Abstract
Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene (-786T >C and 894G >T) enhance endo-thelial dysfunction and have been studied in relation to coronary artery disease (CAD). In the present study, we examined the association of the above polymorphisms with CAD, as well as with myocardial infarction (MI), hypertension, diabetes and smoking in CAD patients. Study subjects consisted of 154 consecutive coronary artery bypass graft (CABG) patients and 155 non-CAD controls. eNOS -786T >C and 894G >T polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism. The estimated frequencies of the -786C and 894T alleles did not differ between the two groups (p = 0.46 and p = 0.84, respectively). The prevalence of eNOS polymorphisms was not associated with MI, hypertension or diabetes in CABG patients; however, we found that the 894TT genotype and 894T allele were significantly more frequent in current/past smoker CABG patients (16.7 per cent and 39.6 per cent, respectively) compared with never smoker CABG patients (6.1 per cent and 24.4 per cent, respectively) (p = 0.01 and p < 0.01, respectively). We found no association of eNOS -786C and 894T variant alleles with CAD; however, within CABG patients, a gene-environment interaction was found between the eNOS 894T allele and smoking.
Highlights
Atherosclerotic coronary artery disease (CAD) is the most common form of cardiovascular disease
The aim of the present study was to evaluate the association of two endothelial nitric oxide synthase (eNOS) gene polymorphisms with CAD in coronary artery bypass graft (CABG) patients compared with non-atherosclerotic individuals
We investigated the association of 2786T
Summary
Atherosclerotic coronary artery disease (CAD) is the most common form of cardiovascular disease. CAD is a multifactorial disease of complex aetiology, influenced by both genetic and environmental determinants.[1] Several risk factors for CAD have been established, such as hypertension, diabetes mellitus, lipid disorders and smoking. To comprehend fully the aetiology of CAD, special attention has been given to genetic factors. Many candidate gene studies have been published in the past decade, the genetic background of CAD remains poorly defined.[2]. Numerous studies suggest that endothelial dysfunction plays a crucial role in the initiation and progression of atherosclerosis, the fundamental pathology of CAD. A key element in endothelial dysfunction is the loss of endothelium-derived nitric oxide (NO)
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