动脉粥样硬化晚期斑块局部应力的流固耦合分析及体外反搏作用干预机制的研究

杜健航; 王梁; 伍贵富; 郑振声; 戴刚; 冯铭哲

doi:10.6052/0459-1879-17-150

动脉粥样硬化晚期斑块局部应力的流固耦合分析及体外反搏作用干预机制的研究

doi: 10.6052/0459-1879-17-150

杜健航^1,2,*, ,,
王梁³,
伍贵富^1,2,
郑振声²,
戴刚²,
冯铭哲²

¹中山大学附属第八医院,广东深圳 518033
²卫生部辅助循环重点实验室,广州 500089
³伍斯特理工学院数学科学系,马萨诸塞州伍斯特市 01609,美国

基金项目: 收稿: 2017-05-02,录用: 2017-12-29, 网络版发表: 2017-12-29.;卫生部临床学科重点专项 (254004);卫生部辅助循环重点实验室开放基金资助项目.

详细信息

作者简介:
*通讯作者：杜健航,副教授,主要研究方向：血管生物力学,心血管辅助循环和体外反搏. E-mail：zsudjhang@163.com

通讯作者:
杜健航

中图分类号: O38;
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出版历程
- 收稿日期: 2017-05-02
- 刊出日期: 2018-01-18

FLUID-STRUCTURE INTERACTION ANALYSIS OF LOCAL STRESSES IN ATHEROSCLEROTIC PLAUQE AND THE INTERVENTION OF ENHANCED EXTERNAL COUNTERPULSATION TREATMENT

¹The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518033,Guangdong, China
²Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou 500089, China
³Department of Mathematics Science, Worcester Polytechnic Institute, Worcester, MA 01609, USA

摘要

摘要: 生物机械力被普遍认为在动脉粥样硬化晚期斑块进程及最终破裂中起着重要的作用. 本文的目的是研究血流灌注、动脉内压、斑块组织和材料特性等因素对斑块局部流动切应力及斑块结构应力水平的影响,同时评价临床中的非介入辅助循环疗法 —— 体外反搏对斑块局部应力水平的干预作用. 采用结合猪动物模型在体测量及三维流固耦合数值仿真的研究方法. 结果显示,当斑块狭窄率一定时 (50%),斑块的流动切应力水平主要由血流灌注决定;而斑块结构应力主要取决于动脉内压及纤维帽厚度. 只有在纤维帽足够薄的情况下,斑块的材料特性才对斑块结构应力有显著影响;当纤维帽最薄同时脂质池材料最软时,临界斑块壁面应力因子达到极值的 257.72 kPa (正常生理状态) 及 300.20 kPa (体外反博状态). 由于最大壁面应力、临界斑块壁面应力及全局最大斑块壁面应力三个应力因子中,只有临界斑块壁面应力明显受纤维帽厚度和脂质池材料特性的影响,因此其可能与斑块进程的关联最为紧密. 此外,体外反博作用明显提高了晚期斑块的应力水平,这是否会给斑块进程及重构带来慢性的影响,需要作更深入的研究.
- 晚期斑块 /
- 流固耦合 /
- 增强型体外反搏
Abstract: It is generally agreed that biomechanical stresses play important roles in advanced atherosclerotic plaque progression and rupture. This paper aims to perform a pilot study to access the influences of blood perfusion, blood pressure, histology and material properties of plaques on the levels of blood flow stress (FSS) and plaque structural stress (PSS), and meanwhile to access the intervention of enhanced external counterpulsation (EECP), a kind of clinical non-invasive assisted circulation therapy. A method combining in vivo measurements performed in a porcine model and 3D fluid-structure interaction (FSI) numerical simulation was adopted. Results showed that, when the stenotic degree was fixed to 50%, FSS level of the plaque depended mainly on blood perfusion, while PWS level was mainly determined by both blood pressure and fibrous cap (FC) length. Only when FC was thin enough, plaque material properties had significant influence on PSS. A thinnest FC together with a softest lipid pool led to the peak critical plaque wall stress (3D CPWS) of 257.72 kPa (normal physiological state) and 300.20 kPa (EECP state). Note that changes in FC length or lipid pool material property only induced the variation of 3D CPWS significantly, we suggested that 3D CPWS was a stress-based factor that might play a much more important role during plaque progression than max WSS (MWSS) or global max plaque stress (GMPWS). Moreover, EECP treatment significantly increased the levels of both FSS and PWS, whether it would intervene the progression and remodeling of advanced plaque, and should be brought the attention in its clinical applications might need more detailed evaluations.
- atherosclerosis /
- advanced plaque /
- fluid-structure interface

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参考文献(1)

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