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Chronic heart failure is a common clinical condition with a high mortality and morbidity. Patients with the condition suffer from shortness of breath and fatigue on exercise. This article reviews the recent advances made in the understanding of the pathophysiology of chronic heart failure and explores further possible research options.
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PMID:The mechanisms underlying the increased ventilatory response to exercise in chronic stable heart failure. 128 2

Chronic heart failure (CHF) is a syndrome of impaired left ventricular (LV) function and cardiac output reserve that is associated with secondary compensatory adaptations including: LV hypertrophy and dilation, neuroendocrine activation, and vasoconstriction and redistribution of peripheral blood flow. The primary limitation in CHF is exercise intolerance characterized by fatigue and/or dyspnea during mild to moderate exertion. These symptoms are primarily attributed to impaired nutrient blood flow, cellular atrophy, and loss of oxidative function in skeletal muscle. Functional capacity in CHF is usually classified into four categories determined by symptom-limited exercise testing: normal > or = 7 METs; mild 5-7 METs; moderate 3-5 METs, severe < 3 METs. Exercise capacity in CHF is frequently unrelated to resting or exercise measures of LV function, e.g., LV ejection fraction (LVEF) and LV end diastolic pressure (LVEDP). Peak exercise heart rate and blood pressure are progressively attenuated in CHF due to baroreflex dysfunction and beta-receptor down regulation. Exercise training studies in selected patients with CHF (mild to moderate) have reported significant increases in peak VO2max, attributed to increases in peak leg blood flow O2 transport. Heart rate and lactate production during submaximal exercise are reduced compared with pretraining values. Potential training complications in patients with CHF include dysrhythmia, hypotension, and deterioration of cardiac status. The major benefit of moderate exercise training is improvement in tolerance to daily activities. However, the long term effect of exercise training on prognosis is currently not established.
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PMID:Exercise testing and training in patients with chronic heart failure. 800 98

Chronic heart failure is a well-recognized syndrome in which left ventricular impairment produces a constellation of secondary changes in other organ symptoms leading to symptoms such as muscular fatigue and dyspnoea and objective limitation to exercise tolerance. With modern drug therapy of diuretics and ACE inhibitors, the majority of patients have minimal if any signs of congestion, and yet severe symptomatic limitation remains. This limitation bears little relationship to conventional measures of either left ventricular function or the haemodynamic profile of the patient. The symptoms limiting exercise are predominantly fatigue or dyspnoea, and yet the classical pathophysiological explanations for their genesis now seem inadequate. Recent investigations, as demonstrated, in part, by the research presented in this symposium, attest to the importance of abnormalities in peripheral blood flow and in skeletal muscle in producing both objective limitation to exercise and in explaining the generation of the exercise-limiting symptoms of the syndrome of stable optimally treated chronic heart failure. In addition it is now evident that these muscle changes may in addition have pathophysiological significance for the maintenance of sympatho-excitation during exercise and potentially therefore in the progression of left ventricular remodelling and in the susceptibility to ventricular arrhythmias. This paper presents some of the background evidence which leads to the hypothesis that a feedback loop links changes in skeletal muscle to abnormal reflex cardiopulmonary control which may both limit exercise and be harmful in the progression of the syndrome.
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PMID:The "muscle hypothesis" of chronic heart failure. 893 79

Chronic heart failure (CHF) is a complex syndrome affecting many body systems. Body wasting (ie, cardiac cachexia) is a serious complication of CHF long known but little investigated. Although no specific diagnostic criteria have been established, we have suggested that cardiac cachexia be defined on the basis of the presence of documented nonintentional and nonedematous weight loss > 7.5% of the premorbid normal weight, occurring over a time period of > 6 months. Using this definition, 16% of an unselected CHF outpatient population was found to be cachectic. The cachectic state is predictive of impaired prognosis independently of age, functional disease classification, left ventricular ejection fraction, and peak oxygen consumption. The mortality in the cachectic cohort is 50% at 18 months. Analyzing body composition in detail, it has been found that patients with cardiac cachexia suffer from a general loss of fat tissue (ie, energy reserves), lean tissue (ie, skeletal muscle), and bone tissue (ie, osteoporosis). Cachectic CHF patients are weaker and fatigue earlier, which is due to both reduced skeletal muscle mass and impaired muscle quality. The pathophysiologic alterations leading to cardiac cachexia remain unclear, but initial cross-sectional studies have suggested that humoral neuroendocrine and immunologic abnormalities are linked, independently of established heart failure severity markers, to the presence of body wasting. Comparing the features of cachectic and noncachectic CHF patients with those of healthy control subjects, it is mainly the cachectic CHF patients who show raised plasma levels of epinephrine, norepinephrine, and cortisol; the highest plasma renin activity and aldosterone plasma concentrations; and the lowest plasma sodium level. Several studies have shown that cardiac cachexia is linked to raised plasma levels of tumor necrosis factor-ac. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. The available evidence suggests that cardiac cachexia is a multifactorial neuroendocrine and metabolic disorder with a poor prognosis. A complex imbalance of different body systems may cause the development of body wasting.
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PMID:Cardiac cachexia: a syndrome with impaired survival and immune and neuroendocrine activation. 1008

