, 154, 154c, 176

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ganglionated subplexuses, 24–25 gastric hypomobility, 12 gastric nerve, periesophageal, 33 giant cell myocarditis, 212c great cardiac vein (GCV) anatomy of, 20, 21c, 54, 156c, 161c, 165c, 202 left phrenic nerve and, 22c H Halo catheter, 88, 115c, 116, 160c heart. See also specific anatomy acute margin of, 182 anteroposterior projection of, 7c, 52, 52c atria of. See atria; left atrium; right atrium base of, 9 borders of, 14 conduction system of. See conduction system inferior border of, 14 left anterior oblique projection of, 52, 52c left border of, 14 membranous septum of, 17, 17c position of, 7 right anterior oblique projection of, 52, 52c right border of, 14 trapezoidal shape of, 14, 15c upper border of, 14 venous return of, 54 ventricles of. See left ventricle; right ventricle heart tube, 133c–134c heart valves, 14, 15c. See also specific valve His bundle. See bundle of His hypertrophic cardiomyopathy, 211c, 211–212 hypoplastic left heart syndrome, 222c I idiopathic ventricular tachycardia description of, 209, 209c right ventricle, 191, 192c image integration fluoroscopy systems, 46 3D imaging systems, 45

246

implantable cardioverter-defibrillator (ICD) cardiac magnetic resonance imaging contraindications, 42 leads of, 36c right ventricular angiogram in patient with, 16c inferior aortic recess, 35 inferior caval vein (ICV/IVC) anatomy of, 8c, 13c, 19c, 21c, 25c, 30c, 57c, 75c, 82c, 98c, 141c, 225c, 236c, 241c catheter insertion through, 80c diaphragm and, 12 orifice of, 72, 100c, 111, 112c right phrenic nerve and, 31 inferior isthmus, 113–114, 117, 119c inferior left ventricular vein, 21c inferior papillary muscles, 184 inferior paraseptal region, 82, 82c inferior pyramidal space, 82c inferior sinus venosus defect, 140, 228 inferior vena cava, 131c inflammatory cardiomyopathy, 212, 212c infundibulum, subpulmonary, 185c, 185–187 interatrial bundles, 68 interatrial communications, 139–140, 226, 227c, 229. See also atrial septal defects interatrial groove, 18c, 25 interatrial septum, 61c interauricular band, 157 interstitial fibrosis, 210c interventricular vein, 32, 202 intracardiac echo probe, 49c invasive intracardiac echocardiography (ICE), 48, 48c ischemic heart disease deaths caused by, 206 left ventricle, 206–208 right ventricle, 191 isthmus cavotricuspid, 112c–113c, 113 central, 113

inferior, 113–114, 117, 119c left atrial, 161, 174 mitral, 161c–162c paraseptal, 113, 114c septal, 113–114 J Jatene procedure, 221 jugular sheath, 235c K Koch’s triangle, 72, 76, 97, 106c, 107. See also triangle of Koch L lateral isthmus, 31, 174 lateral pulmonary vein, 11c leads, left ventricular veins for placement of, 20 left anterior descending coronary artery (LAD) anatomy of, 22c–23c, 202 3D mapping of, 37c left anterior oblique (LAO) projection of atrial septum, 62c of atrioventricular junctions, 79c of catheter positioning, 53c–54c of great cardiac vein-coronary sinus channel, 54c, 55 of heart, 52, 52c of left coronary artery and coronary venous system, 56c of right ventricle, 188, 188c–189c of transseptal puncture, 147 left atrial appendage (LAA) anatomy of, 16c, 18c, 21c–22c, 130c, 137c, 155c, 159–161, 165c, 237c circumferential mapping catheters, 170c Coumadin ridge, 29c description of, 9 flow measurements in, 10 fluoroscopic views of, 160c left atrium and, 159 left phrenic nerve and, 32 ostium of, 125c

