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

Pulmonary embolism (PE) is extremely common and is a leading cause of death in all age groups. Unfortunately the diagnosis is most often missed than it is made. Prompt diagnosis and treatment can dramatically reduce the mortality and morbidity. This study was done to evaluate the patients with acute PE, assess the utility of laboratory tests and potential of high resolution spiral computed tomogram angiography of pulmonary arteries (sCTPA) as the confirmatory diagnostic tool. Twenty six consecutive patients with acute PE admitted to CCU of Narayana Hrudayalaya of Banglore were followed prospectively. There were 15 male and 11 female (M:F=1:3:1); age range was 32-58 yrs. (mean 45+/-13 yrs). Pre-testing probability assessment of PE was done by a combined approach of history, physical examination and presence of risk factors. D-dimer and cardiac troponin I (TnI) estimation and sCPTA done by contrast enhanced 64-slice spiral CT scanner in all patients. In addition to the typical findings of PE, sCTPA included and revealed features of cardiac and venous CT imaging. Doppler study of leg veins were done to exclude deep vein thrombosis. Trans-thoracic echocardiography assessed right ventricular dilatation and presence of pulmonary hypertension. Nineteen patients (73.0%) had sub-massive PE, 5 patients (19.2%) had non-massive and 2 patients (7.6%) presented with massive PE. A raised D-dimer (0.5mugm/ml) was found in all the cases (100.0%). An elevated a trponin I (TnI) was found in 18 patients (69.2%). RV dilatation, (i.e. RV/LV>0.9) was found in 21 patients (80.7%). All patients (100.0%) received unfractionated heparin. Thrombolysis with alteplase, without concomittent heparin was administered in 11 patients (42.3%). Inferior venacaval filter were implanted in 9 patients (34.6%) with sub massive PE and recurrent events despite anticoagulation. Embolectomy done in one patients with massive PE, offered satisfactory recovery. Pulmonary endarterectomy were undertaken in 6 patients with acute on chronic thromboembolic pulmonary hypertension. Thus sCTPA detected PE, source of PE and provided prognostic information.
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PMID:Pulmonary embolism: an observational study at Narayana Hrudayalaya Institute of Cardiac Sciences, Bangalore, India. 2063 34

Normotensive patients with acute pulmonary embolism (PE) who have increased troponin levels and right ventricular (RV) dysfunction are thought to be at high risk of death, but the level of risk is unclear. We retrospectively evaluated outcome in 1,273 stable patients with PE who had echocardiographic evaluations of RV size and/or measurement of cardiac troponin I (cTnI). In-hospital all-cause mortality was higher in those with RV enlargement (8.0%, 19 of 237, vs 3.3%, 22 of 663, p = 0.003). With an increased cTnI, irrespective of RV enlargement, all-cause mortality was 8.0% (28 of 330) versus 1.9% (15 of 835) in patients with a normal cTnI (p <0.0001). In patients with an increased cTnI combined with an enlarged right ventricle, all-cause mortality was 10.2% (12 of 118) compared to 1.9% (8 of 421) in patients who had neither (p <0.0001). These data show that increased levels of cTnI and RV enlargement are associated with an adverse outcome in stable patients with acute PE. In conclusion, increased levels of cTnI in combination with RV enlargement might indicate a group who would benefit from intense monitoring and aggressive treatment if subsequently indicated. The outcomes, however, were not extreme enough to warrant routine thrombolytic therapy.
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PMID:Outcome in stable patients with acute pulmonary embolism who had right ventricular enlargement and/or elevated levels of troponin I. 2069 16

Prognosis of stable patients with acute pulmonary embolism (PE) has been assessed with cardiac troponin I (cTnI) and right ventricular (RV) function or size. Whether creatine kinase-MB isoenzyme (CK-MB) would add to the prognostic assessment is uncertain. We retrospectively assessed in-hospital mortality from PE in 392 stable patients to test the hypothesis that CK-MB would be of greater prognostic value than cTnI or RV size and we assessed whether combinations would increase prognostic value. CK-MB was high in 29 patients (7.4%); cTnI was high in 76 patients (19%) and intermediate in 78 patients (20%). The right ventricle was dilated in 128 patients (33%). Trends showed highest in-hospital mortality from PE in 4 of 29 (14%) with high CK-MB compared to 6 of 76 (7.9%) with high cTnI and 8 of 128 (6.3%) with RV dilatation (differences NS). High CK-MB and high cTnI provided added prognostic information only in patients with RV dilatation. Mortality with high CK-MB plus RV dilatation (4 of 19, 21%) tended to exceed mortality with high cTnI plus RV dilatation (5 of 39, 13%, NS). When CK-MB and cTnI were high and the right ventricle was dilated, PE mortality tended to be highest (4 of 14, 29%, NS). In conclusion, cardiac biomarkers contributed to prognosis only in patients with RV dilatation. CK-MB was the strongest predictor of death from PE but its prevalence was low, thus limiting its value as a single prognostic indicator. The combination of high CK-MB, high cTnI, and RV dilatation tended to indicate the highest mortality.
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PMID:Prognosis based on creatine kinase isoenzyme MB, cardiac troponin I, and right ventricular size in stable patients with acute pulmonary embolism. 2124 22

