Maximal endothelial tissue plasminogen activator release is not impaired in patients with acute coronary syndromes before heparin treatment.

Abstract

Procoagulant and fibrinolytic disturbances are described in patients with acute coronary syndromes (ACS), but whether defective maximal tissue plasminogen activator (t-PA) release from the endothelium is also present is still controversial. Previous studies did not take into consideration the contribution of heparin, which strongly affects fibrinolysis. Accordingly, in this study, we measured maximal t-PA release in patients with ACS before, during, and after heparin treatment. Maximal t-PA release was measured by the venous occlusion test in 38 hospitalized patients with confirmed ACS (18 acute myocardial infarctions and 20 unstable anginas) before starting heparin, during heparin treatment, and 4 and 12 h after discontinuation. Plasma plasminogen activator inhibitor type 1 (PAI-1), D-dimer and prothrombin fragment F1 + 2 were also measured. Eighteen age-matched subjects with no evidence of coronary disease were used as controls. At admission, patients showed significantly higher plasma levels of t-PA, PAI-1, and F1 + 2 than controls. Before heparin, maximal t-PA release was similar in patients and controls. Heparin treatment was associated with a significant increase of plasma t-PA, while it did not affect maximal t-PA release. Coagulative and fibrinolytic disturbances are present in patients with ACS, but these do not include maximal t-PA release. Among our patients, maximal t-PA release appears stable over time and is not affected by heparin treatment.