Atrial Fibrillation in Patients With Brugada Syndrome. Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds

Kengo F. Kusano, Makiko Taniyama, Kazufumi Nakamura, Daiji Miura, Kimikazu Banba, Satoshi Nagase, Hiroshi Morita, Nobuhiro Nishii, Atsuyuki Watanabe, Takeshi Tada, Masato Murakami, Kohei Miyaji, Shigeki Hiramatsu, Koji Nakagawa, Masamichi Tanaka, Aya Miura, Hideo Kimura, Soichiro Fuke, Wakako Sumita, Satoru SakuragiShigemi Urakawa, Jun Iwasaki, Tohru Ohe

Research output: Contribution to journalArticle

123 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1169-1175
Number of pages7
JournalJournal of the American College of Cardiology
Volume51
Issue number12
DOIs
Publication statusPublished - Mar 25 2008

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Brugada Syndrome
Electrophysiology
Atrial Fibrillation
Mutation
Genes
Ventricular Fibrillation
Syncope
Sodium Channels
Incidence
Sudden Death
Cardiac Arrhythmias

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Atrial Fibrillation in Patients With Brugada Syndrome. Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds. / Kusano, Kengo F.; Taniyama, Makiko; Nakamura, Kazufumi; Miura, Daiji; Banba, Kimikazu; Nagase, Satoshi; Morita, Hiroshi; Nishii, Nobuhiro; Watanabe, Atsuyuki; Tada, Takeshi; Murakami, Masato; Miyaji, Kohei; Hiramatsu, Shigeki; Nakagawa, Koji; Tanaka, Masamichi; Miura, Aya; Kimura, Hideo; Fuke, Soichiro; Sumita, Wakako; Sakuragi, Satoru; Urakawa, Shigemi; Iwasaki, Jun; Ohe, Tohru.

In: Journal of the American College of Cardiology, Vol. 51, No. 12, 25.03.2008, p. 1169-1175.

Research output: Contribution to journalArticle

Kusano, KF, Taniyama, M, Nakamura, K, Miura, D, Banba, K, Nagase, S, Morita, H, Nishii, N, Watanabe, A, Tada, T, Murakami, M, Miyaji, K, Hiramatsu, S, Nakagawa, K, Tanaka, M, Miura, A, Kimura, H, Fuke, S, Sumita, W, Sakuragi, S, Urakawa, S, Iwasaki, J & Ohe, T 2008, 'Atrial Fibrillation in Patients With Brugada Syndrome. Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds', Journal of the American College of Cardiology, vol. 51, no. 12, pp. 1169-1175. https://doi.org/10.1016/j.jacc.2007.10.060
Kusano, Kengo F. ; Taniyama, Makiko ; Nakamura, Kazufumi ; Miura, Daiji ; Banba, Kimikazu ; Nagase, Satoshi ; Morita, Hiroshi ; Nishii, Nobuhiro ; Watanabe, Atsuyuki ; Tada, Takeshi ; Murakami, Masato ; Miyaji, Kohei ; Hiramatsu, Shigeki ; Nakagawa, Koji ; Tanaka, Masamichi ; Miura, Aya ; Kimura, Hideo ; Fuke, Soichiro ; Sumita, Wakako ; Sakuragi, Satoru ; Urakawa, Shigemi ; Iwasaki, Jun ; Ohe, Tohru. / Atrial Fibrillation in Patients With Brugada Syndrome. Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds. In: Journal of the American College of Cardiology. 2008 ; Vol. 51, No. 12. pp. 1169-1175.
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abstract = "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.",
author = "Kusano, {Kengo F.} and Makiko Taniyama and Kazufumi Nakamura and Daiji Miura and Kimikazu Banba and Satoshi Nagase and Hiroshi Morita and Nobuhiro Nishii and Atsuyuki Watanabe and Takeshi Tada and Masato Murakami and Kohei Miyaji and Shigeki Hiramatsu and Koji Nakagawa and Masamichi Tanaka and Aya Miura and Hideo Kimura and Soichiro Fuke and Wakako Sumita and Satoru Sakuragi and Shigemi Urakawa and Jun Iwasaki and Tohru Ohe",
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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

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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