Future directions in plasminogen activator therapy

Thrombotic disorders such as myocardial and stroke are the leading causes of death and dis in industrialized nations. Timely institution of therapy can achieve a reduction of infarct, a preservation of left ventricular function, and a in mortality. The administration of streptokinase, and acylated plasminogen‐streptokinase acti‐ complex (APSAC) can be associated with a complete breakdown of the hemostatic system. Tissue‐type activator (t‐PA) and single‐chain urokinase‐ plasmiogen activator (scu‐PA, prourokinase) are fibrin specific; however, at the large dosages of ac‐ needed for therapeutic efficacy, bleeding compli‐ are still a problem. New approaches to optimizing the risk/benefit ratio for the patient by improving without sacrificing specificity include the use of combinations of plasminogen activators, of t‐PA and scu‐PA, chimeric molecules, and ‐targeted thrombolytic agents. The last approach the possibility of targeting several different com‐ of the clot with either fibrinolytic or antiplatelet functions in one optimized molecule.