Abstract
McCully first proposed the idea that, in patients with homocysteinemia, high plasma levels of homocysteine (Hcy) resulted in severe and premature atherosclerosis. Epidemiologic studies indicate that hyperhomocysteinemia is an independent risk factor for atherosclerosis. Meta analysis revealed that for every 5μmol/l increase in homocysteine, men had a 1.6-fold increase in the coronary heart disease risk. A 5μmol/l increase in plasma homocysteine is equivalent to an increase in blood cholesterol of 0.5μmol/l. Increasing in the dietary intake of folic acid by 200μg should reduce homocysteine levels by 4μmol/l. Studies investigating the mechanism of action of homocysteine suggest that an increased level of plasma homocysteine may be a physiological risk factor for thrombosis and arterial injury as well as for increased risk of fibrous plaque formation.
A key enzymes for homocysteine metabolism is cystathionine β-synthase and methylenetetrahydrofolate reductase (MTHFR). Recently, polymorphism of these enzymes has been reported to play an important role in the genesis of hyperhomocysteinemia. There is a polymorphysm of the MTHFR (C677T), Ala/Val and Val/Val genotype associated with coronary artery disease.
