Heart failure (HF) can be classified into ischemic and non-ischemic types based on etiology, with differences in their pathological basis and remodeling patterns. Since 2019, sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown in numerous randomised controlled trials (RCT) to reduce the risk of HF getting worse and of cardiovascular events, with benefits that are not dependent on a person's diabetic status. This article systematically reviews evidence on the consistency of SGLT2i efficacy in ischemic and non-ischemic HF, potential sources of heterogeneity, and their multi-pathway cardio-renal-metabolic mechanisms. It discusses clinical integration strategies based on research progress in Chinese populations, with a focus on the latest findings and advancements in the field. Existing RCT subgroup analyses and meta-studies collectively indicate that SGLT2i significantly reduces HF hospitalization/worsening risk in both etiological groups, with most interaction tests showing no statistical significance. At the mechanism level, cross-etiological benefits may be achieved through common terminal pathways such as decongestion and glomerular hyperfiltration correction, myocardial energy metabolism improvement, ion homeostasis and inflammatory fibrosis inhibition. In the future, it is necessary to carry out prospective studies stratified by etiology under a unified and operable etiology determination framework, combining imaging and biomarkers to promote precise treatment.

心力衰竭（HF）按病因学可分为缺血性与非缺血性HF两大类型，二者在病理基础与重构模式上存在差异。钠-葡萄糖协同转运蛋白2抑制剂（SGLT2i）自2019年以来在多项随机对照试验（RCT）中被证实可降低HF恶化与心血管事件风险，且获益不受糖尿病状态影响。本文系统梳理了SGLT2i在缺血性与非缺血性HF中的疗效一致性证据、潜在异质性来源及其心-肾-代谢多通路机制，并结合中国人群研究进展讨论临床整合应用策略。现有RCT亚组分析与荟萃研究总体提示：SGLT2i在两类病因人群中均可显著降低HF住院/恶化风险，交互作用检验多未见统计学差异；机制层面可能通过纠正充血与肾小球高滤过、改善心肌能量代谢、离子稳态与抑制炎症纤维化等共同终末通路发挥跨病因获益。未来需在统一且可操作的病因判定框架下开展按病因分层的前瞻性研究，结合影像与生物标志物以推进精准治疗。