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

There is no comprehensive theory for the various reasons for dyspnea. It is proposed to regard the disproportion between "input" and "output" as the common cause of the various forms. This disproportion may be located between psychological drive and neural response or between neural excitation and muscular response or between muscular activity and ventilatory effect. Thus insufficient perfusion of respiratory muscles--as in cardiac failure--may cause dyspnea. Arterial oxygen pressure as the criterion of sufficient ventilation is misleading in anemia and CO-poisoning, so that there is no dyspnea despite of insufficient O2-transport.
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PMID:[Dyspnea--disproportion between expense and success]. 180 50

Neuroendocrine activity was studied in 60 consecutive untreated patients with dyspnoea and a clinical suspicion of heart failure. On the basis of the so-called Boston clinical criteria the diagnosis of heart failure was regarded as unlikely in 26 patients, possible in 15 patients, and definite in 19 patients. These groups were studied before any drug treatment was started and were compared with a control group of 69 healthy individuals. Plasma atrial natriuretic peptide concentration was clearly raised in patients with definite heart failure and slightly raised in patients with possible heart failure. Plasma adrenaline concentration was somewhat raised in patients with definite or possible heart failure, whereas plasma noradrenaline concentration was raised only in patients with definite heart failure. Plasma renin activity was not increased in any of the patient groups and plasma aldosterone concentration was slightly increased only in patients with definite heart failure. In the total patient series there were significant correlations between plasma atrial natriuretic peptide concentration and markers of the severity of left ventricular dysfunction. There was some evidence of neuroendocrine activation in untreated heart failure: plasma concentrations of atrial natriuretic peptide and catecholamines were increased but the renin-angiotensin-aldosterone system showed little or no activation.
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PMID:Neuroendocrine activity in untreated heart failure. 182 71

On the basis of a case history, the clinical and paraclinical manifestations of hypothyroidism are reviewed. Exertion dyspnoea without signs of cardiac insufficiency occurs frequently. The minute and stroke volume and heart rate are reduced. The blood pressure may rise (reversible) and hypertension may occur. The function of the left ventricle is reversibly reduced. A tendency to formation of exudates has been observed. X-ray of the thorax may revial massive relatively asymptomatic pleural exudates and cardiomegaly. Pericardial exudate occurs frequently and is demonstrated best by echocardiography. Inter- and intracellular deposits, infiltrations and fibroses have been demonstrated in the myocardium and these probably contribute to some of the non-specific, reversible ECG changes (low voltage, flattening/inversion of T waves, sinus bradycardia). The plasma concentrations of several different enzymes (including creatine kinase (CK), CK-MB and LDH) may be raised in myxoedema. The reason for this is perhaps compromized membrane function in the skeletal muscle cells. The diagnosis of myocardial infarction in myoedema requires that CK-MB constitutes at least 6% of the total CK and that the increase is transient. In patients with coronary sclerosis, substitution treatment should be initiated carefully because the risk of ischaemic symptoms is otherwise considerably increased. It is not elucidated whether the hypothyroidism per se can increase atheroma formation.
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PMID:[Cardiovascular manifestations of hypothyroidism]. 186 65

The most frequently reported symptoms in heart failure are fatigue and dyspnoea, which limit exercise tolerance. However, several surveys reveal other changes in physical and psychological well-being which affect the patient's perception of 'quality of life'. The introduction of new treatments for heart failure has stimulated interest in their impact on quality of life. Until recently, attempts to quantify well-being were restricted to assessment of symptoms which affect exercise capacity or classification of the functional capacity of the patient from his ability to perform everyday tasks. Although drug treatment can improve these measures, they are insensitive to change and also provide little information on the more subtle disturbances which patients may perceive as important determinants of their overall well-being. More comprehensive assessments of quality of life have been devised and validated in heart failure. Early results indicate that inotropic drugs such as digoxin and xamoterol can improve these measures. However, at present there is too little information from studies using these questionnaires to compare the wider benefits of individual drug treatments.
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PMID:Effect of drug treatment on quality of life in mild to moderate heart failure. 188 40

We report a rare occurrence of cardiomyopathy associated with allergic bronchopulmonary aspergillosis (ABPA). A 49-year-old man with a history of bronchial asthma was referred to the Matsuyama Red Cross Hospital for evaluation of the abnormal shadow on his chest X-ray. Laboratory examination showed blood eosinophilia and marked elevation of serum IgE concentration and IgE antibody to A fumigatus. The immediate and late skin reactivities to A fumigatus antigen were both positive. The diagnosis of ABPA was made. Treatment using prednisolone was effective in ameliorating the symptoms. However, he was admitted again due to dyspnea, edema and anorexia 6 months later. Chest X-ray, ECG, UCG and scintigraphy suggested severe cardiac failure. The clinical diagnosis of hypertrophic cardiomyopathy, and the pathohistological diagnosis of endomyocardial fibrosis were made by cardiac catheterization and biopsy of endocardium. Retrospectively, cardiomegaly had gradually increased during the past several months while peripheral blood eosinophilia had continued. All these data strongly suggested that eosinophilia due to ABPA might cause severe cardiac damage.
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PMID:[A case of cardiomyopathy due to allergic bronchopulmonary aspergillosis]. 189 65

