Haehling, Stephan von

[["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Rozentryt, Piotr"],["dc.contributor.author","Niedziela, Jacek T."],["dc.contributor.author","Hudzik, Bartosz"],["dc.contributor.author","Lekston, Andrzej"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","Nowak, Jolanta"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Partyka, Robert"],["dc.contributor.author","Rywik, Tomasz"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Poloński, Lech"],["dc.date.accessioned","2019-07-09T11:42:02Z"],["dc.date.available","2019-07-09T11:42:02Z"],["dc.date.issued","2015"],["dc.description.abstract","Background A higher serum phosphate level is associated with worse outcome. Energy-demanding intracellular transport of phosphate is needed to secure anion bioavailability. In heart failure (HF), energy starvation may modify intracellular and serum levels of phosphate. We analysed determinants of serum phosphates in HF and assessed if catabolic/anabolic balance (CAB) was associated with elevation of serum phosphate. Methods We retrospectively reviewed data from 1029 stable patients with HF and have calculated negative (loss) and positive (gain) components of weight change from the onset of HF till index date. The algebraic sum of these components was taken as CAB. The univariate and multivariable predictors of serum phosphorus were calculated. In quintiles of CAB, we have estimated odds ratios for serum phosphorus above levels previously identified to increase risk of mortality. As a reference, we have selected a CAB quintile with similar loss and gain. Results Apart from sex, age, and kidney function, we identified serum sodium, N-terminal fragment of pro-brain-type natriuretic peptide, and CAB as independent predictors of serum phosphorus. The odds for serum phosphorus above thresholds found in literature to increase risk were highest in more catabolic patients. In most catabolic quintile relative to neutral balance, the odds across selected phosphorus thresholds rose, gradually peaking at 1.30 mmol/L with a value of 3.29 (95% confidence interval: 2.00–5.40, P < 0.0001) in an unadjusted analysis and 2.55 (95% confidence interval: 1.38–2.72, P = 0.002) in a fully adjusted model. Conclusions Metabolic status is an independent determinant of serum phosphorus in HF. Higher catabolism is associated with serum phosphorus above mortality risk-increasing thresholds."],["dc.identifier.doi","10.1002/jcsm.12026"],["dc.identifier.pmid","26672973"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58571"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.euproject","SICA-HF"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Higher serum phosphorus is associated with catabolic/anabolic imbalance in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","403"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","412"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Berger, David"],["dc.contributor.author","Bloechlinger, Stefan"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Takala, Jukka"],["dc.contributor.author","Z'Graggen, Werner J."],["dc.contributor.author","Schefold, Joerg C."],["dc.date.accessioned","2018-11-07T10:09:30Z"],["dc.date.available","2018-11-07T10:09:30Z"],["dc.date.issued","2016"],["dc.description.abstract","Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed ventilator-induced diaphragmatic dysfunction' (VIDD) and should be distinguished from peripheral muscular weakness as observed in ICU-acquired weakness (ICU-AW)'. Interestingly, VIDD and ICU-AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross-sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues."],["dc.identifier.doi","10.1002/jcsm.12108"],["dc.identifier.isi","000383753900004"],["dc.identifier.pmid","27030815"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13783"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39664"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Dysfunction of respiratory muscles in critically ill patients on the intensive care unit"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","956"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","961"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bauer, Juergen"],["dc.contributor.author","Morley, John E."],["dc.contributor.author","Schols, Annemie M.W.J."],["dc.contributor.author","Ferrucci, Luigi"],["dc.contributor.author","Cruz‐Jentoft, Alfonso J."],["dc.contributor.author","Dent, Elsa"],["dc.contributor.author","Baracos, Vickie E."],["dc.contributor.author","Crawford, Jeffrey A."