Key result
The Asp allele of the Glu298Asp eNOS gene polymorphism was significantly associated with an increased risk of coronary artery disease (OR 2.186; 95% CI 1.53-3.125; p=0.001).
Why the study?
Is the Glu298Asp eNOS gene polymorphism associated with an increased risk of coronary artery disease in Asian populations?
Cross-Sectional (n=373)
Is the Glu298Asp eNOS gene polymorphism associated with an increased risk of coronary artery disease in Asian populations?
Odds Ratio: 2.186 (95% CI 1.53–3.125)
p-value: p=0.001
The homozygous Asp genotype of the Glu298Asp eNOS polymorphism is significantly associated with an increased risk of coronary artery disease in Asian populations.
May inform CAD genetic risk assessment in Asians; extends meta-analytic support for Glu298Asp as a susceptibility marker.
Background and Objectives: Glu298Asp endothelial Nitric Oxide Synthase (eNOS) gene polymorphism results in a reduced bioavailability of Nitric Oxide (NO) and prone to atherosclerosis. Even though there were more than 15 studies conducted on Asian populations investigating the role of this polymorphism in Coronary Artery Disease (CAD), however; the representative data from Malaysia still not clear. The aim of this study was to assess the association between Glu298Asp polymorphism and CAD by conducting a cross-sectional comparative study; in addition to a meta-analytic approach of review to overcome the contradicting evidence arising from conflicting studies in East Asia and South East Asia. Methodology: The study included 185 CAD patients and 188 control participants. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to identify the genotype of the study participants. The results were confirmed by nucleotide sequencing of selected genotypes and the association with CAD was tested using SPSS version 19 with Chi-square test. Execution of meta-analysis involved 23 Asian case-control studies using Revman meta-analysis software version 5.3. Results: The study has demonstrated a significant association between Glu298Asp genotype variants and CAD patients (p<0.001). Asp allele was a significant predictor for CAD ([p = 0.001, OR = 2.186 (1.53-3.125; CI = 95%)]. Through meta-analysis the combined cohort data showed significant Glu298Asp risk to CAD [p<0.0001, OR = 2.41 (1.61-3.59); Heterogeneity test (I 2 = 10%, p = 0.33)]. Conclusion: It was concluded that homozygous Asp genotype of Glu298Asp polymorphism potentiates a risk for CAD.
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Ibrahim et al. (2016) conducted a cross-sectional in Coronary Artery Disease (n=373). Glu298Asp eNOS gene polymorphism (Asp allele) vs. Control participants was evaluated on Coronary Artery Disease (OR 2.186, 95% CI 1.53-3.125, p=0.001). The Asp allele of the Glu298Asp eNOS gene polymorphism was significantly associated with an increased risk of coronary artery disease (OR 2.186; 95% CI 1.53-3.125; p=0.001).
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