Elastic properties of human aortas in relation to age and atherosclerosis: a structural model

Abstract

A new structural model is described for the tension-radius relationship of blood vessels, taking into account their mechanically important constituents: collagen, elastin and smooth muscle. The model has four characteristic parameters: EC, the Young's modulus of the collagen fibres; ESE, the Young's modulus of the combined smooth-muscle/elastin network; epsilon mu, the amount of strain at which the high stiffness region on the tension-radius curve is reached, and eta an indicator for the degree of collagen fibre stretching. The structural stiffness of the wall constituents is reflected by EC and ESE whereas the global stiffness of the entire blood vessel is described by epsilon mu and eta. All these elasticity parameters are pressure independent, in contrast to generally quoted values for the incremental modulus or vascular compliance which are strongly pressure dependent. Hence, an objective comparison of the mechanical properties for various types of blood vessel, based on the present model parameters, has been made possible. The model was successfully fitted to tension-radius data of 65 human aortas, age range 30-88 years, with moderate or severe atherosclerosis. The structural as well as the global stiffness changes with age, e.g. collagen stiffness shows a ninefold increase over 60 years. Global stiffness depends on atherosclerosis.

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

“…Often, it is alteration of the quantity and/or architecture of these fibres that leads to the mechanical, and hence functional, changes associated with aortic disease [9,14,34 -42]. For example, structural alterations in the walls of large arteries with progressing age causes a decrease in the total arterial compliance [9,10,[43][44][45][46], which in turn leads to both a decreased distal blood flow and an increase in aortic pulse pressure [30]. This increased pulse pressure has been shown to be the strongest predictor of cardiovascular mortality, because it increases the mechanical load on the left ventricle [47].…”

Synergistic effect of angiotensin II type 1 receptor and endothelial nitric oxide synthase gene polymorphisms on arterial stiffness

“…Turnover (synthesis and degradation) of key extracellular matrix components (elastin, collagen and calcium) is also impaired. 4,5 In muscular-type arteries, arterial stiffening is moreover determined by degree of smooth muscle hypertrophy and smooth muscle tone which represent structural and functional component of stiffness, respectively. 6 Age and BP are major determinants of arterial rigidity.…”

A constitutive model for fibrous tissues considering collagen fiber crimp

“…Among these, a number of structural models have been proposed that characterize the fiber recruitment process by assuming that either the fiber length, [19,38,39,22,36], or the stretch at which the fibers engage [23,21] are statistically distributed. These models use unbounded distributions, which seem non-physiological for quantities such as the fiber length and the stretch.…”

“…Their wavy appearance in the reference configuration motivates the assumption that they are unable to sustain compressive loads. For the modeling of the tensile behavior, we follow the work of others and consider that a given fiber carries load only after unfolding, assuming that the force necessary to perform this 5 A c c e p t e d m a n u s c r i p t is negligible [22,23]. Once the fiber starts to bear load, it is assumed that it follows Hooke's law until rupture [31].…”

“…There is, thus, a distribution in either the stretch of the fibers or their lengths. This idea has also been adopted subsequently by means of constitutive models to describe the mechanical response of, e.g., arterial walls ( [21] with ideas from [22,14]) or tendons and ligaments [23], just to name a few. All these constitutive models, however, assume unbounded statistical distributions for the fiber length (or stretch), which is a bounded quantity.…”