Low‐level transcutaneous vagus nerve stimulation attenuates cardiac remodeling in a rat model of heart failure with preserved ejection fraction

New Findings

What is the central question of this study?

In this study, we investigated the effect of chronic intermittent low‐level transcutaneous vagus nerve stimulation on cardiac inflammation, fibrosis and diastolic dysfunction in a rat model of heart failure with preserved ejection fraction.

What is the main finding and its importance?

In salt‐sensitive rats fed with high salt diet, we show that low‐level transcutaneous vagus nerve stimulation significantly attenuates blood pressure elevation, ameliorates diastolic function and attenuates left ventricular inflammation and fibrosis compared to the sham group. Further studies to examine the efficacy of this novel treatment in humans are warranted.

Abstract

Inflammation and fibrosis play a central role in the development of heart failure with preserved ejection fraction (HFpEF). We previously showed that low‐level, transcutaneous stimulation of the vagus nerve at the tragus (LLTS) is anti‐inflammatory. We investigated the effect of chronic intermittent LLTS on cardiac inflammation, fibrosis and diastolic dysfunction in a rat model of HFpEF. Dahl salt‐sensitive (DS) rats were randomized in 3 groups: low salt (LS, 0.3% NaCl; n = 12; control group without stimulation) and high salt (HS, 4% NaCl) with either active (n = 18) or sham (n = 18) LLTS at 7 weeks of age. After 6 weeks of diet (baseline), sham or active LLTS (20 Hz, 2 mA, 0.2 ms) was implemented for 30 minutes daily for 4 weeks. Echocardiography was performed at baseline and 4 weeks after treatment (endpoint). At endpoint, left ventricle (LV) histology and gene expression were examined. After 6 weeks of diets, HS rats developed hypertension and LV hypertrophy compared to LS rats. At endpoint, LLTS significantly attenuated blood pressure elevation, prevented the deterioration of diastolic function and improved LV circumferential strain, compared to the HS sham group. LV inflammatory cell infiltration and fibrosis were attenuated in the HS active compared to the HS sham group. Pro‐inflammatory and pro‐fibrotic genes [tumor necrosis factor, osteopontin, interleukin (IL)‐11, IL‐18 and IL‐23A] were differentially altered in the 2 groups. Chronic intermittent LLTS ameliorates diastolic dysfunction, and attenuates cardiac inflammation and fibrosis in a rat model of HFpEF, suggesting that LLTS may be used clinically as a novel noninvasive neuromodulation therapy in HFpEF.

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