Anker, Stefan Dietmar

[["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","1050"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","European journal of heart failure"],["dc.bibliographiccitation.lastpage","1056"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Kosiborod, Mikhail"],["dc.contributor.author","Zannad, Faiez"],["dc.contributor.author","Piña, Ileana L."],["dc.contributor.author","McCullough, Peter A."],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","van der Meer, Peter"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Rasmussen, Henrik S."],["dc.contributor.author","Lavin, Philip T."],["dc.contributor.author","Singh, Bhupinder"],["dc.contributor.author","Yang, Alex"],["dc.contributor.author","Deedwania, Prakash"],["dc.date.accessioned","2019-07-09T11:41:57Z"],["dc.date.available","2019-07-09T11:41:57Z"],["dc.date.issued","2015-10-01"],["dc.description.abstract","AIMS: Hyperkalaemia in heart failure patients limits use of cardioprotective renin-angiotensin-aldosterone system inhibitors (RAASi). Sodium zirconium cyclosilicate (ZS-9) is a selective potassium ion trap, whose mechanism of action may allow for potassium binding in the upper gastrointestinal tract as early as the duodenum following oral administration. ZS-9 previously demonstrated the ability to reduce elevated potassium levels into the normal range, with a median time of normalization of 2.2 h and sustain normal potassium levels for 28 days in HARMONIZE-a Phase 3, double-blind, randomized, placebo-controlled trial. In the present study we evaluated management of serum potassium with daily ZS-9 over 28 days in heart failure patients from HARMONIZE, including those receiving RAASi therapies. METHODS AND RESULTS: Heart failure patients with evidence of hyperkalaemia (serum potassium ≥5.1 mmol/L, n = 94) were treated with open-label ZS-9 for 48 h. Patients (n = 87; 60 receiving RAASi) who achieved normokalaemia (potassium 3.5-5.0 mmol/L) were randomized to daily ZS-9 (5, 10, or 15 g) or placebo for 28 days. Mean potassium and proportion of patients maintaining normokalaemia during days 8-29 post-randomization were evaluated. Despite RAASi doses being kept constant, patients on 5 g, 10 g, and 15 g ZS-9 maintained a lower potassium level (4.7 mmol/L, 4.5 mmol/L, and 4.4 mmol/L, respectively) than the placebo group (5.2 mmol/L; P<0.01 vs. each ZS-9 group); greater proportions of ZS-9 patients (83%, 89%, and 92%, respectively) maintained normokalaemia than placebo (40%; P < 0.01 vs. each ZS-9 group). The safety profile was consistent with previously reported overall study population. CONCLUSION: Compared with placebo, all three ZS-9 doses lowered potassium and effectively maintained normokalaemia for 28 days in heart failure patients without adjusting concomitant RAASi, while maintaining a safety profile consistent with the overall study population."],["dc.identifier.doi","10.1002/ejhf.300"],["dc.identifier.pmid","26011677"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12624"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58558"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1879-0844"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Maintenance of serum potassium with sodium zirconium cyclosilicate (ZS-9) in heart failure patients: results from a phase 3 randomized, double-blind, placebo-controlled trial."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","932"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","942"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Abraham, William T."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Brueckmann, Martina"],["dc.contributor.author","Zeller, Cordula"],["dc.contributor.author","Macesic, Hemani"],["dc.contributor.author","Peil, Barbara"],["dc.contributor.author","Brun, Michèle"],["dc.contributor.author","Ustyugova, Anastasia"],["dc.contributor.author","Jamal, Waheed"],["dc.contributor.author","Salsali, Afshin"],["dc.contributor.author","Lindenfeld, JoAnn"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Abraham, William"],["dc.contributor.author","Anker, Stefan"],["dc.contributor.author","Welty, Francine"],["dc.contributor.author","Clayton, Tim"],["dc.contributor.author","Greenberg, Barry"],["dc.contributor.author","Konstam, Marvin"],["dc.contributor.author","Lees, Kennedy"],["dc.contributor.author","Palmer, Mike"],["dc.contributor.author","Parhofer, Klaus"],["dc.contributor.author","Pedersen, Terje"],["dc.contributor.author","Carson, Peter"],["dc.contributor.author","Freston, James"],["dc.contributor.author","Kaplowitz, Neil"],["dc.contributor.author","Lewis, James"],["dc.contributor.author","Mann, Johannes"],["dc.contributor.author","Petrie, John"],["dc.contributor.author","Agostoni, Piergiuseppe"],["dc.contributor.author","Butler, Javed"],["dc.contributor.author","Desai, Akshay"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Howlett, Jonathan"],["dc.contributor.author","Wranicz, Jerzy"],["dc.contributor.author","Mas, Josep Redón"],["dc.contributor.author","Cardoso, José