Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

摘要: Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired risk factors have been described the pathophysiology of venous thrombosis, degree type abnormalities that contribute arterial are less well understood. Endothelial cell with elaboration proinflammatory mediators stimulates process thrombosis. this is most often result attributable atherosclerotic disease, other disease states can elicit similar response as well. Similarly, once has initiated, variations activity coagulation proteins endogenous anticoagulants, kinetics platelet aggregation, may alter effectiveness thrombus formation. Epidemiological studies identified several or inherited endothelial damage altered equilibrium, thereby predisposing patients These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), thrombophilias, hyper-reactivity. This review explores our present understanding these development thrombotic events. At present, literature supports role for fibrinogen suggests lupus anticoagulants titers cardiolipin IgG antibodies predispose vascular In certain subsets patients, including those concomitant cardiac factors, <55 years age, women, thrombophilias such carriership factor V Leiden prothrombin G20210A mutations confer higher However, data on PAI-1, receptor polymorphisms contradictory lacking.