A 26-year-old man was referred to our tertiary cardiovascular centre due to nocturnal agonal respiration and syncope that was occurring with a frequency of four to five episodes/year. The electrocardiogram (ECG) showed type I Brugada pattern with J waves seen on lateral leads ( Fig. 1 ). Although the patient’s previous ECG records were all compatible with Brugada pattern, a specific diagnosis was not made and a specific treatment was not given. The patient’s family history was negative for sudden cardiac death. Echocardiography was free of any sign of structural heart disease, with normal left ventricular function. Cardiac magnetic resonance showed normal right ventricular anatomy and function. The patient was implanted an implantable cardioverter-defibrillator (ICD) for primary prophylaxis. A week after discharge, the patient was readmitted to the emergency department due to frequent ICD shocks. Device interrogation revealed four episodes of polymorphic ventricular tachycardia that initiated with premature ventricular contractions of different coupling intervals ( Fig. 2 ), which were appropriately cardioverted to sinus rhythm during the previous week. Owing to frequent ICD shocks, we planned to give quinidine for arrhythmia control; however, as quinidine was not available in our country, we administered cilostazol at a dose of 100 mg twice daily. On the second day of cilostazol, the patient’s ECG converted from type I to type III Brugada pattern with disappearance of J waves and an increase of 20 beats/min in resting heart rate ( Fig. 3 ). The patient is currently being followed on cilostazol, free of symptoms and ICD discharge for 10 months; follow-up ECGs were all compatible with type III Brugada pattern.
