catheter ablation of atrial fibrillation · 2016-08-12 · 14 catheter ablation of atrial...

Catheter Ablation ofAtrial Fibrillation

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Catheter Ablation of AtrialFibrillationEDITED BY

Etienne AliotMichel HaïssaguerreWarren M. Jackman

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© 2008 by Blackwell PublishingBlackwell Futura is an imprint of Blackwell Publishing

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Catheter ablation of atrial fibrillation / edited by Etienne Aliot, Michel Haissguerre, Warren M. Jackman.p. ; cm.

Includes bibliographical references.ISBN 978-1-4051-6349-1 (Hbk trade version)978-1-4051-8665-0 (Customised version, not for trade sale)

1. Catheter ablation. 2. Atrial fibrillation – Surgery. I. Aliot, Etienne. II. Ha?ssaguerre, Michel. III. Jackman, Warren M.

[DNLM: 1. Atrial Fibrillation – surgery. 2. Atrial Fibrillation – therapy. 3. Catheter Ablation – methods. WG 330 C3628 2008]

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Contributors, vii

Introduction, xi

Part 1 Fundamental concepts of atrialfibrillation

1 Anatomy of the left atrium relevant to atrialfibrillation ablation, 3José Angel Cabrera, Jerónimo Farré, Siew Yen Ho, Damián Sánchez-Quintana

2 Mechanisms and significance of fractionatedelectrograms recorded during atrial fibrillation, 32Sander Verheule, Els Tuyls, Natasja de Groot,Maurits Allessie

3 Computer simulation studies of atrialfibrillation, 43Nathalie Virag, Lam Dang, Patrick Ruchat,Juerg Schlaepfer, Lukas Kappenberger

4 Experimental and theoretical insights intofundamental mechanisms of antiarrhythmicdrug actions on atrial fibrillation: prospects for improved pharmacotherapy, 52Stanley Nattel

5 Mechanisms of atrial fibrillation in animals and humans, 61Omer Berenfeld, Jérôme Kalifa, José Jalife

6 Three-dimensional images in catheter ablation of atrial fibrillation, 75Hsuan-Ming Tsao, Mei-Han Wu, Shih-AnnChen

7 Signal processing of fibrillatory electrograms, 85Thomas H. Everett, IV, Jeffrey E. Olgin

Part 2 Practical approaches in atrialfibrillation

8 Emerging technologies in the treatment ofatrial fibrillation, 105Matthew Wright, Christian de Chillou, EtienneAliot, D. Wyn Davies

9 Techniques targeting the pulmonary veins, 117Sabine Ernst, Feifan Ouyang, Matthias Antz,Julian K. R. Chun, Dietmar Bänsch, Karl-Heinz Kück

10 Techniques of linear lesion for atrial fibrillation ablation, 124Mélèze Hocini, Kang Teng Lim, PrashanthanSanders, Pierre Jaïs, Mark D. O’Neill, YoshihideTakahashi, Anders Jönsson, Seiichiro Matsuo,Sébastien Knecht, Leonardo Arantès, Jacques Clémenty, Michel Haïssaguerre

11 Ablation strategies in paroxysmal atrialfibrillation, 136Isabel Deisenhofer, Claus Schmitt

12 Ablation strategies in chronic atrial fibrillation, 163Mark D. O’Neill, Kang Teng Lim, Pierre Jaïs,Mélèze Hocini, Yoshihide Takahashi, AndersJönsson, Frédéric Sacher, Prashanthan Sanders,Sathish Kodali, Leonardo Arantès, SeiichiroMatsuo, Sébastien Knecht, Thomas Rostock,Martin Rotter, Jacques Clémenty, George J.Klein, Michel Haïssaguerre

Contents

v

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vi Contents

Part 3 Special challenges in atrialfibrillation

13 Diagnostic algorithm of atrial tachycardiafollowing atrial fibrillation ablation:importance of localized reentries, 193Pierre Jaïs, Sébastien Knecht, Seiichiro Matsuo,Mark D. O’Neill, Rajesh Subbiah, LeonardoArantès, Kang Teng Lim, Nicolas Derval,Frédéric Sacher, Antoine Deplagne, PierreBordachar, Mélèze Hocini, Jacques Clémenty,Michel Haïssaguerre

14 Catheter ablation of atrial fibrillation inpatients with heart failure, 212Ibrahim Abu Romeh, Mohammed Nasir Khan,Andrea Natale

15 Morbidity and mortality of ablation versusdrugs, 219Carlo Pappone, Vincenzo Santinelli

16 Atrial mechanical function after atrialfibrillation ablation, 225Prashanthan Sanders, Pierre Jaïs, Glenn D.Young, Frédéric Sacher, Martin Rotter, MélèzeHocini, Li-Fern Hsu, Martin K. Stiles, BobbyJohn, Dennis H. Lau, Yoshihide Takahashi,Thomas Rostock, Pawel Kuklik, LorraineMackenzie, Scott Willoughby, MichelHaïssaguerre

17 Surgery for atrial fibrillation: from scalpel tocatheter . . . and back? 233Fiorenzo Gaita, Antonio Montefusco, DomenicoCaponi, George J. Klein

18 Electrogram-guided approach to ablation ofatrial fibrillation, 240David J. Wilber, Joseph Akar, Peter Santucci,Neil Brysiewicz

Index, 257

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Joseph Akar, MD, PHDCenter for Heart and Cardiovascular Medicine, Loyola University Health System, Maywood, Illinois, USA

Etienne Aliot, MDDepartment of Cardiology,University of Nancy,Vandoeuvre les Nancy,France

Maurits Allessie, MD, PhDDepartment of Physiology,Cardiovascular Research Institute Maastricht (CARIM),Maastricht University, Maastricht, The Netherlands

Matthias Antz, MDOberärztin Magn. Navigation,Hanseatic Heart Center St. Georg,Hamburg, Germary

Leonardo Arantès, MDHôpital Cardiologique du Haut-Lévêque and theUniversité Victor Segalen Bordeaux II,Bordeaux, France

Dietmar Bänsch, MDOberärztin Magn. Navigation,Hanseatic Heart Center St. Georg,Hamburg, Germany

Omer Berenfeld, PhDDepartment of Pharmacology and the Institute forCardiovascular Research,SUNY Upstate Medical University,Syracuse, New York, USA

Pierre Bordachar, MDHôpital Cardiologique du Haut-Lévêque and theUniversité Victor Segalen Bordeaux II,Bordeaux, France

Neil Brysiewicz, BSECenter for Heart and Cardiovascular Medicine, Loyola University Health System, Maywood, Illinois, USA

José Angel Cabrera, MD, PhDArrhythmia Unit, Hospital Quiron-Madrid,Universidad Europea de Madrid, Madrid, Spain

Domenico Caponi, MDCardinal Massaia Hospital,Asti, AT Italy

Shih-Ann Chen, MDDivision of Cardiology and Cardiovascular Research Center, National Yang-Ming University, School of Medicine and Taipei Veterans General Hospital, Taiwan

Julian K.R. Chun, MDOberärztin Magn. Navigation, Hanseatic Heart Center St. Georg, Hamburg, Germany

Jacques Clémenty, MDHôpital Cardiologique du Haut-Lévêque and theUniversité Victor Segalen Bordeaux II,Bordeaux, France

Lam Dang, PhDSwiss Federal Institute of Technology,Lausanne, Switzerland

D. Wyn Davies, MD, FRCPSt. Mary’s Hospital,Waller Department of Cardiology,London, UK

Christian de Chillou, MD, PHDDepartment of Cardiology,Nancy University Hospital,Nancy, France

Natasja de Groot, MD, PHDDepartment of Physiology,Cardiovascular Research Institute Maastricht (CARIM),Maastricht University, Maastricht,The Netherlands

Contributors

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viii Contributors

Isabel Deisenhofer, MDDeutsches Herzzentrum München,Klinik an der Technischen,Universität München,München, Germany

Antoine Deplagne, MDHôpital Cardiologique du Haut-Lévêque and the UniversitéVictor Segalen Bordeaux II,Bordeaux, France

Nicolas Derval, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II,Bordeaux, France

Sabine Ernst, MD, PHDImperial College,National Heart and Lung Institute,Royal Brompton and Harefield Hospital,London, UK

Thomas H. Everett, IV, PhDDivision of Cardiology and the Cardiovascular Research Institute, University of California San Francisco, San Francisco,California, USA

Jerónimo Farré, MD, PhD, FESCDepartment of Cardiology,Fundación Jiménez Díaz-Capio, Universidad Autónoma de Madrid, Madrid, Spain

Fiorenzo Gaita, MDDepartment of Cardiology, Cardinal Massaia Hospital, Asti, AT, Italy

Michel Haïssaguerre, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Siew Yen Ho, PhD, FRCPathNational Heart and Lung Institute, Imperial College and the Royal Brompton and Harefield NHS Trust, London, UK

Mélèze Hocini, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Li-Fern Hsu, MB, BSHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Pierre Jaïs, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

José Jalife, MDDepartment of Pharmacology and Institute forCardiovascular Research, SUNY Upstate Medical University, Syracuse, New York, USA

Bobby John, MDCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Anders Jönsson, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Jérôme Kalifa, MD, PhDDepartment of Pharmacology and Institute forCardiovascular Research, SUNY Upstate Medical University, Syracuse, New York, USA

Lukas Kappenberger, MDCardioMet, Centre Hospitalier Universitaire Vaudois,Lausanne, Switzerland

Mohammed Nasir Khan, MDCardiovascular Associates, Elk Grove Village, Illinois, USA

George J. Klein, MDUniversity of Western Ontario, University Hospital,London, Ontario, Canada

Sébastien Knecht, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Sathish Kodali, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Karl-Heinz Kück, MDOberärztin Magn. Navigation, Hanseatic Heart Center St. Georg, Hamburg, Germany

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Contributors ix

Pawel Kuklik, BSCCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Dennis H. Lau, MB, BSCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Kang Teng Lim, MB, BSHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Lorraine Mackenzie, PHDCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Seiichiro Matsuo, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Antonio Montefusco, MDCardinal Massaia Hospital, Asti, AT, Italy

Andrea Natale, MDAdjunct Professor, Stanford University, Palo Alto, California, USA

Stanley Nattel, MDDepartment of Medicine and Research Center, MontrealHeart Institute and Université de Montréal and Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada

Jeffrey E. Olgin, MDDivision of Cardiology and the Cardiovascular ResearchInstitute, University of California San Francisco, San Francisco, California, USA

Mark D. O’Neill, MB, BCH, DPHILHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Feifan Ouyang, MDOberärztin Magn. Navigation, Hanseatic Heart Center St. Georg, Hamburg, Germany

Carlo Pappone, MD, PHD Department of Cardiology, Electrophysiology and Cardiac Pacing Unit, San Raffaele Scientific Institute, Milan, Italy

Ibrahim Abu Romeh, MDHeart Failure and Transplant Fellow,University of Utah,Utah, USA

Thomas Rostock, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Martin Rotter, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Patrick Ruchat, MDService de Chirurgie Cardio-Vasculaire, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Frédéric Sacher, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Damián Sánchez-Quintana, MD, PhDDepartment of Human Anatomy and Cell Biology, Faculty of Medicine, University of Extremadura, Badajoz, Spain

Prashanthan Sanders, MB, BS, PHDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France and Cardiovascular Research Centre,Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Vincenzo Santinelli, MDDepartment of Cardiology, Electrophysiology and Cardiac Pacing Unit, San Raffaele Scientific Institute, Milan, Italy

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x Contributors

Peter Santucci, MDCenter for Heart and Cardiovascular Medicine, Loyola University Health System, Maywood, Illinois, USA

Juerg Schlaepfer, MDService de Cardiologie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Claus Schmitt, MDMedizinischen Klinik, Klinikum Karlsruhe, Karlsruhe, Germany

Martin K. Stiles, MB, CHBCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Rajesh Subbiah, BSC(MED), MB, BS, PHDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Yoshihide Takahashi, MDHôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France

Hsuan-Ming Tsao, MDDepartment of Internal Medicine, National Yang-MingUniversity Hospital, Taiwan

Els Tuyls, MScDepartment of Physiology, Cardiovascular Research Institute Maastricht (CARIM),Maastricht University, Maastricht, The Netherlands

Sander Verheule, PhDDepartment of Physiology, Cardiovascular ResearchInstitute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands

Nathalie Virag, PhDMedtronic Europe, Tolochenaz, Switzerland

David J. Wilber, MDCenter for Heart and Cardiovascular Medicine, Loyola University Health System, Maywood, Illinois, USA

Scott Willoughby, PHDCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

Matthew Wright, MBBS, PHDSt. Mary’s Hospital,Waller Department of Cardiology,London, UK

Mei-Han Wu, MDDivision of Radiology, National Yang-Ming University, School of Medicine and Taipei Veterans General Hospital,Taiwan

Glenn D. Young, MB, BSCardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia

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Atrial fibrillation (AF) has long been a field forexperimental, pharmacological, and clinical inves-tigations. After initial surgical attempts to cure AF using multiple incisions, the observation thatthe pulmonary veins were mainly involved in thegenesis of AF has promoted the use of cathetertechniques for curative approaches.

This book provides a collective text that inte-grates advances in basic and clinical electrophysio-logy that have emerged in the last 10 years. Our goalis to produce a treatise that electrophysiologists,allied healthcare professionals, and industry per-sonnel will use as a guide to assist in patient care, tostimulate research projects, and to continue theremarkable advances in the treatment of AF.

A major message appears to be the complexity ofunderlying factors initiating and perpetuating AF,and the need for combined approaches to involvethese different mechanisms. Another message is toacknowledge the limitations of present technolo-gies which, despite achieving dramatic terminationof most AF, require additional interventions for tissue recovery or new substrate.

The book is divided into several parts. The firstpart (Chapters 1–7) is devoted to the fundamental

concepts of AF, origin of signals, computer simula-tion, and updated reviews of ablation tools. Theanatomy chapter is richly illustrated by numeroushigh quality images. This information is necessaryfor appropriate clinical practice. The second part(Chapters 8–12) provides the present practicalapproaches to the ablation of specific targets in thefibrillating atria including pulmonary veins, frag-mented electrograms, and linear lesions and detailsthe strategies in paroxysmal or chronic AF or facingleft atrial tachycardias. The final part (Chapters13–18) addresses the special challenge of heart failure patients, the impact of ablation on mortal-ity, atrial mechanical function, and lessons fromsurgical AF ablation.

Each chapter is written by experienced and internationally recognized authors, most being theleading experts in this field.

We hope that this book may become a referencetext for many and will be followed by future editions to provide up to date information in thisrapidly developing area.

Etienne AliotMichel HaïssaguerreWarren M. Jackman

Introduction

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PART 1

Fundamentalconcepts of atrialfibrillation

1

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Introduction

Atrial fibrillation (AF) is an arrhythmia most likelydue to multiple etiopathogenic mechanisms. In spiteof a still incomplete understanding of the anatomo-functional basis for the initiation and maintenanceof AF, various radiofrequency catheter ablation(RFCA) techniques have been shown to modify thesubstrate of the arrhythmia and/or its neuroveget-ative modulators, achieving in a high proportion of cases a sustained restoration of a stable sinusrhythm [1–26]. Catheter ablation techniques inpatients with AF have evolved from an initialapproach focused on the pulmonary veins (PVs)and their junctions with the left atrium (LA), to a more extensive intervention mainly, but notexclusively, on the left atrial myocardium and itsneurovegetative innervation [27–32]. We firmlybelieve that progress is still required to refine thecurrently accepted catheter ablation approaches to AF. Because the LA is the main target of catheterablation in patients with AF, in this chapter wereview the gross morphological and architecturalfeatures of this chamber and its relations withextracardiac structures. The latter have also become

relevant because of some extracardiac complica-tions of AF ablation, such as injuries of the phrenicand vagal plexus nerves, or the devastating left atrioesophageal fistula formation [33–40].

Components of the left atrium

From a gross anatomical viewpoint the LA has four components: (1) a venous part that receivesthe PVs; (2) a vestibule that conducts to the mitralvalve; (3) the left atrial appendage (LAA); and (4) the so-called interatrial septum. We want toemphasize that the true interatrial septum is theoval fossa, a depression in the right atrial aspect ofthe area traditionally considered to be the inter-atrial septum [41–46] (Figures 1.1–1.4). At the leftatrial level, a membranous valve covers this regionand conceptually represents the only true interatrialseptum in the sense that it can be crossed withoutexiting the heart. The rest of the “muscular interatrialseptum” is formed by the apposition of the rightand left atrial myocardia that are separated by vascularized fibro-fatty tissues extending from theextracardiac fat. This is why we prefer to use theterm interatrial groove rather than muscular inter-atrial septum, a concept that is not only of academicinterest because trans-septal punctures to accessthe LA should be performed through the oval fossa (Figure 1.2). Thus, a puncture throughout theinteratrial groove (the muscular interatrial septum)

CHAPTER 1

Anatomy of the left atrium relevant to atrial fibrillationablation

José Angel Cabrera, Jerónimo Farré, Siew Yen Ho, & Damián Sánchez-Quintana

1

3

Catheter Ablation of Atrial Fibrillation Edited by EtienneAliot, Michel Haïssaguerre and Warren M. Jackman © 2008 Blackwell Publishing, ISBN: 978-1-4501-6349-1.

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4 PART 1 Fundamental concepts of atrial fibrillation

may result in hemopericardium in a highly antico-agulated patient because blood will dissect the vascularized fibro-fatty tissue that is sandwichedbetween the right and left atrial myocardium at thislevel [47–49].

The major part of the endocardial LA includingthe septal and interatrial groove component is

relatively smooth walled. The left aspect of theinteratrial groove, apart from a small crescent-likeedge, is almost indistinguishable from the parietalatrial wall. The smoothest parts are the superiorand posterior walls, which make up the pulmonaryvenous component, and the vestibule surroundingthe mitral orifice. Behind the posterior portion of

LAALAASCVSCV

LSPV

(a) (b)

LIPVRSPV

RAARAA

AOAO

PTPT AOAO PTPTSCVSCV

RAARAA

LSPVLIPV

RIPV

RAARAA

SCVSCVAOAO

LSPV

RIPV

(c)

LIPV

RSPVRSPV

RSPVRSPV

Figure 1.1 External appearances of the right and leftatriums viewed from anterior (a), superior (b), and rightlateral (c) views. Note the location of the transverse sinus(white dotted lines) and its relationship to the aorta andatrial walls (a, b). The superior and posterior walls of the LAwere anchored by the entrance of one PV at each of the

septumseptumMVMV

TVTV

CSoCSo MVMV

TVTV

LAALAAPAPA

RAARAA

ICVICV

(a) (b)

**

Figure 1.2 (a) Four-chamber section through the heartshowing the offset arrangement of the mitral valve (MV)and tricuspid valve (TV) which produces the so-calledmuscular atrioventricular septum (*) and the deepinfolding of the atrial wall superior to the floor of the ovalfossa (dotted lines). The true septal area is considerablysmaller. (b) The cardiac base (short axis) is dissected byremoving most of the atrium’s aspects. The right pectinate

four corners. (c) Site of the interatrial groove (Waterston’sgroove, blue dotted line). AO, aorta; LAA, left atrialappendage; LIPV, left inferior pulmonary vein; LSPV, leftsuperior PV; PT, pulmonary trunk; RAA, right atrialappendage; RIPV, right inferior pulmonary vein; RSPV,right superior pulmonary vein; SCV, superior caval vein.

muscles skirt around the vestibule of the right atrium andreach the orifice of the coronary sinus. Note that thepectinate muscles in the LA are limited mostly within theappendage and the dotted line marking the vestibule ofthe mitral annulus. CSo, coronary sinus orifice; ICV, inferiorcaval vein; LAA, left atrial appendage; PA, pulmonaryartery; RAA, right atrial appendage.

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CHAPTER 1 Anatomy of the left atrium in AF 5

the vestibular component of the LA is the anteriorwall of the coronary sinus [41] (Figures 1.3 and 1.4).

The walls of the left atrium and the septum

The left atrial wall and its thicknessThe walls of LA, excluding the LAA, can bedescribed as anterior, superior, left lateral, septal,

and posterior. The anterior wall is located behindthe ascending aorta and the transverse pericardialsinus. From epicardium to endocardium its widthis 3.3 ± 1.2 mm (range 1.5–4.8 mm) in unselectednecropsic heart specimens, but this wall canbecome very thin at the area near the vestibule ofthe mitral annulus where it measures an average of2 mm in thickness in our autopsy studies. The roofor superior wall of the LA is in close proximity to

RSPVRSPV

RIPVRIPV

Mitral valveMitral valve

VenouscomponentVenouscomponent

LSPVLSPV

LAALAA


VestibuleVestibule

LIPVLIPV

RSPVRSPV

RIPVRIPV

(a) (b)

Figure 1.3 (a) Dissection of the posterior wall of the LAclose to Waterston’s groove. The smooth-walled venouscomponent of the LA is the most extensive. The septalaspect of the LA shows the crescentic line of the free edge(dotted line) of the flap valve against the rim of the ovalfossa. (b) The orifices of the right superior and inferior

RSRS

RIPV

CSCS

LAALAA

SCV

HornsofOFHornsofOF

(a) (b)

AoAoPTPT

LungLung

RPA

Coronary sinus

RSRS

RIRI

MVMV

SCVPTPT

RIRI

Rightbronchus

Figure 1.4 Longitudinal sections through the left atrialappendage (LAA) showing the orifices of the right PV; theflap valve of the oval fossa overlaps (arrows) the rim toform the septal aspect of the LA. Note the relation of thesuperior caval vein (SCV) to the right superior pulmonary

pulmonary veins (RSPV and RIPV) are adjacent to the planeof the septal aspect of the LA (dotted line). The dashedblue line marks the hinge of the mitral valve. LAA, leftatrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein.

vein (RS). (b) Longitudinal section to show the relationshipof the roof of the left atrium with the right pulmonaryartery (RPA) and right bronchus. Ao, aorta; CS, coronarysinus; MV, mitral valve; PT, pulmonary trunk; RI, rightinferior pulmonary vein; RS, right superior pulmonary vein.

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the right pulmonary artery and its width rangesfrom 3.5 to 6.5 mm (mean 4.5 ± 0.6 mm). Thethickness of the lateral wall ranges between 2.5 and4.9 mm (mean 3.9 ± 0.7 mm) [41].

As already stated, an anatomic septum is like awall that separates adjacent chambers so that perfo-ration of a septal wall would enable us to enter froma chamber to the opposite one without exiting theheart. Thus, the true atrial septal wall is confined tothe flap valve of the oval fossa. The flap valve ishinged from the muscular rim that, deriving fromthe septum secundum, is seen from the right atrialaspect of the interatrial wall. At its anteroinferiorportion the rim separates the foramen ovale fromthe coronary sinus and the vestibule of the tricuspidvalve [48] (Figure 1.2). On the left atrial aspectthere is no visible rim and the flap valve overlapsthe oval rim quite considerably and two horns markthe usual site of fusion with the rim (Figure 1.3 and1.4). The measurement of the mean thickness of theatrial septum in normal hearts at the level of theanteroinferior portion of the muscular rim is 5.5 ±2.3 mm, and the mean thickness of the flap valve is1.5 ± 0.6 mm [41]. These results agree with previ-ously published echocardiographic studies [50].The major portion of the rim around the fossa is aninfolding of the muscular atrial wall that is filledwith epicardial fat. Superiorly and posteriorly thereis an interatrial groove, also known as Waterston’sgroove, whose dissection permits the separation ofthe right and left atrial myocardial walls and toenter the LA without transgressing into the rightatrium. Anteriorly and inferiorly, the rim and itscontinuation into the atrial vestibules overlies themyocardial masses of the ventricles from whichthey are separated by the fat-filled inferior pyram-idal space [48,51] (Figures 1.2–1.4).

The posterior wall of the LA is a target of cur-rently used ablation procedures in patients with AF.Early surgical interventions aimed at reducing thecritical mass of atrial tissues created long trans-mural linear lesions incorporating the posterior LA wall. The posterior wall of the LA is related tothe esophagus and its nerves (vagal nerves) and thethoracic aorta, and its inferior portion is related tothe coronary sinus. In a previous study in 26 unse-lected human heart specimens the overall thicknessof the posterior LA wall was 4.1 ± 0.7 mm (range2.5–5.3 mm) [41]. In a subsequent study we

measured the thickness of the posterior wall fromthe epicardium to endocardium, obtaining sagittaland transverse sections through the LA at three levels(superior, middle, and inferior close to the coronarysinus) in three different LA regions (right venoatrialjunction, mid-posterior atrial wall, and left venoa-trial junction) [52]. We also analyzed the myocar-dial content of the LA wall at all these predefinedsites. The region with the thickest myocardial con-tent was the mid-posterior LA wall (2.9 ± 0.5 mm,range 0.6–4.2 mm). The inferior level, immediatelysuperior to the coronary sinus and between 6 and15 mm from the mitral annulus, had the thickestposterior LA wall (6.5 ± 2.5 mm, range 2.8–12 mm).The latter thickness was due to a rather bulkymyocardial layer (4.3 ± 0.8 mm) and the presenceof a profuse amount of fibro-fatty tissue, both components being less developed at more superiorlevels of the posterior LA wall. The wall at the planeof the right or left venoatrial junction had thethinnest musculature (2.2 ± 0.3 mm, range 1.2–4.5mm) and a very scanty content of fibro-fatty tissue[52]. In some samples of histological sectionsobtained at the PV and posterior atrial wall, themyocardial layer had small areas of discontinuitiesthat were filled with fibrous tissue [42,53].

The myoarchitecture of the left atrialwall Detailed dissections of the subendocardial andsubepicardial myofibers along the entire thicknessof the LA walls have shown a complex architectureof overlapping bands of aligned myocardial bun-dles [41,51] (Figures 1.5 and 1.6). The term “fibers”describes the macroscopic appearance of strands ofcardiomyocytes. These fibers are circumferentialwhen they run parallel to the mitral annulus andlongitudinal when they are approximately perpen-dicular to the mitral orifice. Although there aresome individual variations, our epicardial dissec-tions of the LA have shown a predominant patternof arrangement of the myocardial fibers [41]. Onthe subepicardial aspect of the LA, the fibers in theanterior wall consisted of a main bundle that wasparallel to the atrioventricular groove. This was thecontinuation of the interatrial bundle (Bachmann’sbundle) [54], which could be traced rightward to the junction between the right atrium and thesuperior caval vein. In the LA, the interatrial bundle

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was joined inferiorly at the septal raphe (the portionthat is buried in the atrial septum) by fibers arisingfrom the anterior rim of the oval foramen. Superiorly,it blended with a broad band of circumferentialfibers that arose from the anterosuperior part of theseptal raphe to sweep leftward into the lateral wall.Reinforced superficially by the interatrial bundle,these circumferential fibers passed to either side ofthe neck of the atrial appendage to encircle theappendage, and reunited as a broad circumferentialband around the inferior part of the posterior wall to enter the posterior septal raphe (Figures 1.5and 1.6). The epicardial fibers of the superior wallare composed of longitudinal or oblique fibers,(named by Papez as the “septopulmonary bundle”in 1920) [55] that arise from the anterosuperiorseptal raphe, beneath the circumferential fibers ofthe Bachmann’s bundle. As they ascend the roof,they fan out to pass in front, between, and behindthe insertions of the pulmonary veins and themyocardial sleeves that surround the venous

orifices. On the posterior wall, the septopulmonarybundle often bifurcates to become two obliquebranches. The leftward branch fused with, andwas indistinguishable from, the circumferentialfibers of the anterior and lateral walls, whereas therightward branch turned into the posterior septalraphe. Often, extensions from the rightward branchpassed over the septal raphe to blend with rightatrial fibers and others toward the septal mitralvalve annulus, forming a line that marked an abruptchange in subendocardial fiber orientation.

On the subendocardial aspect of the LA, mostspecimens showed a common pattern of generalarchitecture. The dominant fibers in the anteriorwall were those orginating from a bundle describedby Papez as the septoatrial bundle [55]. The fibersof this bundle ascended obliquely from the anteriorinteratrial raphe and combined with longitudinalfibers arising from the vestibule. They passed theposterior aspect of the LA between the left and right pulmonary veins, blending with longitudinal

RSPVRSPV

LSPV

RIPV

LAA

LSPV

LAA

SeptoatrialbundleSeptoatrial

bundle

Septopulmonarybundle

(a) (b)

LSPV

LIPV

SCV

Coronary sinusICV

(d)

Posterior view

Interatrial band(Bachmann)

RSPV LSPV

TA

MA

(c)SCV

Anterior view

Lateral view

Figure 1.5 Schematic representation of the generalarrangement of the subepicardial and subendocardialfibers of the LA, viewed from the anterior (a, c) andposterior (b, d) aspect. (b) Note the three majorsubendocardial fascicles of the septoatrial bundle.

ICV, inferior caval vein; LAA, left atrial appendage; LIPV,left inferior pulmonary vein; LSPV, left superior pulmonaryvein; MA, mitral valve; RIPV, right inferior pulmonary vein;RSPV, right superior pulmonary vein; SCV, superior cavalvein; TA, tricuspid valve.

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or oblique fibers of the septopulmonary bundle fromthe subepicardial layer. The septoatrial bundle also passed leftward, superior and inferior to themouth of the atrial appendage to reach the lateraland posterior walls. Some of these fibers encircledthe mouth of the LA appendage and continued intothe pectinate muscles within the appendage (Fig-ures 1.5 and 1.6). The subendocardial fibers at theorifices of the PVs were usually loop-like extensionsfrom the longitudinal fibers. These fibers becamecircular at varying distances into the venous wallsand were continuous with the subepicardial fibers.In some specimens, however, the subendocardialfibers were longitudinal or oblique, whereas thesubepicardial fibers were circular, or vice versa. The

distal margins of the muscular sleeves were highlyirregular in the majority of veins.

Pulmonary veins and their endinginto the left atrium

Clinical imaging studies using magnetic resonanceimaging (MRI) and multislice computed tomo-graphy (CT) demonstrated the complex anatomyof the PVs with significant variability in dimen-sions, shape, and branching patterns [56–63].When assessed in a correct attitudinal orientation,the left PVs are located more superiorly than theright-sided veins [64] (Figure 1.7). The superiorPVs run cranially and more anteriorly, whereas the

(a)

(c)

(b)

(d)

LAALAA

RSPV

LIPV

SCVSCV

LAALAA

SCVSCV

RPVRPVLPVLPV

MVMVRARA

Left-posteriorridge

SeptoatrialbundleLSPV

LIPVLIPV

LAALAA

LAALAA

BB

LSPV

LIPVLIPV

*LSPVLSPV

MVMV

LVLV

SPB

Figure 1.6 (a, b) Dissections of the subepicardial fibersviewed from the anterior and left lateral aspects. Theinteratrial (Bachmann) bundle (BB, white dashed lines)crosses the septal raphe and blends into the circumferentialfibers of the anterior wall (dotted lines), passes to eitherside of the neck of the atrial appendage and runs parallelto the posterolateral aspect (*) of the LA. Oblique fibers ofthe septopulmonary bundle (SPB) become longitudinal asthey cross the roof between the left and right PVs (reddashed lines). (c, d) The left atrium everted to show thesubendocardial fibers and the fiber arrangement of the

septoatrial bundle and its three major fascicles (double-headed arrows). Note that endocardially the myocardialcontent of the left posterior ridge is the prolongation ofleftward fibers from the septoatrial bundle that runtoward the orifices of the left-sided PVs and the mouth of the left atrial appendage (LAA, blue dotted lines). LIPV, left inferior pulmonary vein; LPV, left pulmonary vein;LSPV, left superior pulmonary vein; LV, left ventricle; MV, mitral valve; RA, right atrium; RPV, right pulmonaryvein; RSPV, right superior pulmonary vein; SCV, superiorcaval vein.

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inferior veins have a more posterior and lateralcourse. The right superior PV runs near the poste-rior aspect of the right atrium immediately behindthe superior caval vein. The right PVs are alsorelated to the right pulmonary artery, which passesclose to the roof of the LA [46] (Figure 1.8).

The orifices of the right PVs are directly adjacentto the plane of the atrial septum (see Figures 1.3 and1.4). The left superior PV lies superiorly and poste-riorly to the mouth of the LAA, separated endocar-dially by a posterolateral ridge which, epicardially,is a fold that frequently extends to the origin of theleft inferior PV [41,46,61–63]. Although textbookstypically depict four venous orifices, anatomic

observations confirmed by MRI and CT studies instructurally normal hearts, have demonstrated thevariability of the ending of the PVs into the LA. In our series of 35 postmortem human hearts, wefound 26 specimens (74%) with two PVs on eachside [44]. Of these 26 hearts, 15 (69% ) had fourseparate openings of the PVs into the LA and theremaining 11 specimens (31%) had a “vestibule-like” portion for both PVs before opening via acommon orifice into the atrium (Figures 1.9 and1.10). The venous vestibule is more frequentlyfound on the left than on the right side and itslength ranged from 3 to 15 mm (7 ± 3 mm). A sin-gle common PV, defined as a vein branching at the

LAALAASCVSCV

Ao

LIPVLIPV

(a)

(b) (c)

LA

esophagusesophagus LIPVLIPV

LSPVLSPV

RSPVRSPV

LA

anterioranterior

posteriorposterior

LSPVLSPV

RSPVRSPV

LIPVLIPV RIPVRIPV

*

RSPVLSPV

RIPV

LIPVanterior wallanterior wall

superior wall

LAALAA

LIPVLIPV

Figure 1.7 Left atrial anatomy as depicted on axial slicesobtained with the “Visible Human Slice and Surface Server”[46] and three-dimensional reconstruction of the leftatrium (LA) and pulmonary veins (PV) using the NavX®system from data obtained with a 32-slice multidetector CTscanner. (a) Four successive slides obtained from a cranial tocaudal direction. Note that the left PVs are located moresuperiorly than the right-sided veins. The superior PVs runcranially and more anteriorly and the inferior veins have amore posterior and lateral course. (b) The NavX system

allows better geometric visualization of the LA, left atrialappendage (LAA), and PVs in a correct attitudinalorientation. The LAA is anterior to the left superior PV(LSPV). (c) The right superior PV (RSPV) is seen behind thesuperior caval vein (SCV). Note the posterior wall of the LArelated to the esophagus and aorta and the infold (*) ofthe posterolateral atrial wall protuding into theendocardial LA surface as a prominent ridge. Ao, aorta;LIPV, left inferior pulmonary vein; RIPV, right inferiorpulmonary vein.

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AoAo

RSPVRSPV

Right pulmonary artery

LALA

Posterior WallPosterior Wall

RPARPALPALPA

roofroof

RIPVRIPV

RSPVRSPVLSPVLSPV

LIPVLIPV

(a) (b)

Figure 1.8 (a, b) The right superior pulmonary vein (RSPV)is related to the right pulmonary artery (RPA) that passesclose to the roof of the left atrium (LA). Ao, aorta; LIPV, left

LSPVLSPV

LSPVLSPV

RSPVRSPV

LIPVLIPVRIPVRIPV

LPVLPV

LIPVLIPV

LSPVLSPV

(b)(a)

(c) (d)

LIPVLIPV

RIPVRIPV

RSPVRSPV

RSPVRSPV

RIPVRIPV

Figure 1.9 Four heart specimens sectioned tranversallywith the roof of the LA removed and viewed from above toshows the entrance of the pulmonary veins (PVs). (a) Thearrangement of four individualized ending of the PVs intothe LA. (b) A single left PV (LPV). (c) Four PVs; the left PVhas a “vestibule-like” portion (white arrow) for both the

inferior pulmonary vein; LPA, left pulmonary artery; LSPV, left superior pulmonary vein; RIPV, right inferiorpulmonary vein.

left superior PV (LSPV) and left inferior PV (LIPV) beforeopening via a common orifice into the left atrium. (c) Thisheart displayed more than four PVs: three orifices on theright (yellow arrows) and two on the left. RIPV, rightinferior pulmonary vein; RSPV, right superior pulmonaryvein.

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level of the hilum of the lung, was found in threehearts (9%), two on the left side and one on theright. Six hearts (17%) displayed more than fourpulmonary veins (three orifices on the right andtwo on the left). Clinical examination demonstr-ated four venous orifices in 81% of patients, while3% had three orifices and 16% had five orifices[59]. The most common variation is a separate origin of the vein coming from the right middlelobe of the lung (Figure 1.9). The distance betweenthe orifices of the right PVs ranged from 3 to 14 mm (mean 7.3 ± 2.7 mm), and in the left PVsfrom 2 to 16 mm (mean 7.5 ± 2.8 mm). A thininter-orifice left atrial rim between the superior and inferior PVs (measuring from 1 to 3 mm) wasfound in 50% of the hearts. Endocardial examina-tion of the LA using three-dimensional MRI hasshown that the shortest distance between the right and left PVs, the so-called roof line, was 29.9 ±5.9 mm, ranging between 18.9 and 39.2 mm [62].

Anatomic studies and clinical imaging investiga-tions have shown that the PV ending in the LA isnot perfectly cylindrical but has a funnel-shapedmorphology, making it difficult to identify a sharplandmark for the anatomic limits of the PV ostium[41,56,57]. Discounting the common vestibule, thediameter of the venous orifices at the venoatrial

junction ranged in our anatomic specimens from 8 to 21 mm (12.5 ± 3 mm). The transversal diame-ter of the common vestibule is longer than itssuperoinferior diameter (19.5 ± 3 mm vs.13.5 ± 1mm) [41]. Early studies demonstrated a strong cor-relation between the degree of left atrial dilationand both occurrence and duration of AF [65].Imaging studies of the PVs demonstrated that theostial diameters of the superior PV were greater inpatients with AF than in controls [60,66].

Gross anatomy of the leftposterolateral ridge

The posterolateral ridge between the orifices of theleft PVs and the mouth of the LAA is the most relev-ant structural prominence of the endocardial LA(Figure 1.11). Although already described in 1907by Arthur Keith [67] as the “left tænia terminalis”(terminal band or strip) and 13 years later by James Papez [55] as the “left posterior crest”, theLA posterolateral ridge actually is a fold of the post-erolateral left atrial wall protruding into the endocardial LA surface as a prominent crest orridge (Figure 1.11). Epicardially, this broad bundle is in continuity with the uppermost and distal part of the interatrial band (Bachmann’s bundle).

MVMV

LSPVLSPV

LIPVLIPVLAALAA

SS

PP AA

II

LAALAA

superior wallsuperior wall

po

ster

ior

wal

lp

ost

erio

r w

all

ante

rio

r w

all

ante

rio

r w

all

(a) (b)

LSLSLILI


LA isthm

us

LA isthm

us

Figure 1.10 Longitudinal sections of two hearts illustratingendings of the pulmonary veins (PVs) into the LA. (a) Anindividualized ending of the left superior PV (LSPV) and theleft inferior PV (LIPV) into the LA. The left PVs lie superiorand posterior to the mouth of the left atrial appendage(LAA), both separated by a muscular fold. (b) Heart

showing a common vestibule for both left PVs. Note thelarger anteroposterior diameter than the superoinferiorone and the line connecting the inferior margin of the ostiumof the left inferior PV to the mitral annulus called the leftatrial isthmus. The red arrow marks the coronary sinus. LI, left inferior PV; LS, left superior PV; MV, mitral valve.

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Endocardially, the myocardial content is the pro-longation of leftward fibers from the septoatrialbundle that run toward the orifices of the left-sidedPVs and the mouth of the LAA (see Figure 1.6). Theshape and size of this posterolateral LA ridge is ofrelevance during catheter ablation of AF whenencircling the orificies of the left PVs or duringablation of extrapulmonary vein triggers arisingaround or inside the LAA. Anatomic informationof this structure may be useful in order to perform ablation techniques more efficiently and safely, and it can be obtained with current multislice CTand MRI reconstructions of the endocardial aspect of the LA [61–63]. The ridge extends along the lateral wall of the LA from the anterosuperior toposteroinferior region. A recent three-dimensionalMRI study showed that the ridge was narrowestbetween the left superior PV and the LAA in 84% ofpatients. In this study, the mean distance betweenthe left superior PV and the LAA, and between theleft inferior PV and the LAA, were found to be 3.8 ±1.1 mm and 5.8 ± 2.0 mm, respectively. The ridgewas narrower than 5 mm in the majority of patients,thus determining the possibility of obtaining stablecatheter position in this region [61]. Our recentanatomic study of 32 structurally normal human

heart necropsic specimens also revealed a thickermyocardial wall of the ridge at its inferior level adjacent to the inferior PV, with a range between1.5 and 4.2 mm (mean 2.8 ± 1.1 mm). The meanlength of the ridge was 24.2 ± 5.3 mm (range14.2–32.5 mm) with a constant superior insertionat the lateral roof of the LA extending inferiorly toreach the posteroinferior margin of the inferior PVin 88% of hearts (unpublished observations). A CTscan study showed a prominent ridge in all sub-jects extending from the superior part of the leftsuperior PV to the inferior PV in 70–72% of patients[63]. These investigators also found no significantdifferences in the length and width of the ridgebetween patients with AF and controls [63].

