Role of platelets and thrombosis in coronary atherosclerotic disease and sudden death.

During the last decade, significant advances have been made in the understanding of the pathogenesis of coronary atherosclerotic disease. Two facts are important: 1) the early and some of the advanced coronary atherosclerotic lesions progress very slowly, probably by means of a complex stepwise biologic process with one of the steps being an interaction between platelets and the arterial wall; the process can be favored by the so-called risk factors of atherosclerotic disease, and 2) some of the advanced coronary atherosclerotic lesions progress very rapidly, probably by means of complicating anatomic events, one of which is related to a thrombogenic process. From a clinical point of view, technologic improvements, such as serial coronary arteriography, reperfusion during the acute coronary artery syndromes, postmortem coronary arteriography, and methods for serial histopathologic and histochemical studies, have brought to light the clinical importance of the processes of plaque rupture, dissecting hemorrhage and, most important, thrombosis. These complicated processes appear to be of paramount importance in the pathogenesis of some of the acute coronary syndromes including unstable angina, myocardial infarction and sudden coronary death. Antithrombotic and platelet inhibitor therapy is under investigation and appears promising in some of these patient subsets.