Janssen-Telders Carolina, Eringa Etto C, de Groot Joris R, de Man Frances S, Handoko M Louis
Department of Cardiology Amsterdam UMC, Heart Centre, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.
Amsterdam Cardiovascular Sciences, De Boelelaan 1108, 1081 HZ Amsterdam, The Netherlands.
Cardiovasc Res. 2025 Jun 12;121(6):860-870. doi: 10.1093/cvr/cvaf056.
Heart failure with preserved ejection fraction (HFpEF) is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammation and lipotoxic infiltration of the myocardium. However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. This review explores the dynamic role of EAT in health and disease. Drawing upon insights from studies in other conditions, we discuss potential EAT-mediated inflammatory pathways in HFpEF and how they may contribute to functional and structural myocardial and endothelial derangements, including intramyocardial lipid infiltration, fibrosis, endothelial dysfunction, cardiomyocyte stiffening, and left ventricular hypertrophy. Lastly, we propose potential targets for novel therapeutic avenues.
射血分数保留的心力衰竭（HFpEF）是一个日益严重的全球健康问题，其特点是发病率和死亡率高，有效治疗方法有限。肥胖主要通过内脏脂肪组织的积累和作用，显著影响心肌和血管的血流动力学和结构变化。特别是，心外膜脂肪组织（EAT）通过炎症和心肌脂毒性浸润导致HFpEF。然而，导致HFpEF舒张期僵硬的确切信号通路仍需进一步阐明。本综述探讨了EAT在健康和疾病中的动态作用。借鉴其他疾病研究的见解，我们讨论了HFpEF中潜在的EAT介导的炎症途径，以及它们如何导致心肌和内皮功能及结构紊乱，包括心肌内脂质浸润、纤维化、内皮功能障碍、心肌细胞僵硬和左心室肥厚。最后，我们提出了新治疗途径的潜在靶点。