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Heymsfield, Steven B."],["dc.contributor.author","Jatoi, Aminah"],["dc.contributor.author","Kalantar‐Zadeh, Kamyar"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Landi, Francesco"],["dc.contributor.author","Laviano, Alessandro"],["dc.contributor.author","Mancuso, Michelangelo"],["dc.contributor.author","Muscaritoli, Maurizio"],["dc.contributor.author","Prado, Carla M."],["dc.contributor.author","Strasser, Florian"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Coats, Andrew J.S."],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2020-12-10T14:06:45Z"],["dc.date.available","2020-12-10T14:06:45Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jcsm.12483"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16637"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70011"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Sarcopenia: A Time for Action. An SCWD Position Paper"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","10"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC neurology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Scherbakov, Nadja"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Meisel, Andreas"],["dc.contributor.author","Haeusler, Karl Georg"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D"],["dc.contributor.author","Dirnagl, Ulrich"],["dc.contributor.author","Joebges, Michael"],["dc.contributor.author","Doehner, Wolfram"],["dc.date.accessioned","2019-07-09T11:42:18Z"],["dc.date.available","2019-07-09T11:42:18Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND: Patients with stroke are at a high risk for long-term handicap and disability. In the first weeks after stroke muscle wasting is observed frequently. Early post-stroke rehabilitation programs are directed to improve functional independence and physical performance. Supplementation with essential amino acids (EAAs) might prevent muscle wasting and improve rehabilitation outcome by augmenting muscle mass and muscle strength. We aim to examine this in a double blinded, randomized placebo-controlled clinical trial. METHODS: Patients with ischemic or haemorrhagic stroke will be enrolled at begin of the early post-stroke rehabilitation in a parallel group interventional trial. Oral supplementation of EAAs or placebo will be given for 12 weeks in a double blinded manner. Physical and functional performance will be assessed by exercise testing before supplementation of EAAs as well as at discharge from the in-patient rehabilitation, at 12 weeks and 1 year afterwards. DISCUSSION: This is the first randomized double-blinded placebo-controlled clinical study aiming to assess the effect of the EAAs supplementation on muscle strength, muscle function and physical performance in stroke patients during early post-stroke rehabilitation. Supplementation of EAAs could prevent muscle mass wasting and improve functional independence after stroke. TRIAL REGISTRATION: The study is registered at the German registry for clinical trials as well as at World Health Organization (WHO; number DRKS00005577 )."],["dc.identifier.doi","10.1186/s12883-016-0531-5"],["dc.identifier.pmid","26793971"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58637"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2377"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Influence of essential amino acids on muscle mass and muscle strength in patients with cerebral stroke during early rehabilitation: protocol and rationale of a randomized clinical trial (AMINO-Stroke Study)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","611"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","620"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Scherbakov, Nadja"],["dc.contributor.author","Pietrock, Charlotte"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Norman, Kristina"],["dc.contributor.author","Haeusler, Karl Georg"],["dc.date.accessioned","2021-06-01T10:50:54Z"],["dc.date.available","2021-06-01T10:50:54Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jcsm.12400"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86821"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Body weight changes and incidence of cachexia after stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","85"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Turhan, Guelistan"],["dc.contributor.author","Leyva, Francisco"],["dc.contributor.author","Rauchhaus, Mathias"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2019-07-09T11:41:23Z"],["dc.date.available","2019-07-09T11:41:23Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Chronic heart failure (CHF) is associated with insulin resistance, indicating impairment in the control of energy metabolism. Insulin resistance in CHF relates to symptomatic status and independently predicts poor prognosis. We sought to determine whether insulin sensitivity is related to skeletal muscle strength in patients with CHF, taking into account muscle size and perfusion. Methods Quadriceps muscle size (square centimetre cross-sectional area at mid-femur level, computed tomography), isometric quadriceps muscle strength [absolute (in N) and strength per unit muscle area (N/cm2)], resting-leg blood flow (plethysmography) and maximal oxygen consumption (treadmill exercise test) were measured in 33 patients with CHF (left ventricular ejection fraction 28 ± 3.2%, mean ± Standard Error of the mean (SEM)) and 20 healthy controls. Insulin sensitivity was assessed by intravenous glucose