Through mechanobiological control of the extracellular matrix, and hence local stiffness, smooth muscle cells of the media and fibroblasts of the adventitia play important roles in arterial homeostasis, including adaptations to altered hemodynamics, injury, and disease. We present a new approach to model arterial wall mechanics that seeks to define better the mechanical environments of the media and adventitia while avoiding the common prescription of a traction-free reference configuration. Specifically, we employ the concept of constituent-specific deposition stretches from the growth and remodeling literature and define a homeostatic state at physiologic pressure and axial stretch that serves as a convenient biologically and clinically relevant reference configuration. Information from histology and multiphoton imaging is then used to prescribe structurally motivated constitutive relations for a bi-layered model of the wall. The utility of this approach is demonstrated by describing in vitro measured biaxial pressure–diameter and axial force–length responses of murine carotid arteries and predicting the associated intact and radially cut traction-free configurations. The latter provides a unique validation while confirming that this constrained mixture approach naturally recovers estimates of residual stresses, which are fundamental to wall mechanics, without the usual need to prescribe an opening angle that is only defined conveniently on cylindrical geometries and cannot be measured in vivo. Among other findings, the model suggests that medial and adventitial stresses can be nearly uniform at physiologic loads, albeit at separate levels, and that the adventitia bears increasingly more load at supra-physiologic pressures while protecting the media from excessive stresses.

There has been a growing awareness over the past decade that stiffening of the aorta, and its attendant effects on hemodynamics, is both an indicator and initiator of diverse cardiovascular, neurovascular, and renovascular diseases. Although different clinical metrics of arterial stiffness have been proposed and found useful in particular situations, there remains a need to understand better the complex interactions between evolving aortic stiffness and the hemodynamics. Computational fluid–solid-interaction (FSI) models are amongst the most promising means to understand such interactions for one can parametrically examine effects of regional variations in material properties and arterial geometry on local and systemic blood pressure and flow. Such models will not only increase our understanding, they will also serve as important steps towards the development of fluid–solid-growth (FSG) models that can further examine interactions between the evolving wall mechanics and hemodynamics that lead to arterial adaptations or disease progression over long periods. In this paper, we present a consistent quantification and comparison of regional nonlinear biaxial mechanical properties of the human aorta based on 19 data sets available in the literature and we calculate associated values of linearized stiffness over the cardiac cycle that are useful for initial large-scale FSI and FSG simulations. It is shown, however, that there is considerable variability amongst the available data and consequently that there is a pressing need for more standardized biaxial testing of the human aorta to collect data as a function of both location and age, particularly for young healthy individuals who serve as essential controls.

Spontaneous dissection of the human thoracic aorta is responsible for significant morbidity and mortality, yet this devastating biomechanical failure process remains poorly understood. In this paper, we present finite element simulations that support a new hypothesis for the initiation of aortic dissections that is motivated by extensive histopathological observations. Specifically, our parametric simulations show that the pooling of glycosaminoglycans/proteoglycans that is singularly characteristic of the compromised thoracic aorta in aneurysms and dissections can lead to significant stress concentrations and intra-lamellar Donnan swelling pressures. We submit that these localized increases in intramural stress may be sufficient both to disrupt the normal cell-matrix interactions that are fundamental to aortic homeostasis and to delaminate the layered microstructure of the aortic wall and thereby initiate dissection. Hence, pathologic pooling of glycosaminoglycans/proteoglycans within the medial layer of the thoracic aortic should be considered as a possible target for clinical intervention.

The medial layer of large arteries contains aggregates of the glycosaminoglycan hyaluronan and the proteoglycan versican. It is increasingly thought that these aggregates play important mechanical and mechanobiological roles despite constituting only a small fraction of the normal arterial wall. In this paper, we offer a new hypothesis that normal aggregates of hyaluronan and versican pressurize the intralamellar spaces, and thereby put into tension the radial elastic fibres that connect the smooth muscle cells to the elastic laminae, which would facilitate mechanosensing. This hypothesis is supported by novel computational simulations using two complementary models, a mechanistically based finite-element mixture model and a phenomenologically motivated continuum hyperelastic model. That is, the simulations suggest that normal aggregates of glycosaminoglycans/proteoglycans within the arterial media may play equally important roles in supporting (i.e. a structural role) and sensing (i.e. an instructional role) mechanical loads. Additional simulations suggest further, however, that abnormal increases in these aggregates, either distributed or localized, may over-pressurize the intralamellar units. We submit that these situations could lead to compromised mechanosensing, anoikis and/or reduced structural integrity, each of which represent fundamental aspects of arterial pathologies seen, for example, in hypertension, ageing and thoracic aortic aneurysms and dissections.

Finite plane strain bending is solved for a multilayered elastic-incompressible thick plate. This multilayered solution, previously considered only in the case of homogeneity, is in itself interesting and reveals complex stress states such as the existence of more than one neutral axis for certain geometries. The bending solution is employed to investigate possible incremental bifurcations. The analysis reveals that a multilayered structure can behave in a completely different way from the corresponding homogeneous plate. For a thick plate of neo-Hookean material, for instance, the presence of a stiff coating strongly affects the bifurcation critical angle. Experiments designed and performed to substantiate our theoretical findings demonstrate that the theory can be effectively used as a design tool for predicting the capability of an elastic multilayered structure to be subject to a finite bending without suffering localized crazing.