Marimuthu Sathish Kumar, Luraghi Giulia, Maclean Craig, Brodie Robbie, Migliavacca Francesco, McGinty Sean, Hill Nicholas A
School of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8QQ, UK.
Computational Biomechanics Laboratory - LaBS, Department of Chemistry, Materials and Chemical Engineering 'Giulio Natta', Politecnico di Milano, Piazza L. da Vinci 32, 20133, Milan, Italy.
Biomech Model Mechanobiol. 2025 Oct;24(5):1767-1780. doi: 10.1007/s10237-025-01991-2. Epub 2025 Jul 31.
Aortic dissection is a life-threatening disease with high mortality rates. The degradation of the layers of the aorta wall causes tears, which then propagate further due to high-pressure blood penetrating the vessel wall, creating a false lumen. The intimal flap separating the true and false lumen can either bulge inwards constricting the true lumen's blood flow or bulge outwards leading to catastrophic rupture and internal bleeding. Therefore, to understand the role of critical pressure on tear propagation, a computational study of the initiation and propagation of tears of various sizes and at multiple depths and locations in three-dimensional aortas was conducted. Tears were modelled using the extended finite element method, and the wall of the aortas is an anisotropic hyperelastic material. Blood-pressure-loaded aorta geometries were obtained from the corresponding unloaded geometries using an iterative procedure to match the in vivo geometries. Pressure-driven tear initiation and propagation were studied. Our results show that when the tear surface's normal is perpendicular to the blood flow, the critical pressure required to cause further propagation is higher for the shorter and deeper tears and reduces when the initial tear size increases. When the normal is parallel to the blood flow, the difference in critical pressure with an increase in tear depth is small and is more likely to propagate transversely. Also, the critical pressure decreases with an increase in the diameter of the aorta for all the tear orientations. This study concludes that tear size, depth inside the medial layer and the diameter of the aorta near the tear location are critical parameters in assessing the risk of further propagation.
主动脉夹层是一种死亡率很高的危及生命的疾病。主动脉壁各层的降解会导致撕裂，随后由于高压血液穿透血管壁，撕裂会进一步扩展，形成假腔。分隔真腔和假腔的内膜瓣可能向内凸出，限制真腔的血流，或者向外凸出，导致灾难性的破裂和内出血。因此，为了了解临界压力对撕裂扩展的作用，对三维主动脉中不同大小、多个深度和位置的撕裂的起始和扩展进行了计算研究。使用扩展有限元方法对撕裂进行建模，主动脉壁是一种各向异性的超弹性材料。通过迭代过程从相应的无负载几何形状中获取血压加载的主动脉几何形状，以匹配体内几何形状。研究了压力驱动的撕裂起始和扩展。我们的结果表明，当撕裂表面的法线垂直于血流时，较短和较深的撕裂导致进一步扩展所需的临界压力较高，并且随着初始撕裂尺寸的增加而降低。当法线平行于血流时，临界压力随撕裂深度增加的差异较小，并且更有可能横向扩展。此外，对于所有撕裂方向，临界压力都随着主动脉直径的增加而降低。本研究得出结论，撕裂尺寸、中层内部深度以及撕裂位置附近主动脉的直径是评估进一步扩展风险的关键参数。
