Zhang Will, Sacks Michael S
Center for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, Department of Biomedical Engineering, University of Texas at Austin, Austin, TX 78712-0027, USA.
Center for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, Department of Biomedical Engineering, University of Texas at Austin, Austin, TX 78712-0027, USA.
J Mech Behav Biomed Mater. 2017 Nov;75:336-350. doi: 10.1016/j.jmbbm.2017.07.013. Epub 2017 Jul 11.
Bioprosthetic heart valves (BHVs), fabricated from exogenously crosslinked collagenous tissues, remain the most popular heart valve replacement design. However, the life span of BHVs remains limited to 10-15 years, in part because the mechanisms that underlie BHV failure remain poorly understood. Experimental evidence indicates that BHVs undergo significant changes in geometry with in vivo operation, which lead to stress concentrations that can have significant impact on structural damage. These changes do not appear to be due to plastic deformation, as the leaflets only deform in the elastic regime. Moreover, structural damage was not detected by the 65 million cycle time point. Instead, we found that this nonrecoverable deformation is similar to the permanent set effect observed in elastomers, which allows the reference configuration of the material to evolve over time. We hypothesize that the scission-healing reaction of glutaraldehyde is the underlying mechanism responsible for permanent set in exogenously crosslinked soft tissues. The continuous scission-healing process of glutaraldehyde allows a portion of the exogenously crosslinked matrix, which is considered to be the non-fibrous part of the extra-cellular matrix, to be re-crosslinked in the loaded state. Thus, this mechanism for permanent set can be used to explain the time evolving mechanical response and geometry of BHVs in the early stage. To model the permanent set effect, we assume that the exogenously crosslinked matrix undergoes changes in reference configurations over time. The changes in the collagen fiber architecture due to dimensional changes allow us to predict subsequent changes in mechanical response. Results show that permanent set alone can explain and, more importantly, predict how the mechanical response of the biomaterial change with time. Furthermore, we found is no difference in permanent set rate constants between the strain controlled and the stress controlled cyclic loading studies. An important finding we have is that the collagen fiber architecture has a limiting effect on the maximum changes in geometry that the permanent set effect can induce. This is due to the recruitment of collagen fibers as the changes in geometry due to permanent set increase. This means we can potentially optimize the BHV geometry based on the predicted the final BHV geometry after permanent set has largely ceased. Thus, we have developed the first structural constitutive model for the permanent set effect in exogenously crosslinked soft tissue, which can help to simulate BHV designs and reduce changes in BHV geometry during cyclic loading and thus potentially increasing BHV durability.
生物人工心脏瓣膜(BHVs)由外源性交联的胶原组织制成,仍然是最受欢迎的心脏瓣膜置换设计。然而,BHVs的使用寿命仍然限制在10至15年,部分原因是BHVs失效的潜在机制仍知之甚少。实验证据表明,BHVs在体内运行时几何形状会发生显著变化,这会导致应力集中,进而对结构损伤产生重大影响。这些变化似乎不是由于塑性变形,因为瓣叶仅在弹性范围内变形。此外,在6500万次循环时间点未检测到结构损伤。相反,我们发现这种不可恢复的变形类似于在弹性体中观察到的永久变形效应,这使得材料的参考构型随时间演变。我们假设戊二醛的断链-愈合反应是外源性交联软组织中永久变形的潜在机制。戊二醛的持续断链-愈合过程使得一部分外源性交联基质(被认为是细胞外基质的非纤维部分)在加载状态下重新交联。因此,这种永久变形机制可用于解释BHVs在早期阶段随时间演变的力学响应和几何形状。为了模拟永久变形效应,我们假设外源性交联基质随时间在参考构型上发生变化。由于尺寸变化导致的胶原纤维结构变化使我们能够预测随后的力学响应变化。结果表明,仅永久变形就能解释,更重要的是,预测生物材料的力学响应如何随时间变化。此外,我们发现应变控制和应力控制的循环加载研究之间的永久变形速率常数没有差异。我们的一个重要发现是,胶原纤维结构对永久变形效应可引起的最大几何形状变化具有限制作用。这是由于随着永久变形导致的几何形状变化增加,胶原纤维会被募集。这意味着我们可以根据永久变形基本停止后预测的最终BHVs几何形状,潜在地优化BHVs的几何形状。因此,我们开发了第一个用于外源性交联软组织中永久变形效应的结构本构模型,该模型有助于模拟BHVs设计,并减少循环加载期间BHVs几何形状的变化,从而潜在地提高BHVs的耐久性。