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

A pressure-overload model in the rat by banding the pulmonary trunk (PT) was developed to investigate alterations in gene expression in left- and right-ventricular compartments during the transition from compensated right-ventricular (RV) hypertrophy to right heart failure. Right heart failure in rat is characterized by liver cirrhosis, hydrothorax and ascites. The diameter of constriction was found to determine the time course of heart failure development. Only the RV free wall and the right atrium increased in weight, without a difference between compensated and failing RV. An increase in circulating ANP revealed a hypertrophic response of the myocardium, while increased circulating ammonia levels discriminated between compensated hypertrophy and failure. As parameters for stress, fibrosis and Ca2+-handling, changes in the pattern and level of the mRNAs encoding atrial natriuretic peptide (ANP), collagenIIIalpha1, and sarcoplasmic endoplasmic reticular calcium ATPase 2 (SERCA2), phospholamban (PLB) and calsequestrin (CSQ) were studied by Northern blot and in situ hybridization analyses. Pulmonary trunk banding resulted in an induction of ANP mRNA, a moderate increase in collagenIII alpha1 mRNA and a decrease in SERCA2 and PLB mRNA levels in both the left and right ventricles, but changes were most pronounced in the myocardium surrounding the RV cavity. Increased ammonia blood levels are a promising prognostic marker to detect the development of right heart failure.
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PMID:Changing patterns of gene expression in the pulmonary trunk-banded rat heart. 976 42

Clinical course of infectious endocarditis (IE) was analysed for 43 intravenous drug abusers. 42 of them had primary IE, one patient--secondary. Acute course and high activity of the disease were registered in 86% of the patients. IE was provoked by Staphylococcus aureus (50%), Staphylococcus epidermidis 920%), Staphylococcus haemolyticus (11%), E. coli (8%), Pseudomonas aeruginosa (2%), Candida albicans (2%), mixed microflora (7%). Vegetations were detected on the tricuspid, mitral and aortic valves (52, 23 and 19%, respectively), on more than one valve (6%). Pneumonia, pleuricy, hydrothorax, enlargement of the liver, spleen, nephritis and anemia were found in 76, 44, 9, 100, 75, 70 and 88% of the patients, respectively. Cardiac failure aggravated the disease in half of the patients, lethality was 18%. Thus, IE in intravenous drug abusers is characterized by a primary form, acute active course, prevalent damage to the tricuspid valve, polyorganic involvement, high lethality. IE cure in such patients is feasible only in adequate antibacterial therapy, timely surgical correction and giving up drug abuse.
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PMID:[Infectious endocarditis in intravenous drug abusers]. 1101 26

The prognosis of a fetus with hydrothorax at mid-trimester is extremely poor. We encountered a fetus who developed bilateral chylothoraxes at 23 weeks of gestation. Bilateral pleuroamniotic shunts with double-basket catheters were successfully installed at 25 weeks of gestation. Hydrothorax did not recur in this fetus. After the shunting, however, polyhydroamnios, fetal hypoproteinemia, and placental edema developed, and the hydrops worsened. The drainage of the fetal pleural effusion into the amniotic cavity was believed to have contributed to these complications. The infant, born at 29 weeks of gestation, died of cardiac failure and pulmonary hypoplasia. Thus, the shunts did not ameliorate the adverse conditions in this patient.
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PMID:Severe hypoproteinemia in a fetus after pleuro-amniotic shunts with double-basket catheters for treatment of chylothorax. 1114 26

Increased angiotensin II signaling in the brain has been shown to play a critical role in the excessive sympathoexcitation and development of heart failure (HF) after myocardial infarction (MI). We have recently demonstrated that reactive oxygen species mediate the actions of angiotensin II in the brain. In this study, we tested the hypothesis that increased redox signaling in central cardiovascular control regions is a key mechanism in the neurocardiovascular dysregulation that follows MI. Ligation of the left coronary artery induced a large MI and subsequent HF in adult C57BL/6 mice, as demonstrated by cardiac hypertrophy, hydrothorax, and ascites. Immunohistochemical analysis of Fos, a marker of neuronal activation, revealed a significant increase in the number of Fos-positive neurons in the paraventricular nucleus and supraoptic nucleus at 2 and 4 weeks after MI compared with sham mice. Intracerebroventricular injection of an adenoviral vector encoding superoxide dismutase (Ad-Cu/ZnSOD) caused a significant decrease in the number of Fos-positive neurons in the paraventricular nucleus and supraoptic nucleus at 2 weeks after MI compared with mice receiving either saline or a control vector (Ad-LacZ). There was also a diminished role of sympathetic drive in post-MI mice treated centrally with Ad-Cu/ZnSOD, as demonstrated by significantly attenuated falls in heart rate and mean arterial pressure to the ganglionic blocker hexamethonium and decreased urinary norepinephrine levels in these mice compared with Ad-LacZ-treated MI mice. These results suggest that superoxide plays a key role in the central activation and sympathetic hyperactivity after MI in mice and that oxygen radicals in the brain may be important new targets for therapeutic treatment of heart failure.
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PMID:Superoxide is involved in the central nervous system activation and sympathoexcitation of myocardial infarction-induced heart failure. 1468 26

