Elevated plasma homocysteine level (tHcy) is one of the risk factors for coronary artery disease (CAD). It has been demonstrated that doses of folate as low as 0.25 mg/d significantly decreased tHcy in healthy, young women. Homozygosity for C-677T polymorphism in the Methylenetetrahydrofolate reductase (MTHFR) gene seems to be correlated with an elevated tHcy in the situation of low blood folate concentrations. In this study, we evaluated the response of the low dose folate treatment on the tHcy and whether genetic variation of MTHFR gene might influence the response of the folate treatment in korean CAD patients.

CAD patients (n=3), confirmed by coronary angiography, and controls were analyzed for CAD risk factors including tHcy and MTHFR gene C-677T polymorphism. Patients were treated with daily 0.25mg folate for 4weeks and the level of folate and tHcy was reevaluated.

Low dose folate treatment for 4weeks significantly increased folate level (38%, p<0.05), but did not influence tHcy. Patients whose tHcy was decreased with folate replacement (n=1) were characterized by low basal folate level (7.0±2.6 vs 9.1±2.7 nmol/L, p<0.05) and high basal tHcy (12.6±4.4 vs 8.6±2.4 micromol/L, p<0.05) compared to the patients whose tHcy was unaffected or increased with folate. tHcy was decreased 11.2% and 12.6% each in patients with high basal tHcy (>10 micromol/L) and low folate level (<7 nmol/L), but increased 7.3% and 4.5% in patients with low tHcy and high folate level (p<0.05, each). MTHFR C-677T polymorphism was not a significant contributing factor for tHcy and for the response to folate treatment.

Low dose folate treatment can decrease tHcy in CAD patients with low basal folate level and high basal tHcy. C-677T MTHFR gene mutation does not influence the effects of low dose folate treatment on tHcy in Korean CAD patients.