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

A group of ten acromegalic patients, who had no history of heart failure, was studied to determine whether subtle carciac impairment may also be common. None had clinical evidence of coronary artery disease or severe hypertension. Systolic time intervals were recorded in each patient and compared with normal values predicted for sex and heart rate by our own controls and published data. The results indicate that measurable abnormalities in left ventricular performance are common in this sampling. Known duration and activity of disease (growth hormone levels at time of study) did not correlate with the time intervals. The results are consistent with cardiomyopathic effect of excessive growth hormone.
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PMID:Evidence of subclinical heart muscle dysfunction in acromegaly. 12 91

Unexplained cardiomegaly with cardiac failure was observed in a 42-year-old woman in whom a pituitary tumour had been treated by radiotherapy five years previously. She had been amenorrhoeic for 10 years. Thyroid and adrenal function was normal. Despite treatment with digitalis and diuretic, her cardiac disease progressed until she died suddenly at the age of 45. Hyperprolactinaemia was evident some weeks before death, her serum concentration of 68 ng/ml being well above both the reported normal range (2--20 ng/ml) and the concentrations in eight female controls being treated for severe cardiac failure (5--25 ng/ml). Although the association of these two disorders might merely represent coincidence, heart disease with similar features is common in acromegaly and does not correlate with plasma growth hormone concentration. Since prolactin is known to exert metabolic growth hormone-like effects in animals and in man, the possibility should be considered that prolactin hypersecretion might induce or maintain cardiac disease in some patients with pituitary tumours. A preliminary survey of 35 subjects with hyperprolactinaemia has shown five with raised blood pressure and four, two of whom were normotensive, with cardiomegaly on chest radiography.
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PMID:Cardiomegaly and heart failure in a patient with prolactin-secreting pituitary tumour. 15 31

Effects of different broiler stocks, ambient temperatures (Ta), dietary energy content (AME), and dietary levels of unsaturated fat on plasma thyroid and growth hormone concentrations and energy metabolism were studied. An experiment with a 2 x 2 x 2 x 2 factorial split-plot arrangement of treatments with 96 groups of 12 male broilers each was performed. Blood samples were taken at 3, 4, and 5 wk of age. Energy metabolism parameters were determined over an entire period from 1 to 5 wk of age. Chickens from a line selected for fast growth rate and low feed conversion ratio but also more sensitive to heart failure syndrome (HFS) and ascites (Line SS) than commercial birds (Line BC) exhibited the greatest responses to experimental factors. Differences in levels of plasma thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3), and growth hormone (GH) between stocks at different ages were highly dependent on Ta and dietary fat content. Differences in heat production per metabolic weight, percentage of retained fat energy in retained energy, and efficiency of AME intake for retained energy between stocks corresponded to differences in hormone levels. High-fat diets (polyunsaturated fatty acids) inhibited the extra thyroidal conversion of T4 to T3 in both stocks. Differences between stocks in T3 and rT3 levels in plasma indicated that BC birds (in contrast to SS birds) were better able to compensate for an inhibited T4 conversion to T3 by producing more T4. Overall results suggest that the occurrence of HFS and ascites in SS birds could be initiated independently by different factors. These factors might be a limited thyroid hormone production and a lower capacity for oxygen consumption. An inverse relationship between T3 and GH levels found in particular combinations of experimental factors, together with changes in fat deposition, support published concepts about the positive effects of T3 on lipogenesis and GH on lipolysis.
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PMID:Ascites in broilers. 2. Disturbances in the hormonal regulation of metabolic rate and fat metabolism. 147 May 83

Continuous ambulatory measurement of pulmonary arterial pressure was used to investigate changes following right heart catheterisation in patients with chronic heart failure. Ten males, mean age 56 years, with chronic heart failure, underwent 24 hour pressure recording using a micromanometer tipped catheter with in vivo calibration and frequency modulated recording. Eight patients were taking diuretics and 3 vasodilators. Blood was drawn for catecholamines, plasma renin activity and atrial natriuretic peptide 1 hour before catheterisation (-1 h), at the time of catheterisation (0 h) and 1, 2, 3, 4 and 6 hours later and aldosterone, cortisol and growth hormone at -1, 0 and 6 hours. Analysis of variance was used to determine changes in pulmonary arterial pressure, heart rate and hormones from the time of catheterisation in lying, sitting and standing postures. There was no significant change in pulmonary arterial pressure or heart rate over the 12 hours following or 24 hours after catheterisation in any posture. In the majority of patients plasma noradrenaline, plasma renin activity, atrial natriuretic peptide, aldosterone and cortisol were elevated. There was no significant change in hormone levels during the 6 hours following catheterisation. These findings suggest that the effect of invasive haemodynamic monitoring and chronic medical therapy on central haemodynamics is minor, and that a delay between insertion of catheters and measurement of pressure is unnecessary.
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PMID:The influence of right heart catheterisation on pulmonary arterial pressure in chronic heart failure: relationship to neuroendocrinal changes. 183 9

