title: Glu298Asp polymorphism of the eNOS gene is associated with coronary collateral development.
abstract: OBJECTIVE
  We examined the endothelial nitric oxide (eNOS) gene Glu298Asp polymorphism to assess its possible association with the extent of coronary collaterals.
  
  
  METHODS
  A total of 473 consecutive patients who had high grade coronary stenosis or occlusion were evaluated for the extent of coronary collaterals by using Rentrop classification. Patients with grade 0 or 1 collaterals were identified as having poor collaterals. The relation between collateral status and eNOS Glu298Asp polymorphism was studied by multivariate logistic regression analysis.
  
  
  RESULTS
  Subjects with poor collaterals were more likely to have diabetes mellitus (p<0.001) and unstable angina pectoris as clinical presentation (p=0.014) and more likely to carry Asp298 variant (p=0.02) but they were less likely to have received statins (p=0.031). Multivariate analysis demonstrated that Asp298 allele carriers were 1.7 times more likely to have poor collaterals than patients with GluGlu genotype (95% CI: 1.09-2.69, p=0.024). There was a significant interaction between diabetes mellitus and eNOS Glu298Asp polymorphism in the analysis of collateral development. Among 145 diabetic patients Asp298 allele was the only predictor of poor collateral development with OR of 5.38 (95% CI: 2.41-11.98, p<0.001). Once diabetic patients were excluded from the analysis Asp298 allele was no longer a significant correlate of poor collateral formation.
  
  
  CONCLUSIONS
  The present study suggests that the Asp298 allele of the eNOS gene is significantly associated with impaired collateral development, especially in patients with diabetes mellitus. Treatment strategies that modulate eNOS activity and/or NO production may improve coronary collateral development.
authors.affiliation: Ankara University School of Medicine, Cardiology Department, Turkey.
authors.forename: Sadi
authors.initials: S
authors.lastname: Gulec
authors.forename: Halil
authors.initials: H
authors.lastname: Karabulut
authors.forename: Aydan Ongun
authors.initials: AO
authors.lastname: Ozdemir
authors.forename: Cagdas
authors.initials: C
authors.lastname: Ozdol
authors.forename: Sibel
authors.initials: S
authors.lastname: Turhan
authors.forename: Timuçin
authors.initials: T
authors.lastname: Altin
authors.forename: Eralp
authors.initials: E
authors.lastname: Tutar
authors.forename: Yasemin
authors.initials: Y
authors.lastname: Genc
authors.forename: Cetin
authors.initials: C
authors.lastname: Erol
mesh_terms: D000368:Aged; D000483:Alleles; D019943:Amino Acid Substitution; D001224:Aspartic Acid / Q000737:chemistry / Q000235:genetics; D054059:Coronary Occlusion / Q000503:physiopathology*; D023921:Coronary Stenosis / Q000503:physiopathology*; D003331:Coronary Vessels / Q000254:growth & development*; D048909:Diabetes Complications / Q000235:genetics; D005260:Female; D018698:Glutamic Acid / Q000737:chemistry / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D018919:Neovascularization, Physiologic / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D011110:Polymorphism, Genetic; D012044:Regression Analysis
chemical_list: D001224:Aspartic Acid; D018698:Glutamic Acid; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III