3D mapping of, 44c transesophageal echocardiography of, 11c 2D transesophageal image of, 47c velocity measurements in, 10 left atrial ridge, 164 left atrium (LA) ablation of, 174, 176 anatomy of, 21c, 25c, 30c, 53c, 62c, 75c, 92c, 108c, 113c, 126c, 141c, 174, 175c, 198c anterior wall of, 19c, 155 body of, 130, 130c, 154, 154c, 157, 173 cardiac magnetic resonance imaging of, 42c, 208c coronary sinus catheter assessment of, 172c descending thoracic aorta and, 11c–12c epicardial aspect of, 154c esophagus and, spatial relationship between, 10, 11c–12c, 28c, 32c, 176, 177c focal atrial tachycardia in, 124, 124c frontal silhouette of, 14 inferior wall of, 19c interatrial region of, 154c, 159c isthmus of, 161, 174 left atrial appendage and, 159 location of, 16, 16c–17c, 173, 173c mitral valve junction with, 62c musculature of, 158, 166 perforation sites in, 241, 241c posterior wall of, 11c, 16, 158c right atrium connection to, 18, 18c, 173 rotational angiography of, 43c septum of, 130–137. See also atrial septum size assessments, 172c surgical access to, 126c 3D mapping of, 49c three-dimensional (3D) imaging of, 10c, 46c transesophageal echocardiography of, 11c 2D transesophageal image of, 47c venoatrial junction, 166 venous component of, 161

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vestibule of, 161, 161c, 165c walls of, 155–158, 164–166, 165c left bundle branch (LBB) anatomy of, 70c–71c, 73c–74c, 76c, 78c, 200c–201c fascicles of, 76–77, 209 left coronary aortic sinus, 25c, 199 left coronary artery (LCA) anatomy of, 23, 23c, 24, 187c, 197c coronary venous system and, 56c course of, 23–24 left coronary cusp, 204, 204c left gastric vessels, 12, 13c left inferior pulmonary vein, 8c–9c, 12c, 19c, 25c, 130c, 161c, 165c left phrenic nerve anatomy of, 8c–9c, 20, 29, 31–32 course of, 32 great cardiac vein and, 22c injury to, 29 left pulmonary artery, 242c left pulmonary venous recess, 35 left recurrent laryngeal nerve, 33–34 left-sided accessory pathways, 90–92 left superior caval vein anatomy of, 20 persistent, 72, 237, 237c left superior pulmonary vein (LSPV) anatomy of, 8c–9c, 11c–12c, 18c–19c, 20, 25c, 130c, 149, 157c, 165c, 167c, 241c–242c “big loop” approach to, 175c, 238 3D mapping of, 44c left superior vena cava, 109c left upper pulmonary vein, 161c left vagus nerve, 9c, 13c left ventricle (LV) ablation of, 195, 205c anatomy of, 21c, 25c, 52c, 75c–76c, 84c, 132c, 196–202, 211c anterior wall of, 24 apex of, 194c, 198 atrioventricular conduction bundle, 198c

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cardiac magnetic resonance imaging of, 208c catheter identification of, 203–204 conduction tissues of, 201 coronary artery supply of, 202 coronary veins of, 202 description of, 9 dilatation of, 210c dilated cardiomyopathy of, 210, 210c hypertrophic cardiomyopathy of, 211c, 211–212 hypertrophy of, 210c hypoplasia of, 222c inferior wall of, 23 inlet portion of, 194c ischemic heart disease of, 206–208 left border of heart created by, 14 location of, 16 magnetic resonance imaging of, 208c mapping of, 195, 205, 205c muscular wall of, 198 outlet portion of, 194c retrograde mapping approach to, 205, 205c right ventricle and, spatial relationship between, 194c rotational angiography of, 43c septal portion of, 194c substrate map of, 207c 3D mapping of, 207 trabeculations in, 198, 198c transesophageal echocardiography of, 11c transseptal mapping approach to, 205, 205c ventricular tachycardia of, 209 wall of, 194c, 211 left ventricular angiogram, 203c left ventricular outflow tract (LVOT) anatomy of, 16c, 17, 185, 194, 194c, 198 obstruction of, 218, 221 ligament of Marshall, 166, 202 lung left, 8c, 13c right, 13c lymph nodes, 10

