Case ReportEarly Response after Catheter Ablation of the EpicardialSubstrate inaPatientwithBrugadaSyndromeCanBePredictedbyHigh Precordial Leads

Yae Min Park,1 Mi Sook Cha,1 Hanul Choi,1 Woong Chol Kang,1 Seung Hwan Han,1

In Suck Choi,1 Eak Kyun Shin,1 and Young-Hoon Kim 2

1Cardiology Division, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Republic of Korea2Cardiology Division, Department of Internal Medicine, Korea University Anam Hospital, Seoul, Republic of Korea

Correspondence should be addressed to Young-Hoon Kim; yhkmd@unitel.co.kr

Received 30 October 2017; Revised 3 February 2018; Accepted 4 March 2018; Published 29 April 2018

Academic Editor: Hajime Kataoka

Copyright © 2018 Yae Min Park et al. .is is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

A 52-year-old male with Brugada syndrome presented with repeated and appropriate shock from an implantable cardioverterdefibrillator (ICD). Catheter ablation for substrate elimination targeting low-voltage, complex, and fractionated electrocar-diograms and late potentials in the epicardial right ventricular outflow tract was successfully performed. Brugada phenotype in theright precordial leads from the third intercostal space disappeared in the early stage after catheter ablation and that from thestandard fourth intercostal space disappeared later. He remained free from ventricular fibrillation over the next fourteen months.We suggest that this novel ablation strategy is effective in Brugada syndrome patients with ICD, and early response after catheterablation can be predicted by high precordial leads.

1. Introduction

Brugada syndrome is characterized by a typical electro-cardiogram (ECG) abnormality in the right precordialleads and a high risk of ventricular fibrillation- (VF-) re-lated sudden cardiac death. .e cornerstone to preventsudden cardiac death is implantation of an implantablecardioverter defibrillator (ICD) in the high-risk patients[1]. Recently, a novel approach of substrate modification inthe anterior epicardial region of the right ventricular outflowtract (RVOT) reduces VF episodes and even eliminates theBrugada phenotype in ECG [2]. .e ST segment elevationin a Brugada syndrome patient is the most prominent in theleads overlying the RVOT and closely follows its anatomicposition. Here, we present the case of successful substrateelimination in the epicardial RVOT in a patient with Brugadasyndrome whose Brugada phenotype of high precordialleads in ECG disappeared in the early stage after catheterablation.

2. Case Report

A 52-year-old male presented with aborted sudden cardiacarrest and was referred to our electrophysiology departmentfor further workup. .e initial ECG at the emergency roomrevealed VF. Biphasic 200-Joule defibrillation restored sinusrhythm, and cardiopulmonary function recovered withoutneurologic sequelae. He suffered from several episodes ofthe agonal breathing pattern and generalized tonic-clonicmovement prior to admission. .e family history and pasthistory including structural heart disease, syncope, orsudden cardiac death were unremarkable. His ECG afterstabilization showed sinus rhythm with type I Brugadapattern (Figure 1). Echocardiography demonstrated nostructural heart disease with normal left ventricular ejec-tion fraction, and cardiac magnetic resonance imaging scandemonstrated normal biventricular function with no lategadolinium enhancement. Laboratory findings did not showany electrolyte abnormalities. He received ICD implantation

HindawiCase Reports in CardiologyVolume 2018, Article ID 5980380, 5 pageshttps://doi.org/10.1155/2018/5980380

for the secondary prevention of sudden cardiac death. Geneticstudies were recommended, although declined by his familydue to high cost.

Later, regular ECG exams showed consistently un-provoked type I Brugada pattern. Six months after the ICDimplantation, he experienced appropriate shock due to VF.Medication with quinidine was started, and the dose wastitrated up to 200mg tid. However, he su�ered from re-peated appropriate shocks 10 months after starting quin-idine. Premature ventricular complexes (PVCs) were rareduring continuous ECGmonitoring, and VF-triggering PVCswere absent. �erefore, he was o�ered radiofrequency cath-eter ablation for substrate elimination.

