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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aortic valve lesions in progressive systemic sclerosis (PSS) are very uncommon. To our knowledge, aortic regurgitation (AR) associated with PSS has not been reported previously. We would like to report the case of a 58-year-old woman who had PSS with AR due to Raynaud's symptom, fever, positive ANA, accelerated ESR, and diastolic blowing murmur along the left sternal border. After treatment with adreno-cortico steroid and an immunosuppressive agent, the patient improved serologically and symptomatically. However, she was later admitted to our hospital again due to heart failure with progressive AR. She died of refractory heart failure with severe AR and tricuspid regurgitation (TR). The former was caused by aortic cusp lesions and the latter by pulmonary hypertension. An autopsy confirmed the diagnosis of PSS, which was found to have involved the heart, lungs and pancreas. Vasculitis with infiltration and fibrotic changes were noted in these organs. Moreover, there were fibrotic thickenings and shortenings in the aortic cusps with cell infiltration. There were no indications of rheumatic disease. These results suggest that the cause of our patient's aortic valve disease may have been PSS vasculitis.
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PMID:[Report of a case with aortic regurgitation in progressive systemic sclerosis]. 151 78

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
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PMID:Pulmonary and pleural complications of cardiac disease. 268 66

A case of Takayasu's disease presenting in a young man as a solid abdominal mass is described. The literature is reviewed and classifications of the disease are discussed. Occlusive thromboaortopathy, also known as "pulseless disease" or Takayasu's disease, was first described in 1908 by Takayasu, who observed cataracts and peculiar arteriovenous anastamoses around the optic papillae in a young woman. It is a vasculitic disorder of uncertain etiology occurring mainly in young women and may involve part or most of the aorta, as well as the pulmonary artery. Early features include fever, malaise, weight loss, and a high ESR, and, later on, absent pulses, aneurysms, hypertension, and heart failure may occur. The authors describe an unusual case of Takayasu's disease in a young black South African man.
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PMID:An unusual case of occlusive thromboaortopathy (Takayasu's disease)--a case report. 289 76

Thirty-one patients with proven acute myocardial infarction (MI) were studied prospectively at the time of admission to hospital and at 3, 7 and 18 days using 4 immune complex (IC) assays. Each assay showed an increased incidence of IC activity in MI with 76% of patients being positive in at least 1 assay on one or more of the sampling days. A positive IC assay did not show a significant correlation with cardiac failure, pericarditis, post MI syndrome or previous infarction. The presence of IC was found to correlate with serum C-reactive protein (CRP), serum enzymes and ESR and suggested that complexed CRP or other acute phase proteins may account for some of the IC activity found with less specific assays. The measurement of IC levels in MI has not proved helpful in the diagnosis, management or prediction of outcome in this disorder.
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PMID:Circulating immune complexes in myocardial infarction. 660 58

The natural history of acute rheumatic fever (ARF) in adults has been studied from an analysis of 23 patients together with a review of a further 466 published cases. In contrast to the picture in juvenile ARF, in our patients (average age 55 yr), only arthritis (83%) and carditis (35%) were major criteria for the diagnosis. All patients had at least 3 minor criteria. To summarize, 39% of the patients, average age 56 yr were seen in their initial attack of ARF. In those patients with a previous history of rheumatic fever, the mean interval between the index attack and the first illness was 20.5 yr. Contact with young children appeared to be an important predisposing factor. None had an ESR of less than 50 mm in the first hour, even in the presence of cardiac failure. Findings in the acute illness included anemia (70%), hyperglobulinemia (70%), urinary sediment (66%), and hypercalcemia in 7 out of 12 cases. The response to treatment was good and only 1 patient of 13 followed-up developed a new valvular lesion. A survey of the literature shows that attacks of ARF may occur at any age; death in the acute episode is rare and occurs only in patients with severe preexisting valvular disease with congestive failure. The problem of diagnosing active carditis in the presence of rheumatic heart disease (RHD) is discussed. While juvenile ARF may be overdiagnosed, the diagnosis may be missed in the adult rheumatic patient whose cardiac state inexplicably deteriorates. In such patients evidence for a preceding streptococcal infection should be sought. Patients with a high risk of developing ARF include those with carditis in previous attacks, with preexistent RHD, and with several children in the family. These factors should be considered when advising on the duration of antibiotic prophylaxis.
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PMID:Acute rheumatic fever in adults over the age of 45 years: an analysis of 23 patients together with a review of the literature. 729 18

