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May 27, 1983

Platelets and Prostaglandins in Coronary Artery Disease: Rationale for Use of Platelet-Suppressive Drugs

Author Affiliations

From the Department of Medicine, University of Florida College of Medicine, and the Veterans Administration Medical Center, Gainesville, Fla.

JAMA. 1983;249(20):2818-2823. doi:10.1001/jama.1983.03330440056034

THE ROLE of platelets in the genesis of atherosclerosis and its manifestations has received considerable attention. Based on the recognition of platelet "hyperactivity" in patients with coronary artery disease, several platelet-suppressive drugs have been used in a large number of patients. The purpose of this article is to review the role of platelets, the mechanisms of platelet activation, and the results of platelet-inhibitory drug trials in patients with coronary artery disease.

PLATELETS AND HEMOSTASIS  Platelets, small disklike cells circulating in the blood, have a primary role in hemostasis. With stress to the endothelium and its subsequent disruption, platelets adhere to the subendothelial collagen. Circulating platelets are attracted to the adhering platelets, resulting in platelet aggregation and formation of a platelet thrombus. In this thrombus, RBCs, WBCs, and other components of blood are incorporated, resulting in an occlusive clot. On activation, platelets also release potent hormones, prostaglandins, polypeptides, and other vasoactive