Dispersion of Recovery and Vulnerability to Re-entry in a Model of Human Atrial Tissue With Simulated Diffuse and Focal Patterns of Fibrosis.
Dispersion of Recovery and Vulnerability to Re-entry in a Model of Human Atrial Tissue With Simulated Diffuse and Focal Patterns of Fibrosis.
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DOI：
10.3389/fphys.2018.01052
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发表时间：
2018
影响因子：
4
通讯作者：
Clayton RH
中科院分区：
文献类型：
--
作者：
Clayton RH
心房组织纤维化可作为持续性心房颤动的底物，可为局灶性或弥漫性。纤维化区域与传导减慢或阻滞有关，已有几种方法用于模拟这些影响。本研究采用二维心房组织计算模型，研究模拟纤维化区域的空间尺度如何影响模拟正常人类心房组织和因持续性心房颤动而经历重构的人类组织的动作电位持续时间（APD）离散度和再入易感性。电活动模拟在一个10 × 10平方厘米的二维区域内，扩散系数随空间变化，如下所述。细胞电生理采用人心房细胞Courtemanche模型表示，模型参数设置为正常细胞和重构细胞。纤维化的影响是用平滑变化的扩散系数来模拟的，扩散系数是通过采样一个长度尺度在1.25到10.0 mm之间的高斯随机场（GRF）得到的。从每个领域抽取20个样本，并将扩散系数分配在0.05 ~ 0.2 mm2/ms之间。每个样本的APD弥散度通过起搏周期长度为1,000 ms，然后是耦合间隔为400 ms的早搏来评估。采用积极的起搏方案评估重新进入的脆弱性，起搏周期长度从450毫秒减少到250毫秒，正常组织间隔25毫秒，重塑组织间隔300-150毫秒。较小空间尺度的模拟纤维化倾向于延长APD，增加APD弥散，并且相对于较大空间尺度的纤维化，增加持续再入的易感性。本研究表明，当纤维化表现为平滑变化的组织弥散时，纤维化的空间尺度对恢复的弥散性和再入脆弱性都有重要影响。
Fibrosis in atrial tissue can act as a substrate for persistent atrial fibrillation, and can be focal or diffuse. Regions of fibrosis are associated with slowed or blocked conduction, and several approaches have been used to model these effects. In this study a computational model of 2D atrial tissue was used to investigate how the spatial scale of regions of simulated fibrosis influenced the dispersion of action potential duration (APD) and vulnerability to re-entry in simulated normal human atrial tissue, and human tissue that has undergone remodeling as a result of persistent atrial fibrillation. Electrical activity was simulated in a 10 × 10 cm square 2D domain, with a spatially varying diffusion coefficient as described below. Cellular electrophysiology was represented by the Courtemanche model for human atrial cells, with the model parameters set for normal and remodeled cells. The effect of fibrosis was modeled with a smoothly varying diffusion coefficient, obtained from sampling a Gaussian random field (GRF) with length scales of between 1.25 and 10.0 mm. Twenty samples were drawn from each field, and used to allocate a value of diffusion coefficient between 0.05 and 0.2 mm2/ms. Dispersion of APD was assessed in each sample by pacing at a cycle length of 1,000 ms, followed by a premature beat with a coupling interval of 400 ms. Vulnerability to re-entry was assessed with an aggressive pacing protocol with pacing cycle lengths decreasing from 450 to 250 ms in 25 ms intervals for normal tissue and 300–150 ms for remodeled tissue. Simulated fibrosis at smaller spatial scales tended to lengthen APD, increase APD dispersion, and increase vulnerability to sustained re-entry relative to fibrosis at larger spatial scales. This study shows that when fibrosis is represented by smoothly varying tissue diffusion, the spatial scale of fibrosis has important effects on both dispersion of recovery and vulnerability to re-entry.
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影响因子：
2.9
作者：
Biktashev, VN;Holden, AV
通讯作者：
Holden, AV
心房颤动引起的电重塑的致心律失常效应：来自三维虚拟人体心房的见解
DOI：
10.1113/jphysiol.2013.254987
发表时间：
2013-09-01
期刊：
The Journal of physiology
影响因子：
--
作者：
Colman MA;Aslanidi OV;Kharche S;Boyett MR;Garratt C;Hancox JC;Zhang H
通讯作者：
Zhang H
人体心脏组织弥漫性纤维化数学模型中的非平衡心律失常状态和转变。
影响因子：
3.7
作者：
Majumder R;Nayak AR;Pandit R
通讯作者：
Pandit R
影响因子：
20.1
作者：
Ashihara T;Haraguchi R;Nakazawa K;Namba T;Ikeda T;Nakazawa Y;Ozawa T;Ito M;Horie M;Trayanova NA
通讯作者：
Trayanova NA
影响因子：
8.4
作者：
Engelman, Zoar J.;Trew, Mark L.;Smaill, Bruce H.
通讯作者：
Smaill, Bruce H.