Biomarker-based prognostication of adverse cardiac remodeling after STEMI: the role of single nucleotide polymorphism T786C in endothelial NO-synthase gene

Abstract

Background: Endothelial NO-synthase (eNOS) is constitutive enzyme, which expresses in mature endothelial cells and promotes direct vascular dilatation. Single nucleotide polymorphism (SNP) of T786C in eNOS gene may influence on adverse cardiac remodeling after ST-elevation myocardial infarction (STEMI).

Purpose of the study was to investigate possible associations between SNP Т786С in eNOS gene and adverse cardiac remodeling after STEMI.

Methods: 177 acute STEMI patients treated with percutaneous coronary intervention and thrombolysis that were admitted to intensive care unit of GI “L.T.Malaya TNI NAMSU” were enrolled in the study. Anthropometry, cardiovascular risk assay, coronary angiography, echocardiography and biomarkers’ measure were performed at baseline. The DNA extraction was performed with a commercial kit using real-time polymerase chain reaction PCR.

Results: There were correlations between 786СС polymorphism in eNOs gene and adverse cardiac remodeling (r=0.48; P=0.001), LDL cholesterol (r=0.32; P=0.012), type 2 diabetes mellitus (r=0.30; P=0.042), diastolic BP (r=-0.26; P=0.048), unstable angina prior to STEMI (r=0.25; P=0.047) and total quantity of complicated STEMI (r=0.23; P=0.042). Additionally, there were not significant relations between 786СС polymorphism in eNOs gene and multiple coronary vessel injury, STEMI localization, levels of circulating biomarkers of myocardial injury, and amount of damaged coronary arteries. Using univariate and multivariate regressive logistic analysis (Table 4) we found that 786СС genotype of eNOS was independent predictor for late adverse LV remodeling (β-coefficient=1.57342; odds ration =4.8231; 95% confidence interval = 1.5349 – 15.1552; P=0.0071).

In conclusion, the polymorphism 786СС in eNOs gene was found as an independent predictor for late adverse cardiac remodeling after STEMI