
Thrombolytic therapy mimics and enhances physiological fibrinolysis. The following substances are presently available for clinical use: the nonphysiological thrombolytics streptokinase, the APSAC (acylated plasminogen-streptokinase activator complex), the physiological plasminogen activators urokinase and tissue plasminogen activator (t-PA). Whereas the first three systematically activate the fibrinolytic system, t-PA possesses relative fibrin selectivity. The fibrin-selective active pro-urokinase has not yet been officially approved for the treatment of thromboembolic diseases, but it is being clinically tested. Fibrinolytic therapy has an established place in the management of acute myocardial infarction and of massive pulmonary embolism. When an acute deep venous thrombosis is diagnosed with a proximal extension into the popliteal vein, thrombolytic therapy is clearly superior to heparin. The lysis has proven to be an effective form of treatment of peripheral occlusive arterial disease. Local thrombolytic therapy is an option for acute and chronic femoro-popliteal occlusions involving the trifurcation into the calf arteries and for embolic occlusions of the same segment in patients with contraindications to surgical therapy. First study results of thrombolytic therapy of stroke are promising.
Enzyme Precursors, Fibrinolytic Agents, Anistreplase, Thromboembolism, Tissue Plasminogen Activator, Myocardial Infarction, Humans, Streptokinase, Thrombosis, Pulmonary Embolism, Urokinase-Type Plasminogen Activator, Recombinant Proteins
Enzyme Precursors, Fibrinolytic Agents, Anistreplase, Thromboembolism, Tissue Plasminogen Activator, Myocardial Infarction, Humans, Streptokinase, Thrombosis, Pulmonary Embolism, Urokinase-Type Plasminogen Activator, Recombinant Proteins
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