title: Percutaneous interventions alter the hemostatic profile of patients with unstable versus stable angina.
abstract: OBJECTIVE
  The objectives of this study were to define the hemostatic profiles of patients with unstable angina compared with patients with stable angina and to investigate the effect of percutaneous interventions on the follow-up hemostatic profiles of these patients.
  
  
  BACKGROUND
  Disturbances in hemostatic factors have been shown to be present in various clinical syndromes involving coronary artery disease. However, their role in stable angina versus unstable angina is less well defined.
  
  
  METHODS
  We studied 61 patients with either stable or unstable angina undergoing percutaneous coronary interventions. Blood samples were drawn immediately before the intervention and at 1-month follow-up. Plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and von Willebrand factor (vWF) were measured by enzyme-linked immunosorbent assays.
  
  
  RESULTS
  Patients with unstable angina had significantly higher t-PA levels (mean [+/-SE] 23.7 +/- 3.4 vs. 14.3 +/- 1.4 ng/ml, respectively, p = 0.02) and vWF antigen concentrations (2,231 +/- 157 vs. 1,792 +/- 108 mU/ml, respectively, p = 0.03) than patients with stable angina. No statistically significant differences were observed in the PAI-1 levels between the two groups (27.9 +/- 5.5 vs. 21.4 +/- 2.5 ng/ml, respectively, p = 0.25). At 1-month follow-up, there were no longer any significant differences in the t-PA or vWF levels between the two groups (15.7 +/- 1.2 vs. 13.6 +/- 0.6 ng/ml, p = 0.13; 1,962 +/- 170 vs. 1,809 +/- 88 mU/ml, p = 0.39, respectively). There were no significant differences between the hemostatic profiles of patients undergoing percutaneous transluminal coronary angioplasty or coronary stenting initially and at 1-month follow-up.
  
  
  CONCLUSIONS
  These data suggest that elevated plasma levels of t-PA and vWF may correlate with instability of atheromatous plaques, and that their decrease after coronary interventions may reflect plaque reendothelialization and stabilization.
authors.affiliation: Department of Medicine, Columbia-Presbyterian Medical Center, New York 10032, USA.
authors.forename: S
authors.initials: S
authors.lastname: Yazdani
authors.forename: A D
authors.initials: AD
authors.lastname: Simon
authors.forename: L
authors.initials: L
authors.lastname: Kovar
authors.forename: W
authors.initials: W
authors.lastname: Wang
authors.forename: A
authors.initials: A
authors.lastname: Schwartz
authors.forename: L E
authors.initials: LE
authors.lastname: Rabbani
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood*; D000789:Angina, Unstable / Q000097:blood*; D015906:Angioplasty, Balloon, Coronary; D005260:Female; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D015607:Stents; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator