Cardiac cachexia: A systematic overview

Applied Cachexia Research, Department of Cardiology, Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany.
Pharmacology [?] Therapeutics (Impact Factor: 9.72). 12/2008; 121(3):227-52. DOI: 10.1016/j.pharmthera.2008.09.009
Source: PubMed


Cardiac cachexia as a terminal stage of chronic heart failure carries a poor prognosis. The definition of this clinical syndrome has been a matter of debate in recent years. This review describes the ongoing discussion about this issue and the complex pathophysiology of cardiac cachexia and chronic heart failure with particular focus on immunological, metabolic, and hormonal aspects at the intracellular and extracellular level. These include regulators such as neuropeptide Y, leptin, melanocortins, ghrelin, growth hormone, and insulin. The regulation of feeding is discussed as are nutritional aspects in the treatment of the disease. The mechanisms of wasting in different body compartments are described. Moreover, we discuss several therapeutic approaches. These include appetite stimulants like megestrol acetate, medroxyprogesterone acetate, and cannabinoids. Other drug classes of interest comprise angiotensin-converting enzyme inhibitors, beta-blockers, anabolic steroids, beta-adrenergic agonists, anti-inflammatory substances, statins, thalidomide, proteasome inhibitors, and pentoxifylline.

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    • "Heart failure (HF) is a complex syndrome which results from structural and/or functional alterations that limit the ability to respond to physiological demands [1]. These abnormalities involve metabolic and neuro-hormonal factors such as tumor necrosis factor-a (TNF-a), one of the most important catabolic cytokines related with changes in body composition, interleukin 1 (IL-1), IL-6, interferon Y, and transmission growth factor b [2], which produce catabolic and anabolic imbalance and promote loss of fat free mass (FFM) with or without loss of fat mass (FM) in patients with HF. This syndrome is called " Cardiac Cachexia " (CC) [3]. "
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    ABSTRACT: Heart Failure (HF) is a complex syndrome, which can include the physiological, neural hormonal and metabolic complications known as "Cardiac Cachexia" (CC). In the development of CC there is a release of catabolic cytokines (Tumor Necrosis Factor-α, interleukins 1 and 6) that cause a decrease of fat free mass and fat mass. These changes in body composition might be reversed with a therapeutic combination of resistance exercise and branched chain amino acid supplementation (BCAA). Evaluate changes in body composition after a resistance exercise program and BCAA supplementation in patients with HF. In a randomized clinical trial with 3 month of follow-up anthropometric body composition analysis and stress tests were evaluated at the beginning and in the end of the study. Patients were divided into two groups; the experimental group performed the resistance exercise program and received 10 g/day BCAA supplementation, and the control group only performed the resistance exercise program. Both groups were provided with individualized diets and conventional medical treatment. Changes were found in hip circumference between the groups (p = 0.02), and muscle strength was increased in the experimental group (8%) and the control group (11.4%) with no difference between them. METS and VO2Max also increased in experimental and control groups (16.6% and 50.1% respectively). Regarding changes in symptoms, improvements in fatigue (45.4%), decubitus intolerance (21.8%) and dyspnea (25.4%) were observed in the overall sample. Improvements in physical and functional capacities are attributed to resistance exercise program but not to the BCAA supplementation. Clinical Trials Identifier: NCT02240511. Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
    Clinical nutrition (Edinburgh, Scotland) 02/2015; DOI:10.1016/j.clnu.2015.02.004 · 4.48 Impact Factor
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    • "Up-regulation of FABP4 expression and other adipokines in heart failure has been demonstrated in recent studies [26-28], indicating complex neurohormonal and metabolic abnormalities associated with heart failure. Of note, up-regulation of inflammatory cytokines, catecholamines and natriuretic peptides in heart failure is known to mediate increased lipolysis and insulin resistance [29]. It has been reported that lipolysis is mediated in part through the interaction of FABP4 with hormone-sensitive lipase in adipocytes [30]. "
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    ABSTRACT: Background Fatty acid-binding protein 4 (FABP4) is expressed in both adipocytes and macrophages. Recent studies have shown secretion of FABP4 from adipocytes and association of elevated serum FABP4 level with obesity, insulin resistance, hypertension, and atherosclerosis. However, little is known about role of FABP4 in cardiac function.Methods From the database of the Tanno-Sobetsu Study, data for 190 subjects (male/female: 82/108) who were not treated with any medication and underwent echocardiography in 2011 or 2012 were retrieved for analyses of relationships between serum FABP4 concentration, metabolic markers and parameters of echocardiography.ResultsSerum FABP4 level was positively correlated with age, body mass index (BMI), blood pressure (BP), LDL cholesterol, HOMA-R and mean left ventricular (LV) wall thickness (LVWT, males: r¿=¿0.315, females: r¿=¿0.401, p¿<¿0.01) and was negatively correlated with HDL cholesterol, estimated glomerular filtration rate (eGFR) and peak myocardial velocity during early diastole (e¿; males: r¿=¿¿0.434, females: r¿=¿¿0.353, p¿<¿0.01), an index of LV diastolic function. However, no significant correlation was found between FABP4 level and LV end-diastolic dimension, LV ejection fraction or LV mass index. There were significant correlations of e¿ with age, BMI, BP, eGFR, brain natriuretic peptide (BNP), FABP4, metabolic markers and LVWT. Multivariate regression analysis adjusted by HOMA-R, BMI, eGFR, BNP or LVWT in addition to age, gender and BP revealed that serum FABP4 concentration was independently correlated with e¿.Conclusions Elevation of circulating FABP4 may contribute to LV diastolic dysfunction in a general population.
    Cardiovascular Diabetology 08/2014; 13(1):126. DOI:10.1186/s12933-014-0126-7 · 4.02 Impact Factor
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    • "In the present study, we found that the sedentary infarcted group exhibited lower body weight than the other groups. The weight loss observed in the infarcted model animals may lead to cardiac cachexia [26, 27]. Haehling et al. [27] have reported that weight loss in the cachectic patient predominantly affects muscle protein; however, bone and fat tissue are likewise affected later in the course of the disease. "
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    ABSTRACT: The aim of this study was to evaluate the effects of exercise training (ET, 50-70% of VO2 max, 5 days/week) and detraining (DT) on inflammatory and metabolic profile after myocardial infarction (MI) in rats. Male Wistar rats were divided into control (C, n = 8), sedentary infarcted (SI, n = 9), trained infarcted (TI, n = 10; 3 months of ET), and detrained infarcted (DI, n = 11; 2 months of ET + 1 month of DT). After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis), and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI.
    Mediators of Inflammation 06/2014; 2014:207131. DOI:10.1155/2014/207131 · 3.24 Impact Factor
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