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

Experimental models of heart failure can be used to address specific questions not easily answered in patients, but no single model can reproduce exactly any of the clinical syndromes of heart failure since these are dominated by fatigue and breathlessness. Heart failure may be induced experimentally by pressure loading, volume loading, myocardial infarction, or by the creation of other disease states within the myocardium. Pressure loading may be especially useful in the study of ventricular hypertrophy, cellular derangements and vascular changes. Volume loading may be useful when examining the pathogenesis of hormone and electrolyte disturbances. Models of myocardial infarction or destruction are likely to be the most suitable for assessing novel therapy provided that peripheral reflexes are maintained. Experimental cardiomyopathy can provide an important means of identifying pathological subcellular mechanisms. They may be of use in the evaluation of vasodilator drugs but caution should be exercised in the study of inotropic agents. Any one model may be useful if it permits study of a single factor or variable in isolation or at a time when information is not obtainable from patients. For greatest clinical relevance, studies should be made in conscious animals with intact reflexes.
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PMID:Experimental models of heart failure. 315 77

The reduced maximal exercise capacity of patients with heart failure has been attributed to skeletal muscle underperfusion with resultant intramuscular lactic acidosis and muscular fatigue. To investigate this hypothesis, the effect of dichloroacetate, a drug that decreases lactate formation by increasing pyruvate oxidation, on the maximal exercise performance of 18 patients with heart failure and reduced ejection fraction (25 +/- 9%) was examined. Exercise tests after parenteral dextrose (control) and dichloroacetate were performed 1 week apart. The sequence of interventions was randomized in a double-blind manner. Dichloroacetate decreased blood lactate at rest (control 8.0 +/- 2.5 versus dichloroacetate 5.6 +/- 2.9 mg/dl), throughout exercise and at peak exercise (control 26.0 +/- 14.3 versus dichloroacetate 19.4 +/- 10.8) (all p less than 0.05). In contrast, dichloroacetate had no effect on exercise time (control 15.2 +/- 6.0 versus dichloroacetate 15.9 +/- 6.2 min) or peak exercise oxygen consumption (control 1,280 +/- 498 ml/min versus dichloroacetate 1,312 +/- 530 ml/min) (both p = NS). In six subjects, dichloroacetate also had no effect at peak exercise on leg blood flow (control 2.8 +/- 1.1 versus dichloroacetate 3.0 +/- 0.6 liters/min) or femoral oxygen vein saturation (control 12.7 +/- 4.1% versus dichloroacetate 12.5 +/- 5.7%). These data suggest that intramuscular lactate accumulation is not responsible for muscular fatigue during exercise in patients with heart failure.
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PMID:Effect of dichloroacetate on the exercise performance of patients with heart failure. 319 43

Patients with heart failure frequently report leg fatigue during exercise. At present, however, there is no objective method of detecting leg muscle abnormalities in such patients. To determine if phosphorus-31 nuclear magnetic resonance spectroscopy can provide such information, this technique was used to compare calf responses to stair climbing and plantarflexion in 20 patients with heart failure (peak oxygen consumption (VO2) of 13.6 +/- 5 ml/kg/min, ejection fraction 20 +/- 5%) and 9 age-matched normal subjects. Work was quantified by measuring VO2. At rest, both groups exhibited similar inorganic phosphorus to phosphocreatine (Pi/PCr) ratios (patients with heart failure 0.21 +/- 0.07, normal subjects 0.21 +/- 0.06, difference not significant) and pH levels (patients with heart failure 7.06 +/- 0.17, normal subjects 7.05 +/- 0.11, difference not significant). In both normal subjects and patients with heart failure, exercise resulted in a progressive rise in Pi/PCr as VO2 increased. However, examination of the relation of VO2 versus Pi/PCr revealed steeper slopes in patients with heart failure during both stair climbing and plantar-flexion. Neither form of exercise decreased calf pH in normal subjects. In the patients with heart failure, significant decreases in pH were noted during the highest work level of plantarflexion (pH of heart failure patients 6.86 +/- 0.20, pH of normal subjects 7.07 +/- 0.14, p less than 0.01). Metabolic recovery time was also prolonged in the patients with heart failure versus normal subjects (3.3 +/- 0.8 vs 2.1 +/- 0.5 minutes, respectively, p less than 0.002). These findings indicate that phosphorus-31 nuclear magnetic resonance provides objective evidence of leg muscle abnormalities in patients with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of abnormal calf muscle metabolism in patients with heart failure using phosphorus-31 nuclear magnetic resonance. 319 84

