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 Medical Patients with Enoxaparin (MEDENOX) trial was a randomized, placebo-controlled study that defined the risk of venous thromboembolism (VTE) in acutely ill, immobilized, general medical patients and the efficacy of the low-molecular-weight heparin, enoxaparin, in preventing thrombosis. We performed a post-hoc analysis to evaluate the effect of 40 mg enoxaparin once daily on MEDENOX patient outcome in different types of acute medical illness (heart failure, respiratory failure, infection, rheumatic disorder and inflammatory bowel disease) and pre-defined risk factors (chronic heart and chronic respiratory failure, age, immobility, previous VTE and cancer). The primary outcome was the occurrence of documented VTE between days 1 and 14. The relative risk reduction [95% confidence intervals (CI)] for VTE comparing 40 mg enoxaparin with placebo in the subgroups were: acute heart failure, 0.29 (95% CI, 0.10-0.84); acute respiratory failure, 0.25 (95% CI, 0.10-0.65); acute infectious disease, 0.28 (95% CI, 0.09-0.81); and acute rheumatic disorder, 0.48 (95% CI, 0.11-2.16). The relative risk reduction for VTE in the pre-defined risk factor subgroups were: chronic heart failure, 0.26 (95% CI, 0.08-0.92); chronic respiratory failure, 0.26 (95% CI, 0.10-0.68); age, 0.22 (95% CI, 0.09-0.51); immobility, 0.53 (95% CI, 0.14-1.72); previous VTE, 0.49 (95% CI, 0.15-1.68); and cancer, 0.50 (95%o CI, 0.14-1.72). The beneficial effects of enoxaparin extend to a wide range of acutely ill medical patients.
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PMID:Prevention of venous thromboembolism in medical patients with enoxaparin: a subgroup analysis of the MEDENOX study. 1294 75

Myocarditis may result from a wide variety of acute infectious diseases, but electrocardiographic abnormalities interpreted as indicating myocarditis may arise from a number of other causes. Among the factors which may cause myocarditis are direct invasion by an organism, the toxic products of an organism, hypersensitivity to the products of an organism, drugs used in therapy, deficiency in nutrients, electrolyte imbalance, and, rarely, fever. Recently emphasis has been placed on the finding that circulatory failure in acute infectious diseases is often primarily peripheral, although heart failure due to myocarditis is not uncommon.
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PMID:The cardiovascular system in acute infectious disease. 1309 45

We recently showed that angiotensin (ANG) II as well as mechanical stretch stimulated production of tumor necrosis factor (TNF) in cardiac fibroblasts. Presently, we examined the molecular mechanisms by which ANGII and lipopolysaccharide (LPS) upregulate TNF-alpha gene expression. In neonatal rat cardiac fibroblasts, increased transcription of TNF-alpha mRNA was detected as luciferase activity associated with activity of the TNF-alpha promoter. Progressive deletion from this promoter located the LPS-responsive region between -200 and -120 bp from the transcription initiation site, while the sequence between -120 and -70 bp was required for ANGII-induced expression. Next, we examined which cis-acting sequences in the TNF-alpha promoter region were essential for induction of TNF-alpha transcription. Competition analysis by electrophoretic mobility shift assay with and without specific antibodies showed that LPS increased binding of Sp1 and Sp3 to the Sp1-binding site, while Egr-1 was unimportant. With ANGII, binding of ATF-2/c-jun to the CRE site was required for TNF-alpha gene induction; neither Ets nor NF-kappaB was essential. Mutation analysis confirmed that response to LPS relied upon the Sp1 site in the TNF-alpha promoter, while the CRE-binding site was essential for stimulation by ANGII. We concluded that since TNF-alpha gene expression is transcriptionally activated by ANGII or LPS in cardiac fibroblasts via different cis-acting sequences in the TNF-alpha promoter and different transcriptional factors, mechanisms inducing TNF production differ between heart failure or cardiac hypertrophy and infectious disease.
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PMID:Regulation of the human tumor necrosis factor-alpha promoter by angiotensin II and lipopolysaccharide in cardiac fibroblasts: different cis-acting promoter sequences and transcriptional factors. 1451 26

