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(Circulation. 2005;111:3209-3216.)
© 2005 American Heart Association, Inc.

Arrhythmia/Electrophysiology

Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

Atul Verma, MD; Fethi Kilicaslan, MD; Robert A. Schweikert, MD; Gery Tomassoni, MD; Antonio Rossillo, MD; Nassir F. Marrouche, MD; Volkan Ozduran, MD; Oussama M. Wazni, MD; Samy C. Elayi, MD; Luis C. Saenz, MD; Stephen Minor, MD; Jennifer E. Cummings, MD; J. David Burkhardt, MD; Steven Hao, MD; Salwa Beheiry, RN; Patrick J. Tchou, MD; Andrea Natale, MD

From the Section of Pacing and Electrophysiology (A.V., F.K., R.A.S., N.F.M., V.O., O.M.W., S.C.E., L.C.S., S.M., J.E.C., J.D.B., P.J.T., A.N.), Cleveland Clinic Foundation, Cleveland, Ohio; Lexington Cardiology Consultants (G.T.), Lexington, Ky; Umberto I Hospital (A.R.), Mestre (Venice), Italy; and Sutter Pacific Heart Centers (S.H., S.B.), San Francisco, Calif.

Correspondence to Andrea Natale, MD, Electrophysiology Laboratory, Cleveland Clinic Foundation, Desk F15, 9500 Euclid Ave, Cleveland, OH 44195. E-mail natalea{at}ccf.org

Received September 30, 2004; revision received February 18, 2005; accepted March 3, 2005.

Background— Multiple morphologies, hemodynamic instability, or noninducibility may limit ventricular tachycardia (VT) ablation in patients with arrhythmogenic right ventricular dysplasia (ARVD). Substrate-based mapping and ablation may overcome these limitations. We report the results and success of substrate-based VT ablation in ARVD.

Methods and Results— Twenty-two patients with ARVD were studied. Traditional mapping for VT was limited because of multiple/changing VT morphologies (n=14), nonsustained VT (n=10), or hemodynamic intolerance (n=5). Sinus rhythm CARTO mapping was performed to define areas of "scar" (<0.5 mV) and "abnormal" myocardium (0.5 to 1.5 mV). Ablation was performed in "abnormal" regions, targeting sites with good pace maps compared with the induced VT(s). Linear lesions were created in these areas to (1) connect the scar/abnormal region to a valve continuity or other scar or (2) encircle the scar/abnormal region. Eighteen patients had implanted cardioverter defibrillators, 15 had implanted cardioverter defibrillator therapies, and 7 had sustained VT (6 with syncope). VTs (3±2 per patient) were induced (cycle length, 339±94 ms), and scar was identified in all patients. Scar areas were related to the tricuspid annulus, proximal right ventricular outflow tract, and anterior/inferior-apical walls. Lesions connected abnormal regions to the annulus (n=12) or other scars (n=4) and/or encircled abnormal regions (n=13). Per patient, a mean of 38±22 radiofrequency lesions was applied. Short-term success was achieved in 18 patients (82%). VT recurred in 23%, 27%, and 47% of patients after 1, 2, and 3 years’ follow-up, respectively.

Conclusions— Substrate-based ablation of VT in ARVD can achieve a good short-term success rate. However, recurrences become increasingly common during long-term follow-up.

Key Words: arrhythmogenic right ventricular dysplasia • ventricular tachycardia • ablation

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