Cardiovascular Engineering Research Laboratory (CERL), School of Mechanical and Design Engineering, University of Portsmouth, Anglesea Road, Portsmouth PO1 3DJ, United Kingdom.
Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary, University of London, Mile End Road, London E1 4NS, United Kingdom.
J Mech Behav Biomed Mater. 2019 May;93:230-245. doi: 10.1016/j.jmbbm.2019.02.011. Epub 2019 Feb 12.
Viscoelastic attributes of the aortic valve (AV) tissue are, in part, reflected in stress-relaxation and creep behaviours observed in vitro. While the extent of AV time-dependent behaviour under physiological conditions is not yet fully understood, in vitro the tissue exhibits clear stress-relaxation but minimal creep under equi-biaxial loading, in contrast to uniaxial loading where creep is evidently exhibited. Tissue-level stress-relaxation behaviour follows the form of (single and double) Maxwell-type exponential decay relaxation modes, and creep occurs in the form of exponential primary followed by linear secondary creep modes. This paper aims to provide an explanation for these behaviours based on the AV microstructural (i.e. fibre-level) mechanics. The kinematics of AV microstructural reorganisation is investigated experimentally using confocal microscopy to track the interstitial cell nuclei as markers of AV microstructural reorganisation under uniaxial loading. A theoretical framework is then applied to describe the experimentally observed kinematics in mathematical terms. Using this framework it is shown that at the microstructural level, AV stress-relaxation and creep behaviours both stem from the same dissipative kinematics of fibre-fibre and fibre-matrix interactions, that occur as a consequence of microstructural reorganisation due to the applied tissue-level loads. It is additionally shown that the proposed dissipative kinematics correctly predict the nature of relaxation and creep behaviours, i.e. the type and the number of modes involved. Further analysis is presented to demonstrate that the origin of the minimal creep behaviour under equi-biaxial loading can be explained to stem from tissue-level loading boundary conditions. These key findings help to better understand the underlying causes of AV stress-relaxation and creep behaviours in vivo, and why these may differ from the behaviours observed under non-physiological in vitro loading.
主动脉瓣 (AV) 组织的黏弹性特性部分反映在体外观察到的应力松弛和蠕变行为中。虽然在生理条件下 AV 时变行为的程度尚不完全清楚，但在体外，组织在等双轴加载下表现出明显的应力松弛但最小的蠕变，与单轴加载下明显表现出的蠕变形成对比。组织水平的应力松弛行为遵循（单和双）麦克斯韦型指数衰减松弛模式，而蠕变以指数型初级随后线性次级蠕变模式发生。本文旨在基于 AV 微观结构（即纤维水平）力学来解释这些行为。使用共聚焦显微镜实验研究 AV 微观结构重组的运动学，以跟踪作为 AV 微观结构重组标志物的间质细胞核在单轴加载下的运动学。然后应用理论框架以数学术语描述实验观察到的运动学。使用该框架表明，在微观结构水平上，AV 应力松弛和蠕变行为均源自纤维-纤维和纤维-基质相互作用的相同耗散运动学，该运动学是由于施加的组织水平载荷导致微观结构重组而发生的。还表明，所提出的耗散运动学正确地预测了松弛和蠕变行为的性质，即涉及的模式的类型和数量。进一步的分析表明，解释在等双轴加载下最小蠕变行为的起源可以归因于组织水平的加载边界条件。这些关键发现有助于更好地理解体内 AV 应力松弛和蠕变行为的潜在原因，以及为什么这些行为可能与非生理体外加载下观察到的行为不同。
