title: The relationship between endothelial nitric oxide synthase 4a/4b gene polymorphism and premature coronary artery disease.
abstract: BACKGROUND
  Nitric oxide (NO) plays a major role in the regulation of endothelial functions and reduced NO synthesis has been implicated in the development of coronary atherosclerosis. Endothelial nitric oxide synthase (eNOS) intron 4a/b polymorphism has been shown to be related to plasma nitric oxide concentrations and coronary artery disease in various population studies. The aim of this study is to assess the relationship between eNOS 4a/b polymorphism and premature CAD.
  
  
  METHODS
  A total of 70 patients under age 35 who presented with ST-segment elevation myocardial infarction (STEMI) were included in this study.The control group included 50 age- and gender-matched subjects with normal coronary arteries on angiography.The eNOS 4a/b polymorphism was assessed with polymerase chain reaction (PCR).The frequencies of eNOS 4a/b genotypes and alleles were compared. Multivariate regression analysis was used for estimation of the independent predictors of premature CAD.
  
  
  RESULTS
  Frequency of eNOS4a/b gene, aa and ab genotypes were significantly higher in STEMI patients when compared to control group. Presence of allele'a'of the eNOS gene was an independent predictor of STEMI in a young population (OR: 2.78 95% CI: 1.02-7.56 P = 0.044). A significant correlation of eNOS gene polymorphism with other clinical properties of subjects was not established.
  
  
  CONCLUSIONS
  The eNOS4a/b gene polymorphism may be associated with early development of atherosclerosis and myocardial infarction possibly secondary to deterioration of the endothelial function.
authors.affiliation: Dept. of Cardiology, Siyami Ersek Cardiovascular and Thoracic Surgery Center, Istanbul, Turkey.
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ekmekçi
authors.forename: Kazim Serhan
authors.initials: KS
authors.lastname: Ozcan
authors.forename: Bariş
authors.initials: B
authors.lastname: Güngör
authors.forename: Neslihan
authors.initials: N
authors.lastname: Abaci
authors.forename: Damirbek
authors.initials: D
authors.lastname: Osmonov
authors.forename: Aycan
authors.initials: A
authors.lastname: Zencirci
authors.forename: Ercan
authors.initials: E
authors.lastname: Toprak
authors.forename: Cevdet
authors.initials: C
authors.lastname: Dönmez
authors.forename: Duran
authors.initials: D
authors.lastname: Ustek
authors.forename: Cağri
authors.initials: C
authors.lastname: Güleç
authors.forename: Mehmet
authors.initials: M
authors.lastname: Eren
mesh_terms: D000328:Adult; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000150:complications / Q000201:enzymology / Q000235:genetics*; D004247:DNA / Q000235:genetics*; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000201:enzymology / Q000209:etiology / Q000235:genetics; D009569:Nitric Oxide / Q000097:blood; D052250:Nitric Oxide Synthase Type III / Q000097:blood / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D011446:Prospective Studies; D014664:Vasodilation / Q000235:genetics*
chemical_list: D009569:Nitric Oxide; D004247:DNA; D052250:Nitric Oxide Synthase Type III