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

In patients with heart failure there are distinct functional abnormalities in the myocytes themselves. This review deals with the deteriorations in the myocardial energy metabolism and the recently found alterations in the neurohumoral and hormonal signal transduction and signal realization within the cardiac cells. Beside the reduction in the volume of mitochondria in the overloaded myocardium the energy starvation is also reflected by a decrease in the content of high energy phosphates. Studies on nonfailing and failing human ventricular myocardium identified significant alterations in the neurohumoral regulation of the heart including the fluxes and the transport processes of Ca2+ as well as the beta-adrenoceptors, G-proteins, cAMP levels and cAMP-mediated processes. Recent data on the existence of auto-antibodies against the ADP/ATP translocator of the mitochondrial membrane and of stimulatory acting autoantibodies against i) the L-type calcium channel and ii) the beta 1-adrenoceptor, respectively, in patients with dilated cardiomyopathy, may open a new view in the etiology of heart failure and for consequences in the therapeutic concept of these diseases.
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PMID:[Cellular and molecular mechanisms in heart failure]. 172 87

It is well appreciated that theophylline pharmacokinetics exhibits wide intersubject variation. Within-subject changes in clearance have been generally reported in patients with acute exacerbations of disease states such as cor pulmonale or heart failure. Apparent random changes in theophylline clearance within the same patient have recently been reported. This report describes a case of suspected changes in the clearance of theophylline in a morbidly obese patient (250 kg) over a two-month period of time. Frequent dosage adjustments were required to maintain theophylline concentrations within the range of 8.2 to 27.3 micrograms/ml. Possible explanations for these changes included hypoxia and medically induced starvation. Daily theophylline doses ranged from 600 to 1600 mg/d. It is concluded that in some individuals, within-subject changes in theophylline clearance can be substantial, thus requiring frequent monitoring of theophylline concentration.
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PMID:Intrasubject variability of theophylline clearance in a morbidly obese patient. 378 Apr 17

In most patients with heart failure, an imbalance between energy production and energy utilization leads to a state of chronic energy starvation. This imbalance is due both to increased energy demands caused by overloading of myocardial cells in the failing heart, and to a decreased energy supply caused by reduced perfusion, altered cell architecture, and molecular changes in the hypertrophied heart. Energy starvation has important therapeutic implications in the failing heart. Because the systems that relax the heart are especially sensitive to energetic state, inotropic agents could exacerbate relaxation abnormalities and promote arrhythmias. More important is the likelihood that inotropic agents, which increase cardiac energy expenditure, accelerate cell damage and so worsen prognosis in this condition. Vasodilators and negative inotropic agents, on the other hand, by decreasing energy utilization should improve the balance between energy delivery and energy expenditure in the failing heart.
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PMID:Mechanisms and abnormalities of contractility and relaxation in the failing heart. 802 41

The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.
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PMID:Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. 824 97

Our understanding of the pathogenesis and therapy of heart failure has evolved through three paradigms. Organ physiology, the first paradigm, focused therapy of heart failure on salt and water retention and vasoconstriction, which represent major circulatory responses to, cardiac pumping. The second paradigm of cell biochemistry led to the development of powerful inotropic agents designed to increase myocardial contractility. The third paradigm, gene expression (molecular biology), describes regulatory mechanisms that are both primitive and complex; in the setting of heart failure, this paradigm focuses on the roles of altered myocardial cell growth and composition in explaining the accelerated deterioration of the hypertrophied, failing heart. This review focuses on one aspect of the second paradigm: factors that contribute to a state of energy-starvation and the resulting functional consequences in the failing heart.
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PMID:Metabolism of the failing heart. 829 61

Preweaning losses: During the period from September 1991 to August 1992, from 18021 piglets born alive 3417 died until weaning. Major causes of death were crushing by the sow, low birth weight, starvation, splay-leg disease and enteritis. Of these animals 51.6% died during the first three days of life. Mortality decreased during the preweaning period. Litters with more than 11 pigs had elevated death rates of piglets. Mortality was higher during the cold season (except January). Postweaning losses: During the postweaning period 6.4% of the weaned piglets were lost. Of these piglets 4.1% died and the remaining 2.3% were sold due to umbilical hernia. Diseases of the gastrointestinal tract were the main cause of death. Losses of gilts: During the one-year surveillance period 373 gilts were lost. Most of 18 deceased animals died from bleeding due to gastric ulcers and from purulent bronchopneumonia. 314 (91.1%) of the remaining 355 gilts were sold, the residual 9.9% of the animals were slaughtered mainly because of diseases of the musculoskeletal system. Losses of sows: In the breeding herd of 950 to 1035 animals, 35 sows died and 492 were culled in the course of one year. Most deaths resulted from cardiac failure and splenic torsion. Urogenital and locomotor diseases were the main reason for culling. The sows removed from the herd had produced an average of 3.6 litters, but 52.8% had produced no more than 3 litters. Losses of boars: During the survey 10 boars were slaughtered.
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PMID:[Causes of mortality in a swine breeding establishment]. 830 62

