Cebral Juan R, Mut Fernando, Löhner Rainald, Marsh Laurel, Chitsaz Alireza, Bilgin Cem, Bayraktar Esref, Kallmes David, Kadirvel Ramanathan
Bioengineering Department, George Mason University, Fairfax, Virginia, USA.
Physics Department, George Mason University, Fairfax, Virginia, USA.
Int J Numer Method Biomed Eng. 2025 Jan;41(1):e3904. doi: 10.1002/cnm.3904.
As the number of cerebral aneurysms treated with flow diverters continues to increase, it is important to understand what factors influence not only thrombus formation within the aneurysm cavity but also fibrin accumulation across the device and its associated disruption and blockage of the inflow stream. Both processes contribute to the eventual occlusion of the aneurysm or its continued patency and incomplete occlusion which may require future re-treatment. To investigate fibrin accumulation on flow diverters placed across the neck of cerebral aneurysms, a previously developed computational model that couples flow and fibrin dynamics is used in combination with experimental in vitro models of cerebral aneurysms treated with flow diverters. Fibrin accumulation was previously investigated in four glass models of cerebral aneurysms with varying parent artery geometries placed in a flow loop at different flow rates. Corresponding computational models were constructed and compared with the experimental findings. The computational model based on fibrin production stimulated from flow shear stress and subsequent adhesion to device wires was able to reproduce and explain the fibrin accumulation patterns observed in the experimental aneurysms treated with flow diverters. Specifically, these models indicated that increasing vessel curvature, flow rate, and thrombin concentration induced faster fibrin accumulation and associated aneurysm inflow disruption and blockage. The models described and tested in this paper are valuable to understand the detailed mechanisms leading to aneurysm occlusion and healing or incomplete occlusions after treatment with flow diverting devices.
随着采用血流导向装置治疗的脑动脉瘤数量不断增加,了解哪些因素不仅影响动脉瘤腔内血栓形成,还影响纤维蛋白在装置上的积聚及其对流入血流的相关破坏和阻塞,这很重要。这两个过程都有助于动脉瘤最终闭塞或持续通畅以及不完全闭塞,而不完全闭塞可能需要未来再次治疗。为了研究放置在脑动脉瘤颈部的血流导向装置上的纤维蛋白积聚情况,将先前开发的耦合血流和纤维蛋白动力学的计算模型与血流导向装置治疗的脑动脉瘤体外实验模型相结合使用。先前在四个玻璃材质的脑动脉瘤模型中进行了纤维蛋白积聚研究,这些模型具有不同的母动脉几何形状,并以不同流速放置在血流循环中。构建了相应的计算模型,并与实验结果进行比较。基于血流剪切应力刺激产生纤维蛋白并随后附着于装置金属丝的计算模型,能够重现并解释在接受血流导向装置治疗的实验性动脉瘤中观察到的纤维蛋白积聚模式。具体而言,这些模型表明,增加血管曲率、流速和凝血酶浓度会导致更快的纤维蛋白积聚以及相关的动脉瘤流入破坏和阻塞。本文描述和测试的模型对于理解使用血流导向装置治疗后导致动脉瘤闭塞、愈合或不完全闭塞的详细机制很有价值。