title: Randomized coronary patency trial of double-bolus recombinant staphylokinase versus front-loaded alteplase in acute myocardial infarction.
abstract: One hundred two patients with evolving myocardial infarction of 6 hours' duration were given aspirin and intravenous heparin and randomly allocated to intravenous front-loaded, weight-adjusted rTPA administration over a 90-minute period (52 patients) or to two 15 mg doses of recombinant staphylokinase, 30 minutes apart (50 patients). Thrombolysis in Myocardial infarction (TIMI) perfusion grade 3 at 90 minutes was achieved in 68% (95% confidence interval, 55% to 81%) of patients treated with staphylokinase versus 57% (95% confidence interval, 43% to 72%) of patients treated with rTPA (p = not significant). Double-bolus staphylokinase was significantly more fibrin-specific than accelerated rTPA with residual fibrinogen at 90 minutes of 105% +/- 4.1% and 68% +/- 7.5%, respectively (p < 0.0001). Thirteen patients in each study group underwent angioplasty of the culprit coronary artery within the first 24 hours because of suboptimal recanalization (TIMI < 3). In the patients without prior coronary intervention, TIMI 3 at 24 hours was 100% after staphylokinase administration (n = 35) versus 79% after rTPA (n = 34) (p = 0.005). The distribution of inhospital events did not significantly differ between both groups. One patient receiving rTPA died in the hospital from ischemic stroke. Staphylokinase administration did not induce allergic reactions, but significant staphylokinase-neutralizing activity (> 5 micrograms/ml) and specific anti-staphylokinase IgG developed in 73% of patients after 2 weeks. Thus two 15 mg doses of staphylokinase induce early, complete, and sustained coronary artery patency at least as frequently as accelerated rTPA without associated fibrinogen degradation but with subsequent induction of circulating neutralizing antibodies.
authors.affiliation: Center for Molecular and Vascular Biology, University of Lauven, Belgium.
authors.forename: S
authors.initials: S
authors.lastname: Vanderschueren
authors.forename: J
authors.initials: J
authors.lastname: Dens
authors.forename: P
authors.initials: P
authors.lastname: Kerdsinchai
authors.forename: W
authors.initials: W
authors.lastname: Desmet
authors.forename: M
authors.initials: M
authors.lastname: Vrolix
authors.forename: F
authors.initials: F
authors.lastname: De Man
authors.forename: P
authors.initials: P
authors.lastname: Van den Heuvel
authors.forename: L
authors.initials: L
authors.lastname: Hermans
authors.forename: D
authors.initials: D
authors.lastname: Collen
authors.forename: F
authors.initials: F
authors.lastname: Van de Werf
mesh_terms: D005260:Female; D005340:Fibrinogen / Q000187:drug effects; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use*; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008666:Metalloendopeptidases / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D010960:Plasminogen Activators / Q000009:adverse effects / Q000627:therapeutic use; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use; D010959:Tissue Plasminogen Activator / Q000009:adverse effects / Q000627:therapeutic use*; D014654:Vascular Patency / Q000187:drug effects
chemical_list: D005343:Fibrinolytic Agents; D011994:Recombinant Proteins; D005340:Fibrinogen; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator; D008666:Metalloendopeptidases; C022653:auR protein, Staphylococcus aureus