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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pulmonary embolism (PE) is a potentially life-threatening condition, with an overall 3-month mortality rate of 15% and with right ventricular failure as the most common cause of early death. Risk stratification facilitates identification of high-risk patients and may be helpful in guiding the initial and long-term management. In patients with massive PE and hemodynamic instability, rapid risk assessment is paramount and bedside echocardiography and multislice chest computed tomography (CT) are useful for identifying patients who may benefit from thrombolysis or embolectomy. Cardiac biomarkers, including troponin and the natriuretic peptides, are sensitive markers of right ventricular function. Low levels of troponin, B-type natriuretic peptide (BNP), and NT-terminal proBNP are all highly sensitive assays for identifying patients with an uneventful clinical course. Multislice chest CT is not only useful to diagnose or exclude PE; it also is useful for risk assessment. A right-to-left ventricular dimension ratio > 0.9 on the reconstructed CT four-chamber view identifies patients at increased risk of early death. This article focuses on risk stratification tools, including the clinical examination, electrocardiography, echocardiography, cardiac biomarkers, and chest CT.
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PMID:Risk stratification of acute pulmonary embolism. 1717 98

Early diagnosis and treatment are pivotal for patients with acute aortic dissection (AAD). D-dimer is a rule-out diagnostic test for pulmonary embolism but there is evidence that it may also be applicable to AAD. We evaluated plasma D-dimer, white cell blood count (WBC), C-reactive protein (CRP) and N-terminal pro-B-type natriuretic peptide (BNP) in 18 consecutive patients with established AAD, 21 consecutive patients with dilated ascending aortas scheduled for elective surgery and 8 normal subjects. Patients with AAD had significantly higher elevated D-dimer, compared to chronic aneurysms and normal controls (p<0.0001). D-dimer level higher than 700 ng/ml had a sensitivity of 94% and specificity of 59% for diagnosis of AAD. The WBC count was also significantly increased compared to the other groups (p<0.01). CRP and BNP values were significantly higher compared to normal controls but these parameters did not distinguish between AAD and chronic aneurysms. D-dimer can be used as a 'rule-out' test in patients with suspected AAD and seems useful in the discrimination between AAD and chronic uncomplicated aneurysms, unlike CRP and BNP plasma levels.
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PMID:D-dimer and BNP levels in acute aortic dissection. 1723 84

B-Type natriuretic peptide (BNP) is elevated in states of increased ventricular wall stress. BNP is most commonly used to rule out congestive heart failure (CHF) in dyspneic patients. BNP levels are influenced by age, gender and, to a surprisingly large extent, by body mass index (BMI). In addition, it can be elevated in a wide variety of clinical settings with or without CHF. BNP is elevated in other cardiac disease states such as the acute coronary syndromes, diastolic dysfunction, atrial fibrillation (AF), amyloidosis, restrictive cardiomyopathy (RCM), and valvular heart disease. BNP is elevated in non-cardiac diseases such as pulmonary hypertension, chronic obstructive pulmonary disease, pulmonary embolism, and renal failure. BNP is also elevated in the setting of critical illness such as in acute decompensated CHF (ADHF) and sepsis. This variation across clinical settings has significant implications given the increasing frequency with which BNP testing is being performed. It is important for clinicians to understand how to appropriately interpret BNP in light of the comorbidities of individual patients to maximize its clinical utility. We will review the molecular biology and physiology of natriuretic peptides as well as the relevant literature on the utilization of BNP in CHF as well as in other important clinical situations, conditions that are commonly associated with CHF and or dyspnea.
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PMID:Interpretation of B-type natriuretic peptide in cardiac disease and other comorbid conditions. 1734 60

