(Stroke. 1999;30:2101-2104.)
© 1999 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology (K.F., O.M., M. Daffertshofer, C.E., M.H.) and First Department of Medicine (C-E.D., M. Dollman), University of Heidelberg, Clinic Mannheim, Mannheim, Germany.
Correspondence to Dr K. Fassbender, Department of Neurology, Clinic Mannheim, University of Heidelberg, 68135 Mannheim, Germany.
Background and PurposeShifts of the balance between coagulation and fibrinolysis play a crucial role in pathogenesis and treatment of cerebral ischemia. In this study, we characterized the kinetics of hemostatic abnormalities induced by acute ischemic stroke and its thrombolytic (recombinant tissue plasminogen activator [rtPA]) or anticoagulant (heparin) treatment.
MethodsSystemic generation of molecular markers of hemostasis (fibrin monomer, D-dimer, thrombin-antithrombin complex, and fibrinopeptide 1.2) was monitored in acute ischemic stroke, and the effects of thrombolytic and anticoagulant treatments were analyzed.
ResultsThrombolysis with rtPA induced a massive response of markers of coagulation activation and fibrin formation that peaked after 1 to 3 hours and persisted for up to 72 hours. In contrast, only minor hemostatic changes were induced by acute ischemic stroke itself. Administration of heparin did not significantly affect these hemostatic abnormalities.
ConclusionsThis first characterization of the coagulation activation induced by rtPA treatment for acute ischemic stroke and the failure to abolish such hemostatic abnormalities by heparin may be of value for further refinement of the currently discussed thrombolytic therapy and the controversial adjunctive anticoagulant prophylaxis in stroke patients.
Key Words: coagulation stroke, ischemic thrombolysis tissue plasminogen activator, recombinant
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