TY - JOUR
T1 - A combination of experimental and numerical methods to investigate the role of strain rate on the mechanical properties and collagen fiber orientations of the healthy and atherosclerotic human coronary arteries
AU - Karimi, Alireza
AU - Rahmati, Seyyed Mohammadali
AU - Sera, Toshihiro
AU - Kudo, Susumu
AU - Navidbakhsh, Mahdi
N1 - Publisher Copyright:
© 2017 Taylor & Francis.
PY - 2017/3/4
Y1 - 2017/3/4
N2 - Atherosclerosis enables to alter not only the microstructural but also the physical properties of the arterial walls by plaque forming. Few studies so far have been conducted to calculate the isotropic or anisotropic mechanical properties of the healthy and atherosclerotic human coronary arteries. To date there is a paucity of knowledge on the mechanical response of the arteries under different strain rates. Therefore, the objective of the concurrent research was to comprehend whether the alteration in the strain rates of the human atherosclerotic arteries in comparison with the healthy ones contribute to the biomechanical behaviors. To do this, healthy and atherosclerotic human coronary arteries were removed from 18 individuals during autopsy. Histological analyses by both an expert histopathologist and an imaged-based recognizer software were performed to figure out the average angle of collagen fibers in the healthy and atherosclerotic arterial walls. Thereafter, the samples were subjected to 3 diverse strain rates, i.e., 5, 20, and 50 mm/min, until the material failure occurs. The stress-strain diagrams of the arterial tissues were calculated in order to capture their linear elastic and nonlinear hyperelastic mechanical properties. In addition, Artificial Neural Networks (ANNs) was employed to predict the alteration of mean angle of collagen fibers during load bearing up to failure. The findings suggest that strain rate has a significant (p < 0.05) role in the linear elastic and nonlinear hyperelastic mechanical properties as well as the mean angle of collagen fibers of the atherosclerotic arteries, whereas no specific impact on the healthy ones. Furthermore, the mean angle of collagen fibers during the load bearing up to the failure at each strain rate was well predicted by the proposed ANNs code.
AB - Atherosclerosis enables to alter not only the microstructural but also the physical properties of the arterial walls by plaque forming. Few studies so far have been conducted to calculate the isotropic or anisotropic mechanical properties of the healthy and atherosclerotic human coronary arteries. To date there is a paucity of knowledge on the mechanical response of the arteries under different strain rates. Therefore, the objective of the concurrent research was to comprehend whether the alteration in the strain rates of the human atherosclerotic arteries in comparison with the healthy ones contribute to the biomechanical behaviors. To do this, healthy and atherosclerotic human coronary arteries were removed from 18 individuals during autopsy. Histological analyses by both an expert histopathologist and an imaged-based recognizer software were performed to figure out the average angle of collagen fibers in the healthy and atherosclerotic arterial walls. Thereafter, the samples were subjected to 3 diverse strain rates, i.e., 5, 20, and 50 mm/min, until the material failure occurs. The stress-strain diagrams of the arterial tissues were calculated in order to capture their linear elastic and nonlinear hyperelastic mechanical properties. In addition, Artificial Neural Networks (ANNs) was employed to predict the alteration of mean angle of collagen fibers during load bearing up to failure. The findings suggest that strain rate has a significant (p < 0.05) role in the linear elastic and nonlinear hyperelastic mechanical properties as well as the mean angle of collagen fibers of the atherosclerotic arteries, whereas no specific impact on the healthy ones. Furthermore, the mean angle of collagen fibers during the load bearing up to the failure at each strain rate was well predicted by the proposed ANNs code.
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U2 - 10.1080/21655979.2016.1212134
DO - 10.1080/21655979.2016.1212134
M3 - Article
C2 - 27588460
AN - SCOPUS:84984889778
SN - 1949-1018
VL - 8
SP - 154
EP - 170
JO - Bioengineered
JF - Bioengineered
IS - 2
ER -