PLATELET-FUNCTION DURING THROMBOLYTIC THERAPY WITH ANISTREPLASE

Platelets are likely to play a role during thrombolytic therapy of acute myocardial infarction, but their exact involvement is not fully understood at present. The effects of thrombolytic agents on platelet function have mainly been studied using in vitro experiments and results are rather controversial; data from in vivo studies are rare. We studied 10 patients with acute myocardial infarction, who were treated with intravenous anistreplase. Use of aspirin or other anti-platelet drugs were not allowed. Before and after thrombolysis, blood was collected for determining ex vivo platelet aggregation and platelet factor 4, beta-thromboglobulin and thromboxane-B2 in plasma. Immediately after anistreplase, the aggregation of platelets was significantly inhibited: aggregation induced by ADP decreased to 67+/-36% (mean+/-SD) of pretreatment (P<0.05), by arachidonic acid to 29+/-29% (P<0.005) and by collagen to 58+/-46% (P<0.05). The aggregation defect was transient; after 6-12 h aggregation had returned to normal. Then, a significant stimulation of ADP-induced aggregation became apparent, lasting until 24-48 h after thrombolysis; possibly this was mediated by heparin. The platelet proteins and thromboxane-B2 were significantly elevated before thrombolysis and showed a steady decrease after anistreplase. In the first phase of anistreplase therapy, we found no indications of platelet activation. Additional in vitro studies confirmed these findings. Antibodies to streptokinase did not affect platelet function in these patients.