TY - JOUR
T1 - Atrial Fibrillation in Patients With Brugada Syndrome. Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds
AU - Kusano, Kengo F.
AU - Taniyama, Makiko
AU - Nakamura, Kazufumi
AU - Miura, Daiji
AU - Banba, Kimikazu
AU - Nagase, Satoshi
AU - Morita, Hiroshi
AU - Nishii, Nobuhiro
AU - Watanabe, Atsuyuki
AU - Tada, Takeshi
AU - Murakami, Masato
AU - Miyaji, Kohei
AU - Hiramatsu, Shigeki
AU - Nakagawa, Koji
AU - Tanaka, Masamichi
AU - Miura, Aya
AU - Kimura, Hideo
AU - Fuke, Soichiro
AU - Sumita, Wakako
AU - Sakuragi, Satoru
AU - Urakawa, Shigemi
AU - Iwasaki, Jun
AU - Ohe, Tohru
N1 - Funding Information:
This work was supported, in part, by Grant-in-Aid for Scientific Research (No. 18790501), Grant-in-Aid for Young Scientists (No. 17689026) from the Ministry of Education, Culture, Sports, Science and Technology, Japan and Health Sciences Research grants (H18-Research on Human Genome-002) from the Ministry of Health, Labor and Welfare, Japan. This work was also supported, in part, by a grant from the Japan Foundation of Cardiovascular Research, Tokyo, Japan. Drs. Kusano and Taniyama contributed equally to this study.
PY - 2008/3/25
Y1 - 2008/3/25
N2 - Objectives: 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.
AB - Objectives: 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.
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U2 - 10.1016/j.jacc.2007.10.060
DO - 10.1016/j.jacc.2007.10.060
M3 - Article
C2 - 18355654
AN - SCOPUS:40749133744
SN - 0735-1097
VL - 51
SP - 1169
EP - 1175
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 12
ER -