ABSTRACT
Atherosclerosis predisposes to arterial thrombosis and thrombosis superimposed on a disrupted plaque is the proximate event that triggers acute ischemic syndromes and sudden death. A number of studies have focused on novel risk factors, predominantly related to hemostasis and coagulation, to identify a potential role for primary hemostatic abnormalities and cardiovascular risk. Fibrinogen, precursor of fibrin, is an important coagulation protein that plays an important role in plasma viscosity and platelet aggregation. Thrombomodulin is an endothelial cell surface receptor for thrombin that accelerates thrombin-induced activation of the natural anticoagulant protein C. The relationship between hemostatic factors and risk for arterial atherothrombosis, after correction for all known risk factors and confounding variables, is at best weak and at worst unconvincing. Inflammation is critically linked to various pathophysiologic events leading to initiation, progression, and destabilization of atherosclerosis. Several prospective studies have examined the relationship between FVII mediated pro-coagulant activity and atherothrombosis, but the results have been inconsistent.
