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Modelling peeling- and pressure-driven propagation of arterial dissection

机译:模拟剥离和压力驱动的动脉夹层传播

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摘要

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.
机译:动脉夹层是血管壁的纵向撕裂,可形成虚假的内腔供血流,并可能迅速传播,导致死亡。我们使用一个扩展的有限元方法对泪液面采用凝聚力-分离-分离定律的解剖模型。各向异性的超弹性Holzapfel–Gasser–Ogden材料模型描述了动脉壁,该模型解释了胶原纤维和地面基质,而损伤的演化则受线性内聚牵引力-分离定律的控制。我们在剥离测试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圆盘。发现传播优先发生在具有最大刚度的材料轴上,该刚度由纤维方向决定。在压力驱动传播的情况下,我们检查一个圆柱模型,其初始撕裂为弧形。长而浅的夹层会导致内腔在真管腔和夹层之间弯曲。各种屈曲结构与临床CT扫描中看到的结构紧密匹配。我们的结果还表明,更深的眼泪更可能传播。

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