ARTERIAL WALL MECHANICS – A REVIEW

Sarangi Somnath 1; DasBakshi Somnath 2; Bhattacharyya Ranjan 3; Mohanty Akhandal 4

Department of Mechanical Engineering, Indian Institute of Technology Kharagpur
Kharagpur-721302, India,
Email: 1 somsara@mech.iitkgp.ernet.in
2
@iitkgp.ac.in
3
rbmail@mech.iitkgp.ernet.in
4
rakhandal@iitkgp.ac.in

Abstract: The paper attempts a review of various recent advances in the field of Arterial wall mechanics starting with a
detailed description of the composition and microstructure of the artery .The various forces that influence arterial wall
mechanics are also discussed. The mechanical properties and various constitutive models are also discussed. Finally
various experimental techniques, applications and future perspectives have also been looked at.

Keywords: composition, microstructure, arterial wall mechanics, constitutive models, applications, future perspectives.

1. INTRODUCTION It’s the subendothelial layer which is mainly responsible

Arteries have thicker walls and tend to have narrower
lumens. The lumen diameter varies with position of
artery in body. Diameter decreases with increasing
distance from heart. Other properties like stiffness also
changes with changing diameter. Arteries have to
constrict and dilate to control how much blood flows
where, and they must bear the powerful force generated
by the heart. Because of the large amount of muscle in
their walls, they are usually round when cut in cross-
section. Though arteries collected from different region
of body shows different characteristics artery walls
mainly composed of three layers tunica intima, tunica
media and tunica adventitia.
2. ARTERIAL COMPOSITION AND MICR-
OSTRUCTURE
2.1. TUNICA INTIMA
Intima is the innermost layer of artery. A single layer of
endothelial cell, linked by numerous junctions providing
mechanical and electrochemical connection (1, 2), in
intima prevents blood from adhering to lumenal surface
thus acting as a non-thrombogenic interface between
blood and vessel wall. Apart from that it also controls the
vessel wall permeability to macro molecules and white
blood cells. It has also been observed that endothelial
cells are responsible in vascular smooth muscle cells
response to change in stress due to bl ood flow (3, 4, 5,
6). Though detail study in this field is still unavailable it
has been found that a short term response is generated
due to alternation in flow and changes in vessel diameter
(7, 8, 9) as well as a long term effect aligns the
endothelial cell with the direction of flow (10).
Endothelial cells are composed of type IV collagen,
fibronectine and laminin . In addition to that a
subendothelial layer of varying thickness is also present.
for load carrying capacity of the artery. The presence of
Type I and type III collagen confirms mechanical
dominance of subendothelial layer. Orientation of
collagen fiber varies, and thus acts as a separator, with
the thickness in subendothelial layer (11, 12).
2.2. TUNICA MEDIA
It is the middle layer of artery which is of greatest
volume and responsible for most of arterial properties
consist of a three dimensional network of smooth muscle
cells, elastin. and bundles of collagen fibrils (type I about
30% and type III about 70%) (13, 14, 15). For arteries
closer to heart the elastin proportion is higher (called
elastin arteries and have larger diameter) and for arteries
away from heart muscle cell proportion is higher (called
muscular arteries located near the periphery). The
former are elastic “storage” vessels, while
the latter are controllable “resistance”
vessels Elastin, collagen and smooth muscle cells
together form a continuous fibrous helix which is almost
circumferentially oriented within the media. Smooth
muscle cells regulate blood flow locally by modifying
wall properties.
2.3. TUNICA ADVENTITIA
Adventitia means the outermost connective tissue
covering any organ, vessel or any other structure. The
outermost layer of artery is called adventitia because it is
considered extraneous to artery. It consists of type I
collagen, nerves, fibroblast (a cell capable of forming
collagen fibre) and some elastin fibers (16). The collagen
fibres form two helically arranged families of fibres
within which the individual collagen fibres have large
deviation from their mean orientation. Apart from
connecting blood vessel to surrounding tissues adventitia
acts as a protective sheath which prevents over distension
of media. It is also believed that adventitia has
contribution in elastic modulus of vessel wall (17).
