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To the Editor- Misuse of null hypothesis testing: Analysis of biophysical model simulations.致编辑——零假设检验的误用:生物物理模型模拟分析
Heart Rhythm. 2017 Apr;14(4):e50. doi: 10.1016/j.hrthm.2016.12.012. Epub 2016 Dec 9.
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Patient-derived models link re-entrant driver localization in atrial fibrillation to fibrosis spatial pattern.患者来源的模型将心房颤动中折返驱动因素的定位与纤维化空间模式联系起来。
Cardiovasc Res. 2016 Jun 1;110(3):443-54. doi: 10.1093/cvr/cvw073. Epub 2016 Apr 7.
3
Percolation as a mechanism to explain atrial fractionated electrograms and reentry in a fibrosis model based on imaging data.基于成像数据,渗流作为一种机制来解释纤维化模型中的心房碎裂电图和折返。
Heart Rhythm. 2016 Jul;13(7):1536-43. doi: 10.1016/j.hrthm.2016.03.019. Epub 2016 Mar 11.
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Virtual electrophysiological study of atrial fibrillation in fibrotic remodeling.纤维化重塑中房颤的虚拟电生理研究
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Reentry near the percolation threshold in a heterogeneous discrete model for cardiac tissue.心脏组织非均匀离散模型中渗流阈值附近的折返
Phys Rev Lett. 2013 Apr 12;110(15):158101. doi: 10.1103/PhysRevLett.110.158101. Epub 2013 Apr 9.
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Fractional diffusion models of cardiac electrical propagation: role of structural heterogeneity in dispersion of repolarization.心脏电传播的分数阶扩散模型:结构异质性在复极离散中的作用。
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A brief history of tissue models for cardiac electrophysiology.心脏电生理学组织模型简史。
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A microstructural model of reentry arising from focal breakthrough at sites of source-load mismatch in a central region of slow conduction.源自中央缓慢传导区源-负载失配对部位局灶突破的折返微结构模型。
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An efficient finite element approach for modeling fibrotic clefts in the heart.一种用于心脏纤维化裂隙建模的高效有限元方法。
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10
Patient-specific modeling of atrial fibrosis increases the accuracy of sinus rhythm simulations and may explain maintenance of atrial fibrillation.针对患者的心房纤维化建模提高了窦性心律模拟的准确性,并可能解释心房颤动的维持机制。
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患病心脏组织中的动力学建模:模型选择的影响。

Modeling dynamics in diseased cardiac tissue: Impact of model choice.

作者信息

Gokhale Tanmay A, Medvescek Eli, Henriquez Craig S

机构信息

Department of Biomedical Engineering, Duke University, Durham, North Carolina 27708-0281, USA.

出版信息

Chaos. 2017 Sep;27(9):093909. doi: 10.1063/1.4999605.

DOI:10.1063/1.4999605
PMID:28964161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5568867/
Abstract

Cardiac arrhythmias have been traditionally simulated using continuous models that assume tissue homogeneity and use a relatively large spatial discretization. However, it is believed that the tissue fibrosis and collagen deposition, which occur on a micron-level, are critical factors in arrhythmogenesis in diseased tissues. Consequently, it remains unclear how well continuous models, which use averaged electrical properties, are able to accurately capture complex conduction behaviors such as re-entry in fibrotic tissues. The objective of this study was to compare re-entrant behavior in discrete microstructural models of fibrosis and in two types of equivalent continuous models, a homogenous continuous model and a hybrid continuous model with distinct heterogeneities. In the discrete model, increasing levels of tissue fibrosis lead to a substantial increase in the re-entrant cycle length which is inadequately reflected in the homogenous continuous models. These cycle length increases appear to be primarily due to increases in the tip path length and to altered restitution behavior, and suggest that it is critical to consider the discrete effects of fibrosis on conduction when studying arrhythmogenesis in fibrotic myocardium. Hybrid models are able to accurately capture some aspects of re-entry and, if carefully tuned, may provide a framework for simulating conduction in diseased tissues with both accuracy and efficiency.

摘要

传统上,心律失常是使用连续模型来模拟的,这些模型假定组织具有同质性,并采用相对较大的空间离散化。然而,据信在微米水平上发生的组织纤维化和胶原沉积是患病组织中心律失常发生的关键因素。因此,使用平均电学特性的连续模型能够多准确地捕捉诸如纤维化组织中的折返等复杂传导行为,仍不明确。本研究的目的是比较纤维化离散微观结构模型以及两种等效连续模型(均匀连续模型和具有明显异质性的混合连续模型)中的折返行为。在离散模型中,组织纤维化程度的增加会导致折返周期长度大幅增加,而这在均匀连续模型中未得到充分体现。这些周期长度的增加似乎主要是由于尖端路径长度的增加和恢复行为的改变,这表明在研究纤维化心肌中的心律失常发生时,考虑纤维化对传导的离散效应至关重要。混合模型能够准确捕捉折返的某些方面,并且如果仔细调整,可能会提供一个既能准确又能高效模拟患病组织中传导的框架。