Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The operative approach to constrictive pericarditis still remains a surgical challenge. Subtotal pericardiectomy through median sternotomy was analyzed retrospectively in a series of 84 patients operated on for chronic constrictive pericarditis at our institution between 1979 and 1989. The mean duration of symptoms prior to diagnosis was 20 +/- 6 months (1-264 months). Preoperatively, 72% of patients were in NYHA class III or IV, presented signs of right cardiac failure (88%) or anasarca (18%). Chest X-ray showed pericardial calcifications in 40% of the patients. Echocardiography revealed pericardial thickening in 62%. Among 62 patients in whom cardiac catheterization was performed, a characteristic dip-and-plateau was found in 47 patients (76%). A specific etiologic factor was identified in only 37 patients: tuberculosis (12%), recurrent acute pericarditis (9%), hemopericardium (9%), radiotherapy (5%), previous cardiac surgery (4%), bacterial infection (2%), myocardial infarction (2%) and connective tissue disease (2%). In 47 patients (55%), the constrictive pericarditis remained idiopathic. In seven patients we performed a redo-operation for previous incomplete pericardiectomy. Subtotal pericardiectomy (from phrenic nerve to phrenic nerve) was performed in 75 patients. A palliative procedure consisting of pericardial "meshing" was performed in nine patients due to an unsatisfactory cleavage plane. Cardiopulmonary bypass was used in four patients for coexistent cardiac lesions. The operative mortality was 2.3% (two patients: septicemia and pulmonary embolism). Seven patients (8.2%) developed early on-lethal complications. The probability of survival for patients discharged for the hospital was 94% at 3 years and 87% at 7 years. There were four late deaths and no reoperation for recurrent constriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Results of subtotal pericardiectomy for constrictive pericarditis. 851 53

To investigate the etiology of pleural effusions in our region, we undertook a prospective study of patients with this condition in our centers. During a 5-year period, we studied 642 pleural effusion patients aged 57.1 +/- 21.1 years, of whom 401 were men aged 56.5 +/- 21 years and 241 were women aged 57.8 +/- 21.4 years; the male/female ratio was 1.6:1. The most frequent cause of pleural effusion was tuberculosis (25%), followed by neoplasia (22.9%) and congestive heart failure (17.9%). The etiology of 48 cases (7.5%) remained uncertain. In the neoplastic effusion group, the most frequent locations of the primary tumor were lung (32.6%), breast (11.5%), lymphoma (10.8%), and ovary (7.5%); in 21 cases (14.3% of the neoplastic group), it was not possible to identify the primary tumor. The 111 patients aged younger than 40 years with tuberculous effusions made up 69.4% of tuberculous effusion cases and the same percentage of patients younger than 40 years; the proportion of effusions that were tuberculous peaked in the 11- to 30-year-old age group and declined steadily thereafter. Of the patients with neoplastic effusions, 83% were older than 50 years; the proportion of effusions that were neoplastic rose steadily from zero in the 0- to 30-year-old age group to a peak among 60- to 70-year-olds. The age-wise distribution of effusions secondary to congestive heart failure was similar to that of neoplastic effusions. Of the effusions secondary to congestive heart failure, 86% (99/115) affected the right pleura or both, and 83% of effusions secondary to pulmonary thromboembolism (15/18) affected the right side. Neoplastic, tuberculous, parapneumonic, empyematous, and other exudative effusions showed no preference for either side. Of the 97 bilateral effusions, 77 (79.4%) were secondary to heart failure (59, 60.8%) or neoplasia (18, 18.6%). We conclude that in our region, the most frequent cause of pleural effusion is tuberculosis, followed by neoplasia and congestive heart failure. We suggest that all those interested in pleural disease should determine the etiologic pattern of pleural effusion in their region with a view to the adoption of regionally optimized diagnostic and therapeutic attitudes.
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PMID:The etiology of pleural effusions in an area with high incidence of tuberculosis. 854 79

Tuberculous pericarditis is one of the commonest causes of cardiac failure in Transkei and the surrounding regions in southeast Africa. About 20% of patients with clinically diagnosed tuberculous pericardial effusion go on to develop pericardial fibrosis (i.e., construction), a complication which is associated with significant mortality and morbidity. The pathological mechanisms underlying this aberrant inflammatory response are poorly understood, and there is a lack of reliable pointers (clinical or laboratory) in predicting the likelihood of development of constriction. We studied the humoral response to mycobacterial heat shock proteins (65 and 71 kDa) in 25 patients with culture-positive tuberculous pericardial effusion and found a significant correlation between high anti-mycobacterial hsp60 antibody titers (before treatment) and subsequent development of fibrosis (P = 0.035 by logistic regression), which is independent of the effect of the use of prednisolone as adjuvant therapy. Possible mechanisms underlying the pathogenesis of pericardial constriction in tuberculosis are postulated.
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PMID:Humoral response to mycobacterial heat shock proteins in patients with constrictive pericarditis caused by tuberculosis and its implications for pathogenesis. 855