A 77-year-old woman with hypertension was admitted to our hospital because of exertional dyspnea end peripheral edema. Chest X-ray showed cardiomegaly, pulmonary congestion and right pleural effusion. Hypertensive heart failure was diagnosed and treated, and right pleural effusion disappeared in 2 weeks. Abnormalities on laboratory data, i.e. anemia and increased ESR et al. continued after the improvement of heart failure. Serum IgG was elevated (2570 mg/dl), while IgA and IgM were decreased. Immunoelectrophoresis indicated the presence of monoclonal IgG-lambda in the serum. Bone marrow puncture revealed an increase in atypical plasma cells (38.4%). Multiple myeloma was diagnosed from these findings and treated with melphalan and prednisolone. But increases in atypical plasma cells (43.2%) and serum IgG (2573 mg/dl) continued. During treatment, right pleural effusion increased again. Thoracocentesis showed bloody effusion with numerous atypical plasma cells, and the presence of monoclonal IgG-lambda was indicated by immunoelectrophoresis. The patient died of renal and heart failure 2 months after the onset of malignant pleural effusion. Cytological examination and immunoelectrophoresis are necessary for pleural effusion in multiple myeloma.
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PMID:[A case of multiple myeloma associated with abnormal plasma cells and M-protein in pleural effusion]. 864 97

Heart failure (HF) is a complex clinical syndrome due to ischaemic heart disease, idiopathic cardiomyopathy, hypertension, valve heart disease and others. It is not clear if the etiology of HF influences decreased in this syndrome exercise tolerance. Controversial is also dependence of cytokine levels on etiology of HF. The aim of the study was to compare exercise capacity and cytokines levels in pts with ischaemic and dilated cardiomyopathy. We analyzed circulating levels of TNF-alpha and its soluble receptors sTNF-RI and sTNF-RII, and interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) in 41 pts with CHF, functional class NYHA I-IV, mean EF--25.2 +/- 7.1%. For determination of cytokines level (using R & D System tests) venous blood was withdrawn after 30 minutes of supine rest. All underwent echocardiography and cardiopulmonary exercise stress testing. Dilated cardiomyopathy (DCM) was diagnosed in 21 pts, ischaemic (ICM) in 20 pts. Pts with DCM were younger then with ICM (48 +/- 6.6 vs 56 +/- 6.6 yrs; p = 0.001). There were no significant differences between groups concerning BMI and EF. There were no significant differences in the level of TNF-alpha and sTNF-RI between groups. There was a trend of increased sTNF-RII in pts with ICM (3179.7 +/- 832.7 vs 2699 +/- 680.1 pg/ml; p = 0,07), IL-1beta (2.55 +/- 2.41 vs 1.49 +/- 1.68 pg/ml; p = 0.087) and IL-6 (6.25 +/- 2.21 vs 4.98 +/- 3.64 pg/ml; p = 0.065), and significant increased ESR (11.2 +/- 9.5 vs 5.5 +/- 4.7 mm/h; p = 0.04). Peak VO2 was reduced in pts with ICM group as compared to those with DCM (14.1 +/- 3.7 vs 18.1 +/- 4.8 ml/kg/min; p = 0.0069). In chronic heart failure circulating levels of cytokines tended to be higher in pts with ischaemic origin of the syndrome. The exercise capacity is lower in ischaemic cardiomyopathy.
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PMID:[Cardiopulmonary exercise testing and cytokines in chronic heart failure. Comparison of patients with ischaemic and with dilated cardiomyopathy]. 1550 92

