双撕裂破裂前后非牛顿流体血液对腹主动脉的血流动力学效应

IF 1.7 4区 医学 Q3 ENGINEERING, BIOMEDICAL
Yiwen Wang , Changli Zhou , Xuefeng Wu , Lijia Liu , Li Deng
{"title":"双撕裂破裂前后非牛顿流体血液对腹主动脉的血流动力学效应","authors":"Yiwen Wang ,&nbsp;Changli Zhou ,&nbsp;Xuefeng Wu ,&nbsp;Lijia Liu ,&nbsp;Li Deng","doi":"10.1016/j.medengphy.2024.104205","DOIUrl":null,"url":null,"abstract":"<div><h3>Objectives</h3><p>Intimal tears caused by aortic dissection can weaken the arterial wall and lead to aortic aneurysms. However, the effect of different tear states on the blood flow behaviour remains complex. This study uses a novel approach that combines numerical haemodynamic simulation with in vitro experiments to elucidate the effect of arterial dissection rupture on the complex blood flow state within the abdominal aneurysm and the endogenous causes of end-organ malperfusion.</p></div><div><h3>Materials and methods</h3><p>Based on the CT imaging data and clinical physiological parameters, the overall arterial models including aortic dissection and aneurysm with single tear and double tear were established, and the turbulence behaviours and haemodynamic characteristics of arterial dissection and aneurysm under different blood pressures were simulated by using non-Newtonian flow fluids with the pulsatile blood flow rate of the clinical patients as a cycle, and the results of the numerical simulation were verified by in vitro simulation experiments.</p></div><div><h3>Results</h3><p>Hemodynamic simulations revealed that the aneurysm and single-tear false lumen generated a maximum pressure of 320.591 mmHg, 267 % over the 120 mmHg criterion. The pressure differential generates reflux, leading to a WSS of 2247.9 Pa at the TL inlet and blood flow velocities of up to 6.41 m/s inducing extend of the inlet. DTD Medium FL instantaneous WP above 120 mmHg Standard 151 % Additionally, there was 82.5 % higher flow in the right iliac aorta than in the left iliac aorta, which triggered malperfusion. Thrombus was accumulated distal to the tear and turbulence. These results are consistent with the findings of the in vitro experiments.</p></div><div><h3>Conclusions</h3><p>This study reveals the haemodynamic mechanisms by which aortic dissection induces aortic aneurysms to produce different risk states. This will contribute to in vitro simulation studies as a new fulcrum in the process of moving from numerical simulation to clinical trials.</p></div>","PeriodicalId":49836,"journal":{"name":"Medical Engineering & Physics","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Haemodynamic effects of non-Newtonian fluid blood on the abdominal aorta before and after double tear rupture\",\"authors\":\"Yiwen Wang ,&nbsp;Changli Zhou ,&nbsp;Xuefeng Wu ,&nbsp;Lijia Liu ,&nbsp;Li Deng\",\"doi\":\"10.1016/j.medengphy.2024.104205\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objectives</h3><p>Intimal tears caused by aortic dissection can weaken the arterial wall and lead to aortic aneurysms. However, the effect of different tear states on the blood flow behaviour remains complex. This study uses a novel approach that combines numerical haemodynamic simulation with in vitro experiments to elucidate the effect of arterial dissection rupture on the complex blood flow state within the abdominal aneurysm and the endogenous causes of end-organ malperfusion.</p></div><div><h3>Materials and methods</h3><p>Based on the CT imaging data and clinical physiological parameters, the overall arterial models including aortic dissection and aneurysm with single tear and double tear were established, and the turbulence behaviours and haemodynamic characteristics of arterial dissection and aneurysm under different blood pressures were simulated by using non-Newtonian flow fluids with the pulsatile blood flow rate of the clinical patients as a cycle, and the results of the numerical simulation were verified by in vitro simulation experiments.</p></div><div><h3>Results</h3><p>Hemodynamic simulations revealed that the aneurysm and single-tear false lumen generated a maximum pressure of 320.591 mmHg, 267 % over the 120 mmHg criterion. The pressure differential generates reflux, leading to a WSS of 2247.9 Pa at the TL inlet and blood flow velocities of up to 6.41 m/s inducing extend of the inlet. DTD Medium FL instantaneous WP above 120 mmHg Standard 151 % Additionally, there was 82.5 % higher flow in the right iliac aorta than in the left iliac aorta, which triggered malperfusion. Thrombus was accumulated distal to the tear and turbulence. These results are consistent with the findings of the in vitro experiments.</p></div><div><h3>Conclusions</h3><p>This study reveals the haemodynamic mechanisms by which aortic dissection induces aortic aneurysms to produce different risk states. This will contribute to in vitro simulation studies as a new fulcrum in the process of moving from numerical simulation to clinical trials.</p></div>\",\"PeriodicalId\":49836,\"journal\":{\"name\":\"Medical Engineering & Physics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-07-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical Engineering & Physics\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1350453324001061\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENGINEERING, BIOMEDICAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Engineering & Physics","FirstCategoryId":"5","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1350453324001061","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
引用次数: 0

