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

Chronic heart failure is characterized as a clinical disorder by exercise intolerance. There are two factors that are independently responsible for the reduced exercise capacity: (a) a shift from myosin heavy chain 1 (MHC1) to MHC2a and MHC2b and (b) muscle atrophy. We have demonstrated, both in experimental models of heart failure and in man, that the more severe the heart failure, the greater the magnitude of skeletal muscle apoptosis. In the monocrotaline treated rat, that develops a severe right-sided heart failure, the increased number of apoptotic nuclei was paralleled by increasing levels of circulating TNFalpha. In agreement with some recent observations showing that sphingolipids can mediate programmed cell death, we found that in animals with heart failure and high number of apoptotic nuclei, circulating levels of sphingosine were significantly increased. In a study conducted in patients with heart failure we found a correlation between exercise capacity limitation and skeletal myocytes apoptosis. There was also a correlation between degree of muscle atrophy and magnitude of apoptosis. The shift in MHCs, although with a different mechanism, is also responsible for the reduced exercise capacity in these patients. In fact there is a strong correlation between indices of severity of CHF and MHC composition. Muscle fatigue, appears earlier in patients that have a greater skeletal muscle expression of 'fast' MHCs. We have also demonstrated that MHCs shift and apoptosis can be prevented by using angiotensin II converting enzyme inhibitors and angiotensin II receptor blockers.
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PMID:Apoptosis and changes in contractile protein pattern in the skeletal muscle in heart failure. 1141 42

Chronic heart failure (CHF) studies investigating the clinical, hemodynamic, and therapeutic importance of endothelin-1 (ET-1), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) are largely based on resting plasma levels, which may vary with prior exertion and postprandial status. This study investigated the importance of peak-exercise plasma levels of ET-1, ANP, and BNP in the assessment of left ventricular (LV) systolic function. Thirty-six male-patients ages 58 +/- 10 (mean +/- SD ) with NYHA class I-IV CHF due to coronary artery disease or idiopathic dilated cardiomyopathy were enrolled. LV systolic function was assessed by echocardiography and radionuclide ventriculography. Resting and peak cardiopulmonary exercise venous blood sampling and treadmill exercise testing were performed in the fasting state. Resting plasma levels of ET-1, ANP, and BNP were elevated compared with reference laboratory normal values. Exercise induced significant (p < 0.0001) increase in plasma levels of ET-1, ANP, and BNP. On univariate analysis peak-exercise plasma levels of ET-1, ANP, and BNP were more closely related to echocardiographically determined LV end-diastolic diameter and end-systolic diameter than their resting values. Multiple step-wise regression models identified resting and peak-exercise plasma levels of ET-1 and ANP but only the resting BNP as independent predictors of LV dimensions and systolic function. Peak exercise plasma levels of ANP and ET-1 are potentially more reliable and important than their resting levels as markers of LV systolic dysfunction and LV dimensions in patients with heart failure.
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PMID:Incremental importance of peak-exercise plasma levels of endothelin-1 and natriuretic peptides in chronic heart failure. 1148 51

Chronic heart failure has emerged as an important public health problem. The consequent increase in the sanitary services has induced an increased consumption of financial resources and conditioned the need to investigate new sanitary models that guarantee, by integrating the inpatient and outpatient health care delivery, the continuity of health assistance. Cardiac rehabilitation in the context of a day-hospital Heart Failure Unit allows for the organization of a rehabilitation program including various health approaches aimed at guaranteeing a multidisciplinary program and the relief continuity. This article describes the experience developed in the Heart Failure Unit of Montescano.
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PMID:[Rehabilitation day-hospital of the heart failure unit: structure and functions]. 1150 94

Chronic heart failure is associated with a bad prognosis with considerably shortened survival and repeated hospitalisations. Patients suffering from heart failure also have symptoms that can affect their food intake, for example, tiredness when strained, breathing difficulties and gastrointestinal symptoms like nausea, loss of appetite and ascites. Pharmacological therapy can lead to a loss of appetite, which will make the intake of food inadequate to fill the required energy and nutritional needs. The nurse's interest in and knowledge of diet issues can improve these patients' nutritional status. The aim of this literature review was to describe the nurse's interventions regarding malnutrition in patients suffering from chronic heart failure. The literature search gave 13 articles, which were analysed, and sentences whose content was related to the aim were identified. Three areas of content appeared; drug treatment and consequences, gastrointestinal effects, and information and education. The results show that the nutritional status of these patients can be significantly improved by means of simple nursing interventions. Future research should focus on controlled experimental studies to evaluate differences in body weight, body mass index and quality of life between patients suffering from chronic heart failure, who are taking part in a fully enriched nutrition intervention, and patients suffering from chronic heart failure, who are eating their normal diet.
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PMID:Malnutrition in patients suffering from chronic heart failure; the nurse's care. 1151 31

Chronic heart failure (CHF) is a common condition with a poor prognosis, commonly associated with poor exercise tolerance and debilitation symptoms despite optimal modern therapy. Recent investigations have shown that the degree of exercise limitation may be related to pathophysiological changes that occur systemically in the patient with CHF. Exercise training in carefully selected stable patients with heart failure has been shown to be safe to correct many of these pathophysiological changes in the periphery and to lead to worthwhile improvements in exercise capacity. Recent studies have suggested a possible improvement in mortality and morbidity with exercise training in this patient group. This article discusses the factors limiting exercise capacity in CHF and reviews the controlled clinical trial of exercise testing in this condition.
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PMID:Exercise and heart failure. 1157 Jan 21