Common models of chronic heart failure (CHF) do not always result in parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure. The aim of this study was to establish and validate a new model of CHF in the rat. CHF was induced in Wistar Kyoto (WKY/NHsd) and spontaneously hypertensive (SHR/NHsd) rats by creating a permanent (8-week) occlusion of the left coronary artery 2 mm distal to the origin from the aorta by a modified technique. This resulted in a large infarction of the free left ventricular wall. The focus of attention was the validation of the geometric properties of the left ventricle and its contractility. The validation of the geometric properties of the left ventricle was done by a non-invasive magnetic resonance imaging (MRI) technique and by planimetry (stereology). Cardiodynamics (e.g. contractility) were evaluated in the isolated 'working heart' model. We were able to establish a new and predictive model of heart failure in the spontaneously hypertensive rat 8 weeks after coronary artery ligation. At this time point, the WKY rat did not show any symptoms of CHF. The model represents characteristic parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure (NYHA III-IV). Upon inspection, severe clinical symptoms of congestive heart failure were prominent, such as dyspnoea, subcutaneous oedema, pale-bluish limbs and impaired motion. Non-invasive sequential measurements by NMR techniques showed lung oedema, hydrothorax, large dilated left and right ventricular chambers and hypertrophy of the septum. The infarcted animals showed a reduced heart power, diminished contractility and enhanced heart work, much more so in the SHR/NHsd rat than in the WKY/NHsd rat. Furthermore the infarcted animals showed enhanced levels of hydroxyproline/proline ratios, again much more so in the SHR/NHsd rat than in the WKY/NHsd rat.
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PMID:A model of chronic heart failure in spontaneous hypertensive rats (SHR). 1507 Apr 53

Dilated cardiomyopathy is a primary disease of the heart muscle that has been reported in Holstein-Friesian cattle worldwide in the past 20 years. Nine cases of the condition were compared in terms of their clinical and pathological characteristics with nine unaffected animals matched for age, sex and breed. Their clinical signs included right-sided heart failure with severe subcutaneous oedema, ascites and/or hydrothorax and distended jugular veins. There were no characteristic biochemical or haematological changes. Postmortem, the affected hearts were enlarged with all the chambers dilated and walls of variable thickness. In most cases the kidneys were pale with a pitted surface. Histologically there was marked perimysial and endomysial fibrosis, extensive loss of cardiomyocytes by coagulative or colliquative necrosis, increased variation in the cross-sectional area of the myocardial fibres, and multifocal disarray and vacuolation of myocytes. Scanning electron microscopy showed that in all cases there was a mild myocardial inflammatory infiltrate, either diffuse or multifocal, which was identified by immunohistochemical labelling as T cells.
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PMID:Clinical and pathological features of dilated cardiomyopathy in Holstein-Friesian cattle. 1549 3

