Marked procoagulant activity and attenuation of physiologic fibrinolytic activity appear to be critical risk factors for the progression of coronary thrombosis and acute myocardial infarction.
The development of coronary thrombosis in response to rupture of atherosclerotic plaques is the primary determinant of the evolution of stable atherosclerotic coronary disease to unstable ischemic syndromes and acute myocardial infarction. Activation of the tissue factor pathway of coagulation and adhesion of platelets are critical events in the initiation of thrombosis. However, subsequently, other factors may determine the extent of thrombosis by modulating the intensity of procoagulant and fibrinolytic activity. Marked procoagulant activity, attenuation of physiologic fibrinolytic activity, or both appear to be risk factors for myocardial infarction. The results of recent studies have provided considerable insight into potential mechanisms for thrombosis in response to rupture of atherosclerotic plaque and have identified potential novel antithrombotic interventions to inhibit the progression of coronary thrombosis.
Paul R. Eisenberg (Tue,) conducted a review in Acute Myocardial Infarction. Marked procoagulant activity and attenuation of physiologic fibrinolytic activity appear to be critical risk factors for the progression of coronary thrombosis and acute myocardial infarction.