PLATELET-FUNCTION DURING THROMBOLYTIC THERAPY WITH ANISTREPLASE

Platelets are likely to play a role during thrombolytic therapy of acu te myocardial infarction, but their exact involvement is not fully und erstood at present. The effects of thrombolytic agents on platelet fun ction have mainly been studied using in vitro experiments and results are rather controversial; data from in vivo studies are rare. We studi ed 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, be ta-thromboglobulin and thromboxane-B2 in plasma. Immediately after ani streplase, the aggregation of platelets was significantly inhibited: a ggregation induced by ADP decreased to 67+/-36% (mean+/-SD) of pretrea tment (P<0.05), by arachidonic acid to 29+/-29% (P<0.005) and by colla gen to 58+/-46% (P<0.05). The aggregation defect was transient; after 6-12 h aggregation had returned to normal. Then, a significant stimula tion of ADP-induced aggregation became apparent, lasting until 24-48 h after thrombolysis; possibly this was mediated by heparin. The platel et proteins and thromboxane-B2 were significantly elevated before thro mbolysis and showed a steady decrease after anistreplase. In the first phase of anistreplase therapy, we found no indications of platelet ac tivation. Additional in vitro studies confirmed these findings. Antibo dies to streptokinase did not affect platelet function in these patien ts.