Elevated homocysteine levels have been confirmed as an independent risk factor for thrombosis and atherosclerotic cardiovascular disease. Putative mechanisms of atherothrombosis in hyperhomocysteinemia include endothelial cell injury, endothelial dysfunction, increased vascular smooth muscle cell growth, increased platelet adhesiveness, enhanced LDL oxidation and deposition in the arterial wall, and direct activation of the coagulation cascade. The vascular changes in hyperhomocysteinemia are likely to be multifactorial. The treatment of hyperhomocysteinemia varies with the underlying cause; however, vitamin supplementation (with folic acid, pyridoxine, and vitamin B12) is generally effective in reducing homocysteine concentrations.