A large body of literature suggests a relationship between hyperhomocysteinemia and coronary events. Several mutations in the enzymes involved in homocysteine accumulation correlate with thrombosis and, in some studies, with coronary risk.Prospective studies have not shown a robust utility of hyperhomocysteinemia in CHD risk stratification. Clinical trials have not shown that intervention to lower homocysteine levels reduces CHD events. Fortification of the U.S. diet with folic acid to reduce neural tube defects has lowered homocysteine levels in the population at large. Measurement of homocysteine levels should be reserved for individuals with atherosclerosis at a young age or out of proportion to established risk factors. Physicians who advise consumption of supplements containing folic acid should consider that this treatment may mask pernicious anemia.

(Chapter 241. The Pathogenesis, Prevention, and Treatment of Atherosclerosis, Harrison’s Principles of Internal Medicine, 18th edition, Editor: Casa Editrice Ambrosiana)