Link Between SCN5A Mutation and the Brugada Syndrome ECG Phenotype Simulation Study
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- Miyoshi Shunichiro
- Advanced Cardiac Therapeutics, Keio University School of Medicine
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- Mitamura Hideo
- Advanced Cardiac Therapeutics, Keio University School of Medicine
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- Fukuda Yukiko
- Cardiopulmonary Division, Keio University School of Medicine
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- Tanimoto Kojiro
- Cardiopulmonary Division, Keio University School of Medicine
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- Hagiwara Yoko
- Cardiopulmonary Division, Keio University School of Medicine
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- Kanki Hideaki
- Cardiopulmonary Division, Keio University School of Medicine
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- Takatsuki Seiji
- Cardiopulmonary Division, Keio University School of Medicine
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- Murata Mitsushige
- Cardiopulmonary Division, Keio University School of Medicine
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- Miyazaki Toshihisa
- Cardiopulmonary Division, Keio University School of Medicine
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- Ogawa Satoshi
- Cardiopulmonary Division, Keio University School of Medicine
書誌事項
- タイトル別名
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- Simulation Study
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Background The specific changes in the gating kinetics of the sodium current (INa) responsible for its phenotype have remained to be elucidated. In the present study the effect of changes in the gating kinetics of INa on early repolarization (ER) and initiation of phase 2 reentry (P2R) were evaluated in a theoretical epicardial ventricular fiber model. Methods and Results Miyoshi-ICaL was incorporated into the modified Luo-Rudy dynamic (LRd) model. Dispersion at Ito-density was set within a theoretical fiber composed of serially arranged epicardial cells with gap junctions. The following changes in INa kinetics were made: (1) a -10 mV shift in steady-state inactivation, (2) a +10 mV shift in steady-state activation curve, (3) a small inactivation time constant (DEC); P2R and ER were observed. A conduction disturbance within the fiber was simulated and only when the INa-density was decreased did DEC, especially, show a marked increase in the likelihood of causing ER and P2R. Conduction disturbance significantly increased the likelihood causing ER or P2R. Conclusions In this one-dimension model with Ito-density dispersion, DEC-INa precipitates INa-blocker inducible ER. This suggests that the characteristic ST-segment elevation in the Brugada syndrome with SCN5A mutation can be interpreted in part by DEC-INa. Concomitant conduction disturbance may be required to cause P2R at physiological Ito density. (Circ J 2005; 69: 567 - 575)<br>
収録刊行物
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- Circulation Journal
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Circulation Journal 69 (5), 567-575, 2005
一般社団法人 日本循環器学会
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詳細情報 詳細情報について
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- CRID
- 1390282680081584256
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- NII論文ID
- 10015657926
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- NII書誌ID
- AA11591968
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- ISSN
- 13474820
- 13469843
- http://id.crossref.org/issn/13469843
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- PubMed
- 15849444
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 使用不可