Homocysteine and atherothrombosis: diagnosis and treatment.
Hyperhomocysteinemia has long been recognized as a risk factor for cardiovascular disease. Many cross-sectional and retrospective case-control studies have shown an association between elevated total homocysteine levels and coronary, peripheral, and cerebral vascular disease; prospective studies, however, have been inconsistent. Overall, there is evidence to suggest a modest association between elevated homocysteine levels and cardiovascular disease risk. Folate supplementation has been shown to reduce plasma homocysteine even when levels are in the normal range. Clinical studies suggest that lowering plasma homocysteine may improve endothelial dysfunction, a marker of atherothrombotic risk. The long-term effects of folate supplementation on homocysteine levels and cardiovascular disease risk await the results of ongoing clinical trials. However, several recent studies suggest a benefit for reduction of plasma homocysteine levels, as individuals with lower homocysteine have reduced cardiovascular event rates.
Handy
Diane E
DE
Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
Loscalzo
Joseph
J
D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D003327:Coronary Disease / Q000235:genetics; D004730:Endothelium, Vascular / Q000503:physiopathology; D005492:Folic Acid / Q000627:therapeutic use; D006397:Hematinics / Q000627:therapeutic use; D006710:Homocysteine / Q000378:metabolism*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications* / Q000188:drug therapy / Q000209:etiology; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D018384:Oxidative Stress / Q000502:physiology; D011110:Polymorphism, Genetic; D013927:Thrombosis / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control
D006397:Hematinics; D006710:Homocysteine; D005492:Folic Acid; D042965:Methylenetetrahydrofolate Reductase (NADPH2)