PMC5412659_01
Twelve-lead electrocardiogram (ECG). A: At the beginning of electrophysiological study, BrS type 2 pattern. B: After flecainide acetate intravenous infusion. C: During radiofrequency onset. D: Final ECG at the end of electrophysiological study. E: Twelve-lead ECG 5 months after epicardial ablation.
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Dynamic ECG manifestations of Brugada syndrome were clearly observed in this patient (Figure 1A-E). At the beginning of electrophysiological study, BrS type 2 pattern was evident (Figure 1A). Flecainide acetate was infused intravenously over 10 minutes (dose of 100 mg) under ECG monitoring, and type 1 BrS was unmasked with a 3 mm elevation of ST segment in V1-V2 (Figure 1B). Radiofrequency (RF) ablation with 30 W was performed, with progressive slowing of potentials until disappearance (Figure 3), presenting transient ST ascendant elevation in V1-V2 (Figure 1C). After 4 days the patient was discharged with no BrS ECG pattern (Figure 1D). Five months after the electrophysiological study, the patient remained asymptomatic, with no VT/VF episodes and no BrS ECG pattern persisting (Figure 1E).
Anteroposterior view of right ventricle epicardial voltage map. Different late electrograms are shown before ablation, located predominantly in the anterior wall and outflow tract. A: Before flecainide acetate infusion. B: After flecainide acetate infusion.
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Late, fragmented, double, and triple potentials were localized in the RV anterior region (Figure 2A). A new epicardial map was performed, and a wider area of target potentials was localized (a total area of approximately 42.56 cm2), with manifest double and triple potentials (Figure 2B).
Anteroposterior view of the right ventricle epicardial voltage map after radiofrequency (RF) ablation. Electrograms displayed before and after RF delivery.
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Radiofrequency (RF) ablation with 30 W was performed, with progressive slowing of potentials until disappearance (Figure 3), presenting transient ST ascendant elevation in V1-V2 (Figure 1C).