Simulation of abdominal aortic aneurysm growth with updating hemodynamic loads using a realistic geometry

• Published in: Medical engineering & physics 2011-01, Vol.33 (1), p.80-88
• Main Authors: Sheidaei, A, Hunley, S.C, Zeinali-Davarani, S, Raguin, L.G, Baek, S
• Format: Article
• Language: English
• Subjects: Aortic Aneurysm, Abdominal - pathology; Aortic Aneurysm, Abdominal - physiopathology; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Computerized, statistical medical data processing and models in biomedicine; Diseases of the aorta; Fluid–solid-growth interaction; Growth and remodeling; Hemodynamics; Humans; Medical sciences; Models and simulation; Models, Anatomic; Models, Biological; Patient-specific model; Radiology; Time Factors; Vascular adaptation
• ISSN: 1350-4533; 1873-4030
• DOI: 10.1016/j.medengphy.2010.09.012

Abstract 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.