This case study describes epicardial radiofrequency catheter ablation of an arrhythmogenic substrate in a 54-year-old man with spontaneous BrS type I (Figure 1) who experienced recurrent VT and syncope. Multiple appropriate therapies were triggered by the implantable cardioverter defibrillator (ICD) (30 shocks in six months with two hospitalizations due to an electrical storm).

The procedure was conducted under general anesthesia with invasive blood pressure monitoring. Access to the epicardium was achieved via an anterior subxiphoid puncture using a 17 G-Tuohy needle, following established techniques.⁵ High-density multipolar mapping of the epicardial surface was performed using a PENTARRAY® mapping catheter (Biosense Webster, Dmond Bar, CA, USA) coupled with voltage mapping (CARTO®; Biosense Webster). Due to the unavailability of sodium channel blockers (ajmaline, flecainide, procainamide) to enhance phenotypic expression and improve mapping accuracy by increasing fractionated potentials, we opted to infuse 50 ml of warm saline solution (39-40 ºC) into the pericardial space.⁶ Specific reports have shown that this technique slows conduction in diseased areas and accelerates it in healthy ones, thus helping to identify areas of interest. Areas of late, fractionated, and prolonged potentials were noted on the epicardial substrate map and were shown to be confined to the free wall and RVOT. The infusion of warm saline extended the areas of late potentials to lower areas of the epicardial region of the RV⁷ (Figure 2). Endocardial mapping did not demonstrate abnormal potentials. Coronary angiography confirmed a safe distance from the main coronary arteries. We conducted radiofrequency ablation (30-40W; 10-20g; 10-20s) over a broad area encompassing the epicardial free wall and RVOT (Figure 3), aiming to eliminate identified late potentials, leading to the resolution of the coved-shaped ST-segment elevation in leads V1–V2 (Figure 4). Immediately following ablation, the remaining electrocardiographic pattern showed alterations in ventricular repolarization that did not meet the criteria for a classic Brugada type II (saddleback) pattern.

After 40 days, the electrocardiogram (ECG) returned to a normal appearance, suggesting that some of the immediate changes might have been due to pericardial inflammation resulting from the extensive treatment area. This normalized ECG persisted throughout all subsequent outpatient evaluations over the following 12-month follow-up (Figure 5). During this period, there were no documented instances of ventricular arrhythmias, ICD shocks, or syncope.