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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of descending thoracic aortomyoplasty using conditioned latissimus dorsi muscle on cardiac output in five mongrel dogs with pharmacologically induced congestive heart failure was evaluated. A neurovascular left latissimus dorsi flap was lifted and through a left thoracotomy placed around the proximal descending thoracic aorta. The flap was conditioned for 4-6 weeks with a neurostimulator using the following parameters: amplitude 0.5 V, pulse width 210 microseconds and frequency 2 Hz. The neurostimulator was then removed and a cardiomyostimulator inserted and programmed to burst-stimulate the muscle during diastole. Baseline measurements of central venous pressure, heart rate, mean arterial blood pressure, pulmonary capillary wedge pressure, and cardiac output were obtained with the cardiomyostimulator off and on (study 1). Heart failure was induced with a combination of propranolol and verapamil, and measurements again taken with the stimulator off and on. The neurostimulator was reimplanted to continue stimulation of the latissimus dorsi muscle, and another set of measurements taken at 6 weeks with the cardiomyostimulator off and on (study 2). Counterpulsation in control conditions (before cardiac failure) in both studies demonstrated no significant increase in cardiac output. However, mean(s.d.) cardiac output was significantly (P < 0.1) increased by muscle stimulation in dogs with heart failure (study 1: from 2.39(1.10) to 3.14(1.41)l/min; study 2: from 1.89(0.64) to 2.38(0.57)l/min). There was no significant difference in the increase in cardiac output associated with muscle stimulation between studies 1 and 2. The results indicate that the model can increase cardiac output in heart failure and that this improvement is constant over a 4-6 week period, suggesting that muscle fatigue may not occur.
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PMID:Descending thoracic aortomyoplasty: effect of chronically conditioned muscle on heart failure. 807 47

Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups. CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment. 824 99

Cases of hypothyroidism and hyperthyroidism associated with amiodarone therapy are described, and the mechanisms, clinical appearance, and management of amiodarone-induced thyroid dysfunction are discussed. A 72-year-old man with a history of recurrent ventricular tachycardia unresponsive to conventional antiarrhythmic drugs was started on amiodarone therapy. Initially he responded well, but after three months he began to have fatigue, dry skin, and intolerance of cold. His serum thyroid-stimulating hormone (TSH) concentration had risen from 4.4 microU/mL before amiodarone therapy began to 20 microU/mL, consistent with hypothyroidism. He was started on sodium levothyroxine for thyroid hormone replacement; the dosage was adjusted in accordance with subsequent TSH measurements. His hospital course was complicated by congestive heart failure. The second patient was a 43-year-old man with a history of atrial fibrillation who developed hyperthyroidism when placed on amiodarone therapy. He had persistent sweating, intolerance of heat, restlessness, and tachycardia. Thyroid function tests confirmed the presence of hyperthyroidism. The patient was treated with propylthiouracil and propranolol, and amiodarone was discontinued. He remained unresponsive to the propylthiouracil, which was discontinued, and was scheduled for radioactive iodine treatment. The mechanism of amiodarone-induced thyroid dysfunction may involve the large iodine content of the drug. Amiodarone-induced hypothyroidism may range in severity from mild symptoms to severe myxedema; the skin, hair, and nails are particularly affected. Persons with clinical hyperthyroidism secondary to amiodarone treatment show the signs and symptoms of a hypermetabolic state resulting from thyroid hormone excess. Amiodarone-induced hypothyroidism is treated with levothyroxine and hyperthyroidism with antithyroid drugs. Amiodarone can cause thyroid dysfunction, which can have serious consequences.
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PMID:Amiodarone-induced thyroid dysfunction. 825 59

