Anker, Stefan Dietmar

[["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","278"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of cachexia, sarcopenia and muscle"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Calvani, Riccardo"],["dc.contributor.author","Marini, Federico"],["dc.contributor.author","Cesari, Matteo"],["dc.contributor.author","Tosato, Matteo"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Miller, Ram R."],["dc.contributor.author","Bernabei, Roberto"],["dc.contributor.author","Landi, Francesco"],["dc.contributor.author","Marzetti, Emanuele"],["dc.date.accessioned","2019-07-09T11:42:33Z"],["dc.date.available","2019-07-09T11:42:33Z"],["dc.date.issued","2015-12-01"],["dc.description.abstract","Physical frailty and sarcopenia are two common and largely overlapping geriatric conditions upstream of the disabling cascade. The lack of a unique operational definition for physical frailty and sarcopenia and the complex underlying pathophysiology make the development of biomarkers for these conditions extremely challenging. Indeed, the current definitional ambiguities of physical frailty and sarcopenia, together with their heterogeneous clinical manifestations, impact the accuracy, specificity, and sensitivity of individual biomarkers proposed so far. In this review, the current state of the art in the development of biomarkers for physical frailty and sarcopenia is presented. A novel approach for biomarker identification and validation is also introduced that moves from the 'one fits all' paradigm to a multivariate methodology."],["dc.identifier.doi","10.1002/jcsm.12051"],["dc.identifier.pmid","26675566"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58691"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["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","Biomarkers for physical frailty and sarcopenia: state of the science and future developments."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","965"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","973"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Markousis‐Mavrogenis, George"],["dc.contributor.author","Tromp, Jasper"],["dc.contributor.author","Ouwerkerk, Wouter"],["dc.contributor.author","Devalaraja, Matt"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","Dickstein, Kenneth"],["dc.contributor.author","Filippatos, Gerasimos S."],["dc.contributor.author","Harst, Pim"],["dc.contributor.author","Lang, Chim C."],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","Ng, Leong L."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Samani, Nilesh J"],["dc.contributor.author","Zannad, Faiez"],["dc.contributor.author","Zwinderman, Aeilko H."],["dc.contributor.author","Hillege, Hans L."],["dc.contributor.author","Veldhuisen, Dirk J."],["dc.contributor.author","Kakkar, Rahul"],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Meer, Peter"],["dc.date.accessioned","2020-12-10T14:06:17Z"],["dc.date.available","2020-12-10T14:06:17Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/ejhf.1482"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16656"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69840"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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","The clinical significance of interleukin‐6 in heart failure: results from the BIOSTAT‐CHF study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1117"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","1125"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Eckardt, Kai-Uwe"],["dc.contributor.author","Gillespie, Iain A."],["dc.contributor.author","Kronenberg, Florian"],["dc.contributor.author","Richards, Sharon"],["dc.contributor.author","Stenvinkel, Peter"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Wheeler, David C."],["dc.contributor.author","de Francisco, Angel L."],["dc.contributor.author","Marcelli, Daniele"],["dc.contributor.author","Froissart, Marc"],["dc.contributor.author","Floege, Juergen"],["dc.date.accessioned","2018-11-07T09:49:34Z"],["dc.date.available","2018-11-07T09:49:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Early mortality is high in hemodialysis (HD) patients, but little is known about early cardiovascular event (CVE) rates after HD initiation. To study this we analyzed data in the AROii cohort of incident HD patients from over 300 European Fresenius Medical Care dialysis centers. Weekly rates of a composite of CVEs during the first year and monthly rates of the composite and its constituents (coronary artery, cerebrovascular, peripheral arterial, congestive heart failure, and sudden cardiac death) during the first 2 years after HD initiation were assessed. Of 6308 patients that started dialysis within 7 days, 1449 patients experienced 2405 CVEs over the next 2 years. The first-year CVE rate (30.2/100 person-years; 95% CI, 