Biomedical Engineering Reference
In-Depth Information
microvascular changes are closely related to proximal arterial behavior [ 16 ]. An
example was shown in hemodialysis patients, where larger amplitude pressure
waves, caused by stiffer arteries, led to other cardiovascular diseases such as
peripheral artery disease, ischemic heart disease, and heart failure [ 17 ]. Pulmonary
hypertensive patients will also experience increased pulsatile flow into the small
arteries and capillaries due to large artery stiffness, eliciting changes in the vessel
wall which in turn cause an increase in arterial resistance. Pressure and flow induce
wall distensibility by influencing: pulse patterns which are also distorted by
branching of the arterial tree, the resistance to forward motion of flow, and the
configuration and velocity of flow through the arterial tree [ 18 ]. However, the
cellular mechanism underlying the role of vascular stiffening and pulsatile flow in
the vascular remodeling process is still poorly understood, possibly due to the lack
of a model system that can be used to examine the relationship between pulse flow
waves and vascular cells. In addition, this is further complicated by the lack of
understanding of the crosstalk and integration required between length-scales as
one moves from sub-cellular genotype to cellular behavior to disease phenotype.
An excellent example of this the set of diseases described by mutations in the
LMNA gene, collectively known as laminopathies [ 19 ]. The most understood of
these is progeria, where patients exhibit accelerated aging and have notable sim-
ilarities in cardiovascular disease incidence [ 20 ] but surprising differences in
disease ultrastructure [ 21 ].
A biomechanical study comparing the pulmonary arteries of a normo-tensive
and a hypertensive (stiff artery) rat suggested that increased crosslinking of the
extracellular matrix structural proteins may be a mechanism for the pulmonary
artery stiffening [ 22 ]. The elastic modulus (E) determines the stiffness of the vessel
wall; the modulus varies both longitudinally and circumferentially throughout the
arteries. These changes reflect changes in material composition and configuration
of the collagen, elastin and smooth muscle fibers. The elastic modulus can be
calculated from the stress and strain of the artery:
E ¼ dr
de ;
where r is the stress and e is the strain. Changes in arterial stiffness alter the
arterial pressure; Lame's equation for stress in thick walled tubes can relate strains
to pressures as a result of changes in stiffness:
r 1 ¼ P i ½ r 2 þð r þ T Þ 2
ð r þ T Þ 2 r 2
; r ¼ r 0 ð 1 þ e Þ
where r l is the stress in a thick walled artery, P i is the mean pressure, T is the
vessel thickness, r o is the internal radius of the artery in the initial state and r is the
internal radius of the artery in a strained state. Lame's equation can be used to
calculate the systolic and diastolic arterial moduli [ 23 ]. Thus, from Lame's
equation, the stress due to a change in pressure can be calculated and the elastic
modulus can be determined to assess the impact of change in pressure on arterial
Search WWH ::




Custom Search