A case-control study of the interaction of the eNOS gene polymorphisms rs1799983 and rs1800780 with acute coronary syndrome (ACS) risk factors

一项关于eNOS基因多态性rs1799983和rs1800780与急性冠脉综合征(ACS)危险因素相互作用的病例对照研究

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Abstract

BACKGROUND: Endothelial nitric oxide synthase (eNOS) gene polymorphisms may affect its enzymatic activity and nitric oxide (NO) production, which in turn interfere with endothelial function, regulate vascular tone, and participate in inflammatory responses. This ultimately affects the risk and prognosis of acute coronary syndrome (ACS). The aim of this study is to explore the association of eNOS gene polymorphisms with ACS risk factors. METHODS: Patients who were hospitalized for coronary angiography in the First Affiliated Hospital of Xinjiang Medical University from January 2016 to December 2019 were selected. According to the appropriate inclusion and exclusion criteria. ACS and control groups were matched for general information such as gender, age, smoking, and alcohol consumption. 718 patients with ACS and 1008 controls were finally included. Genotyping was detected using the SNPscanTM Multiple SNP Typing Kit. The χ2 test was used to compare baseline information and gene model distribution between the ACS and control groups. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI). RESULTS: This study included 718 patients with ACS and 1008 controls. The results of the analysis of the clinical baseline data after adjusting for confounders showed: age (OR = 1.025; 95%CI: 1.011–1.039; P < 0.001), gender (OR = 1.434; 95%CI: 1.012–2.032; P = 0.042), smoking (OR = 5.665; 95%CI: 3.954–8.117; P < 0.001), diabetes: (O R = 1.741;95%CI: 1.252–2.421,P = 0.001), NLR (OR = 1.387; 95%CI: 1.271–1.513; P < 0.001), PAR (OR = 1.269,95%CI: 1.177–1.369, P < 0.001), TyG (OR = 2.229; 95%CI. 1.847–2.689; P < 0.001), alcohol consumption (OR = 0.410; 95%CI: 0.292–0.577; P < 0.001), and the dominant model of the rs1799983 locus of the eNOS gene (TTvsGG + TG, OR = 3.157, 95%CI: 1.045–9.533, P = 0.042) were all significant influences on ACS. CONCLUSION: ACS interacted significantly with eNOS gene polymorphisms and was strongly associated with NLR, PAR, and TyG levels. Traditional risk factors were significantly different between the ACS and control groups. The dominant model of rs1799983 influences the development of ACS.

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