EDITORIALS Platelet Aggregation and Thrombotic Vascular Disease

frequently the final event in coronary or cerebral arterial occlusion, is a result of the interplay of abnormalities of the vessel wall, hemodynamic forces, plasma coagulant proteins, and platelets. Platelets are thought to initiate a series of intricate reactions by ad-hering to the injured arterial lining, aggregating irreversibly to form a platelet plug, and releasing vasoactive metabolites and hydrolytic enzymes that might in turn alter both the function and structure of the vessel. Heightened platelet function thus might not only participate in the formation of thrombi but also may play a role in the development or progression of some forms of atherosclerosis. The paper in this issue by Sagel and associates (p. 733) reports on the finding that 39 prediabetic, latent, or frankly diabetic subjects had increased platelet aggregation to th