Effects of electrical and structural remodeling on atrial fibrillation maintenance: a simulation study.
Effects of electrical and structural remodeling on atrial fibrillation maintenance: a simulation study.
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DOI：
10.1371/journal.pcbi.1002390
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发表时间：
2012
影响因子：
4.3
通讯作者：
Christini DJ
中科院分区：
文献类型：
--
作者：
Krogh-Madsen T;Abbott GW;Christini DJ
房颤是一种常见的心律失常，通常进展不利：在长期房颤患者中，相对于健康对照组，房颤发作的持续时间和发生频率通常增加。这是由于电、结构和收缩重构过程。我们研究了电重构和结构重构如何促进模拟房颤永久化的机制，使用人体心房动作电位的数学模型，将其纳入人体心房的解剖学上真实的三维结构模型。电重构和结构重构都缩短了心房波长-电重构主要通过减少动作电位时程，而结构重构主要减慢传导。波长的减小与心房颤动/扑动发作的平均持续时间的增加相关。折返持续时间对波长的依赖性对于电重构与结构重构是相同的。然而，心房折返期间的动力学在电重构、结构重构以及电重构和结构重构的组合之间以几种方式变化，包括：（i）与电重构期间相比，结构重构中有更多的碎片波前发生，因此有更多的细丝;（ii）在电重构与结构重构中，主导波锚定在不同的解剖障碍物周围;（iii）主导波通常不锚定在组合的电重构和结构重构中。我们的结论是，在模拟心房颤动，折返持续时间的波长依赖性是相似的电和结构重构，尽管在整体动力学，包括最大数量的细丝，波破碎，恢复特性，以及是否占主导地位的波锚定到解剖障碍或螺旋自由的重大差异。心房颤动是一种以心脏上腔室的快速和不规则激活为特征的异常心律。房颤通常表现为自然进展，发作时间更长，频率更高，通常发生在现有心脏病患者中。由于心房颤动有几种变体，性质复杂，并且随着时间的推移而演变，因此在大型动物模型中进行全面研究非常困难和昂贵，部分原因是体内成像全心房电生理学的固有技术困难。预测多尺度计算模型有可能填补这一研究空白。我们已经纳入了慢性房颤的各个方面，以模拟其各种疾病状态。因此，这项研究代表了第一个全面的计算研究慢性房颤维持在一个生物解剖学详细的细胞模型在一个现实的三维解剖。我们的模拟表明，对细胞过程以及细胞之间的耦合的疾病样修改通过加速节律和/或增加循环激活波的数量来维持模拟的心房颤动。鉴于该模型能够再现许多临床和实验上重要的特征，我们相信它为未来心房电动力学的研究提供了一个有用的框架，离子通道突变和各种药物。
Atrial fibrillation, a common cardiac arrhythmia, often progresses unfavourably: in patients with long-term atrial fibrillation, fibrillatory episodes are typically of increased duration and frequency of occurrence relative to healthy controls. This is due to electrical, structural, and contractile remodeling processes. We investigated mechanisms of how electrical and structural remodeling contribute to perpetuation of simulated atrial fibrillation, using a mathematical model of the human atrial action potential incorporated into an anatomically realistic three-dimensional structural model of the human atria. Electrical and structural remodeling both shortened the atrial wavelength - electrical remodeling primarily through a decrease in action potential duration, while structural remodeling primarily slowed conduction. The decrease in wavelength correlates with an increase in the average duration of atrial fibrillation/flutter episodes. The dependence of reentry duration on wavelength was the same for electrical vs. structural remodeling. However, the dynamics during atrial reentry varied between electrical, structural, and combined electrical and structural remodeling in several ways, including: (i) with structural remodeling there were more occurrences of fragmented wavefronts and hence more filaments than during electrical remodeling; (ii) dominant waves anchored around different anatomical obstacles in electrical vs. structural remodeling; (iii) dominant waves were often not anchored in combined electrical and structural remodeling. We conclude that, in simulated atrial fibrillation, the wavelength dependence of reentry duration is similar for electrical and structural remodeling, despite major differences in overall dynamics, including maximal number of filaments, wave fragmentation, restitution properties, and whether dominant waves are anchored to anatomical obstacles or spiralling freely. Atrial fibrillation is an abnormal heart rhythm characterized by rapid and irregular activation of the upper chambers of the heart. Atrial fibrillation often shows a natural progression towards longer and more frequently occurring episodes and often occurs in patients with existing heart disease(s). Because atrial fibrillation has several variants, is complex in nature, and evolves over time, it is very difficult and expensive to study comprehensively in large-animal models, in part due to the inherent technical difficulties of imaging whole-atria electrophysiology in vivo. Predictive multiscale computational modeling has the potential to fill this research void. We have incorporated aspects of chronic atrial fibrillation to model some of its various disease states. As such, this study represents the first comprehensive computational study of chronic atrial fibrillation maintenance in a biophysically detailed cell model in a realistic three-dimensional anatomy. Our simulations show that disease-like modifications to cellular processes, as well as to the coupling between cells, perpetuate simulated atrial fibrillation by accelerating the rhythm and/or increasing the number of circulating activation waves. Given the model's ability to reproduce a number of clinically and experimentally important features, we believe that it presents a useful framework for future studies of atrial electrodynamics in response to, e.g., ion channel mutations and various drugs.
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影响因子：
4.6
作者：
Harada, A;Sasaki, K;Shoji, T
通讯作者：
Shoji, T
DOI：
10.1152/ajpheart.01128.2005
发表时间：
2006-12-01
影响因子：
4.8
作者：
Everett, Thomas H.;Wilson, Emily E.;Olgin, Jeffrey E.
通讯作者：
Olgin, Jeffrey E.
影响因子：
6.1
作者：
Jacquemet, V;Virag, N;Kappenberger, L
通讯作者：
Kappenberger, L
影响因子：
37.8
作者：
Atienza, Felipe;Almendral, Jesus;Berenfeld, Omer
通讯作者：
Berenfeld, Omer
影响因子：
8.4
作者：
Allessie, Maurits A.;de Groot, Natasja M. S.;Crijns, Harry J.
通讯作者：
Crijns, Harry J.