28.7-31.7) greatly exceeded the second-year rate (19.4/100; 95% CI, 18.1-20.8). Composite CVEs were highest during the first week with increased risk compared with the second year, persisting until the fifth month. Except for sudden cardiac death, temporal patterns of rates for all CVE categories were very similar, with highest rates during the first month and a high-risk period extending to 4 months. Higher or lower cumulative weekly dialysis dose, lower blood flow, and lower net ultrafiltration during dialysis were associated with CVE during the high-risk period, but not during the post high-risk period. Thus, the incidence of CVE in the first weeks after HD initiation is much higher than during subsequent periods which raises concerns that HD initiation may trigger CVEs."],["dc.description.sponsorship","Amgen (Europe) GmbH, Zug, Switzerland"],["dc.identifier.doi","10.1038/ki.2015.117"],["dc.identifier.isi","000364799200024"],["dc.identifier.pmid","25923984"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35536"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","High cardiovascular event rates occur within the first weeks of starting hemodialysis"],["dc.type","journal_article"],["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.issue","1"],["dc.bibliographiccitation.journal","Lipids in Health and Disease"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Bielecka-Dabrowa, Agata"],["dc.contributor.author","Bytyçi, Ibadete"],["dc.contributor.author","Von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan"],["dc.contributor.author","Jozwiak, Jacek"],["dc.contributor.author","Rysz, Jacek"],["dc.contributor.author","Hernandez, Adrian V."],["dc.contributor.author","Bajraktari, Gani"],["dc.contributor.author","Mikhalidis, Dimitri P."],["dc.contributor.author","Banach, Maciej"],["dc.date.accessioned","2020-12-10T18:38:59Z"],["dc.date.available","2020-12-10T18:38:59Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s12944-019-1135-z"],["dc.identifier.eissn","1476-511X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16859"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77502"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Association of statin use and clinical outcomes in heart failure patients: a systematic review and meta-analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","482"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","489"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Schroeder, Stefan"],["dc.contributor.author","Atar, Dan"],["dc.contributor.author","Bax, Jeroen J."],["dc.contributor.author","Ceconi, Claudio"],["dc.contributor.author","Cowie, Martin R."],["dc.contributor.author","AdamCrisp, AdamCrisp"],["dc.contributor.author","Dominjon, Fabienne"],["dc.contributor.author","Ford, Ian"],["dc.contributor.author","Ghofrani, Hossein-Ardeschir"],["dc.contributor.author","Gropper, Savion"],["dc.contributor.author","Hindricks, Gerhard"],["dc.contributor.author","Hlatky, Mark A."],["dc.contributor.author","Holcomb, Richard"],["dc.contributor.author","Honarpour, Narimon"],["dc.contributor.author","Jukema, J. Wouter"],["dc.contributor.author","Kim, Albert M."],["dc.contributor.author","Kunz, Michael"],["dc.contributor.author","Lefkowitz, Martin"],["dc.contributor.author","Le Floch, Chantal"],["dc.contributor.author","Landmesser, Ulf"],["dc.contributor.author","McDonagh, Theresa A."],["dc.contributor.author","McMurray, John J. V."],["dc.contributor.author","Merkely, Bela"],["dc.contributor.author","Packer, Milton"],["dc.contributor.author","Prasad, Krishna"],["dc.contributor.author","Revkin, James"],["dc.contributor.author","Rosano, Giuseppe M. C."],["dc.contributor.author","Somaratne, Ransi"],["dc.contributor.author","Stough, Wendy Gattis"],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Ruschitzka, Frank"],["dc.date.accessioned","2018-11-07T10:14:33Z"],["dc.date.available","2018-11-07T10:14:33Z"],["dc.date.issued","2016"],["dc.description.abstract","Composite endpoints are commonly used as the primary measure of efficacy in heart failure clinical trials to assess the overall treatment effect and to increase the efficiency of trials. Clinical trials still must enrol large numbers of patients to accrue a sufficient number of outcome events and have adequate power to draw conclusions about the efficacy and safety of new treatments for heart failure. Additionally, the societal and health system perspectives on heart failure have raised interest in ascertaining the effects of therapy on outcomes such as repeat hospitalization and the patient's burden of disease. Thus, novel methods for using composite endpoints in clinical trials (e.g. clinical status composite endpoints, recurrent event analyses) are being applied in current and planned trials. Endpoints that measure functional status or reflect the patient experience are important but used cautiously