The vast majority of patients who undergo mechanical ventilation are able to discontinue ventilatory assistance within a few days. Typically, patients who require only short-term mechanical ventilation do not have severe underlying lung disease, and the problem for which they require ventilatory support is most commonly rapidly reversible. In these patients on short-term ventilatory support, parameters of spontaneous ventilatory requirements and respiratory muscle strength, including minute ventilation, maximal voluntary ventilation, vital capacity, and maximal inspiratory pressure, are useful in predicting the success of discontinuation of mechanical ventilation. Ventilatory support can generally be discontinued by a variety of techniques in these patients without the need for weaning from the ventilator per se. The smaller group of patients in whom it is not possible to discontinue mechanical ventilation within less than 7 days comprises individuals who frequently have severe acute or chronic lung disease, multisystem extrapulmonary disease, or neuromuscular disease. After a period of prolonged mechanical ventilatory support, these complicated patients require a process of progressive weaning in which they gradually become able to support spontaneous ventilation. Spontaneous ventilatory parameters do not correlate well with weaning ability in patients on long-term ventilatory support. A systematic and comprehensive approach in which attention is focused on optimizing pulmonary and nonpulmonary factors that affect the weaning process provides the best chance for successful withdrawal of ventilatory support after long-term mechanical ventilation. Inadequate ventilatory drive, respiratory muscle weakness and fatigue, increased work of breathing, excessive CO2 production, and cardiac failure are potential mechanisms that may play a role in inhibiting successful weaning. Adverse factors relevant to each of these mechanisms must be addressed and corrected to whatever extent possible. Studies have not demonstrated the superiority of either classic T-piece weaning or IMV weaning methods in difficult-to-wean patients on long-term ventilatory support. Both techniques may be used successfully as long as all patient variables that may adversely affect weaning ability are corrected or optimized and close care and attention to the details of the weaning process itself are provided.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Discontinuation of mechanical ventilation. 328 Feb 25

Static or dynamic work in patients with chronic cardiac failure elicits a variety of pathophysiologic responses that impair the ability of the cardiopulmonary unit to sustain O2 delivery at a rate that is commensurate with the O2 requirements of working skeletal muscle. Regional abnormalities in the circulation of skeletal muscle may further compromise nutritive blood flow to muscle. As a result, the patient experiences a sense of fatigue during physical activity. Dyspnea, or an abnormal awareness of breathing, may also accompany exercise in these patients. This sense of breathlessness may be due to an abnormally elevated work of breathing secondary to decreased pulmonary compliance, a heightened chemical drive to ventilation, and a possible imbalance in the O2 supply and demand of the respiratory muscles. The ambulatory monitoring of physical activity in patients with chronic cardiac failure has not been systematically examined. Potential monitoring techniques that may provide accurate and reproducible results regarding the exercise response in these patients include the thoracic impedance principle to measure minute ventilation and portable O2 uptake sensors.
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PMID:Monitoring physical activity in ambulatory patients with chronic cardiac failure. 328 62

The most common symptoms of patients with heart failure are shortness of breath and fatigue. The causes of these symptoms may be different in various entities encompassed by the general term heart failure, such as acute pulmonary edema, circulatory collapse and chronic heart failure. In patients with acute heart failure, shortness of breath is closely related to left atrial pressure. In patients with chronic heart failure, optimally treated with diuretics, the body fluid compartments are usually of normal size. Recent work strongly suggests that, in such patients, central hemodynamic abnormalities are not the sole determinants of symptoms. Impaired vasodilation and altered metabolism in skeletal muscle, circulating metabolites and pulmonary ventilation-perfusion mismatch with consequent increased physiologic dead space may all contribute to the genesis of symptoms. Consequently, it may be possible to alleviate symptoms by treatments that are not aimed directly at improving central hemodynamics. Whether such an approach could also modify prognosis is unknown.
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PMID:Causes of symptoms in chronic congestive heart failure and implications for treatment. 329 93

