Streptokinase, but not tissue plasminogen activator, attenuates platelet aggregation in patients with acute myocardial infarction.

OBJECTIVES: To investigate if tissue plasminogen activator (tPA) and streptokinase given during acute myocardial infarction (AMI) have different effects on platelet aggregation which could contribute to the higher reocclusion rate observed after tPA. DESIGN: Open labelled on consecutive patients. SETTING: Coronary care unit. SUBJECTS: Twenty patients with chest pain and ST elevations on an electrocardiogram suggestive of AMI. INTERVENTIONS: Ten patients were treated with tPA (100 mg 3 h-1), 10 patients with streptokinase (1.5 x 10(6) IU 1 h-1). MAIN OUTCOME MEASURES: Before, immediately after and 24 h after fibrinolytic therapy, platelet aggregation was estimated with filtragometry and whole blood aggregometry. Fibrinogen, beta-thromboglobulin, elastase and the fibrinogen-derived peptide B beta 30-43 were also measured. RESULTS: The groups were comparable at baseline. Directly after treatment, streptokinase prolonged aggregation time in filtragometry with 112 +/- 140 s (P < 0.03) and reduced conductance in whole blood aggregometry by 6.2 +/- 6.1 omega (P < 0.03), both tests indicating inhibited platelet function. Fibrinogen decreased 2.5 +/- 1.0 g l-1 (P < 0.02). In the tPA-treated group corresponding changes were 68 +/- 225 s (NS) and 2.5 +/- 7 omega (NS) with no significant reduction in fibrinogen. After 24 h, at which time every patient was on acetylsalicylic acid, aggregation was inhibited in both groups as measured by aggregometry. Directly after fibrinolytic treatment, neutrophils were similarly activated in both groups with increments of elastase and B beta 30-43 by 26 +/- 46 micrograms l-1 (P < 0.03) and 280 +/- 381 pmol l-1 (P < 0.03) respectively (streptokinase) and by 12 +/- 6 micrograms l-1 (P < 0.02) and 919 +/- 856 pmol l-1 (P < 0.02) respectively (tPA). CONCLUSIONS: Despite similar degrees of platelet and leucocyte activation, streptokinase but not tPA treatment appears to inhibit platelet aggregation. One possible reason could be a streptokinase-induced pronounced decrease of fibrinogen and increase of fibrinogen split products. Therefore, further development of adjuvant antiplatelet therapy could be of clinical importance.