tolerance tests and minimal modelling analysis. Results Right quadriceps strength (−27.0%, P < 0.0001), strength per muscle area (−18.0%, P < 0.003) and insulin sensitivity (−64.2%, P < 0.001) were lower in patients with CHF. The correlation between insulin sensitivity and absolute muscle strength was significant in the CHF group (r = 0.54, P = 0.001) and borderline in controls (r = 0.47, P = 0.06). This association remained significant between insulin sensitivity and strength per muscle area (CHF: r = 0.52, P < 0.01; controls: r = 0.62, P < 0.05). In stepwise regression analyses in CHF, only insulin sensitivity emerged as a predictor of strength per unit area of muscle [standardized coefficient (SC) = 0.45, P = 0.006; diuretic dose, SC = −0.31, P = 0.051; R2 = 0.37, P = 0.001], while age, left ventricular ejection fraction, maximal oxygen consumption, fasting glucose and insulin and blood flow were excluded. In controls, only insulin sensitivity remained in the final regression model (SC = 0.62, P = 0.004; R2 = 0.39, P = 0.004). Conclusions The myofibril contractile function of the quadriceps, i.e. functional quality of skeletal muscle, is strongly related to insulin sensitivity in patients with CHF and in healthy controls, independently of muscle size. Therapies aimed at improving insulin sensitivity in patients with CHF may clarify whether this relationship is causal."],["dc.identifier.doi","10.1002/ehf2.12035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58415"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Skeletal muscle weakness is related to insulin resistance in patients with chronic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1242"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","1249"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Garfias Macedo, Tania"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Cleland, John G. F."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2021-04-14T08:24:54Z"],["dc.date.available","2021-04-14T08:24:54Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Skeletal muscle wasting is an extremely common feature in patients with heart failure, affecting approximately 20% of ambulatory patients with even higher values during acute decompensation. Its occurrence is associated with reduced exercise capacity, muscle strength, and quality of life. We sought to investigate if the presence of muscle wasting carries prognostic information. Methods Two hundred sixty‐eight ambulatory patients with heart failure (age 67.1 ± 10.9 years, New York Heart Association class 2.3 ± 0.6, left ventricular ejection fraction 39 ± 13.3%, and 21% female) were prospectively enrolled as part of the Studies Investigating Co‐morbidities Aggravating Heart Failure. Muscle wasting as assessed using dual‐energy X‐ray absorptiometry was present in 47 patients (17.5%). Results During a mean follow‐up of 67.2 ± 28.02 months, 95 patients (35.4%) died from any cause. After adjusting for age, New York Heart Association class, left ventricular ejection fraction, creatinine, N‐terminal pro‐B‐type natriuretic peptide, and iron deficiency, muscle wasting remained an independent predictor of death (hazard ratio 1.80, 95% confidence interval 1.01–3.19, P = 0.04). This effect was more pronounced in patients with heart failure with reduced than in heart failure with preserved ejection fraction. Conclusions Muscle wasting is an independent predictor of death in ambulatory patients with heart failure. Clinical trials are needed to identify treatment approaches to this co‐morbidity."],["dc.identifier.doi","10.1002/jcsm.12603"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81461"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Muscle wasting as an independent predictor of survival in patients with chronic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","594"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","605"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Pötsch, Mareike S."],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2021-06-01T10:50:56Z"],["dc.date.available","2021-06-01T10:50:56Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jcsm.12537"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17186"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86832"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","MT‐102 prevents tissue wasting and improves survival in a rat model of severe cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Arzt, Michael"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Edelmann, Frank"],["dc.contributor.author","Evertz, Ruben"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Garfias Macedo, Tania"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Noutsias, Michel"],["dc.contributor.author","Schulze, P. Christian"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Laufs, Ulrich"],["dc.date.accessioned","2020-12-10T14:06:20Z"],["dc.date.available","2020-12-10T14:06:20Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Endpoints of large‐scale trials in