Figure1 Diagrammatic model of major components of
healthy, elastic artery
2.4. MICROSTRUCTURE
2.4.1. COLLAGEN
Collagen is fibrous protein constituent of bone, cartilage
and other connective tissues. Collagen imparts
mechanical integrity and strength. It is main constituent
of artery wall. Collagen is synthesized by cells with high
metabolic activity. In blood vessel they are synthesized
by vascular muscle cells and by endothelial cell as well
(18). First procollagen is synthesized intracellular and
then extracellular procollagen is combined with
tropocollagen which self assembles into collagen fibres
spontaneously. Collagens are of various types (19) like
type I, II, III, IV. Collagen type II is found in hyaline and
elastic cartilage and as its index of reflection is very
similar to that of ground substance it is masked but they
are visible in polarizing microscope and electron
microscopy. While type III collagens are of reticular
fiber type help in stabilization of reticular connective
tissue in fat cells type IV collagens are without a fibre
structure and have amorphous structure synthesized by
endothelial cells. While the former are found in media
surrounding elastic fibres the latter are found in basement
membrane. Type I collagen is most common in human
artery (20) they are of high tensile strength, occurs in
wavy bundles and is stiffer than other varieties. It is
composed of collagen fibres which in turn are composed
of microfibrils. Microfibrils are composed of
tropocollagen molecules.
2.4.2. ELASTIN
Elastin is a protein similar to collagen and is the principal
component of elastic fibres. Elastic fibres occur as
accompanying structure of collagen fibre in vascular
wall. Elastin is a type of chemically inert protein and has
some properties similar to rubber. Among biosolid
materials it has the most linear elastic curve. It can
ramify hence forms networks. It is synthesized by
smooth muscle cells in vascular wall with decreasing rate
of synthesis with increasing age (21, 22, 23).
In arteries ratio of elastin to collagen is not constant and
it falls with increasing distance from heart while the
muscle cell proportion increases (24, 25, 26). In artery
cross section ring of elastin can be found between which
muscle cells are embedded that are surrounded by
collagen fibres.
3. IDENTIFICATION OF FORCES INFLUENCING
THE MECHANICS
Transmural pressure is the pressure difference between
inside and outside of any structure for example of blood
vessel. Perfusion pressure is the pressure head or
difference in pressure between two points in a fluid flow
tube. In blood vessel perfusion pressure between two
points can be obtained by subtracting the transmural
pressure corresponding to those two points. The degree
of pressure present in the cavity of the colon is called
intraluminal pressure. When a shear force is applied,
the layer nearer the wall than a layer inside it tends to
slow its movement, while it in turn slows the movement
of the layer just inside it nearer the axis. Higher relative
velocity of the layers with respect to one another occurs
in smaller tubes such as arterioles, because there are
fewer layers with smaller diameters. Residual stress is
observed in many parts of the cardiovascular system and
is thought to reduce transmural stress gradients due to
intravascular pressure. Its development is closely
associated with normal growth and pathological
remodelling. The residual stress increases with growth
and ageing. Pulse wave plays a dominant role in
regulating flow across blood vessel. If the flow wave
generated by the heart comes across a change in
characteristic impedance due to stiffness or lumen cross
sectional area or both a reflective wave generates. When
the impedance increase then reflection is said to be
positive and in this case pressure increases and flow
decreases. Alternatively if pulse wave faces decrease in
impedance then negative reflection occurs and this leads
to fall in pressure and increase in flow.
4. MODELLING MECHANICAL PROPERTIES
4.1. HETEROGENITY
On the microscopic level, healthy arteries are not
homogeneous. The wall is comprised of cells, elastin,
and collagen, and the distribution of these elements
varies from the inner wall to the outer wall, as well as
along the vascular tree. Ultimately, the unknown
interaction of the fibrous constituents determines the
mechanical properties of the extracellular matrix (27). To
complicate matters further, the orientations of elastin and
collagen are load dependent making it likely that the
measured mechanical properties also change with load.
