Davis Lindsey A, Stewart Samantha E, Carsten Christopher G, Snyder Bruce A, Sutton Michael A, Lessner Susan M
Biomedical Engineering Program, University of South Carolina, Columbia, SC 29208 USA; Department of Cell Biology and Anatomy, University of South Carolina, School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29209 USA.
Division of Vascular Surgery, Greenville Health System, 701 Grove Road, Greenville, SC 29605 USA.
Acta Biomater. 2016 Oct 1;43:101-111. doi: 10.1016/j.actbio.2016.07.027. Epub 2016 Jul 16.
One well-established cause of ischemic stroke is atherosclerotic plaque rupture in the carotid artery. Rupture occurs when a tear in the fibrous cap exposes highly thrombogenic material in the lipid core. Though some fibrous cap material properties have been measured, such as ultimate tensile strength and stress-strain responses, there has been very little, if any, data published regarding the fracture behavior of atherosclerotic fibrous caps. This study aims to characterize the qualitative and quantitative fracture behavior of human atherosclerotic plaque tissue obtained from carotid endarterectomy samples using two different metrics. Uniaxial tensile experiments along with miniature single edge notched tensile (MSENT) experiments were performed on strips of isolated fibrous cap. Crack tip opening displacement (CTOD) and stress in the un-cracked segment (UCS) were measured at failure in fibrous cap MSENT specimens subjected to uniaxial tensile loading. Both CTOD and the degree of crack blunting, measured as the radius of curvature of the crack tip, increased as tearing propagated through the tissue. Higher initial stress in the UCS is significantly correlated with higher collagen content and lower macrophage content in the fibrous cap (ρ=0.77, P=0.009; ρ=-0.64, P=0.047; respectively). Trends in the data show that higher CTOD is inversely related to collagen content, though the sample size in this study is insufficient to statistically substantiate this relationship. To the authors' knowledge, this is the pioneering study examining the fracture behavior of fibrous caps and the first use of the CTOD metric in vascular tissue.
A tear in the fibrous cap of atherosclerotic plaque can lead to ischemic stroke or myocardial infarction. While there is some information in the literature regarding quantitative measures of fibrous cap failure, there is little information regarding the behavior of the tissue during failure. This study examines the failure behavior of fibrous caps both qualitatively, by examining how and where the tissue fails, and quantitatively, by measuring (a) crack tip opening displacement (CTOD) in vascular tissue for the first time and (b) uniaxial stress in the un-cracked segment (UCS). This study shows that both metrics should be evaluated when assessing plaque vulnerability.
缺血性中风的一个公认病因是颈动脉粥样硬化斑块破裂。当纤维帽出现撕裂,使脂质核心中具有高血栓形成性的物质暴露时,就会发生破裂。尽管已经测量了一些纤维帽材料的特性,如极限抗拉强度和应力应变响应,但关于动脉粥样硬化纤维帽断裂行为的数据(即便有)也非常少。本研究旨在使用两种不同指标来表征从颈动脉内膜切除术样本中获取的人类动脉粥样硬化斑块组织的定性和定量断裂行为。对分离出的纤维帽条带进行单轴拉伸实验以及微型单边切口拉伸(MSENT)实验。在承受单轴拉伸载荷的纤维帽MSENT样本失效时,测量裂纹尖端开口位移(CTOD)和未开裂段(UCS)的应力。随着撕裂在组织中扩展,CTOD以及作为裂纹尖端曲率半径测量的裂纹钝化程度均增加。UCS中较高的初始应力与纤维帽中较高的胶原蛋白含量和较低的巨噬细胞含量显著相关(分别为ρ = 0.77,P = 0.009;ρ = -0.64,P = 0.047)。数据趋势表明,较高的CTOD与胶原蛋白含量呈负相关,尽管本研究中的样本量不足以从统计学上证实这种关系。据作者所知,这是第一项研究纤维帽断裂行为的开创性研究,也是首次在血管组织中使用CTOD指标。
动脉粥样硬化斑块纤维帽的撕裂可导致缺血性中风或心肌梗死。虽然文献中有一些关于纤维帽失效定量测量的信息,但关于组织在失效过程中的行为信息很少。本研究通过研究组织如何以及在何处失效来定性地检查纤维帽的失效行为,并通过首次测量(a)血管组织中的裂纹尖端开口位移(CTOD)和(b)未开裂段(UCS)中的单轴应力来定量地进行检查。本研究表明,在评估斑块易损性时,这两个指标都应进行评估。