Specific Platelet Mediators and the Abrupt Progression of Coronary Artery Stenoses

Abstract

Acute coronary heart disease syndromes, including unstable angina and acute myocardial infarction, are usually caused by a primary decrease in coronary blood flow and myocardial oxygen delivery.1–15 Unstable angina occurs in patients with endothelial injury or ulceration at the site of an atherosclerotic plaque and some patients have an intraluminal coronary artery thrombosis.4–6,9–11 Falk7 and Davies and Thomas8 have shown that atherosclerotic plaque Assuring or rupture may lead to coronary arterial thrombosis and the development of unstable angina, acute myocardial infarction, or sudden death. Patients with Q-wave myocardial infarcts often have ulcerated or atherosclerotic plaques and the subsequent development of occlusive coronary artery thrombi.2,3 Patients with non-Q-wave infarcts (usually subendocardial infarcts) much less commonly have coronary artery thrombi that are permanently occlusive, but instead these patients have transient reductions in coronary blood flow followed by reperfusion and sometimes partially occlusive thrombi.3,16 We believe that transient reductions in coronary blood flow are most likely related to intermittent platelet aggregation and vasoconstriction contributed to by the release of selected mediators from aggregating platelets at sites of coronary artery endothelial injury and stenosis.4,5,17