Acute heart failure: mechanisms and pre-clinical models-a Scientific Statement of the ESC Working Group on Myocardial Function.
Acute heart failure
New strategies
Phenotypes
Pre-clinical models
Scientific statement
Therapeutic management
Trajectories
Journal
Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427
Informations de publication
Date de publication:
15 11 2023
15 11 2023
Historique:
received:
12
11
2022
revised:
16
02
2023
accepted:
06
03
2023
medline:
17
11
2023
pubmed:
15
11
2023
entrez:
15
11
2023
Statut:
ppublish
Résumé
While chronic heart failure (CHF) treatment has considerably improved patient prognosis and survival, the therapeutic management of acute heart failure (AHF) has remained virtually unchanged in the last decades. This is partly due to the scarcity of pre-clinical models for the pathophysiological assessment and, consequently, the limited knowledge of molecular mechanisms involved in the different AHF phenotypes. This scientific statement outlines the different trajectories from acute to CHF originating from the interaction between aetiology, genetic and environmental factors, and comorbidities. Furthermore, we discuss the potential molecular targets capable of unveiling new therapeutic perspectives to improve the outcome of the acute phase and counteracting the evolution towards CHF.
Identifiants
pubmed: 37967390
pii: 7421377
doi: 10.1093/cvr/cvad088
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2390-2404Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
Déclaration de conflit d'intérêts
Conflict of interest: T.T. received speaker fees and/or holds advisory board seats from Böhringer Ingelheim, Sanofi-Genzyme, Takeda, Novo-Nordisk, Amicus Therapeutics, KSILINK not related to the present article. T.T. filed and licensed patents about non-coding RNAs, and he is founder and shareholder of Cardior Pharmaceuticals (not related to this article). P.R. received travel support, speaker fees, honoraria from Novartis, Vifor, Böhringer, and Daiichi Sankyo (not related to this article). L.W.V.L. received Consultancy fees to UMCU from Abbott, Medtronic, Vifor, Novartis (not related to the present article). W.L. received honoraria from Bristol-Myers Squibb (MyoKardia), Merck, Sharp& Dohme (MSD, USA), and Servier, as well as a research grant from MSD (not related to the present article). J.B. received honoraria for lectures/consulting from Novartis, Vifor, Bayer, Pfizer, Boehringer Ingelheim, AstraZeneca, Cardior, CVRx, BMS, Amgen, Corvia, not related to the present article; and research support for the department from Zoll, CVRx, Abiomed, not related to the present article. C.G.T. reports Receipt of honoraria or consultation fees: VivaLyfe, Univers Formazione, Solaris, Myocardial Solutions; and is listed as an inventor of 2 patents related to HF. All other authors have nothing to disclose.