An arterial dissection is a longitudinal tear in the vessel wall, which can create a false lumen for blood flow and may propagate quickly, leading to death. We employ a computational model for a dissection using the extended finite element method with a cohesive traction-separation law for the tear faces. The arterial wall is described by the anisotropic hyperelastic Holzapfel–Gasser–Ogden material model that accounts for collagen fibres and ground matrix, while the evolution of damage is governed by a linear cohesive traction-separation law. We simulate propagation in both peeling and pressure-loading tests. For peeling tests, we consider strips and discs cut from the arterial wall. Propagation is found to occur preferentially along the material axes with the greatest stiffness, which are determined by the fibre orientation. In the case of pressure-driven propagation, we examine a cylindrical model, with an initial tear in the shape of an arc. Long and shallow dissections lead to buckling of the inner wall between the true lumen and the dissection. The various buckling configurations closely match those seen in clinical CT scans. Our results also indicate that a deeper tear is more likely to propagate.

中文翻译：

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模拟剥离和压力驱动的动脉夹层传播

动脉夹层是血管壁的纵向撕裂，它可以为血流创造假腔，并可能迅速传播，导致死亡。我们使用扩展有限元方法对撕裂面采用内聚牵引分离定律进行解剖计算模型。动脉壁由各向异性超弹性 Holzapfel-Gasser-Ogden 材料模型描述，该模型考虑了胶原纤维和地面基质，而损伤的演变由线性内聚牵引-分离定律控制。我们在剥离和压力加载测试中模拟传播。对于剥离测试，我们考虑从动脉壁切下的条带和盘。发现传播优先沿具有最大刚度的材料轴发生，这由纤维取向决定。在压力驱动传播的情况下，我们检查圆柱形模型，初始撕裂呈弧形。长而浅的夹层导致真腔和夹层之间的内壁屈曲。各种屈曲配置与临床 CT 扫描中看到的非常匹配。我们的结果还表明，更深的撕裂更有可能传播。