M magnetic resonance imaging description of, 42 of Ebstein anomaly, 225c of left atrium, 208c of tricuspid atresia, 224c manubrium, 7c mapping. See also 3D mapping atrial flutter activation sequence imaged using, 117, 118c left ventricle, 195, 205, 205c pulmonary valve, 188 right ventricular outflow tract, 188 ventricular septum, 191 marginal veins acute, 23c imaging of, 21c, 22 obtuse, 21c–23c, 55c, 202 medial papillary muscle, 183c–184c, 184 mediastinum anatomy of, 7c extracardiac nerves from, 24 middle, 7c superior, 7c membranous septum, 17, 17c, 68c, 71c, 80c, 102c, 114c, 183c–184c, 184, 200c middle cardiac vein (MCV), 20, 21c, 22, 55c middle mediastinum, 7c mitral annulus (MA) anatomy of, 49c, 85c description of, 55, 81 displacement of, 240c focal atrial tachycardia origins, 124c hinge of, 197 transseptal mapping of, 92, 92c–93c mitral isthmus, 161c–162c mitral valve (MV) anatomy of, 21c, 125c, 126c, 132c, 137c, 157c, 162c, 165c, 184c, 242c animal specimens of, 77c anterior leaflets of, 81c, 197c, 198–199 aortic valve and, fibrous continuity between, 81c, 197c

leaflets of, 81c, 92, 197, 197c, 198 left atrial junction with, 62c location of, 15c, 17c orifice of, 14, 55, 81 posterior leaflets of, 197c, 198 transesophageal echocardiography of, 11c moderator band (MB), 185, 191 monomorphic ventricular ectopy, 204c monomorphic ventricular tachycardia, 199 mustard procedure, 218c–220c myocardial infarction, 207c–208c myocardial sleeve, 164c, 166, 167c myocardial strands, 167c myocarditis, 212, 212c myocardium atrial, 17c, 70c, 72, 81 internodal, 68, 68c ventricular, 17c, 81, 212 myocytes in Bachmann’s bundle, 18 infarction effects on, 206 vacuolated, 206c N narrow QRS complex tachycardia, 104 nodal artery, 69, 69c nodofascicular accessory pathways, 96c nodoventricular accessory pathways, 96c, 226 noncoronary aortic sinus, 200, 200c noncoronary cusp, 143c O oblique left atrial vein, 20 oblique pericardial sinus, 8c, 13c, 35, 176, 177c oblique vein, 166 obtuse marginal vein (OMV), 21c–23c, 55c, 202 Ortner syndrome, 33 ostium primum atrial septal defect of, 228 description of, 133c ostium secundum, 133c outlet septum, 216c, 218c

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oval fossa. See also fossa ovale anatomy of, 68, 68c, 100c, 101, 112c, 131c, 157c–158c, 236c aneurysmal valve of, 132c probe patent, 137c–138c, 137–138 transillumination of, 135c P P wave, 123 papillary muscles anatomy of, 77c, 92c, 198 anterior, 184–185 anterolateral, 197c catheter entrapment in, 240c inferior, 184 insertion of, 198 medial, 183c–184c, 184 posteromedial, 197c paraseptal accessory pathways, 93 paraseptal isthmus, 113, 114c paraseptal wall, of right ventricular outflow tract, 186, 186f parietal atrioventricular junction, 197 parietal junctions, 79–81 parietal pericardium, 34. See also fibrous pericardium paroxysmal tachycardia, 86 patent foramen ovale (PFO), 131, 138c, 226–228, 241c pectinate muscles, 68c, 100, 114 perforation left atrium, 241, 241c transseptal puncture, 242, 242c pericardial cavity, 34–35 pericardial fluid, 36 pericardial sac anteroposterior view of, 13c description of, 9 fibrous, 12 pericardial sinus oblique, 8c, 13c, 35, 176, 177c transverse, 16 pericardial space, 34–36

248

pericardium fibrous. See fibrous pericardium function of, 9 serous, 8c, 34 periesophageal gastric nerve, 33 periesophageal plexus, 10, 13c periesophageal vagus nerve, 33 perimembranous ventricular septal defect, 216c persistent left superior caval vein (LSVC), 72, 237, 237c phrenic nerves anatomy of, 9c course of, 10, 10c left. See left phrenic nerve right, 9c, 30c, 31, 32c, 173–174 right superior pulmonary vein and, 10c, 30c, 174 superior vena cava and, 10c three-dimensional (3D) imaging of, 10c pigtail catheter, 188c pleura, 9 posterior descending coronary artery, 20, 23c, 23–24, 82c posterior esophageal plexus, 33 posterior fibrous pericardium, 13c posterior septum, 79 posteroseptal accessory pathways, 94c probe patent oval fossa, 137c–138c, 137–138, 228. See also patent foramen ovale pulmonary artery (PA) anatomy of, 52c cardiac magnetic resonance imaging of, 42c puncture of, 242c rotational angiography of, 43c pulmonary atresia, 222c pulmonary infundibulum, 199 pulmonary trunk anatomy of, 13c, 16c, 17, 23c, 160c, 242c cardiac magnetic resonance imaging of, 42c pulmonary valve anatomy of, 60c, 156c, 189c, 199c, 242c

