Abstract

See Article by Yamada et al Idiopathic ventricular arrhythmias (VAs) most often arise from the outflow tract regions of the right ventricle (RV) and left ventricle (LV).1–4 Outcomes of catheter ablation with the current technological developments are overall high, with curing rates exceeding 80%,5 and ablation has become a first-line therapy for patients who are symptomatic or have a decreased ejection fraction because of frequent ventricular tachycardia/premature ventricular contractions (PVCs).6 However, there are 2 groups of idiopathic VAs where ablation results particularly challenging and outcomes remain modest, even in high-volume centers. The first one is LV summit arrhythmias, where ablation is limited by proximity to the major coronary arteries, the presence of epicardial fat, and sometimes a deep origin of the arrhythmogenic source within the LV wall.7 The second one is VAs originating from intracavitary structures within both ventricles, including the papillary muscles (PMs) of the tricuspid valve (TV) and mitral valve apparatus,8–10 false tendons11 and in the RV also the moderator band,11,12 and other muscular bands or ridges crossing the endocardial surface, such as the crista supraventricularis and the infundibular muscles.13 These structures are highly variable in anatomy and cannot be visualized by fluoroscopy or standard electroanatomic mapping. In addition, catheter contact and stability becomes an issue when targeting a mobile structure or a narrow ridge in a beating heart. In this issue of Circulation: Arrhythmia and Electrophysiology , Yamada et al14 report 19 patients with idiopathic VAs originating from the RV infundibular muscles: 14 cases from the parietal band (PB) and 5 cases from the septal band. Anatomic …

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