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

Skeletal muscle possesses inherent plasticity of gene expression. Low frequency pulse-train stimulation can remodel the biochemical machinery that confers physiological expression and fatigue resistance approaching that of the myocardium. This fatigue-resistant muscle can generate sufficient force to meet the power requirements for useful cardiac work. This ultimate goal is currently being pursued in models of cardiomyoplasty and muscle-powered cardiac assist devices. In this article, we review the three major subcellular systems subserving canine skeletal muscle transformation and compare them to those of cardiac muscle. The magnitude of the problem of clinical heart failure and the feasibility of fatigue-resistant skeletal muscle joining the therapeutic armamentarium are addressed. The adaptation and transformation of fast-twitch skeletal muscle in response to chronic electrical stimulation augers therapeutic potential as an endogenous, readily available power source for myocardial assistance. The basis mechanisms of skeletal muscle fatigue require elucidation to gain a complete and thorough understanding of how to manipulate this property to provide continuous hemodynamic work.
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PMID:The remodelling of skeletal muscle for indefatigable hemodynamic work. 205 39

The mechanism of exertional fatigue in heart failure appears to be considerably more complex than was originally thought. Although it still seems likely that muscle underperfusion is the major culprit, the possibility that skeletal muscle changes contribute to the fatigue suggests that several new therapeutic modalities may improve exercise capacity in heart failure. If muscle atrophy due to de-conditioning or malnutrition is found to contribute to fatigue, exercise capacity in heart failure could be improved, at least in part, by exercise training or nutritional supplementation. Alternatively, agents such as anabolic steroids or growth hormone could be used to stimulate muscle hypertrophy and, thereby, help to improve the fatigue. Heart failure is a common disorder, affecting over three million Americans and many more people throughout the world. One of the most disabling problems experienced by these patients is exertional fatigue. Patients report that they are easily fatigued during normal daily activity. During maximal exercise testing, patients usually terminate exercise early due to fatigue of the legs associated with an early increase in the concentration of lactate in the blood. Traditionally, such exertional fatigue has been attributed to skeletal muscle underperfusion. Over the past five years, however, there has been increasing evidence that heart failure is associated with intrinsic skeletal muscle changes which may also contribute to the exertional fatigue. Nuclear magnetic resonance studies using 31P have demonstrated abnormal skeletal muscle metabolic responses to exercise that do not appear to be due to muscle under-perfusion. Skeletal muscle biopsy studies have demonstrated a variety of changes in patients. Anthropometric studies suggest that a generalized loss of muscle mass may occur in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of extertional fatigue in heart failure. 210 92

Clinical experience with long-term nifedipine treatment in 23 patients aged between 1 1/12 and 14 8/12 years is reported. The cardiopulmonary diseases comprised primary pulmonary diseases with pulmonary hypertension (n = 4), congenital heart defects with intracardiac shunts and pulmonary hypertension which either were inoperable as a result of an Eisenmenger reaction (n = 7) or presented a high surgical risk (n = 5), or defects in which pulmonary hypertension did not regress despite corrective (n = 1) or palliative surgery (n = 3), and congenital defects without pulmonary hypertension (n = 3). Subjective improvement with an increase in physical performance was clearly observed in 15 cases. Echocardiography and cardiac catheter examinations showed no progression of the pulmonary arterial diseases, except in 1 patient with severe primary pulmonary hypertension and an 11-year observation period with nifedipine treatment during the last 4 years. No complications occurred during the 4 corrective operations. A patient aged 14 8/12 years with the Down syndrome and atrioventricular septal defect developed easily controllable heart failure during 7-day administration of nifedipine without additional cardiotherapy. 4 children initially suffered from flushed face and scalp, in one case with headache; 2 children reported fatigue. Long-term treatment with nifedipine should begin with strict 7-day supervision in hospital and possibly additional digitalization. Success of the treatment was determined by an improved quality of life in patients with primary pulmonary hypertension and inoperable defects, and by a reduced perioperative risk and postoperative regression of pulmonary hypertension in patients with operable defects.
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PMID:Experience with long-term nifedipine therapy in paediatric cardiological patients. 211 16

