Search

In the first part of this study we develop a realistic subject-specific aorta finite element model derived from a dual-venc MRI scan. We investigate if spontaneous dissection will occur under extreme hypertensive lumen blood pressure loading, or if significant reduction in interface strength must occur in order for dissection to initiate. Importantly, we also demonstrate that dissection initiation is a pure mode II fracture process, rather than a mixed mode or mode I process. In the second part of this study we construct a parameterised idealised aorta model in order to assess the relative contribution for several anatomical and physiological factors to dissection risk. Such parametric analyses provide fundamental insight into the mechanics of stress localisation and delamination in the aorta. Overall, our detailed series of simulations suggest that variations in anatomical features and hypertensive loading will not result in a sufficient elevation of the stress state in the aorta wall to initiate dissection. Our results suggest that initiation of aortic dissection requires a significant reduction in the mode II fracture strength of the aortic wall, suggesting that dissection is preceded by structural and biomechanical remodelling.

Advancement of subject-specific in-silico medicine requires new imaging protocols tailored to specific anatomical features, paired with new constitutive model development based on structure/function relationships. In this study we develop a new dual-VENC 4D Flow MRI protocol that provides unprecedented spatial and temporal resolution of in-vivo aortic deformation. All previous dual-VENC 4D Flow MRI studies in the literature focus on an isolated segment of the aorta, which fail to capture the full spectrum of aortic heterogeneity that exists along the vessel length. The imaging protocol developed provides high sensitivity to all blood flow velocities throughout the entire cardiac cycle, overcoming the challenge of accurately measuring the highly unsteady non-uniform flow field in the aorta. Cross sectional area change, volumetric flow rate, and compliance are observed to decrease with distance from the heart, while pulse wave velocity is observed to increase. A non-linear aortic lumen pressure-area relationship is observed throughout the aorta, such that a high vessel compliance occurs during diastole, and a low vessel compliance occurs during systole. This suggests that a single value of compliance may not accurately represent vessel behaviour during a cardiac cycle in-vivo. This high-resolution MRI data provides key information on the spatial variation in non-linear aortic compliance which can significantly advance the state-of-the-art of in-silico diagnostic techniques for the human aorta.

This paper, the second of two parts, presents a novel subject-specific in-silico framework in which we uncover the relationship between the spatially varying constituents of the aorta and the non-linear compliance of the vessel during the cardiac cycle uncovered in Part I. In Part II a novel microstructurally motivated constitutive model is developed, and simulations reveal that internal vessel contractility, due to pre-stretched elastin and actively generated smooth muscle stress, must be incorporated, along with collagen strain stiffening, in order to accurately predict the non-linear pressure-area relationship observed in-vivo. Modelling of elastin and smooth muscle contractility allows for the identification of the reference vessel configuration at zero-lumen pressure, in addition to accurately predicting high- and low-compliance regimes under a physiological range of pressures. This modelling approach is also shown to capture the key features of elastin and SMC knockout experiments. The volume fractions of the constituent components of the aortic material model were computed so that the in-silico pressure-area curves accurately predict the corresponding MRI data at each location. Simulations reveal that collagen and smooth muscle volume fractions increase distally, while elastin volume fraction decreases distally, consistent with reported histological data. Furthermore, the strain at which collagen transitions from low to high stiffness is lower in the abdominal aorta, again supporting the histological finding that collagen waviness is lower in this distally. The analyses presented in this paper provides new insights into the heterogeneous structure-function relationship that underlies aortic biomechanics. This novel subject-specific MRI/FEA methodology provides a foundation for personalised in-silico clinical analysis and tailored aortic device development.