α2-antiplasmin consumption and fibrinogen breakdown during thrombolytic therapy

Abstract

The role of α 2-antiplasmin, the fast-acting plasmin inhibitor of human plasma, in the occurrence of systemic fibrinogen breakdown during thrombolytic therapy (evidenced by a rapid decrease of plasma fibrinogen and the generation of high amounts of fibrin-(ogen) degradation products in serum) was studied in patients with vascular occlusive disease. Depletion of α 2-antiplasmin either by infusion of high doses of streptokinase or of 8,000 CTA units of plasmin was consistently accompanied by systemic fibrinogenolysis. Infusion of urokinase or of 4,000 CTA units of plasmin, resulting in a decrease of α 2-antiplasmin to about 50 percent of the pre-infusion value, was not accompanied by rapid systemic fibrinogen breakdown although a progressive decrease of fibrinogen to about 50 percent of the preinfusion value was observed over a period of 6–12 hours. Thus systemic fibrinogenolysis only occurred in association with a depletion of the circulating α 2-antiplasmin pool. It is concluded that α 2-antiplasmin constitutes an important parameter which should be taken into account in the interpretation of changes in laboratory tests occurring during thrombolytic therapy.