Key result
eNOS Glu298Asp TT genotype linked to ~11-fold higher coronary no-reflow risk during STEMI PCI.
Why the study?
Endothelial nitric oxide synthase gene variants reduce enzyme activity and confer risk for coronary heart disease, but their role in coronary no-reflow phenomenon has not been revealed.
Is the endothelial nitric oxide synthase Glu298Asp gene variant associated with the development of coronary no-reflow phenomenon in patients with STEMI undergoing primary PCI?
Case-Control (n=116)
Is the endothelial nitric oxide synthase Glu298Asp gene variant associated with the development of coronary no-reflow phenomenon in patients with STEMI undergoing primary PCI?
Effect estimate: OR 10.85 (95% CI 1.22-96.39)
Absolute Event Rate: 11.54% vs 1.56%
p-value: p=0.016
The homozygous TT allele of the eNOS Glu298Asp gene variant is associated with a significantly increased risk of developing the no-reflow phenomenon during primary PCI for STEMI.
TT genotype associated with higher no-reflow risk after STEMI PCI; hypothesis-generating and requires prospective validation before clinical use.
No-reflow phenomenon is an important complication of primary percutaneous coronary intervention. Several variants in the endothelial nitric oxide synthase gene, which reduce endothelial nitric oxide synthase activity, are a risk factor for coronary heart disease. However, its role in no-reflow phenomenon has not yet been revealed. This study aimed to investigate whether there is a relationship between endothelial nitric oxide synthase Glu298Asp gene variant and the development of coronary no-reflow phenomenon in patients with ST elevation myocardial infarction. The study was conducted among 116 patients undergoing primary percutaneous coronary intervention for ST elevation myocardial infarction. Group 1 included 52 ST elevation myocardial infarction patients undergoing no-reflow phenomenon as a study group. Group 2 comprised 64 ST elevation myocardial infarction patients without no-reflow phenomenon as a control group. Endothelial nitric oxide synthase was tested using polymerase chain reaction-restriction fragment length variant. The prevalence of TT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was found to be significantly higher in patients developing coronary no-reflow when compared to those without no-reflow (p = 0.016; 11.54% vs. 1.56%) (OR = 10.85, 95% CI = 1.22–96.39). However, a similar association for the heterozygous GT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was not observed between the two groups. The results of this preliminary study indicate that there is an association between Glu298Asp variant in endothelial nitric oxide synthase gene and the development of no-reflow phenomenon in ST elevation myocardial infarction. The presence of homozygous TT allele may contribute to tendency to the development of no-reflow phenomenon.
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Yalçın et al. (2019) conducted a case-control in ST elevation myocardial infarction (n=116). Endothelial nitric oxide synthase Glu298Asp gene variant (TT genotype) vs. Absence of TT genotype was evaluated on Prevalence of TT genotype of endothelial nitric oxide synthase Glu298Asp gene variant (OR 10.85, 95% CI 1.22-96.39, p=0.016). The TT genotype of the eNOS Glu298Asp gene variant was significantly associated with coronary no-reflow in STEMI patients undergoing primary PCI (11.54% vs 1.56%; OR 10.85; 95% CI 1.22-96.39).
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