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Despite considerable progress in defining the role of hypercoagulable states in venous thromboembolic disease, the contribution of hypercoagulability to arterial vascular disease remains less clear. It is now well established that thrombophilic conditions such as factor V Leiden and the prothrombin G20210A mutation are risk factors for deep vein thrombosis, pulmonary embolism, and other venous thromboembolic events.1 By contrast, these thrombophilic factors have not been found to be clinically important risk factors for arterial thrombotic events such as ischemic stroke or acute coronary syndromes,2–4 despite the fact that arterial thrombosis is a frequent complication of atherosclerosis and plaque rupture.5 A commonly accepted explanation for the markedly different influences of hypercoagulability on venous versus arterial thrombotic events is that thrombosis in the deep veins, which occurs at low shear stress, is mediated primarily by activation of the coagulation cascade, whereas thrombosis in arteries is mediated primarily by activation of platelets under conditions of high shear stress.2 This explanation fits well with the clinical observation that antiplatelet drugs, such as aspirin or clopidogrel, are effective in the prevention of arterial events, whereas anticoagulant therapies, such as vitamin K antagonists, are the mainstay of treatment for venous thromboembolic disease. On the other hand, the observation that men with hemophilia are relatively protected from mortality due to ischemic heart disease in comparison with the general male population6 suggests that impaired coagulation can impede thrombosis formation in coronary arteries.Article see p 774 In this issue of Circulation , Seehaus et al7 report an intriguing series of observations from murine models that may …

Countervailing Effects on Atherogenesis and Plaque Stability