Ergot derivative dopamine agonists, e.g. pergolide, bromocriptine, dihydroergocriptine used in treatment of Parkinson's disease can cause pleural, pericardial, retroperitoneal and valvular fibrotic changes. Case No 1: A 56-year-old woman with PD was treated with pergolide 3mg/24h since July 2002. In June 2003, edema of lower extremities was first noticed and echocardiography found a minor mitral regurgitation without any morphological changes of the valve. In January 2004, left- sided cardiac failure rapidly developed and echocardiography revealed multivalvular insufficiency with predominating severe mitral regurgitation. Mitral valve replacement was performed and pergolide was changed to ropinirole. Until now, neither cardiac functions nor motor status are sufficiently compensated. Case No 2: A 66-year-old-man with PD since 1996 was treated with pergolide 3 mg/day since 1999. In the beginning of 2004, leg edema appeared. On examination, bilateral hydronephrosis with ureteric strictures and incipient renal insufficiency was found. Bilateral ureteroplasty was performed and the histology showed periureteric fibrosis. Treatment with steroids was initiated and pergolide was changed to pramipexole. Despite the treatment, the fibrosis progressed, requiring ureteral stenting. Based on the literature review and on our own experience, we propose following guidelines to minimize the risk of complications: A. Not to use EAD as the first-line dopamine agonists. B. Regularly follow all patients treated with EAD, especially monitor the majorsymptoms: dyspnea, cough, fatigue, leg edema (also asymmetric), symptoms of urinary outflow obstruction, cardiac insufficiency, chest pain, heart murmur. An elevated ESR, C-reactive protein or anemia support the diagnosis. C. All symptomatic patients should undergo workup for serosal fibrosis (according to type of complication): chest X-ray or CT scan, spirometry, renal functions, renal ultrasound, CT of retroperitoneum. D. Before the introduction of EAD therapy, examine the renal functions, perform chest X-ray and echocardiography. Screening echocardiography should be performed in 3-6 months and subsequently in every 6-12 months.
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PMID:[Organ changes induced by ergot derivative dopamine agonist drugs: time to change treatment guidelines in Parkinson's disease?]. 1580

The prognostic implications of NT-proBNP measured on admission in patients with the ST-elevation myocardial infarction (STEMI) are not so far well elucidated. The present investigation, performed in 198 STEMI patients submitted to percutaneous coronary intervention (PCI), was aimed at assessing the prognostic value of NT-proBNP measured on admission to Intensive Cardiac Care Unit (ICCU) and its relation with the extension of myocardial infarction (indicated by cardiac biomarkers and ejection fraction) and inflammatory markers (C-reactive protein - CRP, erythrocyte sedimentation rate - ESR, leucocytes, fibrinogen). All patients who died during ICCU stay had increased values of NT-proBNP. Each quartile of NT-proBNP resulted directly correlated with age, heart rate, peak Tn I, admission creatinine serum levels, ESR, fibrinogen, and inversely correlated with ejection fraction. At backward logistic regression analysis, NT-proBNP values showed a significative correlation with peak Tn I (OR 1.013; 95% CI 1.001-1.025; p=0.036), and CRP positive (OR 6.450; 95% CI 1.714-24.272; p=0.006); age was close to reaching statistical significance (OR 1.043; 95% CI 0.999-1.089; p=0.055). At long term-follow-up NT-proBNP lacks any prognostic role in predicting adverse events such as hospitalization for rePCI, re-infarction and heart failure. Kaplan-Meier curves showed that all patients dead at follow-up were in the highest NT-proBNP quartiles.
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PMID:NT-proBNP on admission for early risk stratification in STEMI patients submitted to PCI. Relation with extension of STEMI and inflammatory markers. 1820 87

Vertebral osteomyelitis is a rare entity. Its diagnosis is often difficult because of nonspecific symptons and the high frequency of back pain in general population. Aetiologic diagnosis is essential in order to perform specific treatment. Thus, blood cultures, serology, and culture of samples obtained by bone biopsy are the basis of the diagnosis. Magnetic resonance imaging permits an accurate diagnosis showing neurological involvement when it is present. ESR and CRP are good outcome markers. Endocarditis must be suspected in patients with predisposing heart condition, heart failure, positive blood cultures and infectyions caused by gram-positive organisms. Indications of surgery are severe neurological involvement, spinal instability and drainage of big abscesses. In Spain, as well as bacteria, we should consider M. tuberculosis, B. melitensis, and fungi as a potential aetiologic agents causing the infection.
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PMID:[Infectious spondylodiskitis]. 2179 58


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