Publications

  • Stephan von Haehling
    [Show abstract] [Hide abstract]
    ABSTRACT: To the Editor: Kress and Hall (April 24 issue)(1) describe neuromuscular problems commonly observed in the intensive care unit (ICU) during critical illness. Critical illness polyneuropathy is a generalized axonal neuropathy with predominance in the lower extremities.(2) Entrapment neuropathy is also quite common in the ICU. Loss of subcutaneous fat during a long stay in the ICU makes peripheral nerves susceptible to compression injury, particularly at the fibular head (leading to diminished power of the anterior tibialias) and at the ulnar groove (leading to diminished power in the intrinsic hand muscles). The problem can be avoided simply by awareness and . . .
    New England Journal of Medicine 07/2014; 371(3):287-8. · 51.66 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Matrix metalloproteinase 9 (MMP-9) is crucial for physiological tissue repair and pathophysiological myocardial remodeling. The regulation of its functioning has been shown to be mediated by formation of complexes with tissue inhibitor of metalloproteinases 1 (TIMP-1) and neutrophil gelatinase associated lipocalin (NGAL). We investigated the mRNA and protein expression of MMP-9, TIMP-1 and NGAL, the formation of complexes, their gelatinolytic activity and cellular localization in left ventricle (LV) from 10 female pigs with induced systolic heart failure (HF), 5 control pigs, and a woman with severe HF. The MMP-9, TIMP-1 and NGAL mRNA in LV did not differ between diseased and healthy pigs. In all pigs MMP-9, TIMP-1 and NGAL proteins were present in LV as high molecular weight (HMW) complexes (115, 130, 170 and 220 kDa), and no monomers were found. A 80 and 115 kDa gelatinolytically active bands were present in all LV homogenates. A 130-kDa active band was seen only in LV from pigs with severe HF. Similar results were found in the explanted heart of a female patient with severe HF. The incubation of the homogenates of porcine LV at 37°C resulted in appearance of 88 kDa active band, which was accompanied by a decreased intensity of HMW bands. The incubation of the homogenates of porcine LV (depleted of active MMP-9) with trypsin generated 80 and 115 kDa active bands. Immunohistochemistry revealed the presence of MMP-9 in the cytoplasm of porcine cardiomyocytes, but not in cardiofibroblasts. Our data suggest that MMP-9 originates from cardiomyocytes, forms the gelatinolytically inactive complexes with TIMP-1 and NGAL, present in normal and failing myocardium, likely serving as a reservoir of active MMP-9. Further studies are needed to elucidate the role of these HMW complexes in the extracellular matrix remodeling during the progression of HF, which presence should be considered when developing efficient strategies inhibiting myocardial matrix metalloproteinases.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 06/2014; 65(3):365-75. · 2.48 Impact Factor
  • Source
    John E Morley, Stephan von Haehling, Stefan D Anker
    [Show abstract] [Hide abstract]
    ABSTRACT: The two most common muscle wasting diseases in adults are sarcopenia and cachexia. Despite differences in their pathophysiology, it is believed that both conditions are likely to respond to drugs that increase muscle mass and muscle strength. The current gold standard in this regard is exercise training. This article provides an overview of candidate drugs to treat muscle wasting disease that are available or in development. Drugs highlighted here include ghrelin agonists, selective androgen receptor molecules, megestrol acetate, activin receptor antagonists, espindolol, and fast skeletal muscle troponin inhibitors.
    Journal of cachexia, sarcopenia and muscle. 05/2014;
  • S von Haehling, S D Anker
    [Show abstract] [Hide abstract]
    ABSTRACT: Anaemia and iron deficiency are frequent co-morbidities in patients with chronic heart failure. Both are bound to worsen an already reduced exercise capacity in these patients. Recent data have demonstrated that iron deficiency alone, i. e. without concomitant anaemia, reduces quality of life, exercise capacity and likely also surivival. Two clinical entities should be differentiated in this context: absolute and functional iron deficiency, the first being an absolute deficiency of iron, the second representing a disturbed mobilisation capacity. The FAIR-HF study has shown that intravenous iron administration can improve quality of life and exercise capacity in affected patients. A correct diagnosis can easily be arrived at using parameters such as serum ferritin and transferrin saturation. Replenishing iron stores is most useful using the intravenous route, and administered doses need to be adjusted to individual needs.
