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.Graphical Abstract Assembling the acute heart failure (AHF) in a translational view. Different causes of AHF can be reproduced in pre-clinical models to unveil novel pathophysiological and molecular mechanisms. Identifying novel molecular targets amongst organelles and cellular compartments can be tested again in the pre-clinical models. Effective strategies can be exploited in human scenarios. Image was partially created with BioRender.com.