because heart failure treatments may improve function yet have adverse effects on mortality. This paper discusses the use of traditional and new composite endpoints, identifies qualities of robust composites, and outlines opportunities for future research."],["dc.identifier.doi","10.1002/ejhf.516"],["dc.identifier.isi","000379258400007"],["dc.identifier.pmid","27071916"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14326"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40642"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.haserratum","/handle/2/69867"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Traditional and new composite endpoints in heart failure clinical trials: facilitating comprehensive efficacy assessments and improving trial efficiency"],["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","2303"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Albrecht, Annemarie"],["dc.contributor.author","Porthun, Jan"],["dc.contributor.author","Eucker, Jan"],["dc.contributor.author","Coats, Andrew J.S."],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Pezzutto, Antonio"],["dc.contributor.author","Karakas, Mahir"],["dc.contributor.author","Riess, Hanno"],["dc.contributor.author","Keller, Ulrich"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Landmesser, Ulf"],["dc.contributor.author","Haverkamp, Wilhelm"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2021-07-05T15:00:42Z"],["dc.date.available","2021-07-05T15:00:42Z"],["dc.date.issued","2021"],["dc.description.abstract","Aims: It is largely unknown whether cancer patients seen in routine care show ventricular arrhythmias in 24 h electrocardiograms (ECGs), and whether when they are detected they carry prognostic relevance. Methods and Results: We included 261 consecutive cancer patients that were referred to the department of cardiology for 24 h ECG examination and 35 healthy controls of similar age and sex in the analysis. To reduce selection bias, cancer patients with known left ventricular ejection fraction <45% were not included in the analysis. Non–sustained ventricular tachycardia (NSVT) episodes of either ≥3 and ≥4 beats duration were more frequent in cancer patients than controls (17% vs. 0%, p = 0.0008; 10% vs. 0%, p = 0.016). Premature ventricular contractions (PVCs)/24 h were not more frequent in cancer patients compared to controls (median (IQR), 26 (2–360) vs. 9 (1–43), p = 0.06; ≥20 PVCs 53% vs. 37%, p = 0.07). During follow-up, (up to 7.2 years, median 15 months) of the cancer patients, 158 (61%) died (1-/3-/5-year mortality rates: 45% [95%CI 39–51%], 66% [95%CI 59–73%], 73% [95%CI 64–82%]). Both non-sustained ventricular tachycardia of ≥4 beats and ≥20 PVCs/24 h independently predicted mortality in univariate and multivariate survival analyses, adjusted for all other univariate predictors of mortality as well as relevant clinical factors, including cancer stage and type, performance status (ECOG), prior potentially cardiotoxic anti-cancer drug therapy, coronary artery disease, potassium concentration, and haemoglobin (multivariate adjusted hazard ratios: NSVT ≥4 beats [HR 1.76, p = 0.022], ≥20 PVCs/24 h [HR 1.63, p < 0.0064]). Conclusions: NSVT ≥4 beats and ≥20 PVCs/day seen in routine 24 h ECGs of patients with cancer carry prognostic relevance."],["dc.description.abstract","Aims: It is largely unknown whether cancer patients seen in routine care show ventricular arrhythmias in 24 h electrocardiograms (ECGs), and whether when they are detected they carry prognostic relevance. Methods and Results: We included 261 consecutive cancer patients that were referred to the department of cardiology for 24 h ECG examination and 35 healthy controls of similar age and sex in the analysis. To reduce selection bias, cancer patients with known left ventricular ejection fraction <45% were not included in the analysis. Non–sustained ventricular tachycardia (NSVT) episodes of either ≥3 and ≥4 beats duration were more frequent in cancer patients than controls (17% vs. 0%, p = 0.0008; 10% vs. 0%, p = 0.016). Premature ventricular contractions (PVCs)/24 h were not more frequent in cancer patients compared to controls (median (IQR), 26 (2–360) vs. 9 (1–43), p = 0.06; ≥20 PVCs 53% vs. 37%, p = 0.07). During follow-up, (up to 7.2 years, median 15 months) of the cancer patients, 158 (61%) died (1-/3-/5-year mortality rates: 45% [95%CI 39–51%], 66% [95%CI 59–73%], 73% [95%CI 64–82%]). Both non-sustained ventricular tachycardia of ≥4 beats and ≥20 PVCs/24 h independently predicted mortality in univariate and multivariate survival analyses, adjusted for all other univariate predictors of mortality as well as relevant clinical factors, including cancer stage and type, performance status (ECOG), prior potentially cardiotoxic anti-cancer drug therapy, coronary artery disease, potassium concentration, and haemoglobin (multivariate adjusted hazard ratios: NSVT ≥4 beats [HR 1.76, p = 0.022], ≥20 PVCs/24 h [HR 1.63, p < 0.0064]). Conclusions: NSVT ≥4 beats and ≥20 PVCs/day seen in routine 24 h ECGs of patients with cancer carry prognostic relevance."],["dc.identifier.doi","10.3390/cancers13102303"],["dc.identifier.pii","cancers13102303"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87884"],["dc.language.iso","en"],["dc.notes.intern","DOI Import DOI-Import GROB-441"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Spontaneous Non-Sustained Ventricular Tachycardia and Premature Ventricular Contractions and Their Prognostic Relevance in Patients with Cancer in Routine Care"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","621"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","628"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Okonko, Darlington O."],["dc.contributor.author","Jouhra, Fadi"],["dc.contributor.author","Abu‐Own, Huda"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Colet, Josep Comin"],["dc.contributor.author","Suki, Chainey"],["dc.contributor.author","Mori, Claudio"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2020-12-10T14:06:11Z"],["dc.date.available","2020-12-10T14:06:11Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/ehf2.12462"],["dc.identifier.eissn","2055-5822"],["dc.identifier.issn","2055-5822"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69807"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Effect of ferric carboxymaltose on calculated plasma volume status and clinical congestion: a FAIR‐HF substudy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of cachexia, sarcopenia and muscle"],["dc.bibliographiccitation.lastpage","365"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Stewart Coats, Andrew J."],["dc.contributor.author","Ho, Gwo Fuang"],["dc.contributor.author","Prabhash, Kumar"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Tilson, Julia"],["dc.contributor.author","Brown, Richard"],["dc.contributor.author","Beadle, John"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2019-07-09T11:42:31Z"],["dc.date.available","2019-07-09T11:42:31Z"],["dc.date.issued","2016-06-01"],["dc.description.abstract","BACKGROUND: Cancer cachexia is a major cause of morbidity and mortality with no widely approved treatment. METHODS: The ACT-ONE trial is a randomized, double-blind, parallel group, placebo-controlled, phase II multicentre trial in patients (25-80 years) with stages III or IV colorectal cancer or non-small cell lung cancer-related cachexia that tested two doses of espindolol (a novel non-selective β blocker with central 5-HT1a and partial β2 receptor agonist effects). The primary endpoint was the difference in the rate of weight change over 16 weeks (linear mixed-effect model for repeated measures) between high-dose espindolol and placebo. RESULTS: Eighty-seven patients were randomized centrally in blocks in a ratio 3:2:1 [42 high dose, 10 mg twice daily (bd):31 placebo:14 low dose, 2.5 mg bd]. High-dose espindolol produced a statistically and clinically significant weight gain (+0.54 kg/4 weeks, 95% CI 0.38-0.70) compared with a weight loss on placebo (-0.21 kg/4 weeks, 95% CI -0.37-0.05); P < 0.0001. High-dose espindolol produced a statistically significant increase in lean body mass, whilst changes in fat mass were neutral. Hand grip strength significantly (high dose -1.15 ± 0.7 kg, placebo -3.51 ± 0.8 kg change per 4 weeks; P = 0.0134), stair climbing power, and 6-min walk test non-significantly were all directionally in favour of high-dose espindolol. There were no clinically significant differences in safety signals or survival between treatment groups, although a numerical excess of dyspnoea was seen with high-dose espindolol (19.1%) compared with placebo (3.2%). CONCLUSIONS: This positive trial showed that espindolol 10 mg bd significantly reversed weight loss, improved fat free mass, and maintained fat mass in advanced colorectal cancer and non-small cell lung cancer-related cachexia. This was associated with a significant improvement in handgrip strength, supporting the further investigation of 10 mg bd espindolol for the treatment of cancer cachexia. Although not powered to look at dose response, most treatment effects for low dose lay between high dose and placebo, suggesting that there may be a dose response in the effects of espindolol."],["dc.identifier.doi","10.1002/jcsm.12126"],["dc.identifier.pmid","27386169"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58685"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Espindolol for the treatment and prevention of cachexia in patients with stage III/IV non-small cell lung cancer or colorectal cancer: a randomized, double-blind, placebo-controlled, international multicentre phase II study (the ACT-ONE trial)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]