    DMW - Deutsche Medizinische Wochenschrift 04/2014; 139(16):841-4. · 0.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Muscle wasting and cachexia are the ultimate consequence of aging and a variety of acute and chronic illnesses. Significant efforts are made by many stakeholders to develop effective therapies. An important aspect of successful therapeutic development research is a common nomenclature for effective communication between researchers and clinicians, to the public, and also with regulatory bodies. Despite several efforts to develop consensus definitions for cachexia and sarcopenia, including such new terms for muscle wasting as myopenia, a common conceptual approach and acceptable vocabulary and classification system are yet to be established. Notwithstanding the potential need to translate such disease definitions and terminologies into different languages, we advocate the use of the term "muscle wasting" as the unifying entity that represents the single most common disease process across a large spectrum of cachexia and in sarcopenia-associated disorders. In this paper, we outline a first proposal for the disease nomenclature and classification of "Muscle Wasting Diseases." This concept can be applied in acute and chronic disease settings. It is pertinent for wasting diseases, cachexia, and sarcopenia of any severity and due to any underlying illness. The concept of muscle wasting disease underscores the most common denominator of the underlying wasting processes, i.e., muscle wasting, without ignoring the advanced disease states that are also accompanied by fat tissue wasting. The term muscle wasting disease is easily understood by both the scientific community and the lay public. This may promote its general use and efforts to heighten education and awareness in the field.
    Journal of cachexia, sarcopenia and muscle. 03/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This article highlights preclinical and clinical studies in the field of wasting disorders that were presented at the 7th Cachexia Conference held in Kobe, Japan, in December 2013. This year, the main topics were the development of new methods and new biomarkers in the field of cachexia and wasting disorders with particular focus on inflammatory pathways, growth differentiation factor-15, myostatin, the ubiquitin proteasome-dependent pathway, valosin and the regulation of ubiquitin-specific protease 19 that is involved in the differentiation of myogenin and myosin heavy chain. This article presents highlights from the development of drugs that have shown potential in the treatment of wasting disorders, particularly the ghrelin receptor agonist anamorelin, the myostatin antagonist REGN1033, the selective androgen receptor modulators enobosarm and TEI-E0001, and the anabolic catabolic transforming agent espindolol. In addition, novel data on the prevalence and detection methods of muscle wasting/sarcopenia are presented, including the D3-creatine dilution method and several new biomarkers.
    Journal of cachexia, sarcopenia and muscle. 03/2014;
  • Source
    John E Morley, Stephan von Haehling, Stefan D Anker, Bruno Vellas
    [Show abstract] [Hide abstract]
    ABSTRACT: The physical frailty phenotype consists of fatigue, weight loss, and loss of muscle power. Sarcopenia has been shown to be a major cause of frailty. Six societies including SCWD published a consensus suggesting that all persons older than 70 years of age should be screened for frailty when seeing health professionals. Simple screening tests such as the FRAIL (fatigue, resistance, aerobic, illness, and loss of weight) scale can be used. It is felt that frailty can be treated by exercise (resistance and aerobic), high quality protein, vitamin D, and treatment of the common causes of fatigue. It is expected that this approach will decrease disability in older persons.
    Journal of cachexia, sarcopenia and muscle. 02/2014;
  • Miroslava Valentova, Stephan von Haehling
    [Show abstract] [Hide abstract]
    ABSTRACT: The European Society of Cardiology held their annual congress in Amsterdam between the 31st of August and 4 September 2013 to discuss the latest developments in the field. The meeting included an update of the latest treatments currently under investigation for the treatment of heart failure. Updates were provided on the RELAX-AHF study that had, for the first time, demonstrated an improvement in post-discharge outcome in patients with acute heart failure treated with seralaxin. The meeting also gave the opportunity to highlight the latest goings on from the promising agent omecamtiv mecarbil as shown in the ATOMIC-AHF study. Indeed, its unique inotropic effect showed a potential to improve dyspnea without increasing myocardial oxygen consumption. Other presentations at the meeting included: a recent study evaluating ultrafiltration in the treatment of acute HF with renal impairment and the effects of the vasodilator cinaciguat. The unremarkable results from the recent ASTRONAUT study with aliskiren were also touched upon. It is important to note that while the data from seralaxin and omecamtiv mecarbil has been promising, the long term benefits of these therapies in heart failure still need to be evaluated. The authors also highlight the need for these promising agents to be further evaluated in women and other ethnic groups.
