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(Circulation. 2007;116:2241-2252.)
© 2007 American Heart Association, Inc.

Arrhythmia/Electrophysiology

Catheter Ablation of Ventricular Tachycardia After Repair of Congenital Heart Disease

Electroanatomic Identification of the Critical Right Ventricular Isthmus

Katja Zeppenfeld, MD; Martin J. Schalij, MD; Margot M. Bartelings, MD; Usha B. Tedrow, MD; Bruce A. Koplan, MD; Kyoko Soejima, MD; William G. Stevenson, MD

From the Departments of Cardiology and Anatomy, Leiden University Medical Center, Leiden, the Netherlands (K.Z., M.J.S., M.M.B.), and the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass (U.B.T., B.A.K., K.S., W.G.S.).

Correspondence to Katja Zeppenfeld, MD, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands. E-mail k.zeppenfeld{at}lumc.nl

Received June 25, 2007; accepted August 22, 2007.

Background— Catheter ablation of ventricular tachycardia (VT) after repair of congenital heart disease can be difficult because of nonmappable VTs and complex anatomy. Insights into the relation between anatomic isthmuses identified by delineating unexcitable tissue using substrate mapping techniques and critical reentry circuit isthmuses might facilitate ablation.

Methods and Results— Sinus rhythm voltage mapping of the right ventricle was performed in 11 patients with sustained VT after repair of congenital heart disease. Unexcitable tissue from patch material, valve annulus, or dense fibrosis, identified from bipolar voltage (<0.5 mV) and pacing threshold (>10 mA), was defined as an anatomic isthmus boundary bordering 4 isthmuses between (1) the tricuspid annulus and scar/patch in the anterior right ventricular outflow, (2) the pulmonary annulus and right ventricular free wall scar/patch, (3) the pulmonary annulus and septal scar/patch, and (4) the septal scar/patch and tricuspid annulus. The reentry circuit isthmuses of all induced 15 VTs (mean cycle length, 276±78 ms; 73% poorly tolerated), identified by activation, entrainment, and/or pace mapping, were located in an anatomic isthmus (11 of 15 VTs in anatomic isthmus 1). Transecting the anatomic isthmuses by ablation lesions abolished all VTs. During 30.4±29.3 months of follow-up, 91% of patients remained free of VT.

Conclusions— Reentry circuit isthmuses in VT late after repair of congenital heart disease are located within anatomically defined isthmuses bordered by unexcitable tissue. The boundaries can be identified with 3-dimensional substrate mapping and connected by ablation lines during sinus rhythm. These findings should facilitate catheter and surgical ablation of stable and unstable VTs.

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CLINICAL PERSPECTIVE

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