HENRI BOUNAMEAUX, M.D.; JOSEPH VERMYLEN, M.D.; COLLEN DÉSIRÉ, M.D.; Ph.D.
Physiologic thrombolysis appears to be regulated via adsorption of tissue-type plasminogen activator and plasminogen on the fibrin surface, and generation of plasmin out of reach of circulating alpha 2-antiplasmin (1). The thrombolytic agents streptokinase and urokinase, which have no specific affinity for fibrin, activate circulating and fibrin-bound plasminogen without preference. Extensive plasminogen activation and plasmin generation will exhaust alpha 2-antiplasmin, and then free circulating plasmin will degrade several plasma coagulation proteins such as fibrinogen, factor V, and factor VIII. This hemostatic breakdown may cause bleeding. Therefore, fibrinspecific plasminogen activators could constitute safer thrombolytic agents. Promising results have been reported in
BOUNAMEAUX H, VERMYLEN J, DÉSIRÉ C. Thrombolytic Treatment with Recombinant Tissue-Type Plasminogen Activator in a Patient with Massive Pulmonary Embolism. Ann Intern Med. ;103:64–65. doi: 10.7326/0003-4819-103-1-64
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Published: Ann Intern Med. 1985;103(1):64-65.
Emergency Medicine, Pulmonary Embolism, Pulmonary/Critical Care, Venous Thromboembolism.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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