[Pathophysiology of acute coronary syndromes]

Abstract

Coronary atherosclerosis and plaque disruption with superimposed thrombosis are the main causes of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death. Coronary artery spasm has also been implicated in the pathogenesis of acute coronary syndromes. Other researchers and we have reported that the plasma levels of fibrinopeptide A, a sensitive marker of thrombin generation, and plasminogen activator inhibitor activity, an indicator of the impairment of fibrinolysis, increase in patients with unstable angina and acute myocardial infarction. We also showed that coronary artery spasm induced fibrinopeptide A generation and may lead to thrombus formation in the coronary artery involved, and plasminogen activator inhibitor activity increased after coronary spasm. Tissue factor is the primary initiator of the extrinsic coagulation cascade. We have recently demonstrated that the plasma TF antigen levels increase in patients with acute myocardial infarction and unstable angina. Furthermore, we examined directional coronary atherectomy specimens from 24 patients with unstable angina and 23 with stable exertional angina. We have shown that tissue factor expression on macrophages was more frequent in coronary atherosclerotic plaques in patients with unstable angina. Tissue factor expressed on macrophages may play an important role in the thrombogenicity in coronary atherosclerotic plaques of these patients. In conclusion, increased coagulation cascade and impaired fibrinolysis occurs and leads to coronary thrombosis in patients with acute coronary syndromes. These phenomena also occur in patients with coronary spasm.