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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 may affect cardiac function. In rats, chronic hypersecretion of growth hormone leads to increased maximum isometric contractile force of the left ventricular papillary muscle in vitro. In humans, administration of growth hormone can increase myocardial contractility. However, cardiac effects of growth hormone in heart failure or cardiac dysfunction have not been studied to date. The current study was to evaluate the cardiac effects of growth hormone in conscious rats with postinfarction left ventricular dysfunction and sham controls. Ligation of the left coronary artery or sham operation was performed, then 4 weeks after surgery, recombinant human growth hormone (2 mg/kg/day, SC) or vehicle was administered for 15 days. Catheters were implanted 13 days after treatment with growth hormone or vehicle. Hemodynamic parameters were measured in conscious rats 2 days after catheterization. In vehicle-treated rats, left ventricular systolic pressure, maximum dP/dt, and arterial pressure were significantly decreased and left ventricular end-diastolic pressure was significantly increased in the ligation group compared with sham controls. Growth hormone treatment increased left ventricular systolic pressure (p < 0.05) and dP/dt (p < 0.05) and reduced left ventricular end-diastolic pressure (p < 0.05), significantly in the ligated rats. In sham rats, growth hormone tended to decrease arterial pressure but did not alter ventricular contractility. Neither ligation nor growth hormone significantly altered heart rate and right atrial pressure. These results suggest that growth hormone treatment may improve cardiac function by increasing myocardial contractility in cardiac dysfunction or heart failure.
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PMID:Effects of growth hormone in rats with postinfarction left ventricular dysfunction. 778 32

We report experiences in 3 patients with acromegaly while using the somatostatin analogue octreotide. In case 1, a 44 year old male developed pneumococcal meningitis 3 months after having transphenoidal surgery for a pituitary tumour. This occurred with the re-emergence of communication between the surgical tract and the C.S.F. In case 2 a 52 year old male with insulin resistant diabetes mellitus requiring 240 units/day, with greatly elevated growth hormone concentrations was able to stop insulin within 5 days of starting octreotide. In case 3, a 52 year old male with sleep apnoea syndrome, respiratory failure and resistant heart failure made a dramatic improvement which is maintained 2 years later. All cases were associated with substantial falls in growth hormone and insulin like growth factor-1 concentrations.
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PMID:Experiences with octreotide in acromegaly. 844 80

It is possible that growth hormone can offer therapeutic benefits for treating some forms of heart failure.
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PMID:Cardiac performance: growth hormone enters the race. 856 31

The effects of growth hormone (GH) plus insulin-like growth factor-1 (IGF-1) were tested in an experimental model of cardiac failure treated with chronic angiotensin-converting enzyme (ACE) inhibition. Myocardial infarction was induced in rats by left coronary artery ligation. Two weeks after ligation, the animals received either captopril (2 g/L in drinking water) or water for 3 months. The rats were then given either GH (2 mg/kg/day) plus IGF-1 (2 mg/kg/day) or vehicle for 14 days. Captopril treatment decreased mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP) and systemic vascular resistance (SVR) (p < 0.05), and increased cardiac index (CI) and stroke volume index (SVI) (p < 0.05). GH/IGF-1 or captopril+GH/IGF-1 treatment decreased MAP, LVEDP, and SVR (p < 0.05), and increased left ventricular maximum dP/dt, CI, and SVI (p < 0.05). The increases in CI and SVI were significantly greater in the captopril+GH/IGF-1-treated animals than in those treated with captopril alone (p < 0.05). The beneficial effect of captopril in reducing cardiac hypertrophy was preserved in the captopril+GH/IGF-1 group. The results indicate that GH/IGF-1 and captopril can improve cardiac performance in congestive heart failure by independent and complementary mechanisms.
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PMID:Beneficial effects of growth hormone and insulin-like growth factor-1 in experimental heart failure in rats treated with chronic ACE inhibition. 858 84