In this study we tested the hypothesis that the ryanodine-binding Ca-release channel activity and density of the sarcoplasmic reticulum (SR) terminal cisternae were decreased in congestive heart failure (CHF) that occurs spontaneously in doberman pinschers or experimentally with rapid ventricular pacing of mongrels. We used a novel, sensitive, and easy-to-perform microassay and demonstrated a 50% decrease in activity of the myocardial SR Ca pump and a 75% reduction in SR Ca-release channel activity in CHF. Decreases in Ca channel content were associated with increases in net Ca sequestration. 45Ca-release experiments from passively loaded SR terminal cisternae and ryanodine-binding studies confirmed a 53-68% downregulation of the Ca-release channel activity. As a consequence of release channel downregulation, there was partial restoration of net Ca sequestration activity in dogs with CHF and complete compensation in dogs with mild cardiac dysfunction. Deterioration of Ca cycling correlated with deterioration of myocardial performance, apparently due to decreased Ca-adenosinetriphosphatase (ATPase) pump and not Ca channel content. One-half the reduction in Ca-release activity could be attributed to decreased Ca sequestration and one-half to decreased Ca channel density. Downregulation of Ca channel content decreases the amplitude of the Ca cycle and maximizes the downregulation of Ca pumps that may occur. Although these adaptations may reduce cellular energy expenditure, they are likely to render the myocardium more susceptible to fatigue and failure.
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PMID:Compensatory downregulation of myocardial Ca channel in SR from dogs with heart failure. 838 26

This study aimed to refine and extend the findings of an original study which focused on the description of fatigue associated with congestive heart failure. A descriptive approach based on Levine's Conservation Model provided both quantitative and qualitative data. Qualitative data addressed personal integrity and quantitative data measured energy conservation, structural and social integrity. Patients described fatigue as being tired and exhausted and containing both physical and emotional components. Fatigue occurred as a result of stress, physical activity and disease. Patient-identified interventions included rest, distraction, medicine, and physical and spiritual activities. Age, pH and oxygen saturation were significantly related to fatigue. The findings are examined using the concept of adaptation as defined by Levine. Implications for nursing are discussed within the framework of the Conservation Model with emphasis on a holistic approach to patient care.
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PMID:Fatigue associated with congestive heart failure: use of Levine's Conservation Model. 843 16

Atrial fibrillation is most the common sustained arrhythmia seen by the cardiologist. Therapy to prevent this arrhythmia is often prescribed so as to eliminate associated symptoms which include palpitations, fatigue, dizziness and presyncope, shortness of breath, congestive heart failure and emboli, especially those that result in a cerebrovascular accident. Pharmacologic therapy is the only effective therapy for preventing atrial fibrillation and the class 1 antiarrhythmic drugs remain the most frequently used agents. Although each of these agents has been reported to be effective for preventing atrial fibrillation, they are associated with frequent side effects, some of which are potentially serious, especially aggravation of arrhythmia. Prior to treatment the benefit vs risk of these drugs for each patient must be established.
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PMID:Class 1 antiarrhythmic agents for therapy of atrial fibrillation. 845 55

To determine the level of daily physical activity routinely performed by patients with congestive heart failure (CHF) and the ability of clinical and laboratory assessments of function to predict peak daily activity levels, 45 patients with CHF were evaluated in the laboratory and during 2 days of usual activity. Subjects performed symptom-limited treadmill exercise tests with respiratory gas analysis and wore a Vitalog activity monitor with continuous measurement of heart rate and body motion. Mean maximal oxygen uptake for this sample was 16.8 ml/kg/min. Peak daily physical activity involved walking on a flat surface (44%), or general activities (housework/yardwork, 42%). Most subjects were asymptomatic (49%) during daily physical activity, 22% noted dyspnea, 16% fatigue and 13% sore muscles/joints. Perceived intensity of peak daily physical activity (mean = 4.19, SD = 2.21) was similar to perceived exertion (mean = 3.73, SD = 1.37) reported at ventilatory threshold measured during treadmill exercise testing. Subjects may control their peak daily physical activity to minimize symptoms experienced. It was further observed that current methods of assessing functional capacity in these patients were inadequate for estimating the peak level of daily activity. In conclusion, daily physical activity levels are low in patients with congestive heart failure and a gap exists between exercise capacity and actual performance of daily physical activity.
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PMID:Daily physical activity levels in congestive heart failure. 846 82

