Frequent Outflow Tract PVCs Suppressed by Sedation
A 47-year-old woman with palpitations and fatigue has a 22% premature ventricular contraction burden on a 14-day monitor. The PVCs have a left bundle branch block morphology, an inferior axis, and a transition at V3; there is a notched intrinsicoid deflection in the inferior leads. Echocardiography and cardiac magnetic resonance imaging are normal. Metoprolol succinate 50 mg daily and diltiazem 120 mg daily have failed to control symptoms, and she is reluctant to take amiodarone. She is referred for catheter ablation. At the start of the procedure, the PVCs are frequent, but after induction of deep sedation with propofol and fentanyl, the burden falls to fewer than one PVC per minute. The electrophysiologist has placed a catheter at the right ventricular outflow tract and records an earliest local activation time 18 ms before QRS onset, with a pace map match of 9 of 12 leads at 10 mA and 2 ms.
1. What is the most likely anatomic origin of the PVCs, and how would you map and ablate them?
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LBBB morphology with an inferior axis indicates an outflow tract origin, and transition at V3 favors the septal right ventricular outflow tract, though an aortic cusp or epicardial site can mimic it; the notched inferior intrinsicoid deflection suggests a free-wall or epicardial component. I would perform activation mapping with a multipolar catheter, looking for the earliest bipolar signal preceding QRS by at least 20 to 30 ms, and pace mapping at 10 mA and 2 ms to compare 12-lead morphology. I would use intracardiac echocardiography to define the RVOT, aortic root, and coronary anatomy, and I would consider coronary angiography or CT integration if the earliest site is near the left main or right coronary artery. Ablation would start at the earliest activation and pace-map site with low power, typically 30 to 40 W, and careful impedance monitoring. Success is elimination of the target PVC and no inducible clinical PVC with isoproterenol. I would also screen for a second morphology, because multiple outflow tract foci occur.
2. The PVCs become rare under deep sedation and the earliest activation is only 18 ms pre-QRS. How do you proceed?
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An 18 ms pre-QRS activation and a 9 of 12 pace map are not sufficient to justify ablation, especially when the clinical PVC is suppressed. Deep sedation with propofol can suppress automaticity and make mapping unreliable. I would lighten sedation, stop propofol if possible, and use isoproterenol or epinephrine to provoke the PVC. If the PVC remains absent, I would not ablate empirically; the risk of an unnecessary lesion in the RVOT, including perforation or coronary injury, outweighs the benefit. I would consider remapping on another day or using a non-contact mapping system, and I would review the Holter to confirm the burden and morphology. If a second morphology is present, I would map both. The patient should be counseled that a repeat procedure may be needed rather than accepting a low-confidence ablation.