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Artery bent buckling has been suggested as a possible mechanism that leads to artery tortuosity, which is associated with aging, hypertension, atherosclerosis, and other pathological conditions. It is necessary to understand the relationship between microscopic wall structural changes and macroscopic artery buckling behavior. To this end, the objectives of this study were to develop arterial buckling equations using a microstructure-based 4-fiber reinforced wall model, and to simulate the effects of vessel wall microstructural changes on artery buckling. Our results showed that the critical pressure increased nonlinearly with the axial stretch ratio, and the 4-fiber model predicted higher critical buckling pressures than what the Fung model predicted. The buckling equation using the 4-fiber model captured the experimentally observed reduction of critical pressure induced by elastin degradation and collagen fiber orientation changes in the arterial wall. These results improve our understanding of arterial stability and its relationship to microscopic wall remodeling, and the model provides a useful tool for further studies. [ABSTRACT FROM AUTHOR]

Abstract: A new mass transfer model has been formulated and implemented for predicting the penetration of liquid medication into an arterial wall. The model takes separate account of the transport of medication in the tissue and in the liquid stream. The transport equations take into consideration both diffusion and advection. An original lateral transport mechanism relating the drug concentrations in the tissue and in the advecting liquid stream is postulated and calibrated with experimental data from the literature. The special features of the mechanism are its non-Fickian nature and the accounting of the affinity (binding) of the drug to the tissue. Once established, the model was applied by means of numerical simulation to the in-artery distribution of Paclitaxel, a drug whose function is to minimize restenosis of the artery wall. The application encompassed parametric values of the duration of the drug therapy, the viscosity of the advecting fluid, and the pressure used to drive the drug into the tissue. It was found that the drug concentration at a clinically relevant depth in the artery wall varied linearly with the duration of the therapy, increased with increasing values of the driving pressure, and decreased for higher viscosities of the advecting fluid. In addition to its capabilities for predicting drug concentrations during the therapy duration period, the simulations also were able to follow the temporal variations of the drug distribution after the cessation of the therapy. [Copyright &y& Elsevier]

Abstract: Background: Estrogen therapy that is started at the time of menopause seems to protect against the development of atherosclerosis and cardiovascular diseases, in contrast to the initial increased cardiovascular risk when hormone therapy is initiated in older women. With increased aging and degree of atherosclerosis, the thickness of the artery intima increases and that of the media decreases. These changes can be noninvasively estimated using high-frequency ultrasound. Methods and results: The thickness of carotid and femoral artery intima and media was assessed, using noninvasive high-frequency ultrasound (25MHz). Long-term estrogen users (mean treatment duration 20 years) had a significantly thinner mean carotid intima layer (−25%; P =0.0002), a thicker media layer (+74%; P =0.0002) and a substantially lower intima/media thickness ratio (−54%; P <0.0001) than 17 age-matched nonusers, with values closer to those in 20 premenopausal women. Similar but less pronounced differences between the postmenopausal groups were found for the femoral artery. Conclusions: A preserved thin artery wall intima and a low intima/media thickness ratio, at values close to those in young women might be partially responsible for the beneficial cardiovascular effects of estrogen therapy when it is initiated at the time of menopause. [Copyright &y& Elsevier]