Congestive heart failure (CHF) is one of the most common causes of death in western countries. The aim of this study was to establish and validate the working heart model in rat hearts with CHF. In the rat model the animals show parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure. The focus of attention was the evaluation of cardiodynamics (e.g.contractility) in the isolated 'working heart' model. The geometric properties of the left ventricle were measured by planimetry (stereology). Formulae available in the past for determining certain parameters in the working heart model (e.g.external heart work) have to be fitted to the circumstances of the infarcted rat hearts with its different organ properties.CHF was induced in Wistar Kyoto (WKY/NHsd) and spontaneously hypertensive rats (SHR/NHsd) by creating a permanent (8 week) occlusion of the left coronary artery, 2 mm distal to the origin from the aorta, by a modified technique (Itter et al. 2004). This resulted in a large infarction of the free left ventricular wall. We were able to establish and adapt a new and predictive working heart model in spontaneously hypertensive rat hearts with myocardial infarction (MI) 8-12 weeks after coronary artery ligation. At this stage the WKY rat did not show any symptoms of CHF. The SHR rat represented characteristic parameters and symptoms that could be extrapolated to the clinical situation of patients with end-stage heart failure (NYHA III-IV). Upon inspection, severe clinical symptoms of CHF such as dyspnoea, subcutaneous oedema, palebluish limbs and impaired motion were prominent. On necropsy the SHR showed lung oedema, hydrothorax, large dilated left and right ventricular chambers and hypertrophy of the septum. In the working heart model the infarcted animals showed reduced heart power, diminished contractility and enhanced heart work, much more so in the SHR/NHsd than in the Wistar Kyoto rat (WKY/NHsd). The aim for the future is to find a causal therapy of heart failure treatment. At present, only palliative therapy is possible for patients with heart failure. For this reason the working heart model in CHF rat hearts should provide a valuable method for early testing of new therapeutic approaches for patients with CHF.
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PMID:The isolated working heart model in infarcted rat hearts. 1590 61

We report an extremely rare case of pseudo-Meigs' syndrome caused by a retroperitoneal tumor in a patient with Ebstein anomaly. A 60-year-old woman was admitted because of marked hydrothorax and ascites. She also had pleural effusion. Because echocardiography revealed Ebstein anomaly, medical treatment was performed, under the diagnosis of heart failure. However, her pleural effusion and ascites did not completely disappear. Computed tomography (CT) scan showed a round solid retroperitoneal pelvic mass, with a diameter of approximately 5 cm in the vesicouterine fossa. After resection of the tumor, which was histologically found to be fibroma, her pleural effusion and ascites disappeared.
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PMID:Pseudo-Meigs' syndrome caused by retroperitoneal tumor in a patient with Ebstein anomaly. 1613 73

Concurrent infection with bovine leukaemia virus (BLV) and Theileria annulata was diagnosed in a Friesian calf about 6 months of age at a dairy farm at the Qassim region of central Saudi Arabia. The disease ended fatally with signs of liver and heart failure. There was anorexia, pyrexia, anaemia, generalized oedema and jaundice. Haematology showed low RBC counts, PCV percentage and haemoglobin concentration and WBC counts. Lymphocyte differential was high. Examination of blood smears stained with Giemsa's stain showed the presence of piroplasms in red blood cells. Autopsy showed enlarged lymph nodes and lymphosarcoma lesions in the omentum and the heart. There was hydroperitoneum, hydropericardium and hydrothorax. The liver was pale yellow and friable. Impression smears from sliced lymph nodes and stained with Giemsa's stain showed presence of Koch's blue bodies in lymphoblasts. Histopathological examination revealed fatty degeneration of hepatocytes and pleomorphic lymphoblasts and giant cells in lymph nodes. Lymphoblasts infiltrated the omentum and heart tissues. Amyloid was found around blood vessels in the liver, kidneys and lymph nodes. BVL infection was diagnosed by demonstrating antibodies against the virus in serum using agar gel immunodiffusion and was confirmed with ELISA.
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PMID:Concurrent infection with bovine leukaemia virus and Theileria annulata in a Friesian calf. 1831 46

A 28-year-old woman was diagnosed by transvaginal ultrasound at 9+6 weeks with early fetal cardiac failure (hydrothorax and bradycardia). Doppler analysis of ductus venosus showed a negative A-wave pattern. The follow-up sonogram obtained at 11+6 weeks documented a missed abortion. A transvaginal ultrasound-guided coelocentesis was performed under local cervical anesthesia before uterine suction and 8 mL of clear extracoelomic fluid were successfully aspirated. Cytogenetic analysis demonstrated a 45,X karyotype. Ultrasound and Doppler waveform analysis of ductus venosus allowed early diagnosis of fetal cardiac failure. Coelocentesis may be the method of choice for early fetal karyotyping and may be used in the future to induce immunologic tolerance.
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PMID:Early detection (9+6 weeks) of cardiac failure in a fetus diagnosed as Turner syndrome by 2D transvaginal ultrasound-guided coelocentesis. 1933 87


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