Rezvani-Sharif Alireza, Tafazzoli-Shadpour Mohammad, Avolio Alberto
Faculty of Biomedical Engineering, Amirkabir University of Technology, Tehran, Iran.
Department of Biomedical Science, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Cardiovasc Eng Technol. 2019 Mar;10(1):181-192. doi: 10.1007/s13239-018-0370-1. Epub 2018 Jul 13.
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.
动脉粥样硬化是心血管疾病的主要危险因素。然而，动脉粥样硬化斑块发展与动脉壁层状结构局部硬度之间的相互作用机制尚未完全明确。在本研究中，测定了三组不同的健康、轻度病变和晚期动脉粥样硬化人类腹主动脉壁及斑块成分的局部杨氏模量。进行组织学染色以突出动脉粥样硬化斑块成分和主动脉中膜的层状结构，中膜由弹性蛋白同心层和层间区域组成。利用原子力显微镜的力谱模式在微米水平上测定主动脉壁薄片和斑块成分的杨氏模量。观察到动脉粥样硬化斑块不同位置的杨氏模量（E）存在高度变异性，如纤维帽（E = 15.5±2.6 kPa）、钙化区（E = 103.7±19.5 kPa）和脂质池（E = 3.5±1.2 kPa）。与健康动脉相比，腹主动脉壁中层病变部分的弹性蛋白薄片硬度降低（18.6%），层间区域硬度增加（50%）。此外，在不完全斑块中，病变壁和无病变壁之间的弹性蛋白薄片和层间区域硬度均存在显著差异。我们的结果阐明了人类腹主动脉壁不同薄片硬度随动脉粥样硬化斑块发展的变化情况，并可能为动脉粥样硬化进展过程中主动脉壁重塑提供新的见解。
