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Thrombolytic therapy with tissue plasminogen activator or streptokinase
induces transient thrombin activity
J Owen, KD Friedman, BA Grossman, C Wilkins, AD Berke and ER Powers
Department of Medicine, College of Physicians and Surgeons, Columbia
University, New York, NY 10032.
We have determined the plasma level of fibrinopeptide A as a specific index
of thrombin activity during the infusion of a thrombolytic agent in
patients with acute myocardial infarction. Peripheral venous plasma levels
of fibrinopeptide A increased following the initiation of thrombolytic
therapy from 2.7 nmol/L to a peak of 13.0 nmol/L at 30 minutes with
streptokinase and from 1.1 nmol/L to a peak of 10.7 nmol/L at 90 minutes
with tissue plasminogen activator. The amount of fibrinogen converted to
fibrin I was determined by integration of the plasma level of
fibrinopeptide A over time. The amount of fibrin I formed over the
five-hour period from the start of drug infusion was approximately 10 mg/dL
in response to either streptokinase or recombinant tissue plasminogen
activator. We conclude that activation of coagulation occurs in response to
thrombolytic therapy despite heparin administration. This thrombin action,
though transient, would be sufficient to cause rethrombosis if localized
and incompletely opposed by fibrinolytic activity.
Volume 72,
Issue 2,
pp. 616-620,
08/01/1988
Copyright © 1988 by The American Society of Hematology
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