Structural strain energy function applied to the ageing of the human aorta

Zulliger, Martin A.; Stergiopulos, Nikolaos

doi:10.1016/j.jbiomech.2007.03.011

Cited by 75 publications

(72 citation statements)

References 31 publications

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“…Scale bar 100 μm individual fibrils, underlies age-related arterial stiffening (Zulliger and Stergiopulos 2007). In the same study, the authors present evidence that alterations in the microstructure of elastic fibre are likely to play an important role in determining tissue mechanical properties and that, as a consequence, the model of elastin as an isotropic solid is over-simplified.…”

Section: Vascularmentioning

confidence: 80%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

265

189

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The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

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Section: Vascularmentioning

confidence: 80%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

265

189

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“…Attaching fibers to one another can stiffen the fiber ensemble by shifting the recruitment of the fibers to lower strains and forcing the engagement to occur more abruptly. Evidently, the datafitting study of Zulliger and Stergiopulos (72) revealed that the elastic modulus of the individual collagen fiber does not vary with age; however, there is a clear decrease in the mean fiber engagement strain and an even more pronounced decrease in fiber engagement variance with age. We introduced the function C AGE to account for the accumulation of AGEs over time.…”

Section: Prescribed Model Parametersmentioning

confidence: 99%

“…Zulliger and Stergiopulos (72) examined the changes in elastic and structural properties of the human aortic wall with aging by applying a structure-based constitutive law to the experimental data published by Langewouters et al (36) and Wuyts (69). The data referred to 43 human thoracic aortas obtained postmortem from subjects 30 -88 yr old.…”

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confidence: 99%

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A constituent-based model of age-related changes in conduit arteries

Tsamis

Rachev

Stergiopulos

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Tsamis A, Rachev A, Stergiopulos N. A constituent-based model of age-related changes in conduit arteries. Am J Physiol Heart Circ Physiol 301: H1286 -H1301, 2011. First published July 1, 2011; doi:10.1152/ajpheart.00570.2010.-In the present report, a constituent-based theoretical model of age-related changes in geometry and mechanical properties of conduit arteries is proposed. The model was based on the premise that given the time course of the load on an artery and the accumulation of advanced glycation end-products in the arterial tissue, the initial geometric dimensions and properties of the arterial tissue can be predicted by a solution of a boundary value problem for the governing equations that follow from finite elasticity, structure-based constitutive modeling within the constrained mixture theory, continuum damage theory, and global growth approach for stress-induced structure-based remodeling. An illustrative example of the age-related changes in geometry, structure, composition, and mechanical properties of a human thoracic aorta is considered. Model predictions were in good qualitative agreement with available experimental data in the literature. Limitations and perspectives for refining the model are discussed. arterial remodeling; vascular mechanics; elastin fatigue damage; collagen cross-linking AGING AFFECTS THE MECHANICAL FUNCTION of human conduit arteries such as the aorta, the iliac arteries, and the carotid arteries. It manifests as a change in the vessel geometry and material properties of the vascular tissue, accompanied by alterations in loading conditions. Geometric and structural alterations in the tissue of conduit vessels with progressing age cause a decrease in the total arterial compliance (66), which, in turn, leads to an increase in pulse pressure. The increase in pulse pressure has been shown to be the strongest predictor for cardiovascular mortality, for it augments the mechanical load on the left ventricle (9). Furthermore, the decrease in diastolic pressure observed in late middle age, which reduces the coronary arterial perfusion, raises the demands on the left ventricle (25).Geometric changes observed in aging are associated with an increase in arterial volume (7) characterized by increased lumen area (63) and wall thickening (43) and decreased axial stretch associated with loss in longitudinal stiffness (65). An increase in the opening angle has been observed, which was obtained after residual stress was relieved in an isolated arterial ring by a radial cut (54). Simultaneously, the content of collagen increases and the number of smooth muscle (SM) cells decreases (55). Furthermore, mean aortic pressure gradually increases with advanced age (27). The interrelation among the aforementioned processes is unknown. Additionally, the stiffness of the elastin structure gradually increases with advanced age due to a nonatherosclerotic mineralization mechanism called the medial elastocalcinosis (MEC), during which calcium salts bind to the elastin of the aortic media (15). Also, ela...

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“…For the most recent models, the aim is to take into account a higher degree of complexity. For instance, in Zulliger and Stergiopulos, 104 the stiffening of the aorta with progressing age is investigated. On the question of the stiffening of the arteries due to age, Astrand et al 105 used an in vivo technique to study the stiffening of elastin and collagen.…”

Section: Solid Physical Propertiesmentioning

confidence: 99%

Evolution and rupture of vulnerable plaques: a review of mechanical effects

Assemat¹,

Hourigan²

2013

CPT

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Atherosclerosis occurs as a result of the buildup and infiltration of lipid streaks in artery walls, leading to plaques. Understanding the development of atherosclerosis and plaque vulnerability is of critical importance, since plaque rupture can result in heart attack or stroke. Plaques can be divided into two distinct types: those that rupture (vulnerable) and those that are less likely to rupture (stable). In the last few decades, researchers have been interested in studying the influence of the mechanical effects (blood shear stress, pressure forces, and structural stress) on the plaque formation and rupture processes. In the literature, physiological experimental studies are limited by the complexity of in vivo experiments to study such effects, whereas the numerical approach often uses simplified models compared with realistic conditions, so that no general agreement of the mechanisms responsible for plaque formation has yet been reached. In addition, in a large number of cases, the presence of plaques in arteries is asymptomatic. The prediction of plaque rupture remains a complex question to elucidate, not only because of the interaction of numerous phenomena involved in this process (biological, chemical, and mechanical) but also because of the large time scale on which plaques develop. The purpose of the present article is to review the current mechanical models used to describe the blood flow in arteries in the presence of plaques, as well as reviewing the literature treating the influence of mechanical effects on plaque formation, development, and rupture. Finally, some directions of research, including those being undertaken by the authors, are described.

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Structural strain energy function applied to the ageing of the human aorta

Cited by 75 publications

References 31 publications

Tissue elasticity and the ageing elastic fibre

Tissue elasticity and the ageing elastic fibre

A constituent-based model of age-related changes in conduit arteries

Evolution and rupture of vulnerable plaques: a review of mechanical effects

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