Pulmonary embolism and deep vein thrombosis

Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Cardiovascular Division, Boston, MA 02115, USA.
The Lancet (Impact Factor: 45.22). 04/2012; 379(9828):1835-46. DOI: 10.1016/S0140-6736(11)61904-1
Source: PubMed


Pulmonary embolism is the third most common cause of death from cardiovascular disease after heart attack and stroke. Sequelae occurring after venous thromboembolism include chronic thromboembolic pulmonary hypertension and post-thrombotic syndrome. Venous thromboembolism and atherothrombosis share common risk factors and the common pathophysiological characteristics of inflammation, hypercoagulability, and endothelial injury. Clinical probability assessment helps to identify patients with low clinical probability for whom the diagnosis of venous thromboembolism can be excluded solely with a negative result from a plasma D-dimer test. The diagnosis is usually confirmed with compression ultrasound showing deep vein thrombosis or with chest CT showing pulmonary embolism. Most patients with venous thromboembolism will respond to anticoagulation, which is the foundation of treatment. Patients with pulmonary embolism should undergo risk stratification to establish whether they will benefit from the addition of advanced treatment, such as thrombolysis or embolectomy. Several novel oral anticoagulant drugs are in development. These drugs, which could replace vitamin K antagonists and heparins in many patients, are prescribed in fixed doses and do not need any coagulation monitoring in the laboratory. Although rigorous clinical trials have reported the effectiveness and safety of pharmacological prevention with low, fixed doses of anticoagulant drugs, prophylaxis remains underused in patients admitted to hospital at moderate risk and high risk for venous thromboembolism. In this Seminar, we discuss pulmonary embolism and deep vein thrombosis of the legs.

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Available from: Henri Bounameaux, Aug 25, 2014
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    • "Venous thrombosis, including deep vein thrombosis (DVT) and pulmonary embolism, is a major source of morbidity and mortality worldwide [1]. Although it is accepted that the combination of so-called virchow triad, namely 1) vascular abnormalities and endothelial dysfunction, 2) hypercoagulability and 3) stasis, may play a pivotal role in the pathogenesis of venous thrombosis, the underlying mechanisms are not fully elucidated. "
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    ABSTRACT: Recently, evidence indicated that the rapamycin-eluting stent which was used worldwide may contribute to an increased risk for thrombosis. On the contrary, other researchers found it was safe. Thus, it is necessary to clarify the effect of rapamycin on thrombosis and the corresponding mechanisms. The effects of rapamycin in vivo were evaluated by modified deep vein thrombosis animal model. The platelets were from healthy volunteers and the platelet-endothelium (purchased from ATCC) adhesion in cultured endothelial cells was assessed. Membrane rufflings in endothelial cells were examined by confocal and electron microscope. Thrombus formation increased in rats that were injected with rapamycin. Electron microscope analysis exhibited microvilli on the rapamycin-treated endothelium in rats. Rapamycin enhanced membrane ruffling in human umbilical vein endothelial cells (HUVECs) and adhesion of platelets to HUVECs. The platelet-HUVECs adhesion was attenuated when cells were treated with cytochalacin B. Inhibition of autophagy by 3-methyladenine led to suppression of membrane ruffles in HUVECs and augmentation of platelet-endothelial adhesion. In conclusion, we found that endothelial membrane remodeling induced by rapamycin is crucial for the adhesion of platelets to endothelial cells and thereby for thrombosis in vivo, and that the endothelial membrane remodeling is autophagy dependent.
    BMC Cell Biology 02/2014; 15(1):7. DOI:10.1186/1471-2121-15-7 · 2.34 Impact Factor
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    • "According with their scores, patients with PE can be assigned to one of the following different classes of risk: a) high-risk patients, who represent about 5% of all symptomatic patients, with about a 15% short-term mortality; these patients should be treated aggressively with thrombolytic drugs or surgical or catheter embolectomy [46]; b) low-risk patients, with a short-term mortality of about 1%; they might benefit from early discharge or even outpatient treatment [47]; c) intermediate risk patients, who represent about 30% of all symptomatic patients and should be admitted to hospital, with potential benefit of thrombolytic treatment. Both low-risk and intermediate risk categories are referred to as non-massive pulmonary embolism [24]. "
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    ABSTRACT: The diagnosis of pulmonary embolism (PE) is frequently considered in patients presenting to the emergency department or when hospitalized. Although early treatment is highly effective, PE is underdiagnosed and, therefore, the disease remains a major health problem. Since symptoms and signs are non specific and the consequences of anticoagulant treatment are considerable, objective tests to either establish or refute the diagnosis have become a standard of care. Diagnostic strategy should be based on clinical evaluation of the probability of PE. The accuracy of diagnostic tests for PE are high when the results are concordant with the clinical assessment. Additional testing is necessary when the test results are inconsistent with clinical probability. The present review article represents the consensus-based recommendations of the Interdisciplinary Association for Research in Lung Disease (AIMAR) multidisciplinary Task Force for diagnosis and treatment of PE. The aim of this review is to provide clinicians a practical diagnostic and therapeutic management approach using evidence from the literature.
    Multidisciplinary respiratory medicine 12/2013; 8(1):75. DOI:10.1186/2049-6958-8-75 · 0.15 Impact Factor
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    • "Deep-vein thrombosis (DVT) and pulmonary embolism (PE) are two different clinical manifestations of venous thromboembolism (VTE) (incidence 1–1.5 per 1,000 person years) [1]. PE is the third most common cause of cardiovascular mortality, after acute coronary syndromes and stroke [2]. The reported all-cause mortality after acute PE is 5–15% [3], driven by the severity of the initial presentation, recurrent PE, and associated comorbidities. "
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    ABSTRACT: With the advent of new oral anticoagulants (NOACs) for the treatment of deep-vein thrombosis (DVT) and/or pulmonary embolism (PE), a new era of oral anticoagulation for patients with venous thromboembolism (VTE) has begun. Rivaroxaban is the first NOAC to receive regulatory approval for the acute and continued treatment of DVT and PE, and for the secondary prevention of VTE. Here, the clinical trials of rivaroxaban in patients with VTE are reviewed, and the clinical use of rivaroxaban for patients with PE is discussed. Even though rivaroxaban will facilitate the therapeutic management of PE, its use in specific clinical situations needs further study.
    Advances in Therapy 06/2013; 30(6). DOI:10.1007/s12325-013-0041-4 · 2.27 Impact Factor
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