title: The Glu298Asp polymorphism in endothelial nitric oxide synthase gene is associated with coronary in-stent restenosis.
abstract: BACKGROUND
  Reduced or impaired synthesis of nitric oxide promotes the proliferation of vascular smooth muscle cells, and thus may induce the neointimal formation leading to coronary in-stent restenosis. Recent reports have suggested that the Glu298Asp polymorphism in exon 7 of the endothelial nitric oxide synthase gene is associated with coronary spasm and acute myocardial infarction. In this study, we have examined the implication of this polymorphism with regard to coronary restenosis after Palmaz-Schatz stent deployment.
  
  
  METHODS
  Eighty-nine lesions in 85 consecutive patients were treated with Palmaz-Schatz stents, and were prospectively followed up for 6 months. The lesions were classified into a restenosis group (% diameter stenosis=50%) and a non-restenosis group. Assessment was made using an automated quantitative angiographic system. We performed polymerase chain reaction-restriction fragment length polymorphism analysis to detect the missense Glu298Asp variant in exon 7 of the endothelial nitric oxide synthase gene.
  
  
  RESULTS
  Coronary risk factors and angiographic findings of stenotic lesions did not differ between the groups. Univariate analyses showed that the missense Glu298Asp variant was the only statistically significant predictor of restenosis (odds ratio, 4.27; P=0.025). In addition, multiple logistic regression analysis revealed the missense Glu298Asp variant as the only independent predictor for in-stent restenosis (odds ratio, 3.90; P=0.036).
  
  
  CONCLUSIONS
  The missense Glu298Asp variant may be an independent risk factor for in-stent restenosis.
authors.affiliation: Internal Medicine II, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Japan.
authors.forename: Tomomichi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Kenji
authors.initials: K
authors.lastname: Okumura
authors.forename: Takahito
authors.initials: T
authors.lastname: Sone
authors.forename: Tai
authors.initials: T
authors.lastname: Kosokabe
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Tsuboi
authors.forename: Junichiro
authors.initials: J
authors.lastname: Kondo
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Mukawa
authors.forename: Hiroki
authors.initials: H
authors.lastname: Kamiya
authors.forename: Takahito
authors.initials: T
authors.lastname: Tomida
authors.forename: Hajime
authors.initials: H
authors.lastname: Imai
authors.forename: Hideo
authors.initials: H
authors.lastname: Matsui
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Hayakawa
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001224:Aspartic Acid / Q000235:genetics; D023903:Coronary Restenosis / Q000235:genetics*; D004730:Endothelium, Vascular / Q000201:enzymology*; D005260:Female; D005838:Genotype; D018698:Glutamic Acid / Q000235:genetics; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D020125:Mutation, Missense; D019001:Nitric Oxide Synthase / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D015607:Stents / Q000009:adverse effects
chemical_list: D001224:Aspartic Acid; D018698:Glutamic Acid; D019001:Nitric Oxide Synthase