摘要

目标主动脉夹层造成的内膜撕裂会削弱动脉壁,导致主动脉瘤。然而,不同撕裂状态对血流行为的影响仍然很复杂。本研究采用数值血流动力学模拟与体外实验相结合的新方法,来阐明动脉夹层破裂对腹部动脉瘤内复杂血流状态的影响,以及造成内脏器官灌注不良的内源性原因。材料与方法根据CT成像数据和临床生理参数,建立了包括主动脉夹层和单撕裂、双撕裂动脉瘤在内的整体动脉模型,并以临床患者的搏动性血流速率为循环,采用非牛顿流体模拟了动脉夹层和动脉瘤在不同血压下的湍流行为和血流动力学特征,并通过体外模拟实验验证了数值模拟的结果。结果血流动力学模拟显示,动脉瘤和单撕裂假腔产生的最大压力为 320.591 mmHg,比 120 mmHg 标准高出 267%。压差产生回流,导致 TL 入口处的 WSS 达到 2247.9 Pa,血流速度高达 6.41 m/s,从而诱导入口扩展。此外,右侧髂主动脉的血流量比左侧髂主动脉高 82.5%,导致灌注不良。血栓在撕裂和湍流远端积聚。结论这项研究揭示了主动脉夹层诱发主动脉瘤产生不同风险状态的血流动力学机制。这将有助于体外模拟研究,成为从数值模拟到临床试验过程中的一个新支点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Haemodynamic effects of non-Newtonian fluid blood on the abdominal aorta before and after double tear rupture

Haemodynamic effects of non-Newtonian fluid blood on the abdominal aorta before and after double tear rupture

Objectives

Intimal tears caused by aortic dissection can weaken the arterial wall and lead to aortic aneurysms. However, the effect of different tear states on the blood flow behaviour remains complex. This study uses a novel approach that combines numerical haemodynamic simulation with in vitro experiments to elucidate the effect of arterial dissection rupture on the complex blood flow state within the abdominal aneurysm and the endogenous causes of end-organ malperfusion.

Materials and methods

Based on the CT imaging data and clinical physiological parameters, the overall arterial models including aortic dissection and aneurysm with single tear and double tear were established, and the turbulence behaviours and haemodynamic characteristics of arterial dissection and aneurysm under different blood pressures were simulated by using non-Newtonian flow fluids with the pulsatile blood flow rate of the clinical patients as a cycle, and the results of the numerical simulation were verified by in vitro simulation experiments.

Results

Hemodynamic simulations revealed that the aneurysm and single-tear false lumen generated a maximum pressure of 320.591 mmHg, 267 % over the 120 mmHg criterion. The pressure differential generates reflux, leading to a WSS of 2247.9 Pa at the TL inlet and blood flow velocities of up to 6.41 m/s inducing extend of the inlet. DTD Medium FL instantaneous WP above 120 mmHg Standard 151 % Additionally, there was 82.5 % higher flow in the right iliac aorta than in the left iliac aorta, which triggered malperfusion. Thrombus was accumulated distal to the tear and turbulence. These results are consistent with the findings of the in vitro experiments.

Conclusions

This study reveals the haemodynamic mechanisms by which aortic dissection induces aortic aneurysms to produce different risk states. This will contribute to in vitro simulation studies as a new fulcrum in the process of moving from numerical simulation to clinical trials.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Medical Engineering & Physics
Medical Engineering & Physics 工程技术-工程:生物医学
CiteScore
4.30
自引率
4.50%
发文量
172
审稿时长
3.0 months
期刊介绍: Medical Engineering & Physics provides a forum for the publication of the latest developments in biomedical engineering, and reflects the essential multidisciplinary nature of the subject. The journal publishes in-depth critical reviews, scientific papers and technical notes. Our focus encompasses the application of the basic principles of physics and engineering to the development of medical devices and technology, with the ultimate aim of producing improvements in the quality of health care.Topics covered include biomechanics, biomaterials, mechanobiology, rehabilitation engineering, biomedical signal processing and medical device development. Medical Engineering & Physics aims to keep both engineers and clinicians abreast of the latest applications of technology to health care.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信