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肥厚型心肌病伴心室中部梗阻时心尖部动脉瘤形成机制的数值模拟研究

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction.

作者信息

Deng Long, Zuo Heng, Li An, Yang Chun, Huang Xueying

机构信息

Department of Cardiac Surgery, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing, China.

School of Mathematical Sciences, Sichuan Normal University, Chengdu, China.

出版信息

Front Physiol. 2021 Jul 21;12:717717. doi: 10.3389/fphys.2021.717717. eCollection 2021.

DOI:10.3389/fphys.2021.717717
PMID:34366902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8334850/
Abstract

Apical aneurysm was observed to be associated with midventricular obstruction (MVO) in hypertrophic cardiomyopathy (HCM). To investigate the genesis of the apical aneurysm, the idealized numerical left ventricular models (finite-element left ventricle models) of the healthy left ventricle, subaortic obstruction, and midventricular obstruction in HCM of left ventricle were created. The mechanical effects in the formation of apical aneurysm were determined by comparing the myofiber stress on the apical wall between these three models (healthy, subaortic obstruction, and midventricular obstruction models). In comparing the subaortic obstruction model and MVO model with HCM, it was found that, at the time of maximum pressure, the maximum value of myofiber stress in MVO model was 75.0% higher than that in the subaortic obstruction model (654.5 kPa vs. 373.9 kPa). The maximum stress on the apex of LV increased 79.9, 69.3, 117.8% than that on the myocardium around the apex in healthy model, subaortic obstruction model, and MVO model, respectively. Our results indicated that high myofiber stress on the apical wall might initiate the formation process of the apical aneurysm.

摘要

在肥厚型心肌病(HCM)中,观察到心尖部动脉瘤与心室中部梗阻(MVO)有关。为了研究心尖部动脉瘤的发生机制,构建了健康左心室、主动脉瓣下梗阻以及HCM左心室的心室中部梗阻的理想化数值左心室模型(有限元左心室模型)。通过比较这三种模型(健康、主动脉瓣下梗阻和心室中部梗阻模型)心尖壁上的肌纤维应力,确定心尖部动脉瘤形成过程中的力学效应。在将主动脉瓣下梗阻模型和HCM的MVO模型进行比较时发现,在最大压力时,MVO模型中肌纤维应力的最大值比主动脉瓣下梗阻模型高75.0%(654.5 kPa对373.9 kPa)。与健康模型、主动脉瓣下梗阻模型相比,左心室心尖部的最大应力分别比心尖周围心肌处的最大应力增加了79.9%、69.3%、117.8%。我们的结果表明,心尖壁上较高的肌纤维应力可能启动心尖部动脉瘤的形成过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/e5f32c0383d8/fphys-12-717717-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/be4dac1ef831/fphys-12-717717-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/03d27a1ac379/fphys-12-717717-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/af80b74e582d/fphys-12-717717-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/e5f32c0383d8/fphys-12-717717-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/be4dac1ef831/fphys-12-717717-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/03d27a1ac379/fphys-12-717717-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/af80b74e582d/fphys-12-717717-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e9/8334850/e5f32c0383d8/fphys-12-717717-g004.jpg

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