## 3 Results
### Biomechanical Behaviour of Healthy and Diseased Aortas
#### 3.4.3 Aortic Dissection  
The real pathogenesis of AD is still an open debate. Several numerical models provided great contributions towards a better understanding of the main contributors to the development and progression of AD. [PERSON] et al. [82] evidenced that AD induced abnormal haemodynamics with the presence of recirculation zones both in True Lumen (TL) and False Lumen (FL). Geometrical features were also identified as a primary cause of disturbed haemodynamics. [PERSON] et al. [37] focused on studying the underlying haemodynamics responsible for the longitudinal propagation of AD by developing CFD models with pulsatile flow conditions. Tear (entry point towards the FL ) size and location impacted the FL blood flow patterns. The transmural pressure gradient, specifically in the circumferential direction, was suggested as one of the mechanisms responsible for the cleavage of lamellar units. Abnormal WSS distributions were proposed as the main cause of intimal tear initiation, justified by the elevated values of Time-Averaged Wall Shear Stress (TAWSS) found near the tear. [PERSON] et al. [83] studied the influence of anatomical risk factors in 14 idealised models of AD (tear size and location, number of entries and FL location). Evidence pointed out that FL increases flow resistance and revealed significant differences in the haemodynamics between the TL and FL. These differences diminish with the increase in the tear size. [PERSON] et al. [26] also assessed the influence of tear location on haemodynamics with CFD simulations on patient-specific geometric models. Their results proved that aortic root proximity induces more turbulence in the FL. Pressure and WSS distributions seem to be well correlated with tear location since the tear usually occurred in regions where these quantities presented higher magnitude. [PERSON] et al. [64] also investigated the haemodynamics of pulsatile flow on AD. Their results suggested that a high WSS gradient between TL and FL acts as the main contributor to layer delamination and consequent AD progression and that high vorticity may be associated with intimal tear initiation and growth. [PERSON] et al. [45] investigated the most influential factors in AD propagation. CSM simulations on idealised models with two uniform thickened layers (media and adventia layers) were accomplished. Failure criteria based on Hashin failure theory, hyperelastic anisotropic constitutive models and residual and prestresses were considered. The authors postulated that initial tearing is correlated with tissue fatigue and that tissue ultimate tensile stress can be achieved during intense workouts (e.g., weight lifting). Media layer strength appeared as a fundamental factor in AD propagation and the shear fracture was identified as a key process in delamination. [PERSON] et al. [84] published a comprehensive overview on the topic of AD numerical modelling with a focus on the biomechanical factors leading to the initial tear.  
Besides the study of the effects of AD in the haemodynamics, the interaction between the blood flow and tear is also important as it may provide further insight into the mechanisms that induce the development of AD. [PERSON] et al. [85] applied FSI simulations to study this interaction in an idealised aortic model that included the TL and FL was applied. The haemodynamic parameters at the TL and FL tend to homogeneity as the FL increase in size. Smaller FL presents lower velocities and may be stagnant. Moreover, stress analysis around the flap evidenced an elevated concentration of stress, which may lead to AD progression.