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J. Thromb. Thrombolysis · May 2001
ReviewPlasminogen activator inhibitor type-1 (part two): role for failure of thrombolytic therapy. PAI-1 resistance as a potential benefit for new fibrinolytic agents.
- K Huber.
- Department of Cardiology, University of Vienna-General Hospital, Währinger Gürtel 18/20, A-1090 Vienna, Austria. kurt.huber@univie.ac.at
- J. Thromb. Thrombolysis. 2001 May 1; 11 (3): 195-202.
AbstractRapid and sustained reperfusion of an occluded coronary artery is the goal of thrombolytic therapy in acute myocardial infarction. However, the clot-dissolving efficacy of fibrinolytic agents such as tissue-type plasminogen activator (t-PA) is limited, in vivo, in part by the action of plasminogen activator inhibitor type-1 (PAI-1). A new generation of fibrinolytic agents has been genetically engineered to have greater resistance to PAI-1 inhibition. This article reviews the pathophysiologic role of PAI-1 in failure of thrombolytic therapy and describes the advantages that PAI-1-resistance may confer upon fibrinolytic agents such as TNK-t-PA, the new fibrinolytic agent with the most powerful PAI-1 resistance.
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