In conscious sedation with intravenous propofol andmidazolam, a VF induction test was attempted with pro-grammed ventricular stimulation with three basal cyclelengths (600–500–400ms) with up to three extra stimulidecremented to ventricular refractoriness or 200ms fromthe RV apex prior to the ablation procedure, and VF wasreproducibly inducible. Endocardial substrate mapping ofthe RV and RVOT was performed (NavX System; St. JudeMedical Inc., St. Paul, MN, USA), which showed no sig-ni�cant low-voltage area or fragmented potential. Epicardialaccess was obtained using �uoroscopy-guided subxiphoidpuncture, and a long sheath (SL1; St. Jude Medical Inc.,St. Paul, MN, USA) was introduced. Epicardial mapping(173 points) including RV and left ventricular areas wasperformed, revealing an extensive area of low voltage de�nedas bipolar signal amplitude <0.5mV with wide duration(>80ms) and fragmentation (≥3 distinct components) andlate potential in the anterior RVOT. �ese areas were mea-sured at 34.4mm2, with the longest total duration of ab-normal fractionated potential up to 468ms and up to 326msafter the end of the surface QRS. Unipolar mapping showedJ-point elevation identical to the typical Brugada pattern(Figure 2(a)). Epicardial ablation was performed by an openirrigated tip catheter (Cool�ex; St. JudeMedical, Minnetonka,MN, USA) targeting these areas (35W; total ablation time:19.8minutes) (Figure 2(b)).�is resulted in elimination of thefractionated potentials and drastic reduction of the localamplitude.

Remapped epicardial voltage mapping revealed that theseareas were replaced with scar tissue (<0.1mV; Figure 2(c)).

Slight changes in morphologies of V1–V3 were detected,although the Brugada pattern remained in surface ECG rightafter the ablation procedure. An evaluation for the remnantsubstrate was performed after �ecainide infusion (2mg/kg for10 minutes), revealing no signi�cant changes in local am-plitude in epicardial RVOT, although coved-type STelevationin surface ECGwas accentuated.�e programmed ventricularstimulation was repeated, resulting in noninducibility of VF.�e patient was discharged on the third day after the pro-cedure with resumed quinidine therapy.

Right precordial leads from the third intercostal spaceshowed disappearance of coved-type ST elevation on thethird day after ablation, while those from the fourth in-tercostal space still showed the Brugada pattern. Onemonth later, the Brugada pattern of precordial leads fromeither the third or fourth intercostal space disappeared(Figures 3(a)–3(c)). �e �ecainide provocative test (2mg/kgfor 10 minutes) was performed after three months of catheterablation which revealed unmasking of type I Brugada pattern(Figure 3(d)). He remained free from palpitations, fainting, orsyncopal episodes over the next fourteen months withoutquinidine treatment. �ere was no ventricular arrhythmiadetected by the ICD.

3. Discussion

We report the case of Brugada syndrome patient withsuccessful substrate elimination in the epicardial RVOT,who had been su�ering from repeated appropriate ICDshocks. �e Brugada phenotype in the high right precordialleads disappeared in the early stage after catheter ablationand that in the standard precordial leads disappeared later.Epicardial ablation in the anterior RVOT suppressed fur-ther VF episodes and completely eliminated the Brugadaphenotype in this patient.

Catheter ablation for the management of Brugadasyndrome has not been extensively reported. �e epicardialablation technique targeting the potential substrate in theRVOT for the Brugada syndrome was �rst introduced byNademanee et al. in 2011 [3]. Delayed depolarization overthe anterior aspect of the RVOTepicardium was suggestedas the underlying electrophysiological mechanism in Brugadasyndrome, and catheter ablation over this abnormal area

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Figure 1: ECG after stabilization showed sinus rhythm with type I Brugada pattern, resulting in the diagnosis of Brugada syndrome.ECG� electrocardiogram.

2 Case Reports in Cardiology

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Figure 2: (a) Epicardial mapping revealed an extensive area of low voltage with fragmented and late potential in the anterior RVOT. Graycolor of 3D mapping indicates scar tissue, and these areas were measured at 34.4mm2, with the longest total duration of abnormalfractionated potential up to 468ms and up to 326ms after the end of the surface QRS. (b) Epicardial ablation was performed targeting thearea of low voltage with fragmented and late potential in the anterior epicardial RVOT. (c) Remapped epicardial voltage mapping revealedthat these areas were substituted with a scar. RVOT�right ventricular out�ow tract.

Case Reports in Cardiology 3

resulted in normalization of the Brugada ECG patternand prevented VF episodes [3]. A combined epicardialand endocardial ablation strategy for Brugada syndrometargeting low-voltage, fractionated late potentials in theRVOT was reported recently [4]. We performed endo-cardial substrate mapping before attempting the epicardialapproach; however, there were no abnormal electrocar-diograms to target.

�e STsegment elevation in a Brugada syndrome patientis the most prominent in the leads overlying the RVOT andclosely follows its anatomic position [5, 6]. Recording ECGsby placing the right precordial leads at higher intercostalspaces increases the sensitivity for detecting Brugada syn-drome. Regional epicardial �brosis and electrocardiogramabnormalities a�ecting the RVOT correspond to the highprecordial leads where the Brugada phenotype is best seenand also an ablation e�ect is best seen in our patient.

We con�rmed noninducibility of VF by programmedelectric stimulation at the end of the procedure. However,noninducibility might not be the proper endpoint because ofseveral shortcomings of the induction test. Recently, Papponeet al. published the catheter ablation of Brugada syndromewith endpoints of elimination of all abnormal electric ven-tricular potentials before and after ajmaline, leading to ECG

normalization and noninducibility of VT/VF [7]. However,acute normalization of the Brugada ECG pattern during theablation procedure needs further evaluation as an endpoint[8]. Despite normalization of spontaneous type I Brugadapatterns after successful ablation, VF recurrence persistedin 27% of patients [9], and a substantial number of patientsshowed normalization of the Brugada pattern within threemonths of ablation [3]. Previous studies demonstrated thatelimination of the arrhythmogenic substrate associated withdisappearance of the Brugada ECG pattern as con�rmed by�ecainide testing indicates successful outcome [2, 7]. How-ever, our patient showed unmasking of type I Brugada patternby �ecainide testing after three months of catheter ablationeven though we ablated all abnormal substrates con�rmed bythe sodium channel blocker at the time of the ablationprocedure. Currently, the best endpoint is to eliminate allsubstrate areas that harbor abnormal low-voltage fractionatedsignals detected after the sodium channel blocker challenge[8]. And we suggest that early disappearance of the Brugadapattern at high precordial leads is helpful to assess the successof ablation before disappearance of the Brugada pattern atstandard precordial leads.

Epicardial ablation was e�ective in eliminating thesubstrate and the Brugada phenotype in our patient, andearly successful response after catheter ablation can be pre-dicted by high precordial leads.

Conflicts of Interest

�e authors declare that they have no con�icts of interest.

References

[1] K. Nademanee, G. Veerakul, M. Mower et al., “De�brilla-tor versus beta-blockers for unexplained death in �ailand(DEBUT): a randomized clinical trial,” Circulation, vol. 107,no. 17, pp. 2221–2226, 2003.

[2] J. Brugada, C. Pappone, A. Berruezo et al., “Brugada syndromephenotype elimination by epicardial substrate ablation,” Cir-culation: Arrhythmia and Electrophysiology, vol. 8, no. 6,pp. 1373–1381, 2015.

[3] K. Nademanee, G. Veerakul, P. Chandanamattha et al.,“Prevention of ventricular �brillation episodes in Brugadasyndrome by catheter ablation over the anterior right ven-tricular out�ow tract epicardium,” Circulation, vol. 123, no. 12,pp. 1270–1279, 2011.

[4] S. A. Saha, K. Krishnan, C. Madias, and R. G. Trohman,“Combined right ventricular out�ow tract epicardial and en-docardial late potential ablation for treatment of Brugadastorm: a case report and review of the literature,” Cardiologyand erapy, vol. 5, no. 2, pp. 229–243, 2016.

[5] C. Veltmann, T. Papavassiliu, T. Konrad et al., “Insights intothe location of type I ECG in patients with Brugada syn-drome: correlation of ECG and cardiovascular magneticresonance imaging,”Heart Rhythm, vol. 9, no. 3, pp. 414–421,2012.

[6] S. Savastano, R. Rordorf, A. Vicentini et al., “A compre-hensive electrocardiographic, molecular, and echocardio-graphic study of Brugada syndrome: validation of the 2013diagnostic criteria,” Heart Rhythm, vol. 11, no. 7, pp. 1176–1183, 2014.

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Figure 3: ECGs of the Brugada syndrome patient showing re-cordings of the anterior precordial leads: V1-2 leads from the4th intercostal space and high precordial leads (V5 and V6positioned cranially from V1 and V2) from the 3rd intercostalspace. (a) Baseline before catheter ablation; (b) three days afterablation; (c) one month after ablation. Note the disappearance ofthe Brugada pattern at high precordial leads (V5-6) in the earlystage and then at standard precordial V1-2 leads after catheterablation. (d) �e �ecainide provocative test after three months ofablation revealed unmasking of type I Brugada pattern.ECG � electrocardiogram.

4 Case Reports in Cardiology

[7] C. Pappone, J. Brugada, G. Vicedomini et al., “Electricalsubstrate elimination in 135 consecutive patients with Brugadasyndrome,” Circulation: Arrhythmia and electrophysiology,vol. 10, no. 5, p. e005053, 2017.

[8] K. Nademanee, M. Hocini, and M. Haissaguerre, “Epicardialsubstrate ablation for Brugada syndrome,” Heart Rhythm,vol. 14, no. 3, pp. 457–461, 2017.

[9] P. Zhang, R. Tung, Z. Zhang et al., “Characterization of theepicardial substrate for catheter ablation of Brugada syn-drome,” Heart Rhythm, vol. 13, no. 11, pp. 2151–2158, 2016.

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