title: Thrombolytic treatment of acute pulmonary embolism.
abstract: Many investigators have reported about beneficial results with thrombolytic therapy in patients with acute pulmonary embolism. Streptokinase and urokinase have been used for more than 15 years, but the conditions of use of these agents still remain controversial. Optimal dosage and treatment schedule are still evolving. For streptokinase most investigators adopt a fixed dosage schedule: a loading dose of 250,000 units followed by a maintenance infusion of 100,000 units per hour for 24 to 72 hours. For urokinase numerous dosage regimens have been used such as: high dosage schedule 4,400 units per kilogram per hour for twelve to 24 hours with or without loading dose; moderate dosage 1,600 to 2,000 units per kilogram per hour for 24 hours and low dosage in bolus. With these treatments there is a trend to reduced in-hospital-mortality in massive pulmonary embolism; the early pulmonary revascularization and the hemodynamic improvement are higher than those noticed with heparin. These results are obtained with a minimum of complication essentially bleeding in 10 or 15%; most bleeding being located at puncture site. More recently, new thrombolytic agents have been used in acute pulmonary embolism. Only four studies have tested rt-PA which is effective and relatively safe, but the optimal dose regimens remain to be determined. Less information is available concerning Anisoylated Plasminogen Streptokinase Activator Complex (APSAC), the angiographic improvement seems to be rapid and important (50% on average) but the decrease of fibrinogen is important too and comparable with streptokinase. Considering the good results of thrombolytic treatment of acute submassive and massive pulmonary embolism, there is a doubt as to whether the pulmonary embolectomy has any place in the pulmonary embolism patients except in those with cardiac arrest. In the near future new thrombolytic drugs could be more efficient on pulmonary embolism and deep venous thrombosis, and thus the bleeding risk might be decreased.
authors.affiliation: Cardiology Department, University Hospital Tours, France.
authors.forename: B
authors.initials: B
authors.lastname: Charbonnier
authors.forename: G
authors.initials: G
authors.lastname: Meyer
authors.forename: M
authors.initials: M
authors.lastname: Stern
authors.forename: H
authors.initials: H
authors.lastname: Sors
authors.forename: M L
authors.initials: ML
authors.lastname: Brochier
mesh_terms: D000208:Acute Disease; D016255:Anistreplase; D005343:Fibrinolytic Agents / Q000008:administration & dosage*; D006801:Humans; D010958:Plasminogen / Q000008:administration & dosage; D011655:Pulmonary Embolism / Q000188:drug therapy*; D011994:Recombinant Proteins / Q000008:administration & dosage; D013300:Streptokinase / Q000008:administration & dosage; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage; D014568:Urokinase-Type Plasminogen Activator / Q000008:administration & dosage
chemical_list: D005343:Fibrinolytic Agents; D011994:Recombinant Proteins; D016255:Anistreplase; D010958:Plasminogen; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator