A 48-year-old female patient without any past medical history was referred to our hospital for frequent PVCs. The patient had no history of smoking or excessive alcohol or caffeine intake. Physical examination showed no signs of heart failure. Blood tests showed a slightly elevated brain natriuretic peptide level of 57.1 pg/mL, but no other abnormalities were found. The PVC was monomorphic, and the morphology was right bundle branch block and right inferior axis. Based on the previous report, ALPM was suspected as the origin (Figure 1A). Holter electrocardiogram showed 29,332 beats of monomorphic PVC per day. This is equivalent to 27.0% of the total heartbeats. It occurred more frequently from night to morning, and >3 lasting beats were not confirmed. Echocardiography revealed a 60.4% ejection fraction, no enlargement of chamber size or valvular disease, and relatively thick ALPM chordae tendineae attached to the AML (Figure 1B). Given the lack of structural heart disease, this PVC was diagnosed as idiopathic. Because of the failure in suppressing the PVCs and the worsening of symptoms by oral beta blocker, we performed a catheter ablation.
Frequent PVCs were observed throughout the case. The CARTO  3 system (Biosense Webster, Inc, Irvine, CA) was used for 3D mapping, and the right internal jugular vein, right femoral veins, and right femoral artery were punctured under local anesthesia. A decapolar catheter (EPstar; Japan Lifeline Co, Ltd, Tokyo, Japan) was inserted into the coronary sinus, and another decapolar catheter (Scooper; FUKUDA DENSHI Co, Ltd, Tokyo, Japan) was placed into the right ventricle to record both His and right ventricle electrogram.
An intracardiac ultrasound catheter (SOUNDSTAR; Biosense Webster, Inc) was used to create an anatomical shell of the LV, the aortic valve, and the papillary muscles at the beginning of the procedure. A trabeculated structure was noted from the ALPM to the AML (Figure 2A). Then, a mapping catheter (PentaRay; Biosense Webster, Inc) was inserted into the LV for the activation mapping of the PVC. Contrary to what we anticipated, the earliest activation was at the AMLAMFC (Figure 2B), where a discrete prepotential preceded the QRS onset of the PVC by 84 ms (Figure 2C). This site coincided with the trabeculated structure noted by the intracardiac ultrasound (Figure 2A). The discrete potential noted during PVC could be observed after the offset of the QRS during sinus rhythm, which suggested the retrograde conduction via the trabeculated structure (Figure 2C). No prepotential was noted around the ALPM, and the 3D mapping showed later activation (Supplemental Video 1).
Pace mapping score obtained by the PaSoTM module (Biosense Webster, Inc) was the best at the base of the ALPM; however, the score was low at the AMLAMFC (Figure 2D). Radiofrequency (RF) ablation was first applied using a 3.5 mm irrigation catheter (THERMOCOOL SMARTTOUCHTM SF; Biosense Webster, Inc) at the ALPM where the best pace mapping score was obtained (Figure 2E). However, this failed to suppress the PVCs.
Considering the instability of the ablation catheter and the possible intramural origin, RF ablation was performed at the tip of the ALPM. However, this also failed to suppress the PVCs. Given the evidence of the discrete prepotential at the AMLAMFC and the result of pace mapping, we postulated that the origin of this PVC was at the AMLAMFC and the exit was at the ALPM. RF application at the AMLAMFC successfully eliminated the PVC after accelerated PVCs with the same morphology (Figure 2E). No PVC was observed after RF ablation even with isoproterenol infusion.