LAUSR

Premature ventricular contractions (PVCs) originate from left ventricle (LV) papillary muscle (PM) in 5%– 10% of idiopathic PVCs and 14% of those origins are located in the basal third of the PM.1,2 Treatment of such PMrelated PVCs is challenging; the recurrence rate following percutaneous radiofrequency catheter ablation (RFCA) is higher than that for other types of idiopathic PVCs due to the vigorous movement and tissue thickness, i.e., evidence remains scarce on the treatment of PMrelated PVCs; several reports have demonstrated the usefulness of intracardiac echocardiography and pace mapping.3,4 Here, we report a unique form of PMrelated PVCs that emerged from PMtendon transitions, which were successfully treated with RFCA. A combination of intracardiac echocardiography and PASO® Module mapping with a DecaNav catheter critically contributed to the success. A 55yearold woman was referred to our hospital for RFCA of frequent PVCs with a QRS width of 220 ms, complete right bundle branch block, and a superior axis (Figure 1A,B). She had a past medical history of a posterolateral myocardial infarction and was treated for chronic heart failure since then. A Holter electrocardiography revealed frequent monomorphic PVCs at 45 000 beats/day. The LV ejection fraction was further reduced to 35% from 50%, which was already reduced before the PVCs became frequent. Carvedilol 20 mg failed to suppress the PVC burden. In the first attempt at catheter ablation, a 3D mapping system (CARTO3®, Biosense Webster) and openirrigated tip radiofrequency catheter (SMARTTOUCH®SF, Biosense Webster) were used to create an activation map, which exhibited a centrifugal propagation pattern from the inferior LV wall near the posterior PM (Figure 1E). The local potential at the earliest activation site preceded the QRS onset of the surface 12lead ECG by 20 ms at 0.09 mV (Figure 1C). The PVCs were mechanically suppressed when the ablation catheter made strong contact with the earliest activation site (Figure 1D,E). Following transient reactive firings, ablation with 30 W apparently abolished the PVC. The procedure was concluded after a 30min waiting period. Because the same morphology of PVCs recurred 3 months after the first session (Figure 2A,B), a second ablation session was performed. To better determine the source of the origin, a linear decapolar mapping catheter (DecaNav, Biosense Webster) was used. In addition to a conventional activation map, we created a “pacemap” (Figure 2C– F, dubbed “PASO® mapping”), in which the PASO® score (calculated by the PASO® Module and ranged from 0.00 to 1.00 with 1.00 being the highest, CARTO 3 system, Biosense Webster) for each point was displayed in a color, to help visualize the spatial distribution of the PASO® scores. The scores tended to be high in the area close to the posterior PM (Figure 2C– F). We discovered that the score was markedly high at 0.97 at an inner point floating in the LV chamber (Figure 2E, “E” in Figure 2F). An ultrasound catheter with an intracardiac magnetic sensor (SOUND STAR®, Biosense Webster) clearly demonstrated that the earliest point was exactly at the junction between the posterior PM and chordae tendineae (Figure 3A,B, Video S1). The onset of the local potential at that point preceded that of the surface 12lead ECG QRS by 43 ms with 0.05 mV (Figure 3C). While monitoring the catheter contact with intracardiac echocardiography, RF energy (30 W) was delivered at that point with an average