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.