Clive Handler Michael Cleman Editors. Classic Papers in Coronary Angioplasty

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2 Clive Handler Michael Cleman Editors Classic Papers in Coronary Angioplasty

3 Classic Papers in Coronary Angioplasty

4 Clive Handler and Michael Cleman (Eds) Classic Papers in Coronary Angioplasty With 18 Figures

5 Clive Handler, MD, FACC, FESC Consultant Cardiologist and Physician The National Pulmonary Hypertension Unit The Royal Free Hospital London, UK and Consultant Cardiologist Highgate Hospital London, UK Michael Cleman, MD, FACC Professor of Medicine Director Cardiac Catheterization Laboratory and Angioplasty Services Yale University School of Medicine/Yale-New Haven Hospital New Haven, Connecticut, USA British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: ISBN-10: e-isbn: Printed on acid-free paper ISBN-13: Springer-Verlag London Limited 2006 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licences issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature. Whilst we have made considerable efforts to contact all holders of copyright material contained in this book, we may have failed to locate some of them. Should holders wish to contact the Publisher, we will be happy to come to some arrangement with them. Printed in the United States of America (EB) Springer Science+Business Media springer.com

6 Contents Editors Contributors Acknowledgements Preface Foreword vi vi viii ix xi Chapter 1 Vascular biology of atherosclerosis 1 Peter F. Bodary, Daniel T. Eitzman Chapter 2 Chapter 3 Quantification of coronary atherosclerosis for cardiovascular risk assessment: the hole in the doughnut? 21 Paul Schoenhagen, Steven E. Nissen Primary angioplasty (PPCI) in ST-elevation myocardial infarction 39 Iqbal Saeed Malik, Rodney Foale Chapter 4 Coronary angioplasty for acute coronary syndromes 65 Steven Pfau Chapter 5 High-risk coronary intervention: a selective literature review of high-risk subsets 89 Jeffrey J. Popma, Hung Ly Chapter 6 Stenting in coronary angioplasty 115 Jeptha P. Curtis, John F. Setaro Chapter 7 Ancillary techniques in interventional cardiology 141 John M. Lasala, George Chrysant, Adrian Messerli Chapter 8 Anti-thrombotic management in interventional cardiology 163 James Tcheng, Steve Kindsvater Chapter 9 Coronary artery bypass grafts in the era of percutaneous coronary angioplasty 191 Thanos Athanasiou, Brian Glenville Chapter 10 Epilogue 217 Gerry Coghlan Frequently cited papers in coronary angioplasty 229 Index 231

7 Editors Clive Handler MD, FACC, FESC Consultant Cardiologist and Physician, The National Pulmonary Hypertension Unit, The Royal Free Hospital, London, UK and Consultant Cardiologist, Highgate Hospital, London, UK Michael Cleman MD, FACC Professor of Medicine, Director, Cardiac Catheterization Laboratory and Angioplasty Services, Yale University School of Medicine/Yale-New Haven Hospital, New Haven, Connecticut, USA Contributors Thanos Athanasiou MD, PhD, FETCS Consultant Cardiothoracic Surgeon, St. Mary s Hospital, London, UK Peter F. Bodary PhD Research Investigator of Internal Medicine/Cardiology, University of Michigan, Ann Arbor, Michigan, USA George Steven Chrysant MD Director, Advanced Cardiac Imaging, Integris Heart Hospital, Oklahoma City, Oklahoma, USA Gerry Coghlan MD, FRCP Consultant Cardiologist, The Royal Free Hospital, London, UK Jeptha P. Curtis MD Instructor of Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA Daniel T. Eitzman MD, FACC Associate Professor of Internal Medicine/Cardiology, University of Michigan, Ann Arbor, Michigan, USA Rodney Foale MBBS, FRCP, FACC, FESC, FCSANZ Consultant Cardiologist and Clinical Director of Surgery, Cardiovascular Science and Critical Care, Waller Department of Cardiology, St. Mary s Hospital, London, UK Brian Glenville BSc(Hons), MS Professor and Head of Department of Cardiothoracic Surgery, Hadassah University Hospital, Jerusalem, Israel Steven Michael Kindsvater MD Keesler Medical Center, Keesler AFB, Mississippi, USA John M. Lasala MD, PhD Associate Professor of Cardiology, Washington University School of Medicine, St Louis, Missouri, USA Hung Ly MD Interventional Cardiology Fellow, Cardiology Division, Brigham and Women s Hospital, Boston, Massachusetts, USA vi

