Journal
ANNALS OF BIOMEDICAL ENGINEERING
Volume 39, Issue 7, Pages 2027-2045Publisher
SPRINGER
DOI: 10.1007/s10439-011-0287-4
Keywords
Aneurysms; Vascular growth; Remodeling; Elastin fatigue; Collagen turnover; Stress
Categories
Funding
- NIH [HL-086418, HL-105297]
- National Centers for Biomedical Computing (SimBios at Stanford University)
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Arterial responses to diverse pathologies and insults likely occur via similar mechanisms. For example, many studies suggest that the natural process of aging and isolated systolic hypertension share many characteristics in arteries, including loss of functional elastin, decreased smooth muscle tone, and altered rates of deposition, and/or crosslinking of fibrillar collagen. Our aim is to show computationally how these coupled effects can impact evolving aortic geometry and mechanical behavior. 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. Moreover, it is suggested that collagenous stiffening, although itself generally an undesirable process, can play a key role in attenuating excessive dilatation, perhaps including the enlargement of abdominal aortic aneurysms.
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