Abstract
Several lines of evidence point to an important role for platelets in the pathogenesis of sudden death, acute myocardial infarction, and unstable angina.1 These acute coronary events usually occur on a background of advanced coronary atherosclerosis. Observations made at autopsy,2 by angiography,1 and by angioscopy3 suggest that these acute coronary events are precipitated by rupture of an atherosclerotic plaque, which exposes platelets and other blood elements to reactive components, such as collagen, in the depths of the plaque. These interactions result in the adhesion of platelets to the exposed subendothelium and the release by platelets of chemical mediators that induce . . .