Endothelial nitric oxide synthase Asp298Glu (894G/T) gene polymorphism as a possible risk factor for the coronary slow flow phenomenon among Iranians

Abstract

Background Mounting evidence indicates an association between endothelial dysfunction and the coronary slow flow phenomenon (CSFP). In the present study, we aimed to evaluate the possible role of endothelial nitric oxide synthase (eNOS) 894G/T and interleukin-1β (IL-1β) 315C/T polymorphisms as possible risk factors for CSFP. Methods This prospective study enrolled patients with CSFP and individuals with normal coronary arteries. Genotypes were assessed using regular polymerase chain reaction and direct Sanger-sequencing techniques. Results The study population consisted of 267 individuals: 180 patients with CSFP (49 women [27.2%]) at a median age of 55 (48–62) years and 87 controls with normal coronary arteries (56 women [64.4%]) at a median age of 47 (41–58) years. The allelic distribution of eNOS 894G/T was significantly associated with CSFP (odds ratio [OR], 1.58; 95% confidence interval (CI), 1.04–2.42; P = 0.03). This polymorphism increased the risk of CSFP under the dominant model (OR 1.73; 95% CI I.02–2.95; P = 0.04). However, the allelic frequencies (1.05; 95% CI 0.68–1.59; P = 0.83) and genotypic frequencies (0.88; 95% CI 0.52–1.49; P = 0.63) of the IL-1β 315C/T polymorphism were not associated with the incidence of CSFP in the Iranian population. Conclusions The CSFP and control groups were statistically different regarding the eNOS 894G/T polymorphism. Our findings also demonstrated that the IL-1β 315C/T polymorphism was not a risk factor for CSFP.

Relationship between uric acid/ albumin ratio and coronary slow flow

“…In addition to arterial endothelial dysfunction, endotheliumdependent vasodilation is also weak in this group. In comparison to persons with normal coronary flow, these patients showed higher plasma levels of asymmetric dimethyl-arginine, endothelin-1, and homocysteine, and lower plasma levels of nitric oxide [4]. Furthermore, a link between microalbuminuria and endothelial dysfunction has been observed in the literature [5].…”