Related Experiment Video
Updated: Oct 3, 2026
Location, Dissection, and Analysis of the Murine Stellate Ganglion
Published on: December 22, 2020
Left Stellate Ganglion Pulsed Radiofrequency Suppresses Ischemic Ventricular Arrhythmias: A Translational Study
Zhou Xu1, Shu Yang2, Xiaokai Zhou3
1Department of Cardiology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Background:
Cardiac sympathetic hyperactivity originating from the left stellate ganglion (LSG) drives ischemic ventricular arrhythmias (VAs). Stellate ganglion block provides only transient relief, whereas surgical denervation is invasive and irreversible. A minimally invasive approach with potentially sustained effects is needed.
Objectives:
This study sought to investigate whether pulsed radiofrequency (PRF) of the LSG-a nonthermal neuromodulatory technique-safely suppresses ischemic VAs, and to characterize its mechanism using integrated neural and cardiac transcriptomics.
Methods:
Safety was first assessed in healthy rats (n = 15) randomized to control, LSG-PRF (42 °C, 2 Hz, 20 milliseconds), or surgical LSG excision. In a rat myocardial infarction (MI) model (n = 24; Sham, MI, MI + PRF), cardiac sympathetic nerve activity, programmed electrical stimulation, echocardiography, and histology were evaluated, complemented by bulk RNA-seq of the LSG and single-cell RNA-seq of cardiac tissue. Translational feasibility was tested in 4 patients with drug-refractory electrical storm using ultrasound-guided LSG-PRF.
Results:
In contrast to LSG excision, PRF produced only transient Horner's syndrome and did not cause hypotension. In MI rats, PRF reduced cardiac sympathetic nerve activity, attenuated ventricular tachycardia/ventricular fibrillation inducibility and duration on programmed stimulation, lowered serum norepinephrine and angiotensin II, improved left ventricular function, and reduced myocardial fibrosis. LSG transcriptomics showed down-regulation of inflammation- and sprouting-related genes including S100a9 and Ngf. Single-cell analysis of the infarcted heart revealed attenuation of a proinflammatory Grik2+ Schwann cell subset, with computationally inferred reductions in neuro-immune signaling. In all 4 patients, no sustained ventricular tachycardia recurrence was observed during a median follow-up of 12 months.
Conclusions:
LSG-PRF is a minimally invasive neuromodulatory strategy associated with suppression of sympathetic hyperactivity and post-MI VAs, accompanied by attenuated ganglionic inflammation and modulated cardiac neuro-immune signaling. Preliminary clinical experience supports feasibility and warrants prospective trials.
