Increasing Flow Diversion for Cerebral Aneurysm Treatment Using a Single Flow Diverter

动脉瘤 医学 剪应力 血流动力学 血流 脉动流 生物医学工程 心脏病学 材料科学 外科 复合材料
作者
Jianping Xiang,Ding Ma,Kenneth V. Snyder,Elad I. Levy,Adnan H. Siddiqui,Hui Meng
出处
期刊:Neurosurgery [Lippincott Williams & Wilkins]
卷期号:75 (3): 286-294 被引量:52
标识
DOI:10.1227/neu.0000000000000409
摘要

A neurovascular flow diverter (FD), aiming at inducing embolic occlusion of cerebral aneurysms through hemodynamic changes, can produce variable mesh densities owing to its flexible mesh structure.To explore whether the hemodynamic outcome would differ by increasing FD local compaction across the aneurysm orifice.We investigated deployment of a single FD using 2 clinical strategies: no compaction (the standard method) and maximum compaction across the aneurysm orifice (an emerging strategy). Using an advanced modeling technique, we simulated these strategies applied to a patient-specific wide-necked aneurysm model, resulting in a relatively uniform mesh with no compaction (C1) and maximum compaction (C2) at the aneurysm orifice. Pre- and posttreatment aneurysmal hemodynamics were analyzed using pulsatile computational fluid dynamics. Flow-stasis parameters and blood shear stress were calculated to assess the potential for aneurysm embolic occlusion.Flow streamlines, isovelocity, and wall shear stress distributions demonstrated enhanced aneurysmal flow reduction with C2. The average intra-aneurysmal flow velocity was 29% of pretreatment with C2 compared with 67% with C1. Aneurysmal flow turnover time was 237% and 134% of pretreatment for C2 and C1, respectively. Vortex core lines and oscillatory shear index distributions indicated that C2 decreased the aneurysmal flow complexity more than C1. Ultrahigh blood shear stress was observed near FD struts in inflow region for both C1 and C2.The emerging strategy of maximum FD compaction can double aneurysmal flow reduction, thereby accelerating aneurysm occlusion. Moreover, ultrahigh blood shear stress was observed through FD pores, which could potentially activate platelets as an additional aneurysmal thrombosis mechanism.

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