title: Association of the eNOS E298D polymorphism and the risk of myocardial infarction in the Greek population.
abstract: 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.
authors.affiliation: Department of Pharmaceutical Technology, School of Pharmacy, University of Athens, Panepistimiopolis Zografou, 15771 Athens, Greece.
authors.forename: Chaido
authors.initials: C
authors.lastname: Dafni
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Drakoulis
authors.forename: Olfert
authors.initials: O
authors.lastname: Landt
authors.forename: Dimitris
authors.initials: D
authors.lastname: Panidis
authors.forename: Martin
authors.initials: M
authors.lastname: Reczko
authors.forename: Dennis V
authors.initials: DV
authors.lastname: Cokkinos
mesh_terms: D016022:Case-Control Studies; D004252:DNA Mutational Analysis; D005838:Genotype; D006115:Greece / Q000453:epidemiology; D006801:Humans; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D011110:Polymorphism, Genetic; D012306:Risk; D012307:Risk Factors
chemical_list: C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III