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of torsemide are reviewed. Torsemide belongs to the pyridine-sulfonylurea class of loop diuretics. Its primary site of activity is the thick ascending limb of the loop of Henle, where it blocks active reabsorption of sodium and chloride, resulting in diuresis, natriuresis, and other effects. Torsemide has high bioavailability, a relatively long half-life, and a prolonged duration of activity. It is highly protein bound. Clinical trials indicate that torsemide is effective in the treatment of hypertension and of edema and other symptoms in patients with chronic renal failure (CRF), hepatic dysfunction, or congestive heart failure (CHF). Torsemide has infrequent, mild, and transient adverse effects; among the most common are orthostatic hypotension, fatigue, dizziness, and nervousness. The recommended initial oral dosages of torsemide are 10-20 mg/day for CHF, 20 mg/day for CRF, 5 mg/day for hypertension, and 5-10 mg/day (in combination with a potassium-sparing diuretic or aldosterone antagonist) for hepatic cirrhosis. In most patients, the pharmacokinetic advantages of torsemide over other loop diuretics are unlikely to translate into a substantial edge in clinical outcomes, and in practice there may be no cost advantages. Although torsemide does not offer major advantages over other loop diuretics, it may be of benefit in patients who do not respond to or cannot tolerate other agents.
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PMID:Torsemide: a new loop diuretic. 852 33

Patients with congestive heart failure (CHF) suffer from respiratory muscle weakness which may contribute to dyspnea. Nasal continuous positive airway pressure (NCPAP) can improve left ventricular ejection fraction (LVEF) and reduce dyspnea in patients with CHF and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) but its effects on respiratory muscle strength are not known. We therefore studied the effects of NCPAP on maximal inspiratory and expiratory pressures (MIP and MEP, respectively), LVEF, dyspnea, and fatigue in patients with chronic CHF and CSR-CSA over 3 mo. Eight patients were randomized to control and nine to nightly NCPAP. There were no significant changes in any of these factors in the control group during the study. In contrast, among the NCPAP group, MIP increased from 79.3 +/- 8.1 to 90.7 +/- 10.4 cm H2O (mean +/- SEM; p < 0.02), LVEF increased from 24.0 +/- 4.0 to 32.6 +/- 6.6% (p < 0.02) and symptoms of dyspnea and fatigue were alleviated. However, MEP did not change. In addition, the number of apneas and hypopneas decreased from 49 +/- 11 to 17 +/- 7 per hour of sleep (p < 0.001) and mean low Sao2 during sleep increased from 87.9 +/- 1.0 to 93.0 +/- 1.0% (p < 0.01). Our data indicate that nightly application of NCPAP in patients with CHF and CSR-CSA improves inspiratory muscle strength and LVEF, and relieves dyspnea and fatigue.
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PMID:CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea. 854 29

Overt congestive heart failure (CHF) has a prevalence of 1% of the population. The predominant symptoms of patients with CHF are fatigue and dyspnoea. Fatigue is thought to result from changes in peripheral muscle metabolism secondary to decrease vasodilative capacity and physical inactivity. An increase of peripheral perfusion by vasodilator therapy and physical activity are therefore recommended. Beside overt decompensation, where dyspnoea results from acute pulmonary congestion due to backward failure, increased physiological dead space ventilation caused by pulmonary ventilation/perfusion mismatch accounts, to a large degree, for dyspnoea, and can be improved by vasodilator therapy. According to the pathophysiology of CHF, normalisation of loading conditions and myocardial inotropy are the parameters addressed by various pharmacological agents in order to alleviate symptoms and slow progression of the disease. Diuretics are rapidly acting and effective agents to improve congestion and decrease filling pressures. Digitalis improves haemodynamics and symptomatology by increasing inotropy and slowing resting heart rate in atrial fibrillation; however, prognostic effects have yet to be proved. The introduction of vasodilators has significantly improved the prognosis of the disease, and the administration of ACE inhibitors in particular has been shown to slow progression of CHF. This results in a substantial decrease in morbidity and mortality. The present article appraises the role of the currently used drugs in the treatment of CHF, considering effects on pathophysiology and clinical outcome and provides an approach to a differential drug regimen.
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PMID:Current guidelines for the treatment of congestive heart failure. 874 Dec 34


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