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

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).