    Expert Opinion on Investigational Drugs 02/2014; · 4.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This article aims to describe molecular pathways involved in the development of muscle wasting and cachexia, diagnostic possibilities, and potential treatments that have seen clinical testing in recent heart failure trials. An understanding of the specific changes that cause a catabolic-anabolic imbalance is an essential first step in the development of pharmaceutical intervention strategies aimed at blocking muscle wasting. Skeletal muscle mass and muscle strength are the most important determinants of exercise capacity in patients with heart failure. In contrast with cachexia, muscle wasting is not usually associated with weight loss, implying the need for sophisticated assessment methods to correctly diagnose muscle wasting, for example the use of computed tomography, magnetic resonance imaging, or dual energy X-ray absorptiometry. Simpler techniques such as handgrip strength, exercise testing, or even a biomarker may help in determining patients with a high pre-test probability of muscle wasting. Despite intensive research efforts in the field of muscle wasting during the last couple of decades, no effective treatment of muscle wasting currently exists other than exercise training. This situation remains true even though study of the molecular pathways involved in muscle wasting suggests many therapeutic targets. Easily applicable diagnostic tools may help to identify patients at risk of developing muscle wasting.
    Current opinion in supportive and palliative care 01/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Acute renal failure (ARF) requiring renal replacement therapy (RRT) occurs frequently in ICU patients and significantly affects mortality rates. Previously, few large clinical trials investigated the impact of RRT modalities on patient outcomes. Here we investigate the effect of two major RRT strategies (intermittent hemodialysis (IHD) and continuous veno-venous hemofiltration (CVVH)) on mortality and renal-related outcome measures. This single-center prospective randomized controlled trial ("CONVINT") included 252 critically ill patients (159 male, mean age 61.5 +/- 13.9 years, Acute Physiology and Chronic Health Evaluation (APACHE) II score 28.6 +/- 8.8) with dialysis-dependent ARF treated in the ICUs of a tertiary care academic center. Patients were randomized to receive either daily IHD or CVVH. The primary outcome measure was survival at 14 days after the end of RRT. Secondary outcome measures included 30-day-, intensive care unit- and intra-hospital mortality as well as course of disease severity/biomarkers and need for organ support therapy. At baseline, no differences in disease severity, distribution of age and gender, or suspected reason of acute renal failure were observed. Survival rates at 14 days after RRT were 39.5% (IHD) versus 43.9% (CVVH) (odds ratio (OR) 0.84, 95% confidence interval (CI) 0.49 to 1.41; P = 0.50). 14-day-, 30-day, and all-cause intra-hospital mortality rates were not different between the two groups (all P >0.5). No differences were observed in days on RRT, vasopressor days, days on ventilator or ICU-/ intra-hospital length of stay. In a monocentric RCT, we observed no statistically significant differences between the investigated treatment modalities regarding mortality, renal-related outcome measures, or survival at 14 days after RRT. Our findings add to mounting data demonstrating that intermittent and continuous RRTs may be considered equivalent approaches for critically ill patients with dialysis-dependent acute renal failure.Trial registration: NCT01228123, clinicaltrials.gov.
    Critical care (London, England) 01/2014; 18(1):R11. · 4.72 Impact Factor
  • Journal of Cardiac Failure. 01/2014; 20(8):S3.
