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心肌梗死区域内纤维化分布对心室组织中波传播的影响。

Influence of the distribution of fibrosis within an area of myocardial infarction on wave propagation in ventricular tissue.

机构信息

School of Computer Science and Technology, Harbin Institute of Technology, Harbin, Heilongjiang, China.

School of Physics and Astronomy, The University of Manchester, Manchester, UK.

出版信息

Sci Rep. 2019 Oct 2;9(1):14151. doi: 10.1038/s41598-019-50478-5.

DOI:10.1038/s41598-019-50478-5
PMID:31578428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6775234/
Abstract

The presence of fibrosis in heart tissue is strongly correlated with an incidence of arrhythmia, which is a leading cause of sudden cardiac death (SCD). However, it remains incompletely understood how different distributions, sizes and positions of fibrotic tissues contribute to arrhythmogenesis. In this study, we designed 4 different ventricular models mimicking wave propagation in cardiac tissues under normal, myocardial infarction (MI), MI with random fibrosis and MI with gradient fibrosis conditions. Simulation results of ideal square tissues indicate that vulnerable windows (VWs) of random and gradient fibrosis distributions are similar with low levels of fibrosis. However, with a high level of fibrosis, the VWs significantly increase in random fibrosis tissue but not in gradient fibrosis tissue. In addition, we systematically analyzed the effects of the size and position of fibrosis tissues on VWs. Simulation results show that it is more likely for a reentry wave to appear when the length of the infarcted area is greater than 25% of the perimeter of the ventricle, when the width is approximately half that of the ventricular wall, or when the infarcted area is attached to the inside or outside of the ventricular wall.

摘要

心脏组织中的纤维化存在与心律失常的发生率密切相关,心律失常是心脏性猝死(SCD)的主要原因。然而,不同分布、大小和位置的纤维化组织如何导致心律失常的发生仍不完全清楚。在这项研究中,我们设计了 4 种不同的心室模型,模拟正常、心肌梗死(MI)、MI 伴随机纤维化和 MI 伴梯度纤维化条件下心脏组织中的波传播。理想正方形组织的模拟结果表明,随机和梯度纤维化分布的易损窗口(VWs)在纤维化水平较低时相似。然而,在纤维化水平较高时,随机纤维化组织中的 VWs 显著增加,而梯度纤维化组织中的 VWs 则没有显著增加。此外,我们系统地分析了纤维化组织的大小和位置对 VWs 的影响。模拟结果表明,当梗死区域的长度大于心室周长的 25%、宽度约为心室壁的一半、或者梗死区域附着在心室壁的内侧或外侧时,折返波更有可能出现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/02ac63940b62/41598_2019_50478_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/e67d27d4639b/41598_2019_50478_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/5b391cb71b67/41598_2019_50478_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/60a983fad1aa/41598_2019_50478_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/982a462b59d2/41598_2019_50478_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/d95f57ef1bd2/41598_2019_50478_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/37ca59cfe9cd/41598_2019_50478_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/840ce151d630/41598_2019_50478_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/02ac63940b62/41598_2019_50478_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/e67d27d4639b/41598_2019_50478_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/5b391cb71b67/41598_2019_50478_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/60a983fad1aa/41598_2019_50478_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/982a462b59d2/41598_2019_50478_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/d95f57ef1bd2/41598_2019_50478_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/37ca59cfe9cd/41598_2019_50478_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/840ce151d630/41598_2019_50478_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7164/6775234/02ac63940b62/41598_2019_50478_Fig8_HTML.jpg

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2
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Europace. 2016 Dec;18(suppl 4):iv60-iv66. doi: 10.1093/europace/euw351.
3
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4
Cardiovascular involvement in Erdheim-Chester diseases is associated with myocardial fibrosis and atrial dysfunction. Erdheim-Chester 病的心血管受累与心肌纤维化和心房功能障碍有关。
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5
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6
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