The Severity of Coronary Artery Disease and Methylenetetrahydrofolate Reductase (MTHFR) Enzyme Gene Polymorphism
Journal Title: International Cardiovascular Research Journal - Year 2016, Vol 10, Issue 4
Abstract
Background: Some mutations of Methylenetetrahydrofolate Reductase (MTHFR) gene cause a decrease in MTHFR activity. Decreased MTHFR activity may, in turn, be associated with increased plasma homocysteine level and vascular disease. Objectives: This study aimed to assess the effect of homocysteine, MTHFR C677T, and A1298C gene polymorphisms on the extent and severity of Coronary Artery Disease (CAD). Patients and Methods: This study was conducted on 53 patients with the diagnosis of myocardial infarction. According to the results of coronary angiography, Reardon coronary artery scoring was applied to assess the extent and severity of atherosclerosis. MTHFR C677T and A1298C gene mutations and serum homocysteine, folate, and vitamin B12 levels were analyzed, as well. Results: TT genotype of MTHFR C677T gene polymorphism was not found in any of the patients. On the other hand, the incidence of CC and CT genotypes in MTHFR C677T gene polymorphism was 47.2% and 52.8%, respectively. Besides, the incidence of AA, AC, and CC genotypes in MTHFR A1298C gene polymorphism was 37.7%, 45.3%, and 17%, respectively. The results showed no significant difference among different MTHFR genotypes regarding the extent and severity of CAD. Additionally, serum homocysteine, folate, and vitamin B12 levels were not associated with the extent and severity of CAD. Conclusions: Although most studies have found a relationship between homocysteine and MTHFR C677T and A1298C gene polymorphism, this relationship was not observed in our study. According to the results, the severity of CAD was not affected by homocysteine level or MTHFR genotypes. Thus, investigation of different MTHFR gene polymorphisms in a larger number of participants would help understand the genetic basic of CAD.
Authors and Affiliations
Fatma Demet Ince, Aysenur Atay, Mehmet Hicri Koseoglu, Hamit Yasar Ellidag, Murat Yesil, Erdal Deveci
Keywords
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