TY - JOUR
T1 - Acute heart failure
T2 - mechanisms and pre-clinical models-a Scientific Statement of the ESC Working Group on Myocardial Function
AU - Ciccarelli, Michele
AU - Pires, Inês Falcão
AU - Bauersachs, Johann
AU - Bertrand, Luc
AU - Beauloye, Christophe
AU - Dawson, Dana
AU - Hamdani, Nazha
AU - Hilfiker-Kleiner, Denise
AU - van Laake, Linda W.
AU - Lezoualc'h, Frank
AU - Linke, Wolfgang A.
AU - Lunde, Ida G.
AU - Rainer, Peter P.
AU - Rispoli, Antonella
AU - Visco, Valeria
AU - Carrizzo, Albino
AU - Dal Ferro, Matteo
AU - Stolfo, Davide
AU - van der Velden, Jolanda
AU - Zacchigna, Serena
AU - Heymans, Stephane
AU - Thum, Thomas
AU - Tocchetti, Carlo Gabriele
PY - 2023/10/1
Y1 - 2023/10/1
N2 - 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.
AB - 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.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85178355589&origin=inward
U2 - 10.1093/cvr/cvad088
DO - 10.1093/cvr/cvad088
M3 - Review article
C2 - 37967390
SN - 0008-6363
VL - 119
SP - 2390
EP - 2404
JO - Cardiovascular research
JF - Cardiovascular research
IS - 14
ER -