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eISSN: 1643-3750

Role of Endothelial Nitric Oxide Synthase Polymorphisms in Atrial Fibrillation: A PRISMA-Compliant Meta-Analysis

Yi-Qing Zhang, Yu-Feng Jiang, Lu Hong, Hua-Jia Yang, Jun-Yi Zhang, Ya-Feng Zhou

Department of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China (mainland)

Med Sci Monit 2019; 25:2687-2694

DOI: 10.12659/MSM.913528

Available online:

Published: 2019-04-12


#913528

BACKGROUND: Research interest in endothelial nitric oxide synthase(eNOS) polymorphisms and atrial fibrillation (AF) has grown in last recent years, but the results of individual studies are inconsistent due to their small sample sizes.
MATERIAL AND METHODS: We searched databases for eligible studies on eNOS and AF, extracted the relevant data, and rigorously screened them according to inclusion and exclusion criteria. Then, we evaluated the study quality according to the Newcastle-Ottawa scale score, and we pooled the odds ratios (ORs) and 95% confidence intervals (CIs) by using a random-effects model or fixed-effects model based on inter-study heterogeneity. In addition, we performed subgroup analysis and sensitivity analysis and assessed publication bias.
RESULTS: According to the inclusion and exclusion criteria, we finally found 8 studies in this search. The recessive (OR=0.81; 95% CI=0.67 to 0.97; p=0.988; I²=0.0%) model showed that the eNOS 786T/C polymorphism was relevant to AF. We also found that the eNOS 786T/C polymorphism decreases the risk of AF, especially in white people (OR=0.81; 95% CI=0.67 to 0.97; P=0.023 for recessive model) and in the control population (OR=0.79; 95% CI=0.65 to 0.97; P=0.022 for recessive model). We found no obvious publication bias.
CONCLUSIONS: The eNOS gene loci 786T/C polymorphism is relevant to the risk of AF. Our results suggest that the 786T/C polymorphism significantly decreases AF risks in white people and control populations. Larger studies are required for further evaluation.

Keywords: Atrial Fibrillation, meta-analysis, Nitric Oxide Synthase Type III



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