The relationship between endothelial nitric oxide synthase gene polymorphism (T-786 C) and coronary artery disease in the Turkish population

Abstract

Previous studies revealed that there were various mutations on endothelial nitric oxide synthase (eNOS) gene and these mutations might be a risk factor for coronary artery disease (CAD), myocardial infarction (MI), and hypertension (HT). In this study, we aimed to investigate the relationship between eNOS gene polymorphism (T-786 C) and coronary artery disease in the Turkish population. Two hundred and eleven unrelated individuals (152 male, 59 female, mean age 59 years, range 27-85) whose angiographic examinations were performed in our hospital were enrolled into the study; 159 of these had angiographically determined coronary artery lesions (>or=50% stenosis at least in one vessel). Fifty-two individuals were free of coronary artery disease on their coronary angiography. The Gensini scoring system was used to determine the severity of the CAD. The polymerase chain reaction (PCR) method was used for genotyping the individuals. To determine the independent risk factors for coronary artery disease, multivariate logistic regression analysis was used. The variant distribution of the T-786 C polymorphism was as follows. For all individuals: TT 94 (44.5%), TC 88 (41.7%), CC 29 (13.8%); in CAD patients: TT 63 (39.6%), TC 73 (45.9%), CC 23 (14.5%); and in normal individuals: TT 31 (59.6%), TC 15 (28.8%), CC 6 (11.5%). There was a statistically significant difference in the variant distribution between CAD and normal individuals (P<0.05). On the other hand, when we compared the frequency of the at-least-one-C-allele carriers (CC+TC, dominant model) and TT homozygous, those with at least one C allele were more prevalent in CAD patients. The results were as follows. In coronary artery disease patients: CC+TC 96 (60.4%), TT 63 (39.6%); in normals: TC+CC 21 (40.4%), TT 31 (59.6%) (P<0.01). When we compared the allele distribution (T vs C, additive model) between CAD patients and normal controls, the results were as follows: T 0.625 vs 0.740, C 0.375 vs 0.260; there was also a statistically significant association between CAD and C allele (P<0.05). When we compared the means of the Gensini scores between each genotype of the T-786 C mutation, there was a statistically significant difference. The results were TT (48.6+/-37.3, median 43.0), TC (55.4+/-41.2, median 41.0), CC (77+/-43.6, median 80.0) (P<0.05). Multivariate logistic regression analysis revealed that C-dominant (CC+TC) individuals had 2.9-fold more likelihood to suffer from CAD (odds ratio: 2.902; confidence interval: 1.272-6.622) (P<0.05). We conclude that the T-786 C polymorphism of eNOS gene might be a risk factor for coronary artery disease in the Turkish population.

The −665 C>T polymorphism in the eNOS gene predicts cardiovascular mortality and morbidity in white Europeans

“…A few case-control studies 12-14 addressed the issue whether coronary heart disease might be associated with genetic variation in eNOS. Cases were patients referred for coronary angiography 14 or patients with myocardial infarction 12,13 or angiographically confirmed coronary lesions. 12 The studied single-nucleotide polymorphisms included rs2070744 (T786C) 14 and rs1799983 (glu298asp).…”

“…Cases were patients referred for coronary angiography 14 or patients with myocardial infarction 12,13 or angiographically confirmed coronary lesions. 12 The studied single-nucleotide polymorphisms included rs2070744 (T786C) 14 and rs1799983 (glu298asp). 12,13 These studies with the number of cases ranging from 159 14 to 547 13 reported association with genetic variation in eNOS.…”

Poly (ADP-ribose) Polymerase Inhibition Improves Endothelial Dysfunction Induced by Hyperhomocysteinemia in Rats

“…NO is a vasoactive substance and a major mediator of endothelium-dependent vasodilation [27]. ET-1 was endothelium derived constrictive factor.…”

Association between eNOS polymorphisms and risk of coronary artery disease in a Korean population: a meta-analysis

“…Several recent case-control studies have evaluated the roles of eNOS polymorphisms in CAD development (Tangurek et al, 2006;Rios et al, 2007;Han et al, 2010). The purpose of this study is to replicate previously published data in a larger population (Kim et al, 2007).…”