In a double-blind study comparing two active treatments (digoxin and xamoterol) and placebo in patients with heart failure, improvements in exercise capacity and quality of life were observed in all three groups, with no significant differences. The substantial benefits seen in the placebo group were probably the result of increased attention from the medical and research staff and suggest the therapeutic value of special heart failure clinics. The relationship between exercise and symptomatic/functional status has been unclear. We developed quantitative measures of quality-of-life variables and examined their relationship with exercise capacity. There were significant relationships between change in exercise duration and changes in breathlessness, tiredness, chest pain, walking difficulty, rate of walking, difficulty with daily tasks, speed of daily tasks, mood, and sleeping. This study confirms the validity of measuring change in exercise capacity and demonstrates that specific measurements of quality of life make an important contribution to the evaluation of the treatment of heart failure.
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PMID:Exercise capacity and quality of life in the treatment of heart failure. 214 3

To assess whether an inotropic agent may affect quality of life in severe heart failure, a double-blind, placebo-controlled crossover study was performed in 10 patients over three periods of 3 weeks, including an initial control period of 3 weeks and periods on placebo or enoximone, 150 mg t.d.s. Quality of life was assessed by a questionnaire following initial training of patients to evaluate their symptoms after certain stresses, by visual analogue scales of symptoms, and by objective assessments during graded exercise. Daily dyspnoea score decreased from 33.2 +/- 2 (placebo) to 27.7 +/- 4 (enoximone) (P less than 0.01) and daily fatigue score decreased from 14.8 +/- 2.5 (placebo) to 12.6 +/- 2 (enoximone) (P less than 0.05). There were also significant beneficial responses in the mean daily NYHA class and in the duration of a walking test. Self-assessed global quality of life score increased from 2.7 +/- 0.6 (placebo) to 3.6 +/- 0.8 (enoximone) (P less than 0.05). It was concluded that over periods of 3 weeks, enoximone significantly improved self-assessed quality of life.
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PMID:Effects of enoximone on quality of life. 214 35

The current techniques of respiratory gas-exchange monitoring during stress testing in patients with congestive heart failure have provided new physiopathologic and clinical data. The "breath-by-breath" measurement of oxygen consumption and carbon dioxide production and the evaluation of the relationship between these parameters and respiratory volumes, allow to determine both ventilatory and metabolic responses during exercise, thus giving a precise estimate of the effective cardiopulmonary functional capacity. The demonstration of peripheral vascular and metabolic abnormalities by these techniques have provided new insights into the mechanism of dyspnea and fatigue in patients with heart failure. Although the relationship between respiratory and metabolic parameters and hemodynamics has been extensively studied, its mechanisms are still unclear. Moreover, controversy still exists as to the link between functional capacity and prognosis. Finally, recent studies on the cardiopulmonary adaptations to exercise training in patients with left ventricular dysfunction, have clearly demonstrated clinical and hemodynamic improvement after conditioning. These data, if confirmed, may provide a new approach in the management of patients with this disorder.
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PMID:[Monitoring of respiratory exchange during ergometric test in patients with heart failure: current aspects and prospects]. 219 41

Recently there has been extensive development of orally active angiotensin converting enzyme (ACE) inhibitors in addition to those already marketed, for example, captopril, enalapril, lisinopril and ramipril. It was initially thought that ACE inhibitors were likely to be most useful as antihypertensive agents in conditions in which circulating renin and angiotensin II were elevated. However, it is now clear that they can also lower arterial pressure when plasma renin is not high. In addition, they have beneficial effects in cardiac failure. Thus, captopril, enalapril, lisinopril and ramipril can be used in the treatment of mild to moderate hypertension either alone or in conjunction with diuretics or calcium antagonists. Broadly speaking, efficacy appears to be similar to that of beta-blockers or diuretics. Unfortunately, however, there are no long term studies comparing one ACE inhibitor with another or with other classes of antihypertensive agents. Furthermore, there are no prognostic studies which show that use of ACE inhibitors reduces morbidity or mortality in hypertension. Many new ACE inhibitors are undergoing clinical assessment, including alacepril, cilazapril, fosenopril, perindopril, quinapril and ramipril. The drugs vary, in that some exist in the active form whereas others are prodrugs which are converted to the active agent following absorption. In addition they each possess one of several ligands, for example, carboxyl, phosphinyl or sulfhydryl groups, and so vary in their affinity for ACE. Although many of these agents are renally excreted, a small number are metabolised via the liver (e.g. quinapril and spirapril) and this may prove advantageous in the presence of renal impairment. In common with captopril and enalapril, the new ACE inhibitors inhibit the renin-angiotensin system and initial results suggest that they are effective in lowering blood pressure in essential hypertension. Furthermore, they reduce systemic vascular resistance in the absence of a reflex tachycardia. There are a number of adverse effects which are attributable to the pharmacological mechanism of the ACE inhibitors as a group; these include hypotension, particularly in patients with high renin levels, prior diuretic use, renal impairment or in the elderly. Additional adverse effects may relate to chemical structure. The high incidence of adverse effects noted in early studies related to excess dosage and to the presence of a sulfhydryl group, which the more recently developed ACE inhibitors lack. The adverse effects most commonly reported with established and new ACE inhibitors include headache and fatigue, cough, skin rashes, hypotension and diarrhoea. As a group, ACE inhibitors have an acceptable but not negligible adverse effect burden.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin converting enzyme inhibitors and moderate hypertension. 222 19

