Key result
The eNOS E298D TT genotype was associated with a significantly increased risk of myocardial infarction compared to the GG and GT genotypes (OR 2.06).
Why the study?
Does the eNOS E298D polymorphism increase the risk of myocardial infarction in the Greek population?
Case-Control (n=422)
No
Does the eNOS E298D polymorphism increase the risk of myocardial infarction in the Greek population?
Odds Ratio: 2.06 (95% CI 1.06–4)
Absolute Event Rate: 13.2% vs 6.9%
p-value: p=0.032
The eNOS E298D TT genotype is associated with an approximately two-fold increased risk of myocardial infarction in the Greek population, independent of traditional cardiovascular risk factors.
Should not yet guide MI risk assessment; extends eNOS-MI association in Greeks but remains hypothesis-generating.
BACKGROUND: Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays a key role in the regulation of vascular tone. Endothelium-derived NO exerts vasoprotective effects by suppressing platelet aggregation, leukocyte adhesion and smooth muscle cell proliferation. The E298D polymorphic variant of eNOS has been associated with myocardial infarction (MI), but data relating to this variant are divergent in Greece. Accordingly, we examined a possible association between the E298D polymorphism of the eNOS gene and MI in a subgroup of the Greek population. METHODS: The study population consisted of 204 patients with a history of MI and 218 control subjects. All subjects were of Greek origin and were selected from the general population of the greater Athens area. Genotyping was performed with melting curve analysis (Lightcycler system) of polymerase chain reaction amplified products using hybridization probes. RESULTS: According to the univariate findings, the risk for MI in E298D TT was 2.06 (95%CI: 1.06-4.00, p = 0.032) versus GG+GT and 2.34 (95%CI: 1.17-4.68, p = 0.016) versus GG. The risk for the T allele was estimated at 1.42 (95%CI, 1.06-1.89, p = 0.022) as compared to G allele. Regarding the additive model, one allele increase was associated with 43% higher risk of MI (OR = 1.43, 95%CI: 1.07-1.93, p = 0.018) as compared to the baseline category of homozygous GG. The positive association of TT versus GG+GT with MI risk remained even after adjusting for the main study covariates. Moreover, strong evidence was found for an increased risk for MI among carriers of the TT genotype who were smokers, hypertensive and had a family history of CAD. CONCLUSIONS: This study indicates that E298D polymorphism of the eNOS gene seems to be associated with MI occurrence in the Greek population. It is possible that TT genotype is closely linked to the etiology of MI even after adjusting for known MI risk factors.
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Dafni et al. (2010) conducted a case-control in Myocardial Infarction (n=422). eNOS E298D polymorphism (TT genotype) vs. GG and GT genotypes was evaluated on Risk of myocardial infarction (OR 2.06, 95% CI 1.06-4.00, p=0.032). The eNOS E298D TT genotype was associated with a significantly increased risk of myocardial infarction compared to the GG and GT genotypes (OR 2.06).
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