Brugada syndrome is associated with a high risk of sudden cardiac death. Currently, the cornerstone of therapy is implantation of an implantable cardioverter defibrillator (ICD). Recently, a novel approach to preventively ablate the substrate located in the anterior epicardial region of the right ventricular outflow tract showed promising results by reducing the number of ventricular fibrillation episodes in patients with ICD. Here we report on a patient with Brugada syndrome who refused ICD therapy in whom a successful epicardial right ventricular outflow tract substrate ablation was performed. In some special cases, ablation therapy might be considered as the sole therapeutic option for these patients.
R ESUM ELe syndrome de Brugada est associe à un risque eleve de mort cardiaque subite. Actuellement, la pierre angulaire du traitement est l'implantation d'un defibrillateur cardioverteur implantable (DCI). Recemment, une nouvelle approche pour proceder de manière preventive à l'ablation du substrat localise dans la region epicardique anterieure de la chambre de chasse du ventricule droit a montre des resultats prometteurs en reduisant le nombre d'episodes de fibrillation auriculaire chez les patients portant un DCI. Nous rapportons ici le cas d'un patient souffrant du syndrome de Brugada qui a refuse le traitement par DCI chez qui une ablation du substrat epicardique de la chambre de chasse du ventricule droit a ete reussie. Dans certains cas particuliers, le traitement par ablation pourrait être considere comme la seule option therapeutique chez ces patients.A 31-year-old male patient with recurrent short lasting paroxysmal palpitations, once leading to syncope, was referred to our Electrophysiology Department for evaluation. Apart from congenital hypoplasia of both upper and lower extremities he had no known disease in his medical history and physical examination did not reveal any other abnormalities. His family history of sudden cardiac death (SCD) was unknown because he was adopted in infancy. Twelve-lead resting electrocardiogram (ECG) showed a type II Brugada pattern, with a characteristic "saddle back" pattern ST segment elevation most prominently in V 2 and V 3 and a negative T-wave in lead V 1 without fragmentation or inferolateral early repolarization (Fig. 1). Echocardiography and routine laboratory tests were normal. A 24-hour Holter ECG recording revealed short runs of atrial ectopy only.During the electrophysiology study, atrial fibrillation developed during catheter positioning, which terminated spontaneously. No other supraventricular or ventricular arrhythmia was inducible by pacing manoeuvres (2 extrasystoles with a coupling interval until refractoriness or reaching 200 ms at 550, 400, and 330 ms base drive, respectively). Then ajmaline with a dose of 1 mg/kg of body weight was given intravenously over 10 minutes and we recorded a > 0.2 mV ST segment elevation in V 2 and evolution of a type I Brugada pattern (Fig. 1), however, no arrhythmia could be induced after the drug test. On the...