Abstract
It is generally held that impairment of coronary-artery blood flow is a major cause of angina pectoris, myocardial infarction, ventricular arrhythmias, and sudden cardiac death. These events may be precipitated through several mechanisms that affect the coronary vessels, such as atherosclerotic narrowing, vasospasm, rupture of an atherosclerotic plaque with consequent hemorrhage or thrombosis, and increased sensitivity to autonomic or sympathomimetic stimuli. Platelet activation could be important in one or more of these mechanisms. The role of platelets in initiating arterial thrombosis is well established. Activated platelets also synthesize THROMBOXANE A2, which is a potent platelet aggregant and vasoconstrictor . . .