Most computational models of abdominal aortic aneurysms address either the hemodynamics within the lesion or the mechanics of the wall. More recently, however, some models have appropriately begun to account for the evolving mechanics of the wall in response to the changing hemodynamic loads. Collectively, this large body of work has provided tremendous insight into this life-threatening condition and has provided important guidance for current research. Nevertheless, there has yet to be a comprehensive model that addresses the mechanobiology, biochemistry, and biomechanics of thrombus-laden abdominal aortic aneurysms. That is, there is a pressing need to include effects of the hemodynamics on both the development of the nearly ubiquitous intraluminal thrombus and the evolving mechanics of the wall, which depends in part on biochemical effects of the adjacent thrombus. Indeed, there is increasing evidence that intraluminal thrombus in abdominal aortic aneurysms is biologically active and should not be treated as homogeneous inert material. In this review paper, we bring together diverse findings from the literature to encourage next generation models that account for the biochemomechanics of growth and remodeling in patient-specific, thrombus-laden abdominal aortic aneurysms.

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Adaptations of large arteries to sustained alterations in hemodynamics that cause changes in both caliber and stiffness are increasingly recognized as important initiators or indicators of cardiovascular risk to high flow, low resistance organs such as the brain, heart, and kidney. There is, therefore, a pressing need to understand better the underlying causes of geometric and material adaptations by large arteries and the associated time courses. Although such information must ultimately come from well designed experiments, mathematical models will continue to play a vital role in the design of these experiments and their interpretation. In this paper, we present a new multilayered model of the time course of basilar artery growth and remodeling in response to sustained alterations in blood pressure and flow. We show, for example, that single- and multi-layered models consistently predict similar changes in caliber and wall thickness, but multilayered models provide additional insight into other important metrics such as the residual stress related opening angle and the axial prestress, both of which are fundamental to arterial homeostasis and responses to injury or insult.

We present a three-dimensional mathematical framework for modeling the evolving geometry, structure, and mechanical properties of a representative straight cylindrical artery subjected to changes in mean blood pressure and flow. We show that numerical predictions recover prior findings from a validated two-dimensional framework, but extend those findings by allowing effects of transmural gradients in wall constituents and vasoactive molecules to be simulated directly. Of particular note, we show that the predicted evolution of the residual stress related opening angle in response to an abrupt, sustained increase in blood pressure is qualitatively similar to measured changes when one accounts for a nonlinear transmural distribution of pre-stretched elastin. We submit that continuum-based constrained mixture models of arterial adaptation hold significant promise for deepening our basic understanding of arterial mechanobiology and thus for designing improved clinical interventions to treat many different types of arterial disease and injury.

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