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增强型体外反搏对脑动脉血流动力学的影响:多尺度研究。

Hemodynamic effects of enhanced external counterpulsation on cerebral arteries: a multiscale study.

机构信息

Department of Biomedical Engineering, College of Life Science and Bioengineering, Beijing University of Technology, No. 100 Pingleyuan, Chaoyang District, Beijing, 100124, China.

Sino-Dutch Biomedical and Information Engineering School, Northeastern University, Shenyang, 110004, China.

出版信息

Biomed Eng Online. 2019 Aug 28;18(1):91. doi: 10.1186/s12938-019-0710-x.

DOI:10.1186/s12938-019-0710-x
PMID:31462269
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6714389/
Abstract

BACKGROUND

Enhanced external counterpulsation (EECP) is an effective method for treating patients with cerebral ischemic stroke, while hemodynamics is the major contributing factor in the treatment of EECP. Different counterpulsation modes have the potential to lead to different acute and long-term hemodynamic changes, resulting in different treatment effects. However, various questions about appropriate counterpulsation modes for optimizing hemodynamic effects remain unanswered in clinical treatment.

METHODS

A zero-dimensional/three-dimensional (0D/3D) geometric multiscale model of the cerebral artery was established to obtain acute hemodynamic indicators, including mean arterial pressure (MAP) and cerebral blood flow (CBF), as well as localized hemodynamic details for the cerebral artery, which includes wall shear stress (WSS) and oscillatory shear index (OSI). Counterpulsation was achieved by applying pressure on calf, thigh and buttock modules in the 0D model. Different counterpulsation modes including various pressure amplitudes and pressurization durations were applied to investigate hemodynamic responses, which impact acute and long-term treatment effects. Both vascular collapse and cerebral autoregulation were considered during counterpulsation.

RESULTS

Variations of pressure amplitude and pressurization duration have different impacts on hemodynamic effects during EECP treatment. There were small differences in the hemodynamics when similar or different pressure amplitudes were applied to calves, thighs and buttocks. When increasing pressure amplitude was applied to the three body parts, MAP and CBF improved slightly. When pressure amplitude exceeded 200 mmHg, hemodynamic indicators almost never changed, demonstrating consistency with clinical data. However, hemodynamic indicators improved significantly with increasing pressurization duration. For pressurization durations of 0.5, 0.6 and 0.7 s, percentage increases for MAP during counterpulsation were 1.5%, 23.5% and 39.0%, for CBF were 1.2%, 23.4% and 41.6% and for time-averaged WSS were 0.2%, 43.5% and 85.0%, respectively.

CONCLUSIONS

When EECP was applied to patients with cerebral ischemic stroke, pressure amplitude applied to the three parts may remain the same. Patients may not gain much more benefit from EECP treatment by excessively increasing pressure amplitude above 200 mmHg. However, during clinical procedures, pressurization duration could be increased to 0.7 s during the cardiac circle to optimize the hemodynamics for possible superior treatment outcomes.

摘要

背景

增强型体外反搏(EECP)是治疗脑缺血性中风患者的有效方法,而血流动力学是 EECP 治疗的主要影响因素。不同的反搏模式有可能导致不同的急性和长期血流动力学变化,从而产生不同的治疗效果。然而,在临床治疗中,关于优化血流动力学效果的合适反搏模式仍存在诸多问题。

方法

建立了一个零维/三维(0D/3D)的脑动脉几何多尺度模型,以获得包括平均动脉压(MAP)和脑血流量(CBF)在内的急性血流动力学指标,以及包括壁面切应力(WSS)和脉动剪切指数(OSI)在内的脑动脉局部血流动力学细节。在 0D 模型中,通过对小腿、大腿和臀部模块施加压力来实现反搏。应用不同的反搏模式,包括不同的压力幅度和加压持续时间,以研究对急性和长期治疗效果的影响。在反搏过程中考虑了血管塌陷和脑自动调节。

结果

压力幅度和加压持续时间的变化对 EECP 治疗期间的血流动力学效果有不同的影响。当对小腿、大腿和臀部施加相似或不同的压力幅度时,血流动力学的差异很小。当向三个身体部位施加逐渐增大的压力幅度时,MAP 和 CBF 略有改善。当压力幅度超过 200mmHg 时,血流动力学指标几乎不再变化,与临床数据一致。然而,随着加压持续时间的增加,血流动力学指标显著改善。对于加压持续时间为 0.5、0.6 和 0.7s,反搏期间 MAP 的百分比增加分别为 1.5%、23.5%和 39.0%,CBF 分别为 1.2%、23.4%和 41.6%,时均壁面切应力分别为 0.2%、43.5%和 85.0%。

结论

当 EECP 应用于脑缺血性中风患者时,施加于三个部位的压力幅度可能保持不变。通过将压力幅度过度增加到 200mmHg 以上,患者可能不会从 EECP 治疗中获得更多益处。然而,在临床操作中,可以将加压持续时间在心动周期内增加到 0.7s,以优化血流动力学,从而获得更好的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/22b038d0d072/12938_2019_710_Fig14_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/4cffa00520a1/12938_2019_710_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/541051c57b4f/12938_2019_710_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/d7dbbbf016dc/12938_2019_710_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/564a3bfe2e14/12938_2019_710_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/c89c92a53a72/12938_2019_710_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/e2f4bb3abc70/12938_2019_710_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/d303aec61fc5/12938_2019_710_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/2a02bcb070f7/12938_2019_710_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/6714389/22b038d0d072/12938_2019_710_Fig14_HTML.jpg

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