Previous studies showed increased growth hormone (GH) plasma levels in patients with severe heart failure. It has been hypothesized that the activation of adenohypophysis determines the enhanced release of GH. The present study was designed to verify whether impaired hepatic function, due to biventricular cardiac failure and hepatic stasis, by reducing synthesis and release of insulin-like growth factor-1 (IGF-1), may affect the negative feedback mechanism of the IGF-1 on GH secretion. We studied 20 normotensive, non diabetic patients without primitive liver disease; 10 patients in NYHA functional class IV with clinical signs of biventricular cardiac impairment and hepatic stasis (Group A); 10 patients in NYHA functional class III with prevalent left ventricular dysfunction (Group B). Blood samples for radioimmunologic determination of GH, IGF-1, atrial natriuretic factor (ANF), proteins, albumin plasma levels and transaminase plasma levels measurements, were collected 24 hours before hemodynamic study. Group A patients had clinical and hemodynamic signs of hepatic stasis with impaired liver function (SGOT 68 +/- 5.5 U/l; SGPT 89 +/- 4.3 U/1; proteins 4.56 +/- 0.4 g/dl with albumin/globulin ratio < 1; albumin plasma levels 2.8 +/- 0.7 g/dl). The parameters were normal in Group B (SGOT 16 +/- 3.7 U/l;SGPT 13 +/- 1.9 U/l; proteins 7.5 +/- 0.7 g/dl with albumin/globulin ratio > or = 1.5;albumin plasma levels 4.2 +/- 1.2 g/dl). ANF values, over normal range in both groups, were significantly higher in Group A (157.9 +/- 43.9 vs 65.6 +/- 14.6 fmol/ml.p < 0.0001). In Group A GH values were increased (4.9 +/- 4.5 vs 0.12 +/- 0.04 ng/ml); on the contrary IGF-1 values were lower (187.9 +/- 98.2 vs 260.4 +/- 141.4 ng/ml, p < 0.01). The comparison between IGF-1 and albumin plasma levels showed a high correlation either in Group A (r = 0.88, p < 0.001;) or in Group B (r = 0.81, p < 0.001). Our findings allow to hypothesize that the reduced hepatic synthesis and release of IGF-1 may be responsible for the lack of trophic action of GH on cardiac myocytes in patients with biventricular heart failure and hepatic stasis.
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PMID:[Changes in growth hormone/insulin-like growth factor-1 axis in patients with normal pituitary function and biventricular cardiac failure and hepatic stasis]. 876 34

The physiologic trophic factors growth hormone (GH) and insulin-like growth factor 1 (IGF-1) generally increase body weight and cardiac mass proportionately, and several studies suggest that both growth factors cause vasodilation and increased myocardial contractility. Established clinical benefits of ACE inhibitors can be explained, at least in part, by inhibition of cell hypertrophy, lowered systemic vascular resistance (SVR) and afterload, leading to reduction of progressive left-ventricular (LV) enlargement. An alternative approach would be to administer IGF-1 or GH to stimulate compensatory hypertrophy and reduce afterload by their vasodilator action, as well as through potential favorable effects on myocardial contractility. In our initial study in the rat myocardial infarction (MI) model, when IGF-1 was administered early (at 2 days) post-MI and continued for 2 weeks, body weight (BW) increased and LV weight/BW remained unchanged, the LV end-diastolic volume (EDV) and stroke volume increased (but not when normalized to BW), and the LV ejection fraction increased in rats with large infarctions. These findings suggested a beneficial rather than detrimental effect of such treatment, and we then studied the action of combined IGF-1 and GH starting after infarct healing at 4-weeks' post-MI. BW increased substantially and LVEDV/BW was lower in treated rats than in control rats, suggesting relatively less LV dilation with little remodeling in this setting; IGF-1/GH increased the cardiac output by 46%, systemic vascular resistance (SVR) fell and the cardiac index (CI) was significantly elevated in treated rats with a large MI. Recently, others have used the rat MI model to study the effects of 2-weeks' of GH started at 4-weeks' post-MI, as well as IGF/GH for 2-weeks in rats treated with an ACE inhibitor for 3-month's post-MI. In both studies, in conscious treated rats the BW increased, LV/BW was not different compared to the control rats, but the CI increased, SVR fell, and estimated LV dP/dtmax was significantly augmented. Preliminary data in our laboratory suggest that beneficial effects may also occur with GH administration in the setting of chronic angiotensin II receptor blockade (losartan) after MI in the rat. Thus, growth factor therapy appears to have favorable effects in heart failure early and late after MI in the rat. Additional cardiac hypertrophy occurs early after MI, but the later beneficial effects appear to relate primarily to systemic vasodilation, improved cardiac output, and enhanced myocardial contractility.
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PMID:The role of hypertrophy and growth factors in heart failure. 895 69

