title: Atrial fibrillation in patients with Brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds.
abstract: OBJECTIVE
  The goal of our work was to examine the relationships of atrial fibrillation (AF) with genetic, clinical, and electrophysiological backgrounds in Brugada syndrome (BrS).
  
  
  BACKGROUND
  Atrial fibrillation is often observed in patients with BrS and indicates that electrical abnormality might exist in the atrium as well as in the ventricle. SCN5A, a gene encoding the cardiac sodium channel, has been reported to be causally related to BrS. However, little is known about the relationships of atrial arrhythmias with genetic, clinical, and electrophysiological backgrounds of BrS.
  
  
  METHODS
  Seventy-three BrS patients (49 +/- 12 years of age, men/women = 72/1) were studied. The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes. Genetic and clinical variables were also compared with electrophysiologic (EP) parameters: atrial refractory period, interatrial conduction time (CT), repetitive atrial firing, and AF induction by atrial extra-stimulus testing.
  
  
  RESULTS
  Spontaneous AF occurred in 10 (13.7%) of the BrS patients and SCN5A mutation was detected in 15 patients. Spontaneous AF was associated with higher incidence of syncopal episodes (60.0% vs. 22.2%, p < 0.03) and documented VF (40.0% vs. 14.3%, p < 0.05). SCN5A mutation was associated with prolonged CT (p < 0.03) and AF induction (p < 0.05) in EP study, but not related to the spontaneous AF episode and other clinical variables. In patients with documented VF, higher incidence of spontaneous AF (30.8% vs. 10.0%, p < 0.05), AF induction (53.8% vs. 20.0%, p < 0.03), and prolonged CT was observed.
  
  
  CONCLUSIONS
  Spontaneous AF and VF are closely linked clinically and electrophysiologically in BrS patients. Patients with spontaneous AF have more severe clinical backgrounds in BrS. SCN5A mutation is associated with electrical abnormality but not disease severity.
authors: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. kusanokengo@hotmail.com
authors: Kengo F
authors: KF
authors: Kusano
authors: Makiko
authors: M
authors: Taniyama
authors: Kazufumi
authors: K
authors: Nakamura
authors: Daiji
authors: D
authors: Miura
authors: Kimikazu
authors: K
authors: Banba
authors: Satoshi
authors: S
authors: Nagase
authors: Hiroshi
authors: H
authors: Morita
authors: Nobuhiro
authors: N
authors: Nishii
authors: Atsuyuki
authors: A
authors: Watanabe
authors: Takeshi
authors: T
authors: Tada
authors: Masato
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authors: Murakami
authors: Kohei
authors: K
authors: Miyaji
authors: Shigeki
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authors: Hiramatsu
authors: Koji
authors: K
authors: Nakagawa
authors: Masamichi
authors: M
authors: Tanaka
authors: Aya
authors: A
authors: Miura
authors: Hideo
authors: H
authors: Kimura
authors: Soichiro
authors: S
authors: Fuke
authors: Wakako
authors: W
authors: Sumita
authors: Satoru
authors: S
authors: Sakuragi
authors: Shigemi
authors: S
authors: Urakawa
authors: Jun
authors: J
authors: Iwasaki
authors: Tohru
authors: T
authors: Ohe
mesh_terms: D000328:Adult; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology*; D053840:Brugada Syndrome / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology*; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006329:Heart Conduction System; D006801:Humans; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel; D012720:Severity of Illness Index; D015222:Sodium Channels; D017180:Tachycardia, Ventricular / Q000235:genetics*
chemical_list: D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels