Key result
Left stellate ganglion pulsed radiofrequency safely suppresses post-MI ventricular arrhythmias in early translational testing.
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Why the study?
Cardiac sympathetic hyperactivity from the left stellate ganglion drives ischemic ventricular arrhythmias, and current treatments are either transient or invasive, necessitating a minimally invasive approach with sustained effects.
Does pulsed radiofrequency of the left stellate ganglion suppress ischemic ventricular arrhythmias in post-MI models and patients with electrical storm?
Does pulsed radiofrequency of the left stellate ganglion suppress ischemic ventricular arrhythmias in post-MI models and patients with electrical storm?
Left stellate ganglion pulsed radiofrequency is a promising, minimally invasive neuromodulatory strategy to suppress sympathetic hyperactivity and ischemic ventricular arrhythmias.
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 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.
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Xu et al. (2026) studied Ischemic ventricular arrhythmias (n=43). Left stellate ganglion pulsed radiofrequency (LSG-PRF) vs. Control, surgical LSG excision, and sham was evaluated on Safety, cardiac sympathetic nerve activity, and ventricular arrhythmia inducibility. Left stellate ganglion pulsed radiofrequency safely suppressed sympathetic hyperactivity and post-myocardial infarction ventricular arrhythmias in rats, with preliminary feasibility in 4 patients.
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