In a heterogeneous model, parameters depend on the wall
constituents and their spatial distribution. Heterogeneity
has been modeled using approaches of increasing
complexity: from a model having a two-layered cross
section that represents the distinct wall layers in healthy
vessels (28), to models that account for healthy and
diseased histologic components (29), to models that
further include tissue microstructure (e.g., extracelular
matrix fiber distributions) (30).
4.2. INCOMPRESSIBLITY
The incompressibility constraint requires the
conservation of wall volume during the deformation of a
material (31, 32, 33). Incompressibility is a reasonable
assumption in that biological tissues contain mostly
water, which is incompressible at physiologic pressures.
Incompressibility has been modeled either by
constraining constitutive equations directly or using
Lagrange multipliers. Both approaches make use of the
fact that, for an incompressible deformation, the
determinant of the deformation gradient is unity.
4.3. RESIDUAL STRESS
If an artery piece is cut longitudinally it gets opened up
and this testifies the existence of residual stress (34). It
was first observed by Bergel (35). Vaishnav and
Vossoughi (36, 37) were the first to incorporate residual
stress and strain in theoretical models, followed by Fung
and co-workers (38, 39, 40). Inclusion of residual stress
in arterial models results in a more uniform distribution
of stress, noticeably decreasing stress at the intimal layer,
as compared to models without residual stress. Current
models incorporate residual stress using a cut-open ring
segment as the zero-stress state. In one approach, the
opening angle is measured and included in the
circumferential stretch ratio used to calculate strain (41).
This method uses incompressibility to relate the radii and
opening angle. Alternatively, strain is referred to inner
and outer surfaces in the stress-free configuration without
the use of the incompressibility assumption. Although
individual arterial layers may each have their own
opening angles, all of the reviewed studies use a single
opened configuration to represent all layers. Despite the
existence of axial residual stress (42), only one model
includes it (43).
4.4. SMOOTH MUSCLE CONTRACTIBILITY
Smooth muscle contractibility was modelled by Rachev
& Hayashi (44) using different functional forms for the
active and passive circumferential stress.
∂W
σ θ p = λθ2 +q
∂E 0
σ θ a = Mλθ f (λθ ),
where σθp represents the passive circumferential stress,
and σθa represents the active circumferential stress, λθ is
the circumferential stretch, q is an unknown scalar
function determined from equilibrium and boundary
conditions, W is the strain energy density function, Eθ is
the circumferential Green’s strain, M reflects the level of
smooth muscle contractile activity, and f(λθ) is a
normalized function accounting for the length-tension
relationship. The total circumferential stress is the sum of
the active and passive components. Active axial and
radial components were not modelled.
4.5. PRESSURE RELATED DYNAMIC WALL
MOTION
Demiray & Vito (45) introduced dynamic radial wall
motion in an elastic, homogeneous, isotropic,
incompressible, cylindrical artery. If (R, Θ, Z) and (r, θ,
z) are the cylindrical polar coordinates of a body before
and after deformation, wall motion caused by time-
dependent internal pressure and axial force may be
described as
R2
r = r ( R, t ) = [ + C (t )]1 / 2
λz (t )
θ =Θ
z = λz (t ) Z ,
where C(t) is an unknown function, assumed to be of the
sinusoidal form with diastolic and systolic boundary
conditions used to solve for the unknown parameters, and
λz is the axial stretch, further assumed to be constant for
simplicity.
4.6. SUMMARY OF BIOMECHANICAL BEHAVI-
OUR
Blood vessels exhibit numerous complex characteristics.
