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Proteolysis of von Willebrand factor after thrombolytic therapy in patients
with acute myocardial infarction
AB Federici, SD Berkowitz, TS Zimmerman and PM Mannucci
Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, IRCCS Maggiore
Hospital, Milano, Italy.
In 20 patients with acute myocardial infarction (AMI) treated with
streptokinase (SK, n = 7), recombinant single-chain tissue plasminogen
activator (rt-PA, n = 7) or urokinase (UK, n = 6), the behavior of plasma
von Willebrand factor (vWF) was studied before and 1.5, 3, 24, 48, and 72
hours after beginning thrombolytic therapy. vWF antigen (vWF:Ag) was high
in plasma, especially after SK. The ristocetin cofactor (RiCof) activity of
vWF, high before therapy, tended to decrease soon after therapy. This
pattern of vWF changes was paralleled by the early loss of higher molecular
weight multimers. By immunoblotting of immunopurified and reduced vWF and
monoclonal antibody epitope mapping, we found that vWF was degraded after
thrombolysis, especially after SK, as indicated by the higher values of two
plasmin-generated fragments of 176 and 145 Kd. There were more
plasmin-generated fragments in the five patients who had bleeding
complications than in the remaining 15 who did not. In conclusion,
quantitative and qualitative changes of vWF compatible with proteolytic
degradation of the protein occur during thrombolytic therapy. Such
degradation, roughly proportional to the degree of the general lytic state
induced by each agent, might be a cofactor of the bleeding complications
occurring in treated patients.
Volume 79,
Issue 1,
pp. 38-44,
01/01/1992
Copyright © 1992 by The American Society of Hematology
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