This double-blind, randomized, multicenter clinical study assessed the efficacy and safety of ibopamine 100 mg t.i.d. as monotherapy vs. placebo in 52 patients with mild chronic heart failure aged over 60 years during a 12-week treatment period. Ibopamine produced a statistically significant increase in exercise tolerance and reduction in fatigue during effort compared to placebo. A trend towards decreased requirement of concomitant diuretic therapy was noted in the ibopamine-treated group. Ibopamine was well tolerated throughout the study. This study indicated that ibopamine is an effective and safe agent as monotherapy in the treatment of mild chronic heart failure in elderly patients.
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PMID:Ibopamine in the treatment of mild chronic heart failure in elderly patients. A double-blind, placebo-controlled study. 227 58

Recent studies in patients with long-term heart failure have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. The present study provides an analysis of substrate and enzyme content, fiber typing, and capillarization in skeletal muscle biopsy samples obtained at rest from the vastus lateralis in 11 patients with long-term heart failure (left ventricular ejection fraction, 21 +/- 8%) and nine normal subjects. Patients demonstrated a reduced peak exercise oxygen consumption (13.0 +/- 3.3 ml/kg/min) when compared with normals (30.2 +/- 8.6 ml/kg/min, p less than 0.001) and had an accelerated rise in blood lactate levels during exercise. In mixed fiber skeletal muscle, total phosphorylase and glycolytic enzyme activities were not different in the two groups, whereas mitochondrial enzymes involved in terminal oxidation were decreased in patients as compared with normal subjects as indicated by reductions in succinate dehydrogenase (51 +/- 15 vs. 81 +/- 17 microM/g protein/min, p less than 0.001) and citrate synthetase (26 +/- 7 vs. 43 +/- 20 microM/g protein/min, p less than 0.05). 3-Hydroxyacyl-CoA-dehydrogenase, an important enzyme mediating beta-oxidation of fatty acids, was also reduced in patients as compared with normals (18 +/- 7 vs. 27 +/- 10 microM/g protein/min, p less than 0.05). There was no difference in high-energy phosphagens or lactate concentration of mixed muscle in the two groups, whereas glycogen content was decreased in patients (262 +/- 29 vs. 298 +/- 35 microM glucosyl units/kg dry wt, p = 0.01). Patients demonstrated a reduced percentage of slow twitch type I fibers (36 +/- 7% vs. 52 +/- 22%, p less than 0.05) and had a higher percentage of type IIb fast twitch fibers (24 +/- 9% vs. 11 +/- 12%, p = 0.02), which were smaller than the type IIb fibers seen in normal subjects (p less than 0.05). In patients, the number of capillaries per fiber was decreased for type I and type IIa fibers (both, p less than 0.03), but the ratio of capillaries to cross-sectional fiber area was not different for the two groups. These data demonstrate major alterations in skeletal muscle histology and biochemistry in patients with long-term heart failure, including fiber atrophy, a decrease in percentage of composition of type I fibers, and an increase in type IIb fibers accompanied by a decrease in oxidative enzyme capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. 229 59

Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and metabolic basis of impaired exercise tolerance in patients with severe left ventricular dysfunction. 231 88


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