Chronic heart failure is one of the most serious medical problems in the United States, affecting some 4 million persons. In spite of its common occurrence, and comprehensive literature regarding this condition, no unifying hypothesis has been accepted to explain the signs and symptoms of chronic heart failure. The cardiocirculatory and neurohormonal models place an emphasis on left ventricular ejection fraction and cardiac output and do not provide appropriate explanations for the symptoms of breathlessness and fatigue. The muscle hypothesis supplements these conventional models. It proposes that abnormal skeletal muscle in heart failure results in activation of muscle ergoreceptors, leading to an increase in ventilation and sensation of breathlessness, the perception of fatigue, and sympathetic activation. At least one fourth of patients with chronic heart failure are limited by skeletal muscle abnormalities rather than cardiac output. Cardiac rehabilitation exercise can lead to an increase in exercise capacity that is superior to that gained from digitalis or angiotensin-converting enzyme inhibitors. Exercise tends to reverse the skeletal muscle myopathy of chronic heart failure and reduces the abnormal ergoreflex. Other interventions that have been shown to have a favorable outcome include localized muscle group training, respiratory muscle training, and dietary approaches. The possibility that osteopathic manipulative treatment might be of benefit is an attractive, but untested, possibility.
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PMID:The muscle hypothesis: a model of chronic heart failure appropriate for osteopathic medicine. 1168 Nov 64

Chronic heart failure is a dominant problem not only in cardiology but also from the political and economical points of view in civilized countries. The paper describes general and specific methods of heart failure therapy such as reconstruction of coronary artery disease, valve disease, cardiomyoplasty remodelling of left ventricular cavity, ventricular assist-control devices, artificial heart and heart transplantation.
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PMID:[Non-pharmacologic treatment of heart failure]. 1172 65

Chronic heart failure is characterized by increased vascular systemic resistances secondary to activation of various vasoconstrictor systems and to decreased endothelium-dependent vasodilatation. Endothelial dysfunction, described both in animals and in humans, may be caused by an increased inactivation of nitric oxide (NO) by reactive oxygen species, leading to decreased NO bioavailability and impaired vasodilatation. Increased levels of free radicals in heart failure may result either from increased production or a decrease in the cellular antioxidant reserves. Free radicals are produced by three enzymatic systems: NADH/NADPH oxidase (after stimulation by angiotensin II or TNF-alpha), xanthine oxidase or endothelial NO-synthase (NOS) itself. However, oxidative stress alone cannot explain endothelial dysfunction. Other mechanisms involved in the regulation of the production of NO (e.g. decreased expression and/or activity of the NOS) and/or changes in production of vasoconstrictors may participate in this impaired endothelium-dependent vasodilatation in heart failure.
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PMID:[Oxidative stress and endothelial dysfunction in heart failure]. 1180 96

Chronic heart failure is a complex disorder with interactions among the cardiovascular, immune, and neurohormonal systems. The concept that the progression of heart failure is due to neurohormonal abnormalities has received the greatest attention to date, leading to substantial therapeutic benefits. Although many current therapies are also thought to exert a variety of immunologic effects, this has been much less studied. In this review, the authors discuss a number of interactions among immune pathways and neurohormonal abnormalities relevant to heart failure. Cytokines, in particular tumor necrosis factor-alpha, have tremendous interactive opportunities within a regulatory network of energy metabolism, immune function, and neuroendocrine and hormonal function. Inflammatory cytokines are known to contribute to the progression of heart failure, and have been related to patients' prognosis. Advanced heart failure can be considered a state of chronic (low-grade) inflammation, and there are many reasons to suggest that anticytokine therapy could be successful in these patients. These novel approaches are certainly not without some risk, and many of them are very expensive, which may limit their application to certain subgroups of patients. In the future, it may not be enough to monitor cardiac function alone. Rather, the immune and neurohormonal status of patients may also need to be included in the performance of a complete assessment.
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PMID:Immune and neurohormonal pathways in chronic heart failure. 1182 25

Chronic heart failure is a common, disabling disorder with high mortality. Oxidative stress may have both functional and structural effects on the myocardium, leading to myocardial decompensation. In this study, the authors examined the relationship of oxidative stress and functional capacity in patients with varying degrees of heart failure. Fifty-one patients with chronic heart failure and 31 control subjects were studied. The functional capacity of patients was determined. Plasma malondialdehyde, vitamin E, and beta-carotene levels were measured. The malondialdehyde levels were significantly different between control subjects and heart failure patients (p=0.03). There was a positive correlation between patients' malondialdehyde levels and New York Heart Association functional class (r=0.59; p<0.0001). There was a negative correlation between the functional class and vitamin E and beta-carotene levels (r=20.43; p<0.0001 and r=20.25; p<0.01, respectively). These data demonstrate that oxidative stress is increased systemically in patients with chronic heart failure. It seems that this increase correlates with functional class. (c)2001 CHF, Inc.
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PMID:Relation of functional capacity with the oxidative stress and antioxidants in chronic heart failure. 1182 75


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