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).
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 related the 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 less than 0.05), C-reactive protein (day three, p less than 0.01), fibrinogen (day six, p less than 0.01), and C1-inactivator (day eight, p less than 0.01). Tissue-type plasminogen activator activity measured as C1-inactivator resistant fibrinolytic activity showed a minimum day two after the acute attack (p less than 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).
D000209:Acute-Phase Proteins / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D003174:Complement C1 Inactivator Proteins / Q000097:blood; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood* / Q000150:complications; D013924:Thrombophlebitis / Q000097:blood / Q000209:etiology; D010959:Tissue Plasminogen Activator / Q000037:antagonists & inhibitors / Q000097:blood*
D000209:Acute-Phase Proteins; D003174:Complement C1 Inactivator Proteins; D005340:Fibrinogen; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator