Abstract
Background: The purpose of this study was to investigate the associations between variants of a promoter polymorphism of the endothelial nitric oxide synthase (eNOS) gene and clinical outcomes in acute ST-segment elevation myocardial infarction (STEMI) patients after a successful primary percutaneous coronary artery intervention (PCI).
 Methods: 177 patients with acute STEMI, 82 patients with angiographically proven stable coronary artery disease, and healthy volunteers were included in the study. The primary end-point was a combined event (follow-up major adverse cardiac events –MACEs and hospitalization) that occurred within 6-month of the discharge from the hospital.
 Results: The combined end-point was determined in 72 patients from the entire acute STEMI population (40.6%), including 24 events for 786TT genotype, 23 events for 786TC genotype and 25 events for 786CC genotype. Kaplan-Meier curves demonstrated that acute STEMI patients with 786CC eNOs genotype had lower MACEs free accumulation when compared to those with 786TC and 786TT eNOs genotypes at 6-month follow up period (Log-rank p < 0.001). Multivariate Cox regression analyses identified 786CC in eNOs gene as an independent predictor of clinical outcomes in STEMI after PCI.
 Conclusions: the 786CC polymorphism in eNOs gene is an independent predictor for clinical outcomes after a successful primary PCI in acute STEMI.
Highlights
Nitric oxide (NO) is an established factor in maintaining endothelial function and vascular wall integrity 1–4
Previous studies have shown that polymorphism in promoter region of endothelial NO synthase (eNOs) gene (T786C) in segment elevation myocardial infarction (STEMI) patients is corresponding with impaired pleiotropic effect of NO, which led to adverse cardiac remodeling, early stent thrombosis and restenosis after percutaneous coronary artery intervention (PCI) 11–14
Plasma levels of NO(x) were significantly lower in acute STEMI patients with 786CC genotype compared to others, but there was no significant difference in biomarker levels between patients with 786TT and 786TT genotypes
Summary
Nitric oxide (NO) is an established factor in maintaining endothelial function and vascular wall integrity 1–4. Genetic polymorphisms of endothelial NO synthase (eNOs) is associated with altered NO levels in peripheral blood, increased levels of plasma low-density lipoproteins (LDL) and oxidized lipids, suppressed the production of vascular endothelial growth factor and increased fasting glucose 5–7 These findings were reported to have clinical significance in acute ST-segment elevation myocardial infarction (STEMI), stable coronary artery disease (CAD), asymptomatic atherosclerosis, heart failure (HF), abdominal obesity, hypertension, diabetes mellitus, and restenosis and thrombosis after primary percutaneous coronary artery intervention (PCI) 8–10. The purpose of this study was to investigate the associations between variants of a promoter polymorphism of the endothelial nitric oxide synthase (eNOS) gene and clinical outcomes in acute ST-segment elevation myocardial infarction (STEMI) patients after a successful primary percutaneous coronary artery intervention (PCI).
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