  • Goran Loncar, Stephan von Haehling
    [Show abstract] [Hide abstract]
    ABSTRACT: Novel biochemical markers may improve the estimation of overall risk in subjects at a high risk of adverse cardiac events. Measurement of some of these markers, including pregnancy-associated plasma protein A (PAPP-A), brings significant prognostic information independent of traditional risk factors. PAPP-A has been recently identified as a marker of plaque destabilization with growing interest in cardiovascular research. Our group has recently demonstrated that higher levels of serum PAPP-A were independently associated with an increased short-term risk of cardiovascular events in a large sample of 2568 consecutive patients presenting with cardiac chest pain. PAPP-A levels above 34.6 mIU/l in cardiac chest-pain patients sets alarm bells ringing as a warning for higher risk of short-term cardiovascular adverse events, including stent thrombosis, myocardial infarction, ischemic stroke or cardiovascular-related death within 90 days, the combined primary end point of this study. Cardiac chest pain patients with PAPP-A levels above 34.6 mIU/l may suffer from adverse cardiovascular events five times more frequently within 90 days than those with lower PAPP-A levels (hazard ratio: 5.28; 95% CI: 3.81-7.31). However, current data do not support the diagnostic role of PAPP-A for acute coronary syndrome in comparison to the gold standard biomarker troponin. Additionally, PAPP-A is known to interact with heparin, which may diminish its potential utility in every day clinical life. Future multicenter and large-volume studies are warranted to validate the use of PAPP-A in routine clinical practice.
    Expert Review of Cardiovascular Therapy 12/2013;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sarcopenia, the age-related, progressive loss of skeletal muscle mass, strength, and function, is a considerable socioeconomic burden by increasing risks of falls, fractures, and frailty. Moreover, sarcopenic patients are often obese and therapeutic options are very limited. Here, we assessed the efficacy of espindolol on muscle mass in 19-month-old male Wistar Han rats (weight, 555 ± 18 g), including safety issues. Rats were randomized to treatment with 3 mg/kg/day espindolol (n = 8) or placebo (n = 14) for 31 days. Placebo-treated rats progressively lost body weight (-15.5 ± 7.2 g), lean mass (-1.5 ± 4.2 g), and fat mass (-15.6 ± 2.7 g), while espindolol treatment increased body weight (+8.0 ± 6.1 g, p < 0.05), particularly lean mass (+43.4 ± 3.5 g, p < 0.001), and reduced fat mass further (-38.6 ± 3.4 g, p < 0.001). Anabolic/catabolic signaling was assessed in gastrocnemius muscle. Espindolol decreased proteasome and caspase-3 proteolytic activities by approximately 50 % (all p < 0.05). Western blotting showed a reduced expression of key catabolic regulators, including NFκB, MuRF1, and LC-3 (all p < 0.01). The 50- and 26-kDa forms of myostatin were downregulated fivefold and 20-fold, respectively (both p < 0.001). Moreover, 4E-BP-1 was reduced fivefold (p < 0.01), while phospho-PI3K was upregulated fivefold (p < 0.001), although Akt expression and phosphorylation were lower compared to placebo (all p < 0.05). No regulation of p38 and expression of ERK1/2 were observed, while phosphorylation of p38 was reduced (-54 %, p < 0.001) and ERK1/2 was increased (115 and 83 %, respectively, both p < 0.01). Espindolol did not affect cardiac function (echocardiography) or clinical plasma parameters. Espindolol reversed the effects of aging/sarcopenia, particularly loss of muscle mass and increased fat mass. Thus, espindolol is an attractive candidate drug for the treatment of sarcopenia patients.
    Journal of cachexia, sarcopenia and muscle. 11/2013;
  • Journal of the American College of Cardiology 11/2013; · 14.09 Impact Factor
  • Source
    Stephan von Haehling, Stefan D Anker
    [Show abstract] [Hide abstract]
    ABSTRACT: A striking discrepancy exists in the number of publications on obesity as compared to cachexia or wasting disorders. In PubMed, the number of entries that contain "cachexia" as a title word is only 1,825, whereas the number of entries for "obesity" in the title is 47,828, giving a ratio of 1:26 in favor of "obesity" publications. The difference in publication activities in these two fields has further broadened over the last years. Looking at guidance from national or international guidelines, PubMed analysis is even more depressing with 147 entries for obesity, but only four for cachexia. None of the latter provides guidance for the everyday care of cachectic patients. This publication activity is in stark contrast to the mortality impact of cachexia vs obesity at the time of diagnosis, which is at least 20 times higher for cachexia over the first 5 years. We assume, the mismatch is even bigger when it comes to public research support for these two medical conditions, which likely is a big part of the reason for this publication imbalance. Another reason may be that there is a perception bias in the research community, the public and hence also among healthcare providers and politicians as to what is important in medicine. We think, cachexia is at least as big an unmet need as is obesity. For shorter-term outcomes, cachexia is certainly a much bigger medical need than obesity. We hope that the current research efforts will change the situation for the better of our patients.
