More on thrombolysis and hemorrhagic stroke.

Abstract

Bleeding complications, including catastrophic intracranial hemorrhage, have always been the inevitable downside of thrombolytic therapy. When the concept of early reperfusion was introduced into the therapy of acute myocardial infarction,1 2 previous intravenous thrombolytic regimens were drastically shortened to a 1-hour high-dose infusion, not only to increase efficacy but also to reduce bleeding risks.3 4 From subsequent large-scale trials,5 6 however, a persistent significant hazard of intracranial hemorrhage was observed. With the advent of the more fibrin-specific thrombolytic tissue-type plasminogen activator (TPA) along with an improved efficacy, a lower bleeding risk was anticipated. Again, the incidence of hemorrhagic strokes turned out to be even higher with the new drug than with streptokinase.7 8 9 We still do not know whether TPA is just not sufficiently fibrin specific or whether fibrin specificity per se does not help to reduce the bleeding risk. The answer will be given in the near future by new, completely fibrin-specific thrombolytics such as staphylokinase10 or TNK, a mutant of wild-type TPA,11 which currently are being investigated in phase II clinical trials. With currently available drugs, thrombolytic therapy saves about 30 lives per 1000 patients with acute myocardial infarction presenting with ST-segment elevation or …