2017 Fiscal Year Final Research Report
Novel Non-invasive risk stratification of sudden cardiac death in patients with inherited arrhythmias
Project/Area Number |
15K09150
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cardiovascular medicine
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Research Institution | National Cardiovascular Center Research Institute |
Principal Investigator |
AIBA TAKESHI 国立研究開発法人国立循環器病研究センター, 病院, 医長 (40574348)
|
Co-Investigator(Kenkyū-buntansha) |
稲田 慎 姫路獨協大学, 医療保健学部, 准教授 (50349792)
松浦 博 滋賀医科大学, 医学部, 教授 (60238962)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 不整脈 / 電気生理学 / シミュレーション / 右室流出路 / 伝導 |
Outline of Final Research Achievements |
Local conduction abnormalities at the right ventricular outflow tract epicardium (RVOT-Epi) are one of the potent arrhythmogenic substrates in many heart diseases. However, how much delay at RVOT-Epi develops ventricular arrhythmias (VAs) is not quantitatively investigated. We constructed a 3-D human ventricular model to investigate the role of conduction delay in the RVOT-Epi on initiation and maintenance of the VAs. No VAs occurred in the mild to moderate conduction delay of 2.3cm φ in the RVOT-Epi, but in the severe delay, propagation of the wave front was broken up into the multiple wavelets in the RVOT-Epi, thus, maintained the VAs. The VAs inducibility is much easier in the larger delayed size (3.0cmφ). In contrast, these findings could not be reproduced in the delayed conduction set at RV free wall (RVFW). These findings suggest that the structural vulnerability for VAs in RVOT-Epi as an arrhythmic risk of arrhythmogenic right ventricular cardiomyopathy or Brugada syndrome.
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Free Research Field |
循環器内科
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