Summary
Thrombolytic therapy has become the mainstay of treatment for acute transmural myocardial
infarction. Present fibrinolytic regimens have a number of shortcomings, including
the failure to induce early and sustained reperfusion in as many as 40-50% of the
patients, and to prevent reocclusion in another 10-20% of the patients. The efforts
for improving thrombolysis are focused on the development of new agents (fibrinolytics,
anticoagulants, and antiplatelet agents). TNK-tPA is a triple combination mutant of
wild-type tissue plasminogen activator that exhibits a longer plasma half-life, an
enhanced fibrin-specificity, and an increased resistance to the plasminogen activator
inhibitor-1. This paper summarizes the results of clinical trials with TNK-tPA in
acute myocardial infarction.
Key words
Thrombolysis - TNK-tPA - acute myocardial infarction