title: New-onset atrial fibrillation as first clinical manifestation of latent Brugada syndrome: prevalence and clinical significance.
abstract: OBJECTIVE
  To evaluate the prevalence, clinical significance, and prognosis of latent Brugada syndrome (BrS) in patients with new-onset atrial fibrillation (AF) unmasked by class 1C antiarrhythmic drugs.
  
  
  RESULTS
  Between January 2000 and June 2008, all consecutive patients with new-onset AF, who after flecainide exhibited typical Brugada ECG pattern, underwent electrophysiologic, pharmacologic, and genetic testing. Among 346 patients [median age 53 years; interquartile range (IQR), 15], 11 (3.2%; median age 51 years; IQR, 19) diagnosed as lone AF exhibited typical Brugada ECG pattern. Genetic testing was negative. Ventricular tachycardia/ventricular fibrillation (VT/VF) was induced by electrophysiologic testing (five patients) or during flecainide infusion (one patient). Six patients with type 1 ECG pattern and inducible VT/VF underwent ICD implantation. During a median follow-up of 31.5 months (range: 10-85) after ICD implantation, three patients developed BrS and one of them experienced VF. Patients without ICD (five patients) remained asymptomatic during a median follow-up of 74 months. Persistent type 1 pattern occurred only in the three patients who developed BrS.
  
  
  CONCLUSIONS
  This study, for the first time, reveals the prevalence of latent BrS in patients with new-onset lone AF, which may precede VT/VF. Persistence of type 1 and ventricular tachyarrhythmias inducibility represents a marker of electrical instability leading to sudden death.
authors.affiliation: Division of Electrophysiology and Cardiac Pacing, Department of Cardiology, San Raffaele University Hospital, Via Olgettina 60, 20132 Milan, Italy. carlo.pappone@hsr.it
authors.forename: Carlo
authors.initials: C
authors.lastname: Pappone
authors.forename: Andrea
authors.initials: A
authors.lastname: Radinovic
authors.forename: Francesco
authors.initials: F
authors.lastname: Manguso
authors.forename: Gabriele
authors.initials: G
authors.lastname: Vicedomini
authors.forename: Simone
authors.initials: S
authors.lastname: Sala
authors.forename: Francesco Maria
authors.initials: FM
authors.lastname: Sacco
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ciconte
authors.forename: Massimo
authors.initials: M
authors.lastname: Saviano
authors.forename: Maurizio
authors.initials: M
authors.lastname: Ferrari
authors.forename: Elena
authors.initials: E
authors.lastname: Sommariva
authors.forename: Stefania
authors.initials: S
authors.lastname: Sacchi
authors.forename: Cristiano
authors.initials: C
authors.lastname: Ciaccio
authors.forename: Eleftherios M
authors.initials: EM
authors.lastname: Kallergis
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Santinelli
mesh_terms: D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000209:etiology*; D053840:Brugada Syndrome / Q000150:complications* / Q000188:drug therapy / Q000235:genetics; D004562:Electrocardiography; D005260:Female; D005424:Flecainide / Q000627:therapeutic use; D005820:Genetic Testing; D006801:Humans; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins / Q000235:genetics*; D009154:Mutation / Q000235:genetics; D062554:NAV1.5 Voltage-Gated Sodium Channel; D015222:Sodium Channels / Q000235:genetics*
chemical_list: D000889:Anti-Arrhythmia Agents; D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels; D005424:Flecainide