Gross anatomy of the left atrialappendage

The LAA is characteristically a small finger-likeextension of the LA with a multilobulated appear-ance in 80% of hearts [68,69] (Figure 1.12). A quan-titative study of the normal LAA in 500 autopsyhearts showed that the mean length, width, and sizeof the appendage increased with age up 20 years[69]. In adult postmortem hearts the mean orifice

(a) (b) (c)

LSPVLSPV

LAALAA

LSPVLSPVLSPVLSPV

Mitral v

alve

Mitral v

alve

CSCSMitra

l valve

Mitral va

lve

post

erio

r po

ster

ior

ante

rio

ran

teri

or

superiorsuperior

****

LAALAA

post

ero-

late

ral r

idge

post

ero-

late

ral r

idge

LIPVLIPV

Figure 1.11 Endocardial visualization of the leftposterolateral wall. (a) Three-dimensional reconstructionof the endocardial left atrium using the NavX system fromdata obtained with a 32-slice multidetector CT scanner.Note the prominent posterolateral ridge (*) between theleft atrial appendage (LAA) and the left superiorpulmonary vein (LSPV) along the lateral wall from itsanterosuperior to posteroinferior region. (b, c) Twopostmortem heart specimens showing prominent

endocardial posterolateral ridges, extending in (b) to theinferior margin of the left inferior pulmonary vein (LIPV).Observe the muscular trabeculations extending inferiorlyfrom the left appendage to the vestibule of the mitral valve(red arrows). (c) Transillumination of the left lateral wall toillustrate the extra-appendicular posterior pectinate muscleand the thinnest muscular wall in between the musculartrabeculae. CS, coronary sinus.

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diameter of the LAA was 1.07 cm in women and1.16 cm in men, in contrast with morphologicalexaminations of LAA orifices using CT scans thatshowed a mean longitudinal and transverse dia-meter of 3.2 ± 0.6 mm and 1.9 ± 0.5 mm, respectively[63,69]. The greater diameters in the in vivo humanstudies as compared to necropsic measurementsmost likely is due to tissue retraction produced bythe fixation of the specimens in the latter studies.The LAA orifice and volume of patients with AF isgreater than that observed in controls.

Reinforced superficially by the interatrial bundle,circumferential fibers that arise from the antero-superior part of the septal raphe pass to either sideof the neck of the left appendage to form broadbundles of muscular connections between the appendage and the body of the LA. A recent study has shown that to electrically disconnect the LAA it isnecessary to apply long-lasting radiofrequency pulsesthat gradually change the activation sequence, thussuggesting a dense circumferential connection ofthe appendage to the LA [32]. A narrow, oval-shaped mouth marks the junction between the LAAand the venous component of the LA. The myo-cardial ridge and an inflection of the endocardialsurface bounded the ostial borders of the append-age in most hearts. In the LA, the pectinate muscles are mostly confined within the left appendage.They form a complicated network of muscularstrips lining the endocardial surface. In some 28%

of our human heart specimens the anterior ostialmargin of the appendage does not present as aclear-cut border and muscular trabeculations canbe found extending inferiorly from the appendageto the vestibule of the mitral valve (see Figure 1.11).These extra-appendicular myocardial bands cor-respond to the small posterior set of pectinate muscles originating from the septoatrial bundle toembrace the left appendage. In those hearts withextra-appendicular posterior pectinate muscles,the areas in between the muscular trabeculae hadthe thinnest muscular walls (0.5 ± 0.2 mm) (seeFigures 1.6 and 1.11). In other specimens (15%),remnants of pectinate muscles between the ostiumof the left inferior PV and vestibule of the mitralannulus can be found. A previous histological studyof the mitral isthmus described “small isthmuscrevices” present in almost all patients that mayentrap the tip of the ablation catheter, which maylead to excessive tissue heating and tamponade.

The left circumflex coronary artery runs epi-cardially in the fat-filled atrioventricular groove,related to the smooth anterior vestibule and in closeproximity to the inferior border of the orifice of theLAA (Figure 1.12). The shortest distance from theleft appendage orifice and the circumflex artery was< 3–5 mm in 80% of our unselected human heartnecropsic specimens. In CT in vivo studies the leftcircumflex coronary artery ran < 2 mm from theLAA orifice in 74% of cases, an anatomic detail to

(a) (b) (c)

LS PV

LS PV

LAA

LSPVLSPV

LAALAA

postero-lateralridge

LVLV

PLR

**

LCXMV

MV

vest

ibul

e


LIPVLIPV

10 mm

Figure 1.12 (a) Longitudinal section through left atrialappendage (LAA) showing the orifices of the leftpulmonary veins, and the left posterolateral ridge. (b, c)Longitudinal sections through the left superior pulmonaryvein (LSPV) and left atrial appendage (LAA) and leftsuperior pulmonary vein (LSPV) stained with Masson’s

trichrome. Note the myocardium and fat tissue (*) of theposterolateral ridge and the left circumflex artery (LCX)closer to the vestibule of the left atrium in (b). LIPV, leftinferior pulmonary vein; LV, left ventricle; MV, mitral valve;PLR, posterolateral ridge.

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be considered when ablating inside or around theorifice of the LAA.

Architecture of the leftposterolateral ridge: the Marshallstructures

The posterolateral ridge is more than a simpleendocardial fold of the lateral LA wall thatinfluences the stability of the contact of the tip of the catheter with the endocardium during anablation procedure. Electrophysiological and sur-gical investigations demonstrated extra-PV atrialfoci after PV isolation originating from the LAA[22,32]. In addition, the junctional area betweenthe LAA and the LA body has a relevant impact onthe fibrillatory process, acting as a source of activityspreading to the rest of the atrium and contributingto the maintenance of atrial fibrillation [19,21–23,70–72]. Because of the potential relevance for current and future endocardial catheter ablationtechniques we will describe the architecturalarrangement of myocardial bundles forming theposterolateral LA ridge and its vascular and autonomic nervous system content, as well as theanatomic relations with the Marshall structures(the oblique vein and ligament).

