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

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

Apoptosis has been found in skeletal muscles of patients with chronic heart failure (CHF) and has been associated with exercise intolerance. In CHF, cachexia is characterized by neurohormonal activation and muscle wasting. Neurohormonal activation can lead to cell death and fibrosis. The purpose of the study was to determine the severity of apoptosis and fibrosis in skeletal muscles of patients with CHF and cachexia and its relationship to exercise intolerance in these patients. Skeletal muscle biopsies of 21 patients with CHF (eight with cachexia) and four healthy controls of similar age have been studied by in situ end labeling (ISEL) for apoptosis and by the Picrosirius Red technique for collagen. Apoptosis in skeletal muscles was detected by ISEL in 52% of the patients with CHF (11 out of 21) and in none of the controls. CHF patients with apoptosis-positive skeletal muscles had impaired exercise tolerance (peak oxygen consumption 11.4+/-5.7 vs. 16.91+/-6.6, P=0.029). Increased collagen was detected by Picrosirius Red in eight out of 21 patients with CHF and in none of the controls. Increased collagen (fibrosis) was detected in six out of eight patients with cachexia and in two out of 13 patients without cachexia (P=0.01). Peak oxygen consumption and apoptosis were similar in cachectic and non-cachectic patients. Thus, the skeletal musculature of patients with cardiac cachexia is characterised by the presence of fibrosis. Apoptosis was not found to be more frequent in cachectic CHF patients. Our data support the hypothesis that cachexia contributes by a different mechanism to skeletal muscle myopathy of CHF patients and different mechanisms are implicated in deterioration of exercise tolerance and progression to cardiac cachexia.
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PMID:Studies on apoptosis and fibrosis in skeletal musculature: a comparison of heart failure patients with and without cardiac cachexia. 1282 Dec 25

Skeletal muscle disuse with space-flight and ground-based models (e.g., hindlimb unloading) results in dramatic skeletal muscle atrophy and weakness. Pathological conditions that cause muscle wasting (i.e., heart failure, muscular dystrophy, sepsis, COPD, cancer) are characterized by elevated "oxidative stress," where antioxidant defenses are overwhelmed by oxidant production. However, the existence, cellular mechanisms, and ramifications of oxidative stress in skeletal muscle subjected to hindlimb unloading are poorly understood. Thus we examined the effects of hindlimb unloading on hindlimb muscle antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase), nonenzymatic antioxidant scavenging capacity (ASC), total hydroperoxides, and dichlorohydrofluorescein diacetate (DCFH-DA) oxidation, a direct indicator of oxidative stress. Twelve 6 month old Sprague Dawley rats were divided into two groups: 28 d of hindlimb unloading (n = 6) and controls (n = 6). Hindlimb unloading resulted in a small decrease in Mn-superoxide dismutase activity (10.1%) in the soleus muscle, while Cu,Zn-superoxide dismutase increased 71.2%. In contrast, catalase and glutathione peroxidase, antioxidant enzymes that remove hydroperoxides, were significantly reduced in the soleus with hindlimb unloading by 54.5 and 16.1%, respectively. Hindlimb unloading also significantly reduced ASC. Hindlimb unloading increased soleus lipid hydroperoxide levels by 21.6% and hindlimb muscle DCFH-DA oxidation by 162.1%. These results indicate that hindlimb unloading results in a disruption of antioxidant status, elevation of hydroperoxides, and an increase in oxidative stress.
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PMID:Hindlimb unloading increases oxidative stress and disrupts antioxidant capacity in skeletal muscle. 1282 51

Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-alpha (TNF-alpha) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not yet clear. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After 2 wk, 2 groups of rats were treated with GH (0.2 mg.kg(-1).day(-1) and 1.0 mg.kg(-1).day(-1)) subcutaneously. A third group of controls had saline. After 2 additional weeks, rats were killed. Tibialis anterior cross-sectional area, myosin heavy chain (MHC) composition, and a study on myocyte apoptosis and serum levels of TNF-alpha and SPH were carried out. The number of apoptotic nuclei, muscle atrophy, and serum levels of TNF-alpha and SPH were decreased with GH at high but not at low doses compared with CHF rats. Bcl-2 was increased, whereas activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slowed down both contraction and relaxation but did not affect specific tetanic force, whereas absolute force was decreased. GH treatment restored contraction and relaxation to control values and brought muscle mass and absolute twitch and tetanic tension to normal levels. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF to improve exercise capacity.
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PMID:Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure. 1367 2

In this paper the perspective for nutritional modulation of systemic impairment in patients with chronic obstructive pulmonary disease (COPD) is discussed. Progressive weight loss is characterised by disease-specific elevated energy requirements unbalanced by dietary intake. Weight gain per se can be achieved by caloric supplementation while future studies may prove efficacy of amino acid modulation to stimulate protein synthesis and enhance muscle anabolism. Disproportionate muscle wasting resembles the cachexia syndrome as described in other chronic wasting diseases (cancer, chronic heart failure, acquired immunodeficiency syndrome (AIDS)). There is yet no adequate nutritional strategy available to treat cachexia in COPD. Muscle substrate metabolism has hardly been investigated, but the few data available point towards a decreased fat oxidative capacity that may show similarities with the "metabolic syndrome" as described in type II diabetes and obesity and could theoretically benefit from polyunsaturated fatty acid modulation. To adequately target the different therapeutic options, clearly more clinical (intervention) studies are needed in chronic obstructive pulmonary disease patients that are adequately characterised by local and systemic impairment and in which molecular and metabolic markers are linked to functional outcome.
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PMID:Nutritional and metabolic modulation in chronic obstructive pulmonary disease management. 1462 Nov 10

