Vertebral Vein Electrical Stimulation to Provoke Ventricular Ectopy During Ablation in the Electrophysiology Lab
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EP LAB DIGEST. 2025;25(2):6.
Bradley P Knight, MD, FACC, FHRS
Dear Readers,
A 71-year-old man presented for a repeat ablation procedure for frequent, highly symptomatic premature ventricular contractions (PVCs) refractory to antiarrhythmic drugs. He also has a history of atrial fibrillation, constrictive pericarditis, and mitral regurgitation, and had previously undergone atrial ablation procedures, left atrial appendage closure with a Watchman device (Boston Scientific), transcatheter edge-to-edge repair of the mitral valve with a MitraClip (Abbott), and surgical pericardiectomy. Two years ago, he underwent his first ablation for frequent PVCs that arose from the left ventricular anterolateral papillary muscle. He did well for 2 years but then began having recurrent highly symptomatic PVCs documented on his recording device. A monitor showed a 21% burden of unifocal PVCs.
However, when he arrived for his repeat ablation procedure, he only had 2 PVCs while he was being prepped for his procedure. After being placed in the EP lab, he had 2 more unifocal PVCs before being placed under anesthesia and then had none. Infusion of isoproterenol and burst pacing from the right ventricular apex did not trigger any PVCs. Fortunately, using a transseptal approach, an excellent pace map could be obtained with a high-density mapping catheter, and that site was successfully targeted with radiofrequency ablation. The patient did well in the immediate days after the procedure.
Pace-mapping is known to have a lower resolution and accuracy to localize PVCs compared to activation mapping, but is often used when there is infrequent intraprocedural ectopy. What more could have been done in the EP lab to trigger this patient’s PVCs? Multiple drugs have been used to increase sympathetic tone in the EP lab to facilitate induction of arrhythmias, including isoproterenol, dobutamine, epinephrine, calcium, and caffeine. These all have limitations including hypotension, at times requiring phenylephrine, and an increase in contractility making it more challenging to safely manipulate catheters in the heart and to achieve catheter stability during ablation. It can be helpful to minimize sedation and avoid general anesthesia, but this strategy also has limitations.
In December 2024, Timothy Markman and colleagues from the University of Pennsylvania published an interesting study1 using a new technique to trigger PVCs to facilitate catheter ablation in the EP lab: stimulation of the sympathetic nervous system from the vertebral veins (VVs). Apparently, the VVs typically course anteriorly from the spinal column at the level of the stellate ganglion. Using a deflectable sheath from the femoral vein, the left VV was cannulated, and a multipolar electrophysiological catheter was positioned distally within the vein. Electrical stimulation was performed at a frequency of 20 Hz. Initially, stimulation was performed at 1 mA and a pulse width of 2 milliseconds. The amplitude was gradually increased up to 25 mA or until frequent PVCs occurred for up to 15 minutes. If the patient experienced discomfort, stimulation intensity was reduced. They used the technique in 15 patients with rare intraprocedural PVCs despite attempted induction with isoproterenol, pacing, and minimal sedation over a 3-year period. Seven of 15 had undergone at least 1 prior unsuccessful ablation. During the initial 10 minutes of the procedure, 1 patient had 2 spontaneous PVCs, and the remainder of the patients had no PVCs. Patients had a mean of 1.3 PVCs throughout the 10-minute period before VV stimulation compared to 8.2 PVCs per minute during VV stimulation. Stimulation from VVs was safely used to induce PVCs, facilitating activation mapping in 7 patients and, ultimately, successful ablation in 9 patients. There were no complications related to VV stimulation. It is not clear how much of an increase in cardiac contractility was seen on fluoroscopy or intracardiac echocardiography during VV stimulation.
Patients with a high burden of PVCs causing symptoms or ventricular dysfunction are good candidates for catheter ablation, but a limitation of the procedure is the variability in PVC frequency over time, which can result in infrequent intraprocedural ectopy that limits the ability to perform activation mapping. Often, the procedure is cancelled or aborted. Based on the data from the Penn group, electrical stimulation of the VVs using a multielectrode EP catheter may be a promising new technique to provoke PVCs in the EP lab to facilitate mapping and successful catheter ablation.
Disclosures: Dr Knight has served as a paid consultant to Medtronic and was an investigator in the PULSED AF trial. In addition, he has served as a consultant, speaker, investigator, and/or has received EP fellowship grant support from Abbott, AltaThera, AtriCure, Baylis Medical, Biosense Webster, Biotronik, Boston Scientific, CVRx, Philips, and Sanofi; he has no equity or ownership in any of these companies.
Reference
1. Markman TM, Tschabrunn CM, Callans D, Marchlinski FE, Nazarian S. Intravascular sympathetic stimulation to facilitate catheter ablation of premature ventricular complexes. JAMA Cardiol. Published online December 23, 2024. doi:10.1001/jamacardio.2024.4447
