title: Plasminogen activator inhibitor-1 4G4G genotype is associated with myocardial infarction but not with stable coronary artery disease.
abstract: BACKGROUND
  A case control study was conducted to test the hypothesis that plasminogen activator inhibitor type-1 (PAI-1) 4G/5G gene polymorphism confers an increased risk for myocardial infarction (MI) in patients with known coronary atherosclerosis.
  
  
  METHODS
  One hundred fifty-six consecutive patients who presented with acute MI and 111 stable coronary artery disease (SCAD) patients with documented critical coronary artery stenoses were prospectively enrolled. PAI-1 4G/5G gene polymorphism and conventional atherosclerotic risk factors were studied in all patients. PAI-1 4G/5G gene polymorphism was studied in another 281 healthy blood bank donors.
  
  
  RESULTS
  The frequency 4G4G genotype was significantly higher in the MI group as compared to SCAD group (32.7% vs. 15.3%, P = 0.001) while it was not statistically significant between MI and healthy control groups (32.7% vs. 26.0%, P = 0.136). Comparing with healthy controls SCAD group had significantly lower frequency of 4G4G genotype (P = 0.024). In comparison with SCAD group PAI-1 4G/4G genotype, male sex and smoking habits favored to MI in univariate analysis with a P value of less than 0.2. These variables were included in multivariate regression model to estimate the associated risk for MI. PAI-1 4G/4G genotype was the only independent variable (OR 2.67, 95%CI 1.43-4.96, P = 0.002) associated with MI in this regression model. Comparing with healthy control group 4G4G genotype was not associated with MI (OR 1.38, 95%CI 0.90-2.12). However, presence of 4G4G genotype had a protective effect against development of SCAD (OR 0.52, 96%CI 0.29-0.92).
  
  
  CONCLUSIONS
  Compared to patients with critical coronary stenoses, PAI-1 4G/4G genotype was found to be an independent predictor for development of MI in this population. PAI-1 4G4G genotype have a protective effect against development of high grade stable coronary stenoses.
authors.affiliation: Faculty of Medicine, Department of Cardiology, Hacettepe University, Ankara, Turkey. oonalan@gmail.com
authors.forename: Orhan
authors.initials: O
authors.lastname: Onalan
authors.forename: Gunay
authors.initials: G
authors.lastname: Balta
authors.forename: Ali
authors.initials: A
authors.lastname: Oto
authors.forename: Giray
authors.initials: G
authors.lastname: Kabakci
authors.forename: Lale
authors.initials: L
authors.lastname: Tokgozoglu
authors.forename: Kudret
authors.initials: K
authors.lastname: Aytemir
authors.forename: Cigdem
authors.initials: C
authors.lastname: Altay
authors.forename: Aytemiz
authors.initials: A
authors.lastname: Gurgey
authors.forename: Nasih
authors.initials: N
authors.lastname: Nazli
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006720:Homozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*
chemical_list: D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human