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Reentry and Ectopic Pacemakers Emerge in a Three-Dimensional Model for a Slab of Cardiac Tissue with Diffuse Microfibrosis near the Percolation Threshold

机译:再入和异位起搏器出现在渗流阈值附近弥漫性微纤维化的心脏组织平板的三维模型中

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摘要

Arrhythmias in cardiac tissue are generally associated with irregular electrical wave propagation in the heart. Cardiac tissue is formed by a discrete cell network, which is often heterogeneous. Recently, it was shown in simulations of two-dimensional (2D) discrete models of cardiac tissue that a wave crossing a fibrotic, heterogeneous region may produce reentry and transient or persistent ectopic activity provided the fraction of conducting connections is just above the percolation threshold. Here, we investigate the occurrence of these phenomena in three-dimensions by simulations of a discrete model representing a thin slab of cardiac tissue. This is motivated (i) by the necessity to study the relevance and properties of the percolation-related mechanism for the emergence of microreentries in three dimensions and (ii) by the fact that atrial tissue is quite thin in comparison with ventricular tissue. Here, we simplify the model by neglecting details of tissue anatomy, e. g. geometries of atria or ventricles and the anisotropy in the conductivity. Hence, our modeling study is confined to the investigation of the effect of the tissue thickness as well as to the comparison of the dynamics of electrical excitation in a 2D layer with the one in a 3D slab. Our results indicate a strong and non-trivial effect of the thickness even for thin tissue slabs on the probability of microreentries and ectopic beat generation. The strong correlation of the occurrence of microreentry with the percolation threshold reported earlier in 2D layers persists in 3D slabs. Finally, a qualitative agreement of 3D simulated electrograms in the fibrotic region with the experimentally observed complex fractional atrial electrograms (CFAE) as well as strong difference between simulated electrograms in 2D and 3D were found for the cases where reentry and ectopic activity were triggered by the micro-fibrotic region.
机译:心脏组织中的心律不齐通常与心脏中不规则的电波传播有关。心脏组织是由离散的细胞网络形成的,该网络通常是异质的。最近,在心脏组织的二维(2D)离散模型的仿真中显示,如果传导连接的分数刚好高于渗滤阈值,则穿过纤维化,异质区域的波可能会产生折返和短暂或持续的异位活动。在这里,我们通过模拟代表心脏组织薄板的离散模型来研究三维中这些现象的发生。这是由于(i)有必要研究渗流相关机制在三个方面出现微折返的相关性和性质,以及(ii)与心室组织相比,心房组织非常薄的事实。在这里,我们通过忽略组织解剖细节来简化模型。 G。心房或心室的几何形状以及电导率的各向异性。因此,我们的建模研究仅限于研究组织厚度的影响,以及将2D层中的电激发动力学与3D平板中的电激发动力学进行比较。我们的结果表明,即使是薄薄的组织平板,其厚度对微折返和异位搏动发生的可能性也有很强的影响。在3D平板中,微折返的发生与早期在2D层中报告的渗透阈值之间的密切相关性仍然存在。最后,在纤维化区域的3D模拟电图与实验观察到的复杂心房分数电图(CFAE)的定性吻合,以及在2D和3D模式下模拟电图之间的强差异,发现了折返和异位活动是由纤维化触发的。微纤维化区域。

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