elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Exercise training reduces plasma levels of homocysteine and improves endothelial function, however without evidence of a better outcome. Larger studies are needed in order to demonstrate that the reduction of plasma levels of homocysteine by oral supplementation with folates and vitamins B6 and B12 translates into a decreased incidence of ischemic events, in particular in patients with documented coronary artery disease and ischemic encephalopathy.
hyperhomocysteinemia, arteriosclerotic vascular disease, cardiovascular risk factors, folic acid, 5-methyltetrahydrofolate