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Updated: Feb 10, 2026

Chronic Ovine Model of Right Ventricular Failure and Functional Tricuspid Regurgitation
Published on: March 17, 2023
Chronic median nerve modulation reduces ventricular arrhythmia and improves ventricular function in a postmyocardial
Zhengqin Zhai1, Shuang Zhao1, Min Tang1
1The Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, National Clinical Research Center of Cardiovascular Diseases, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Aim:
Median nerve stimulation (MNS) is a novel neuromodulation approach for treatment of ventricular arrhythmia, but little is known about its chronic effects. The aim of this study was to investigate the effects of chronic MNS on ventricular arrhythmia and ventricular dysfunction postmyocardial infarction (MI).
Method:
Two weeks after MI, 12 rabbits were randomly divided into control and MNS groups, and chronic MNS was performed in MNS group for 2 weeks. Ventricular function and arrhythmias; sympathetic innervation and activity; and interleukin-1 β (IL-1 β) and norepinephrine (NE) levels were analyzed.
Results:
Both the total number of premature ventricular complex and episodes of ventricular tachycardia were lower in MNS group than in control group (20 560 ± 10 314 beats vs 70 079 ± 37 184 beats, P = .021, and 115 ± 63 episodes vs 307 ± 164 episodes, P = .034, respectively). Compared with control group, MNS decreased the cardiac sympathetic nerve density and level of circulating NE in MNS group (1798.42 ± 644.07 μm2 /mm2 vs 1003.79 ± 453.00 μm2 /mm2, P = .041, and 20.86 ± 4.54 pg/mL vs 11.07 ± 1.43 pg/mL, P = .002, respectively). MNS also improved the left ventricular ejection fraction (59.07 ± 1.91% vs 49.77 ± 3.47%, P = .003) and inhibited the level of IL-1 β in serum (69.19 ± 4.71 pg/mL vs 85.93 ± 12.80 pg/mL, P = .013).
Conclusion:
Chronic MNS appears to protect against ventricular arrhythmia and improves ventricular function post-MI, which may be mediated by suppressing cardiac sympathetic activity and anti-inflammatory effects.
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