Thromb Haemost 1996; 76(06): 0857-0859
DOI: 10.1055/s-0038-1650675
Rapid Communications
Schattauer GmbH Stuttgart

Procoagulant Properties of Intravenous Staphylokinase Versus Tissue-Type Plasminogen Activator

Authors

  • K Okada

    The Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, Leuven, Belgium
  • H R Lijnen

    The Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, Leuven, Belgium
  • H Moreau

    The Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, Leuven, Belgium
  • S Vanderschuere

    The Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, Leuven, Belgium
  • D Collen

    The Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, Leuven, Belgium
Further Information

Publication History

Received 04 July 1996

Accepted after revision 30 August 1996

Publication Date:
11 July 2018 (online)

Summary

The fibrin-specificity and procoagulant effects of recombinant staphylokinase (Sak42D) were compared with those of recombinant tissue-type plasminogen activator (rt-PA) in patients with acute myocardial infarction. Plasma samples were obtained at baseline and at 25 and 90 min, from 24 patients who were randomly assigned to a double bolus (15 mg each, 30 min apart) administration of Sak42D or to accelerated weight-adjusted rt-PA (maximum of 100 mg over 90 min). Baseline levels of fibrinopeptide A (FPA), prothrombin fragment 1+2 and thrombin-antithrombin III complex (TAT) were comparable in the Sak42D and rt-PA groups (p ≥ 0.6). In patients treated with Sak42D, plasma levels of FPA, prothrombin fragment 1+2 and TAT did not markedly increase during treatment (p = 0.06, p = 0.4 and p = 0.03, respectively). In contrast, during administration of rt-PA the levels of FPA, prothrombin fragment 1+2 and TAT increased significantly over baseline (p = 0.003, p < 0.0001 and p = 0.001, respectively). As a result, the levels of all three procoagulant parameters were significantly lower during treatment with Sak42D as compared to rt-PA. Thus, FPA levels in the Sak42D group (median values) were 40 ng/ml at 25 min and 11 ng/ml at 90 min, as compared to 88 ng/ml and 50 ng/ml in the rt-PA group (p = 0.0007 and p = 0.009, respectively). Prothrombin fragment 1+2 levels in the Sak42D group were 1.3 nM at 25 min and 1.2 nM at 20 min, as compared to 11 nM and 5.3 nM in the rt-PA group (both p < 0.0001). TAT levels were 4.7 ng/ml at 25 min and 6.2 ng/ml at 90 min in the Sak42D group, with corresponding values of 16 ng/ml and 9.6 ng/ml in the rt-PA group (p = 0.02 and p = 0.03, respectively).

In the patients treated with Sak42D, no significant systemic fibrinolytic activation was observed, as revealed by unaltered levels of clotta-ble fibrinogen, plasminogen and a2-antiplasmin up to 90 min after the start of therapy. In contrast, the corresponding residual levels at 90 min in patients treated with rt-PA decreased to (mean ± SEM; n = 12) 62 ± 6%, 45 ± 5% and 52 ± 10%, respectively (all p < 0.01 versus the Sak42D group)

These data confirm the high degree of fibrin-specificity of Sak42D and demonstrate that this is associated with significantly less generation of procoagulant activity in plasma after intravenous administration in patients with acute myocardial infarction