8 Iqbal Saeed Malik MA, MRCP, PhD Consultant Interventional Cardiologist, Waller Department of Cardiology, St. Mary s Hospital, London, UK Adrian W. Messerli MD Cardiology Associates of Kentucky, Lexington, Kentucky, USA Steven E. Nissen MD, FACC Medical Director, Cleveland Clinic Cardiovascular Research Coordinating Center, The Cleveland Clinic Foundation, Cleveland, Ohio, USA Steven Pfau MD Associate Professor of Medicine, Yale University School of Medicine, Cardiology Section, New Haven, Connecticut, USA Jeffrey J. Popma MD Director, Interventional Cardiology, Brigham and Women s Hospital, Associate Professor of Medicine, Harvard Medical School, Boston, Massachusetts, USA Paul Schoenhagen MD, FAHA Cardiovascular Imaging, Departments of Radiology and Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA John F. Setaro MD Associate Professor of Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA James E. Tcheng MD, FACC, FBCAI, FESC Associate Professor of Medicine; Associate Professor of Community & Family Medicine, Duke Clinical Research Institute, Duke University Medical Center Durham, North Carolina, USA vii

9 Acknowledgements Both Clive Handler and Michael Cleman would like to thank Professor Lawrence Cohen for writing the foreword to this book and for arranging the transatlantic link between London and New Haven, which was essential for this project, and for his encouragement and wise counsel. Clive Handler would like to acknowledge the support of his wife, Caroline, and their three children, Charlotte, Sophie and Julius, during the production of this book. The idea for this book came from his colleague from school, Dr Neil Soni, who co-edited the first book in this series, Classic Papers in Critical Care. He is also grateful to his colleague from the Royal Free Hospital, Dr Gerry Coghlan, who not only contributed the final chapter but also proof read the book. Michael Cleman would like to acknowledge his wife Marilyn, and his children, Jake and Katie for their patience and support in this project. The support and expertise of his interventional colleagues at Yale has been invaluable in collating the material. viii

10 Preface Percutaneous coronary intervention (PCI) is one of the most commonly performed cardiac procedures. Physicians, all healthcare professionals and healthcare managers, as well as patients and their families, the world over, are aware that it is a very useful and powerful tool to help improve the lives of patients with coronary heart disease. But how did we get here? Cardiologists of our generation were in training when PCI was in its infancy. There was no evidence base to guide us and we witnessed and practiced with comparatively primitive equipment. We all had to learn from our own successes and failures as well as from the experiences of colleagues. The residents and trainees of today may not fully appreciate the anxieties of interventionists during procedures during those early years. Inherent problems included imaging and evaluating the significance of a coronary artery lesion; lack of data on what constituted high risk lesions and patients which made case selection difficult (this, in turn added uncertainty when discussing and quantifying the procedural risks to patients); arterial access problems and bleeding (particularly during the anticoagulation era); primitive and traumatic hardware complicating target lesion access; the sinking feeling of dealing with abrupt vessel closure, dissection and haemodynamic collapse before the availability of stents; and the disappointment felt by patients and interventionists with a comparatively high incidence of restenosis. Subacute thrombosis was an infrequent but worrying and unpredictable complication. On-site backup coronary artery surgery was generally considered mandatory and this had a knock-on effect on the work and finances of hospitals and providers. Memories of those early days when our expectations of the procedure, performed mainly for accessible, proximal, comparatively simple lesions in patients with single vessel disease, were that plain old balloon angioplasty would keep our patients away from the surgeons for a little while longer, and that it could be used as a salvage procedure for inoperable patients, have faded and have been replaced with a different, more confident, evidence-based practice. The frontiers have been pushed back; PCI incorporating drug-eluting stents and modern antiplatelet treatments is a routine, low-risk, day-case procedure performed in patients of all ages and co-morbidity, with high patient and clinician expectations for both acute and chronic coronary artery disease, without the necessity of on-site surgery. PCI has changed the way we approach clinical problems. Physicians managing patients with known or suspected coronary heart disease, whether in their office, in the emergency room or in the coronary care unit, understand that prompt diagnosis and treatment are now available. We continually search for improvements and refinements in equipment and pharmacological therapies. We collaborate with our basic science colleagues to find answers to molecular and cellular biological obstacles. Our imaging and vascular colleagues are key members of the multidisciplinary approach to develop and expand the use of the technique and enhance the quality of service we provide our patients. These rapid developments in the management of coronary heart disease, which will eventually affect nearly all of us, have been possible only through the vision, persistence, intellectual curiosity, skill and discipline of our predecessors. Interventionists today have been handed the baton and continue the quest. The aim of this book is not intended to be a birthday party for PCI, although its publication coincides with the 25th anniversary of Grüntzig s paper. We wanted to pause, take breath and try to produce a small, useful and enjoyable book that would remind all those involved in PCI, of some of the major contributions to the literature. Looking back often helps in seeing what may lie ahead. ix