The purpose of this investigation is to assess the prevalence of elevated cardiac biomarkers, with or without estimates of right ventricular (RV) size, in stable patients with acute pulmonary embolism (PE). Our hypothesis is that the combination of high levels of cardiac troponin I (cTnI), high creatine kinase isoenzyme MB (CK-MB), and normal size RV are sufficiently uncommon in stable patients with PE to make the diagnosis of PE unlikely. Retrospective review showed a high cTnI plus high CK-MB in 20 (3.4%) of 585 stable patients with acute PE. A high cTnI plus high CK-MB with normal RV size was shown in 5 (1.9%) of 264 patients. In stable patients with such findings, therefore, PE is unlikely and other diagnoses, particularly acute coronary syndrome, should be considered before pursuing a diagnosis of PE.
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PMID:Elevated cardiac biomarkers with normal right ventricular size indicate an unlikely diagnosis of acute pulmonary embolism in stable patients. 2130 4

Acute pulmonary embolism (PE) is a severe and potentially fatal disease which acutely augments the right ventricle (RV) strain. Development of RV dysfunction (RVD) in the disease process is synonymous with an overall poor prognosis. The diagnosis of PE is usually established by a combination of clinical assessment, D-dimer test and medical imaging with either lung scintigraphy or pulmonary multidetector computer tomography (MDCT) angiography. Which of the two methods to use in PE diagnostic has not been determined and very limited data comparing these modalities are available. Assessment of RV function is cumbersome due to complex geometry. RVD is usually established by echocardiography which is observer dependent, has low reproducibility, and requires expertise. Therefore, a simple and reproducible biochemical method to assess RVD in patients with PE would be desirable. Brain natriuretic peptide (BNP), pro-atrial natriuretic peptide (pro-ANP), cardiac troponin I (TnI), and endothelin-1 (ET-1) have been the most studied plasma biomarkers in the context of risk stratification in PE. BNP is mainly produced in the ventricles of the heart. It is released from the left ventricle in response to increased filling pressure and is increased in chronic left heart failure. Pro-ANP is primarily produced in the atria, is released by atrial distention and is elevated in chronic pulmonary hypertension and could be an early marker for RVD. Plasma level of ET-1 has been shown to correlate with pulmonary pressure and is released from endothelial cells in the pulmonary vessels. Additionally, increases in circulating levels of ET-1 have been reported in an experimental animal model of PE. TnI is part of a complex of regulatory proteins in the cardiac myofilaments and is released upon myocyte injury. It is related to short term clinical outcome, prolonged hypotension, and cardiogenic shock after myocardial infarction and is a predictor of 30-day mortality and RVD using echocardiography in patients with PE. Our hypothesis was therefore that the neuroendocrine activation of BNP, pro-ANP, ET-1, and TnI alone or in combination could serve as markers of RVD in patients with PE. The use of plasma biomarkers would be much simpler than reproducible medical imaging methods such as magnetic resonance imaging (MRI), radionuclide based methods etc.
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PMID:Neuroendocrine activation and diagnostics in pulmonary embolism: Translational studies. 2137 7

Predictors of in-hospital mortality from massive pulmonary embolism (PE) were retrospectively assessed in 78 patients who received thrombolytic therapy. Mortality from PE was 19% (15 of 78). Mortality from PE was higher in those with shock, 36% (12 of 33) versus no shock, 7% (3 of 45; P = .001), 21% (7 of 34) with right ventricle (RV) hypokinesis, and 20% (13 of 64) with RV enlargement. Mortality was 14% (2 of 14) with normal cardiac troponin I (cTnI), 19% (4 of 21) with intermediate cTnI, and 22% (8 of 36) with high cTnI (comparisons between groups nonsignificant [NS]). Trends with combinations of risk factors showed the highest mortality with shock plus high cTnI plus RV hypokinesis (57%) or shock plus high cTnI plus RV enlargement (54%). In conclusion, among the single risk factors, shock was associated with the highest in-hospital mortality from PE and combinations with high cTnI and RV enlargement were associated with higher mortalities.
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PMID:Predictors of in-hospital mortality in patients receiving thrombolytic therapy for pulmonary embolism. 2159 22

Creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and myoglobin (Mb) are biochemical markers of myocardial injury; however, Mb is more abundant in skeletal muscles. The present study involved analysis of these markers in pericardial and cerebrospinal fluids (PCF and CSF) from serial medicolegal autopsy cases (n=295, within 48h) to examine their efficacy in determining the cause of death. Although these markers showed a slight postmortem time-dependent elevation, except for CK-MB in CSF, the distribution depended on the cause of death. Mb levels in PCF and CSF were higher in fatal hyperthermia (heat stroke) and methamphetamine abuse, and CK-MB in both fluids was also higher in the latter. In psychotropic drug intoxication, CK-MB, cTnI and Mb were higher in PCF, but only cTnI was elevated in CSF. In electrocution and cerebrovascular disease, each marker was higher in PCF and also relatively high in CSF. PCF cTnI level was higher in acute pulmonary embolism without significant elevation of any other markers, whereas CSF CK-MB was higher in acute blunt brain injury death and methamphetamine abuse. In most cases of delayed brain injury death, hypothermia (cold exposure) and pneumonia, these markers were low or intermediate in both PCF and CSF; however, sudden cardiac death, asphyxiation and fire fatality cases showed few characteristic findings. These observations suggest that combined analyses of these markers in postmortem PCF and CSF, in addition to blood samples, are helpful for evaluating the severity of myocardial and/or skeletal muscle damage in death processes, in particular for investigating deaths due to hyperthermia, hypothermia, electrocution and intoxication.
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PMID:Combined analyses of creatine kinase MB, cardiac troponin I and myoglobin in pericardial and cerebrospinal fluids to investigate myocardial and skeletal muscle injury in medicolegal autopsy cases. 2168 43

Although cardiac troponin I (cTnI) elevations during acute pulmonary embolism (PE) are predictive of in-hospital death, it is not clear whether cTnI measurements at emergency department (ED) admission are predictive of the occurrence of hypotension. The study subjects included all consecutive patients with acute PE (diagnosed by chest computed tomography angiography) in the ED between January 2006 and December 2011. All underwent cTnI tests at ED admission and were divided into two groups based on the occurrence of hypotension within 24 h. Of 457 stable patients with acute PE who were admitted to the ED during the study period, 301 patients were included. Within 24 h of hospitalization, 27 (9.0%) developed hypotension. The patients who developed hypotension had a significantly higher mean cTnI concentration than did the remaining patients (1.01 vs. 0.14 ng/mL, P < 0.00). They were also more likely to be treated with thrombolytic therapy and had higher 28-day and 6-month mortality rates. Cardiac TnI elevation (>0.05 ng/mL) at ED admission was a strong predictor of the development of hypotension within 24 h (odds ratio, 8.2; 95% confidence interval, 2.6-26.1; P = 0.00). The sensitivity, specificity, positive predictive value, and negative predictive value of elevated cTnI were 85%, 66%, 20%, and 98%, respectively. This study suggests that a normal cTnI nearly rules out subsequent development of hypotension within 24 h. This may help to select those patients who would benefit most from intensive clinical surveillance and escalated treatment.
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PMID:Value of cardiac troponin I for predicting in-hospital occurrence of hypotension in stable patients with acute pulmonary embolism. 2314 66

We analysed a cohort of patients with normotensive pulmonary embolism (PE) in order to assess whether combining echocardiography and biomarkers with the pulmonary embolism severity index (PESI) improves the risk stratification in comparison to the PESI alone. The PESI was calculated in normotensive patients with PE who also underwent echocardiography and assays of cardiac troponin I and brain natriuretic peptide. 30-day adverse outcome was defined as death, recurrent PE or shock. 529 patients were included, 25 (4.7%, 95% CI 3.2-6.9%) had at least one outcome event. The proportion of patients with adverse events increased from 2.1% in PESI class I-II to 8.4% in PESI class III-IV, and to 14.3% in PESI class V (p<0.001). In PESI class I-II, the rate of outcome events was significantly higher in patients with abnormal values of biomarkers or right ventricular dilatation. In multivariate analysis, the PESI (class III-IV versus I-II, OR 3.1, 95% CI 1.2-8.3; class V versus I-II, OR 5.5, 95% CI 1.5-25.5 and echocardiography (right ventricular/left ventricular ratio, OR (for an increase of 0.1) 1.3, 95% CI 1.1-1.5) were independent predictors of an adverse outcome. In patients with normotensive PE, biomarkers and echocardiography provided additional prognostic information to the PESI.
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PMID:Echocardiography and pulmonary embolism severity index have independent prognostic roles in pulmonary embolism. 2438 22

Acute pulmonary embolism is a critical condition associated with increased mortality. Lung embolization causes acute pulmonary hypertension and right ventricle afterload. Global heart ischemia supervenes and may lead to severe shock and death. In this article, we reviewed current literature supporting the idea that abnormal matrix metalloproteinase (MMP) activity contributes to acute pulmonary embolism-induced hemodynamic changes. While low MMP levels are usually found in normal lung tissues, it is well known that inflammation and lung injury increase MMP expression and activity. This is probably due to recruitment and migration of inflammatory cells from the circulation to lung tissues. In addition, recent studies have shown increased MMP levels and activity in the right ventricle from animals with acute pulmonary embolism. Such increases in proteolytic activity were associated with increased cardiac troponin I in serum, suggesting a possible role for MMPs in cardiomyocyte injury during acute pulmonary embolism. These alterations have justified the use of doxycycline as an MMP inhibitor in acute pulmonary embolism. We review current evidence indicating that MMPs are targets in this critical condition. MMP inhibition apparently exerts antihypertensive effects and protects against cardiomyocyte injury caused by acute pulmonary embolism.
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PMID:Matrix metalloproteinases as drug targets in acute pulmonary embolism. 2331 66


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