TY - CHAP
T1 - Multi-scale modelling of vascular disease
T2 - abdominal aortic aneurysm evolution
AU - Watton, Paul N.
AU - Huang, Huifeng
AU - Ventikos, Yiannis
N1 - Funding Information:
Acknowledgments Paul Watton is funded by The Centre of Excellence in Personalized Healthcare (funded by the Wellcome Trust and EPSRC, grant number WT 088877/Z/09/Z). This support is gratefully acknowledged.
Publisher Copyright:
© Springer-Verlag Berlin Heidelberg 2012.
PY - 2013
Y1 - 2013
N2 - We present a fluid-solid-growth (FSG) computational framework to simulate the mechanobiology of the arterial wall. The model utilises a realistic constitutive model that accounts for the structural arrangement of collagen fibres in the medial and adventitial layers, the natural reference configurations in which the collagen fibres are recruited to load bearing and the (normalised) mass-density of the elastinous and collagenous constituents. Growth and remodelling (G&R) of constituents is explicitly linked to mechanical stimuli: computational fluid dynamic analysis produces snapshots of the frictional forces acting on the endothelial cells; a quasi-static structural analysis is employed to quantify the cyclic deformation of the vascular cells. We apply the computational framework to simulate the evolution of a specific vascular pathology: abdominal aortic aneurysm (AAA). Two illustrative models of AAA evolution are presented. Firstly, the degradation of elastin (that is observed to accompany AAA evolution) is prescribed, and secondly, it is linked to low levels of wall shear stress (WSS). In the first example, we predict the development of tortuosity that accompanies AAA enlargement, whilst in the latter, we illustrate that linking elastin degradation to low WSS leads to enlarging fusiform AAAs. We conclude that this computational framework provides the basis for further investigating and elucidating the aetiology of AAA and other vascular diseases. Moreover, it has immediate application to tissue engineering, e.g., aiding the design and optimisation of tissue engineered vascular constructs.
AB - We present a fluid-solid-growth (FSG) computational framework to simulate the mechanobiology of the arterial wall. The model utilises a realistic constitutive model that accounts for the structural arrangement of collagen fibres in the medial and adventitial layers, the natural reference configurations in which the collagen fibres are recruited to load bearing and the (normalised) mass-density of the elastinous and collagenous constituents. Growth and remodelling (G&R) of constituents is explicitly linked to mechanical stimuli: computational fluid dynamic analysis produces snapshots of the frictional forces acting on the endothelial cells; a quasi-static structural analysis is employed to quantify the cyclic deformation of the vascular cells. We apply the computational framework to simulate the evolution of a specific vascular pathology: abdominal aortic aneurysm (AAA). Two illustrative models of AAA evolution are presented. Firstly, the degradation of elastin (that is observed to accompany AAA evolution) is prescribed, and secondly, it is linked to low levels of wall shear stress (WSS). In the first example, we predict the development of tortuosity that accompanies AAA enlargement, whilst in the latter, we illustrate that linking elastin degradation to low WSS leads to enlarging fusiform AAAs. We conclude that this computational framework provides the basis for further investigating and elucidating the aetiology of AAA and other vascular diseases. Moreover, it has immediate application to tissue engineering, e.g., aiding the design and optimisation of tissue engineered vascular constructs.
KW - Abdominal Aortic Aneurysm
KW - Collagen Fibre
KW - Cyclic Deformation
KW - Wall Shear Stress
UR - http://www.scopus.com/inward/record.url?scp=84896345128&partnerID=8YFLogxK
U2 - 10.1007/8415_2012_143
DO - 10.1007/8415_2012_143
M3 - Chapter (Book)
AN - SCOPUS:84896345128
T3 - Studies in Mechanobiology, Tissue Engineering and Biomaterials
SP - 309
EP - 339
BT - Studies in Mechanobiology, Tissue Engineering and Biomaterials
PB - Springer
ER -