Thrombolytic therapy for pulmonary embolism

Department of Geriatrics, West China Hospital, Sichuan University, No. 37, Guo Xue Xiang, Chengdu, Sichuan, China, 610041.
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 02/2009; 8(3):CD004437. DOI: 10.1002/14651858.CD004437.pub3
Source: PubMed


A blood clot that lodges in the main artery of the lungs (pulmonary embolism) strains the right side of the heart, affects blood circulation and can be fatal. Patients are also at risk of new blood clots forming (recurrence). With large blood clots (massive pulmonary embolism), restoring blood flow is urgently required. Heparin thins the blood but newer drugs that actively break up the clots (thrombolytics) may act more quickly and be more effective. These newer drugs include streptokinase, urokinase and recombinant tissue-type plasminogen activator. The major complication of treatment is bleeding. The review authors searched the literature and were able to combine data from eight randomized controlled clinical trials. The trials involved 679 adult patients who were in a stable condition and randomly assigned to a thrombolytic agent or heparin. Thrombolytics did not show any benefit over heparin in terms of deaths and recurrence of blood clots. Limited information from only three of the trials showed that they were better at improving blood flow through the lungs. Major bleeding events were similar with both therapies. The evidence is quite weak and more double-blind trials are needed to show if there is a true benefit of thrombolytic therapy for pulmonary embolism.

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    • "Serial pulmonary angiograms and perfusion lung scans (VQ-scan) in patients diagnosed with acute PE and treated with heparin indicate that, while resolution of thrombi is negligible 2 hours after treatment initiation , it is 10% after 24 hours, 40% after 7 days, and 50% after 2 to 4 weeks [19]. The long term rate of PE resolution remains a matter of debate. "
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    ABSTRACT: Long-term follow-up studies have consistently demonstrated that after an episode of acute pulmonary embolism (PE), half of patients report functional limitations and/or decreased quality of life up to many years after the acute event. Incomplete thrombus resolution occurs in one-fourth to one-third of patients. Further, pulmonary artery pressure and right ventricular function remain abnormal despite adequate anticoagulant treatment in 10-30% of patients, and 0.5-4% is diagnosed with chronic thromboembolic pulmonary hypertension (CTEPH) which represents the most severe long term complication of acute PE. From these numbers, it seems that CTEPH itself is the extreme manifestation of a much more common phenomenon of permanent changes in pulmonary artery flow, pulmonary gas exchange and/or cardiac function caused by the acute PE and associated with dyspnea and decreased exercise capacity, which in analogy to post-thrombotic syndrome after deep vein thrombosis could be referred to as the post-pulmonary embolism syndrome. The acknowledgement of this syndrome would both be relevant for daily clinical practice and also provide a concept that aids in further understanding of the pathophysiology of CTEPH. In this clinically oriented review, we discuss the established associations and hypotheses between the process of thrombus resolution or persistence, lasting hemodynamic changes following acute PE as well as the consequences of a PE diagnosis on long-term physical performance and quality of life.
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    ABSTRACT: The underlying disorder of pulmonary embolism (PE) is venous thromboembolism (VTE), comprising deep vein thrombosis, thrombus in transit, acute pulmonary embolism and chronic thromboembolic pulmonary hypertension (CTEPH). PE may recur and cause serious long-term complications, such as post-thrombotic syndrome and CTEPH. This short overview summarizes current concepts on pathophysiology, epidemiology, diagnosis and treatment of this common disorder.
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