The aim of this study was to evaluate changes of pituitary and adrenal cortex hormones in patients with congestive heart failure according to NYHA functional classes and to detect possible prognostic effects of these changes. We studied 101 patients: 60 with congestive heart failure, in absence of clinical, anamnestic signs of endocrine diseases (Group I, 37 males, 23 females; mean age 62 +/- 7.2 years) and 41 patients with cardiac diseases without signs of congestive heart failure, homogeneous for age and sex (Group II, 23 males, 18 females; mean age 61 +/- 8.5 years). All patients were submitted to a 12 month follow-up in order to evaluate hormonal changes. Hormonal study was performed through radioimmunoassay technique. Plasma levels of insulin, growth hormone (GH), adrenocorticotropine (ACTH), cortisol and prolactin (PRL) were evaluated. We observed in Group I a significant increase of cortisol and GH with respect to Group II. No significant difference occurred in plasma levels of insulin, PRL and ACTH. Subdividing Group I patients on the basis of NYHA classification, significant increase (p < 0.05) in cortisol and GH was observed in IV NYHA functional class with respect to II and III NYHA ones. Moreover a significant reduction (p < 0.02) of ACTH in IV NYHA functional class was also detected. Plasma levels of cortisol and GH were also significantly higher in patients dead during the follow-up with respect to survivors. Statistical analysis showed a linear negative correlation between cortisol and ACTH in III NYHA functional class (p < 0.03), a negative correlation between cortisol and radius/thickness ratio (p < 0.03) and between cortisol and serum glutamic oxalacetic transaminase (p < 0.05). In IV NYHA functional class a significant negative correlation between cortisol and shortening fraction (p < 0.05) also occurred. Plasma levels of cortisol and GH were significantly higher (p < 0.05) in IV NYHA functional class with respect to II and III classes, with associated significant reduction of shortening fraction (p < 0.05). Our data confirm that, besides catecholamines and renin-angiotensin-aldosterone system, in the presence of severe congestive heart failure (IV NYHA functional class), a significant activation of pituitary and adrenal cortex hormones occurs. It is still an open question whether this activation plays a pathogenetic role in the evolution of heart failure, but the significant increase of these hormones (GH and cortisol) seems to be significant negative prognostic markers.
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PMID:[The prognostic value of activation of the hypophyseal and adrenal cortical systems in severe heart failure]. 911 59

Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although concomitant cardiac hypertrophy, generally considered to be a cardiovascular risk factor, has also been reported. In the present study, we combine a rat model with impaired cardiac performance after myocardial infarction (MI) with echocardiographic evaluation of GH effects on cardiac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in subsequent impaired cardiac performance. After 6 weeks' recovery, blind transthoracic echocardiography was performed to determine infarction size, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rats were treated with daily s.c. injections of saline (n = 8) or recombinant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg-1 body weight for 1 week. A new blind echocardiography examination was performed after treatment demonstrating a 13% increase in ejection fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a significant decrease in end-systolic volume. There were no significant changes in left ventricular (LV) or interventricular wall thickness, LV dimensions, heart rate or diastolic function. No effects were seen on LV weight, cardiac insulin-like growth factor (IGF) I, IGF-I receptor and GH receptor mRNA content. GH in a physiological dose improves systolic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in the treatment of heart failure and merits further investigation.
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PMID:Growth hormone improves cardiac function in rats with experimental myocardial infarction. 922 33

A perioperative anesthetic management of a 69 year old woman with acromegaly whose clinical course was characterized by severe heart failure is described. The patient showed symptoms of massive cardiomegaly. Endocrine studies indicated that her pituitary tumor was active with hyperproduction of growth hormone. There was no demonstrable evidence for other known causes of heart disease. Following hormonal therapy using continuous subcutaneous infusion of somatostatin for about two months, there was improvement in daily activity and reduction in heart size. After the improvement of cardiac function, transsphenoidal hypophysectomy was performed under general anesthesia and its perioperative course was quite uneventful. We conclude that because cardiac involvement such as left ventricular dilatation in acromegaly might be reversible with proper treatment, any surgical procedure, as long as the case is elective, should be considered after hormone therapy.
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PMID:[A patient with acromegalic heart disease--a case report]. 925 11

Cytokines have been associated with the pathogenesis of acute coronary syndromes and chronic heart failure (CHF), which are both associated with cardiomyocyte loss. In CHF, increased serum concentrations of proinflammatory cytokines, including tumour necrosis factor alpha (TNF-alpha) and also soluble TNF receptor have been found. Both TNF and Fas-ligand have been able to induce programmed cell death (apoptosis) of cardiomyocytes in various experimental studies. In ischaemic conditions of the heart, increased serum levels of soluble Fas receptor have been found. The proinflammatory cytokines interleukin 1 (IL-1), IL-2 and interferon-gamma can induce TNF production from target cells, including myocytes. TNF and some other cytokines are able to induce nitric oxide production, which depresses cardiac function and can induce apoptosis. However, anti-inflammatory cytokines such as IL-10, IL-4 and IL-13, secreted by T-helper type 2 lymphocytes and other cells, inhibit the production of proinflammatory cytokines. Preliminary studies suggest that cardiotrophin-1, produced by cardiomyocytes, is able to inhibit cytokine-induced cardiomyocyte apoptosis in vitro. As growth hormone is able to inhibit the production of proinflammatory cytokines in many cell types, it may also play an important role in the regulation of apoptosis induced by these cytokines. When the cytokine-induced pathways leading to altered gene expression of cardiomyocytes are understood, this knowledge may aid in the development of drugs that prevent progressive cardiomyocyte loss, in particular by inhibiting cytokine-induced apoptosis.
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PMID:Cytokines and cardiomyocyte death. 937 93


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