title: Relationship of plasminogen activator inhibitor-1 levels following thrombolytic therapy with rt-PA as compared to streptokinase and patency of infarct related coronary artery.
abstract: BACKGROUND
  Type 1 plasminogen activator inhibitor (PAI-1) is considered to be risk factor for acute myocardial infarction (AMI). A rebound of circulating PAI-1 has been reported after rt-PA administration. We investigated the relationships between PAI-1 levels before and after thrombolytic therapy with streptokinase (SK) as compared to rt-PA and the patency of infarct-related arteries.
  
  
  RESULTS
  Fifty five consecutive patients with acute MI were randomized to streptokinase or rt-PA. The plasma PAI-1 levels were studied before and serially within 24 h after thrombolytic administration. Vessel patency was assessed by an angiogram at 5+/-1days. The PAI-1 levels increased significantly with both rt-PA and SK as shown by the levels obtained from a control group of 10 patients treated with coronary angioplasty alone. However, the area under the PAI-1 curve was significantly higher with SK than with rt-PA (p<0.01) and the plasma PAI-1 levels peaked later with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PAI-1 levels on admission, the PAI-1 levels after thrombolysis were related to vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the area under the PAI-1 curve were significantly higher in patients with occluded arteries (p<0.002, p<0.04 and p<0.05 respectively). The same tendency was observed in the t-PA group without reaching significance.
  
  
  CONCLUSIONS
  This study showed that the PAI-1 level increase is more pronounced after SK treatment than after t-PA treatment. There is a relationship between increased PAI-1 levels after thrombolytic therapy and poor patency. Therapeutic approaches aimed at quenching PAI-1 activity after thrombolysis might be of interest to improve the efficacy of thrombolytic therapy for acute myocardial infarction.
authors.affiliation: Division of Cardiology, University of Marseille, School of Medicine, France.
authors.forename: F
authors.initials: F
authors.lastname: Paganelli
authors.forename: M C
authors.initials: MC
authors.lastname: Alessi
authors.forename: P
authors.initials: P
authors.lastname: Morange
authors.forename: J M
authors.initials: JM
authors.lastname: Maixent
authors.forename: S
authors.initials: S
authors.lastname: Lévy
authors.forename: I J
authors.initials: IJ
authors.lastname: Vague
mesh_terms: D015415:Biomarkers; D003331:Coronary Vessels / Q000503:physiopathology; D005343:Fibrinolytic Agents / Q000008:administration & dosage*; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011994:Recombinant Proteins / Q000008:administration & dosage; D013300:Streptokinase / Q000008:administration & dosage*; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage*
chemical_list: D015415:Biomarkers; D005343:Fibrinolytic Agents; D017395:Plasminogen Activator Inhibitor 1; D011994:Recombinant Proteins; D013300:Streptokinase; D010959:Tissue Plasminogen Activator