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覆膜支架治疗主动脉弓极度缩窄所致假性动脉瘤的血流动力学

Hemodynamics in the treatment of pseudoaneurysm caused by extreme constriction of aortic arch with coated stent.

作者信息

Li Lanlan, Wang Yiwei, Jin Ping, Yang Tingting, Zhu Guangyu, Li Yuxi, Tang Jiayou, Liu Yang, Yang Jian

机构信息

Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi, China.

School of Energy and Power Engineering, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

Front Cardiovasc Med. 2024 Aug 20;11:1363230. doi: 10.3389/fcvm.2024.1363230. eCollection 2024.

DOI:10.3389/fcvm.2024.1363230
PMID:39228660
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11368758/
Abstract

OBJECTIVES

To evaluate the changes in distal vascular morphology and hemodynamics in patients with extremely severe aortic coarctation (CoA) after covered palliative (CP) stent dilation with different surgical strategies.

MATERIALS AND METHODS

Perioperative computed tomography angiography and digital subtraction angiography were utilized to construct three aortic models with varying stenosis rates and one follow-up model in a patient with extremely severe CoA. The models included: an idealized non-stenosed model (A: 0%), a model post initial stent deployment (B: 28%), a model post balloon expansion (C: 39%), and a model 18 months after post-balloon expansion (D: 39%). Consistent boundary conditions were applied to all models, and hemodynamic simulation was conducted using the pure fluid method.

RESULTS

The narrowest and distal diameter of the stent increased by 34.71% and 59.29%, respectively, from model B to C. Additionally, the distal diameter of the stent increased by -13.80% and +43.68% compared to the descending aorta diameter, respectively. Furthermore, the ellipticity of the maximum cross-section of the aneurysm region in model A to D continued to increase. The oscillatory shear index at the stenosis to the region of the aneurysm were found to be higher in Models A and B, and lower in Models C and D. At the moment of maximum flow velocity, the blood flow distribution in models A and B was more uniform in the widest section of the blood vessels at the distal end of the stenosis, whereas models C and D exhibited disturbed blood flow with more than 2 eddy currents. The time-averaged wall shear stress (TAWSS) decreased in the distal and basal aneurysms, while it significantly increased at the step position. The aneurysmal region exhibited an endothelial cell activation potential value lower than 0.4 Pa.

CONCLUSION

In patients with extremely severe CoA, it is crucial to ensure that the expanded diameter at both ends of the CP stent does not exceed the native vascular diameter during deployment. Our simulation results demonstrate that overdilation leads to a decrease in the TAWSS above the injured vessel, creating an abnormal hemodynamic environment that may contribute to the development and enlargement of false aneurysms in the early postoperative period.

CLINICAL TRIAL REGISTRATION

ClinicalTrials.gov, (NCT02917980).

摘要

目的

评估采用不同手术策略进行覆膜姑息性(CP)支架扩张术后,极重度主动脉缩窄(CoA)患者远端血管形态和血流动力学的变化。

材料与方法

利用围手术期计算机断层扫描血管造影和数字减影血管造影,为一名极重度CoA患者构建了三个不同狭窄率的主动脉模型和一个随访模型。这些模型包括:理想化的无狭窄模型(A:0%)、初次支架置入后模型(B:28%)、球囊扩张后模型(C:39%)以及球囊扩张后18个月模型(D:39%)。对所有模型应用一致的边界条件,并采用纯流体方法进行血流动力学模拟。

结果

从模型B到模型C,支架最窄处和远端直径分别增加了34.71%和59.29%。此外,与降主动脉直径相比,支架远端直径分别增加了 -13.80%和 +43.68%。此外,模型A到D中动脉瘤区域最大横截面的椭圆率持续增加。在模型A和B中,狭窄部位至动脉瘤区域的振荡剪切指数较高,而在模型C和D中较低。在最大流速时刻,模型A和B中狭窄远端血管最宽处的血流分布在血管最宽处更均匀,而模型C和D表现出血流紊乱,有超过2个涡流。时间平均壁面剪切应力(TAWSS)在远端和基底动脉瘤处降低,而在台阶位置显著增加。动脉瘤区域的内皮细胞激活电位值低于0.4 Pa。

结论

对于极重度CoA患者,在置入CP支架时确保两端扩张直径不超过天然血管直径至关重要。我们的模拟结果表明,过度扩张会导致损伤血管上方的TAWSS降低,产生异常的血流动力学环境,这可能在术后早期促进假性动脉瘤的形成和扩大。

临床试验注册

ClinicalTrials.gov,(NCT02917980)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/2989995307d8/fcvm-11-1363230-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/e1ee65d52761/fcvm-11-1363230-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/145a3c04518a/fcvm-11-1363230-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/5c02572179a8/fcvm-11-1363230-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/81abf634ecf8/fcvm-11-1363230-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/2989995307d8/fcvm-11-1363230-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/e1ee65d52761/fcvm-11-1363230-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/145a3c04518a/fcvm-11-1363230-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/831c5e5416c8/fcvm-11-1363230-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/5c02572179a8/fcvm-11-1363230-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/81abf634ecf8/fcvm-11-1363230-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75f9/11368758/2989995307d8/fcvm-11-1363230-g006.jpg

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