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(Circulation. 2001;104:1451.)
© 2001 American Heart Association, Inc.

Editorials

Platelet Collagen Receptors and Risk Prediction in Stroke and Coronary Artery Disease

Thomas J. Kunicki, PhD; Zaverio M. Ruggeri, MD

From the Roon Research Center for Arteriosclerosis and Thrombosis, Division of Experimental Hemostasis and Thrombosis of the Department of Molecular and Experimental Medicine and the Department of Vascular Biology, The Scripps Research Institute, La Jolla, Calif.

Correspondence to Thomas J. Kunicki, PhD, Associate Professor, Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, Maildrop: MEM 150, La Jolla, CA 92037. E-mail tomk@scripps.edu

Key Words: Editorial • platelets • stroke

The importance of thrombosis as a health hazard cannot be overestimated. Ischemic heart disease and cerebrovascular disease are the leading causes of morbidity and mortality among both adult men and adult women in the developed western world.^1,2 Recent evidence indicates that the incidence of this disease is steadily increasing among Asian populations,³ and cardiovascular disease is now the leading cause of death among native American Indians.⁴ Epidemiological studies indicate that these diseases result from complex interactions between genetic susceptibility factors, long-term environmental influences (for example, hormonal imbalance, smoking, or obesity), and established, intercurrent disorders (such as diabetes, hypertension, dyslipidemia, or hyperhomocysteinemia).

See p 1459

A devastating complication of these disorders is acute myocardial infarction, which results from the formation of an occlusive thrombus at the site of a ruptured atherosclerotic plaque. The critical role of platelets in this process is now well accepted.⁵ Plaque rupture and/or endothelial damage lead to the exposure of von Willebrand factor and collagen, among other platelet-reactive substrates, which facilitate the adhesion of circulating platelets to the damaged vessel wall. Several receptors, each with distinct functions, are involved in this process, including the glycoprotein (GP) Ib-IX-V complex, the integrins ₂ß₁ and ₅ß₁,⁶ and platelet GP VI. As a result of these initial interactions, the platelet is activated, leading to a conformational change in another integrin, _IIbß₃, which contributes in a fundamental way to the homotypic aggregation of platelets into a thrombus. Thrombin generated at the blood-plaque interface converts fibrinogen to fibrin, which stabilizes thrombus . . . [Full Text of this Article]

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