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Thromb Haemost 1987; 58(03): 817-821
DOI: 10.1055/s-0038-1645996
Original Article
Schattauer GmbH Stuttgart

Depression of Tissue Plasminogen Activator (t-PA) Activity and Rise of t-PA Inhibition and Acute Phase Reactants in Blood of Patients with Acute Myocardial Infarction (AMI)[]

Jørgen Gram
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
,
Cornelis Kluft
*   The Gaubius Institute TNO, Leiden, The Netherlands
,
Jørgen Jespersen
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
› Author Affiliations
Further Information

Publication History

Received 12 February 1987

Accepted after revision 08 May 1987

Publication Date:
28 June 2018 (online)

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Summary

We 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).

Keywords

Acute myocardial infarction - Acute phase reactants - Fibrinolysis
 

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