The Severity of Coronary Artery Disease and Methylenetetrahydrofolate Reductase (MTHFR) Enzyme Gene Polymorphism

Background: Some mutations of Methylenetetrahydrofolate Reductase (MTHFR) \ngene cause a decrease in MTHFR activity. Decreased MTHFR activity may, in turn, be \nassociated with increased plasma homocysteine level and vascular disease. \nObjectives: This study aimed to assess the effect of homocysteine, MTHFR C677T, and \nA1298C gene polymorphisms on the extent and severity of Coronary Artery Disease (CAD). \nPatients and Methods: This study was conducted on 53 patients with the diagnosis \nof myocardial infarction. According to the results of coronary angiography, Reardon \ncoronary artery scoring was applied to assess the extent and severity of atherosclerosis. \nMTHFR C677T and A1298C gene mutations and serum homocysteine, folate, and \nvitamin B12 levels were analyzed, as well. \nResults: TT genotype of MTHFR C677T gene polymorphism was not found in any of the \npatients. On the other hand, the incidence of CC and CT genotypes in MTHFR C677T \ngene polymorphism was 47.2% and 52.8%, respectively. Besides, the incidence of AA, \nAC, and CC genotypes in MTHFR A1298C gene polymorphism was 37.7%, 45.3%, and \n17%, respectively. The results showed no significant difference among different MTHFR \ngenotypes regarding the extent and severity of CAD. Additionally, serum homocysteine, \nfolate, and vitamin B12 levels were not associated with the extent and severity of CAD. \nConclusions: Although most studies have found a relationship between homocysteine \nand MTHFR C677T and A1298C gene polymorphism, this relationship was not \nobserved in our study. According to the results, the severity of CAD was not affected by \nhomocysteine level or MTHFR genotypes. Thus, investigation of different MTHFR gene \npolymorphisms in a larger number of participants would help understand the genetic \nbasic of CAD.