Thrombolytic therapy.
Despite their widespread use in patients with acute myocardial infarction, all currently available thrombolytic agents suffer from a number of significant limitations, including resistance to reperfusion, the occurrence of acute coronary reocclusion and bleeding complications. Therefore, the quest for thrombolytic agents with a higher thrombolytic potency, specific thrombolytic activity and/or a better fibrin-selectivity continues. Several lines of research towards improvement of thrombolytic agents are being explored, including the construction of mutants and variants of plasminogen activators, chimeric plasminogen activators, or plasminogen activators from animal or bacterial origin. Several of these new thrombolytic agents have been evaluated in animal models of venous or arterial thrombosis, some in pilot studies in patients with acute myocardial infarction and a few in large clinical trials with mortality end points. Definition of their relative therapeutic benefit, against presently available "classical" thrombolytic agents will require further dose-finding studies and randomized clinical trials.
Collen
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Center for Molecular and Vascular Biology, University of Leuven, Belgium. desire.collen@med.kuleuven.ac.be
D001241:Aspirin / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008666:Metalloendopeptidases / Q000627:therapeutic use; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D013927:Thrombosis / Q000188:drug therapy*; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use
D006493:Heparin; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D008666:Metalloendopeptidases; C022653:auR protein, Staphylococcus aureus; D001241:Aspirin