Models of ventricular arrhythmia mechanisms.

Models of ventricular arrhythmia mechanisms.
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室性心律失常机制模型。

DOI:
10.1109/embc.2013.6609803
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发表时间:
2013
期刊:
Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference
影响因子:
--
通讯作者:
Clayton RH
Clayton RH
中科院分区:
--
文献类型:
--
作者:
Clayton RH

文献摘要

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人类心脏室性心律失常的启动和维持机制具有重要的临床意义,但很难进行实验研究。在这项研究中,电激活的单域模型被用来研究细胞尺度上的电生理动力学如何影响组织尺度上的VF表面激活模式。细胞电生理学描述了人类心室心外膜动作电位的两种现象学模型。组织几何形状为8.0×8.0×1.2 cm三维组织板,具有轴对称各向异性。在这两种情况下,初始重入波都分裂成多个激活小波。动作电位持续时间恢复较陡的模型变异产生了更复杂的激活,其平均纤维数(13.79)高于恢复较陡的模型变异(3.08)。越复杂的激活与越少的跨壁细丝相关,因此每个细丝的心外膜波阵面和相位奇点的平均数量较低。恢复幅度较小的模型变体心外膜相位奇点和波前的平均数目与人类心脏的实验观察结果一致。本研究表明,细胞尺度动力学的微小变化可以对模拟三维组织中再入激活的复杂性以及在心外膜表面观察到的特征产生很大的影响。
The mechanisms that initiate and sustain ventricular arrhythmias in the human heart are clinically important, but hard to study experimentally. In this study, a monodomain model of electrical activation was used to examine how dynamics of electrophysiology at the cell scale influence the surface activation patterns of VF at the tissue scale. Cellular electrophysiology was described with two variants of a phenomenological model of the human ventricular epicardial action potential. The tissue geometry was an 8.0×8.0×1.2 cm 3D tissue slab with axially symmetric anisotropy. In both cases an initial re-entrant wave fragmented into multiple wavelets of activation. The model variant with steep action potential duration restitution produced much more complex activation, with a greater average number of filaments (13.79) than the variant with less steep restitution (3.08). More complex activation was associated with proportionally fewer transmural filaments, and so the average number of epicardial wavefronts and phase singularities per filament was lower. The average number of epicardial phase singularities and wavefronts for the model variant with less steep restitution were consistent with experimental observations in the human heart. This study shows that small changes in cell scale dynamics can have a large influence on the complexity of re-entrant activation in simulated 3D tissue, as well as on the features observed on the epicardial surface.