Parvovirus infection during pregnancy is an important cause of hydrops fetalis. It is attributed to anemia caused by viral-induced destruction of red blood cells. Infection of other organs has been reported including the heart, liver, and lungs. Few of these reports, however, convincingly demonstrate virions within the functional parenchyma of the tissue. This is of particular concern regarding myocardium in the context of hydrops fetalis which is, in part, due to cardiac failure. The problem in routine pathology practice is that most fetuses with the infection are macerated. This, in part, probably explains the paucity of published information on cardiac involvement. This study examined five cases of fatal hydrops fetalis with variable maceration with serologically proven parvovirus B19 infection. Transmission electron microscopy of cardiac tissue demonstrated intranuclear virions in both erythroid precursor cells and in cardiac myocytes in three of these cases. In each of these, immuno-gold electron microscopy provided confirmatory evidence of parvovirus infection. Virions were not identifiable where maceration had caused disintegration of nuclei in the myocytes. In addition, virions were absent in the three negative control cases where retroplacental hemorrhage was confirmed as the cause of death. This study suggests that parvovirus infection of cardiac myocytes may play a more important role in causing hydrops fetalis than previously realized. It also demonstrates that maceration should not discourage the use of electron microscopy.
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PMID:Parvovirus infects cardiac myocytes in hydrops fetalis. 1470 34

Blood culture is a key investigation for the diagnosis of infectious endocarditis (IE). When negative, there are diagnostic and therapeutic problems. The aim of this study was to determine the frequency, the clinical features and the aetiological factors of IE with negative blood cultures compared with IE with positive blood cultures compared with IE with positive blood cultures. The authors undertook a retrospective review of 98 cases of patients admitted for IE from 1991 to 2000 to the Department of Infectious Diseases and Cardiology of Sousse (Tunisia). Of the 98 patients, 48 (48.9%), 29 men and 19 women with an average age of 34.3 years, had negative blood cultures. An infectious agent was identified in 7 cases (14.5%) by serology, valve culture or cerebrospinal fluid including Brucella (2), Coxiella (1) and Candida (1). Therefore, in 41 cases (42%), the cause of IE was not determined. Transthoracic echocardiography was of diagnostic value in 96% of cases and transoesophageal echocardiography showed disease not observed on transthoracic echocardiography in 5 cases. The main complication was cardiac failure (27 cases). The mortality was 14.5%. Comparison of the two groups showed that negative blood cultures were associated with a higher incidence of previous antibiotic therapy, extracardiac signs of IE and cardiac failure. Early surgical indications and mortality were the same in both groups. This report confirmed the high frequency of IE with negative blood cultures. Previous antibiotic therapy seems to be an important aetiological factor but cannot explain this high frequency. Methodological problems of blood cultures and the absence of systematic investigation for rare infectious agents are other possible factors.
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PMID:[Infectious endocarditis with negative blood cultures]. 1503 11

Air passenger miles will likely double by year 2020. The altered and restrictive environment in an airliner cabin can influence haematological homeostasis in passengers and crew. Flight-related deep venous thromboemboli (DVT) have been associated with at least 577 deaths on 42 of 120 airlines from 1977 to 1984 (25 deaths/million departures), whereas many such cases go unreported. However, there are four major factors that could influence formation of possible flight-induced DVT: sleeping accommodations (via sitting immobilisation); travellers' medical history (via tissue injury); cabin environmental factors (via lower partial pressure of oxygen and lower relative humidity); and the more encompassing chair-rest deconditioning (C-RD) syndrome. There is ample evidence that recent injury and surgery (especially in deconditioned hospitalised patients) facilitate thrombophlebitis and formation of DVT that may be exacerbated by the immobilisation of prolonged air travel. In the healthy flying population, immobilisation factors associated with prolonged (>5 hours) C-RD such as total body dehydration, hypovolaemia and increased blood viscosity, and reduced venous blood flow (pooling) in the legs may facilitate formation of DVT. However, data from at least four case-controlled epidemiological studies did not confirm a direct causative relationship between air travel and DVT, but factors such as a history of vascular thromboemboli, venous insufficiency, chronic heart failure, obesity, immobile standing position, more than three pregnancies, infectious disease, long-distance travel, muscular trauma and violent physical effort were significantly more frequent in DVT patients than in controls. Thus, there is no clear, direct evidence yet that prolonged sitting in airliner seats, or prolonged experimental chair-rest or bed-rest deconditioning treatments cause DVT in healthy people.
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PMID:Airline chair-rest deconditioning: induction of immobilisation thromboemboli? 1545 46

