Biomedical Engineering Reference
In-Depth Information
High cycle fatigue. The arterial wall is exposed to over 3.0 x 10 9 cycles of load-
ing during a 75 year lifetime. In 1976, O'Rourke hypothesized this high cycle fa-
tigue was responsible for the frayed appearance of the elastic fibres in aged arteries.
Fractal analysis has been performed on histological sections of elastin lamellae in
arteries [61], with results indicating that elastin fatigue occurred due to increased
cardiac cycles over the same time period [3]. Constituent-based structural models
have been developed to account for aging [31, 124] and fatigue related degradation
of the IEL [74].
Biochemical degradation of elastin. In vitro studies in rabbit carotid arteries have
demonstrated qualitative changes in the mechanical properties of the wall after en-
zymatic damage to arterial elastin [31]. Chemically induced damage to the IEL has
also been hypothesized to arise from self induced enzymatic damage (e.g. [104]). For
example, mechanical factors such as altered wall shear stress and wall shear stress
gradient may trigger a signaling cascade in the endothelial cells lining blood ves-
sels, causing them to initiate the degradation of the IEL seen in cerebral aneurysm
formation.
6.4.1.1 Lack of repair of damaged elastin
Deposition of arterial elastin begins in vivo and peaks early in post natal develop-
ment, driven by hemodynamic factors The creation of elastic fibres in adulthood is
believed to be negligible (see, e.g. [111]) Using tritium-labeled valine, Davis showed
that no elastin turnover or growth occurs in the mouse aorta during adulthood [25].
Shapiro et al. estimated the longevity of elastic fibres in the lung in to be on the or-
der of the human lifetime, using aspartic acid racemization and 14C turnover [103].
These results suggest the detrimental effects of damage to the elastic fibres will not,
in general, be repaired. The inability of cell in the arterial wall to reactivate the many
genes in the proper ratios and sequences required for normal fibre assembly [105]
may prevent its deposition later in life as well as elastic fibre repair.
6.4.1.2 Medical impact of damage to the IEL
Age-associated arterial stiffening has been conjectured to arise as a result of fatigue
damage to elastic fibres that then results in load transfer to the (stiffer) collagen fibres
[85]. The stiffened vessels are less capable of storing elastic energy during the car-
diac cycle resulting in an increase in pressure during diastole and reduced pressure
through diastole. Increases in atherosclerosis, arterial weakening, and detrimental
cardiac changes have been attributed to these changes in pressure waveform [86].
This stiffening leads to an increase in the arterial wave speed [86] and wave reflec-
tions. Studies have indicated that increased arterial wave reflections are predictors
of severe cardiovascular events, and therapeutic attempts to reduce these wave re-
flections to improve prognosis have been suggested [114].
Damage to the elastin in the IEL is associated with pathological disorders such as
cerebral aneurysms [4, 12, 13, 14, 19, 92, 102], spontaneous cervical artery dissec-
tion aneurysms [8, 101], and complications associated with balloon angioplasty [57].
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