11 Preface We have invited some of the world s leading interventionists to help us and they have done a fine job. They were given a difficult task. We asked them to provide us with their personal choice of the papers that have most influenced their practice and understanding of PCI in a number of its components. As busy clinicians, we are not often (if ever) forced to identify the papers that have been the most influential in shaping our practice. It may be considered a somewhat artificial approach, but reading an expert s personal, restricted choice of papers that he would take on a desert island (without internet or library access), is of interest. Dr Mitchell Fink MD, in his preface to Classic Papers in Critical Care, excused the personal choices of the contributors by likening them to the views of a San Francisco restaurant critic. We have also included citation indices for each paper so that our readers have the additional views of the wider PCI community. You may have your own personal choices and may disagree with the choice of our contributors. We would beg your tolerance with this, an inherent weakness of this book. But it is also a strength, because the very nature and enjoyment of this series is that leading world experts allow readers to peep at their academic proclivities and personal perspectives of papers they think are scientifically and clinically useful. We feel that it provides a useful reference for others and has educational and historical value. Our friend and teacher, the eminent Professor Lawrence Cohen, confessed in his foreword, that he got it wrong at his first attempt to 25 years ago. Even he could not have anticipated how things were to turn out. This collection of Classic Papers in Coronary Angioplasty, 25 years down the road, is an opportunity to look behind us as we enter an early lap of a long distance race. Together with our contributors, we hope that you will enjoy this coned-in snapshot of PCI in We have no doubt that the next quarter of a century will bring us more surprises and improved care for our patients. Clive Handler MD, FACC, FESC Michael Cleman MD, FACC x

12 Foreword I am particularly pleased to get a second chance. I refer to the fact that at the time of my first chance, I got it all wrong. The year was 1979 and Dr Andreas Grüntzig had recently published an article in The New England Journal of Medicine entitled Nonoperative Dilation of Coronary Artery Stenosis: Percutaneous Transluminal Coronary Angioplasty. I took the opportunity to write a Letter to the Editor in which I stated: A method for relief of coronary obstructions that did not involve operations would obviously have a major impact on medical, surgical, economic and psychologic aspects of this disease... Although this report is of great interest, it would be wise for cardiologists to maintain a healthy skepticism... This operation is clearly not the answer for most patients with obstructive coronary lesions. It is appropriate for only a fraction of patients with coronary artery disease perhaps between 3 and 10 per cent. It may be successful in some patients with intrinsic coronary lesions and even in some who have previously undergone bypass grafting with subsequent occlusion of the graft. I further went on to say: Even when the obstructive lesion can be reached by the catheter, in how many patients will the dilatation be successful and free from complications such as intimal dissection? Further, if a lesion can be dilated, will the obstruction remain open for an extended period or will it return in days, weeks or months? Perhaps you can understand my relief at being given a second chance to visit the topic of coronary angioplasty. This excellent book explores the growth in our knowledge gleaned over a quarter of a century. It explores the field from perspectives ranging from that of the vascular biologist to that of the surgeon who must thoughtfully reassess the diminishing role of coronary artery bypass surgery now that a non-operative approach is not only possible but in many instances preferable. It would not be a stretch to say that coronary angioplasty is to cardiology as the Rosetta Stone was to Egyptian hieroglyphics, allowing the language to be translated. The opening chapter on Vascular Biology of Atherosclerosis begins with the seminal work of Ross which was the first to identify the vascular smooth muscle cell as playing a critical role in the development of the atherosclerotic plaque. In collaboration with L. Harker, Ross went on to point to the role of hyperlipidemia in causing endothelial injury. The chapter by Schoenhagen and Nissen chronicles our ability to quantify the extent of coronary plaquing and also estimate the composition of coronary plaques. Proudfit s paper of 40 years ago reports on the correlation between clinical findings and selective cine coronary arteriography in 1000 patients. For the first time, a patient s clinical symptoms could be evaluated alongside a picture of the coronary arterial tree. This chapter also contains the 1990 article by Nissen et al. describing the development of intravascular ultrasound (IVUS), a technique that is able not only to quantify the extent of plaque but also its morphology. As experience with coronary angioplasty grew in patients with stable angina, it is not surprising that clinicians would extend this technique to the patient who is in the midst of a myocardial infarction. This approach is compared to the previous gold standard, thrombolytic therapy. It is now generally agreed that although both procedures have their respective roles, primary xi

