title: Plasma urokinase antigen and plasminogen activator inhibitor-1 antigen levels predict angiographic coronary restenosis.
abstract: BACKGROUND
  The fibrinolytic system is intimately involved in several processes that contribute to restenosis, including clot dissolution, cell migration, and tissue remodeling. However, the role of the individual activators (urokinase [uPA] and tissue plasminogen [tPA] activators) and inhibitors (plasminogen activator inhibitor [PAI-1]) of the fibrinolytic system in maintaining patency after coronary artery angioplasty and stenting is unclear.
  
  
  RESULTS
  We prospectively studied 159 patients with stable angina who underwent successful elective angioplasty (n=110) or stenting (n=49) of de novo native coronary artery lesions. Plasma samples were drawn at baseline (before angioplasty) and serially after angioplasty (immediately afterward and 6 hours, 24 hours, 3 days, 7 days, 1 month, 3 months, and 6 months afterward). Antigen and activity assays were performed for uPA, tPA, and PAI-1. Follow-up quantitative coronary angiography was performed in 92% of eligible patients. The overall angiographic restenosis rate (diameter stenosis >50%) was 31% (37% in PTCA patients, 17% in stented patients). At all time periods, including baseline, uPA antigen levels were significantly higher and PAI-1 antigen levels were significantly lower in patients with restenosis. Restenosis rates for patients in the upper tertile of baseline uPA antigen levels were 2-fold higher than for those in the lower 2 tertiles (46% versus 24% and 22%, respectively; P<0.004). In a stepwise regression multivariate analysis, obstruction diameter after the procedure and uPA antigen were significant predictors of follow-up diameter stenosis.
  
  
  CONCLUSIONS
  Plasma uPA antigen levels and PAI-1 antigen levels identify patients at increased risk for restenosis after percutaneous coronary revascularization.
authors.affiliation: Division of Cardiology, Terrence Donnelly Heart Centre, Hematology University of Toronto, Toronto, Ontario, Canada. straussb@smh.toronto.on.ca
authors.forename: B H
authors.initials: BH
authors.lastname: Strauss
authors.forename: H K
authors.initials: HK
authors.lastname: Lau
authors.forename: K A
authors.initials: KA
authors.lastname: Bowman
authors.forename: J
authors.initials: J
authors.lastname: Sparkes
authors.forename: R J
authors.initials: RJ
authors.lastname: Chisholm
authors.forename: M B
authors.initials: MB
authors.lastname: Garvey
authors.forename: L L
authors.initials: LL
authors.lastname: Fenkell
authors.forename: M K
authors.initials: MK
authors.lastname: Natarajan
authors.forename: I
authors.initials: I
authors.lastname: Singh
authors.forename: J M
authors.initials: JM
authors.lastname: Teitel
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000601:surgery / Q000628:therapy; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000517:prevention & control; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis* / Q000276:immunology; D011446:Prospective Studies; D012008:Recurrence; D012307:Risk Factors; D015607:Stents; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014568:Urokinase-Type Plasminogen Activator / Q000097:blood* / Q000276:immunology
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator