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

Fatty acid metabolism has been reported to be impaired earlier than myocardial blood flow in left ventricular hypertrophic myocardium, e.g., in hypertrophic cardiomyopathy or hypertensive heart disease. The purpose of this study was to determine whether impaired fatty acid metabolism also occurs in right ventricular (RV) hypertrophy. The subjects consisted of 6 patients with chronic obstructive pulmonary disease, 4 with primary pulmonary hypertension, 2 each with refractory pulmonary tuberculosis, tricuspid insufficiency, pulmonary embolism, 1 each with atrial septal defect, ventricular septal defect (Eisenmenger complex), Ebstein anomaly, and endocardial defect, and 7 healthy controls. SPECT imaging with Tl-201 (Tl) and I-123 beta-methyliodophenyl pentadecanoic acid (BMIPP), and Tc-99m RBC first pass and gated blood pool scintigraphy were performed. Based on Tl planar images, the subjects were classified into 3 groups: 7 patients with no RV visualization (Group A), 11 with moderate RV visualization (Group B) and 9 with marked RV visualization (Group C). As a semi-quantitative evaluation by Tl myocardial SPECT, 3 regions in 3 representative short axial images were divided into 9 segments, each of which was graded from 0 to +3, and their sum was calculated as the RV score. The right ventricular ejection fraction (RVEF) and the left ventricular ejection fraction were obtained by Tc-99m RBC cardiac scintigraphy. The groups with marked visualization of the right ventricle had lower RVEF (p < 0.01), and there was a good correlation between the RVEF and the RV score with both Tl and BMIPP (Tl: r = -0.79, BMIPP: r = -0.70). Although a good correlation was demonstrated between the RV score with Tl and BMIPP in Groups A and B (r = 0.86, p < 0.001), in Group C, in which there was marked RV T1 visualization, the RV score with BMIPP was significantly smaller than with Tl (BMIPP vs. Tl: 11.5 +/- 3.7 vs. 16.4 +/- 3.8, p < 0.01). These findings suggest that impaired fatty acid metabolism may exist in severely hypertrophic right ventricle due to RV overload.
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PMID:Detection of impaired fatty acid metabolism in right ventricular hypertrophy: assessment by I-123 beta-methyl iodophenyl pentadecanoic acid (BMIPP) myocardial single-photon emission computed tomography. 931 Jan 69

Hemodynamic syncope is caused by an impediment to a necessary increase of the cardiac output; therefore, hemodynamic syncopes most often occur during or shortly after exercise. However, a syncope at rest does not exclude a hemodynamic cause. Moreover, arrhythmias which may directly lead to syncope or accentuate the hemodynamic impediment are often present in cardiac diseases causing hemodynamic syncope. Hemodynamic syncopes are responsible for 2 to 3% of all syncopes leading to medical evaluation. Of these, more than half are caused by aortic stenosis and about one quarter by pulmonary embolism. Other reasons are rare. Hypertrophic cardiomyopathy is more often associated with arrhythmic than with hemodynamic syncope. Syncope in primary pulmonary hypertension is often preceded by dizziness, epigastric distress and faintness. Since the medical therapy may lead to hemodynamic deterioration, it must be started under invasive observation. Primary tumors of the heart are rare; secondary cardiac neoplasms are 6 to 40 times more common. Myxoma is the most common primary tumor of the heart. It is important to promptly undertake surgery in order to improve prognosis. Various other diseases may provoke hemodynamic syncope; however, other symptoms are by far more common.
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PMID:[Hemodynamically-induced syncope]. 933 77

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease resulting from the thromboembolic obstruction of the segmental and/or large size pulmonary arteries, subsequently leading to pulmonary arterial hypertension. Incomplete resolution of acute pulmonary emboli and thrombus organization are believed to be important for the development of the disease. Primary pulmonary hypertension (PPH) is a further disease that at present is poorly understood but shows a clinical picture similar to CTEPH. Since lipoprotein(a) [Lp(a)]. a genetically determined risk factor for atherosclerosis and thrombosis, has been found increased in plasma of patients with deep vein thrombosis and pulmonary embolism, we measured plasma Lp(a) levels in 40 patients with CTEPH and 50 patients with PPH and compared them to 50 matched controls. The median for Lp(a) plasma levels was significantly higher in CTEPH patients (26.6 mg/dl) than in PPH patients (9.6 mg/dl) and controls (7.2 mg/dl). Increased plasma Lp(a) could, therefore. play a significant role in the mechanisms of ongoing thrombosis and thrombus organization in CTEPH, while its possible role in PPH can be limited to a small number of patients.
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PMID:Plasma Lp(a) levels are increased in patients with chronic thromboembolic pulmonary hypertension. 971 43

