ArticleJAMA cardiology2025
Intravascular Sympathetic Stimulation to Facilitate Catheter Ablation of Premature Ventricular Complexes.
Article in JAMA cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Arrhythmia induced by right internal jugular vein catheterization: a case report.BMC cardiovascular disorders · 2026Article
- Pharmacologic parasympathetic withdrawal to facilitate activation mapping and ablation of infrequent intraprocedural premature ventricular contractions.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
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5 authors.
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Abstract
Importance: Infrequent intraprocedural premature ventricular complexes (PVCs) limit the efficacy of catheter ablation. Intravascular stimulation of sympathetic nerves via vertebral veins (VVs) has been used to activate cardiac sympathetic tone and may promote PVCs. Objective: To characterize the ability of direct electrical sympathetic stimulation via VVs to induce PVCs at the time of catheter ablation. Design, Setting, and Participants: This prospective case series involved adult patients undergoing catheter ablation of PVCs, with rare or absent PVCs despite standard provocation, at the Hospital of the University of Pennsylvania between 2022 and 2024. Stimulation was performed via the left VV (20 Hz, up to 25 mA). Main Outcomes and Measures: The primary outcome was PVC frequency, assessed before, during, and after stimulation. A multilevel mixed-effects Poisson regression was used to compare the rate of PVCs during the procedure. Results: Fifteen patients (mean [SD] age, 60 [17] years; 10 male [71%]) had a mean (SD) preprocedure PVC burden of 16.3% (8.6%) (median [IQR], 17.0% [11.5%-21.5%]), and 7 of 15 had undergone at least 1 prior unsuccessful ablation. Provocation of PVCs was attempted with isoproterenol, atrial and ventricular burst pacing, and minimal sedation in all patients before VV stimulation. Throughout the 10-minute period before VV stimulation, patients had a mean (SD) of 1.3 (1.4) PVCs (median [IQR], 1.0 [0.0-2.5] PVCs). During VV stimulation, PVCs were noted in all patients (mean [SD], 8.2 [5.7] PVCs per minute; median [IQR], 6.0 [4.5-13.0] PVCs per minute). In the 10-minute period after VV stimulation, patients had a mean (SD) of 5.1 (6.6) PVCs per minute (median [IQR], 3.0 [0.5-6.5] PVCs per minute). After VV stimulation, ablation was guided by activation mapping in 7 patients and by pace mapping alone in the remaining patients. Postablation monitoring demonstrated a mean (SD) 1.3% (2.3%) burden of PVCs (median [IQR], 0.0% [0.0%-2.5%]), with 9 of 15 patients having less than 1% burden of PVCs. There were no adverse events related to VV stimulation. Conclusions and Relevance: These findings suggest that intravascular sympathetic stimulation via the VV can be used to safely provoke PVCs during catheter ablation.
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