    Journal of cachexia, sarcopenia and muscle. 11/2013;
  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE To investigate the impact of iron status on survival in patients with type 2 diabetes and coronary artery disease (CAD).RESEARCH DESIGN AND METHODS Serum ferritin, transferrin saturation (Tsat), and soluble transferrin receptor (sTfR) were measured in 287 patients with type 2 diabetes and stable CAD (65 ± 9 years of age, 78% men).RESULTSDuring a mean follow-up of 45 ± 19 months, there were 59 (21%) deaths and 60 (21%) cardiovascular hospitalizations. Both serum ferritin and sTfR strongly predicted 5-year all-cause mortality rates, independently of other variables (including hemoglobin, measures of renal function, inflammation, and neurohormonal activation). There was an exponential relationship between sTfR and mortality (adjusted hazard ratio [HR] per 1 log mg/L: 4.24 [95% CI 1.43-12.58], P = 0.01), whereas the relationship between ferritin and mortality was U shaped (for the lowest and the highest quintiles vs. the middle quintile [reference group], respectively: adjusted HR 7.18 [95% CI 2.03-25.46], P = 0.002, and adjusted HR 5.12 [1.48-17.73], P = 0.01). Similar patterns were observed for the composite outcome of all-cause mortality or cardiovascular hospitalization, and in these multivariable models, low Tsat was related to unfavorable outcome.CONCLUSIONS Both low and high serum ferritin (possibly reflecting depleted and excessive iron stores, respectively) along with high serum sTfR (reflecting reduced metabolically available iron) identify patients with type 2 diabetes and CAD who have a poor prognosis.
    Diabetes care 10/2013; · 7.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Stroke is the second leading cause of death and the leading cause of disability in Western countries. More than 60% of patients remain disabled, 50% of patients suffer from hemiparesis and 30% remain unable to walk without assistance. The skeletal muscle is the main effector organ accountable for disability in stroke. This disability is primarily attributed to the brain lesion; however less attention is paid to structural, metabolic and functional alterations of muscle tissue after stroke. Hemiparetic stroke leads to various muscle abnormalities: A combination of denervation, disuse, inflammation, remodelling and spasticity accounts for a complex pattern of muscle tissue phenotype change and atrophy. The molecular mechanisms of muscle degradation after stroke are only incompletely understood. Reinnervation, fibre-type shift, disuse atrophy, and local inflammatory activation are only some of the key features yet to be explained. Only limited data is available today on clinical muscle changes after stroke that results from few studies in a mere 500 patients. Despite its importance for optimum post stroke recovery, stroke-related sarcopenia is not considered in current guidelines for stroke therapy or rehabilitation and measurement tools to address sarcopenia are infrequently used. This lack of robust evidence on muscle pathology after stroke and on treatment strategies needs to be addressed in an interdisciplinary integrated approach. This review provides an overview on current pathophysiologic insights and on clinical relevance of sarcopenia in stroke patients and on measurement tools to address the problem in the clinical setting.
    International journal of cardiology 10/2013; · 6.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cancer cachexia is thought to be the cause of >20% of cancer related deaths. Symptoms of cancer cachexia patients include depression and anorexia significantly worsening their quality of life. Moreover, in rodent models of cancer cachexia atrophy of the heart has been shown to impair cardiac function. Here, we characterize the effects of the antidepressant and anxiolytic drug tandospirone on wasting, cardiac function and survival in experimental cancer cachexia. The well-established Yoshida hepatoma rat model was used and tumor-bearing rats were treated with 1mg/kg/d (LD), 10mg/kg/d (HD) tandospirone or placebo. Weight, body composition (NMR), cardiac function (echocardiography), activity and food intake were assessed. Noradrenalin and cortisol were measured in plasma and caspase activity in skeletal muscle. Ten mg/kg/d tandospirone decreased the loss of body weight (p=0.0003) compared to placebo animals, mainly due to preservation of muscle mass (p<0.001), while 1mg/kg/d tandospirone was not effective. Locomotor activity (p=0.0007) and food intake (p=0.0001) were increased by HD tandospirone. The weight (p=0.0277) and function of heart (left ventricular mass, fractional shortening, stroke volume, ejection fraction, all p<0.05) were significantly improved. In the HD tandospirone group, plasma levels of noradrenalin and cortisol were significantly reduced by 49% and 52%, respectively, which may have contributed to the lower caspase activity in the gastrocnemius muscle. Most importantly, HD tandospirone significantly improved survival compared to placebo rats (HR: 0.34; 95% CI: 0.13-0.86; p=0.0495). Tandospirone showed significant beneficial effects in the Yoshida hepatoma cancer cachexia model and should be further examined as a prospective drug for this syndrome.
