Platelet Aggregation After Thrombolytic Therapy

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Abstract
Using urokinase (UK) in the management of acute myocardial infarction (AMI) and pulmonary embolism (PE), an unexpected side effect of thrombolytic therapy, the enhancement of platelet aggregation, was observed. This platelet hyperaggregation process was studied in 244 subjects, 70 normal blood donors and 174 patients with AMI or PE. A simplified turbidimetric method was used in vivo and in vitro. The patients were divided into 5 groups: Group 1: 70 normal donors; Group 2: 10 AMI patients treated with heparin (HEP); Group 3: 12 AMI patients and 14 PE patients treated with HEP and UK; Group 4: 30 AMI patients treated with HEP and dipyridamole (Dip); Group 5: 108 patients, 44 with AMI and 64 with PE, treated with HEP, UK and Dip. Platelet hyperaggregation was observed in AMI and PE patients, which was already present before treatment and more frequent in PE than in AMI. This hyperaggregation is significantly enhanced in UK group (Group 3). It could be inhibited with Dip (Group 5). The comparison between Groups 3 and 5 shows that with HEP and UK, but without Dip, platelet hyperaggregation increases from 30 to 71%. It decreases from 71 to 40% in the group with Dip (P < 0.0025). The in vitro studies showed that UK and SK can enhance platelet aggregation without the help of ADP. The resulting hyperaggregation could be inhibited with .epsilon.-amino caproic acid and acexamic acid, while Kunitz inhibitor fails to inhibit the aggregating process. The side effect apparently cannot be related to the thrombolytic process, and its mechanism remains unknown. UK-induced platelet hyperaggregation could be a fair model for the assessment of antiaggregant drugs.