13 Foreword percutaneous coronary intervention (PPCI) is the preferable method if the patient can be brought to the catheterization laboratory in a timely manner. Coronary angioplasty has spawned a wealth of research directed at prevention of thrombosis. The work on platelet glycoprotein IIb/IIIa receptor inhibition was stimulated by the need to prevent thrombosis at the site of angioplasty. It is unlikely that this field of research would have been advanced as far as it is today had it not been for the needs brought about by angioplasty. Once balloon angioplasty became an established therapeutic procedure, the addition of coronary stenting was a natural sequence. It was hoped that stenting would help prevent restenosis, a complication that plagued up to 20 per cent of patients undergoing balloon angioplasty. Starting slowly 15 years ago, coronary stents are now placed in 80 per cent of patients undergoing balloon angioplasty. The latest improvement is the development of drug-eluting stents to further prevent smooth muscle proliferation leading to restenosis. Chapter 9 of this important book is a reflective commentary on the respective roles of angioplasty and coronary artery bypass surgery. From its slow beginnings in 1980 where there were about 1000 angioplasties performed, there are currently 900,000 angioplasties performed annually. Most of these angioplasties are performed in patients who could not have been considered candidates when the procedure was first introduced over 25 years ago. It has already become the primary treatment of patients with coronary artery disease. Finally, I want to commend the two editors Drs Clive Handler and Michael Cleman. I first met Dr Handler when I was a Visiting Professor at the Brompton Hospital in He was a member of the Junior Cardiac Club. We became colleagues and friends, a relationship that has been a mutual pleasure for the past 20 years. Dr Cleman is my respected colleague at Yale. I have watched him grow from the time he came to Yale as a Cardiology Fellow 25 years ago, to his becoming a Professor and Head of our Interventional Cardiology Team. As I indicated in the beginning of this piece, I am grateful to both of them for the opportunity of having a second chance to visit coronary angioplasty. This time I believe I got it right. Professor Lawrence S. Cohen The Ebenezer K. Hunt Professor of Medicine Yale University School of Medicine New Haven, CT USA Fellow, British Cardiac Society xii