Refeeding syndromes with electrolyte aberrations, heart failure and arrhythmias may complicate the nutritional rehabilitation of emaciated patients with eating disorders. Therefore, electrocardiographic (ECG) changes and changes in serum electrolyte concentrations following refeeding were studied in 37 admissions of 32 teenage girls with eating disorders. On admission they were all on a weight-losing course and weighed 37.0+/-8.0 kg (mean +/- SD) following a weight loss of 14.2+/-7.2 kg. On ECG recordings there was a prolongation of the QT interval and an increased QT dispersion. Serum concentrations of sodium, potassium and magnesium were with few exceptions normal. Serum concentrations of creatinine were high in relation to the low body weight, indicating protein catabolism. The first 2 wk of refeeding resulted in a weight gain of 1.7+/-0.2 kg without signs of refeeding syndromes or electrolyte aberrations. QT prolongation and dispersion normalized within the 3 d of refeeding. It is concluded that oral refeeding of patients with eating disorders and weight loss can be performed efficiently and without causing refeeding syndromes. QT pathology, a consequence of acute starvation and a risk factor for cardiac arrhythmias, normalizes within days. In view of the need to balance adequate refeeding and reduction of QT pathology against the risks of refeeding syndromes the start of refeeding of severely emaciated patients is best performed in a hospital setting where monitoring of ECG and serum electrolytes is possible.
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PMID:Heart risk associated with weight loss in anorexia nervosa and eating disorders: electrocardiographic changes during the early phase of refeeding. 1083 Apr 58

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral alimentation (continuous or bolus) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.
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PMID:Hepatobiliary abnormalities and parenteral nutrition. 1102 27

Cardiac energy metabolic shifts occur as a normal response to diverse physiologic and dietary conditions and as a component of the pathophysiologic processes which accompany cardiac hypertrophy, heart failure, and myocardial ischemia. The capacity to produce energy via the utilization of fats by the mammalian postnatal heart is controlled in part at the level of expression of nuclear genes encoding enzymes involved in mitochondrial fatty acid beta-oxidation (FAO). The principal transcriptional regulator of FAO enzyme genes is the peroxisome proliferator-activated receptor alpha (PPARalpha), a member of the ligand-activated nuclear receptor superfamily. Among the ligand activators of PPARalpha are long-chain fatty acids; therefore, increased uptake of fatty acid substrate into the cardiac myocyte induces a transcriptional response leading to increased expression of FAO enzymes. PPARalpha-mediated control of cardiac metabolic gene expression is activated during postnatal development, short-term starvation, and in response to exercise training. In contrast, certain pathophysiologic states, such as pressure overload-induced hypertrophy, result in deactivation of PPARalpha and subsequent dysregulation of FAO enzyme gene expression, which sets the stage for abnormalities in cardiac lipid homeostasis and energy production, some of which are influenced by gender. Thus, PPARalpha not only serves a critical role in normal cardiac metabolic homeostasis, but alterations in PPARalpha signaling likely contribute to the pathogenesis of a variety of disease states. PPARalpha as a ligand-activated transcription factor is a potential target for the development of new therapeutic strategies aimed at the prevention of pathologic cardiac remodeling.
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PMID:PPAR signaling in the control of cardiac energy metabolism. 1128 1

Malnutrition, muscle wasting and cachexia are often present in chronic heart failure (CHF). However, malnutrition in CHF patients is not always as severe as muscle wasting. Data in the literature show that 24% of CHF patients have malnutrition (albumin < 3.5 mg/dl) but 68% have muscle atrophy. This apparent discrepancy can be explained by considering the metabolic role of the striate muscle. In fact, the striate muscle maintains the body metabolic performance by continuous exchanges of fuels (amino acids) with the liver. This happens in case of malnutrition or starvation. In such situations, glucose is produced by gluconeogenesis when amino acids are metabolized in the liver. Malnutrition, muscle wasting and the frequent progression through cachexia can be reduced by specific therapy such as cytokine and/or catabolic hormone antagonists. This is because cytokines and catabolic hormones, with consequent insulin resistance, cause muscle wasting. An alternative and/or complementary therapy may be exogenous amino acid supplementation. In fact, amino acids: a) are rapidly absorbed regardless of pancreatic activity, b) reduce insulin resistance, c) induce the hepatic synthesis of anabolic molecules such as growth hormone and insulin-like growth factor, and d) modulate the catabolic hormonal-mediated effects on adipocytes. Research on the best suitable qualitative and quantitative amino acid composition for an alternative and/or complementary therapy is still being studied in different research centers.
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PMID:Malnutrition, muscle wasting and cachexia in chronic heart failure: the nutritional approach. 1278 75


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