chronic heart failure have mostly been defined to evaluate treatments with regard to hospitalizations and mortality. However, patients with heart failure are also affected by very severe reductions in exercise capacity and quality of life. We aimed to evaluate the effects of heart failure treatments on these endpoints using available evidence from randomized trials. Interventions with evidence for improvements in exercise capacity include physical exercise, intravenous iron supplementation in patients with iron deficiency, and – with less certainty – testosterone in highly selected patients. Erythropoiesis‐stimulating agents have been reported to improve exercise capacity in anaemic patients with heart failure. Sinus rhythm may have some advantage when compared with atrial fibrillation, particularly in patients undergoing pulmonary vein isolation. Studies assessing treatments for heart failure co‐morbidities such as sleep‐disordered breathing, diabetes mellitus, chronic kidney disease and depression have reported improvements of exercise capacity and quality of life; however, the available data are limited and not always consistent. The available evidence for positive effects of pharmacologic interventions using angiotensin‐converting enzyme inhibitors, angiotensin receptor blockers, beta‐blockers, and mineralocorticoid receptor antagonists on exercise capacity and quality of life is limited. Studies with ivabradine and with sacubitril/valsartan suggest beneficial effects at improving quality of life; however, the evidence base is limited in particular for exercise capacity. The data for heart failure with preserved ejection fraction are even less positive, only sacubitril/valsartan and spironolactone have shown some effectiveness at improving quality of life. In conclusion, the evidence for state‐of‐the‐art heart failure treatments with regard to exercise capacity and quality of life is limited and appears not robust enough to permit recommendations for heart failure. The treatment of co‐morbidities may be important for these patient‐related outcomes. Additional studies on functional capacity and quality of life in heart failure are required."],["dc.identifier.doi","10.1002/ejhf.1838"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69857"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","John Wiley \\u0026 Sons, Ltd."],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","Improving exercise capacity and quality of life using non‐invasive heart failure treatments: evidence from clinical trials"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","448"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC heart failure"],["dc.bibliographiccitation.lastpage","457"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Dos Santos, Marcelo R."],["dc.contributor.author","Emami, Amir"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2019-07-09T11:44:42Z"],["dc.date.available","2019-07-09T11:44:42Z"],["dc.date.issued","2017-11"],["dc.description.abstract","AIMS: We aimed to assess determinants of anorexia, that is loss of appetite in patients with heart failure (HF) and aimed to further elucidate the association between anorexia, functional capacity, and outcomes in affected patients. METHODS AND RESULTS: We assessed anorexia status among 166 patients with HF (25 female, 66 ± 12 years) who participated in the Studies Investigating Co-morbidities Aggravating HF. Anorexia was assessed by a 6-point Likert scale (ranging from 0 to 5), wherein values ≥1 indicate anorexia. Functional capacity was assessed as peak oxygen uptake (peak VO2 ), 6 min walk test, and short physical performance battery test. A total of 57 patients (34%) reported any anorexia, and these patients showed lower values of peak VO2 , 6 min walk distance, and short physical performance battery score (all P < 0.05). Using multivariate analysis adjusting for clinically important factors, only high-sensitivity C-reactive protein [odds ratio (OR) 1.24, P = 0.04], use of loop diuretics (OR 5.76, P = 0.03), and the presence of cachexia (OR 2.53, P = 0.04) remained independent predictors of anorexia. A total of 22 patients (13%) died during a mean follow-up of 22.5 ± 5.1 months. Kaplan-Meier curves for cumulative survival showed that those patients with anorexia presented higher mortality (Log-rank test P = 0.03). CONCLUSIONS: Inflammation, use of loop diuretics, and cachexia are associated with an increased likelihood of anorexia in patients with HF, and patients with anorexia showed impaired functional capacity and poor outcomes."],["dc.identifier.doi","10.1002/ehf2.12209"],["dc.identifier.pmid","28960880"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14870"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59070"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.issn","2055-5822"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Anorexia, functional capacity, and clinical outcome in patients with chronic heart failure: results from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]