Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with diverse etiologies and pathophysiological factors. Obesity and type 2 diabetes mellitus (T2DM), conditions that coexist frequently, induce a cluster of metabolic and non-metabolic signaling derangements which are in favor to induce inflammation, fibrosis, myocyte stiffness, all hallmarks of HFpEF. In contrast to other HFpEF risk factors, obesity and T2DM are often associated with the generation of enlarged epicardial adipose tissue (EAT). EAT acts as an endocrine tissue that may exacerbate myocardial inflammation and fibrosis via various paracrine and vasocrine signals. In addition, an abnormally large EAT poses mechanical stress on the heart via pericardial restrain. HFpEF patients with enlarged EAT may belong to a unique phenotype that can benefit from specific EAT-targeted interventions, including life-style modifications and pharmacologically via statins and fat modifying anti-diabetics drugs; like metformin, sodium-glucose cotransporter 2 inhibitors, or glucagon-like peptide-1 receptor agonists, respectively.

射血分数保留的心力衰竭（HFpEF）是一种异质性综合征，具有多种病因和病理生理因素。肥胖和 2 型糖尿病 (T2DM) 经常共存，会诱发一系列代谢和非代谢信号紊乱，从而有利于诱发炎症、纤维化、肌细胞僵硬，这些都是 HFpEF 的特征。与其他 HFpEF 危险因素相比，肥胖和 T2DM 通常与增大的心外膜脂肪组织 (EAT) 的产生有关。EAT 作为内分泌组织，可能会加剧心肌炎症和纤维化通过各种旁分泌和血管分泌信号。此外，异常大的 EAT 会对心脏造成机械应力通过心包抑制。EAT 增大的 HFpEF 患者可能属于一种独特的表型，可以从特定的 EAT 靶向干预措施中受益，包括生活方式的改变和药物治疗通过他汀类药物和脂肪调节抗糖尿病药物；分别如二甲双胍、钠-葡萄糖协同转运蛋白 2 抑制剂或胰高血糖素样肽 1 受体激动剂。