Does epicardial radiofrequency ablation eliminate the Brugada syndrome phenotype and VT/VF inducibility in patients with BrS?
14 patients with Brugada syndrome (BrS) and an implantable cardioverter-defibrillator, median age 39 years (30.3-42.3).
Epicardial mapping and radiofrequency ablation of abnormal electrograms identified before and after flecainide administration (2 mg/kg per 10 minutes).
Elimination of abnormal epicardial substrate, BrS ECG pattern, and ventricular tachycardia/ventricular fibrillation inducibility.surrogate
Epicardial substrate ablation guided by flecainide testing successfully eliminates the Brugada syndrome ECG phenotype and VT/VF inducibility.
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.
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Josép Brugada
University of Southern California
Carlo Pappone
Electrophysiology
Antonio Berruezo
Electrophysiology
Circulation Arrhythmia and Electrophysiology
Maria Cecilia Hospital
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Brugada et al. (Wed,) studied this question.
synapsesocial.com/papers/69f14c772811130d0cde2650 — DOI: https://doi.org/10.1161/circep.115.003220