The so-called oblique vein of Marshall is part ofthe ligament of Marshall (LOM), formed by thevenous element and fibro-fatty tissue, muscularbundle and autonomic nerves, all forming a

vestigial fold of the pericardium described by JohnMarshall in 1850 [73] (Figure 1.13). The LOMcourses obliquely above the LAA and can be tracedlaterally to the left superior PV bundle in the epicardial aspect of the left atrial fold that forms the left posterior “crest”. Sherlag et al. [74] firstdemonstrated the existence of muscular left atrial“tracts” within this vestigial fold and found electricalactivity arising from the LOM. In their study,Sherlag et al. recorded double potentials from theligament, advancing the hypothesis that this struc-ture could play a role in arrhythmogenesis [74].More recently, the so-called Marshall bundles havebeen thought to be the origin of certain forms offocal AF and that a considerable percentage of non-pulmonary vein foci may arise from the LOM [30,31,75–79]. Electroanatomic mapping showed acommon pattern of electrical connection betweenthe LOM and coronary sinus muscular sleeves,resulting in early activation of the low posterolat-eral wall of the LA. In addition, some patients haddistal electrical connections at the floor of the leftinferior PV or anterolateral wall of the left superiorPV [75,76].

In an elegant histological examination, Kim et al.[80] demonstrated multiple myocardial “tracts”present within the LOM that directly insert into thecoronary sinus musculature near the origin of thevein of Marshall or distally into the posterior freewall of the LA. They found in 57% of specimensboth superficial and deep muscular “tracts” in

CoronarysinusCoronarysinus

LPVLPV

Vein of MarshallVein of Marshall

LAALAA

LIPVLIPV

(b)(a)

Figure 1.13 (a) Heart specimen showing the spatialrelationship of the coronary sinus and the vein/ligament ofMarshall. The coronary sinus runs along the epicardialportion of the vestibular component of the LA surroundingcircumferentially the orifice of the mitral valve. (b) Note in

the enlarged figure, the left atrial oblique vein of Marshallformed by the venous element with fibro-fatty tissue and small muscular bundles. LAA, left atrial appendage;LIPV, left inferior pulmonary vein; LPV, left pulmonary vein.

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relation to the oblique vein of Marshall with anoverall mean length and diameter of 7.8 ± 3.9 mmand 0.7 ± 0.2 mm, respectively. Electrical activityoriginating from the LOM can be recorded fromthe endocardial aspect of the LA in or around theorifices of the left PV. A recent anatomic studyshowed that Marshall bundles gradually diminishedin density towards the distal venous branch andreached the left inferior PV–LA junction and leftsuperior PV–LA junction in 76% and 24% of cases,respectively [81]. In patients with AF undergoingablation of the LOM, it has been shown that mostarrhythmic episodes arise from the distal segmentof the ligament close to the left superior PVs[75,77,79]. An angiographic study also revealedthat the distal end of the vein of Marshall and itsbranches are likely to be distributed around the leftsuperior PV or the left inferior PV ostia, especially

in patients with arrhythmogenic foci [79]. Studiesof endocardial ablation to eliminate activationfrom Marshall bundles recognize that the most fre-quently successful ablation site is at the inferiorborder of the ostium of the left inferior PV. Wehave studied the Marshall structures, demonstrat-ing that they course along the left posterior ridgeand that they are in close proximity to the endocar-dial aspect of the left atrium (Figure 1.14). In 73%of specimens the oblique vein of Marshall or its ligament runs at a distance less than 3 mm from thesuperior level of the endocardial ridge. Throughoutthe trajectory of the vein in relation to the left pos-terior ridge, we observed in all specimens smallmuscular bundles that crossed the oblique vein toconnect with the left atrial free wall.

The Marshall ligament is richly innervated by sympathetic nerve fibers [80,81]. Adrenergic

(a)

(b) (c)

LAA LAA LAA

LPV

LSPV

LIPV

LAA

LPV

Vein of MarshallVO

M

NGG

epicardialganglionepicardialganglion

NN

(d)

SAB

septoatrial bundleseptoatrial bundle

10 mm

3 mm3 mm 5 mm 2 mm

Figure 1.14 (a) Transverse sections at different levels of themyocardial sleeve of the left pulmonary vein (LPV),septoatrial bundle (SAB), and left atrial appendage (LAA)from a 56-year-old man. (b) Transverse section showing theoblique vein of Marshall (VOM). The arrows (G) and (N)indicate the ganglion and nerve bundles in the vicinity ofthe vein, respectively. (c) An enlargement of the septoatrial

bundle shown in (a). Note that the VOM was found indirect contact with the myocardium of the septoatrialbundle. (d) Transverse section showing the epicardialganglion and nerve bundles (N) in the vicinity of themyocardium of the septoatrial bundle. (Trichrome stain.)LIPV, left inferior pulmonary vein; LSPV, left superiorpulmonary vein.

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sensitivity of the myocardial tissues within theLOM may be responsible for atrial tachyarrhyth-mias arising from the LA [78]. Both focal sourcesarising from Marshall structures and muscularconnections with the epicardial interatrialBachmann’s bundle and the inner septoatrial bun-dle may have implications in the fibrillatory processand spread of AF activity between both atria(Figure 1.14). Recent reports have shown that left-to-right interatrial conduction occurs predomin-antly through the Bachmann bundle and that sinus impulses propagated through this interatrialbundle could excite the Marshall musculature andthe nearby left atrium simultaneously [82,83].

The left atrial isthmus

Linear ablation connecting the inferior margin ofthe ostium of the left inferior PV to the mitral annu-lus appears to increase the success rate of catheterablation in patients with AF [13,84]. Although this

posteroinferior wall of the LA between the orifice ofthe left inferior PV and the mitral annulus cannotbe considered an anatomic entity, it is being namedby electrophysiologist as the left atrial isthmus ormitral isthmus (Figure 1.15). In a recent anatomicstudy of 20 hearts, Anton Becker [85] showed markedvariability in the dimensions of the mitral isthmuswith considerable differences in thickness of the leftatrial myocardium at various levels and among dif-ferent hearts. This study also showed the closeanatomic relation between the isthmus area withthe great cardiac vein and the left circumflex artery.The mean distance between the left inferior PV andthe mitral annulus ranged between 17 and 51 mm(mean 34.6 mm). In some hearts the left atrialmyocardium extended into the atrial aspect of themitral valve leaflets. Gaps in the lesion line mayresult in conduction delay and facilitate left atrialflutter. Therefore, the variable thickness of the leftatrial myocardial tissue is highly relevant to achiev-ing an adequate transmural linear lesion across the

CS

LIPV

PM

MV

Leftventricle

LCX

vestibule

(a) (b)

epic

ardi

umep

icar

dium

endo

card

ium

endo

card

ium

LVLV

MV

CS

(b1)

(b2)

10 mm

“remnant”

Figure 1.15 (a, b) Longitudinal sections at the mitralisthmus to illustrate its anatomic relations with thecoronary sinus (CS) and circumflex artery (LCX). (b) Thecoronary sinus is surrounded by a sleeve of muscle from theleft atrial wall (arrows in b1). Note in (b2) the space

between the pectinate muscles where the left posterioratrial wall becomes thinner (red arrow). Note also thedistance of the coronary sinus to the hingeline of the mitralvalve. (Trichrome stain.) LIPV, left inferior pulmonary vein;LV, left ventricle; MV, mitral valve.

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