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Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy
Published on: October 19, 2016
Mechanical Characterization of the Lamellar Structure of Human Abdominal Aorta in the Development of Atherosclerosis:
Alireza Rezvani-Sharif1,2, Mohammad Tafazzoli-Shadpour3, Alberto Avolio2
1Faculty of Biomedical Engineering, Amirkabir University of Technology, Tehran, Iran.
Abstract:
Atherosclerosis is a major risk factor for cardiovascular disease. However, mechanisms of interaction of atherosclerotic plaque development and local stiffness of the lamellar structure of the arterial wall are not well established. In the current study, the local Young's modulus of the wall and plaque components were determined for three different groups of healthy, mildly diseased and advanced atherosclerotic human abdominal aortas. Histological staining was performed to highlight the atherosclerotic plaque components and lamellar structure of the aortic media, consisting of concentric layers of elastin and interlamellar zones. The force spectroscopy mode of the atomic force microscopy was utilized to determine Young's moduli of aortic wall lamellae and plaque components at the micron level. The high variability of Young's moduli (E) at different locations of the atherosclerotic plaque such as the fibrous cap (E = 15.5± 2.6 kPa), calcification zone (E = 103.7±19.5 kPa), and lipid pool (E = 3.5±1.2 kPa) were observed. Reduction of elastin lamellae stiffness (18.6%), as well as stiffening of interlamellar zones (50%), were detected in the diseased portion of the medial layer of abdominal aortic wall compared to the healthy artery. Additionally, significant differences in the stiffness of both elastin lamellae and interlamellar zones were observed between the diseased wall and disease-free wall in incomplete plaques. Our results elucidate the alternation of the stiffness of different lamellae in the human abdominal aortic wall with atherosclerotic plaque development and may provide new insight on the remodeling of the aortic wall during the progression of atherosclerosis.
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