Alterations in the fibrinolytic system components during acute myocardial infarction.
The purpose of this study was to evaluate the changes in tissue-plasminogen activator (t-PA), plasminogen activator inhibitor - type 1 (PAI-1) and D-dimer (DD) antigen plasma levels in acute myocardial infarction (AMI) patients after thrombolytic therapy with two different thrombolytic agents, rt-PA or acetyl-streptokinase and to find out any correlation between the plasma t-PA, PAI-1 and DD levels with the infarct size as it is estimated from the peak of serum CPK levels. The plasma antigen levels of t-PA, PAI-1 and DD were measured by the enzyme immunoassay method (Stago), in 57 consecutive patients (M = 46, F = 11, mean age 55.6 +/- 8.8 years) and in 25 normal subjects (M = 18, F = 7, mean age 54.0 +/- 5.5 years). In 47 out of the 57 patients who were treated successfully with 100 mg of rt-PA (26 patients) or with 1.5 MU 21 of acetyl-streptokinase, as well as in 10 patients who were not treated, samples were obtained again 4 and 24 hours after the end of thrombolytic therapy or admission, respectively. During the acute phase of myocardial infarction the t-PA, PAI-1 and DD antigen plasma levels were significantly higher than in healthy people. There were no significant changes in the t-PA, PAI-1 and DD plasma levels of the patients who were not treated with a thrombolytic agent. We found a significant elevation of t-PA (p < 0.001), PAI-1 (p < 0.05) and DD (p < 0.001) after 4 hours in comparison with the baseline (at presentation, before therapy). After 24 hours the t-PA and DD plasma levels remained significantly higher (p < 0.001) while the PAI-1 plasma levels returned to the pre-therapy levels. There were no significantly different changes in the t-PA, PAI-1 and DD plasma levels of either group of patients, treated with rt-PA or acetyl-streptokinase while the t-PA and PAI-1 levels were positively correlated with infarct size as estimated from peak serum CPK levels.
Ioannidou-Papayannaki
E
E
Haematology Laboratory of 2nd Dept. of Internal Medicine, Aristotelian University of Thessaloniki, Hippokration Hospital, Greece.
Lefkos
N
N
Boudonas
G
G
Efthimiadis
A
A
Psirropoulos
D
D
Vogas
V
V
Papadopoulos
I
I
Klonizakis
I
I
D004796:Clinical Enzyme Tests; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis*; D005342:Fibrinolysis; D006801:Humans; D007124:Immunoenzyme Techniques; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D010960:Plasminogen Activators / Q000037:antagonists & inhibitors / Q000097:blood / Q000627:therapeutic use*; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood / Q000627:therapeutic use*
D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D003402:Creatine Kinase; D013300:Streptokinase; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator