Atrial electrophysiological and structural remodeling in high-risk patients with Brugada syndrome: Assessment with electrophysiology and echocardiography

Norihisa Toh, Hiroshi Morita, Satoshi Nagase, Manabu Taniguchi, Daiji Miura, Nobuhiro Nishii, Kazufumi Nakamura, Tohru Ohe, Kengo F. Kusano, Hiroshi Itoh

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Atrial fibrillation (AF) often occurs in Brugada syndrome (BrS), and BrS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. Atrial vulnerability providing a substrate for AF is known to be enhanced in BrS, but there are no data on atrial structural attributes. Objective: The objective of this study was to assess atrial electrophysiological and structural characteristics in BrS and their relationships with gene mutations. Methods: We studied 57 patients with BrS. Intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to atrial deflection at the distal portion of the coronary sinus. Left atrial volume index (LAVI) was measured by the modified Simpson method at left ventricular end-systole using echocardiography. SCN5A mutations were analyzed in all patients. Results: In patients with documented VF, spontaneous AF frequently occurred and prolonged CT and increased LAVI were observed compared with those in patients without VF (all P <.05; LAVI: 22 ± 5 vs. 32 ± 7 ml/m2). Even among patients without AF, CT and LAVI were still increased in patients with VF (all P <.05; LAVI: 22 ± 5 vs. 29 ± 5 ml/m2). The presence of SCN5A mutation was associated with prolonged CT (P <.05) and increased LAVI (P <.01), but not with arrhythmic episodes. Conclusion: Both atrial vulnerability and structural remodeling are enhanced in high-risk patients with BrS, even in those without AF. These morphological characteristics suggest that BrS is a form of genetic myocardial disease.

Original languageEnglish
Pages (from-to)218-224
Number of pages7
JournalHeart Rhythm
Volume7
Issue number2
DOIs
Publication statusPublished - 2010

Fingerprint

Brugada Syndrome
Electrophysiology
Echocardiography
Atrial Fibrillation
Ventricular Fibrillation
Mutation
Inborn Genetic Diseases
Coronary Sinus
Systole
Heart Atria
Cardiomyopathies

Keywords

  • Atrial fibrillation
  • Echocardiography
  • Genes
  • Remodeling
  • Sudden cardiac death

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Atrial electrophysiological and structural remodeling in high-risk patients with Brugada syndrome : Assessment with electrophysiology and echocardiography. / Toh, Norihisa; Morita, Hiroshi; Nagase, Satoshi; Taniguchi, Manabu; Miura, Daiji; Nishii, Nobuhiro; Nakamura, Kazufumi; Ohe, Tohru; Kusano, Kengo F.; Itoh, Hiroshi.

In: Heart Rhythm, Vol. 7, No. 2, 2010, p. 218-224.

Research output: Contribution to journalArticle

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abstract = "Background: Atrial fibrillation (AF) often occurs in Brugada syndrome (BrS), and BrS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. Atrial vulnerability providing a substrate for AF is known to be enhanced in BrS, but there are no data on atrial structural attributes. Objective: The objective of this study was to assess atrial electrophysiological and structural characteristics in BrS and their relationships with gene mutations. Methods: We studied 57 patients with BrS. Intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to atrial deflection at the distal portion of the coronary sinus. Left atrial volume index (LAVI) was measured by the modified Simpson method at left ventricular end-systole using echocardiography. SCN5A mutations were analyzed in all patients. Results: In patients with documented VF, spontaneous AF frequently occurred and prolonged CT and increased LAVI were observed compared with those in patients without VF (all P <.05; LAVI: 22 ± 5 vs. 32 ± 7 ml/m2). Even among patients without AF, CT and LAVI were still increased in patients with VF (all P <.05; LAVI: 22 ± 5 vs. 29 ± 5 ml/m2). The presence of SCN5A mutation was associated with prolonged CT (P <.05) and increased LAVI (P <.01), but not with arrhythmic episodes. Conclusion: Both atrial vulnerability and structural remodeling are enhanced in high-risk patients with BrS, even in those without AF. These morphological characteristics suggest that BrS is a form of genetic myocardial disease.",
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AU - Nagase, Satoshi

AU - Taniguchi, Manabu

AU - Miura, Daiji

AU - Nishii, Nobuhiro

AU - Nakamura, Kazufumi

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AU - Kusano, Kengo F.

AU - Itoh, Hiroshi

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N2 - Background: Atrial fibrillation (AF) often occurs in Brugada syndrome (BrS), and BrS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. Atrial vulnerability providing a substrate for AF is known to be enhanced in BrS, but there are no data on atrial structural attributes. Objective: The objective of this study was to assess atrial electrophysiological and structural characteristics in BrS and their relationships with gene mutations. Methods: We studied 57 patients with BrS. Intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to atrial deflection at the distal portion of the coronary sinus. Left atrial volume index (LAVI) was measured by the modified Simpson method at left ventricular end-systole using echocardiography. SCN5A mutations were analyzed in all patients. Results: In patients with documented VF, spontaneous AF frequently occurred and prolonged CT and increased LAVI were observed compared with those in patients without VF (all P <.05; LAVI: 22 ± 5 vs. 32 ± 7 ml/m2). Even among patients without AF, CT and LAVI were still increased in patients with VF (all P <.05; LAVI: 22 ± 5 vs. 29 ± 5 ml/m2). The presence of SCN5A mutation was associated with prolonged CT (P <.05) and increased LAVI (P <.01), but not with arrhythmic episodes. Conclusion: Both atrial vulnerability and structural remodeling are enhanced in high-risk patients with BrS, even in those without AF. These morphological characteristics suggest that BrS is a form of genetic myocardial disease.

AB - Background: Atrial fibrillation (AF) often occurs in Brugada syndrome (BrS), and BrS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. Atrial vulnerability providing a substrate for AF is known to be enhanced in BrS, but there are no data on atrial structural attributes. Objective: The objective of this study was to assess atrial electrophysiological and structural characteristics in BrS and their relationships with gene mutations. Methods: We studied 57 patients with BrS. Intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to atrial deflection at the distal portion of the coronary sinus. Left atrial volume index (LAVI) was measured by the modified Simpson method at left ventricular end-systole using echocardiography. SCN5A mutations were analyzed in all patients. Results: In patients with documented VF, spontaneous AF frequently occurred and prolonged CT and increased LAVI were observed compared with those in patients without VF (all P <.05; LAVI: 22 ± 5 vs. 32 ± 7 ml/m2). Even among patients without AF, CT and LAVI were still increased in patients with VF (all P <.05; LAVI: 22 ± 5 vs. 29 ± 5 ml/m2). The presence of SCN5A mutation was associated with prolonged CT (P <.05) and increased LAVI (P <.01), but not with arrhythmic episodes. Conclusion: Both atrial vulnerability and structural remodeling are enhanced in high-risk patients with BrS, even in those without AF. These morphological characteristics suggest that BrS is a form of genetic myocardial disease.

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KW - Sudden cardiac death

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