    International journal of cardiology 10/2013; · 6.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Reduced peripheral muscle mass was demonstrated in patients with chronic heart failure (HF). Adipokines may have potent metabolic effects on skeletal muscle. The associations between adipokines, peripheral muscle mass, and muscle function have been poorly investigated in patients with HF. We measured markers of fat and bone metabolism (adiponectin, leptin, 25-hydroxy vitamin D, parathyroid hormone, osteoprotegerin, RANKL), N-terminal pro B-type natriuretic peptide (NT-pro-BNP) in 73 non-cachectic, non-diabetic, male patients with chronic HF (age: 68±7years, New York Heart Association class II/III: 76/26%, left ventricular ejection fraction 29±8%) and 20 healthy controls of similar age. Lean mass as a measure of skeletal muscle mass was measured by dual energy X-ray absorptiometry (DEXA), while muscle strength was assessed by hand grip strength measured by Jamar dynamometer. Serum levels of adiponectin, parathyroid hormone, osteoprotegerin, RANKL, and NT-pro-BNP were elevated in patients with chronic HF compared to healthy controls (all p<0.0001), while no difference in serum levels of leptin, testosterone or SHBG was noted. Levels of 25-hydroxy vitamin D were reduced (p=0.002) in HF group. Peripheral lean mass and hand grip strength were reduced in patients with HF compared to healthy subjects (p=0.006 and p<0.0001, respectively). Using backward selection multivariable regression, serum levels of increased adiponectin remained significantly associated with reduced arm lean mass and muscle strength. Our findings may indicate a cross-sectional metabolic association of increased serum adiponectin with reduced peripheral muscle mass and muscle strength in non-cachectic, non-diabetic, elderly HF patients.
    European Journal of Internal Medicine 10/2013; · 2.05 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Muscle wasting is common in patients with chronic heart failure (HF) and worsens functional status. Protein catabolism is characteristic of muscle wasting and contributes to resting energy expenditure (REE). Glucagonlike peptide 1 (GLP-1) is linked to REE in healthy individuals. We aimed to evaluate (1) whether REE is elevated in patients with HF with muscle wasting, and (2) whether basal GLP-1 levels are linked to REE in HF. Cross-sectional study. Ambulatory patients with HF were recruited at the Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany. A total of 166 patients with HF and 27 healthy controls participating in the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) were enrolled. GLP-1 was measured in 55 of these patients. Body composition was measured by dual-energy X-ray absorptiometry (DEXA). Muscle wasting was defined as appendicular lean mass of at least 2 SDs below values of a healthy young reference group. REE was measured by indirect calorimetry. GLP-1 was assessed by ELISA. Thirty-four of 166 patients (mean age 67.4 ± 10.2 years, 77.7% male, New York Heart Association class 2.3 ± 0.6) presented with muscle wasting. REE in controls and patients with muscle wasting was significantly lower than in patients without muscle wasting (1579 ± 289 and 1532 ± 265 vs 1748 ± 359 kcal/d, P = .018 and P = .001, respectively). REE normalized for fat-free mass (FFM) using the ratio method (REE/FFM) and analysis of covariance was not different (P = .23 and .71, respectively). GLP-1 did not significantly correlate with REE (P = .49), even not after controlling for FFM using multivariable regression (P = .15). Differences in REE are attributable to lower FFM. GLP-1 does not relate to REE in patients with HF, possibly because of HF-related effects on REE.
    Journal of the American Medical Directors Association 10/2013; · 5.30 Impact Factor

27 Following View all

107 Followers View all