Department of Applied Mathematics and Theoretical Physics, University of Cambridge, Cambridge, United Kingdom.
Barts Heart Centre, Barts Health NHS Trust, London, United Kingdom.
PLoS Comput Biol. 2023 Oct 18;19(10):e1011479. doi: 10.1371/journal.pcbi.1011479. eCollection 2023 Oct.
Spatial patterns of elevated wall shear stress and pressure due to blood flow past aortic stenosis (AS) are studied using GPU-accelerated patient-specific computational fluid dynamics. Three cases of moderate to severe AS, one with a dilated ascending aorta and two within the normal range (root diameter less than 4cm) are simulated for physiological waveforms obtained from echocardiography. The computational framework is built based on sharp-interface Immersed Boundary Method, where aortic geometries segmented from CT angiograms are integrated into a high-order incompressible Navier-Stokes solver. The key question addressed here is, given the presence of turbulence due to AS which increases wall shear stress (WSS) levels, why some AS patients undergo much less aortic dilation. Recent case studies of AS have linked the existence of an elevated WSS hotspot (due to impingement of AS on the aortic wall) to the dilation process. Herein we further investigate the WSS distribution for cases with and without dilation to understand the possible hemodynamics which may impact the dilation process. We show that the spatial distribution of elevated WSS is significantly more focused for the case with dilation than those without dilation. We further show that this focal area accommodates a persistent pocket of high pressure, which may have contributed to the dilation process through an increased wall-normal forcing. The cases without dilation, on the contrary, showed a rather oscillatory pressure behaviour, with no persistent pressure "buildup" effect. We further argue that a more proximal branching of the aortic arch could explain the lack of a focal area of elevated WSS and pressure, because it interferes with the impingement process due to fluid suction effects. These phenomena are further illustrated using an idealized aortic geometry. We finally show that a restored inflow eliminates the focal area of elevated WSS and pressure zone from the ascending aorta.
利用 GPU 加速的患者特定计算流体动力学研究了血流通过主动脉瓣狭窄 (AS) 时升高的壁切应力和压力的空间模式。模拟了三个中度至重度 AS 病例，一个升主动脉扩张，两个在正常范围内（根部直径小于 4cm），使用从超声心动图获得的生理波形。计算框架基于 sharp-interface Immersed Boundary Method 构建，其中从 CT 血管造影术分割的主动脉几何形状被集成到高阶不可压缩 Navier-Stokes 求解器中。这里要解决的关键问题是，由于 AS 引起的湍流增加了壁切应力 (WSS) 水平，为什么有些 AS 患者的主动脉扩张程度较小。最近对 AS 的病例研究将存在升高的 WSS 热点（由于 AS 对主动脉壁的冲击）与扩张过程联系起来。在这里，我们进一步研究了有扩张和无扩张的病例的 WSS 分布，以了解可能影响扩张过程的可能血流动力学。我们表明，对于扩张的病例，升高的 WSS 分布明显比没有扩张的病例更加集中。我们进一步表明，这个焦点区域容纳了一个持续的高压口袋，这可能通过增加壁向力促进了扩张过程。相反，没有扩张的病例表现出相当振荡的压力行为，没有持续的压力“积累”效应。我们进一步认为，主动脉弓的更近端分支可以解释缺乏升高的 WSS 和压力的焦点区域，因为它通过流体抽吸效应干扰了冲击过程。这些现象在理想的主动脉几何形状中进一步得到说明。最后，我们表明恢复流入可以消除升主动脉中升高的 WSS 和压力区的焦点区域。
