Percutaneous interventions alter the hemostatic profile of patients with unstable versus stable angina

Objectives. 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) mere 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 mere 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. (C) 1997 by the American College of Cardiology.