ENDOTHELIAL TISSUE-TYPE PLASMINOGEN-ACTIVATOR RELEASE IN CORONARY HEART-DISEASE - TRANSIENT REDUCTION IN ENDOTHELIAL FIBRINOLYTIC RESERVE IN PATIENTS WITH UNSTABLE ANGINA-PECTORIS OR ACUTE MYOCARDIAL-INFARCTION

Objectives. We sought to examine whether the disturbed fibrinolytic sy stem in patients with an acute coronary syndrome is associated with a reduced endothelial fibrinolytic capacity. Background. Intracoronary t hrombus formation is a frequent finding in acute coronary syndromes. S ystemic alterations of coagulation and fibrinolysis are known to occur , but possible disturbances of endothelial fibrinolytic function have not been investigated. Methods. We compared 42 patients with an acute coronary syndrome (acute myocardial infarction in 11 and unstable angi na pectoris in 31) with 25 patients with stable angina. Venous blood w as sampled serially for determination of markers of the fibrinolytic s ystem and of hypercoagulability from admission to day 10. An occlusion test to determine the maximal endothelial tissue-type plasminogen act ivator (t-PA) release was also performed. Results. Both on day 0 and d ay 10, patients with an acute coronary syndrome had a marked elevation of t-PA mass concen-tration (mean value +/- SEM 14.4 +/- 1.6 [day 0], 18.9 +/- 2.5 ng/ml [day 10]) and of plasminogen activator inhibitor ( PAI) (9.4 +/- 2.2 [day 0], 11.3 +/- 2.6 AU/liter [day 10], p < 0.05 vs . patients with stable angina). There was also a hypercoagulative stat e with elevated thrombin activity and increased D-dimers (p < 0.05 vs. patients with stable angina). Maximal endothelial t-PA release was in itially reduced (p < 0.05 vs. patients with stable angina) to 2.3 +/- 0.9 ngiml, but levels recovered during follow-up to 4.4 +/- 1.4 ngiml (vs. 5.7 a 1.5 ng/ml in patients with stable angina). Conclusions. Des pite the known prolonged systemic alteration of fibrinolysis in acute coronary syndromes, endothelial fibrinolytic capacity is reduced only during the acute phase and becomes normalized during follow-up, and th us is linked more to intravascular thrombus formation than to steady s tate levels of markers of the fibrinolytic system. (C) 1998 by the Ame rican College of Cardiology.