Background and objective: Post-Stenotic Dilatation (PSD), the common complication of coarctation of the aorta (COA), is a progressive disease involving aortic aneurysm and even rupture. However, there has been no definitive method that could investigate the mechanism of PSD formation, progression and rupture. The purpose of the present work is to analyze the mechanism behind PSD formation and to further assess the risk of COA patients with different coarctation degrees deteriorating into PSD.

Method: Three-dimensional non-Newtonian (Carreau-Yasuda) hemodynamic simulations are performed throughout the cardiac cycle, and a novel parameter ($\overline{{\lambda }_{ci}}$ intensity) is proposed to evaluate the intensity of vortices within the aorta. The PSD geometry is reconstructed from Computed Tomography scans. To analyze the formation mechanism and occurrence possibility of PSD, the computer technology is utilized to restore the expansive and/or narrow regions to obtain its previous state (COA) and control group (Normal), and to modify the minimum diameter to obtain the aortas with different coarctation degrees. The clinical cases of pre- and post-operation are further introduced to verify the analysis.

Results: Compared with the Normal, the vortical structures with higher swirling strength are generated and accumulated at the downstream of the coarctation segment after COA occurrence, and partially disappear in the wake of PSD formation. The sequence of $\overline{{\lambda }_{ci}}$ intensity is COA > PSD > Normal and pre-operation > post-operation. With increasing the degree of coarctation, the $\overline{{\lambda }_{ci}}$ intensity is higher and the jet-flow becomes more drastic.

Conclusions: The formation of PSD is caused by the vortical structures with higher swirling strength accumulating at the downstream of the coarctation segment. An increase in coarctation degree elevates the risk of PSD occurrence and even aneurysmal dilatation.

背景与目的：狭窄后扩张（PSD）是主动脉缩窄（COA）的常见并发症，是一种进行性疾病，涉及主动脉瘤甚至破裂。但是，还没有确定的方法可以研究PSD形成，进展和破裂的机制。本工作的目的是分析PSD形成的机制，并进一步评估具有不同缩窄度的COS患者恶化为PSD的风险。

方法：在整个心动周期进行三维非牛顿（Carreau-Yasuda）血流动力学模拟，并建立一个新的参数（$\overline{{\lambda }_{C\mathrm{一世}}}$强度）被提出来评估主动脉内旋涡的强度。PSD几何结构是从计算机断层扫描扫描重建的。为了分析PSD的形成机理和发生可能性，利用计算机技术恢复了扩张和/或狭窄区域以获得其先前状态（COA）和对照组（正常），并修改了最小直径以获得主动脉具有不同的缩合度。进一步介绍了手术前后的临床病例，以验证分析结果。

结果：与正常相比，COA发生后，在旋流段的下游产生并积累了涡旋强度更高的旋涡结构，并在PSD形成后部分消失。的顺序$\overline{{\lambda }_{C\mathrm{一世}}}$强度为COA> PSD>正常和术前>术后。随着紧缩程度的增加，$\overline{{\lambda }_{C\mathrm{一世}}}$ 强度越高，射流越剧烈。

结论：PSD的形成是由于旋涡强度较高的旋涡结构聚集在缩窄段的下游。缩窄程度的增加会增加PSD发生甚至动脉瘤扩张的风险。