A 32-year-old female is described, who was admitted with symptoms of severe right heart failure. The most likely diagnosis of pulmonary embolism was excluded. Echocardiography and left-right catheterisation confirmed the diagnosis of primary pulmonary hypertension. A possible mediator in the process of PPH could be the appetite suppressants she had taken for some months after her second pregnancy. Before further pharmacologic tests could be performed the patient died in circulatory collapse. Postmortem pathological examination confirmed the diagnosis of PPH by the presence of narrowed pulmonary arterioles, media hypertrophy, thrombotic lesions and normal surrounding pulmonary parenchyma. The literature on primary pulmonary hypertension is revised with special emphasis on diagnosis and treatment algorithms.
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PMID:Primary pulmonary hypertension with fatal outcome in a young woman and review of the literature. 1021 74

Analysis of the systolic flow velocity curve (SFVC) in the right ventricular outflow tract is considered as an alternative to the tricuspid valve pressure gradient (TVPG) method for echo-Doppler assessment of pulmonary arterial pressure (P(pa)). The present study checked whether or not SFVC is affected by the cause of pulmonary hypertension. Doppler recordings of 86 patients (39 female, aged 55.5+/-15.2 yrs) with acute (AP-PE) or chronic (CP-PE) proximal pulmonary embolism, chronic obstructive pulmonary disase (COPD) or primary pulmonary hypertension (PPH) were retrospectively analysed by two observers unaware of the purpose of the study. Despite having the lowest TVPG (48+/-13 mmHg), patients with AP-PE had the shortest acceleration time (t(acc); 56+/-15 ms) and time to midsystolic deceleration (t(msd); 105+/-16 ms). t(acc) <60 ms in patients with TVPG <60 mmHg had 98% specificity and 48% sensitivity for AP-PE. In PPH, SFVC was less abnormal (t(acc) 64+/-14 ms, t(msd) 125+/-25 ms, both p<0.03) despite having a TVPG twice as high (92+/-12 mmHg, p< 0.001). In contrast to t(acc), TVPG showed strong correlation with direct P(pa) measurements whenever performed (r=-0.43, p=0.02, versus r=0.80, p<0.001; n=30). There was no correlation between t(acc) and TVPG in a pooled study group and SFVC seemed strongly affected by the presence of both AP-PE and CP-PE. While potentially useful for evaluation of the true right ventricular afterload during pulsatile flow conditions, the systolic flow velocity curve does not provide a reliable estimate of pulmonary arterial pressure.
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PMID:Proximal pulmonary emboli modify right ventricular ejection pattern. 1023 36

Pulmonary hypertension is the hemodynamic consequence of vascular changes within the precapillary (arterial) or postcapillary (venous) pulmonary circulation. These changes may be idiopathic, as in primary pulmonary hypertension or pulmonary veno-occlusive disease, but more commonly they represent a secondary response to alterations in pulmonary blood flow. The pulmonary and systemic bronchial circulations form broad anastomoses that largely prevent infarction except in settings of markedly elevated pulmonary venous pressure, underlying malignancy, or excessive embolic burden. Causes of precapillary pulmonary hypertension include long-standing cardiac left-to-right shunt, chronic thromboembolic disease, and widespread pulmonary embolism arising from intravascular malignant cells, parasites, or foreign materials. The classic radiologic features of precapillary pulmonary hypertension are central arterial enlargement, sharply pruned peripheral vascularity, and right-sided heart hypertrophy and chamber dilatation. Postcapillary pulmonary hypertension may develop secondary to focal venous constriction or to compromised pulmonary venous drainage due to left atrial neoplasia, mitral stenosis, or left ventricular failure. Radiologic manifestations of postcapillary pulmonary hypertension include prominent septal lines, small pleural effusions, and occasionally air-space opacities. In addition, radiologic evaluation of postcapillary pulmonary hypertension may demonstrate evidence of pulmonary arterial hypertension, secondary to the retrograde transmission of elevated pulmonary venous pressure across the capillary bed.
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PMID:From the archives of the AFIP: pulmonary vasculature: hypertension and infarction. 1071 47

Patients with acute massive pulmonary embolism or primary pulmonary hypertension may develop acute circulatory failure and are therefore admitted in the intensive care. The mortality rate of patients with pulmonary embolism and shock varies between 25 and 35% whereas the corresponding figure in patients with submassive embolism is less than 10%. Spiral computed tomography may be the most convenient test for diagnosing pulmonary embolism in the setting of acute circulatory failure. In the few patients who remain unstable despite adequate symptomatic treatment, transthoracic echocardiography combined with clinical judgement is appropriate. Inotropic support and thrombolytic therapy are clearly indicated for patients with massive embolism and shock. The role of the latter is more controversial in patients with right ventricular distension and normal blood pressure. The optimal duration of anticoagulant therapy for pulmonary embolism remains to be defined. Most patients are adequately treated with a six-month course of oral anticoagulants. A shorter duration may be sufficient when a transient risk factor is the cause of the initial event whereas patients with cancer or antithrombin deficiency may require a life long treatment. Primary pulmonary hypertension is a much more uncommon disease which can also lead to right ventricular failure. Symptomatic treatment combines oxygen, inotropic drugs, as well as the optimisation of right ventricular filling pressure. Specific treatment includes inhaled nitric oxide or intravenous epoprostenol followed by anticoagulants with either calcium channel blockers in patients responding acutely to vasodilators or a continuous infusion of epoprostenol in those who do not respond to acute challenge or who are not improving with calcium channel blockers. Although the long term survival has markedly improved as a result of epoprostenol treatment, some patients with refractory primary pulmonary hypertension remain candidates for lung transplantation.
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PMID:[Acute circulatory failure caused by primary pulmonary hypertension or pulmonary embolism]. 1075 56

