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高血压引起的主动脉壁生物力学改变及其在 Stanford B 型主动脉夹层中的作用

Hypertension-Induced Biomechanical Modifications in the Aortic Wall and Their Role in Stanford Type B Aortic Dissection.

作者信息

Wei Yuhao, Li Da, Weng Chengxin, Wang Jiarong, Yuan Ding, Zheng Tinghui

机构信息

Department of Mechanics & Engineering, College of Architecture & Environment, Sichuan University, Chengdu 610065, China.

Yibin Institute of Industrial Technology, Sichuan University Yibin Park, Yibin 644000, China.

出版信息

Biomedicines. 2024 Oct 2;12(10):2246. doi: 10.3390/biomedicines12102246.

DOI:10.3390/biomedicines12102246
PMID:39457560
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11504259/
Abstract

OBJECTIVE

Hypertension is a major risk factor for the type B aortic dissection (TBAD), while many patients do not manage or regulate their hypertension consistently, leading to stable or unstable hypertension. Currently, the effects of stable and unstable hypertension on the biomechanical properties of the aorta remain unclear. The objective was to identify a blood pressure state that represents a greater risk for TBAD development.

METHODS

A total of 183 samples (108 axial and 75 circumferential) were divided into three groups. Fatigue tensile tests were carried out to simulate normotension, stable hypertension, and unstable hypertension conditions, respectively. Uniaxial tensile tests were performed; thus, the elastic modulus, energy loss, and the peeling force were assessed to evaluate the biomechanical properties.

RESULTS

Compared with normal blood pressure, the modulus of elastic fibers decreased under stable hypertension (0.05 ± 0.02 MPa vs. 0.11 ± 0.03 MPa, < 0.001) and unstable hypertension (0.08 ± 0.02 MPa, = 0.008), while collagen fibers increased under stable hypertension (2.14 ± 0.51 MPa vs. 1.10 ± 0.24 MPa, < 0.001) but decreased under unstable hypertension (0.52 ± 0.14 MPa, < 0.001) in the axial direction. Similar trends were observed circumferentially. Energy loss was highest under unstable hypertension (0.16 ± 0.03 vs. 0.08 ± 0.03, < 0.001). Peeling force was significantly reduced under stable hypertension (81.69 ± 12.72 N/m vs. 111.10 ± 27.65 N/m, < 0.001) and further under unstable hypertension (71.37 ± 16.13 N/m, < 0.001).

CONCLUSIONS

Stable and unstable hypertension significantly impair the biomechanical properties of the aortic wall, with unstable hypertension leading to greater damage. Hypertensive patients are recommended to strictly follow medical advice to control blood pressure to avoid a higher risk of TBAD due to improper blood pressure management.

摘要

目的

高血压是B型主动脉夹层(TBAD)的主要危险因素,然而许多患者并未持续有效地管理或控制高血压,导致血压处于稳定或不稳定状态。目前,稳定型和不稳定型高血压对主动脉生物力学特性的影响尚不清楚。本研究旨在确定一种代表TBAD发生风险更高的血压状态。

方法

共183个样本(108个轴向样本和75个周向样本)被分为三组。分别进行疲劳拉伸试验以模拟正常血压、稳定型高血压和不稳定型高血压状态。进行单轴拉伸试验,评估弹性模量、能量损失和剥离力,以评价生物力学特性。

结果

与正常血压相比,在轴向方向上,稳定型高血压(0.05±0.02兆帕 vs. 0.11±0.03兆帕,P<0.001)和不稳定型高血压(0.08±0.02兆帕,P = 0.008)状态下弹性纤维模量降低,而稳定型高血压状态下胶原纤维增加(2.14±0.51兆帕 vs. 1.10±0.24兆帕,P<0.001),不稳定型高血压状态下胶原纤维减少(0.52±0.14兆帕,P<0.001)。周向方向观察到类似趋势。不稳定型高血压状态下能量损失最高(0.16±0.03 vs. 0.08±0.03,P<0.001)。稳定型高血压状态下剥离力显著降低(81.69±12.72牛/米 vs. 111.10±27.65牛/米,P<0.001),不稳定型高血压状态下进一步降低(71.37±16.13牛/米,P<0.001)。

结论

稳定型和不稳定型高血压均显著损害主动脉壁的生物力学特性,不稳定型高血压造成的损害更大。建议高血压患者严格遵循医嘱控制血压,以避免因血压管理不当而导致TBAD风险升高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/5fd8a333adc4/biomedicines-12-02246-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/157b1a162fe3/biomedicines-12-02246-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/277db4d33605/biomedicines-12-02246-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/324df30f5ec9/biomedicines-12-02246-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/5fd8a333adc4/biomedicines-12-02246-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/157b1a162fe3/biomedicines-12-02246-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/277db4d33605/biomedicines-12-02246-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/324df30f5ec9/biomedicines-12-02246-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a50/11504259/5fd8a333adc4/biomedicines-12-02246-g004.jpg

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本文引用的文献

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