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Intravascular Sympathetic Stimulation to Facilitate Catheter Ablation of Premature Ventricular Complexes. | LitMetric

Intravascular Sympathetic Stimulation to Facilitate Catheter Ablation of Premature Ventricular Complexes.

JAMA Cardiol

Section for Cardiac Electrophysiology, Division of Cardiovascular Medicine, Department of Medicine, University of Pennsylvania, Philadelphia.

Published: December 2024

AI Article Synopsis

  • This study investigates the effect of stimulating sympathetic nerves via vertebral veins (VVs) on premature ventricular complexes (PVCs) during catheter ablation in patients with infrequent PVCs.
  • In a case series of 15 patients, stimulation led to a significant increase in PVC frequency from an average of 1.3 PVCs per minute before stimulation to 8.2 PVCs during stimulation.
  • The results indicate that direct electrical stimulation can successfully induce PVCs, potentially aiding in more effective catheter ablation procedures by enabling better mapping of PVC origins.

Article 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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Source
http://dx.doi.org/10.1001/jamacardio.2024.4447DOI Listing

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