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

The term ventricular remodeling has been coined to describe the geometrical changes in size and shape of the left ventricle occurring after large myocardial infarcts. We do not exactly know what initiates this process. Slipping of myofilaments following destruction of connective tissue--probably due to metalloproteinase activation--could be the initial event. As a consequence, wall stress is increased triggering deleterious adaptation processes, such as: - intracardiac angiotensin II generation; - cardiac endothelin formation and release; - pro-apoptotic signals for cardiomyocytes; - hypertrophic signals for fibroblasts and cardiomyocytes. This cascade of events is not only observed in the process of remodeling following myocardial infarction but is also operating during the progression of heart failure. Therapeutic principles therefore are similar in both conditions: - reduction of wall stress (pharmacological or mechanical unloading of the heart); - blockade of angiotensin II generation or of AT1-receptors (ACE-inhibitors or AT1 antagonists); - blockade of endothelin receptors (ET(A)-blockers); - blockade of adrenergic receptors (preferably beta1-adrenergic receptor blockers). Better understanding of the molecular mechanisms of the remodeling process already has fueled the search for new therapeutic interventions (such as endothelin receptor blockers, aldosterone antagonists and growth hormone application). Continuous research in this field may be especially rewarding if we will succeed in identifying the very first step in the cascade.
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PMID:Ventricular remodeling after acute myocardial infarction. 1069 91

It has been reported that growth hormone may benefit selected patients with congestive heart failure. A 63-year-old man with refractory congestive heart failure waiting for heart transplantation, depending on intravenous drugs (dobutamine) and presenting with progressive worsening of the clinical status and cachexia, despite standard treatment, received growth hormone replacement (8 units per day) for optimization of congestive heart failure management. Increase in both serum growth hormone levels (from 0.3 to 0.8 microg/l) and serum IGF-1 levels (from 130 to 300ng/ml) was noted, in association with clinical status improvement, better optimization of heart failure treatment and discontinuation of dobutamine infusion. Left ventricular ejection fraction (by MUGA) increased from 13 % to 18 % and to 28 % later, in association with reduction of pulmonary pressures and increase in exercise capacity (rise in peak VO2 to 13.4 and to 16.2ml/kg/min later). The patient was "de-listed" for heart transplantation. Growth hormone may benefit selected patients with refractory heart failure.
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PMID:Growth hormone for optimization of refractory heart failure treatment. 1075 93

Experimental data suggests that growth hormone and IGF-1 have beneficial effects on myocardial function in animal models of heart failure. Preliminary evidence suggests an abnormality in the growth hormone-IGF-1 axis in heart failure with relative growth hormone resistance. Beneficial effects of growth hormone and IGF-1 include vasodilatation, stimulation of cardiac hypertrophy, increase in calcium sensitivity of cardiac myofilaments and prevention of apoptosis. Recently, cardiac cachexia has been shown to be a powerful negative predictive factor in heart failure. Cachectic patients have higher angiotensin II levels. In the rat there is an important interaction between the renin-angiotensin system and IGF-1. Thus, angiotensin II infusion causes weight loss in part through a catabolic effect. This effect results from increased protein degradation. Angiotensin II reduces circulating and skeletal muscle IGF-1 but increases IGF-1 and the IGF-IR expression in cardiac muscle. Preliminary data suggest a potential beneficial effect of growth hormone in heart failure. Further trials are necessary to test the potential beneficial effect of growth hormone and/or IGF-1 in heart failure.
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PMID:The growth hormone and insulin-like growth factor 1 axis in heart failure. 1079 May 88

In most large scale trials the prognosis of ischemic heart failure is worse than in patients with non-ischemic etiology. The therapeutic effect of essential drugs such as ACE-inhibitors, betablockers and diuretics is similar, but response to some other drugs (amiodarone, amlodipine, digoxin, growth hormone) is better in non-ischemic heart failure. Of great practical importance is the recognition of hibernating myocardium in coronary artery disease, since revascularisation may significantly improve left ventricular function. Specific therapeutic interventions are possible in hypertensive heart disease, alcoholic cardiomyopathy and LV-dysfunction to tachyarrhythmias. The etiology of heart failure should therefore be cleared in all patients.
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PMID:[Ischemic vs nonischemic heart failure--does etiology matter?]. 1085 92

Since left ventricle can cope well with volume overload and patients remain asymptomatic for years, the pharmacological interventions which prolong this period and inhibit heart failure development may be possible. However, understanding the heart failure development in chronic aortic regurgitation is a prerequisite. In this review currently postulated mechanisms of the slow but continuous development of ventricular insufficiency in chronic aortic regurgitation are examined. Based on this analysis the preventive competence of some drugs with remodelling potential is postulated: vasodilators, growth hormone, thyroxin analogues and carnitinepalmitoyltransferase-1 inhibitors. (Ref. 36.)
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PMID:Heart failure development in aortic valve insufficiency. 1091 41

