Book Review

New Horizons in Coronary Heart Disease

N Engl J Med 1995; 332:756March 16, 1995

Article

New Horizons in Coronary Heart Disease
Edited by Gustav V.R. Born and Colin J. Schwartz. 292 pp. London, Current Science, 1993. £44.95. ISBN: 1-85922-164-5

This book lives up to its ambitious title. The editors avoid the usual approach of collecting authoritative views on what is known. Instead, they focus on how the flood of knowledge about atherosclerosis can be used to look ahead. Their book provides an invaluable resource for all those working to improve the prevention and treatment of atherosclerosis, whether in molecular biology, vascular biology, clinical investigation, cardiology, cardiac surgery, or epidemiology.

The book's 23 chapters, each written by an internationally recognized authority, cover topics ranging from apolipoprotein E polymorphism to antiplatelet therapy. A special meeting of the chapter authors contributed to the coherence and minimal overlapping of material in the book. The bulk of the writing appears to have been completed in 1993, since most of the recent work cited is from 1992.

The shortcomings of the book are limited. There are more typographic errors than might be expected. All the chapters are readable, but the description of apolipoprotein B is the least accessible to a nonspecialist.

A great strength of the book is its presentation of the themes currently guiding research on atherogenesis. Through the presentation of the potential contributions of lipids, macrophages, and inflammation to the development of atherosclerotic lesions, it is possible to reconcile the lipid-infiltration hypothesis with a revised response-to-injury hypothesis.

For those who demand facts before jumping on intellectual bandwagons, there are detailed descriptions of the evidence that generated the present interest in oxidized low-density lipoprotein, antioxidant therapy, nitric oxide as a mediator of vascular tone, and platelet activity and macrophage function.

Inclusion of the valuable studies performed by Michael Davies expands the limited knowledge about how advanced coronary artery lesions cause the onset of clinical disease. The need for methods to identify and treat nonstenotic plaques that rupture and cause occlusive thrombosis is highlighted.

The following sample of the ideas in this book can only suggest its novelty. Some syndromes of low high-density lipoprotein levels do not increase the risk of cardiac disease. Not all foam cells come from macrophages. The circadian variation in the onset of myocardial infarction may not reflect the daily variation of plaque rupture. Coronary vascular geometry may be a risk factor, since turbulence leads to lesions. Macrophage infiltration of a plaque may be good, because it removes lipids, or bad, because it increases oxidized low-density lipoprotein and adds to the weakening of the plaque cap. Young plaques rupture at the edge of a lipid pool, whereas older plaques may rupture at the border of a calcified area.

In summary, this book engages the reader in the challenge of understanding the complex disease of atherosclerosis. The editors, Drs. Born and Schwartz, who have contributed extensively to the scientific progress described in the book and inspired junior colleagues for many years, have extended their beneficial efforts against atherosclerosis even further with this fine work.

James E. Muller, M.D.
Deaconess Hospital, Boston, MA 02215