Affiliation:
1. The Section of Coagulation and Fibrinolysis, Department of Clinical Chemistry and Department of Internal Medicine, Ribe Country Hospital in Esbjerg; the Section for Thrombosis Research, South Jutland University Center, Esbjerg, Denmark
2. The Gaubius Institute TNO, Leiden, The Netherlands
Abstract
SummaryWe determined during the acute stage of myocardial infarction selected fibrinolysis variables (tissue-type plasminogen activator, intrinsic plasminogen activators, tissue-type plasminogen activator inhibition, C1-inactivator) and relatedthe observed changes to changes in two acute phase reactants (C-reactive protein, fibrinogen). Acute myocardial injury induce significant increases in blood of tissue-type plasminogen activator inhibition (day one, p <0.05), C-reactive protein (day three, p <0.01), fibrinogen (day six, p <0.01), and C1-inactivator (day eight, p <0.01). Tissue-type plasminogen activator activity measured as C1-inactivator resistant fibrinolytic activity showed a minimum day two after the acute attack (p <0.01), whereas plasminogen activator activities arising from the intrinsic system of fibrinolysis remained constant. The observed changes did not parallel the occurrence of deep vein thrombosis indicated by a positive Tc-plasmin test (41% of the patients).
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