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Augmented plasma protein C activity after coronary thrombolysis with urokinase in patients with acute myocardial
1Cardiopulmonary Division, Keio University School of Medicine, Tokyo, Japan.
Insights
Urokinase for heart attack treatment causes bleeding and clotting. Increased thrombin activity is counteracted by enhanced protein C, suggesting a complex effect on blood clotting.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Coronary thrombolysis is vital for acute myocardial infarction, reducing patient mortality.
- The precise impact of thrombolytic drugs on the body's natural blood clotting system (intrinsic hemostasis) remains unclear.
Purpose of the Study:
- To investigate the effects of urokinase on thrombin and protein C activity in patients experiencing acute myocardial infarction.
Main Methods:
- Serial blood samples were collected from 6 acute myocardial infarction patients undergoing urokinase treatment.
- Plasma levels of thrombin-antithrombin III complex, protein C, and protein S were measured.
Main Results:
- Urokinase induced rapid fibrinolysis and increased thrombin-antithrombin III complex levels, indicating thrombin generation.
- Plasma protein C activity rose concurrently, while protein S levels remained unchanged.
Conclusions:
- Urokinase therapy for coronary thrombolysis triggers both clot breakdown and thrombin generation.
- Elevated protein C activity may serve as a natural counterbalance to urokinase-induced procoagulant effects.
Abstract:
Coronary thrombolysis reduces morbidity and mortality in patients with acute myocardial infarction, however, the exact effects of thrombolytic agents on the status of intrinsic hemostases are not fully understood. In the present study, we examined serial changes in plasma thrombin and protein C activities of 6 patients with acute myocardial infarction treated with urokinase. Fibrinolysis occurred immediately after urokinase injection with an increase in the plasma thrombin-antithrombin III complex, suggesting a subsequent procoagulant state due to thrombin generation. Correspondent increases in plasma protein C activity were observed, however, protein S levels did not change at all. Our findings suggest that urokinase administration for coronary thrombolysis not only causes fibrinolysis, but also induces thrombin activity, which may be antagonized by augmented intrinsic protein C activity.