The associations between exercise capacity, symptoms and specific aspects of quality of life were examined in subjects participating in a trial of the treatment of heart failure. Patients were assessed on entry and after three months treatment. The principle symptoms were fatigue, breathlessness and chest pain. These limited the extent and speed of physical activities, restricted social, leisure and family life and were associated with emotional distress. There were associations between baseline exercise capacity and measures of quality of life. Change in exercise capacity during three months treatment was correlated with changes in measures of symptoms, limitation of activity and quality of life. The findings confirm the value of change in exercise capacity as a measure of functional status and suggest that it should be supported by a limited number of specific measures of quality of life.
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PMID:Cardiac failure: symptoms and functional status. 192 Jan 71

Ultrasonography revealed a renal tumour (4 x 4 cm) in a 67-year-old man with right-sided lumbar pain and macrohematuria. In addition he had marked nocturnal dyspnoea with dry cough. He had lost about 10 kg in weight. On admission he had atrial fibrillation with an irregular ventricular rate (140 beats/min) and engorgement of the neck veins. Two-dimensional echocardiography, undertaken because of signs of increasing heart failure and a fall of systolic blood pressure to below 100 mm Hg, demonstrated a space-occupying lesion in the right ventricle, 4 x 2 x 1 cm, indicating an intracardiac thrombus or solid tumour. The heart failure continued to worsen, despite treatment with cardiac glycosides, verapamil and diuretics. Hence an exploratory thoracotomy was performed. This revealed an intracardiac tumour which had markedly displaced the right ventricular inflow tract and infiltrated the entire myocardium, but not the tricuspid valve. As much of the tumour as possible was resected, but the patient died postoperatively of heart failure. The intracardiac tumour proved to be a metastasis from the papillary carcinoma of the kidney. This had infiltrated the renal capsule and pelvis and invaded the branches of the right renal vein.
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PMID:[Cardiac metastasis as cause of therapy-resistant heart failure]. 193 45

Most research in the field of chronic heart failure during the last 20 years has been directed toward defining and understanding the abnormalities of systolic function seen in this disorder, but systolic performance is not a determinant of effort tolerance. Several lines of evidence, however, suggest a strong relation between exercise capacity and abnormalities of diastolic function in chronic heart failure. Of all the commonly measured hemodynamic variables, effort tolerance (whether limited by dyspnea or fatigue) varies more closely with the level of left ventricular filling pressure than the left ventricular ejection fraction. Consequently, drugs that lower ventricular filling pressures are more likely to enhance exercise capacity than drugs that primarily increase cardiac output and left ventricular ejection phase indexes. Vasodilator drugs do not reduce left ventricular filling pressure, however, by simply redistributing central blood volume to the peripheral capacitance circuits because these agents do not predictably decrease left ventricular volumes. Instead, clinically effective drugs seem to reduce left ventricular filling pressure primarily by producing a favorable shift in the left ventricular diastolic pressure-volume relation. Conversely, agents that adversely affect the diastolic pressure-volume relation frequently cause clinical deterioration. These findings suggest that abnormalities of diastolic rather than systolic performance may be the most important determinants of the clinical status and exercise intolerance of patients with chronic heart failure.
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PMID:Abnormalities of diastolic function as a potential cause of exercise intolerance in chronic heart failure. 196 59

The sympathetic nervous system becomes activated in heart failure, and while this is initially beneficial, the consequences of prolonged raised levels of catecholamines can be counterproductive. Xamoterol, a partial agonist that acts on the cardiac beta 1-adrenergic receptor, modifies the response of the heart to variations in sympathetic activity. At rest, it produces modest improvements in cardiac contractility, relaxation, and filling without increase in myocardial oxygen demand. The improvements are maintained during exercise although the attendant tachycardia is attenuated. The beneficial effects of xamoterol on both systolic and diastolic function suggested that it would be effective in patients with mild-to-moderate heart failure, and this was demonstrated in small placebo-controlled studies where effort tolerance and symptoms were improved. A large multicenter study program comprised of four studies demonstrated that patients with mild-to-moderate heart failure randomized to xamoterol (n = 617) 200 mg b.i.d. for 3 months significantly (p less than 0.0001) improved exercise capacity by 37% as compared with the placebo group (n = 300) with an increase of 18%. The xamoterol group also showed significant improvements in symptoms of breathlessness, fatigue, and life values as compared with the placebo group. In one of the multicenter studies in which 433 patients were randomized to xamoterol (n = 220), placebo (n = 109), and a positive control, digoxin 0.125 mg b.i.d. (n = 104), the percentages of improvement in exercise work were 33%, 5%, and 17%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Review of clinical experience with xamoterol. Effects on exercise capacity and symptoms in heart failure. 196 61

The long term effects of treatment with xamoterol in 14 patients aged 44-73 with mild to moderate heart failure as a result of ischaemic heart disease are reported. After 18 months' treatment with xamoterol, patients were assessed in a randomised double blind crossover comparison of xamoterol (200 mg twice a day) and placebo, each given for one month. Compared with placebo, xamoterol significantly increased exercise duration and work done on a bicycle ergometer and reduced the maximum exercise heart rate. Assessment of symptoms and activities at 12 months by visual analogue and Likert scales showed a trend towards the relief of symptoms of breathlessness and tiredness and an improvement in activity. There was an improvement in the clinical signs of heart failure and no haemodynamic deterioration over a 12 month period as assessed by ejection fraction. The improvement in exercise tolerance, symptoms, and activities was sustained for 18 months without side effects or development of tolerance.
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PMID:Ischaemic left ventricular failure: evidence of sustained benefit after 18 months' treatment with xamoterol. 197 39


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