Because of persistently elevated growth hormone levels, acromegaly gives rise to various changes in organs mediated by insulin-like growth factor-I. In the heart, it causes myocardial hypertrophy, and, with time, heart failure. The authors performed pituitary adenomectomy in a patient with acromegalic cardiomyopathy who had heart failure; after operation, the blood growth hormone levels decreased to within the normal range and there was a marked improvement in left ventricular function by gated blood pool scintigraphy. Pre- and postoperative fluorine-18 fluorodeoxyglucose (FDG) myocardial positron emission tomography showed increased accumulation of FDG in the myocardium before surgery, but accumulation within the normal range after operation. Myocardial glucose metabolism changed when the long-term effects of growth hormone and insulin-like growth factor-I were eliminated, and this appears to be accurately reflected by FDG positron emission tomography.
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PMID:Fluorine-18 FDG myocardial positron emission tomographic findings before and after pituitary adenoma resection in a patient with acromegalic cardiomyopathy. 1094 18

Many pathologic processes that accelerate the progression of heart failure, such as cardiac remodeling and impaired contractility, may be modulated by administration of recombinant growth hormone. The agent improves structural and functional aspects of the failing heart both in the short term and after several months of therapy. However, conflicting clinical results cast doubt on whether it has a clear benefit in all of these patients. In addition, growth hormone therapy may be associated with cardiac and noncardiac adverse effects. Many questions must be addressed before its place in heart failure therapy is established. Optimal patient population, dosing regimen, duration of therapy, and effect on patient survival are unknown. Until larger, blinded studies are completed, growth hormone therapy remains an investigational approach to managing refractory heart failure.
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PMID:Growth hormone: a promising treatment for the failing heart? 1099 3

Heart disease is the major cause of mortality in the developed world. Despite recent advances in the therapy of heart failure due to ACE inhibitors and beta-blockers, the prognosis of this syndrome is still poor. In the past few years, the effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I) on heart morphology and function were extensively studied. Some studies dealing with experimental heart failure of animals and one controversial study dealing with human heart failure suggest positive hemodynamic effects of GH and/or IGF-I treatment. This review summarizes the physiological effects of GH/IGF-I on the myocardium, their signal transduction mechanisms, and the data currently available on the therapeutic use of these agents.
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PMID:[Hormone therapy in heart failure: growth hormone and insulin-like growth factor I]. 1102 Dec 70

L-Arginine (Arg) is the substrate for the synthesis of nitric oxide (NO), the endothelium-derived relaxing factor essential for regulating vascular tone and hemodynamics. NO stimulates angiogenesis, but inhibits endothelin-1 release, leukocyte adhesion, platelet aggregation, superoxide generation, the expression of vascular cell adhesion molecules and monocyte chemotactic peptides, and smooth muscle cell proliferation. Arg exerts its vascular actions also through NO-independent effects, including membrane depolarization, syntheses of creatine, proline and polyamines, secretion of insulin, growth hormone, glucagon and prolactin, plasmin generation and fibrinogenolysis, superoxide scavenging and inhibition of leukocyte adhesion to nonendothelial matrix. Compelling evidence shows that enteral or parenteral administration of Arg reverses endothelial dysfunction associated with major cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes, obesity/insulin resistance and aging) and ameliorates many common cardiovascular disorders (coronary and peripheral arterial disease, ischemia/reperfusion injury, and heart failure). Dietary Arg supplementation may represent a potentially novel nutritional strategy for preventing and treating cardiovascular disease.
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PMID:Arginine nutrition and cardiovascular function. 1105 97

These two issues of Progress in Pediatric Cardiology comprehensively illustrate the wealth of currently available information on the pathophysiology of heart failure, age-related myocardial responsiveness, energy metabolism, cardiopulmonary interactions, the pressure-volume relationship, the systemic inflammatory response, the management of heart failure, pediatric pharmacology, the use of heart failure therapies including digoxin, ACE inhibitors, beta-adrenergic blockers, inotropic agents, diuretics, vasodilators, calcium sensitizers, angiotensin and aldosterone receptor blockers, growth hormone, and future gene therapy. The etiology and course of ventricular dysfunction in children is poorly characterized. Furthermore, many changing developmental properties of the pediatric myocardium and differences in the etiologies of ventricular dysfunction in children compared with adults are illustrated in these articles, invalidating the concept that children can safely be considered small adults for the purpose of understanding heart failure pathophysiology and treatment. However, these articles reveal that strikingly little research in children with ventricular dysfunction exists in terms of well-designed large-scale studies of the epidemiology or multicenter controlled clinical therapeutic trials. A future research agenda is proposed to improve understanding etiologies, course and treatment of ventricular dysfunction in children that is based on organized and funded cooperative groups since no one pediatric cardiac center treats enough children with a particular etiology of ventricular dysfunction. In conclusion, significant understanding of basic mechanisms of pediatric ventricular dysfunction and effective therapies for adults with ventricular dysfunction exist. A multicenter pediatric cardiac ventricular dysfunction network would allow improved understanding of diseases and treatments, and result in evidence-based medicine for pediatric patients with ventricular dysfunction.
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PMID:Ventricular dysfunction clinical research in infants, children and adolescents. 1111 43


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