Biomedical Engineering Reference
In-Depth Information
rial collagen and elastin without the destructive processing typical of previous ap-
proaches.
In this work, we consider damage in arteries, with particular emphasis on cerebral
vessels. A brief introduction to the structure of the healthy arterial wall is given
in the Sect. 6.2. In Sect. 6.3, an overview of structural constitutive models for the
arterial wall are discussed, with particular emphasis on modelling fibre recruitment
and distribution of fibre orientation. This section ends with a discussion of the UA-
MPM device and its application to the healthy arterial wall. In Sect. 6.4, we turn
attention to damage in the arterial wall, beginning with a discussion of sources of
damage and clinical relevance of this subject. We then discuss a continuum damage
theory for the arterial wall. This section ends with a brief overview of the application
of the UA-MPM system to study damage in cerebral vessels. Finally, in Sect. 6.5,
we consider the an application of the continuum damage model to the subject of
cerebral angioplasty.
6.2 Background - structure of the undamaged arterial wall
The healthy artery wall consists of three concentric layers which, moving outward
from the lumen, are 1) the tunica intima, including endothelial cells and a fenestrated
sheet of elastin fibres called the internal elastic lamina (IEL); the tunica media, con-
taining mostly smooth muscle cells, some elastin fibres and collagen fibres; and 3)
the tunica adventitia, composed mainly of a network of type I collagen fibres and
fibroblasts, Fig. 6.1a. An external elastic lamina (EEL) is found interior to the ad-
ventitia. It should be noted that the microstructure varies with location in the arterial
tree, age and disease state. For example, in cerebral arteries the EEL is absent and
nearly all the elastin is confined in the IEL. Further, the microstructure of the wall can
change in response to changes in stimuli through growth, remodelling or damage.
Structure/function relationship in healthy arteries
It has long been recognized that the passive mechanical response of arteries is largely
due to the collagen and elastin found in the arterial wall, and in some cases smooth
muscle cells [6, 90, 93]. The typical stress strain curve from mechanical tests of ar-
terial walls, for example under uniaxial stretch, is highly nonlinear, characterized by
high flexibility at low loads (the toe region) and rapidly increasing stiffness at higher
loads. The toe region has been conjectured to arise from the loading of elastic fibres
and the highly nonlinear response at increasing loads to the recruitment of collagen
fibres [11, 90, 92]. Samila et al. morphologically observed the gradual unfolding of
crimped collagen fibres in human carotid artery strips that were stretched uniaxi-
ally [100]. It is believed that collagen fibres contribute little resistance during this
unfolding process, [92]. As loading intensifies, the collagen contribution takes on
an increasing role as seen by the heightened vessel stiffness. If the elastic fibres are
significantly damaged, the region of high flexibility at low loads will be lost and the
mechanical properties of the vessel will change significantly.
