Streptokinase Efficacy in Patients with Acute Myocardial Infarction with Low Level Antistreptokinase Antibody and High Level LP (a) Lipoprotein

Document Type : Original Article


Background- Lp (a) lipoprotein has structural homology with plasminogen and has been shown to
inhibit plasminogen activation in vitro and, therefore, the effect of streptokinase (SK). SK’s
effect is also inhibited by anti-streptokinase antibody (anti SK Ab). We sought to determine
whether the serum concentration of Lp (a) lipoprotein present when SK was given in acute
myocardial infarction (AMI) influenced the outcome in spite of low anti-streptokinase
antibody, as judged by electrocardiography methods.
Methods- Serum Lp (a) lipoprotein concentration was measured in 135 consecutive patients
admitted with a diagnosis of AMI who received SK treatment. Recovery and non-recovery
from myocardial injury was assessed by the reduction in sum of ST segment elevation
measured from the J point (STJ) and Q wave formation in electrocardiography immediately
before SK was given compared with two hours later.
Results- Serum Lp (a) lipoprotein concentration was measured within 6 hours of onset of symptoms
and before SK was administrated, and was higher than that in healthy reference populations.
Thirty-one patients with high anti-streptokinase antibody levels were excluded. In patients
with Q wave AMI and low anti-streptokinase antibody levels, 31 patients (50%) had high
level Lp (a) lipoprotein (34.2mg/dl), whereas patients with non-Q wave AMI and reduction in
ST segment elevation after SK >50% (median decrease) had a mean serum Lp (a) lipoprotein
concentration of 18mg/dl. The difference was not statistically significant.
Conclusion- In this study, Lp (a) lipoprotein concentration did not significantly influence the
outcome of thrombolytic treatment with SK (Iranian Heart Journal 2008; 9 (1): 34-39).


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