Anker, Stefan Dietmar

[["dc.bibliographiccitation.firstpage","800"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","808"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Di Tullio, Marco R."],["dc.contributor.author","Qian, Min"],["dc.contributor.author","Thompson, John L.P."],["dc.contributor.author","Labovitz, Arthur J."],["dc.contributor.author","Mann, Douglas L."],["dc.contributor.author","Sacco, Ralph L."],["dc.contributor.author","Pullicino, Patrick M."],["dc.contributor.author","Freudenberger, Ronald S."],["dc.contributor.author","Teerlink, John R."],["dc.contributor.author","Graham, Susan"],["dc.contributor.author","Lip, Gregory Y.H."],["dc.contributor.author","Levin, Bruce"],["dc.contributor.author","Mohr, Jay P."],["dc.contributor.author","Buchsbaum, Richard"],["dc.contributor.author","Estol, Conrado J."],["dc.contributor.author","Lok, Dirk J."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Homma, Shunichi"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.12331"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69796"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Left atrial volume and cardiovascular outcomes in systolic heart failure: effect of antithrombotic treatment"],["dc.title.alternative","Left atrial volume and outcome in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Elsner, Sebastian"],["dc.contributor.author","Sliziuk, Veronika"],["dc.contributor.author","Steinbeck, Lisa"],["dc.contributor.author","Kube, Jennifer"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Scherbakov, Nadja"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2020-12-10T14:24:29Z"],["dc.date.available","2020-12-10T14:24:29Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.ijcard.2015.11.178"],["dc.identifier.issn","0167-5273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72267"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The impact of iron deficiency and anaemia on exercise capacity and outcomes in patients with chronic heart failure. Results from the Studies Investigating Co-morbidities Aggravating Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","ehy600"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","19"],["dc.contributor.author","Maack, Christoph"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Heinzel, Frank R."],["dc.contributor.author","Lyon, Alexander R."],["dc.contributor.author","Manstein, Dietmar J."],["dc.contributor.author","Metzger, Joseph"],["dc.contributor.author","Papp, Zoltán"],["dc.contributor.author","Tocchetti, Carlo G."],["dc.contributor.author","Yilmaz, M. Birhan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Balligand, Jean-Luc"],["dc.contributor.author","Bauersachs, Johann"],["dc.contributor.author","Brutsaert, Dirk"],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Chlopicki, Stefan"],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","de Boer, Rudolf A."],["dc.contributor.author","Dietl, Alexander"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","Harjola, Veli-Pekka"],["dc.contributor.author","Heymans, Stephane"],["dc.contributor.author","Hilfiker-Kleiner, Denise"],["dc.contributor.author","Holzmeister, Johannes"],["dc.contributor.author","de Keulenaer, Gilles"],["dc.contributor.author","Limongelli, Giuseppe"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Lund, Lars H."],["dc.contributor.author","Masip, Josep"],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","Mueller, Christian"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Ristić, Arsen"],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Seferović, Petar M."],["dc.contributor.author","Skouri, Hadi"],["dc.contributor.author","Zimmermann, Wolfram H."],["dc.contributor.author","Mebazaa, Alexandre"],["dc.date.accessioned","2019-02-20T13:50:51Z"],["dc.date.available","2019-02-20T13:50:51Z"],["dc.date.issued","2018"],["dc.description.abstract","Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation–contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term."],["dc.identifier.doi","10.1093/eurheartj/ehy600"],["dc.identifier.pmid","30295807"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57605"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/235"],["dc.language.iso","en"],["dc.notes.status","fcwi"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Treatments targeting inotropy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","391"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","412"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Tschöpe, Carsten"],["dc.contributor.author","Boer, Rudolf A."],["dc.contributor.author","Fraser, Alan G."],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Donal, Erwan"],["dc.contributor.author","Edelmann, Frank"],["dc.contributor.author","Fu, Michael"],["dc.contributor.author","Guazzi, Marco"],["dc.contributor.author","Lam, Carolyn