A 26-year-old man who had suffered from intermittent chills and fever over a two month period was quite clear of heart or kidney involved developed acute deterioration of renal function. A new pansystolic murmur over the apex of the heart was heard on auscultation, and echocardiography clearly showed a vegetation about 0.7-0.9 cm in size on the atrial site of the mitral value. Laboratory investigation displayed normochromic anemia with negative Coombs' test. Immunological studies were positive for rheumatoid factor and circulating immune complex. High serum levels of erythrocyte sedimentation rate and C-reactive protein, nephritic sediment of urinalysis and negative blood cultures for bacteria, tuberculosis or fungus were also noted. Abdominal sonography showed normal kidney size, bilaterally. Renal biopsy revealed typical crescentic glomerulonephritis. After intravenous penicillin therapy for two weeks, the serum creatinine level recovered from 6.7 mg/dl to 2.0 mg/dl and circulating immune complex disappeared. In consideration of cardiac insufficiency and the potential risk for complications of the vegetation, the patient underwent mitral valve replacement. Four weeks after operation, all the abnormal data had resolved completely. These data suggested that infective endocarditis with rapidly progressive glomerulonephritis is curable by antibiotic therapy and surgical intervention.
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PMID:Infective endocarditis complicated with rapidly progressive glomerulonephritis: a case report. 880 7

With the advent and the introduction of effective antimicrobial therapy, the mortality for tuberculosis pericarditis decreased in number dramatically. The problems, however, remains in several severe cases. We have experienced a rare case of 74 year old male with subacute effusive-constrictive pericarditis accompanied with miliary tuberculosis. The patient revealed improvement immediately after early an emergent pericardiectomy. However cardiac failure recurred thereafter because of fibrous epicarditis of tuberculous inflammation. Management of subacute effusive-constrictive pericarditis as this has many problems including surgical intervention such as operative timing and indication and/or role of corticosteroids together with antituberculotic drugs.
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PMID:[Subacute effusive-constrictive pericarditis accompanied with miliary tuberculosis: a case report]. 891 70

In this study, total cytoplasmic (Cu,Zn-SOD) and mitochondrial (Mn-SOD) superoxide dismutase activities were measured in sera and pleural fluids from patients with squamous cell carcinoma of the lung. The results were compared with those of control subjects and those of patients with tuberculosis and chronic heart failure. Serum activities were found higher in all patient groups compared to control group. Highest values were however in tuberculosis group. In the correlation analysis, meaningful intra- and inter-correlations were established between enzyme activities in the samples. Results suggest that high serum and pleural fluid SOD activities are not specific biochemical parameters for carcinogenesis and, activities may also increase in some other degenerative diseases such as tuberculosis, chronic heart failure, etc. Therefore, we believe that it is not useful to use serum and pleural fluid SOD activities for diagnostic purposes in cancer. However, the activities of these enzymes in the biological samples might be used as nonspecific prognostic markers in assessing cellular and mitochondrial tissue destruction.
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PMID:Activities of total, cytoplasmic, and mitochondrial superoxide dismutase enzymes in sera and pleural fluids from patients with lung cancer. 892 62

IL-6, soluble IL-6 receptor (sIL-6R) and soluble gp130 (sgp130) levels were measured in sera and pleural effusions from 42 patients with metastatic carcinoma, non-Hodgkin's lymphoma, tuberculosis, cardiac failure and miscellaneous diseases. Pleural IL-6 levels measured by ELISA were very high in all patient groups (mean 34.8 +/- 15.3 ng/ml) without significant difference according to diseases. IL-6 was shown to be biologically active in a proliferative assay. Serum IL-6 levels were low (0.049 +/- 0.014 ng/ml) and did not correlate with pleural fluid levels. Pleural IL-6 levels correlated with the number of polymorphonuclear cells in pleural fluid (P < 0.03). Pleural sIL-6R levels (76 +/- 8 ng/ml) were always lower than serum levels (196 +/- 12 ng/ml; P < 0.0001) but correlated with them (P < 0.01). Pleural sIL-6R and albumin levels correlated (P < 0.01), suggesting a transudation of sIL-6R from the serum. Pleural sgp130 levels (10.9 +/- 1.0 ng/ml) were lower than serum levels (24.6 +/- 2.8 ng/ml; P < 0.002). After gel filtration of pleural fluid, the bulk of IL-6 (> 90%) was recovered in a 15,000-30,000 fraction, corresponding to the expected mol. wt of free IL-6. These results suggest a production and a sequestration of IL-6 in the pleural cavity in all studied conditions.
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PMID:IL-6 and soluble IL-6 receptors (sIL-6R and sgp130) in human pleural effusions: massive IL-6 production independently of underlying diseases. 901 Feb 74

