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Circ Arrhythm Electrophysiol. 2015 Dec;8(6):1373-81. doi: 10.1161/CIRCEP.115.003220. Epub 2015 Aug 19.

Brugada Syndrome Phenotype Elimination by Epicardial Substrate Ablation.

Author information

1
From the Arrhythmia Section, Cardiology Department, Thorax Institute, Hospital Clinic and IDIBAPS (Institut d'Investigació Agustí Pi i Sunyer), Barcelona, Catalonia, Spain (J.B., A.B.); and Arrhythmology Department, Maria Cecilia Hospital, Cotignola and Policlinico San Donato, University of Milan, Milan, Italy (C.P., G.V., F.M., G.C., L.G., V.S.).
2
From the Arrhythmia Section, Cardiology Department, Thorax Institute, Hospital Clinic and IDIBAPS (Institut d'Investigació Agustí Pi i Sunyer), Barcelona, Catalonia, Spain (J.B., A.B.); and Arrhythmology Department, Maria Cecilia Hospital, Cotignola and Policlinico San Donato, University of Milan, Milan, Italy (C.P., G.V., F.M., G.C., L.G., V.S.). carlo.pappone@af-ablation.org.

Abstract

BACKGROUND:

Whether Brugada syndrome (BrS) depends on functional epicardial substrates, which may be definitively eliminated by radiofrequency ablation, remains unknown.

METHODS AND RESULTS:

Patients with BrS underwent epicardial mapping to identify areas of abnormal electrograms as target for radiofrequency ablation. Substrate identification consisted in mapping right ventricle epicardial surface before and after flecainide (2 mg/kg per 10 minutes). After radiofrequency ablation, flecainide and remap confirmed elimination of abnormal substrate, BrS ECG pattern, and ventricular tachycardia/ventricular fibrillation inducibility. Flecainide testing was performed at each follow-up visits ≤6 months. Fourteen patients with BrS, median age 39 years (30.3-42.3) with implantable cardioverter-defibrillator were enrolled. Low-voltage areas (<1.5 mV) were commonly identified on the anterior right free wall and right ventricular outflow tract, which increased after flecainide from 17.6 cm(2) (12.1-24.2) to 28.5 cm(2) (21.6-30.2; P=0.001). Similarly, areas with abnormal electrograms increased after flecainide from 19.0 (17.5-23.6) to 27.3 cm(2) (24.0-31.2; P=0.001). After 23.8 minutes (18.1-28.5) of radiofrequency ablation, abnormal electrograms disappeared, whereas low-voltage areas were replaced by scar areas (<0.5 mV) of 25.9 cm(2) (19.6-31.0). Substrate elimination resulted in BrS ECG pattern disappearance and no ventricular tachycardia/ventricular fibrillation inducibility without complications. After a median follow-up of 5 months (3.8-5.3), ECG remained normal despite flecainide.

CONCLUSIONS:

In patients with BrS, there is a relationship between abnormal ECG pattern, the extent of abnormal epicardial substrate, and ventricular tachycardia/ventricular fibrillation inducibility. Ablation of the substrate identified in the presence of flecainide can eliminate the BrS phenotype and warrants further study.

KEYWORDS:

Brugada syndrome; flecainide; heart; phenotype; sudden cardiac death

PMID:
26291334
DOI:
10.1161/CIRCEP.115.003220
[Indexed for MEDLINE]

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