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

Growth hormone (GH) has been attracted as a possible adjunctive treatment for severe heart failure. However, its treatment effects have been still controversial. To assess severity of basal cardiac disease states in which GH might be effective, we analyzed the relation of treatment effects of GH following chronic angiotensin-converting enzyme (ACE) inhibition on cardiac function and structures to infarct size in rat model of chronic heart failure after myocardial infarction. One day after coronary occlusion, rats were randomized to either an ACE inhibitor, temocapril (T) (80 mg/L in drinking water) or placebo for 12 weeks. The animals received concomitant recombinant human (rh) GH (2 mg/kg/day, SC) (T + GH) or vehicle during the final 2 weeks. Compared with the T group, the T + GH group with large MI had smaller increments of left ventricular (LV) dP/dt(max) (0 vs 17%) and cardiac output (9 vs 49%), less improvement of LV relaxation (tau) (-3 vs 29%) and systemic vascular resistance (8 vs 29%), and a greater increase in LV end-diastolic pressure (123 vs -5%) than did the T+GH group with moderate MI. In the T + GH group when compared with the T group, these functional alterations were associated with a 12% reduction in the LV capillary density and a 21% increase in hydroxyproline contents in rats with large MI, whereas a 12% increase in the density and similar collagen contents were found in rats with moderate MI. Thus, prominent beneficial cardiovascular effects of the additive short-term, high-dose GH to chronic high-dose ACE inhibition were obtained in rats with moderate MI, whereas little additional benefit or even detrimental effects of GH were found in rats with large MI. The present study may provide an insight into the therapeutic strategy of GH given late after MI in the presence of chronic ACE inhibition in congestive heart failure.
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PMID:Effects of growth hormone following chronic angiotensin-converting enzyme inhibition in chronic heart failure: their relation to infarct size. 1171 92

Growth hormone (GH) application is a new strategy in the treatment of heart failure. However, clinical and experimental investigations have shown contradictory effects of GH on cardiac performance. We tested the hypothesis that GH could improve cardiac and renal function in volume overload-induced heart failure. The effect of 4 weeks of GH treatment (2 mg/kg daily) was investigated in Wistar rats with aortocaval shunt. GH application did not influence left ventricular contractility and end-diastolic pressure in rats with aortocaval shunt. In contrast, GH treatment normalized impaired diuresis (vehicle 10.8+/-0.6 mL/d, GH 15.8+/-0.7 mL/d; P<0.05) and sodium excretion (vehicle 1.5+/-0.1 mmol/d, GH 2.2+/-0.1 mmol/d; P<0.001) in shunt-operated rats, with a similar increase of fractional sodium excretion. The urinary excretion of cGMP, the second messenger of atrial natriuretic peptide and NO, was higher in animals with shunts than in sham-operated animals and was further increased by GH (vehicle 293+/-38 nmol/d, GH 463+/-57 nmol/d; P<0.01). Although the atrial natriuretic peptide plasma levels were unchanged after GH, the excretion of NO metabolites (nitrate/nitrite) was elevated (vehicle 2020+/-264 nmol/d, GH 2993+/-375 nmol/d; P<0.05) in parallel with increased renal mRNA levels of inducible NO synthase 2. The changes of renal function after GH and the increased excretion of NO metabolites and cGMP were abolished by simultaneous treatment with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester. GH treatment did not influence cardiac function in rats with aortocaval shunts. However, GH improved renal function by increasing diuresis and sodium excretion. The responsible mechanism might be the enhanced activity of the renal NO system.
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PMID:Cardiac and renal effects of growth hormone in volume overload-induced heart failure: role of NO. 1179 79

Growth hormone is a pituitary polypeptide hormone regulating growth in paediatric age as well as inducing anabolic actions directly or IGF-I mediated in adult age. Particularly, in many animals GH and IGF-I receptors were observed in cardiac myocyte membrane. GH modifies left ventricle structure and function. As concerns spontaneous GH secretion, some data suggest that pituitary gland can have a compensatory role on endocrine response to heart failure. Heart failure stage was directly correlated to nocturnal GH levels. All GH spontaneous night secretion parameters as well as IGF-I levels showed a range between normal people and very high spontaneous secretion. Therefore in these patients there are either a GH peripheric resistance or a reduction of the activity of GH/IGF-I axis. Anyhow in our patients, GH 24 hour infusion was inducing a 5 fold increase in GH concentration and a 50% increase in basal IGF-I levels. Anker et al. suggested to evaluate nutritional state in heart failure patients, observing no differences in non-cachectic patients vs controls, while cachectic patients presented a typical GH resistance syndrome. Interestingly, cardiovascular effects of GH administration seem to be only marginally correlated to hemodynamic basal state. On the other hand basal hormonal setting of the patient seems to correlate to the GH-induced cardiovascular response. In fact, low basal IGF-I but high basal GH patients presented the worst endocrine and cardiovascular response to GH infusion. In literature there are controversial data about GH treatment in patients with chronic heart failure. The heterogeneity of the population could be the reason for this discrepancy. Besides very different IGF-I responses to GH have been reported. Therefore, as there is good clinical evidence that GH acute infusion can improve heart failure, it seems to be necessary firstly to evaluate the basal endocrine status of the patients. Particularly attention should be given to those patients that present a peripheric GH resistance. On the other hand, those patients with a reduced pituitary GH reserve are supposed to have very beneficial effects from GH treatment.
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PMID:[Growth hormone secretion in heart failure]. 1262 59

Despite improvement in survival with angiotensin-converting enzyme inhibitors and beta blockers, clinical events for patients with heart failure remain elevated. New therapies for heart failure are needed to improve functional capacity, quality of life, and prognosis. Growth hormone exerts direct and indirect effects on cardiac structure and function. Experimental models of heart failure and small studies have demonstrated significant improvements in cardiac function, hemodynamic parameters, functional capacity, and quality of life. Despite the lack of benefit demonstrated in small, short-term, randomized clinical trials, further studies are needed to assess the potential role of this adjuvant therapy in heart failure patients.
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PMID:Growth hormone therapy in heart failure: where are we now? 1267 39

Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-alpha (TNF-alpha) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not yet clear. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After 2 wk, 2 groups of rats were treated with GH (0.2 mg.kg(-1).day(-1) and 1.0 mg.kg(-1).day(-1)) subcutaneously. A third group of controls had saline. After 2 additional weeks, rats were killed. Tibialis anterior cross-sectional area, myosin heavy chain (MHC) composition, and a study on myocyte apoptosis and serum levels of TNF-alpha and SPH were carried out. The number of apoptotic nuclei, muscle atrophy, and serum levels of TNF-alpha and SPH were decreased with GH at high but not at low doses compared with CHF rats. Bcl-2 was increased, whereas activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slowed down both contraction and relaxation but did not affect specific tetanic force, whereas absolute force was decreased. GH treatment restored contraction and relaxation to control values and brought muscle mass and absolute twitch and tetanic tension to normal levels. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF to improve exercise capacity.
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PMID:Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure. 1367 2

Growth hormone (GH) acting through locally produced insulin--like growth factors stimulates myocardial hypertrophy and increases myocyte contractility. Many people with growth hormone deficiency (GHD) present a lower left ventricular mass, reduced ejection fraction and lower exercise tolerance. Recombinant human growth hormone (rhGH) administration gives a chance to correct these disturbances. On the other hand excessive levels of GH (for example in acromegaly) may induce heart failure too. Initially, cardiac hypertrophy is an adaptive response, but with time, in untreated cases, it leads to congestive heart failure. Mentioned information inclined many authors to undertake researches on rhGH application in severe heart failure in patient with idiopathic dilated cardiomyopathy and coronary disease. RhGH improved treatment let these patients reach heart transplantation.
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PMID:[Clinical and metabolic effects of recombinant human growth hormone in cardiac insufficiency]. 1459 78

Growth hormone therapy in patients with idiopathic dilated cardiomyopathy and ischemic cardiac failure has revealed varying effects on systolic function, probably related to the response in serum insulin-like growth factor I (IGF-I) levels. As diastolic function has not been studied thoroughly, we studied the effects of 6 months of recombinant human growth hormone (rh GH) treatment on systolic and diastolic function in patients with ischemic cardiac failure, using cardiovascular magnetic resonance (MR) imaging. Nineteen patients with ischemic cardiac failure (left ventricular ejection fraction (LVEF), <40%) were studied in a randomized trial. Nine patients received 6 months treatment with growth hormone (2 IU/day). Systolic and diastolic function were assessed at baseline and after 26 weeks by cardiovascular MR imaging. No differences were found in systolic and diastolic function between rh GH treated patients and controls. No change was observed in left ventricular mass index (LVMI), end-diastolic volume, end-systolic-volume and ejection fraction. The treated patients showed no clinical improvement. Six months of treatment with growth hormone therapy in ischemic cardiac failure has no favorable effects on LVMI, on systolic and diastolic function.
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PMID:Six-months of recombinant human GH therapy in patients with ischemic cardiac failure. 1505 21

Growth hormone (GH) replacement therapy for children and adults with proven GH deficiency due to a pituitary disorder has become an accepted therapy with proven efficacy. GH is increasingly suggested, however, as a potential treatment for frailty, osteoporosis, morbid obesity, cardiac failure, and various catabolic conditions. However, the available placebo controlled studies have not reported many significant beneficial effects, and it might even be dangerous to use excessive GH dosages in conditions in which the body has just decided to decrease GH actions. GH can indeed induce changes in body composition that are considered to be advantageous to GH deficient and non-GH deficient subjects. In contrast to GH replacement therapy in GH deficient subjects, however, excessive GH action due to GH misuse seems to be ineffective in improving muscle power. Moreover, there are no available study data to indicate that the use of GH for non-GH deficient subjects should be advocated, especially as animal data suggest that lower GH levels are positively correlated with longevity.
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PMID:Justified and unjustified use of growth hormone. 1546 91

Growth hormone (GH) deficiency decreases left ventricular (LV) contractility, induces LV chamber dilatation and promotes progression to congestive heart failure. It is, however, controversial, whether GH replacement therapy in addition to standard medical heart failure therapy should be considered as routine treatment in GH deficient patients with heart failure. In the present report of a 64-year-old GH deficient patient with heart failure, we demonstrate by using Doppler echocardiography, magnetic resonance imaging and 31P NMR spectroscopy that even a 12 month period of GH replacement therapy had no sustained effect on morphometric or functional parameters of LV performance nor on clinical signs or symptoms of heart failure. It is concluded that GH replacement therapy should currently not be regarded as standard heart failure therapy in patients with GH deficiency and should only be employed under careful monitoring including close follow-up in a standardized way.
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PMID:Failure of recombinant human growth hormone treatment to improve congestive heart failure in hypopituitarism. 1550 63

Growth hormone (GH)-releasing peptides (GHRP), a class of synthetic peptidyl GH secretagogues, have been reported to exert a cardioprotective effect on cardiac ischemia. However, whether GHRP have a beneficial effect on chronic heart failure (CHF) is unclear, and the present work aims to clarify this issue. At 9 wk after pressure-overload CHF was created by abdominal aortic banding in rats, one of four variants of GHRP (GHRP-1, -2, and -6 and hexarelin, 100 mug/kg) or saline was injected subcutaneously twice a day for 3 wk. Echocardiography and cardiac catheterization were performed to monitor cardiac function and obtain blood samples for hormone assay. GHRP treatment significantly improved left ventricular (LV) function and remodeling in CHF rats, as indicated by increased LV ejection fraction, LV end-systolic pressure, and diastolic posterior wall thickness and decreased LV end-diastolic pressure and LV end-diastolic dimension. GHRP also significantly alleviated development of cardiac cachexia, as shown by increases in body weight and tibial length in CHF rats. Plasma CA, renin, ANG II, aldosterone, endothelin-1, and atrial natriuretic peptide were significantly elevated in CHF rats but were significantly decreased in GHRP-treated CHF rats. GHRP suppressed cardiomyocyte apoptosis and increased cardiac GH secretagogue receptor mRNA expression in CHF rats. GHRP also decreased myocardial creatine kinase release in hypophysectomized rats subjected to acute myocardial ischemia. We conclude that chronic administration of GHRP alleviates LV dysfunction, pathological remodeling, and cardiac cachexia in CHF rats, at least in part by suppressing stress-induced neurohormonal activations and cardiomyocyte apoptosis.
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PMID:GH-releasing peptides improve cardiac dysfunction and cachexia and suppress stress-related hormones and cardiomyocyte apoptosis in rats with heart failure. 1595 41


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