Propagation of dissection in a residually-stressed artery model.

This paper studies dissection propagation subject to internal pressure in a residually-stressed two-layer arterial model. The artery is assumed to be infinitely long, and the resultant plane strain problem is solved using the extended finite element method. The arterial layers are modelled using the anisotropic hyperelastic Holzapfel-Gasser-Ogden model, and the tissue damage due to tear propagation is described using a linear cohesive traction-separation law. Residual stress in the arterial wall is determined by an opening angle [Formula: see text] in a stress-free configuration. An initial tear is introduced within the artery which is subject to internal pressure. Quasi-static solutions are computed to determine the critical value of the pressure, at which the dissection starts to propagate. Our model shows that the dissection tends to propagate radially outwards. Interestingly, the critical pressure is higher for both very short and very long tears. The simulations also reveal that the inner wall buckles for longer tears, which is supported by clinical CT scans. In all simulated cases, the critical pressure is found to increase with the opening angle. In other words, residual stress acts to protect the artery against tear propagation. The effect of residual stress is more prominent when a tear is of intermediate length ([Formula: see text]90[Formula: see text] arc length). There is an intricate balance between tear length, wall buckling, fibre orientation, and residual stress that determines the tear propagation.