Subacute motor neuropathy involving bulbar nerves is an unusual complication of hyperthyroidism. Clinical and neurophysiologic follow-up of such patients has been rarely reported. We describe a 41-year-old Colombian patient who developed respiratory failure associated with motor neuropathy and severe weight loss. The major clinical features included diffuse amyotrophy, bilateral facial paresis, and fasciculations, suggesting motor neuropathy. Electromyography confirmed the presence of axonal neuropathy, with predominant motor involvement. Goiter with hypervascularization was noticed, associated with pure T3 hyperthyroidism (T3l=26 pg/ml; N<3.8). The patient was given carbimazole which induced a severe skin vasculitis 10 days later. Carbimazole was stopped and replaced by propylthiouracile, which also induced vasculitis with secondary cardiac failure. Total thyroidectomy was then performed. General status improved rapidly as well as motor deficit, amyotrophy and pyramidal syndrome. Electromyographic abnormalities improved significantly within 3 months. This observation demonstrates that hyperthyroidism can produce motor axonal neuropathy, curable with radical surgery.
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PMID:[Subacute motor neuropathy induced by T3 hyperthyroidism]. 1473 39

Cachexia is a complex syndrome. The main components of this pathological state are anorexia and metabolic abnormalities such as glucose intolerance, fat depletion, and muscle protein catabolism among others. The aim of the present article is to review the different therapeutic approaches that have been designed to fight and counteract muscle wasting in different pathological states such as cancer, AIDS and chronic heart failure.
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PMID:The pharmacological treatment of cachexia. 1505 12

Over the last 2 decades the clinical application of physical exercise as a therapeutic strategy has developed from rehabilitation to prevention and treatment of cardiovascular diseases. This shift in clinical application was accompanied by a more systematic research approach of the involved mechanisms and the objective clinical assessment of sport interventions using prospective randomized clinical trials. This ongoing process established physical exercise as an evidence-based and guideline-oriented treatment option. In stable coronary artery disease (CAD), exercise therapy has long been used for rehabilitation purposes following an acute myocardial infarction. A recent meta-analysis revealed a significant 27% reduction of total mortality among training patients. Four mechanisms are considered important mediators of the reduced cardiac event rate: improvement of endothelial function, reduced progression of coronary lesions, reduced thrombogenic risk, and improved collateralization. The therapeutic benefit of regular physical exercise has also been confirmed in direct comparison with an interventional strategy: a 12-month exercise therapy in stable CAD patients was associated with a higher event-free survival as compared to conventional percutaneous coronary intervention. In stable chronic heart failure (CHF), physical activity was traditionally discouraged-with negative consequences for the patients: exercise intolerance worsened, the progression of disease-related muscular atrophy accelerated. A carefully designed exercise program at 50-70% of the maximal oxygen uptake was effective in improving exercise capacity by 12-32%. In a recent meta-analysis, exercise therapy reduced the relative risk of CHF mortality by 35% and CHF-related hospitalizations by 28%. Considering the growing body of evidence in favor of sport as a therapy, training interventions should be considered additional/alternative therapeutic strategies as compared with established pharmacological/interventional options.
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PMID:[Sports as therapy]. 1524 37

Heart failure is a severe pathology, which has displayed a dramatic increase in the occurrence of patients with chronic heart disease in developed countries, as a result of increases in the population's average age and in survival time. This pathology is associated with severe malnutrition, which worsens the prognosis. Although the cachexia associated with chronic heart failure is a well-known complication, there is no reference animal model of malnutrition related to heart failure. This study was designed to evaluate the nutritional status of rats in a model of loss of cardiac function obtained by ascending aortic banding. Cardiac overload led to the development of cardiac hypertrophy, which decompensates to heart failure, with increased brain natriuretic peptide levels. The rats displayed hepatic dysfunction and an associated renal hypotrophy and renal failure, evidenced by the alteration in renal function markers such as citrullinemia, creatininemia, and uremia. Malnutrition has been evidenced by the alteration of protein and amino acid metabolism. A muscular atrophy with decreased protein content and increased amino acid concentrations in both plasma and muscle was observed. These rats with heart failure displayed a multiorgan failure and malnutrition, which reflected the clinical situation of human chronic heart failure.
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PMID:Aortic banding in rat as a model to investigate malnutrition associated with heart failure. 1563 66

Human aging is characterized by debilitating diseases, including heart failure, cardiac pacemaker defects, muscle wasting, and osteoporosis, in heart, skeletal muscle, and bone. Recent studies are identifying pathways for these aging-related diseases by examining how the process of aging influences tissue-specific progenitors and differentiated cell lineages in these organ systems. These advances form a foundation for new therapeutic strategies to delay the onset of aging-related disorders.
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PMID:Longevity and lineages: toward the integrative biology of degenerative diseases in heart, muscle, and bone. 1573 85


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