Historically, observed characteristics have been
implemented using simplifications of the actual
behaviour, such as layered or otherwise distinct
structures to represent the heterogeneity of the wall, a
single stress-relieving cut through the entire wall to
account for residual stress and strain, assigning different
stress equations to account for active and passive
responses, and utilizing sinusoidal equations to account
for wall motion. Even though the simplified mechanisms
cannot completely explain the actual behaviour,
important information is often revealed when the
simplifications are included.
5. CONSTITUTIVE MODELS
A constitutive relation is to be formed to describe the
behavior of an artery. Constitutive equation does not
describe a material in particular but it describe its
behavior under particular condition. So for different
condition different constitutive equations are required.
As far as artery material is concerned to model its
viscoelasticity, pseudoelasticity we need to have different
constitutive relations. Here only relations for
pseudoelastic behavior will be studied as this is sufficient
to quantify stress field in an artery under physiological
loading condition.
Blood vessels can be treated as pseudoelastic, randomly
elastic, poroelastic, or viscoelastic. Pseudoelasticity
assumes that a material can be modeled using separate
equations describing the loading and unloading behavior.
In most experiments, loading in one direction is generally
accompanied by unloading in another, making a precise
definition of pseudoelasticity problematic. One possible
solution is random elasticity, which assumes that the
strain response for a given load is centered around a
definite value that lies on a well-defined curve, such that
data from both the loading and unloading curves can be
included simultaneously. Poroelastic formulations treat a
material as a fluid-saturated porous medium and are well
suited to model wall transport. Viscoelastic formulations
include time-dependent responses in the constitutive
equation and are useful for modelling creep, stress
relaxation, and hysteresis
6. EXPERIMENTAL TECHNIQUES
Computer controlled experiments now provide more
accurate data measurement and support a greater variety
of testing conditions. The first microprocessor controlled
biaxial experimental system was developed by Vito (46).
More recently systems have been built to control blood
vessel inflation, axial stretch and torsion (47).
In vitro testing conditions have also evolved since the
early experiments to reproduce in vivo ionic balances
using supplemented saline solutions. A noteworthy area
is use of bioreactors or organ culture to maintain a
physiologically relevant environment. These devices
have been shown to maintain cell viability and vascular
tone within an excised artery for up to seven days. (48)
during which the artery is perfused with supplemented
tissue culture media at physiologic pressures and flows.
In vivo studies also yield very important information.
Studies are performed regularly in the clinical setting
using invasive [intravascular ultrasound (IVUS),
angiography] or non-invasive (magnetic resonance
imaging, ultrasound) imaging methods to study blood
pressure; changes to vessel geometry (49); state of
disease; and responses to external stimuli, such as
exercise and pharmacological agents. Increasingly,
clinical instrumentation is also used for in vivo or in vitro
laboratory testing (50, 51).
7. APPLICATIONS
Angioplasty is the medical alteration of a narrowed or
totally obscured vascular lumen generally caused by
atheroma (the lesion of atherosclerosis). In the
angioplasty procedure, the physician threads a balloon-
tipped catheter – a thin, plastic tube—to the site of a
narrow or blocked artery and then inflates the balloon to
open the vessel. The balloon is then deflated and
removed from the artery. Vascular stenting, which is
often performed at the same time as an angioplasty,
involves the placement of a small wire mesh tube called a
stent in the newly opened artery. This may be necessary
after some angioplasty procedures if the artery is very
narrowed or completely blocked. There are many other
interesting and challenging application areas that will
benefit from more comprehensive blood vessel
constitutive models. These include the creation of new
blood vessel substitutes (52), including the emerging
field of vascular tissue engineering (53, 54) and
aneurysm treatment and prevention (55, 56, 57).
8. CONCLUSIONS AND FUTURE DIRECTIONS
Blood vessels exhibit complex interacting mechanical
and biological behaviours that are important but poorly
understood. Experimental models exist to isolate
observed behaviour, whereas mathematical models exist
to model the observed behaviour. The need remains for
models of increasing complexity, and numerical and
experimental data to complement these models. The
predictive value of current and future models will be
assessed through implementation in relevant applications.
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