| description abstract | Abstract. The early development of aortic dissections (AD) is manifested by tear propagation. The direction and extent of tear propagation are important for surgical strategy selection and outcomes, yet the mechanism underlying early tear propagation is largely unknown. Interface damage, leading to in-plane propagation, is modeled using the cohesive zone method. Bulk material damage, causing transmural propagation, is modeled using a strain-energy-based damage criterion. The influences of geometrical parameters are examined with a double-layer finite-element model of a three-dimensional (3D) idealized aorta. With blood pressure in the true lumen fixed at a physiological value, new findings are: Critical pressures for in-plane tear propagation are well within the physiological blood pressure. Initially, in-plane propagation is more likely to propagate as the tear size increases. However, critical pressures increase when reaching geometrical thresholds of the tear. The opening mode (Mode-I) is the leading fracture mode for in-plane propagation. For transmural propagation, three representative locations are identified, and critical pressures drop monotonically with increasing tear size. In-plane propagation is more likely to occur than transmural propagation in the parameter space studied. However, as blood pressure in the true lumen increases, critical pressures for in-plane propagation increase rapidly and transmural propagation prevails. This study successfully integrates interface damage and bulk material damage methods to model tear propagations, identifying possible mechanisms behind dissection progression. The findings can help predict the outcomes of early development of aortic dissections and assist with treatment and management. | |
