title: Hyperhomocysteinemia, endothelial nitric oxide synthase polymorphism, and risk of coronary artery disease.
abstract: BACKGROUND
  Hyperhomocysteinemia is an independent, graded risk factor for coronary artery disease (CAD). The G894T variant of endothelial nitric oxide synthase (eNOS) was postulated to be associated with hyperhomocysteinemia and could influence individual susceptibility to CAD. The aims of this study were to investigate (a) the relationship of the eNOS G894T polymorphism with the presence and the severity of CAD and (b) the possible relationship between hyperhomocysteinemia and the eNOS G894T variant for the risk of CAD severity in a Tunisian population.
  
  
  METHODS
  We used PCR with restriction fragment length polymorphism analysis to detect the G894T variant of the eNOS gene in 100 patients with CAD and 120 healthy controls. The severity of CAD was expressed by the number of affected vessels. Total plasma homocysteine concentrations were determined by direct chemiluminescence assay.
  
  
  RESULTS
  The frequencies of the eNOS GG, GT, and TT genotypes in the CAD group were significantly different from those in the control group (45%, 44%, and 11% vs 60%, 35.8% and 4.2%, respectively; P = 0.035). There was no association between the eNOS G894T genotype frequencies and the number of stenosed vessels (P = 0.149). In the CAD group, the coexistence of the 894 GT or TT genotypes and hyperhomocysteinemia led to an increased risk of CAD severity.
  
  
  CONCLUSIONS
  The G894T polymorphism of the eNOS gene is associated with the presence of CAD, and in conjunction with hyperhomocysteinemia, increased the risk of CAD severity in a Tunisian population.
authors.affiliation: Research Unit 03/UR/08-14, Faculty of Pharmacy, Monastir, Tunisia. m.kerkeni@belgique.com
authors.forename: Mohsen
authors.initials: M
authors.lastname: Kerkeni
authors.forename: Faouzi
authors.initials: F
authors.lastname: Addad
authors.forename: Maryline
authors.initials: M
authors.lastname: Chauffert
authors.forename: Anne
authors.initials: A
authors.lastname: Myara
authors.forename: Mohamed
authors.initials: M
authors.lastname: Ben Farhat
authors.forename: Abdelhedi
authors.initials: A
authors.lastname: Miled
authors.forename: Khira
authors.initials: K
authors.lastname: Maaroufi
authors.forename: François
authors.initials: F
authors.lastname: Trivin
mesh_terms: D003251:Constriction, Pathologic / Q000235:genetics / Q000473:pathology; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D020138:Hyperhomocysteinemia / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D018570:Risk Assessment; D012720:Severity of Illness Index; D014416:Tunisia / Q000453:epidemiology
chemical_list: D052250:Nitric Oxide Synthase Type III