Role of the -786T>C Variant of the Endothelial Nitric Oxide Synthase Gene in Stent Restenosis Following Coronary Stent Deployment

Document Type : Original Article


1 Department of Cardiology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, IR Iran.

2 Endocrinology and Metabolic Research Center, Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, IR Iran.


Background: The role of polymorphisms on the sequences of the endothelial nitric oxide synthase (eNOS) gene has been proposed to predispose coronary artery disease patients to stent restenosis. We conducted the present study to examine the involvement of the role of the -786T>C variant of the eNOS gene in stent restenosis following coronary stent deployment.
Methods: This cross-sectional study was conducted on 100 consecutive patients who underwent coronary stenting. The study population was assigned into a case group, who had restenosis and were candidated for revascularization (n, 50), and a matched control group, who underwent coronary stenting but without evidence of restenosis within 6 months of stenting (n, 50). The -786T>C polymorphism was identified, following polymerase chain reaction (PCR), by restriction enzyme digestion.
Results: The overall prevalence of restenosis was 34.4%. In total, the frequency of the wild genotype (CC) of the -786T>C variant was 41.9%, the frequency of heterozygous genotype (TC) was 41.9%, and the frequency of the mutant genotype (TT) was 40.9%. We found an association between the presence of stent restenosis and the presence of the -786T>C
variant: in the patients with and without restenosis, the frequency of the CC genotype was 24.2% and 51.7%, the frequency of the TC genotype was 12.1% and 20.0%, and the frequency of the TT genotype was 63.6% and 28.3%, respectively (P = 0.023). In the multivariate logistic regression analysis, along with the presence of the -786T>C variant,
the other determinants of stent restenosis included male gender, waist circumference, both systolic and diastolic blood pressures, history of dyslipidemia, left anterior descending artery (LAD) involvement, distal position of stenting, and duration of the concomitant use of aspirin and Plavix®. However, in similar analysis, none of the pointed factors could predict the severity and percentage of restenosis.
Conclusion: The presence of the -786T>C polymorphism of the eNOS gene is a major and serious risk factor for stent restenosis, independent of the effects of other cardiovascular risk factors. The effect of this polymorphism is particularly highlighted in the LAD. Nevertheless, it seems that the -786T>C polymorphism may not have a central role in the progression and severity of stent restenosis.(Iranian Heart Journal 2015; 16(2):35-40)


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