Silva"],["dc.contributor.author","Störk, Stefan"],["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.1486"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16728"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69841"],["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","Rationale and design of the EMPERIAL‐Preserved and EMPERIAL‐Reduced trials of empagliflozin 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","1"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","9"],["dc.contributor.author","Mordi, Ify R."],["dc.contributor.author","Santema, Bernadet T."],["dc.contributor.author","Kloosterman, Mariëlle"],["dc.contributor.author","Choy, Anna-Maria"],["dc.contributor.author","Rienstra, Michiel"],["dc.contributor.author","van Gelder, Isabelle"],["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","van der Harst, Pim"],["dc.contributor.author","Hillege, Hans L."],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","Ng, Leong L."],["dc.contributor.author","Ouwerkerk, Wouter"],["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","Zannad, Faiez"],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Lang, Chim C."],["dc.date.accessioned","2019-07-09T11:51:01Z"],["dc.date.available","2019-07-09T11:51:01Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: In patients with heart failure with reduced ejection fraction (HFrEF) on sub-optimal doses of beta-blockers, it is conceivable that changes in heart rate following treatment intensification might be important regardless of underlying heart rhythm. We aimed to compare the prognostic significance of both achieved heart rate and change in heart rate following beta-blocker uptitration in patients with HFrEF either in sinus rhythm (SR) or atrial fibrillation (AF). METHODS: We performed a post hoc analysis of the BIOSTAT-CHF study. We evaluated 1548 patients with HFrEF (mean age 67 years, 35% AF). Median follow-up was 21 months. Patients were evaluated at baseline and at 9 months. The combined primary outcome was all-cause mortality and heart failure hospitalisation stratified by heart rhythm and heart rate at baseline. RESULTS: Despite similar changes in heart rate and beta-blocker dose, a decrease in heart rate at 9 months was associated with reduced incidence of the primary outcome in both SR and AF patients [HR per 10 bpm decrease-SR: 0.83 (0.75-0.91), p < 0.001; AF: 0.89 (0.81-0.98), p = 0.018], whereas the relationship was less strong for achieved heart rate in AF [HR per 10 bpm higher-SR: 1.26 (1.10-1.46), p = 0.001; AF: 1.08 (0.94-1.23), p = 0.18]. Achieved heart rate at 9 months was only prognostically significant in AF patients with high baseline heart rates (p for interaction 0.017 vs. low). CONCLUSIONS: Following beta-blocker uptitration, both achieved and change in heart rate were prognostically significant regardless of starting heart rate in SR, however, they were only significant in AF patients with high baseline heart rate."],["dc.identifier.doi","10.1007/s00392-018-1409-x"],["dc.identifier.pmid","30610382"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59857"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/242209/EU//BIOSTAT-CHF"],["dc.relation.issn","1861-0692"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Prognostic significance of changes in heart rate following uptitration of beta-blockers in patients with sub-optimally treated heart failure with reduced ejection fraction in sinus rhythm versus atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","238"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Reviews Cardiology"],["dc.bibliographiccitation.lastpage","250"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Brown, David A."],["dc.contributor.author","Perry, Justin B."],["dc.contributor.author","Allen, Mitchell E."],["dc.contributor.author","Sabbah, Hani N."],["dc.contributor.author","Stauffer, Brian L."],["dc.contributor.author","Shaikh, Saame Raza"],["dc.contributor.author","Cleland, John G. F."],["dc.contributor.author","Colucci, Wilson S."],["dc.contributor.author","Butler, Javed"],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Pitt, Bertram"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Greene, Stephen J."],["dc.contributor.author","Gheorghiade, Mihai"],["dc.date.accessioned","2019-07-09T11:43:18Z"],["dc.date.available","2019-07-09T11:43:18Z"],["dc.date.issued","2017"],["dc.description.abstract","Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible. Although the pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important target for therapy to improve cardiac function directly. Mitochondrial abnormalities include impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria."],["dc.identifier.doi","10.1038/nrcardio.2016.203"],["dc.identifier.pmid","28004807"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14415"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58856"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/242209/EU/A systems BIOlogy Study to TAilored Treatment in Chronic Heart Failure/BIOSTAT-CHF"],["dc.relation.issn","1759-5010"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Expert consensus document: Mitochondrial function as a therapeutic target in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]