Atrial fibrillation in patients with Brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds.
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.
Kusano
Kengo F
KF
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. kusanokengo@hotmail.com
Taniyama
Makiko
M
Nakamura
Kazufumi
K
Miura
Daiji
D
Banba
Kimikazu
K
Nagase
Satoshi
S
Morita
Hiroshi
H
Nishii
Nobuhiro
N
Watanabe
Atsuyuki
A
Tada
Takeshi
T
Murakami
Masato
M
Miyaji
Kohei
K
Hiramatsu
Shigeki
S
Nakagawa
Koji
K
Tanaka
Masamichi
M
Miura
Aya
A
Kimura
Hideo
H
Fuke
Soichiro
S
Sumita
Wakako
W
Sakuragi
Satoru
S
Urakawa
Shigemi
S
Iwasaki
Jun
J
Ohe
Tohru
T
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*
D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels