title: The 4G/5G promotor polymorphism of the plasminogen activator inhibitor-1 gene and late lumen loss after coronary stent placement in smoking and nonsmoking patients.
abstract: BACKGROUND
  Instent restenosis remains a significant clinical problem. Identification of patients at risk for instent restenosis may allow selection of individualized appropriate therapeutic approaches. Genetic polymorphisms have been suggested to be associated with the risk of instent restenosis. Smoking is known to influence hemostatic parameters.
  
  
  OBJECTIVE
  This study investigated the influence of the 4G/5G promotor polymorphism of the plasminogen activator inhibitor type I (PAI-1) gene on instent restenosis in smoking and nonsmoking patients.
  
  
  METHODS
  In all, 300 consecutive patients (133 nonsmoking; 167 smoking) with elective coronary stent placement and 6-month angiographic follow-up were studied. Quantitative coronary angiography and genotyping with polymerase chain reaction analysis were performed in all patients.
  
  
  RESULTS
  Nonsmoking PAI-1 4G/4G carriers showed a significantly greater late lumen loss (n = 38; 0.54 +/- 0.53 mm) compared with nonsmoking PAI-1 4G/5G (n = 68; 0.38 +/- 0.45 mm) or 5G/5G (n = 27; 0.19 +/- 0.23 mm) carriers, analysis of variance (ANOVA) p < 0.001. Smoking patients with the genotypes 4G/4G (n = 46; 0.53 +/- 0.54 mm) and 4G/5G (n = 79; 0.37 +/- 0.41 mm) had a late loss similar to that of nonsmoking patients. Smoking 5G/5G carriers had the highest late loss of all smoking patients (n = 42; 0.63 +/- 0.50); ANOVA p < 0.05; nonsmoking 5G/5G vs. smoking 5G/5G p < 0.001.
  
  
  CONCLUSIONS
  The promotor polymorphism of the PAI-1 gene has a significant influence on instent restenosis after coronary stent implantation. The 5G/5G genotype predisposes nonsmoking gene carriers to less late lumen loss, whereas in smoking gene carriers this genotype is associated with the greatest late lumen loss. This might be explained by an altered expression pattern of hemostatic parameters.
authors.affiliation: Medical Clinic I, University Hospital of Aachen, Germany.
authors.forename: J R
authors.initials: JR
authors.lastname: Ortlepp
authors.forename: R
authors.initials: R
authors.lastname: Hoffmann
authors.forename: A
authors.initials: A
authors.lastname: Killian
authors.forename: J
authors.initials: J
authors.lastname: Lauscher
authors.forename: S
authors.initials: S
authors.lastname: Merkelbach-Brese
authors.forename: P
authors.initials: P
authors.lastname: Hanrath
mesh_terms: D000368:Aged; D003327:Coronary Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000601:surgery*; D023903:Coronary Restenosis / Q000209:etiology / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D005787:Gene Frequency / Q000235:genetics; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D011237:Predictive Value of Tests; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011859:Radiography; D012907:Smoking / Q000235:genetics*; D015607:Stents
chemical_list: D017395:Plasminogen Activator Inhibitor 1