Chronic thromboembolic pulmonary hypertension (CTEPH) is an uncommon disease with a severe prognosis. Initially considered as a constantly fatal disease, it can be cured since the advent in the late 80's of thromboendarterectomy. CTEPH occurs in approximately 0.1% of patients who survive acute pulmonary embolism. Such outcome is due to the failure of the normal thrombi resolution in the pulmonary circulation. This disease is observed in both sexes and occasionally as early as in the third decade. Many patients have no history of acute venous thromboembolism which is responsible for the frequent diagnosis delay. Therefore, it is of paramount importance to search for pulmonary vascular disease when patients complain solely of dyspnea on exertion. These patients should undergo echocardiography and, if necessary, right heart catheterization. Once the diagnosis of pulmonary hypertension is established the next step is to find the cause. Ventilation-perfusion scanning is probably the most sensitive non-invasive test to provide evidence that pulmonary hypertension is related to chronic thromboembolism. Angiography and helical computed tomography allow to confirm the diagnosis of CTEPH and to determine whether it is accessible or not to thromboendarterectomy. Most patients who undergo thromboendarterectomy improve clinically and in terms of gas exchange and pulmonary hemodynamics. When thrombi are inaccessible surgically, patients should be placed on the list for lung transplantation if they fulfill the criteria established for primary pulmonary hypertension. When all surgical procedures are contraindicated, anticoagulant and oxygen therapy remain the sole possibility of treatment.
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PMID:[Chronic thromboembolic pulmonary arterial hypertension]. 1090 51

We report a middle-aged woman who died 2 days after presenting with dyspnea and severe pulmonary hypertension of unknown etiology. Her symptoms were highly suggestive of pulmonary embolism, but clinical evaluations for that disease yielded negative results. Autopsy revealed a Krukenberg tumor of the left ovary, representing metastatic gastric carcinoma from an occult primary lesion. Although the lungs exhibited no gross evidence of pulmonary emboli or neoplasia, microscopic examination revealed diffuse microscopic metastases in the pulmonary arterial vasculature. The pulmonary arteries exhibited fibrocellular intimal proliferation with smooth muscle colonization of the luminal neoplastic lesions and associated microthrombi. This disease entity, known as tumor-related thrombotic pulmonary microangiopathy, results in generalized microvascular obliteration and subsequent pulmonary hypertension. It is a rare condition that is distinct from ordinary pulmonary thromboembolism and primary pulmonary hypertension. Tumor-related thrombotic pulmonary microangiopathy should be considered diagnostically by the autopsy pathologist in cases of rapidly evolving pulmonary hypertension in a middle-aged or elderly individual, or respiratory failure of unknown cause, especially if there is a history of a visceral malignancy.
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PMID:Tumor-related thrombotic pulmonary microangiopathy: review of pathologic findings and pathophysiologic mechanisms. 1091 85

Pulmonary thromboembolism presents in two clinical subsets: acute pulmonary embolism (PE) with or without right heart thrombi or paradoxical embolism and chronic thromboembolic pulmonary hypertension (CTEPH). Both PE and CTEPH have been underdiagnosed and carry high mortality rates. Acute massive PE is a hemodynamic entity leading to right ventricular overload readily identified with the use of transthoracic echocardiography. Transesophageal echocardiography (TEE) is a noninvasive bedside technique that has high diagnostic accuracy for the detection of central pulmonary thromboembolism. Due to the high prevalence of central pulmonary thromboembolism in acute PE, TEE is a useful method to provide the necessary proof for the institution of thrombolytic therapy. In the subset of patients with acute PE combined with right heart thrombi or paradoxical embolism, TEE is the technique of choice to guide surgery. CTEPH presents as primary pulmonary hypertension, but it has become a surgically curable disease. TEE is a fast, fairly sensitive, and highly specific diagnostic bedside modality to select surgical candidates with CTEPH. TEE should become a routine test in patients with suspected massive acute PE, suspected right heart thrombi, or paradoxical embolism associated with acute pulmonary embolism and in patients with primary pulmonary hypertension to select those having CTEPH who are suitable for surgery.
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PMID:Should Transesophageal Echocardiography Become a Routine Test in Patients with Suspected Pulmonary Thromboembolism? 1117 12


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