Twenty two patients with heart failure were studied in a double blind crossover trial to compare amiodarone (200 mg/day) with placebo. Each agent was given for three months. Extrasystoles and complex ventricular arrhythmias were common during ambulatory electrocardiographic monitoring and during exercise testing at entry to the study. Breathlessness and tiredness as assessed by visual analogue scores and duration of treadmill exercise did not become worse during amiodarone treatment. During the placebo and amiodarone phases of the study left ventricular ejection fraction and cardiac index determined by first pass radionuclide ventriculography were similar, both at rest and during upright bicycle exercise. Exercise induced ventricular tachycardia was abolished and simple and complex ventricular arrhythmias observed on 24 hour ambulatory monitoring were greatly diminished during amiodarone treatment. Three patients died, all suddenly, during the placebo phase. In two patients amiodarone was withdrawn after a further myocardial infarction in one and a worsening of symptoms of ventricular arrhythmia in the other. In contrast with other antiarrhythmic agents amiodarone is effective in suppressing ventricular arrhythmias in heart failure without causing adverse haemodynamic effects. Because frequent ventricular arrhythmias are known to be associated with a poor prognosis in heart failure, these data suggest that amiodarone may improve the poor prognosis in patients with heart failure.
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PMID:Clinical, haemodynamic, and antiarrhythmic effects of long term treatment with amiodarone of patients in heart failure. 329 21

Ten adult, awake cats were exposed to high pressure (7.5, 9, or 10 MPa) of a heliox (He-O2) or trimix (He-N2-O2) gas mixture. Total duration of the experiment, i.e., duration of compression plus sojourn at maximal pressure, varied between 23 and 59 h. Throughout the experiment, minute ventilation (VE), heart rate, and rectal temperature were recorded. The total mass of gas (Mt) breathed by each animal was determined from the product of VE, gas density (p), and time (t). As previously shown, VE was increased in all animals breathing heliox mixtures, whereas this was never observed in trimix experiments. Ventilatory arrest occurred before cardiac failure in 3 animals breathing heliox mixtures, where the highest values of Mt were measured; the others survived. Rectal temperature, t, or p values did not account for the difference between those animals surviving and those who died. Thus, increased ventilation in high density gas mixtures was responsible for increased values of Mt. Present observations suggest that ventilatory failure associated to the highest values of Mt is related to respiratory muscle fatigue.
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PMID:Ventilatory failure in cats during prolonged exposure to very high pressure. 336 92

The combination of nifedipine and atenolol must be evaluated in terms of risks and benefits to the hypertensive patient. Disadvantages with single-agent therapy justify trials of combination regimens. beta-Blockers may be unacceptable to some patients because of gastrointestinal upset, musculoskeletal symptoms, tiredness, malaise, insomnia, depression or confusion, sweating, breathlessness or cold extremities. The side effect profile varies from patient to patient and between different beta-blockers. Calcium antagonists also have characteristic side effects, including severe headaches, flushing and oedema, tachycardia and possibly worrying palpitations, and polyuria. Combining a calcium antagonist and a beta-blocker can reduce some side effects; for example, tachycardia is offset by addition of beta-blocker to calcium antagonist therapy, and beta-blocker-induced cold extremities may be reversed with a drug such as nifedipine. Moreover, the antihypertensive efficacy is increased, which is useful in previously resistant patients. However, an excessive fall in blood pressure is a possible adverse effect of the combination. There is also the possibility of precipitating heart failure in patients with cardiomegaly and severely compromised left ventricular function. The combination of nifedipine and atenolol was evaluated in 25 patients in a randomised, crossover trial following a month's treatment with atenolol 50mg twice daily. Patients received either atenolol 50mg twice daily alone, or atenolol 50mg twice daily with sustained release nifedipine 20mg or 40mg twice daily, or placebo twice daily during three 4-week treatment periods. Additional antihypertensive benefit was obtained by addition of the low dose of nifedipine compared with atenolol alone, but no further advantage was obtained with the higher nifedipine dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aims of combination therapy--improved quality of life or better blood pressure control? 337 14

The concept of 'reconstructive cardiac surgery' using a stimulated autologous skeletal muscle has been investigated in this research. Our approach has been to investigate the substitution or reinforcement of a ventricular wall by a contractile tissue. The experiments have demonstrated the feasibility of this technique and the long-term adaptability and adequate electrophysiological properties of the Latissimus Dorsi flap transferred to a heterotopic position over the heart. Long-term biocompatible fatigue resistant muscle stimulation has become possible in experimental and clinical cases as a result of the development of specially designed electrodes and the use of a progressive sequential stimulation protocol to adapt the skeletal muscle to a cardiac support function. Autologous pericardium treated with glutaraldehyde was found to be a suitable material to close the ventricular cavity. Cardiomyoplasty with autologous skeletal muscle to restore ventricular contractility seems to be a valid alternative in addition to current methods of treatment for irreversible myocardial failure.
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PMID:Dynamic cardiomyoplasty: a new approach to assist chronic myocardial failure. 343 Nov 52


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