Department of Biomedical Engineering, Yale University, New Haven, CT, USA.
Ann Biomed Eng. 2022 Feb;50(2):183-194. doi: 10.1007/s10439-022-02906-3. Epub 2022 Jan 19.
Computational models of aortic dissection can examine mechanisms by which this potentially lethal condition develops and propagates. We present results from phase-field finite element simulations that are motivated by a classical but seldom repeated experiment. Initial simulations agreed qualitatively and quantitatively with data, yet because of the complexity of the problem it was difficult to discern trends. Simplified analytical models were used to gain further insight. Together, simplified and phase-field models reveal power-law-based relationships between the pressure that initiates an intramural tear and key geometric and mechanical factors-insult surface area, wall stiffness, and tearing energy. The degree of axial stretch and luminal pressure similarly influence the pressure of tearing, which was ~88 kPa for healthy and diseased human aortas having sub-millimeter-sized initial insults, but lower for larger tear sizes. Finally, simulations show that the direction a tear propagates is influenced by focal regions of weakening or strengthening, which can drive the tear towards the lumen (dissection) or adventitia (rupture). Additional data on human aortas having different predisposing disease conditions will be needed to extend these results further, but the present findings show that physiologic pressures can propagate initial medial defects into delaminations that can serve as precursors to dissection.
主动脉夹层的计算模型可以研究这种潜在致命情况发生和传播的机制。我们展示了由经典但很少重复的实验所激发的相场有限元模拟的结果。初步模拟在定性和定量上都与数据一致，但由于问题的复杂性，很难辨别趋势。简化的分析模型被用来获得进一步的见解。简化和相场模型一起揭示了引发壁内撕裂的压力与关键几何和机械因素（损伤表面积、壁刚度和撕裂能）之间的幂律关系。轴向拉伸程度和管腔压力同样会影响撕裂的压力，对于健康和患病的人类主动脉，初始损伤小于亚毫米的情况下，撕裂压力约为 88kPa，但对于较大的撕裂尺寸，压力会降低。最后，模拟表明撕裂的传播方向受到弱化或强化的焦点区域的影响，这可能导致撕裂向管腔（夹层）或外膜（破裂）发展。需要更多关于具有不同易患病况的人类主动脉的数据来进一步扩展这些结果，但目前的发现表明，生理压力可以将初始的中层缺陷传播为可以作为夹层前体的分层。
