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shocks from her implantable cardioverter-defibrillator.Device interrogation confirmed appropriate therapy forventricular tachycardia (VT), cycle length 380 to 400 ms.We elected to perform VT ablation. Prior cardiac magneticresonance imaging showed a dilated right ventricle (RV)with microaneurysms in the RV free wall but no fibrofattyreplacement. The left ventricle was extensively involved(ejection fraction 42%). Resting ECG prior to the ablationshowed minor interventricular conduction delay and flat Twaves in the right precordial leads but no epsilon waves(Figure 1).

RV geometry was created using a standard curve NaviStarablation catheter and CARTO (both Biosense Webster,Diamond Bar, CA). A voltage map showed extensivescarring with fractionated potentials in the RV, especiallyfrom the anterior to high lateral position. The clinical VT waseasily induced and well tolerated. During VT activationmapping, very early signals (75 ms ahead of QRS) wereobserved at the scar anterolaterally. Entrainment demon-strated that this was the exit site. Ablation was performedhere and extended laterally and superiorly until the clinicalVT was terminated. A faster, poorly tolerated VT wasinduced and mapped to the septum. Ablation here producedlocal delayed activation and manifest epsilon waves. ECGpostablation showed more profound interventricular con-duction delay with frank T-wave inversion and new epsilonwaves in the right precordial leads (Figure 1). The epsilonwaves remained static at 12-month follow-up.

Major ECG diagnostic criteria for ARVC can be sub-divided into abnormalities of repolarization (T-wave inver-sion V1–V3 or beyond in absence of right bundle branchblock) or depolarization/conduction, which was recentlyrestricted to the presence of epsilon waves in the rightprecordial leads.1 Epsilon waves are believed to representdelayed activation of the RV free wall and their presence toreflect more diffuse RV involvement.2 In keeping with this,epsilon waves can be dynamic early in ARVC3 and canappear years after the initial diagnosis with disease pro-gression.4 The case reported here is the first to showdevelopment postablation, which by its nature increasesscarring within the RV. The presence of epsilon waves didnot herald an increased risk of ventricular arrhythmia, as hasbeen previously shown.2

References1. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right

ventricular cardiomyopathy/dysplasia: proposed modification of the Task ForceCriteria. Eur Heart J 2010;31:806–814.

2. Nasir K, Bomma C, Tandri H, et al. Electrocardiographic features of arrhythmo-genic right ventricular dysplasia/cardiomyopathy according to disease severity.Circulation 2004;110:1527–1534.

3. Quarta G, Ward D, Tome Esteban MT, et al. Dynamic electrocardiographicchanges in patients with arrhythmogenic right ventricular cardiomyopathy. Heart2010;96:516–522.

4. Jaoude SA, Leclercq JF, Coumel P. Progressive ECG changes in arrhythmogenicright ventricular disease: evidence for an evolving disease. Eur Heart J 1996;17:1717–1722.

CORRIGENDUM

“Corrigendum to ‘Specificity of electrocardiographic criteriafor the differential diagnosis of wide QRS complex tachy-cardia in patients with intraventricular conduction defect.’ byDatino Romaniega T, Almendral J, Avila P, González-Torrecilla E, Atienza F, Arenal A, Fernández-Avilés F,

HeartRhythm 2013 Sep;10(9):1393-401. The first authorwould like to note his name should be recognized as TomásDatino (Datino T) and not as Tomás Datino Romaniega(Datino Romaniega T) in this article.”