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Enhanced platelet function in acute myocardial infarction is attenuated by streptokinase treatment
C Sylvén1, K E Karlberg, J Chen
1Karolinska Institute, Department of Medicine, Huddinge University Hospital, Sweden.
Insights
Platelet activation markers increased in myocardial infarction patients treated with streptokinase. However, platelet aggregation significantly decreased after treatment, indicating a complex response to the therapy.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Myocardial infarction (MI) involves platelet activation and aggregation.
- Streptokinase is a thrombolytic agent used in MI treatment.
- The effect of streptokinase on platelet function in MI requires further elucidation.
Purpose of the Study:
- To investigate platelet activation and aggregation in patients with myocardial infarction treated with streptokinase.
- To assess changes in specific platelet function markers before and after streptokinase infusion.
Main Methods:
- Studied twelve consecutive patients with myocardial infarction.
- Measured plasma fibrinogen, leucocyte count, elastase, beta-thromboglobulin, and platelet aggregation time before and after streptokinase infusion.
- Utilized filtragometer and whole-blood aggregometry for platelet aggregation assessment.
Main Results:
- Before treatment, patients showed enhanced fibrinogen, leucocyte count, elastase, beta-thromboglobulin, and reduced platelet aggregation time.
- After streptokinase infusion, leucocyte count, elastase, and beta-thromboglobulin levels increased further.
- Despite increased activation markers, platelet aggregation significantly decreased, as evidenced by increased aggregation time and decreased electrical impedance.
Conclusions:
- Streptokinase treatment in myocardial infarction leads to increased markers of platelet activation.
- Paradoxically, streptokinase therapy results in a significant decrease in platelet aggregation.
- The findings suggest a complex interplay between streptokinase, inflammatory markers, and platelet function in MI patients.
Abstract:
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 x 10(6) 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 1-1 (P less than 0.03), leucocyte count was 14.3 +/- 3.3 x 10(3) l-1 (P less than 0.0005), elastase was 39 +/- 8 micrograms l-1 (P less than 0.0002), beta-thromboglobulin was 68 +/- 71 micrograms 1-1 (P less than 0.0001) and filtragometer platelet aggregation time was 137 +/- 40 s (P less than 0.0001). After streptokinase the leucocyte count, elastase and beta-thromboglobulin levels increased further, by about 40% (P less than 0.02), 130% (P less than 0.02) and 140% (P less than 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 less than 0.003), and whole-blood aggregometry, in which electrical impedance decreased by about 65% (P less than 0.01).