Arterial thrombosis results from complex gene-gene and gene-environment interactions. While Vichow's triad was traditionally referred to venous thrombosis, the same process has been applied to arterial thrombosis: abnormalities of hemorrheology, abnormal blood constituents and abnormal vessel wall/endothelial dysfunction. Research carried out in the past decade has identified several polymorphisms in genes related to coagulation and fibrinolytic factors, platelet receptors, endothelial dysfunction, homocysteine metabolism, endothelial nitric oxide synthase, abnormal blood flow and oxidative stress. Whereas the individual contribution of each polymorphism to the overall cardiovascular risk seems to be modest, multiple gene-gene and gene-environment interactions appear more relevant in the pathogenesis of arterial thrombosis.