animal specimens of, 77c fluoroscopic imaging of, 188, 189c location of, 14, 15c plane of, 16c, 187 semilunar leaflets of, 186c, 187 sequential mapping of, 188 subpulmonary infundibulum, 185, 185c pulmonary veins (PV) ablation contraindications in, 174 angiography of, 169, 238c–239c atrial fibrillation and, 168–172, 169c circumferential mapping catheters in, 170c, 172c fluoroscopy of, 169c left inferior, 8c–9c, 12c, 19c, 25c, 130c, 161c, 165c left superior. See left superior pulmonary vein ostia of, 163c, 168 right inferior. See right inferior pulmonary vein right superior. See right superior pulmonary vein septal, 169, 239c 3D imaging of, 46c pulmonary venous atrium, 220c pulmonary venous recesses, 35 Purkinje fibers, 70c, 77, 77c, 201c, 209 Q Q-tip sign, 164 R Rastelli procedure, 221 recurrent laryngeal nerve palsy, 33 reentrant tachycardia, 87, 87c right anterior oblique (RAO) projection of atrial septum, 130c of catheter positioning, 53c–54c of heart, 52, 52c of left coronary artery and coronary venous system, 56c of right ventricle, 188, 188c–189c of transseptal puncture, 147

right atrial appendage (RAA) anatomy of, 18c, 98c, 99, 100c, 103c, 130c, 155c, 157c apical portion of, 100, 100c right atrial atriotomy, 31c right atrial isthmus-dependent atrial flutter, 111–121 right atrium (RA) anatomy of, 21c, 25c, 30c, 52c–53c, 75c, 80c, 99–103, 108c, 125c, 126c, 141c, 154c, 182c, 217c anterior wall of, 125c atrioventricular nodal reentrant tachycardia and, 103–110 cardiac magnetic resonance imaging of, 42c catheter positioning in, 110c Chiari network in, 111, 111c embryonic septation of, 133c–134c endocardial anatomy of, 69c epicardial anatomy of, 69c, 98c Eustachian valve, 101c, 101–102, 103c, 111 fast pathways of, 103c, 103–104 flutter of, se atrial flutter focal atrial tachycardia in, 123 free wall of, 62 Halo catheter in, 115c, 116 inferior wall of, 19c intercaval area of, 19c lateral wall of, 100 left atrium connection to, 18, 18c, 173 location of, 16, 16c–17c middle cardiac vein entry into, 22 musculature of, 99–100 pectinate muscles of, 100, 100c, 114 posterior wall of, 101 right border of heart created by, 14 sagittal bundle of, 100 slow pathway of anatomy of, 104, 106, 107c–108c displacement of, 109c terminal crest of, 99–101 three-dimensional (3D) imaging of, 10c, 46c triangle of Koch. See triangle of Koch or Koch’s triangle

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tricuspid valve, 62c vestibule of, 98c, 99–100, 100c, 103, 108c, 112c right brachiocephalic vein, 31 right bundle branch (RBB) anatomy of, 70c–71c, 73c–74c, 76c, 77, 78c block of, 221 right cardiac vein, 21c, 22 right coronary aortic sinus, 199 right coronary arterial dominance, 23 right coronary artery (RCA) anatomy of, 23, 23c, 62c, 82c, 88c, 112c, 182c, 187c origin of, 16c proximal portion of, 88c 3D mapping of, 37c right inferior pulmonary vein anatomy of, 8c–9c, 11c, 19c, 25c, 30c, 32c, 48c, 130c, 135c, 155c, 157c, 238, 241c round projection of, 169c 3D mapping of, 44c, 49c right phrenic nerve, 9c, 29, 30c, 31, 32c, 173–174 right pulmonary artery, 17 right pulmonary venous recess, 35 right-sided accessory pathways, 89, 89c right superior pulmonary vein (RSPV) anatomy of, 8c–9c, 18c–19c, 25c, 32c, 130c, 135c, 140c, 154c–155c, 157c, 167c, 241c phrenic nerve and, 10c, 30c, 174 3D mapping of, 44c, 49c right vagus nerve, 9c right ventricle (RV) anatomy of fluoroscopic, 188–191 general, 21c, 25c, 52c, 75c–76c, 84c, 88c, 103c, 131c–132c, 182–187, 211c angiogram of, 16c body of, 185, 188, 190 cardiac magnetic resonance imaging of, 42c, 208c

