Roles of Elastin, Muscle Contractility and Collagenous Stiffening in Aortic Aging: A Thick-Walled Multi-Layered Model

Abstract

Evolving geometry, composition and mechanical properties in the aging aorta, resulting in part from elastin degradation, decreased smooth muscle tone, and altered rates of turnover of fibrillar collagen, contribute to many cardiovascular diseases. Constrained mixture models permit us to account for individual mass kinetics of structurally significant constituents as well as their individual deposition stretches and mechanical properties and predict salient facets of arterial growth and remodeling (G&R). Thick-walled models can also predict evolving retraction lengths, opening angles, and internal stress distributions. Employing a thick-walled, multi-layered constrained mixture model, we suggest that a coupled loss of elastin and vasoactive function are fundamental mechanisms by which aortic aging occurs. The model predicts that gradual losses of elastin and vasoactivity drive complex G&R sequences and differential growth. The model also suggests that collagenous stiffening, although typically regarded as harmful, can play a role in preventing the development and/or enlargement of abdominal aortic aneurysms.