LAUSR

To the Editor, We read the article with great interest by Itoh et al about the successful ablation of the original premature ventricular contraction (PVC) with induced preferential conduction block between a PVC origin at the aorta‐mitral continuity (AMC) and a breakout site at the left ventricular summit (LVS). As the authors stated, the discrete prepotentials (PPs) can be found at successful ablation sites of idiopathic PVCs arising from the aortic cusps, LVS or AMC. Therefore, these PPs could be caused by the presence of myocardial fibers, possibly representing the “dead‐end tract.” They may reflect an area of depressed conductivity known to be a prerequisite for experimental ventricular ectopy including parasystole. The origin and the preferential pathway, an insulated pathway connected to the exit, may also become targets for eliminating PVCs. In the left or right coronary cusp PVCs, the site of a discrete PP with greater than equals to 50ms activation time may be an indicator of a successful ablation site even if the pace mapping score at the site is poor. Additional circumstantial evidence for the existence of this insulated pathway and its role in arrhythmogenesis can be found in the coincidence of disappearing outflow tract PVCs after accessory pathway ablation and the encounter of PPs and a delta wavelike QRS onset at PVC ablation sites. The remediable ablation site for cusp PVCs may not necessarily be the site of the earliest activation but maybe the site with the PP representing the preferential pathway. In such cases, the detailed mapping is required to reveal the critical discrete PP. The selective capture of such PPs without local ventricular capture by pacing could also be informative. On the other side, the catheter artifacts from mechanical motion or movements frequently occur when the catheter tip contacts valve structures and myocardial walls. An aortic valve closure artifact is observed in up to one‐third of cases during mapping within the aortic cusps. This aortic valve artifact is clinically relevant since during activation mapping this might misrepresent an early site of activation by at least 30 to 40 seconds, timing that could make the difference between a successful or unfavorable PVC ablation. This artifact timing consistently coincides with the terminal portion of the T‐wave and correlates with invasive hemodynamics and aortic valve artifacts. Recognition of this physiological phenomenon is useful when assigning near‐field activation; however, it can be difficult sometimes to differentiate true and pseudo‐PP during activation mapping at the aortic cusp region.