2003 Fiscal Year Final Research Report Summary
Development of Comprehensive Electrophysiological Heart Simulator for In-Silico Study
| Project/Area Number |
14580843
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
NAKAZAWA Kazuo National Cardiovascular Center Research Institute, Laboratory of Development and Evaluation of Biomedical Instruments and Systems, Laboratory Chie, 研究機器管理室, 室長 (50198058)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Takanori Kyorin University Hospital, 医学部附属病院, 講師 (80256734)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Fatal Arrhythmia / Computer Simulation / Spiral Reentry / Luo-Rudy Model / Bidomain Model |
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| Research Abstract |
So far the ventricle morphology data in our simulator were based on the polygon data for the computer graphics. But we have to carry out simulation with a patient's individual ventricle morphology in order to estimate fatal arrhythmia as correct as possible. So we extracted myocardial region manually from MRI images and reconstructed 4-dimensional (3D space + time) heart morphology during one heart-beat. First, we obtained 24 cross-sectional short-axis images that cover the whole heart at each of 17 phases by True FISP sequences. Second, we developed an editor tool to put points manually at the myocardial boundary on each image, and extracted the region. We also developed a 3-dimensional editor tool to link these points between consecutive sections, and reconstructed heart morphological polygon data. To improve the shape and to use it as a simulation model, we performed several processes such as correction of different heart position between MRI images, smoothing of heart polygons, conversion to volume data and so on.
On the other hand, we developed the 2-dimensional bidomain model to clarify the electrical defibrillation mechanism. The model was consisted of a homogeneous and an isotropic bidomain myocardial sheet. Membrane kinetics was represented by a modified version of the Luo-Rudy-1 model and myocardial fibers were considered. Possibilities of the electrical stimulation to control spiral wave reentry were investigated under the effects of stimulus induced virtual electrode polarization. As a result, a set of localized stimulations during spiral wave reentry caused spiral wave shift or capture, which provided insight into mechanistic basis of spiral wave control leading to the new electrical defibrillation mechanism.
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