Platelets: Pathophysiology and Antiplatelet Drug Therapy By Harvey J. Weiss (review)

Abstract

BOOK REVIEWS Platelets: Pathophysiology and Antiplatelet Drug Therapy. By Harvey J. Weiss. New York: Alan R. Liss, 1982. Pp. 165. $22.00. Dr. Harvey J. Weiss is professor of medicine, College of Physicians and Surgeons of Columbia University, and director of the Division of HematologyOncology at St. Luke's-Roosevelt Hospital Center in New York. He has a longstanding interest in many aspects ofplatelet function and in the inhibitory effects of the so-called antiplatelet drugs. In collaboration with a number of investigators , he has made significant contributions to our present knowledge of these subjects. This is die latest in a number of useful reviews of this nature diat Dr. Weiss has written. It provides a detailed overview up to 1981, although Dr. Weiss was able to add some references to articles published in 1982. It is appropriate that this book should be reviewed in Perspectives in Biology and Mediane since it itself provides a perspective. The book is divided into four chapters, the first two, concerning platelet mechanisms and the biological properties of platelets, serving to set the stage for chapters 3 and 4, in which the pharmacological aspects of "antiplatelet drugs" are discussed and their use in clinical medicine is described widi emphasis on the large-scale clinical trials in patients widi cerebrovascular disease and ischemic heart disease. An indication of the comprehensive review provided by this book is die reference list which contains well over 800 citations. A useful index is also included. In general, Dr. Weiss has made appropriate choices of the topics that are necessary to provide an adequate background for the understanding of the effects of"antiplatelet drugs" and their uses. Of necessity, the discussion of each topic is brief, but in most cases it is focused on die key information. Although the history of the development of our understanding of subjects such as ADPinduced aggregation or prostaglandins is of interest, some of the early theories that are no longer accepted might have been omitted to permit more detailed discussion ofsubjects ofcurrent interest, such as the role offibrinogen in aggregation induced by all agents, die reversible nature ofthe complex of membrane glycoproteins that form die fibrinogen receptor, die relationship of this reversibility to platelet deaggregation, the possible role of thrombospondin in platelet aggregation, the synergistic effects among aggregating agents, and the activation of the phosphoinositol-phosphatidic acid cycle in response to release-inducing agents. However, in a relatively short chapter ranging from platelet production through rheology, structure, activation, function, metabolism, to regulation and role in coagulation, diere are bound to be a few Permission to reprint a book review printed in diis section may be obtained only from the author. 314 Book Reviews omissions, and, of course, we tend to notice when topics in which we are most interested are not mentioned. Chapter 2 gives a clear summary of the role of platelets in hemostasis and the platelet abnormalities that result in impairment of hemostasis. Thrombosis and atherogenesis are treated more briefly, with litde consideration of the causes of vessel wall injury that may initiate thrombosis and atherosclerosis, or of die eventual dissolution or resolution of thrombi. The roles of platelets in maintaining vascular integrity, and in inflammation, immunological reactions, and malignancy are quite rightly identified as important biological properties of platelets. The inclusion of platelet-activating factor (PAF) in the section on immunological reactions, rather than as a platelet aggregating agent, is appropriate since it seems unlikely that PAF has much involvement in the aggregation of human platelets. Chapter 3 on the pharmacologic aspects of antiplatelet drugs concentrates on the drugs that are currently in use or have the potential to be used in clinical medicine. It is organized into sections on drugs that inhibit the formation of thromboxane A2 by platelets and PGI2 formation by the vessel wall, agents that raise cyclic AMP in platelets, drugs that act on die platelet membrane, anticoagulants , and a number ofdrugs that act in less well-defined ways. Drugs diat inhibit cyclo-oxygenase receive the most attention since they have been most extensively studied in all respects, including clinical trials. The rationale for the development of thromboxane synthetase inhibitors is not discussed, although, theoretically, their ability...