A passive implantable device developed for the treatment of heart failure, the Myosplint System, has demonstrated therapeutic efficacy in a canine model of pacing induced heart failure. The current study sought to demonstrate chronic device safety and biocompatibility, in vivo, in a normal porcine model. Two devices were implanted into each normal, beating heart of 6 juvenile and 15 adult pigs without cardiopulmonary bypass. Animals survived 90 (juvenile and adult) or 180 days (adult only). Serial hematologic and biochemical profiles were evaluated in each pig during the study period. A comprehensive necropsy study was performed in each pig to evaluate device stability, healing response, thromboembolism, hemorrhage, and intravascular hemolysis related to the Myosplint system. Six adult animals died from infectious disease (four) or perioperative (two) complications unrelated to device design or function and were excluded from the final analysis. No clinical, biochemical or pathologic evidence of significant, device related adverse events was observed in surviving animals. The chronic myocardial healing response appeared normal at term, and all devices maintained their structural integrity throughout the study. The Myosplint system was easily implanted in beating hearts and was rapidly incorporated into host tissues without clinically significant morbidity in this porcine model.
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PMID:Safety and biocompatibility of the Myosplint system--a passive implantable device that alters ventricular geometry for the treatment of heart failure. 1549 82

Clinical toxoplasmosis is commonly reported in the cat, with the most consistent findings being ocular, pulmonic, hepatic, neurological, gastrointestinal and muscular abnormalities. Myocarditis, whilst frequently identified at post-mortem examination, has not been identified ante-mortem. In immunocompromised humans, myocarditis associated with toxoplasmosis is not an uncommon complication. In such cases, lymphocytic myocardial infiltration can lead to depressed myocardial function, which can be associated with congestive heart failure, rhythm disturbances and pericardial effusions. In addition, myocardial failure has been reported in immunocompetent humans associated with active toxoplasmosis [Chandenier J, Jarry G, Nassif D, Douadi Y, Paris L, Thulliez P, Bourges-Petit E, Raccurt C (2000) Congestive heart failure and myocarditis after seroconversion for toxoplasmosis in two immunocompetent patients. European Journal of Clinical Microbiological Infectious Disease 19, 375-379]. Here we describe a cat with echocardiographic changes consistent with infiltrative or inflammatory disease, and elevated IgG and IgM titres to Toxoplasma gondii. There was resolution of these myocardial changes once the toxoplasmosis was treated.
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PMID:Suspected toxoplasma-associated myocarditis in a cat. 1592 27

Emergent mechanical support for the failing ventricle, with eventual transfer for definitive care, is often required at non-transplant centers. Transfer for definitive care, in terms of bridge to transplant, may require ventricular assist device (VAD) placement at the primary institution or at the transplant center. Review of consecutive single transplant center referrals was conducted to decipher optimal management. From January 1997 to December 2000, 104 patients were transferred to the University of Pennsylvania Heart Failure/Transplant Service. Most were transferred from active cardiac surgical programs, with 56 patients having post-cardiotomy failure at the primary site. A VAD was placed in procedures done at the outside hospital (OSH) in 28 patients, most commonly (60%) an Abiomed device. Of the 76 patients that received a VAD at the transplant center (TxpC), 86% received a TCI or Thoratec device. Biventricular support was required in 34 patients. Overall survival was 57%, with 54 patients bridged to transplantation and 5 patients undergoing recovery. Patients having a VAD placed at the OSH had a 32% (9 of 28) survival, whereas at the TxpC survival was 65% (45 of 76) (p < 0.05). Mid-term follow-up showed that all 5 patients weaned are presently alive, and 52 patients are alive at >1-year post-transplant. The most common cause of death was multi-system organ failure (19 of 45), followed by major neurologic event (15 of 45). Infection was the cause of death in only 6 patients. Left ventricular failure can be treated by emergent VAD placement. Overall survival is substantial if these patients are referred to a transplant center with multiple options. In contrast to previous reports, survival rates may be improved by earlier referral, before VAD placement at non-transplant centers and use of a VAD with longer-term capability.
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PMID:Emergent mechanical support in the community: improvement with early transplant center referral. 1594 38

Endocarditis produced by Erysipelothrix rhusiopathiae is an uncommon disease in humans. This bacterial species is found worldwide as a commensal or a pathogen in many animals. Infection in humans is usually due to occupational exposure. The case is reported of a 43-year-old male parrot breeder with native aortic and mitral valve endocarditis and NYHA class II heart failure at six months after wound infection. The patient was discharged after six weeks' treatment with intravenous penicillin G and replacement of the mitral and aortic valves due to severe regurgitation. At one year after surgery the patient was asymptomatic and infection-free.
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PMID:Mitro-aortic infective endocarditis produced by Erysipelothrix rhusiopathiae: case report and review of the literature. 1597 25


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