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

Chronic heart failure is a clinical syndrome of cardiac origin, which affects various organ systems. It is associated with metabolic abnormalities leading to a catabolic syndrome in advanced stages of the disease. As in several other chronic diseases, skeletal muscle dysfunction and structural muscle abnormalities result in progressive muscle wasting and cachexia. These changes are accompanied by increased expression of proinflammatory cytokines, increased rate of apoptosis and activation of the proteolytic ubiquitin-proteasome pathway. Further, reduced expression of the local anabolic insulin-like growth factor-1 has been demonstrated in skeletal muscle of animals and patients with chronic heart failure. This suppression occurs in the presence of normal serum levels of insulin-like growth factor-1. In addition to catabolic effects of proinflammatory cytokines, these recent findings are consistent with reduced anabolism involving altered local insulin-like growth factor-1 levels in progressive muscle atrophy in chronic heart failure. This article describes local effects of insulin-like growth factor-1 on skeletal muscle function and morphology, its role in stem cell recruitment and muscle regeneration as well as its regulation in circumstances of muscle inflammation and wasting.
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PMID:Insulin-like growth factor-1 and muscle wasting in chronic heart failure. 1596 37

Chronic heart failure is characterized by changes in skeletal muscle that contribute to exercise intolerance and muscle weakness. To determine whether changes in the quantity and isoform distribution of key myofibrillar proteins are related to altered gene expression, we measured skeletal muscle myofibrillar mRNA abundance in nine heart failure patients (mean +/- SE; 63 +/- 3 yr) and nine controls (70 +/- 3 yr). In addition, we assessed the relationship of circulating levels of anabolic and catabolic hormones, as well as local expression of insulin-like growth factor (IGF)-I, to myofibrillar mRNA abundance. Heart failure patients were characterized by lower abundance of mRNA encoding the myosin heavy chain (MHC) I isoform (P < 0.01), whereas MHC IIa and MHC IIx mRNA did not differ between groups. Actin mRNA was also lower in heart failure patients compared with controls (P < 0.001). The expression of each MHC isoform transcript correlated with its respective protein product (MHC I: r = 0.656, P < 0.01; MHC IIa: r = 0.489, P < 0.05; MHC IIx: r = 0.505, P < 0.05; n = 18 for all). In addition to changes in myofibrillar transcripts, we found lower (P < 0.01) skeletal muscle IGF-1Ea mRNA content in heart failure patients. Myofibrillar mRNA levels were positively associated with skeletal muscle IGF-1Ea transcript levels (range of r values: 0.663-0.765; P values: <0.01 to <0.001) and modestly associated with circulating markers of immune activation (range of r values: -0.487 to -0.555; P values: <0.05 to <0.03). Our findings suggest that alterations in skeletal muscle MHC content and isoform distribution in heart failure may derive, in part, from changes in MHC gene expression. The relationships of myofibrillar mRNA content to both local and circulating hormones further suggest that alterations in the balance between anabolic and catabolic hormones in heart failure patients may influence skeletal muscle myofibrillar protein phenotype by altering gene expression.
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PMID:Skeletal muscle myofibrillar mRNA expression in heart failure: relationship to local and circulating hormones. 1614 80

Chronic heart failure is a clinical syndrome associated with an ominous long-term prognosis and major economic consequences for Western societies. In recent years, considerable progress has been made in the pharmacological management of heart failure, and several treatments have been confirmed to confer survival and symptomatic benefits. However, pharmaceuticals remain underutilised, and the combination of several different drugs present challenges for their optimal prescription, requiring a thorough knowledge of potential side effects and complex interactions. This article reviews in detail the evidence pertaining to the out-patient pharmacological management of chronic heart failure, and offers recommendations on the use of various drugs in complex clinical conditions, or in areas of ongoing controversy.
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PMID:Out-patient management of chronic heart failure. 1614 7