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 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 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 (CHF) is a common and disabling syndrome with a poor prognosis. It is a major and increasing public health problem. Angiotensin-converting enzyme inhibitors, diuretics, and digitalis are the standards treatments for CHF. Other drugs, such as beta-blockers, spironolactone, calcium antagonists, vasodilators, and antiarrhythmic agents are used to counteract the progression of the syndrome or to improve the hemodynamic profile. Despite optimum treatment with neurohumoral antagonists, prognosis of CHF remains poor; the patients complain of persistent reductions in their exercise capacity and quality of life. Fatigue and shortness of breath, two common and disabling symptoms in patient with CHF, are relatively independent from hemodynamic and neuroendocrine changes, although they seem to be related to the impairment of peripheral muscle metabolism and energetic phosphate production. Therefore, CHF is a complex metabolic syndrome in which the metabolism of cardiac and peripheral muscles is impaired and novel therapeutic strategies have been aimed at positive modulation with compounds such as carnitine, trimetazidine, and ranolazine.
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PMID:Metabolic modulation and optimization of energy consumption in heart failure. 1269 36

Chronic heart failure (CHF) is an important public health care problem and a leading cause of morbidity and mortality world wide. Anemia is a common finding in CHF and known to cause heart failure. Patients with CHF are limited by exercise capacity and fatigue. A low hemoglobin concentration leads to impairment of both. With increasing severity of heart failure, anemia also becomes more frequent and clinically more relevant. There are many potential reasons for development of anemia in chronic heart failure like bone marrow depression, reduced intestinal iron uptake, and the dilution in consequence of sodium and water retention. However, the anemia seen in CHF is generally an "anemia of chronic illness". Furthermore, it has been shown that hemoglobin levels independently predict increased mortality in CHF.
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PMID:Anemia in chronic heart failure--frequency and prognostic impact. 1294 May 40

Chronic heart failure (CHF) impairs muscle O2 delivery (QO2) and, at a given O2 uptake (VO2), lowers microvascular O2 pressures (PmvO2: determined by the QO2-to-VO2 ratio), which may impair recovery of high-energy phosphates following exercise. Because CHF preferentially decreases QO2 to slow-twitch muscles, we hypothesized that recovery PmvO2 kinetics would be slowed to a greater extent in soleus (SOL: approximately 84% type I fibres) than in peroneal (PER: approximately 14% type I) muscles of CHF rats. PmvO2 dynamics were determined in SOL and PER muscles of control (CON: n= 6; left ventricular end-diastolic pressure, LVEDP: approximately 3 mmHg), moderate CHF (MOD: n= 7; LVEDP: approximately 11 mmHg) and severe CHF (SEV: n= 4; LVEDP: approximately 25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recovery PmvO2 values nor the mean response time (MRT; a weighted average of the time to 63% of the overall response) were altered by CHF (CON: 66.8 +/- 8.0, MOD: 72.4 +/- 11.8, SEV: 69.1 +/- 9.5 s). In marked contrast, SOL PmvO2, at recovery onset, was reduced significantly in the SEV group ( approximately 6 Torr) and PmvO2 MRT was slowed with increased severity of CHF (CON: 45.1 +/- 5.3, MOD: 63.2 +/- 9.4, SEV: 82.6 +/- 12.3 s; P < 0.05 CON vs. MOD and SEV). These data indicate that CHF slows PmvO2 recovery following contractions and lowers capillary O2 driving pressure in slow-twitch SOL, but not in fast-twitch PER muscle. These results may explain, in part, the slowed recovery kinetics (phosphocreatine and VO2) and pronounced fatigue following muscular work in CHF patients.
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PMID:Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type. 1513 Oct 70


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