Cardiovascular Research Unit, Department of Medicine and Surgery, University of Salerno, Via Salvador Allende, 84081 Baronissi, Italy.
UnIC@RISE, Department of Surgery and Physiology, Faculty of Medicine of the University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal.
Cardiovasc Res. 2023 Nov 15;119(14):2390-2404. doi: 10.1093/cvr/cvad088.
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.
尽管慢性心力衰竭 (CHF) 的治疗已显著改善了患者的预后和生存率，但急性心力衰竭 (AHF) 的治疗管理在过去几十年中几乎没有变化。这部分是由于缺乏用于病理生理学评估的临床前模型，因此，对不同 AHF 表型中涉及的分子机制的了解有限。本科学声明概述了由病因、遗传和环境因素以及合并症相互作用引起的从急性到 CHF 的不同轨迹。此外，我们讨论了潜在的分子靶点，这些靶点有可能揭示新的治疗前景，以改善急性期的结果并阻止向 CHF 的发展。
