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颅内动脉瘤血流导向装置上纤维蛋白积聚的建模

Modeling Fibrin Accumulation on Flow-Diverting Devices for Intracranial Aneurysms.

作者信息

Cebral Juan R, Mut Fernando, Löhner Rainald, Marsh Laurel, Chitsaz Alireza, Bilgin Cem, Bayraktar Esref, Kallmes David, Kadirvel Ramanathan

机构信息

Bioengineering Department, George Mason University, Fairfax, Virginia, USA.

Physics Department, George Mason University, Fairfax, Virginia, USA.

出版信息

Int J Numer Method Biomed Eng. 2024 Dec;40(12):e3883. doi: 10.1002/cnm.3883. Epub 2024 Nov 5.

Abstract

The mechanisms leading to aneurysm occlusion after treatment with flow-diverting devices are not fully understood. Flow modification induces thrombus formation within the aneurysm cavity, but fibrin can simultaneously accumulate and cover the device scaffold, leading to further flow modification. However, the interplay and relative importance of these processes are not clearly understood. A computational model of fibrin accumulation and flow modification after flow diversion treatment of cerebral aneurysms has been developed under the guidance of in vitro experiments and observations. The model is based on the loose coupling of flow and transport-reaction equations that are solved separately by independent codes. Interaction or reactive terms account for thrombin production from prothrombin stimulated by thrombogenic metallic wires and inhibition by antithrombin as well as fibrin production from fibrinogen stimulated by thrombin and flow shear stress, and fibrin adhesion to device wires and already attached fibrin. The computational model was demonstrated and tested on idealized vessel and aneurysm geometries. The model was able to reproduce the salient features of fibrin accumulation after the deployment of flow-diverting devices in idealized in vitro models of cerebral aneurysms. Namely, fibrin production in regions of high shear stress, initial accumulation at the inflow zone, and progressive occlusion of the device and corresponding flow attenuation. The computational model linking flow dynamics to fibrin production, transport, and adhesion can be used to investigate and better understand the effects that lead to fibrin accumulation and the resulting aneurysm inflow reduction and intra-aneurysmal flow modulation.

摘要

血流导向装置治疗后导致动脉瘤闭塞的机制尚未完全明确。血流改变会诱导动脉瘤腔内血栓形成,但纤维蛋白同时会积聚并覆盖装置支架,从而导致进一步的血流改变。然而,这些过程之间的相互作用及其相对重要性尚不清楚。在体外实验和观察的指导下,已经建立了一个脑动脉瘤血流导向治疗后纤维蛋白积聚和血流改变的计算模型。该模型基于血流与传输 - 反应方程的松散耦合,这些方程由独立的代码分别求解。相互作用项或反应项考虑了由促血栓形成的金属丝刺激凝血酶原产生凝血酶,以及抗凝血酶的抑制作用,还有凝血酶和血流剪切应力刺激纤维蛋白原产生纤维蛋白,以及纤维蛋白与装置金属丝和已附着纤维蛋白的黏附。该计算模型在理想化的血管和动脉瘤几何形状上进行了演示和测试。该模型能够在理想化的脑动脉瘤体外模型中重现血流导向装置植入后纤维蛋白积聚的显著特征。即,在高剪切应力区域产生纤维蛋白,在流入区域初始积聚,以及装置的逐渐闭塞和相应的血流衰减。将血流动力学与纤维蛋白产生、传输和黏附联系起来的计算模型可用于研究并更好地理解导致纤维蛋白积聚以及由此引起的动脉瘤流入减少和动脉瘤内血流调节的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2db/11618230/6e356049b595/CNM-40-e3883-g003.jpg

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