Massive pulmonary embolism (PE) with hemodynamic instability (e.g., hypotension and cardiac shock) is associated with a poor prognosis and high mortality rates (> 50%). Accordingly patients with massive PE should be treated aggressively with thrombolytic agents (or surgical or interventional procedures). Streptokinase, urokinase, and recombinant tissue plasminogen activator (rtPA) have been used, with generally similar results. Among patients with submassive PE [i.e., subclinical right ventricular (RV) dysfunction and normal blood pressure], the role of thrombolytic therapy is controversial. Thrombolytic therapy is generally NOT indicated in normotensive patients without RV dysfunction. In this context, some experts recommend prompt administration of thrombolytic agents to prevent cardiogenic shock but data affirming benefit over heparin alone are lacking. Thrombolytic therapy is generally NOT indicated in normotensive patients without RV dysfunction. The role of echocardiography, computed tomographic (CT) scans, and cardiac biomarkers (e.g., troponins, brain natriuretic peptide, etc.) to identify patients who might benefit from aggressive thrombolytic therapy remains controversial. This article reviews indications for thrombolysis in massive PE, with an emphasis on recent data derived from normotensive patients. Further, we propose a diagnostic and therapeutic algorithm for treating acute PE. Additional studies are required to determine the benefit and safety of thrombolytic therapy for PE.
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PMID:Massive pulmonary embolism: what level of aggression? 1830 86

Dyspnea is a primary clinical manifestation of acute congestive heart failure (CHF) among patients presenting to the emergency department (ED). Unfortunately, other critical illnesses, including acute coronary syndromes, pulmonary embolism, chronic obstructive pulmonary disease, and pneumonia, may present with clinical symptoms and signs similar to acute CHF. N-terminal pro-brain natriuretic peptide (NT-proBNP) has proven to be a powerful tool in the diagnostic assessment of dyspnea as a result of its ability to confirm or exclude the presence of acute CHF. However, many of the disorders that mimic acute CHF may result in elevated NT-proBNP levels as well. Results from the ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) study recently demonstrated that a strategy integrating NT-proBNP testing into routine clinical assessment demonstrated a better diagnostic yield than each strategy used in isolation. We present a diagnostic algorithm integrating NT-proBNP testing with clinical assessment for use in routine clinical practice.
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PMID:A clinical and biochemical critical pathway for the evaluation of patients with suspected acute congestive heart failure: The ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) algorithm. 1834 Jan 69

Massive pulmonary embolism is an uncommon complication of multiple myeloma treated with thalidomide-dexamethasone regimen. In 2006, multiple myeloma was diagnosed in a 72-year-old man, who received thalidomide-dexamethasone therapy. In January 2007, echocardiography and computerized tomography identified massive pulmonary embolism in the pulmonary arteries and a deep vein thrombus of the right leg. The patient also had an elevated concentration of B-type natriuretic peptide. After heparinization and warfarin therapy, the patient's condition improved. This is the first report of a patient with a rare complication of pulmonary embolism from thalidomide-treated multiple myeloma.
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PMID:Pulmonary embolism in a patient with multiple myeloma receiving thalidomide-dexamethasone therapy. 1841 84

Myocardial stretch leads to the natriuretic peptides release in acute or chronic left ventricular dysfunction. However, there is an accumulating evidence that B-type natriuretic peptide (BNP) and its N-terminal fragment (NT-proBNP) may originate from right ventricle and their concentrations are elevated in patients with acute pulmonary embolism (APE) especially when resulting in right ventricular dysfunction (RVD). Recently it is underlined that severity assessment of APE as well as the risk stratification and therapy selection is based both on patients' hemodynamic status and markers of myocardial injury and RVD. BNP and NT-proBNP are helpful in identifying patients with RVD in APE, emerging as an adjunctive tool to echocardiography. Elevated BNP or NT-proBNP levels are also significant predictors of death and/or complicated clinical course in APE.
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PMID:B-type natriuretic peptide in acute pulmonary embolism. 1870 1