The effects of infusing human alpha-calcitonin gene-related peptide were studied in eight patients with congestive heart failure, five normal rabbits and five rabbits with adriamycin-induced cardiomyopathy. In patients with heart failure, calcitonin gene-related peptide caused a dose-dependent increase in cardiac output and decrease in pulmonary and systemic vascular resistance and pulmonary artery pressure. The systemic blood pressure and right atrial and pulmonary wedge pressures decreased only at the highest infusion rate (16 ng/kg per min). Heart rate remained unchanged. Plasma epinephrine increased (p less than 0.05), whereas aldosterone, atrial natriuretic peptide and prolactin concentrations decreased (p less than 0.05). Plasma norepinephrine, renin activity, cortisol and growth hormone concentrations remained unchanged. In both groups of rabbits, the drug decreased blood pressure and increased cardiac output and heart rate. There was a significant increase in renal blood flow (p less than 0.05). The peptide did not affect the contraction amplitude of human and rabbit ventricular myocytes. These findings suggest that calcitonin gene-related peptide is a vasodilator in the rabbit and humans with little direct effect on ventricular myocardium. This peptide may be useful in some forms of heart failure.
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PMID:Cardiovascular and hormonal effects of calcitonin gene-related peptide in congestive heart failure. 198 28

Cardiac hypertrophy and heart failure are common to acromegalic patients who have abnormally high serum growth hormone (GH). While the function of cardiac muscle is clearly affected by chronically elevated GH, the electrical activity of myocytes from hearts with GH-dependent hypertrophy has not been studied. We used adult, female Wistar-Furth rats with induced GH-secreting tumors to study the effect of excessive GH on ion channels of cardiac myocytes. GH-secreting tumors were induced by subcutaneous inoculation of GH3 cells. Eight weeks after inoculation, the rats had doubled their body weight and heart size compared with age-matched controls. There were no differences in either action potential amplitude or resting potential of right ventricular myocytes from control and tumor-bearing rats. However, action potential duration increased significantly in tumor-bearing rats; the time to 50% repolarization was 23 +/- 14 ms (n = 10) compared with 6.6 +/- 1.5 ms (n = 14) in controls. The prolongation of the action potential was mainly due to a decrease in density of a transient outward current (It,o) carried by K+. The normalized conductance for It,o decreased from 0.53 +/- 0.10 nS/pF (n = 25) in controls to 0.33 +/- 0.09 nS/pF (n = 26) in tumor-bearing rats. The decrease in It,o) and increase in heart weight occurred with a similar time course. The increased action potential duration prolongs Ca2+ influx through L-type Ca2+ channels in the tumor-bearing animals; this may be important in cardiovascular adaptation.
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PMID:Decreased transient outward K+ current in ventricular myocytes from acromegalic rats. 200 Sep 88

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

Report on a girl with Seckel-syndrome (bird-headed dwarfism). In addition to the known symptomatology she had a congenital heart failure (ASD II, VSD, PDA). Endocrine evaluation revealed decreased growth hormone stimulation. In the CT-scan of the skull enlarged ventricles were demonstrated.
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PMID:[Seckel dwarfism based on a personal case]. 271 36

The authors report the case of a patient with acromegaly. The clinical history was dominated by left ventricular failure, for which acromegaly was the only evident cause. The cardiac index, pulmonary arterial pressure and the average pulmonary capillary pressure were measured before ablation of the hypophyseal tumour; the measurements were repeated 3 months and 8 years later. The postoperative course followed two phases: transient improvement of the haemodynamic parameters, then relapse of cardiac failure. This case confirms the possibility of a true cardiomyopathy during acromegaly; but the fact that the cardiac failure did not regress despite the decreased growth hormone levels was unusual and raises several physiopathological hypotheses.
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PMID:[Cardiac insufficiency in acromegaly. Apropos of a case]. 383 12

Cardiovascular complications are a major cause of morbidity and mortality in acromegaly and seem to be related to the long duration of the disorder. Conventional external pituitary irradiation for acromegaly produces a consistent, but slow, fall in elevated serum growth hormone (GH) levels. It has not been established whether such treatment is effective in preventing the development of cardiovascular complications. The evolution of cardiovascular disease has therefore been studied in 11 acromegalic patients followed up for a mean 10 years (range 3-17) after external pituitary irradiation. At the final follow-up fasting serum GH were significantly (P less than 0.01) lower than pre-irradiation levels, but cardiovascular events (myocardial infarction, dysrhythmias, hypertension, major arterial disease, heart failure) increased significantly in prevalence (P less than 0.01) during this period. Electrocardiographic abnormalities also increased in prevalence. At the final follow-up 6 patients had cardiomegaly on chest X-ray and echocardiographs (10 patients) were abnormal in every case. All 11 patients had evidence of complete or partial anterior hypopituitarism. We confirm that external pituitary irradiation is effective in reducing elevated serum GH levels in acromegaly, but suggest that such a slow reduction in serum GH levels does not retard the development of cardiovascular complications.
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PMID:Progression of cardiovascular disease in acromegalic patients treated by external pituitary irradiation. 396 7


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