Biomedical Engineering Reference
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possible differential changes in pulse, not mean, pressure throughout the vasculature
might be responsible for different time courses of arterial remodeling. Flow through
the LAD, LCCA, LMCA, and BA increased, whereas flow through the P-Ao de-
creased further. Cardiac workload increased 12 % from 9890 to 11059 mmHg/mL.
15.4 Discussion
Findings over the past few decades have revealed that vessels within the elastic,
muscular arteries, arterioles, capillaries, venules or veins respond markedly differ-
ently to altered biomechanical stimuli. For example, whereas all arteries and ar-
terioles tend to thicken in response to hypertension, the elastic arteries, muscular
arteries, and arterioles tend to do so while increasing, maintaining, and decreasing
their caliber, respectively (Humphrey, 2002 ). More recently, it has become apparent
that differential remodeling responses can even occur within vessels of the same
general classification and within close proximity to one another. For example, the
ascending aorta (an elastic artery) appears to be the first central artery (i.e., of the
rest of the aorta and carotids) to manifest aging related changes in structure that af-
fect overall mechanical properties (Redheuil et al., 2010 ). Amongst the many effects
of aging on arteries, including increased endothelial dysfunction and advanced gly-
cation endproducts (Lakatta et al., 2009 ; Safar, 2010 ), it appears that fatigue-type
damage to elastic fibers is particularly important (Arribas et al., 2006 ; O'Rourke
and Hashimoto, 2007 ). Indeed, it may well be that the increased susceptibility of
the ascending aorta to an aging related loss of elastic fiber integrity may explain in
part the increased susceptibility of the same region to dilatation and dissection in
Marfan syndrome (Pearson et al., 2008 ), which results from a genetic mutation in
the fibrillin-1 gene (FBN1); fibrillin-1 appears to help stabilize elastic fibers, hence
mutations in FBN1 also result in decreased elastic fiber integrity.
Understanding better the spatio-temporal progression of vascular changes in both
adaptive and maladaptive G&R could impact clinical care significantly. For exam-
ple, being able to identify early indicators of vascular disease or subsequent risk
could allow earlier interventions, before the subsequent disease presents symp-
tomatically as heart attack, stroke, or other life threatening condition. A long-term
goal of this work is to build a new class of computational models that aid in under-
standing local and systemic effects of spatially and temporally progressive changes
in large portions of the vascular tree and attendant changes in the hemodynamics,
which in turn serve as strong mechanobiological stimuli for subsequent vascular
growth and remodeling.
Toward that end, here we presented a zeroth order model wherein progres-
sive changes in large segments of the vasculature were introduced based on lim-
ited observations in the literature to study possible consequences on the associated
hemodynamics. Specifically, motivated by animal models of increased blood pres-
sure/pulse pressure (Xu et al., 2000 ;Huetal., 2008 ; Eberth et al., 2009 ; Hayenga,
2010 ), we studied the potential short-term effects of the abrupt creation of a 75 %
coarctation in the human descending thoracic aorta.
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