S.P."],["dc.contributor.author","Lancellotti, Patrizio"],["dc.contributor.author","Melenovsky, Vojtech"],["dc.contributor.author","Morris, Daniel A."],["dc.contributor.author","Nagel, Eike"],["dc.contributor.author","Pieske-Kraigher, Elisabeth"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Solomon, Scott D."],["dc.contributor.author","Vasan, Ramachandran S."],["dc.contributor.author","Rutten, Frans H."],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Seferovic, Petar"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.date.accessioned","2020-12-10T14:06:19Z"],["dc.date.available","2020-12-10T14:06:19Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/eurheartj/ehz641"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69854"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","How to diagnose heart failure with preserved ejection fraction: the HFA–PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1956"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","New England Journal of Medicine"],["dc.bibliographiccitation.lastpage","1964"],["dc.bibliographiccitation.volume","376"],["dc.contributor.author","Packer, Milton"],["dc.contributor.author","O’Connor, Christopher"],["dc.contributor.author","McMurray, John J.V."],["dc.contributor.author","Wittes, Janet"],["dc.contributor.author","Abraham, William T."],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Dickstein, Kenneth"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Holcomb, Richard"],["dc.contributor.author","Krum, Henry"],["dc.contributor.author","Maggioni, Aldo P."],["dc.contributor.author","Mebazaa, Alexandre"],["dc.contributor.author","Peacock, W. Frank"],["dc.contributor.author","Petrie, Mark C."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","van Veldhuisen, Dirk J."],["dc.contributor.author","Kowarski, Lisa S."],["dc.contributor.author","Schactman, Mark"],["dc.contributor.author","Holzmeister, Johannes"],["dc.date.accessioned","2020-12-10T18:12:31Z"],["dc.date.available","2020-12-10T18:12:31Z"],["dc.date.issued","2017"],["dc.description.abstract","BACKGROUND In patients with acute heart failure, early intervention with an intravenous vasodilator has been proposed as a therapeutic goal to reduce cardiac-wall stress and, potentially, myocardial injury, thereby favorably affecting patients' long-term prognosis. METHODS In this double-blind trial, we randomly assigned 2157 patients with acute heart failure to receive a continuous intravenous infusion of either ularitide at a dose of 15 ng per kilogram of body weight per minute or matching placebo for 48 hours, in addition to accepted therapy. Treatment was initiated a median of 6 hours after the initial clinical evaluation. The coprimary outcomes were death from cardiovascular causes during a median follow-up of 15 months and a hierarchical composite end point that evaluated the initial 48-hour clinical course. RESULTS Death from cardiovascular causes occurred in 236 patients in the ularitide group and 225 patients in the placebo group (21.7% vs. 21.0%; hazard ratio, 1.03; 96% confidence interval, 0.85 to 1.25; P=0.75). In the intention-to-treat analysis, there was no significant between-group difference with respect to the hierarchical composite outcome. The ularitide group had greater reductions in systolic blood pressure and in levels of N-terminal pro-brain natriuretic peptide than the placebo group. However, changes in cardiac troponin T levels during the infusion did not differ between the two groups in the 55% of patients with paired data. CONCLUSIONS In patients with acute heart failure, ularitide exerted favorable physiological effects (without affecting cardiac troponin levels), but short-term treatment did not affect a clinical composite end point or reduce long-term cardiovascular mortality. (Funded by Cardiorentis; TRUE-AHF ClinicalTrials.gov number, NCT01661634.)"],["dc.identifier.doi","10.1056/NEJMoa1601895"],["dc.identifier.eissn","1533-4406"],["dc.identifier.isi","000401407500009"],["dc.identifier.issn","0028-4793"],["dc.identifier.pmid","28402745"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74406"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Massachusetts Medical Soc"],["dc.relation.issn","1533-4406"],["dc.relation.issn","0028-4793"],["dc.title","Effect of Ularitide on Cardiovascular Mortality in Acute Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","606"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Heart"],["dc.bibliographiccitation.lastpage","613"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Ferreira, João Pedro"],["dc.contributor.author","Rossignol, Patrick"],["dc.contributor.author","Demissei, Biniyam"],["dc.contributor.author","Sharma, Abhinav"],["dc.contributor.author","Girerd, Nicolas"],["dc.contributor.author","Anker, Stefan D"],["dc.contributor.author","Cleland, John G"],["dc.contributor.author","Dickstein, Kenneth"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Hillege, Hans L"],["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","van Veldhuisen, Dirk J"],["dc.contributor.author","Zwinderman, Aeilko H"],["dc.contributor.author","Voors, Adriaan"],["dc.contributor.author","Zannad, Faiez"],["dc.date.accessioned","2020-12-10T18:37:15Z"],["dc.date.available","2020-12-10T18:37:15Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1136/heartjnl-2017-311750"],["dc.identifier.eissn","1468-201X"],["dc.identifier.issn","1355-6037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76891"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Coronary angiography in worsening heart failure: determinants, findings and prognostic implications"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2468"],["dc.bibliographiccitation.issue","36"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","Kasztura, Monika"],["dc.contributor.author","Sokolski, Mateusz"],["dc.contributor.author","Bronisz, Marek"],["dc.contributor.author","Nawrocka, Sylwia"],["dc.contributor.author","Oleskowska-Florek, Weronika"],["dc.contributor.author","Zymlinski, Robert"],["dc.contributor.author","Biegus, Jan"],["dc.contributor.author","Siwolowski, Pawel"],["dc.contributor.author","Banasiak, Waldemar"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Filippatos, Gerasimos S."],["dc.contributor.author","Cleland, John G. F."],["dc.contributor.author","Ponikowski, Piotr"],["dc.date.accessioned","2018-11-07T09:35:07Z"],["dc.date.available","2018-11-07T09:35:07Z"],["dc.date.issued","2014"],["dc.description.abstract","Aim Acute heart failure (AHF) critically deranges haemodynamic and metabolic homoeostasis. Iron is a key micronutrient for homoeostasis maintenance. We hypothesized that iron deficiency (ID) defined as depleted iron stores accompanied by unmet cellular iron requirements would in this setting predict the poor outcome. Methods and results Among 165 AHF patients (age 65 +/- 12 years, 81% men, 31% de novo HF), for ID diagnosis we prospectively applied: low serum hepcidin reflecting depleted iron stores (<14.5 ng/mL, the 5th percentile in healthy peers), and high-serum soluble transferrin receptor (sTfR) reflecting unmet cellular iron requirements (>= 1.59 mg/L, the 95th percentile in healthy peers). Concomitance of low hepcidin and high sTfR (the most profound ID) was found in 37%, isolated either high sTfR or low hepcidin was found in 29 and 9% of patients, and 25% of subjects demonstrated preserved iron status. Patients with low hepcidin and high sTfR had peripheral oedema, high NT-proBNP, high uric acid, low haemoglobin (P < 0.05), and 5% in-hospital mortality (0% in remaining patients). During the 12-month follow-up, 33 (20%) patients died. Those with low hepcidin and high sTfR had the highest 12-month mortality [(41% (95% CI: 29-53%)] when compared with those with isolated high sTfR [15% (5-25%)], isolated low hepcidin [7% (0-19%)] and preserved iron status (0%) (P < 0.001). Analogous mortality patterns were seen separately in anaemics and non-anaemics. Conclusion Iron deficiency defined as depleted body iron stores and unmet cellular iron requirements is common in AHF, and identifies those with the poor outcome. Its correction may be an attractive therapeutic approach."],["dc.description.sponsorship","National Centre of Science (Poland) [NN 519 654340//6543/B/T02/2011/40]"],["dc.identifier.doi","10.1093/eurheartj/ehu235"],["dc.identifier.isi","000342924900011"],["dc.identifier.pmid","24927731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32323"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.journal","European Heart Journal"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Comin-Colet, Josep"],["dc.contributor.author","Filippatos, Gerasimos S."],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Arutyunov, G. P."],["dc.contributor.author","Motro, M."],["dc.contributor.author","Mori, C."],["dc.contributor.author","Pocock, S. J."],["dc.contributor.author","van Veldhuisen, D. J."],["dc.contributor.author","Ponikowski, Piotr"],["dc.date.accessioned","2018-11-07T09:53:31Z"],["dc.date.available","2018-11-07T09:53:31Z"],["dc.date.issued","2015"],["dc.format.extent","494"],["dc.identifier.isi","000361205103585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36344"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","Congress of the European-Society-of-Cardiology (ESC)"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Ferric carboxymaltose in iron deficient heart failure patients: a meta-analysis on individual patient data"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]