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: Recombinant thrombolytic peptides are mainly represented by recombinant forms of tissue plasminogen activator (t-PA), a proteolytic enzyme that catalyzes the conversion of plasminogen into active plasmin, which then functions to dissolve clots. The three clinically relevant recombinant thrombolytic peptides are alteplase (t-PA), reteplase (r-PA), and tenecteplase (TNK). r-PA and TNK have been structurally modified from native t-PA to increase their half-life and fibrin specificity. Thrombolytics play an important role in several diseases, including ST-segment elevation myocardial infarction (STEMI), deep vein thrombosis (DVT) and pulmonary embolism (PE), ischemic stroke, and peripheral arterial disease. Thrombolytic therapy has evolved into an alternative treatment for STEMI, reserved predominantly for patients who do not have access to timely percutaneous coronary intervention. In patients with DVT/PE or arterial related critical limb ischemia, the use of thrombolytic therapy is limited to specific patient populations. Thrombolytic therapy is the treatment of choice for ischemic stroke in patients who present <or=3 hours following the onset of symptoms. Moreover, thrombolytic therapy is used to restore function to stenotized central venous access devices as well as occluded hemodialysis access grafts.
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    ABSTRACT: Ein Patient mit akuter Lungenembolie ist nur dann auf der Intensivstation zu versorgen, wenn er kreislaufinstabil oder beatmungspflichtig ist oder wenn er bei erhaltenem Kreislauf Zeichen der schweren rechtsventrikulären Dysfunktion aufweist. Für beide Patientengruppen ist die bettseitige Echokardiographie die entscheidende diagnostische Methode. Therapeutisch ist die wesentliche Entscheidungsfindung die zur Thrombolyse. Sie ist bei Kreislaufinstabilität in der Regel indiziert, bei alleiniger Rechtsherzbelastung nur in Einzelfällen, ohne Rechtsherzbelastung gar nicht. Ein weiterer Gefäßnotfall ist das komplexe Krankheitsbild der heparininduzierten Thrombozytopenie TypII, das sowohl arterielle als auch venöse Verschlüsse hervorrufen kann. Die bei Verdacht zu beginnende alternative Antikoagulation muss bei Bestätigung in therapeutischer Dosis fortgesetzt, im viel häufigeren Fall der Nicht-Bestätigung aber zeitgerecht wieder abgesetzt werden. Bezüglich anderer arterieller Verschlüsse (kritische Extremitätenischämie, akrale Läsionen, iatrogene Verletzungen) werden die bei Intensivpflichtigkeit relevanten Vorgehensweisen geschildert. Acute pulmonary embolism requires ICU management only for patients with hemodynamic instability who need artificial ventilation, or for hemodynamically stable patients with significant right ventricular dysfunction. For both patient groups, echocardiography is the most relevant diagnostic method. The main therapeutic consideration is on systemic thrombolysis. It is indicated in almost all patients with hemodynamic instability but only in selected cases of right ventricular dysfunction. All other patients receive standard anticoagulation only. A second vascular emergency scenario is type 2 heparin-induced thrombocytopeniae (HIT II) which may cause venous as well as arterial complications. Alternative anticoagulation has to be established from the first moment of clinical suspicion. It has to be continued in a therapeutic dosage if HITII is confirmed, and has to be stopped if the diagnosis is refuted. The latter case is by far more frequent. Regarding arterial occlusions (acute limb ischemia, acral gangrene, iatrogenic vascular trauma) hints are given for the management in the setting of intensive care. SchlüsselwörterLungenembolie-Heparininduzierte Thrombozytopenie-Intensivtherapie-Thrombolyse-Antikoagulation KeywordsPulmonary embolism-Heparin-induced thrombocytopenia-Intensive care-Thrombolysis-Anticoagulation
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