Zimmermann, Wolfram-Hubertus

[["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","272"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","285"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","de Boer, Rudolf A."],["dc.contributor.author","De Keulenaer, Gilles"],["dc.contributor.author","Bauersachs, Johann"],["dc.contributor.author","Brutsaert, Dirk"],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","Diez, Javier"],["dc.contributor.author","Du, Xiao‐Jun"],["dc.contributor.author","Ford, Paul"],["dc.contributor.author","Heinzel, Frank R."],["dc.contributor.author","Lipson, Kenneth E."],["dc.contributor.author","McDonagh, Theresa"],["dc.contributor.author","Lopez‐Andres, Natalia"],["dc.contributor.author","Lunde, Ida G."],["dc.contributor.author","Lyon, Alexander R."],["dc.contributor.author","Pollesello, Piero"],["dc.contributor.author","Prasad, Sanjay K."],["dc.contributor.author","Tocchetti, Carlo G."],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Sluijter, Joost P.G."],["dc.contributor.author","Thum, Thomas"],["dc.contributor.author","Tschöpe, Carsten"],["dc.contributor.author","Zannad, Faiez"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Lindsey, Merry L."],["dc.contributor.author","Maack, Christoph"],["dc.contributor.author","Heymans, Stephane"],["dc.date.accessioned","2019-07-09T11:50:51Z"],["dc.date.available","2019-07-09T11:50:51Z"],["dc.date.issued","2019"],["dc.description.abstract","Fibrosis is a pivotal player in heart failure development and progression. Measurements of (markers of) fibrosis in tissue and blood may help to diagnose and risk stratify patients with heart failure, and its treatment may be effective in preventing heart failure and its progression. A lack of pathophysiological insights and uniform definitions has hampered the research in fibrosis and heart failure. The Translational Research Committee of the Heart Failure Association discussed several aspects of fibrosis in their workshop. Early insidious perturbations such as subclinical hypertension or inflammation may trigger first fibrotic events, while more dramatic triggers such as myocardial infarction and myocarditis give rise to full blown scar formation and ongoing fibrosis in diseased hearts. Aging itself is also associated with a cardiac phenotype that includes fibrosis. Fibrosis is an extremely heterogeneous phenomenon, as several stages of the fibrotic process exist, each with different fibrosis subtypes and a different composition of various cells and proteins - resulting in a very complex pathophysiology. As a result, detection of fibrosis, e.g. using current cardiac imaging modalities or plasma biomarkers, will detect only specific subforms of fibrosis, but cannot capture all aspects of the complex fibrotic process. Furthermore, several anti-fibrotic therapies are under investigation, but such therapies generally target aspecific aspects of the fibrotic process and suffer from a lack of precision. This review discusses the mechanisms and the caveats and proposes a roadmap for future research."],["dc.identifier.doi","10.1002/ejhf.1406"],["dc.identifier.pmid","30714667"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59843"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/305507/EU//HOMAGE"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602904/EU//FIBRO-TARGETS"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602156/EU//HECATOS"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]