Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience
Kharazi, A.; Emkanjoo, Z.; Alizadeh, A.; Nikoo, M.H.; Jorat, M.V. and Sadr-Ameli, M.A. (2007) Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience. Indian Pacing and Electrophysiology Journal, 7 (1). pp. 33-39. ISSN 0972-6292
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Background: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increase risk of sudden cardiac death. Risk stratification for the life-threatening arrhythmic events in Brugada syndrome is not yet established. In the present study, we report our experience in patients with Brugada syndrome, following an ICD implantation. Methods and Results: A total of 12 patients (11 men, 1 woman) with a mean age of 46.5±11.8 were studied. At diagnosis, 7 patients had syncope of unknown origin, 2 patients were asymptomatic, 2 patients were survivors of cardiac arrest, and 1 had documented clinical VT requiring direct cardioversion for termination. Age was similar between the symptomatic and asymptomatic patients (46.6±13 vs. 46±2.8, respectively). Two patients reported a family history of sudden cardiac death. In 3 patients, spontaneous coved-type ECG was found at baseline. In 9 patients, a class I antiarrhythmic drug administration unmasked the characteristic type I ECG. In 4 patients (2 symptomatic with syncope at presentation and 2 asymptomatic), who underwent PES, sustained polymorphic VT or VF was induced. VF was induced by single extrastimuli in 2 symptomatic patients (1 from RV apex and 1 from RVOT). In 2 asymptomatic patients, VF was induced by two and triple ventricular extrastimli (1 from RV apex and 1 from RVOT). None of them experienced an event during follow-up. No significant difference was found between symptomatic and asymptomatic patients (p=NS). The mean follow-up period for the entire study population was 27.83±11.25 months. During follow-up, 2 patients (one with prior cardiac arrest and another with syncope) had VF. Both of them had a type I ECG after provocation with a class I antiarrhythmic drug. None of them had undergone programmed ventricular stimulation. Five patients (41.7 %) had inappropriate ICD interventions during follow-up. The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient. Conclusions: Knowledge about Brugada syndrome is steadily progressing but there are still unanswered issues dealing with the risk stratification and the management of patients.
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