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Prehospital Thrombolysis: A Manual from Berlin
Published on: November 26, 2013
The thrombolytic paradox
H M Hoffmeister1, S Szabo, U Helber
1Medizinische Klinik, Abteilung Innere Medizin III, Eberhard-Karls-Universität, Tübingen, Germany.
Thrombosis Research
|September 25, 2001
Summary
Thrombolytic drugs can paradoxically increase blood clotting by activating the coagulation system. This "thrombolytic paradox" is linked to non-fibrin-specific drugs and systemic plasmin activation, not fibrin-specific agents like tenecteplase.
Area of Science:
- Biochemistry
- Hematology
- Pharmacology
Background:
- Patients with acute myocardial infarction often have a hypercoagulative state.
- Thrombolytic drugs aim to dissolve clots but can also activate coagulation pathways.
Purpose of the Study:
- To investigate the mechanism behind paradoxical thrombin activation during thrombolytic therapy.
- To test the hypothesis that plasmin-mediated activation of the contact phase causes this procoagulant effect.
Main Methods:
- Evaluation of various thrombolytic regimens in vitro.
- Assessment of thrombin activation and systemic plasmin activation.
- Comparison of fibrin-specific (tenecteplase) and non-fibrin-specific (streptokinase) drugs.
Main Results:
- Non-fibrin-specific thrombolytics, like streptokinase, caused significant thrombin activation and contact phase activation.
- Fibrin-specific tenecteplase did not induce additional thrombin activation.
- The "thrombolytic paradox" correlated with the degree of systemic plasmin activation.
Conclusions:
- Plasmin-mediated activation of the factor XII/kallikrein system is the cause of the thrombolytic paradox.
- Fibrin specificity is crucial in preventing paradoxical thrombin activation during thrombolysis.
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