Streptokinase, but not tissue plasminogen activator, attenuates platelet aggregation in patients with acute myocardial infarction.
OBJECTIVE
To investigate if tissue plasminogen activator (tPA) and streptokinase given during acute myocardial infarction (AMI) have different effects on platelet aggregation which could contribute to the higher reocclusion rate observed after tPA.


METHODS
Open labelled on consecutive patients.


METHODS
Coronary care unit.


METHODS
Twenty patients with chest pain and ST elevations on an electrocardiogram suggestive of AMI.


METHODS
Ten patients were treated with tPA (100 mg 3 h-1), 10 patients with streptokinase (1.5 x 10(6) IU 1 h-1).


METHODS
Before, immediately after and 24 h after fibrinolytic therapy, platelet aggregation was estimated with filtragometry and whole blood aggregometry. Fibrinogen, beta-thromboglobulin, elastase and the fibrinogen-derived peptide B beta 30-43 were also measured.


RESULTS
The groups were comparable at baseline. Directly after treatment, streptokinase prolonged aggregation time in filtragometry with 112 +/- 140 s (P < 0.03) and reduced conductance in whole blood aggregometry by 6.2 +/- 6.1 omega (P < 0.03), both tests indicating inhibited platelet function. Fibrinogen decreased 2.5 +/- 1.0 g l-1 (P < 0.02). In the tPA-treated group corresponding changes were 68 +/- 225 s (NS) and 2.5 +/- 7 omega (NS) with no significant reduction in fibrinogen. After 24 h, at which time every patient was on acetylsalicylic acid, aggregation was inhibited in both groups as measured by aggregometry. Directly after fibrinolytic treatment, neutrophils were similarly activated in both groups with increments of elastase and B beta 30-43 by 26 +/- 46 micrograms l-1 (P < 0.03) and 280 +/- 381 pmol l-1 (P < 0.03) respectively (streptokinase) and by 12 +/- 6 micrograms l-1 (P < 0.02) and 919 +/- 856 pmol l-1 (P < 0.02) respectively (tPA).


CONCLUSIONS
Despite similar degrees of platelet and leucocyte activation, streptokinase but not tPA treatment appears to inhibit platelet aggregation. One possible reason could be a streptokinase-induced pronounced decrease of fibrinogen and increase of fibrinogen split products. Therefore, further development of adjuvant antiplatelet therapy could be of clinical importance.
Karlberg
K E
KE
Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
Chen
J
J
Hagerman
I
I
Bergström
K
K
Wallin
R
R
Saldeen
T
T
Sylvén
C
C
D000368:Aged; D016009:Chi-Square Distribution; D005260:Female; D005340:Fibrinogen / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D009504:Neutrophils / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects*; D013300:Streptokinase / Q000494:pharmacology* / Q000627:therapeutic use; D010959:Tissue Plasminogen Activator / Q000494:pharmacology* / Q000627:therapeutic use; D016896:Treatment Outcome
D005340:Fibrinogen; D013300:Streptokinase; D010959:Tissue Plasminogen Activator