title: PAI-1 4G/5G gene polymorphism is associated with angiographic patency in ST-elevation myocardial infarction patients treated with thrombolytic therapy.
abstract: BACKGROUND
  In this study, we examined the relationship between PAI-1 4G/5G polymorphism and patency of the infarct-related artery after thrombolysis in patients with ST-elevation myocardial infarction (STEMI).
  
  
  METHODS
  Acute STEMI patients who received thrombolytic therapy within first 12 h were included in our study. The PAI-1 4G/5G promoter region insertion/deletion polymorphism was studied from venous blood samples. Patients with the PAI-1 4G/5G gene polymorphism were included in group 1 and the others were included in group 2. Coronary angiography was performed in all patients in the first 24 h after receiving thrombolytic therapy. Thrombolysis in myocardial infarction (TIMI) 0-1 flow in the infarct-related artery was considered as 'no flow', TIMI 2 flow as 'slow flow', and TIMI 3 flow as 'normal flow'.
  
  
  RESULTS
  A total of 61 patients were included in our study. Thirty patients (49.2%) were positive for the PAI-1 4G/5G gene polymorphism, whereas 31 of them (50.8%) were in the control group. There were significantly more patients with 'no flow' (14 vs. 6; P=0.02) and less patients with 'normal flow' (8 vs. 19; P=0.02) in group 1. In addition, time to thrombolytic therapy (TTT) was maximum in the 'no flow' group and minimum in the 'normal flow' group (P=0.005). In the logistic regression analysis, TTT (odds ratio: 0.9898; 95% confidence interval: 0.982-0.997; P=0.004) and the PAI-1 4G/5G gene polymorphism (odds ratio: 4.621; 95% confidence interval: 1.399-15.268; P<0.01) were found to be independently associated with post-thrombolytic 'no flow'.
  
  
  CONCLUSIONS
  The PAI-1 4G/5G gene polymorphism and TTT are associated independently with 'no flow' after thrombolysis in patients with STEMI.
authors: Department of Cardiology, Burdur Bucak State Hospital, Turkey.
authors: Bugra
authors: B
authors: Ozkan
authors: Caglar E
authors: CE
authors: Cagliyan
authors: Zafer
authors: Z
authors: Elbasan
authors: Onur K
authors: OK
authors: Uysal
authors: Gulhan Y
authors: GY
authors: Kalkan
authors: Mehmet
authors: M
authors: Bozkurt
authors: Kamuran
authors: K
authors: Tekin
authors: Sevcan T
authors: ST
authors: Bozdogan
authors: Ozge
authors: O
authors: Ozalp
authors: Mustafa
authors: M
authors: Duran
authors: Durmus Y
authors: DY
authors: Sahin
authors: Murat
authors: M
authors: Cayli
mesh_terms: D000368:Aged; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy / Q000379:methods; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D005343:Fibrinolytic Agents; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D013300:Streptokinase; D010959:Tissue Plasminogen Activator