Key result
The eNOS gene polymorphism Glu298Asp was not significantly associated with STEMI overall (OR 0.9; 95% CI 0.6-1.6), but the 894 TT genotype was significantly associated with STEMI in patients >40 years.
Why the study?
Genetic polymorphisms in endothelial nitric oxide synthase are associated with multiple cardiovascular diseases, but their relationship with STEMI across age groups remained to be evaluated.
Is the eNOS gene polymorphism (Glu298Asp) and plasma nitric oxide level associated with the occurrence of STEMI?
Case-Control (n=600)
Is the eNOS gene polymorphism (Glu298Asp) and plasma nitric oxide level associated with the occurrence of STEMI?
Odds Ratio: 0.9 (95% CI 0.6–1.6)
p-value: p=0.589
The eNOS gene polymorphism Glu298Asp and lower NO levels are associated with STEMI in patients older than 40 years, but not in those with premature CAD.
eNOS 894 TT and lower NO associate with STEMI after age 40; hypothesis-generating and requires prospective confirmation before clinical use.
BACKGROUND: Genetic polymorphism in endothelial Nitric Oxide Synthase (eNOS) are associated with occurrence of multiple cardiovascular diseases (CVDs). METHODS: This study included 300 young ST-segment elevation myocardial infarction (STEMI) patients and 300 healthy controls. STEMI patients were divided into two groups: premature coronary artery disease [CAD] (STEMI<40 years of age) and older STEMI (>40 years of age). Genetic polymorphisms in the eNOS gene (894G/T) was evaluated in both subjects and controls. Plasma levels of nitric oxide (NO) were estimated for both patients as well as controls. RESULTS: Mean age of the study population was 49.7 ± 9.2 years with premature CAD being present in 58 (19.3 %) patients. No significant difference at genotypic (P = 0.589, odds ratio (OR) = 0.9, 95 % CI = 0.6-1.6) and allelic level (P = 0.173, OR = 1.2, 95 % CI = 0.9-1.4) was observed between STEMI patients and healthy controls. Genotype 894 TT had significantly higher frequency in STEMI patients >40 years (P = 0.047, OR: 2.5; 95 % CI = 1.0-6.0). No significant difference at genotypic (P = 0.279) and allelic level (P = 0.493) was observed between premature CAD (STEMI age <40 years) and healthy controls. NO levels (131 ± 59.6 μM vs 118.11 ± 49.96 μM; P = 0.001) was significantly higher in healthy controls as compared to STEMI patients >40 years of age (P= 0.001). CONCLUSION: There was significant association of eNOS gene polymorphism Glu298Asp with STEMI patients > 40 years. However, this association was not observed in premature CAD patients. Lower levels of NO in STEMI patients >40 years suggests its potential role as a marker of CVD.
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Gupta et al. (2024) conducted a case-control in ST-segment elevation myocardial infarction (STEMI) (n=600). eNOS gene polymorphism (894G/T) vs. Healthy controls was evaluated on Genotypic difference in eNOS gene (894G/T) between STEMI patients and healthy controls (OR 0.9, 95% CI 0.6-1.6, p=0.589). The eNOS gene polymorphism Glu298Asp was not significantly associated with STEMI overall (OR 0.9; 95% CI 0.6-1.6), but the 894 TT genotype was significantly associated with STEMI in patients >40 years.
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