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)

Cardiomyopathic hamsters (UM-X7.1) show clinical signs of congestive heart failure and an abnormal EKG pattern. The sarcolemmal fraction obtained from the failing hearts at advanced stages of myopathy exhibited no change in the basal adenylate cyclase activity; however, the activity of this enzyme in the presence of catecholamines or NaF was lower in the failing heart sarcolemma than that in the control. The activities of Ca2+-ATPase, Mg2+-ATPase, and Na+-K+-ATPase in the failing heart sarcolemma were also less than the control values. These results suggest an association of membrane defect with heart failure.
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PMID:Membrane alteration in failing hearts of cardiomyopathic hamsters. 12 77

A patient with the hungry bone syndrome following parathyroidectomy for hyperparathyroidism developed congestive heart failure, probably due to the myocardial depressant effects of hypocalcemia and hypomagnesmia. Calcium and magnesium alone were instrumental in relieving his symptoms, decreasing his heart size, and clearing the pulmonary congestion. A mechanism for the pathogenesis of hypocalcemia and hypomagnesemia induced heart failure is proposed.
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PMID:Case report. Congestive heart failure complicating the hungry bone syndrome. 13 Aug 1

A 45-year-old woman with congestive heart failure, in whom there was no evidence of coronary heart disease, valve disease, or other demonstrable cause of heart failure, was found to have taken high doses of dextroamphetamine over a long period. Withdrawal of amphetamine resulted in deterioration, suggesting a physical cardiac dependence on the drug. The clinical and autopsy findings are presented and the similarities to the myocarditis associated with pheochromocytoma are discussed. The evidence presented suggests a causal relationship between administration of dextroamphetamine and the cardiomyopathy.
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PMID:Cardiomyopathy associated with amphetamine administration. 13 14

Three patients with interruption and seven with hypoplasia of the aortic arch were treated surgically. The subclavian artery and the aortic isthmus were employed for reconstructing the aortic arch in five, and a Dacron prosthesis was used to restore the aortic continuity in five. A ductus arteriosus coexisted in all patients and a ventricular or atrial septal defect in nine. Congestive heart failure and pulmonary hypertension were prominent clinical features, and the role of the ductus and other intracardiac anomalies on their pathogenesis in discussed. Six patients, one with an interrupted and five with a hypoplastic arch survived but three have evidence of either pulmonary vascular disease or significant pulmonary hypertension. Only one patient with hypoplasia of the arch is now considered cured after his ventricular septal defect was closed in a second operation. The analysis of this and other series in the literature indicate a high mortality rate of the conditions; however, early surgical treatment, which is the only effective means to control heart failure and avoid the effects of prolonged pulmonary hypertension, has brought upon a decline in mortality in recent years.
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PMID:[Surgical treatment of congenital interruption and hypoplasia of the aortic arch]. 13 70

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.
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PMID:Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. 13 86

The Ca2+-activated myosin ATPase and the amino acid compositions of actin and myosin were determined for preparations from chronically failing dog hearts. Hypertrophy and congestive heart failure were produced by combined tricuspid valve insufficiency and pulmonary artery stenosis. Control, shamoperated, and noncardiac circulatory failure (inferior vena cava constriction) dogs also were studied. All hearts were divided into right ventricle, septum and left ventricle and each sample was individually analyzed. Calcium-activated ATPase decreased in the failing hearts and showed a distinct gradient of depression from right to left ventricles. There were no changes in ATPase activity among the other groups. The amino acid composition of actin was the same regardless of origin. The amino acid composition of myosin was unaltered except that cystine/2 residues were markedly decreased in failing heart myosin. The same gradient of depression was present as was found for Ca2+-activated myosin ATPase. This study suggests that protein metabolism is abnormal and that altered proteins are produced in hypertrophy and congestive heart failure. It appears that these changes do not affect all proteins, since actin was normal by the parameters studied. It is clear that the stressed ventricle is the most severely involved, but the entire heart is altered to some degree. Thus, we conclude that altered protein metabolism may be an important primary factor in the genesis of heart failure.
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PMID:The amino acid composition of actin and myosin and Ca2+-activated myosin adenosine triphosphatase in chronic canine congestive heart failure. 13 12

To determine whether haemodynamic effective support of the failing heart can prevent spontaneous irreversible ventricular fibrillation (IVF) after experimental cardiogenic shock, 63 open chest dogs were assigned randomly into four groups--two control groups (combined heart failure--CHF) and two MCHSS-treated (combined heart failure and non-pulsatile bypass with intraaortic counterpulsation). The CHF was produced by occlusion of the anterior descending coronary artery (group I) or the left circumflex coronary artery (group II) and by an artificial shunt between the pulmonary artery and right atrium. IVF were observed in 10 out of 22 control dogs (group I) and im 17 out of 21 control dogs (group II). In the 20 dogs with the CHF (10 animals in each group) the MCHSS was performed in the course of two hours. During the heart support no IVF were observed in any of the dogs. The difference between the incidence of IVF in the control and treated animals is statistically significant (Chi square = 21.9767 greater than Chi square 0.005).
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PMID:Mechanical combined heart supporting system for prevention of irreversible ventricular fibrillation after experimental cardiogenic shock. 14 Mar 92

Clinical and necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.
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PMID:Hypertrophic cardiomyopathy in the dog. 15 45

Management of symptomatic atrioventricular canal (AVC) in infancy may be difficult. Between July, 1969, and September, 1977, 31 infants with complete AVC presented in congestive heart failure (CHF) to the University of Minnesota Hospitals. Fifteen of these patients have responded to medical management and have been followed as outpatients. The other 16 patients remained in CHF. Six of them died of persistent heart failure within 4 months. The other 10 infants, aged 3 weeks to 1 year (mean 4 months), underwent pulmonary artery banding and seven survived operation. One of the survivors died with apparent pneumonia 1 month postoperatively. Each of the remaining six patients, who have been followed for 9 months to 9 years, had minimal mitral insufficiency and a large ventricular shunt. The three patients dying after banding had significant mitral insufficiency. We believe that pulmonary artery banding is an effective palliative procedure for infants with complete AVC and CHF who have large ventricular shunts and minimal mitral insufficiency.
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PMID:Pulmonary artery banding in infants with complete atrioventricular canal. 15 89

Recordings were made from left atrial type B receptors in six mongrel dogs after recovery from the cardiac effects of a chronic AV fistula. All animals showed hemodynamic and clinical signs of congestive heart failure after 44.5 +/- 3.6 days with a patent Dacron shunt between the aorta and inferior vena cava below the level of the renal arteries. The stimulus-response curves of the left atrial stretch receptors (change in spikes/cardiac cycle or in spikes/minute vs. change in left atrial pressure) after 45.2 +/- 7.2 days of shunt closure were similar to those seen in sham-operated dogs from a previous study. However, the slope of the stimulus-response curve of the dogs in which the AV fistula was closed was significantly greater than the slope of the curve from the AV fistula dogs with heart failure. Radiographs indicated that after shunt closure, cardiac dilatation had regressed. This study incidates that a decrease in the sensitivity of left atrial receptors in dogs with congestive heart failure is a reversible phenomenon and that the initial depression is most likely related to the concomitant cardiac dilatation that accompanies the failure state.
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PMID:Changes in the sensitivity of left atrial receptors following reversal of heart failure. 15 85


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