A substantial international reference on heart failure. This volume will address the major management issues for patients with acute and chronic heart failure and will guide professional diagnosis.
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Philip A Poole-Wilson BA, MB, BChir, MA, MD, FRCP, FACC, FESC, FMedSci is the British Heart Foundation Simon Marks Professor of Cardiology and Head of Cardiovascular Sciences, National Heart & Lung Institute (NHLI), Imperial College London and Honorary Consultant Physician at the Royal Brompton & Harefield Hospitals, London, UK. He qualified (MB) in 1967. He held clinical positions until 1972 at various hospitals in London and was a British American Travelling Research Fellow at the University of California in Los Angeles (UCLA) from 1973 to 1974. His thesis was accepted for MD (Cantab) in 1975. After holding positions as Senior Lecturer (National Heart Hospital) and Reader in Cardiology he was appointed as Professor of Cardiology at the University of London in 1983. In the period 1990-2000 he served as Clinical Director, Research Director, and Non-Executive Board Director of the Royal Brompton Hospital. He was Head of the Division (National Heart and Lung Institute (NHLI)) in the Faculty of Medicine of Imperial College London from 1997 to 2000. He has been a member of the Council and Senate of Imperial College London.
Professor Poole-Wilson's other appointments include President of the European Society of Cardiology (1994-1996) and President of the World Heart Federation (2003-2005) of which he is currently the Past-President. He has served on many committees within the Department of Health, MRC, Research Assessment Exercise, British Heart Foundation and Welcome Trust in the UK. He is on the Editorial Board of several leading journals and is Chairman/Member of the Steering or Monitoring Committees of several large clinical trials. He was awarded Le Prix Europe et Medecine 2001 de l’Institut des Sciences de la Sante, Paris and has received many other awards. As of March 2006 he had 459 citations in PubMed. His specialist interests are heart failure, coronary heart disease and the global prevention of heart disease and stroke.
Thomas R. Kuhn, in The Structure of Scientific Revolutions (2nd ed. Chicago: University of Chicago Press, 1970), describes scientific progress as a series of revolutions, which he calls paradigm shifts. According to Kuhn, knowledge advances when an established system of beliefs (paradigm) can no longer explain new observations that, when viewed from within the paradigm, represent anomalies. This creates a crisis that ends with the emergence of a new paradigm -- the scientific revolution. Such a paradigm shift began in 1628, when Harvey's description of the heart as a pump challenged the galenic view that the heart's chief function was to heat the blood. When, in 1715, Vieussens relied on Harvey's observations in describing how mitral stenosis caused blood to back up into the lungs, this new paradigm replaced the hippocratic view that phlegm (the cold humor) descending from the brain into the chest caused pleural effusions.
Those who have followed developments in the study of heart failure will recognize that this field is evolving through a paradigm shift as dramatic as that which followed Harvey's description of the circulation. It is now clear that heart failure cannot be viewed simply as a pump disorder (the result of abnormal organ physiology) caused by myocardial weakness (abnormal cell biochemistry). Although these earlier paradigms provide valid explanations for most clinical features of this syndrome, they do not explain the apparently anomalous results of several recent clinical trials. For example, inotropic drugs, although providing immediate symptomatic relief, have been found to worsen prognosis, whereas beta-blockers, which initially weaken the failing heart, cause slow improvement in cardiac function and appear to prolong survival. The paradigms of organ physiology and cell biochemistry also cannot explain why most direct-acting vasodilators, while causing short-term symptomatic improvement, either worsen prognosis or have no effect on survival, whereas angiotensin-converting-enzyme inhibitors have the opposite effect and improve outcome. By creating a Kuhnian crisis, these and other anomalies tell us a new paradigm is needed to understand heart failure.
Such a new paradigm is provided by molecular biology, which over the past decade has given us a novel way to view the failing heart. This paradigm explains many anomalies, notably how the effects of drugs on gene expression might influence long-term prognosis. It also helps us in understanding why fetal genes are reexpressed in the overloaded adult heart, how the addition of sarcomeres at the ends of cardiac myocytes contributes to the progressive dilatation ("remodeling") that puts failing hearts at a mechanical and energetic disadvantage, and how modifying the hypertrophic response can improve symptoms and prolong survival in patients with this condition.
Viewed against the background of a field in rapid transition, an important textbook such as Heart Failure: Scientific Principles and Clinical Practice faces daunting challenges. How well does it bring up to date the many valid aspects of the older paradigms of organ physiology and cell biochemistry? Does the book help the reader understand the growing impact of the new paradigm of molecular biology on patient care? Are these topics presented in a manner that justifies the purchase of such a large and expensive book? Happily, all of these questions can be answered in the affirmative -- and with considerable enthusiasm.
In addition to providing updates on topics such as fluid retention, the causes of dyspnea, receptor abnormalities, cardiac energetics, and endothelial factors, as well as valuable reviews of epidemiology, etiology, diagnosis, and clinical management, this book includes several chapters that describe heart failure in terms of the paradigm of molecular biology. The 55 chapters, written by recognized experts in the many fields covered, are uniformly excellent and up to date; the chapter on beta-blockers, for example, provides a timely discussion that includes data published in 1996. Since most chapters are actually free-standing essays, this multiauthored book can be recommended as a reference for those seeking authoritative discussions of specific aspects of heart failure, rather than an introductory textbook for the nonexpert. At this time, when new concepts regarding the pathophysiology and treatment of heart failure are appearing each year, it is a pleasure to have a book as timely and well written as that edited by Poole-Wilson and his colleagues.
Reviewed by Arnold M. Katz, M.D.
Copyright © 1998 Massachusetts Medical Society. All rights reserved. The New England Journal of Medicine is a registered trademark of the MMS.
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