14 Chapter 1 Vascular biology of atherosclerosis Peter F. Bodary, Daniel T. Eitzman Introduction The pathogenesis of atherosclerosis has been the subject of thousands of articles published over the past several decades. Currently over 5000 papers per year are being published related to atherosclerosis. To identify only eight articles from this vast literature that have had great impact on our understanding of the biology of atherosclerosis is a difficult task. It will be impossible to do justice to the hundreds of investigators that have shaped the field as it is currently viewed. Most of the fundamental concepts shaping the field of atherosclerosis were generated by pathologists through observational studies. The current view of atherosclerosis probably began with the work of Rudolph Carl Virchow, a professor of pathology, who published Cellular Pathology in Virchow put forth the novel notion that cells were affected by outside stimuli and that diseased cells arose from other diseased cells. Virchow suggested that the atherosclerotic lesion resulted from lipid accumulation and cellular proliferation in the arterial wall. During the same time period (1852), von Rokitansky suggested that atherosclerotic lesion development was preceded by fibrin deposition and that persistence of fibrin deposits might contribute to the formation of an atherosclerotic lesion. Many other pathologists preceding and during this time period had made similar observations and it is difficult to determine who should be credited with the original observations. Suffice it to say, many pathologists have described atheromatous changes in the vasculature but experimental data to support specific hypotheses were lacking during this time period. This review will therefore focus on papers from the more modern era of vascular biology. The modern biology of atherosclerosis arguably began with a series of seminal primate studies described by Russell Ross. In 1973, Ross and Glomset described the cellular composition of atherosclerotic lesions and proposed a critical role for the vascular smooth muscle cell in atherogenesis. Ross and Harker went on to propose the response to injury hypothesis to explain the development of atherosclerotic plaques and establish the critical role of hyperlipidemia in the initiation and progression of atherosclerosis. In 1981, Ross Gerrity established the role of the monocyte in atherogenesis using a hypercholesterolaemic swine model. This work de-emphasized the contribution of the vascular smooth muscle cell in the growing atherosclerotic lesion and stressed the importance of foam cells derived from monocytes. In 1983, Erling Falk studied human autopsy specimens and demonstrated that coronary thrombosis developed when plaque rupture occurred at a site of pre-existing coronary stenosis. Further characterization of the vulnerable plaque composition was provided by Michael Davies from an autopsy series of patients who died suddenly of ischaemic coronary disease. Seymour Glagov and co-workers introduced the concept of vascular remodelling when he demonstrated that the vascular wall could actually enlarge to accommodate atherosclerotic lesion growth. Further elucidation of the complexity of atherosclerotic lesions was provided by Herbert Stary when he published results of an autopsy series that included infants through young adults. These studies demonstrated that growth of the atherosclerotic plaque begins very early in life and progresses through various stages of complexity. Following the establishment of the contribution of lipids to atherosclerosis by several investigators, Brown and Goldstein elucidated the major pathway responsible for cholesterol homoeostasis. This work would earn them the Nobel prize and lead to therapeutical breakthroughs towards the battle against atherosclerotic vascular disease.

15 Vascular biology of atherosclerosis Title 1 Author Reference Abstract Summary Atherosclerosis and the arterial smooth muscle cell Ross R, Glomset J Science 1973; 180: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. In this paper, Russell Ross reviews the current data regarding the vascular smooth muscle cell in atherosclerosis. Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. At the time this paper was written, little was known about the genesis of atherosclerosis. Previous studies had demonstrated that blood pressure, smoking and plasma lipid concentrations could influence the development of clinical symptoms of atherosclerotic vascular disease but the sequence of pathological events at the cellular level was largely unknown. Focal accumulation of intimal smooth muscle cells was argued to be critical to the early stages of atherosclerosis. Ross argued that the accumulation of smooth muscle cells necessarily precedes or accompanies both the deposition of lipid and the accumulation of extracellular connective matrix, because the lipid deposits occur either within smooth muscle cells or outside them in association with connective tissue matrix components which are secretory products of smooth muscle cells. Ross stated that smooth muscle cell proliferation began when a breach of endothelial integrity occurred that would allow substances present in the plasma to stimulate cellular proliferation. Studies supporting these observations included the tendency of vascular smooth muscle cells to accumulate in the intima at arterial branch points, where endothelial permeability appeared to be increased. Stemerman and Ross had also demonstrated experimentally using macaques that vascular lesions could be induced by denuding the femoral artery vascular endothelium with balloon catheters. Three months after injury, the lesion contained as many as 15 layers of smooth muscle cells surrounded by collagen and immature elastic fibers. These lesions were described as identical in appearance to the fibromusculoelastic lesions seen in man. Ross also reviews evidence (in vitro and in vivo) that lipids appear to influence proliferation of vascular smooth muscle cells and that vascular smooth muscle cells are responsible for production of extracellular matrix. Citation Count 986 Key message Strengths Vascular smooth muscle cell proliferation plays a critical role in the development and growth of atherosclerotic lesions. The identification of vascular smooth muscle cells and the time course of proliferation and matrix production following vascular injury greatly enhanced the understanding of vascular lesion 2