title: Predictive value of plasma plasminogen activator inhibitor-1 for coronary restenosis: dependence on stent implantation and antithrombotic medication.
abstract: BACKGROUND
  The plasmin activation system is involved in the development of restenosis after percutaneous coronary interventions (PCI). Conflicting data exist concerning the role of plasminogen activator inhibitor-1 (PAI-1) and its predictive value for restenosis.
  
  
  OBJECTIVE
  To evaluate the fibrinolytic response to injury after PCI with or without stent implantation on different antithrombotic medications and its relation to late restenosis.
  
  
  METHODS
  Eighty consecutive patients with successful PCI without (balloon only; n = 37) or with stent implantation (stent; n = 43) on different antithrombotic regimes (balloon only, aspirin; stent, aspirin/coumadin/dipyridamole vs. aspirin/ticlopidine). Blood samples were taken at baseline and up to 7 days after PCI and PAI-1 active antigen and tissue plasminogen activator (t-PA) antigen were determined. Restenosis was angiographically determined after 6 months.
  
  
  RESULTS
  PCI increased both t-PA and PAI-1 levels (P < 0.001), with a significant prolonged and pronounced increase in stent vs. balloon-only patients (P < 0.05). Restenosis (stent 26%; balloon 38%) was significantly correlated to an attenuated PAI-1 increase after 24 h in the ticlopidine group (P = 0.007; restenosis, relative Delta PAI-1 + 50 +/- 28%; non-restenosis, + 139 +/- 50%), but not in the coumadin group. In the balloon-only group late restenosis (ISR) was associated with a trend for an augmented PAI-1 increase after 24 h.
  
  
  CONCLUSIONS
  Coronary stent implantation significantly increases t-PA and PAI-1 plasma levels up to 1 week compared with balloon angioplasty alone. ISR in ticlopidine-treated patients was associated with an attenuated early PAI-1 active antigen increase. A less than 50% increase 24 h after stent implantation under ticlopidine treatment may identify patients at risk for the development of ISR.
authors.affiliation: Department of Cardiology, Medical University of Vienna, Währingergürtel 18-20, A-1090 Vienna, Austria. guenter.christ@meduniwien.ac.at
authors.forename: G
authors.initials: G
authors.lastname: Christ
authors.forename: M
authors.initials: M
authors.lastname: Nikfardjam
authors.forename: R
authors.initials: R
authors.lastname: Huber-Beckmann
authors.forename: M
authors.initials: M
authors.lastname: Gottsauner-Wolf
authors.forename: D
authors.initials: D
authors.lastname: Glogar
authors.forename: B R
authors.initials: BR
authors.lastname: Binder
authors.forename: J
authors.initials: J
authors.lastname: Wojta
authors.forename: K
authors.initials: K
authors.lastname: Huber
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D001241:Aspirin / Q000627:therapeutic use; D003131:Combined Modality Therapy / Q000009:adverse effects / Q000379:methods; D023903:Coronary Restenosis / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D005260:Female; D005342:Fibrinolysis; D005343:Fibrinolytic Agents / Q000009:adverse effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood* / Q000502:physiology; D011237:Predictive Value of Tests; D011725:Pyridines / Q000627:therapeutic use; D012189:Retrospective Studies; D015607:Stents / Q000009:adverse effects; D013988:Ticlopidine / Q000627:therapeutic use; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D005343:Fibrinolytic Agents; D017395:Plasminogen Activator Inhibitor 1; D011725:Pyridines; C446540:thienopyridine; D010959:Tissue Plasminogen Activator; D013988:Ticlopidine; D001241:Aspirin