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Catheter Ablation of Stable and Unstable Ventricular Tachycardias in Patients with Arrhythmogenic Right Ventricular Dysplasia
Author(s) -
SATOMI KAZUHIRO,
KURITA TAKASHI,
SUYAMA KAZUHIRO,
NODA TAKASHI,
OKAMURA HIDEO,
OTOMO KIYOSHI,
SHIMIZU WATARU,
AIHARA NAOHIKO,
KAMAKURA SHIRO
Publication year - 2006
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2006.00434.x
Subject(s) - medicine , cardiology , arrhythmogenic right ventricular dysplasia , ablation , catheter ablation , tachycardia , ventricular tachycardia , ventricular outflow tract , sinus rhythm , electrophysiology , atrial fibrillation , heart failure , cardiomyopathy
A reentrant circuit within an area of abnormal myocardium is suspected as the origin of ventricular tachycardia (VT) in patients with arrhythmogenic right ventricular dysplasia (ARVD). Objectives: To examine the relationship between the reentrant circuits of VT and the abnormal electrograms in ARVD, and to assess the feasibility of a block line formation in the reentrant circuit isthmus utilizing electroanatomical mapping system (CARTO) guidance. Methods and Results: An electrophysiological study and catheter ablation (CA) were performed in 17 ARVD patients (13 men, 47 ± 17 year) using CARTO. Endocardial mapping during sinus rhythm demonstrated electrogram abnormalities extended from the tricuspid annulus (TA) or the right ventricular outflow tract in 16 of 17 patients. In 13 hemodynamically stable VTs, the reentrant circuits and critical slow conduction sites for the CA were investigated during VTs. The entire macro‐reentrant pathway was identified in 6/13 stable VTs (figure‐of‐8 in 4, single loop in 2). In the remaining seven VTs, a focal activation pattern was found in four and an unidentifiable pattern in three. CA successfully abolished all the macro‐reentrant and focal tachycardias, however, not effective in three unidentifiable VTs. In the 13 cases with unstable VT, the linear conduction block zone was produced between the sites with abnormal electrograms and the TA. Ultimately, 23/26 VTs (88%) became noninducible after the CA. During follow‐up (26 ± 15 months), 13/17 patients remained free from any VT episodes. Conclusions: CARTO is useful for characterizing the anatomical and electrophysiological substrates, and for identifying the optimal ablation sites for VT associated with ARVD.