Prothrombotic effects of homocysteine, which have been demonstrated in patients with acute coronary syndromes include attenuation of endothelial cell tissue plasminogen activator binding sites, activation of factor VIIa and V, inhibition of protein C and heparan sulfate, increased fibrinopeptide A and prothrombin fragments 1 and 2, increased blood viscosity, and decreased endothelial antithrombotic activity due to changes in thrombomodulin function. This evidence concerns the gene PLAT and acute coronary syndrome.