doi: 10.1161/CIRCULATIONAHA.106.621623
(Circulation. 2006;113:e853.)
© 2006 American Heart Association, Inc.
Book Reviews |
Molecular Mechanisms of Cardiac Hypertrophy and Failure
University of Texas Southwestern Medical Center, Dallas, Tex
 |
Introduction |
|---|
 Top Introduction DisclosuresReferences |
|---|
Richard A. Walsh, MD, ed
736 pages. London, UK: Taylor & Francis; 2005. $299.95. ISBN 1-84212-488
The heart responds to multiple forms of stress with an adaptive hypertrophic increase in cardiac mass. Under prolonged stress, the heart undergoes an apparent irreversible change, resulting in dilation, diminished performance, and ultimate failure.1 Heart failure is the leading hospital discharge diagnosis in the United States, and despite the application of state-of-the art therapy, mortality remains high at 
50% at 5 years.2
Substantial efforts have been dedicated to the discovery of novel ways to prevent, detect, and treat cardiac hypertrophy and failure. Despite these efforts, however, virtually all the advances in heart failure therapy over the past 3 decades have emanated from other fields.3 The now-bedrock therapies that antagonize prominent signaling cascades (eg, angiotensin-converting enzyme inhibitors, ß-blockers, aldosterone antagonists) were first developed to treat other disorders (eg, hypertension, angina, or edema). The increasing use of device-based therapy can be viewed as a byproduct of electrophysiology. Contrast this with the distressingly large number of potential therapies emanating from basic studies, such as adrenergic agonists, phosphodiesterase inhibitors, Ca2+ sensitizers, and cytokine antagonists, which have failed to emerge as successful therapies for the chronic treatment of heart failure.
Many of us accept that the failure of basic research-derived therapies stems in part from a lack of a full appreciation of the varied and wide-ranging nature of the syndrome we call heart failure. In fact, a multitude of investigators around the world have devoted their life’s work to deciphering molecular mechanisms inherent to heart failure in pursuit of discovering key principles that will guide future therapy. However, given that a multitude of disease mechanisms ultimately culminate in heart failure—including myocardial infarction, chronic pressure or volume overload, excessive electrical activation, over-stimulation by circulating factors, and mutations of genes encoding contractile, cytoskeletal, or Ca2+-handling proteins—it is not too surprising that heart failure remains a highly elusive syndrome.
The new book entitled Molecular Mechanisms of Cardiac Hypertrophy and Failure is an important addition to this field. The editor, Richard Walsh, has amassed an impressive list of expert associate editors and contributors to tackle the job of providing comprehensive and accessible synopses of numerous complex topics. Designed as a compendium of 41 short chapters, it provides en masse an ample overview of a fast-moving field of science. Overall, the book is styled as a collection of discrete, free-standing chapters, rather than as a linear work with a continuous thread. The book is divided logically into 4 sections focusing on mechanisms of (1) cardiac hypertrophy, (2) abnormal cardiac function in heart failure, (3) arrhythmogenesis, and (4) the molecular genetic basis of cardiomyopathy.
Inside, the reader is afforded serial snapshots that canvas most aspects of this area of biology. The chapters are relatively short, making them accessible and inviting. Interested readers seeking more in-depth treatment will find citations to the primary literature in which additional detail can be found. The reader can expect to find a worthwhile and enjoyable read in the great majority of the chapters. Plentiful and informative illustrations are included; however, it is somewhat distracting to turn repeatedly to the front to access color illustrations, a cost-saving move presumably mandated by the publisher.
A major benefit that will be derived from this work is the availability of a well-written and comprehensive source of information that can rapidly propel new investigators to the leading edge of knowledge in this field. Indeed, this book fills a significant void, as no similar book has previously been published.
Given the pace of discovery in cardiovascular biology, we expect that new editions will appear in future years. In those future editions, expanded discussion of the challenge of translating basic insights into clinically relevant interventions and drug discovery will be welcome. The converse challenge of translating clinical observations for use in the basic laboratory will also be an important topic for future consideration.
Not only is the pace of discovery in this field rapid, but the character of heart failure itself is also evolving. For instance, we expect the worldwide epidemic of obesity and metabolic syndrome to change the face of heart failure in ways beyond the emergence of atherosclerotic disease in younger and younger patients. As one example, future editions of the text will be enhanced by expanded treatment of lipotoxic cardiomyopathies.
Because this textbook is a successful compendium of science in a fast-moving, evolving field, we recommend it to both new and seasoned investigators. For the former, it provides a much-needed introduction to a complex area of biological science; for the latter, it provides a snapshot in time and signposts that point the way to more detailed information. The authors and editors are to be commended for a very fine work that will emerge rapidly as an important resource.
|
Disclosures |
|---|
|
TopIntroductionDisclosuresReferences |
|---|
Dr Rothermel received a research grant from the National Institutes of Health. Dr Hill received research grants from the National Institutes of Health, the American Heart Association, and the Reynolds Foundation.
|
References |
|---|
|
TopIntroductionDisclosuresReferences |
|---|
1. Berenji K, Drazner MH, Rothermel BA, Hill JA. Does load-induced ventricular hypertrophy progress to systolic heart failure? Am J Physiol Heart Circ Physiol. 2005; 289: H8–H16.
2. Heart Disease and Stroke Statistics: 2006 Update. Dallas, Tex: American Heart Association; 2006.
3. Packer M. The impossible task of developing a new treatment for heart failure. J Card Fail. 2002; 8: 193–196.[CrossRef][Medline] [Order article via Infotrieve]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||