Site-specific arrhythmogenesis in patients with Brugada syndrome

Hiroshi Morita, Kengo Fukushima-Kusano, Satoshi Nagase, Shiho Takenaka-Morita, Nobuhiro Nishii, Mikio Kakishita, Kazufumi Nakamura, Tetsuro Emori, Hiromi Matsubara, Tohru Ohe

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.

Original languageEnglish
Pages (from-to)373-379
Number of pages7
JournalJournal of Cardiovascular Electrophysiology
Volume14
Issue number4
DOIs
Publication statusPublished - Apr 1 2003

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Brugada Syndrome
Ventricular Fibrillation
Electric Stimulation
Ventricular Premature Complexes
Septum of Brain
Heart Ventricles
Cardiac Arrhythmias
Electrocardiography

Keywords

  • Brugada syndrome
  • Free wall
  • Right ventricular outflow tract
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

Site-specific arrhythmogenesis in patients with Brugada syndrome. / Morita, Hiroshi; Fukushima-Kusano, Kengo; Nagase, Satoshi; Takenaka-Morita, Shiho; Nishii, Nobuhiro; Kakishita, Mikio; Nakamura, Kazufumi; Emori, Tetsuro; Matsubara, Hiromi; Ohe, Tohru.

In: Journal of Cardiovascular Electrophysiology, Vol. 14, No. 4, 01.04.2003, p. 373-379.

Research output: Contribution to journalArticle

Morita, H, Fukushima-Kusano, K, Nagase, S, Takenaka-Morita, S, Nishii, N, Kakishita, M, Nakamura, K, Emori, T, Matsubara, H & Ohe, T 2003, 'Site-specific arrhythmogenesis in patients with Brugada syndrome', Journal of Cardiovascular Electrophysiology, vol. 14, no. 4, pp. 373-379. https://doi.org/10.1046/j.1540-8167.2003.02365.x
Morita, Hiroshi ; Fukushima-Kusano, Kengo ; Nagase, Satoshi ; Takenaka-Morita, Shiho ; Nishii, Nobuhiro ; Kakishita, Mikio ; Nakamura, Kazufumi ; Emori, Tetsuro ; Matsubara, Hiromi ; Ohe, Tohru. / Site-specific arrhythmogenesis in patients with Brugada syndrome. In: Journal of Cardiovascular Electrophysiology. 2003 ; Vol. 14, No. 4. pp. 373-379.
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abstract = "Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29{\%}), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76{\%}). PES at RVA induced VF in only 2 patients (12{\%}), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64{\%} of PVCs occurred at the free-wall region of the RVOT, 18{\%} at the septal region of the RVOT, 9{\%} at RVA, and 9{\%} at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.",
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T1 - Site-specific arrhythmogenesis in patients with Brugada syndrome

AU - Morita, Hiroshi

AU - Fukushima-Kusano, Kengo

AU - Nagase, Satoshi

AU - Takenaka-Morita, Shiho

AU - Nishii, Nobuhiro

AU - Kakishita, Mikio

AU - Nakamura, Kazufumi

AU - Emori, Tetsuro

AU - Matsubara, Hiromi

AU - Ohe, Tohru

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N2 - Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.

AB - Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.

KW - Brugada syndrome

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KW - Right ventricular outflow tract

KW - Ventricular fibrillation

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