Mononuclear cells (MNC) generate cell-bound procoagulant activity (PCA) which shortens recalcification time after incubation with an antigen to which the donor has been sensitized. PCA has been demonstrated in various lung diseases, including exudative pleural effusions. To determine the value of measuring cell-bound PCA in the diagnosis of tuberculous pleural effusions we examined pleural effusion MNC of patients with tuberculosis (n = 19), congestive heart failure (n = 7), and carcinoma (n = 7). MNC were isolated, incubated in 0 or 10 micrograms/ml purified protein derivative (PPD) for 15 min and for 20 h, and recalcification time determined. Incubation with thromboplastin was used as control. The recalcification times in serum incubated for 15 min varied within a wide range, the mean values were longest for tuberculous effusion MNC, incubation for 20 h increased variation. Incubation of cells for 15 min with thromboplastin led to a decrease of mean recalcification time in tuberculous (p < 0.001) and heart failure (p < 0.05), and with no significance in carcinomatous effusions. Incubation with PPD led to decrease of recalcification time which was not significant. Comparisons of the mean relative recalcification times after PPD incubation showed that tuberculosis differed from lung cancer (p < 0.001), lung cancer from heart failure (p < 0.05), but not heart failure from tuberculosis. We conclude from our study that pleural effusion MNC express spontaneous PCA in vitro which is strongest in carcinomatous pleural effusions. Incubation of MNC with thromboplastin and less discernable with PPD leads to an increase in PCA which is more pronounced in tuberculous pleural effusions. However, due to substantial intersubject variability and overlap between the study groups, this test does not allow reliable differentiation of tuberculous from other MNC rich pleural effusions.
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PMID:Procoagulant activity of purified protein derivative-stimulated pleural effusion mononuclear cells in tuberculous pleurisy. 909 51

CTEPH have not been widely recognised until recently. Introduction of the new, sophisticated, non-invasive diagnostic tools accounts for rapid progress in that field. Patients with high pulmonary hypertension have a very poor prognosis. Medical treatment (vasodilators, anticoagulants) does not change outcome. Pulmonary thromboendarterectomy is the only therapeutic option for the patients. It is essential to prevent further episodes of pulmonary embolism both over the long term and during the high risk perioperative period by means of inferior vena cava filters. In the Department of Medicine, Institute of Tuberculosis and Lung Diseases 18 LGM ivc filters have been inserted in patients with CTEPH since 1994. In 7 patients PTE was performed-in 5 cases good result was achieved, 2 patients died after surgery. In the latter group 5 patients died mainly because of severe heart failure. Only one non-fatal episode of pulmonary embolism was observed. It should be concluded that the LGM ivc filters are safe and effective in preventing episodes of pulmonary embolism in patients with CTEPH.
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PMID:[Implantation of LGM inferior vena cava filters in patients with chronic pulmonary hypertension during a course of major vessel thromboembolism--observation of 18 patients]. 918 83

The differential diagnosis of ascites often leads to confusion and an inability to exclude its multitude of causes in many patients. In this review, we outline the clinical features and laboratory investigations that usually elucidate the cause of ascites for the clinician in a simple and logical manner. Roughly 80-85% of cases of ascites are related to underlying chronic liver disease, but cardiac failure, tuberculosis, malignancy-related ascites and other less common causes should always be considered. Careful evaluation of the patient, including a clinical history, physical examination and diagnostic paracentesis should routinely be performed to determine the cause of ascites. Fluid should be sent for cell count and albumin along with simultaneous determination of serum albumin to determine the serum: ascites albumin gradient. This gradient allows classification of the cause of ascites into portal hypertension-related and nonrelated with a diagnostic accuracy of > or = 97%. The causes of ascites are individually discussed in relationship to their clinical features and to the laboratory investigations that are relevant in each situation.
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PMID:Differential diagnosis of ascites. 930 24


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