论文标题

主动脉狭窄患者的壁剪应力和压力模式,有或没有主动脉膨胀,由高性能基于图像的计算流体动力学捕获

Wall shear stress and pressure patterns in aortic stenosis patients with and without aortic dilation captured by high-performance image-based computational fluid dynamics

论文作者

Zolfaghari, Hadi, Andiapen, Mervyn, Baumbach, Andreas, Mathur, Anthony, Kerswell, Rich R.

论文摘要

使用GPU加速的患者特定的计算流体动力学研究了较高的壁剪应力和由于血流经过的血流而引起的空间模式。三种中度AS的病例,一种在正常范围内的升主动脉扩张(根直径小于4厘米)的病例,用于从超声心动图数据中获得的生理节拍周期波形。计算框架是基于尖锐的接口浸入边界方法构建的,其中从CT血管造影分段的主动脉几何形状集成到高阶不可压缩的Navier-Stokes求解器中。我们表明,即使壁剪应力升高并且由于所有情况上升主动脉的湍流而引起的振荡,但其空间分布比没有扩张的情况更为专注于膨胀。该焦点区域与主动脉外主动脉外曲率上的主动脉瓣射流撞击有关,并使用主动脉瓣膨胀患者的4D流动MRI在体内显示(van ooij et al。,J。Am。心脏协会,6(9),2017年,2017年)。我们表明,这个焦点区域还容纳了持续的高压袋,这很可能通过增加的壁正常强迫来促进扩张过程。相反,没有扩张的情况显示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,主动脉弓的近端分支可以解释缺乏较高的壁剪应力和压力的焦点区域,因为它会由于流体吸力效应而干扰撞击过程。使用理想化的主动脉几何形状进一步说明了这些现象。我们最终表明,恢复的流入条件消除了升高主动脉的壁剪应力和压力区域的焦点区域。

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 AS, one with a dilated ascending aorta and two within the normal range (root diameter less than 4cm) are simulated for physiological beat cycle waveforms obtained from echocardiography data. 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. We show that even though the wall shear stress is elevated and oscillatory due to turbulence in the ascending aorta for all the cases, its spatial distribution is significantly more focused for the case with dilation than those without dilation. This focal area is linked to aortic valve jet impingement on the outer curvature of the ascending aorta, and has been shown in vivo using 4D flow MRI of aortic stenosis patients with aortic dilation (van Ooij et al., J. Am. Heart Assoc., 6(9), 2017). We show that this focal area also accommodates a persistent pocket of high pressure, which is likely to 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 wall shear stress 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 condition eliminates the focal area of elevated wall shear stress and pressure zone from the ascending aorta.

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