Advances in modeling vascular tissue growth and remodeling (G&R) as well as medical imaging usher in a great potential for integrative computational mechanics to revolutionize the clinical treatment of cardiovascular diseases. A computational model of abdominal aortic aneurysm (AAA) enlargement has been previously developed based on realistic geometric models. In this work, we couple the computational simulation of AAA growth with the hemodynamics simulation in a stepwise, iterative manner and study the interrelation between the changes in wall shear stress (WSS) and arterial wall evolution. The G&R simulation computes a long-term vascular adaptation with constant hemodynamic loads, derived from the previous hemodynamics simulation, while the subsequent hemodynamics simulation computes hemodynamic loads on the vessel wall during the cardiac cycle using the evolved geometry. We hypothesize that low WSS promotes degradation of elastin during the progression of an AAA. It is shown that shear stress-induced degradation of elastin elevates wall stress and accelerates AAA enlargement. Regions of higher expansion correlate with regions of low WSS. Our results show that despite the crucial role of stress-mediated collagen turnover in compensating the loss of elastin, AAA enlargement can be accelerated through the effect of WSS. The present study is able to account for computational models of image-based AAA growth as well as important hemodynamic parameters with relatively low computational expense. We suggest that the present computational framework, in spite of its limitations, provides a useful foundation for future studies which may yield new insight into how aneurysms grow and rupture.

Despite rapid expansion of our knowledge of vascular adaptation, developing patient-specific models of diseased arteries is still an open problem. In this study, we extend existing finite element models of stress-mediated growth and remodelling of arteries to incorporate a medical image-based geometry of a healthy aorta and, then, simulate abdominal aortic aneurysm. Degradation of elastin initiates a local dilatation of the aorta while stress-mediated turnover of collagen and smooth muscle compensates the loss of elastin. Stress distributions and expansion rates during the aneurysm growth are studied for multiple spatial distribution functions of elastin degradation and kinetic parameters. Temporal variations of the degradation function are also investigated with either direct time-dependent degradation or stretch-induced degradation as possible biochemical and biomechanical mechanisms for elastin degradation. The results show that this computational model has the capability to capture the complexities of aneurysm progression due to variations of geometry, extent of damage and stress-mediated turnover as a step towards patient-specific modelling.