Alterations of endothelial function, inflammatory activation, and nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway are involved in the pathophysiology of heart failure. Metabolic alterations have been studied in the myocardium of heart failure (HF) patients; alterations in ketone body and amino acid/protein metabolism have been described in patients affected by HF, as well as mitochondrial dysfunction and other modified metabolic signaling. However, their possible contributions toward cardiac function impairment in HF patients are not completely known. Recently, sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) have emerged as a new class of drugs designed to treat patients with type 2 diabetes (T2D), but have also been shown to be protective against HF-related events and CV mortality. To date, the protective cardiovascular effects of these drugs in patients with and without T2D are not completely understood and several mechanisms have been proposed. In this review, we discuss on vascular and metabolic effects of SGLT2i and GLP-1 in HF patients.

心力衰竭的病理生理学涉及内皮功能、炎症激活和一氧化氮-环磷酸鸟苷 (NO-cGMP) 通路的改变。已经在心力衰竭 (HF) 患者的心肌中研究了代谢改变；已在受 HF 影响的患者中描述了酮体和氨基酸/蛋白质代谢的改变，以及线粒体功能障碍和其他改变的代谢信号。然而，它们对 HF 患者心功能损伤的可能贡献尚不完全清楚。最近，钠-葡萄糖协同转运蛋白 2 抑制剂 (SGLT2i) 和胰高血糖素样肽-1 (GLP-1) 受体激动剂 (RAs) 已成为一类旨在治疗 2 型糖尿病 (T2D) 患者的新型药物，但也被证明可以预防 HF 相关事件和 CV 死亡率。迄今为止，这些药物对患有和不患有 T2D 的患者的心血管保护作用尚未完全了解，并且已经提出了几种机制。在这篇综述中，我们讨论了 SGLT2i 和 GLP-1 对 HF 患者的血管和代谢影响。