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cardiomyopathy of, 193, 193c hypertrophied wall of, 216c inferior border of heart created by, 14 inferior wall of, 22 inlet portion of, 183 in left anterior oblique projection, 188, 188c–189c left ventricle and, spatial relationship between, 194c location of, 16 morphology of, 182, 182c perforation of, 190 in right anterior oblique projection, 188, 188c–189c roof of, 185 supraventricular crest of, 79, 183c, 185 3D mapping of, 190c trabecular portion of, 184–185 right ventricular apex (RVA) anatomy of, 138c catheter in, 116 fluoroscopic imaging of, 190 right ventricular catheter, 36c right ventricular inflow tract, 198c right ventricular outflow tract (RVOT) anatomy of, 16c, 16–17, 24, 103c, 185, 198c–199c anterior view of, 185c free wall of, 186, 186f, 189 mapping of, 188–189 obstruction of, 215 paraseptal wall of, 186, 186f posterior portion of, 189 sequential mapping of, 188–189 in tetralogy of Fallot, 216c 3D mapping of, 192c ventricular tachycardia arising from, 191 right ventricular tachycardia, 191, 192c rotational angiography, 43 S “sandwich” mapping, 33c, 34 sarcoid heart disease, 212c secundum atrial septal defect, 226

selective angiogram, 37 semilunar leaflets, of pulmonary valve, 186c, 187 senning procedure, 219 septal defects atrial, 139–141, 225, 225c, 226–228 atrioventricular, 227c, 228–229 ventricular. See ventricular septal defects septal isthmus, 113–114 septal pulmonary veins, 169, 239c septoatrial bundle, 158, 158c septomarginal trabeculations (SMT), 183c, 185 septoparietal trabeculations, 215, 216c septopulmonary bundle, 158, 158c septum primum, 132, 133c septum secundum, 132, 133c sequential mapping atrial flutter activation sequence imaged using, 117, 118c pulmonary valve, 188 right ventricular outflow tract, 188 ventricular septum, 191 serous pericardium anatomy of, 8c parietal layer of, 34 single ventricle, 221–224 sinotubular junction, 23 sinus node (SN) anatomy of, 68c–70c, 69, 99 borders of, 70 head of, 69, 69c innervation of, 69 location of, 18c morphology of, 69 tail of, 69, 69c sinus node artery, 24 sinus of Valsalva, 23, 199 sinus septum, 101 sinutubular junction, 199c slow pathway, of right atrium anatomy of, 104, 106, 107c–108c displacement of, 109c

small cardiac vein, 20, 21c subacute haemorrhagic infarction, 206c subclavian sheath, 235c sub-Eustachian pouch, 113c–114c sub-Eustachian sinus, 114 subpulmonary infundibulum, 185c, 185–187, 199c, 200 subxiphoid space, 35 sulcus terminalis, 99 superior aortic recess, 35 superior caval vein (SCV/SVC) anatomy of, 8c, 13c, 18c–19c, 25c, 30c, 98c, 100c, 133, 136c, 138c, 140c–141c, 157c, 217c, 228, 236c description of, 9 orifice of, 57f, 69c, 140, 227c superior cavoatrial junction, 31 superior mediastinum, 7c superior sinus venosus defect, 140c, 227c, 228 superior vena cava. See also superior caval vein (SCV/SVC) anatomy of, 131c, 135c guidewire in, 144c phrenic nerve and, 10c supraventricular crest, 23, 183c, 185 supraventricular tachycardia (SVT), 87 T tachycardia atrial. See atrial tachycardia atrial reentrant, 219, 229 atrioventricular nodal reentrant. See atrioventricular nodal reentrant tachycardia focal atrial. See focal atrial tachycardia narrow QRS complex, 104 right ventricular, 191, 192c ventricular. See ventricular tachycardia tendon of Todaro, 68c, 70c–71c, 72, 102, 102c, 132c terminal crest (TC), 68, 68c–69c, 99–101, 113, 113c, 135c tetralogy of Fallot, 215, 216c–217c