Chronic heart failure (CHF) is a global disease in which beside renin-angiotensin-aldosterone (RAA) system most endocrinal glands are affected. The occurrence of these disorders depends on the degree of heart failure. The influence on prognosis and therapeutic strategy is not known. The aim of this study was to evaluate the frequency of secretion disturbances of chosen hormones: prolactin (PRL), testosterone (TTE), thyroid hormones fT3, fT4 and TSH in a group of male in NYHA functional class II-IV and left ventricular ejection fraction less than 35% dependently on clinical degree of CHF and left ventricular defect. 27 male aged 35-83 years (mean 55,4) with different etiology of heart failure were enrolled in to the study. 3 groups (A, B, C) were selected dependently on NYHA class-group A - NYHA II (9), B - NYHA III (8), C - NYHA IV (10) and D group of healthy volunteers. 3 other groups were selected accordingly to left ventricular ejection fraction - I - 30-35% (14), II - 20-29% (8), III - <20% (5), IV - normal ventricular ejection fraction (10). The immunofluorescent tests were used for measuring chosen hormones concentration in blood serum. In 14 from 27 (52%) hormonal disturbances were found. No changes were noted in group A. All noted disturbances were observed in group B and C (NYHA class III/IV) more frequent in group C (90%) vs B (75%). This relation was not observed in connection with left ventricular ejection fraction. Elevated serum PRL (8) and decreased TTE concentration (5) were the most frequent hormone changes in whole study group. Results of this study confirm that CHE is often accompanied by disturbances in endocrinal glands secretion. The frequency of these disturbances rises with the degree of clinical advance of CHF.
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PMID:[Prolactin (PRL), thyrotropin (TSH), free thyroid hormones (fT4), (fT3) and testosterone (TTE) level in men with chronic heart failure]. 1620 45

Peripheral and central chemoreflexes are the dominant autonomic mechanisms regulating ventilatory patterns in response to changes in partial pressures of oxygen and carbon dioxide in arterial blood and exert powerful effects on neural circulatory control. Both reflex pathways are capable of eliciting increases in sympathetic nerve traffic and consequent increases in blood pressure. Chronic heart failure is accompanied by a sustained elevation in sympathetic nerve traffic, which is thought to be an important component in the pathophysiology and progression of the disease. The role of chemoreflex mechanisms in the control of sympathetic function during heart failure is an important topic for which there are many questions and few answers. This review summarizes available evidence documenting peripheral and central chemoreflex function in heart failure, possible mechanisms for their alteration, and their possible contribution to ventilatory, and circulatory abnormalities that occur in heart failure.
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PMID:Chemoreflex function in heart failure. 1622 15

Activation of the sympathetic nervous system is a compensatory mechanism which initially provides support for the circulation in the face of a falling cardiac output. It has been recognized for some time that chronic elevation of sympathetic outflow with the consequent increase in plasma norepinephrine, is counterproductive to improving cardiac function. Indeed, therapeutic targeting to block excessive sympathetic activation in heart failure is becoming a more accepted modality. The mechanism(s) by which sympathetic excitation occurs in the heart failure state are not completely understood. Components of abnormal cardiovascular reflex regulation most likely contribute to this sympatho-excitation. However, central mechanisms which relate to the elaboration of angiotensin II (Ang II) and nitric oxide (NO) may also play an important role. Ang II has been shown to be a sympatho-excitatory peptide in the central nervous system while NO is sympatho-inhibitory. Recent studies have demonstrated that blockade of Ang II receptors of the AT(1) subtype augments arterial baroreflex control of sympathetic nerve activity in the heart failure state, thereby predisposing to a reduction in sympathetic tone. Ang II and NO interact to regulate sympathetic outflow. Blockade of NO production in normal conscious rabbits was only capable of increasing sympathetic outflow when accompanied by a background infusion of Ang II. Conversely, providing a source of NO to rabbits with heart failure reduced sympathetic nerve activity when accompanied by blockade of AT(1) receptors. Chronic heart failure is also associated with a decrease in NO synthesis in the brain as indicated by a reduction in the mRNA for the neuronal isoform (nNOS). Chronic blockade of Ang II receptors can up regulate nNOS expression. In addition, exercise training of rabbits with developing heart failure has been shown to reduce sympathetic tone, decrease plasma Ang II, improve arterial baroreflex function and increase nNOS expression in the central nervous system. This review summarizes a large number of studies which have concentrated on the mechanisms of sympatho-excitation in heart failure. It now seems clear that one mechanism which is important in regulating sympathetic outflow in this disease state depends upon a central interaction between Ang II and NO at the cellular and nuclear levels.
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PMID:Angiotensin II--nitric oxide interactions in the control of sympathetic outflow in heart failure. 1622 14

