title: Lack of association between the Glu298Asp polymorphism of endothelial nitric oxide synthase and slow coronary flow in the Turkish population.
abstract: BACKGROUND
  Coronary endothelial dysfunction plays an important pathogenetic role in patients with slow coronary flow (SCF). No data exist regarding the possible contribution of the Glu298Asp polymorphism genotype of the endothelial nitric oxide synthase (eNOS) gene to human SCF in the literature.
  
  
  OBJECTIVE
  To investigate the association between SCF and the Glu298Asp polymorphism of the eNOS gene.
  
  
  METHODS
  The study population consisted of 85 consecutive patients. The patient group included 66 patients with angiographically proven normal coronary arteries with SCF, and 19 subjects with normal coronary arteries with no SCF. The thrombolysis in myocardial infarction frame count was used for the diagnosis of SCF. The Glu298Asp polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism.
  
  
  RESULTS
  The baseline characteristics were similar between the two groups, except for high-density lipoprotein cholesterol, which was higher in the SCF group than in the controls. The genotype distribution of Glu298Asp was as follows: GG 26%, GT 56% and TT 12%, where G is guanine and T is thymine. There was no difference in the frequency of the various genotypes or the alleles in patients with SCF versus normal controls.
  
  
  CONCLUSIONS
  The Glu298Asp polymorphism genotype of the eNOS gene is not a risk factor for SCF in the present study population.
authors.affiliation: Department of Medical Genetics, Erciyes University Medical Faculty, Kayseri, Turkey. aocaglayan@erciyes.edu.tr
authors.forename: A O
authors.initials: AO
authors.lastname: Caglayan
authors.forename: N
authors.initials: N
authors.lastname: Kalay
authors.forename: C
authors.initials: C
authors.lastname: Saatci
authors.forename: A
authors.initials: A
authors.lastname: Yalcýn
authors.forename: H
authors.initials: H
authors.lastname: Akalýn
authors.forename: M
authors.initials: M
authors.lastname: Dundar
mesh_terms: D000328:Adult; D000368:Aged; D003324:Coronary Artery Disease / Q000235:genetics*; D003326:Coronary Circulation / Q000235:genetics*; D004730:Endothelium, Vascular / Q000201:enzymology / Q000503:physiopathology*; D005260:Female; D005787:Gene Frequency; D006801:Humans; D008297:Male; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D012307:Risk Factors; D014421:Turkey / Q000453:epidemiology
chemical_list: D052250:Nitric Oxide Synthase Type III