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Thebesian valve, 57c, 95c, 103, 104c, 236 Thebesian veins, 20 thoracic aorta, descending, 11c–13c, 242c thoracic vertebrae, 9 thorax anteroposterior projection of, 7c computed tomography of, 7c 3D imaging cardiac magnetic resonance imaging, 42 computed tomography, 41 description of, 41 image integration, 45 rotational angiography, 43 3D mapping integration with, 46 3D mapping atrial flutter, 117, 118c description of, 44 example of, 44c left atrium, 49c left ventricle, 207 right coronary artery, 37c right ventricle, 190c right ventricular outflow tract, 192c 3D image integration with, 46 total cavopulmonary connection, 223c, 224 trachea (Tr) anatomy of, 7c, 12c bifurcation of, 16 transannular patch, 215, 217c transesophageal echocardiography (TEE/TOE) esophagus, 29c left atrial appendage, 11c mitral valve, 11c

250

transmural infarcts, 207 transposition of the great arteries, 218–221 transseptal puncture landmarks for, 142–143 left anterior oblique projection of, 147, 150c–151c left ventricular mapping, 205 perforation during, 242, 242c right anterior oblique projection of, 147, 150c–151c second, 149, 150c–151c site for, 147c step-by-step technique for, 144–148, 144c–147c, 149c–151c transseptal sheath (TS), 11c, 144c, 146, 149, 238c, 242 transverse pericardial sinus, 8c, 16, 35, 133, 176, 177c triangle of Koch. See also Koch’s triangle anatomy of, 68c, 106 borders of, 72, 102, 102c description of, 17, 70 fluoroscopy of, 106c tricuspid annulus accessory pathway insertion along, 89, 90c anatomy of, 80c, 85c, 106c, 108c, 184, 184c, 224c anterolateral aspect of, 235, 236c description of, 14, 17 difficulty in reaching, 234, 234c–235c mapping of, 190 superior approach to, 90c upper free wall quadrant of, 89 tricuspid atresia, 221, 222c, 224c

tricuspid valve (TV) anatomy of, 21c, 76c, 82c, 100c–101c, 103c, 112c, 125c, 132c, 137c anterosuperior leaflet of, 184 catheter positioning across, 60c hinge line of, 183 imperforate, 222c leaflets of, 68c, 72, 102, 183, 225c location of, 15c, 17c orifice of, 14, 55, 182c, 225c septal leaflet of, 68c, 72, 102, 183, 225 vestibule of, 80 trigones, 197c, 198 troubleshooting catheter maneuvering, 240, 240c coronary sinus, 236, 236c persistent left superior caval vein, 72, 237, 237c pulmonary vein angiography, 238, 238c–239c tricuspid annulus, 234–235, 235c–236c 2D Digital Imaging and Communications in Medicine (DICOM), 45 V vagus nerves esophagus and, 13c left, 9c, 13c periesophageal, 10, 13c, 33 right, 9c valve of Vieussens, 20, 21c vein of Galen, 22 vein of Marshall, 20, 21c, 158, 165c, 166, 202, 237 venoatrial junction, 166

ventricles. See left ventricle; right ventricle ventricular arrhythmias ischemic heart disease, 191 right ventricular tachycardia, 191, 192c ventricular ectopy, 204c ventricular myocardium, 17c, 81, 212 ventricular preexcitation, 86, 86c ventricular septal defects (VSD) aortic root, 216c complete transposition of the great arteries and, 218 muscular, 216c perimembranous, 216c in tetralogy of Fallot, 215 transannular patch for, 217c, 221 ventricular septum anatomy of, 17c, 61c, 78c, 184c basal portion of, 14 blood supply to, 202 curvature of, 16 mapping of, 191 ventricular tachycardia (VT) in dilated cardiomyopathy, 210 idiopathic, 209, 209c left ventricle, 209 monomorphic, 199 ventriculo-infundibular fold, 183c, 199 viral myocarditis, 210c W Waterston’s groove, 157 wide-complex QRS antidromic atrioventricular reentrant tachycardia, 87, 87c Wolff-Parkinson-White (WPW) syndrome, 78, 86–87

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