作者：赵惠奇，张青海，郑昭芬

单位：

1.湖南师范大学附属第一医院湖南省人民医院心血管内科2.湖南省心力衰竭临床医学研究中心

单位（英文）：

1.Department of Cardiology, the First Affiliated Hospital of Hunan Normal University/Hunan Provincial People's Hospital, Changsha 410000, China 2.Hunan Heart Failure Clinical Medical Research Center, Changsha 410000, China Corresponding author: ZHANG Qinghai, E-mail: rock_kinhool@hotmail.com; ZHENG Zhaofen, E-mail: zhaofenz@foxmail. com

关键词：

心力衰竭; 射血分数保留的心力衰竭; 能量代谢; 治疗; 综述;

关键词（英文）：

Heart failure; Heart failure with preserved ejection fraction; Energy metabolism; Therapy; Review

中图分类号：

R 541.6

DOI：

10.12114/j.issn.1008-5971.2023.00.054

基金项目：

湖南省社会发展领域重点研发项目（2019SK2021）；湖南省卫生健康委科研计划项目（202203013494）；湖南省教 育厅优秀青年项目（22B0091）；湖南省中医药管理局重点项目（C2023010）

摘要：

射血分数保留的心力衰竭（HFpEF）是心力衰竭的主要类型之一，50%以上的心力衰竭患者归为HFpEF。目前，血管紧张素转换酶抑制剂、血管紧张素Ⅱ受体阻滞剂、β-受体阻滞剂等心力衰竭常规用药对HFpEF患者的疗效欠佳，亟需寻找新的治疗手段来改善HFpEF患者预后。钠-葡萄糖协同转运蛋白2抑制剂（SGLT2i）目前成为国内外最新推荐的“心力衰竭第四联”药物，其可改善酮体代谢，尤其能改善HFpEF患者的预后，提示靶向调节心肌能量代谢可能是HFpEF治疗的新方向。本文通过分析正常心肌能量代谢及HFpEF心肌能量代谢的特点、HFpEF的代谢疗法，得出减少脂肪酸的摄取和氧化、改善葡萄糖氧化代谢、增加酮体及支链氨基酸氧化代谢可进一步优化心肌能量代谢，更好地保护或改善心功能，可成为HFpEF的潜在治疗靶点。

英文摘要：

　Heart failure with preserved ejection fraction (HFpEF) is one of the main types of heart failure, and more than 50% of heart failure patients are classified as HFpEF. At present, classical heart failure medications such as angiotensin converting enzyme inhibitors, angiotensin Ⅱ receptor blockers and β-receptor blockers, are less effective in HFpEF patients.It is urgent to find new treatment methods to improve the prognosis of patients with HFpEF. Sodium-glucose cotransporter 2 inhibitor (SGLT2i) has become the latest recommended "fourth combination of drugs for heart failure" at home and abroad, which can improve ketone metabolism, especially the prognosis of patients with HFpEF, indicating that targeted regulation of cardiac energy metabolism may be a new therapeutic target for HFpEF. In this review, by analyzing the characteristics of normal myocardial energy metabolism and HFpEF myocardial energy metabolism, as well as the metabolic therapy of HFpEF, concluded that reducing the intake and oxidation of fatty acids, improving glucose oxidative metabolism, and increasing the oxidative metabolism of ketone bodies and branched chain amino acids can further optimize myocardial energy metabolism, better protect or improve cardiac function, and can become potential therapeutic targets of HFpEF.

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