Why the study?
Does streptokinase infusion reduce platelet aggregation in patients with acute myocardial infarction?
Does streptokinase infusion reduce platelet aggregation in patients with acute myocardial infarction?
Streptokinase treatment in acute myocardial infarction attenuates platelet aggregation despite increasing markers of platelet activation.
Streptokinase may attenuate platelet aggregation in AMI despite rising activation markers; hypothesis-generating from single case report and requires confirmation.
The aim of this study was to determine whether platelets are activated and aggregation is increased in myocardial infarction treated with streptokinase. Twelve consecutive patients were studied. Before streptokinase infusion (1.5 times 106 IU i.v. over a period of 1 h), 7 ± 4 h after the onset of symptoms, fibrinogen, leucocyte and platelet functions were enhanced compared to reference values. Plasma fibrinogen was 3.1 ± 0.6 g l‐1 (P < 0.03), leucocyte count was 14.3 ± 3.3 times 103 l‐1 (P < 0.0005), elastase was 39 ± 8 μg l‐1 (P < 0.0002), β‐thromboglobulin was 68 ± 71 μg l‐1 (P < 0.0001) and filtragometer platelet aggregation time was 137 ± 40 s (P < 0.0001). After streptokinase the leucocyte count, elastase and β‐thromboglobulin levels increased further, by about 40% (P < 0.02), 130% (P < 0.02) and 140% (P < 0.005), respectively. Fibrinogen was almost eliminated. Despite signs of increased activation, platelet aggregation was decreased as indicated by both filtragometer aggregation time, which increased by about 480% (P < 0.003), and whole‐blood aggregometry, in which electrical impedance decreased by about 65% (P < 0.01).
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Sylvén et al. (1992) studied this question.
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