Özet:

the objective. Coronary heart disease (CHD) is a complex disease caused by genetic and environmental factors, being one of the major causes of death in the world. Endothelial dysfunction is key for atherosclerosis pathogenesis leading to CHD. Endothelial dysfunction causes the formation of atherosclerotic plaque when endothelial cells do not perform ultimate functions such as vascular homeostasis and nitric oxide (NO) production. In our study, we intended to investigate Endothelial NO synthase (eNOS, NOS3) rs1799983 variation (Glu298Asp) in CHD patients and determine its metabolic effects on CHD development. Materials and Methods. This study was carried out using a sample of 75 CHD patients and 73 healthy controls. eNOS rs1799983 genotypes were determined by polymerase chain reaction, restriction fragment lenght polymorphism and agarose gel electrophoresis. The results. The eNOS rs1799983 genotype distributions were the same between study groups (p>0.05). When the effects of the rs1799983 genotypes were examined on metabolic parameters in the study groups, the body mass index was found to be increased in the subjects with the TT (Asp/Asp) genotypes as compared to G (Glu) allele (GG+GT genotypes). However, eNOS rs1799983 was not associated with metabolic and biochemical parameters in patients with CHD (p>0.05). and Conclusion. Our findings indicate that the eNOS rs1799983 genotypes may be associated with elevated body mass index.

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