Nagai Michiaki, Rommel Karl-Philipp, Po Sunny S, Dasari Tarun W
Cardiovascular section, Department of Medicine, University of Oklahoma, Health Science Center, Oklahoma, USA.
Department of Cardiology, Hiroshima City Asa Hospital, Hiroshima, Japan.
Hypertens Res. 2024 Dec;47(12):3318-3329. doi: 10.1038/s41440-024-01886-2. Epub 2024 Sep 11.
Metabolic syndrome (MetS) induces a systemic inflammatory state which can lead to cardiomyopathy, manifesting clinically as heart failure (HF) with preserved ejection fraction (HFpEF). MetS components are intricately linked to the pathophysiologic processes of myocardial remodeling. Increased sympathetic nervous system activity, which is noted as an upstream factor of MetS, has been linked to adverse myocardial structural changes. Since renal denervation and vagus nerve stimulation have a sympathoinhibitory effect, attention has been paid to the cardioprotective effects of autonomic neuromodulation. In this review, the pathophysiology underlying the relationship between MetS and HF is elucidated, and the evidence regarding autonomic neuromodulation in HFpEF is summarized.
代谢综合征（MetS）会引发一种全身性炎症状态，进而导致心肌病，临床上表现为射血分数保留的心力衰竭（HFpEF）。MetS的各个组成部分与心肌重塑的病理生理过程密切相关。交感神经系统活动增强作为MetS的一个上游因素，已被证实与不良心肌结构变化有关。由于肾去神经支配和迷走神经刺激具有交感神经抑制作用，自主神经调节的心脏保护作用已受到关注。在这篇综述中，阐述了MetS与HF之间关系的病理生理学，并总结了有关HFpEF中自主神经调节的证据。
