Numerous large-scale and prospectively designed epidemiologic studies suggest that hemostatic factors, for instance fibrinogen, D-dimer, VWF, and PAI-1, predict cardiovascular disease (CVD) in apparently healthy subjects as well as recurrent events in patients with established CVD (Lowe et al, 2002). These relationships have been shown to be independent of sociodemographic factors, lifestyle, and established cardiovascular risk factors smoking, diabetes, hypertension, and obesity, all of which may affect hemostasis. Altogether, this abundant epidemiologic research challenges the view that hemostasis factors are mere risk markers of CVD and do not actively contribute to atherosclerosis. It is assumed that a procoagulant milieu, as reflected by increased activity of clotting factors, coagulation activation markers, platelets, and the VWF on the one hand and impaired fibrinolysis on the other will gradually contribute to atherosclerosis progression over many decades by promoting fibrin deposits in the atherosclerotic vessel wall and inflammation (Falk and Fernandez-Ortiz, 1995). Moreover, a procoagulant milieu at the time of atherosclerotic plaque rupturing will accelerate coronary thrombus growth to determine myocardial ischemia and damage.
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