Evidence of increased platelet activation after thrombolysis in patients with acute myocardial infarction

Gundars Rasmanis, Ole Vesterqvist, Krister Gréen, Olof Edhag, Peter Henriksson

Cardiac Division of the Department of Medicine, Karolinska Institutet, Huddinge University Hospital and Department of Blood Coagulation and Clinical Chemistry, Karolinska Hospital, Stockolm, Sweden

Objective—To assess platelet activation after thrombolysis in patients with acute myocardial infarction.

Design—Platelet function was assessed by measurement of the in vivo synthesis of thromboxane by gas chromatography-mass spectrometry of thromboxane's major urinary metabolite, 2,3-dinor-thromboxane-B₂.

Setting—Coronary care unit of Huddinge University Hospital.

Subjects—30 patients with acute myocardial infarction given either streptokinase 1·5 million units intravenously over one hour + 500 mg aspirin (n = 10), 500 mg aspirin (n = 10), or neither thrombolysis nor aspirin (n = 10).

Results—Patients treated by thrombolysis had a 20-fold increase in thromboxane formation during thrombolysis compared with control patients not treated by thrombolysis (p = 0·0001). Until two days after thrombolysis thromboxane production in patients treated with streptokinase did not decrease to a value comparable with patients treated with aspirin but not given thrombolysis.

Conclusions—Thromboxane production increased considerably during thrombolysis, possibly reflecting greatly enhanced platelet activation. The slow decrease in thromboxane formation after treatment with aspirin suggests that the efficacy of thrombolysis might be improved by more efficient antiplatelet treatment.

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