Massive pulmonary embolism is defined by systemic hypotension or cardiogenic shock. Clinically stable patients with right ventricular dysfunction on echocardiography, elevated brain natriuretic peptide or troponin are usually considered as having sub-massive pulmonary embolism, but this definition is not universally accepted. The time-lag to confirm massive pulmonary embolism should be kept as short as possible and every effort should be done to rely on bedside tests and to avoid patient transfer to the radiology department. D-dimer tests are useless in this setting and the diagnosis is mainly based on clinical probability and bedside echocardiography. When clinical probability is high, right ventricular dilatation assessed by echocardiography allows confirming the diagnosis without additional testing. On the other hand a normal echocardiography does not allow excluding pulmonary embolism. In this setting, a spiral computed tomography is mandatory after the patient has been stabilized. Anticoagulant treatment should be started as soon as pulmonary embolism has been suspected. Supportive care includes oxygen, fluid loading and inotropes. There is little doubt that thrombolytic treatment is of value in patients with massive pulmonary embolism. Conversely, the use of thrombolytic therapy in patients with so-called sub-massive pulmonary embolism remains controversial. Current data do not confirm that thrombolytic therapy decreases mortality in those patients but cannot exclude a clinically significant benefit. A large randomised comparison of heparin and thrombolysis in patients with sub-massive pulmonary embolism is underway to answer this question. Surgical or catheter embolectomy is nowadays only rarely performed in patients with pulmonary embolism. This method can be undertaken in the few patients with persisting shock despite supportive care and who have an absolute contraindication for thrombolytic therapy. Before new data are available there is no special indication for vena cava interruption in patients with massive pulmonary embolism.
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PMID:[Massive pulmonary embolism]. 1877 37

Chronic thromboembolic pulmonary hypertension (CTPH) is a potential complication of pulmonary embolism (PE). Only few studies have assessed the role of brain natriuretic peptide (BNP) in patients with chronic pulmonary hypertension, and there are no data on the potential utility of BNP as a preclinical biomarker of CTPH. To assess the correlation between pulmonary artery systolic pressures (PAPs) and amino terminal proBNP (Nt-proBNP) and its value in the diagnosis of CTPH in patients with previous PE. Patients were evaluated with echocardiography at least 6 months after the index event. Pulmonary hypertension was defined as PAPs > or =40 mmHg at rest. Each subject underwent measurement of Nt-proBNP. Forty-nine patients were enrolled (mean age 64.5 +/- 13.1 years; 22 men). Seven patients had CTPH, and two were symptomatic. There was a good correlation between PAP on echocardiography and Nt-proBNP (r 0.64; P = 0.00003). Nt-proBNP was elevated in 6 of 7 patients [sensitivity: 85.7%; 95% confidence interval (CI): 48.7, 97.4] and it was normal in 35 of 42 patients without CTPH (specificity: 76.2%; 95% CI: 61.5, 86.5%). Six of the 13 patients with high Nt-proBNP levels had CTPH, whereas 1 of 36 patients with normal Nt-proBNP levels had pulmonary hypertension. The resulting positive predictive value was 46.1% (95% CI: 19.2, 74.9), and the negative predictive value was 97.2% (95% CI: 85.5-99.9). In conclusion, Nt-proBNP correlates with PAPs and may be used to exclude preclinical or symptomatic CTPH in patients with previous PE. Prospective studies on a larger population are warranted to confirm our preliminary findings.
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PMID:Brain natriuretic peptide as a preclinical marker of chronic pulmonary hypertension in patients with pulmonary embolism. 1965 24

B-type natriuretic peptide (BNP) is increasingly used in emergency departments to assess the cause of acute dyspnea and in cardiology to follow treatments and predict outcome. It is increasingly used in the intensive care unit in situations such as respiratory failure (acute pulmonary edema, exacerbation of chronic obstructive pulmonary disease and difficult weaning from ventilator) or when pulmonary embolism is suspected. BNP has also been used to assess alteration of myocardial function in sepsis. Plasma BNP is very high in septic-shock patients (>1000 pg/ml), which is suggested to relate to both myocardial stretch and to an alteration in one of the BNP clearance pathways. Whether BNP at admission or at discharge may predict outcome requires further investigation.
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PMID:Use of B-type natriuretic peptide in critically ill patients. 2047 21


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