Chronic heart failure is characterised by excess adrenergic activity that augurs a poor prognosis. The reasons for increased adrenergic activity are complex and incompletely understood. The circumstantial evidence relating increased activity to adverse outcome is powerful, but not yet conclusive. In normal subjects, autonomic control of the circulation is predominantly under the control of sympatho-inhibitory inputs from the arterial and cardiopulmonary baroreceptors, with a small input from the excitatory ergo- and chemo-receptors. In heart failure, the situation is reversed, with loss of the restraining input from the baroreceptors and an increase in the excitatory inputs, resulting in excessive adrenergic activity. The circumstantial evidence linking neuroendocrine activation with poor outcome coupled with the clinical success of inhibition of the renin-angiotensin-aldosterone system has long suggested that inhibition of adrenergic activity might be beneficial in heart failure. There is a number of potential ways of achieving this. Improved treatment of heart failure itself may reduce sympathetic drive. There is an interplay between angiotensin II, aldosterone and the sympathetic nervous system, and thus RAAS antagonists, such as angiotensin converting enzyme inhibitors and spironolactone could directly reduce sympathetic activation. Exercise rehabilitation may similarly reduce sympathetic activity.Recently, beta-adrenergic receptor antagonists have been conclusively shown to improve symptoms, reduce hospitalisations and increase survival. However, the demonstration that central reduction of sympathetic activity with agents such as moxonidine increases morbidity and mortality suggests that we do not properly understand the role of sympathetic activation in the pathophysiology of heart failure.
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PMID:The control of adrenergic function in heart failure: therapeutic intervention. 1622 19

Chronic heart failure with its age-dependent prevalence and incidence is one of the most frequent diseases. Due to high mortality and morbidity there is the necessity of early diagnosis and therapeutic measures being as causal as possible. The medical graded therapy is based on the combination of ACE-inhibitors/AT1-blockers, beta-blockers, diuretics and digitalis. Cardiac resynchronization therapy represents a novel option of treatment for only 25% of patients. Nevertheless the prognosis of patients with chronic heart failure with conventional medical therapy is remaining poor. Additional improvement in the treatment of patient with chronic heart failure remains a priority medical task. The results of this case report argues for CPAP as further adjunctive treatment option in patients with chronic heart failure.
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PMID:[CPAP as adjunctive treatment option for chronic heart failure]. 1624 Jan 42

Chronic heart failure remains a leading cause of mortality. Although granulocyte colony-stimulating factor (G-CSF) is reported to have a beneficial affect on postinfarction cardiac remodeling and dysfunction when administered before the onset of or at the acute stage of myocardial infarction (MI), its effect on established heart failure is unknown. We show here that subcutaneous administration of G-CSF greatly improves the function of murine hearts failing due to a large, healed MI. G-CSF changed the geometry of the infarct scar from elongated and thin to short and thick, induced hypertrophy among surviving cardiomyocytes, and reduced myocardial fibrosis. Expression of G-CSF receptor was confirmed in failing hearts and was upregulated by G-CSF treatment. G-CSF treatment also led to activation of signal transducer and activator of transcription-3 and induction of GATA-4 and various sarcomeric proteins such as myosin heavy chain, troponin I and desmin. Expression of metalloproteinase-2 and -9 was also increased in G-CSF-treated hearts, while that of tumor necrosis factor-alpha, angiotensin II type 1 receptor (AT1) and transforming growth factor-beta1 was reduced. Although activation of Akt was noted in G-CSF-treated hearts, vessel density was unchanged, and apoptosis was too rare to exert a meaningful effect. No bone marrow-derived cardiomyocytes or vascular cells were detected in the failing hearts of green fluorescent protein chimeric mice. Finally, beneficial effects of G-CSF on cardiac function were found persisting long after discontinuing the treatment (2 weeks). Collectively, these findings suggest G-CSF administration could be an effective approach to treating chronic heart failure following a large MI.
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PMID:Treatment with granulocyte colony-stimulating factor ameliorates chronic heart failure. 1630 79

Chronic heart failure, secondary to left ventricular hypertrophy or myocardial infarction, is a condition with increasing morbidity and mortality. Although the mechanisms underlying the development and progression of this condition remain a subject of intense interest, there is now growing evidence that redox-sensitive pathways play an important role. This article focuses on the involvement of reactive oxygen species derived from a family of superoxide-generating enzymes, termed NADPH oxidases (NOXs), in the pathophysiology of ventricular hypertrophy, the accompanying interstitial fibrosis and subsequent heart failure. In particular, the apparent ability of the different NADPH oxidase isoforms to define the response of a cell to a range of physiological and pathophysiological stimuli is reviewed. If confirmed, these data would suggest that independently targeting different members of the NOX family may hold the potential for therapeutic intervention in the treatment of cardiac disease.
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PMID:NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology. 1632 3


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