Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation

Masamichi Tanaka, Kazufumi Nakamura, Kengo Fukushima Kusano, Hiroshi Morita, Keiko Ohta-Ogo, Daiji Miura, Aya Miura, Koji Nakagawa, Takeshi Tada, Masato Murakami, Nobuhiro Nishii, Satoshi Nagase, Yoshiki Hata, Kunihisa Kohno, Mamoru Oouchida, Kenji Shimizu, Chikao Yutani, Tohru Ohe, Hiroshi Itoh

Research output: Contribution to journalArticle

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Abstract

Background: Brugada syndrome is a disease known to cause ventricular fibrillation with a structurally normal heart and is linked to SCN5A gene mutation. However, the mechanism by which ventricular fibrillation develops in cases of Brugada-type electrocardiogram without SCN5A mutation has remained unclear. Recently, oxidative stress has been implicated in the pathophysiology of cardiac arrhythmia. We also investigated oxidative stress levels in the myocardia of patients with Brugada-type electrocardiogram. Methods: Endomyocardial biopsy samples were obtained from 68 patients with Brugada-type electrocardiogram (66 males and two females). We performed histological and immunohistochemical analyses for CD45, CD68, and 4-hydroxy-2-nonenal-modified protein, which is a major lipid peroxidation product. Results: SCN5A mutation was detected in 14 patients. Ventricular fibrillation was documented in three patients with SCN5A mutation and in 11 without SCN5A mutation. In patients with SCN5A mutation, 4-hydroxy-2-nonenal-modified protein-positive area was not significantly different between the documented ventricular fibrillation (VF) group (VF+ group) and the group without documented VF (VF- group). However, in patients without SCN5A, the area was significantly larger in the VF+ group than that in the VF- group (P

Original languageEnglish
JournalCardiovascular Pathology
Volume20
Issue number1
DOIs
Publication statusPublished - Jan 2011

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Ventricular Fibrillation
Electrocardiography
Oxidative Stress
Mutation
Brugada Syndrome
Lipid Peroxidation
Cardiac Arrhythmias
Myocardium
Proteins
Biopsy

Keywords

  • Brugada syndrome
  • Oxidative stress
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pathology and Forensic Medicine

Cite this

Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation. / Tanaka, Masamichi; Nakamura, Kazufumi; Kusano, Kengo Fukushima; Morita, Hiroshi; Ohta-Ogo, Keiko; Miura, Daiji; Miura, Aya; Nakagawa, Koji; Tada, Takeshi; Murakami, Masato; Nishii, Nobuhiro; Nagase, Satoshi; Hata, Yoshiki; Kohno, Kunihisa; Oouchida, Mamoru; Shimizu, Kenji; Yutani, Chikao; Ohe, Tohru; Itoh, Hiroshi.

In: Cardiovascular Pathology, Vol. 20, No. 1, 01.2011.

Research output: Contribution to journalArticle

Tanaka, Masamichi ; Nakamura, Kazufumi ; Kusano, Kengo Fukushima ; Morita, Hiroshi ; Ohta-Ogo, Keiko ; Miura, Daiji ; Miura, Aya ; Nakagawa, Koji ; Tada, Takeshi ; Murakami, Masato ; Nishii, Nobuhiro ; Nagase, Satoshi ; Hata, Yoshiki ; Kohno, Kunihisa ; Oouchida, Mamoru ; Shimizu, Kenji ; Yutani, Chikao ; Ohe, Tohru ; Itoh, Hiroshi. / Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation. In: Cardiovascular Pathology. 2011 ; Vol. 20, No. 1.
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AU - Tanaka, Masamichi

AU - Nakamura, Kazufumi

AU - Kusano, Kengo Fukushima

AU - Morita, Hiroshi

AU - Ohta-Ogo, Keiko

AU - Miura, Daiji

AU - Miura, Aya

AU - Nakagawa, Koji

AU - Tada, Takeshi

AU - Murakami, Masato

AU - Nishii, Nobuhiro

AU - Nagase, Satoshi

AU - Hata, Yoshiki

AU - Kohno, Kunihisa

AU - Oouchida, Mamoru

AU - Shimizu, Kenji

AU - Yutani, Chikao

AU - Ohe, Tohru

AU - Itoh, Hiroshi

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N2 - Background: Brugada syndrome is a disease known to cause ventricular fibrillation with a structurally normal heart and is linked to SCN5A gene mutation. However, the mechanism by which ventricular fibrillation develops in cases of Brugada-type electrocardiogram without SCN5A mutation has remained unclear. Recently, oxidative stress has been implicated in the pathophysiology of cardiac arrhythmia. We also investigated oxidative stress levels in the myocardia of patients with Brugada-type electrocardiogram. Methods: Endomyocardial biopsy samples were obtained from 68 patients with Brugada-type electrocardiogram (66 males and two females). We performed histological and immunohistochemical analyses for CD45, CD68, and 4-hydroxy-2-nonenal-modified protein, which is a major lipid peroxidation product. Results: SCN5A mutation was detected in 14 patients. Ventricular fibrillation was documented in three patients with SCN5A mutation and in 11 without SCN5A mutation. In patients with SCN5A mutation, 4-hydroxy-2-nonenal-modified protein-positive area was not significantly different between the documented ventricular fibrillation (VF) group (VF+ group) and the group without documented VF (VF- group). However, in patients without SCN5A, the area was significantly larger in the VF+ group than that in the VF- group (P

AB - Background: Brugada syndrome is a disease known to cause ventricular fibrillation with a structurally normal heart and is linked to SCN5A gene mutation. However, the mechanism by which ventricular fibrillation develops in cases of Brugada-type electrocardiogram without SCN5A mutation has remained unclear. Recently, oxidative stress has been implicated in the pathophysiology of cardiac arrhythmia. We also investigated oxidative stress levels in the myocardia of patients with Brugada-type electrocardiogram. Methods: Endomyocardial biopsy samples were obtained from 68 patients with Brugada-type electrocardiogram (66 males and two females). We performed histological and immunohistochemical analyses for CD45, CD68, and 4-hydroxy-2-nonenal-modified protein, which is a major lipid peroxidation product. Results: SCN5A mutation was detected in 14 patients. Ventricular fibrillation was documented in three patients with SCN5A mutation and in 11 without SCN5A mutation. In patients with SCN5A mutation, 4-hydroxy-2-nonenal-modified protein-positive area was not significantly different between the documented ventricular fibrillation (VF) group (VF+ group) and the group without documented VF (VF- group). However, in patients without SCN5A, the area was significantly larger in the VF+ group than that in the VF- group (P

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