Monomorphic ventricular tachycardia originating from right ventricular outflow tract as a trigger for the recurrent ventricular fibrillation in a patient with brugada syndrome.

INTRODUCTION

Brugada Syndrome is a cardiac ion channel disorder that affects the sodium current. This syndrome is characterized by cove-shaped ST elevation in ECG leads V1 to V3 in the absence of structural heart disease.

CASE PRESENTATION

A 36-year-old man diagnosed with Brugada Syndrome was reffered to our center with frequent implantable cardioverter-defibrillator (ICD) discharges. ICD interrogation showed several appropriate ICD intervention for tachycardia detected in the ventricular fibrillation zone. Unfortunately, quinidine was not available in our country at the time of admission; therefore, we decided to ablate suspicious arrhythmogenic substrates. Programmed ventricular stimulation from right ventricle (RV) reproducibly induced a sustained ventricular tachycardia with left bundle branch block morphology and inferior axis. RV outflow tract (RVOT) endocardially mapped and earliest activation signal (90 milliseconds) achieved at posterior aspect of the RVOT septum. RF energy application at that site terminated the tachycardia and no inducible tachycardia was detected. During two-year follow-up, he had no episodes of ICD therapy and remained symptom-free with any antiarrhythmic drug.

DISCUSSION

This case clearly indicated that catheter ablation might be considered as a viable option in every patient with Brugada syndrome and frequent ICD discharge. During the electrophysiology study, intravenous procainamide may also be used to reveal future arrhythmogenic focus in this group of patients.