Spronck Bart, Heusinkveld Maarten H G, Donders Wouter P, de Lepper Anouk G W, Op't Roodt Jos, Kroon Abraham A, Delhaas Tammo, Reesink Koen D
Department of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands;
Department of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands; Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands;
Am J Physiol Heart Circ Physiol. 2015 Mar 15;308(6):H568-82. doi: 10.1152/ajpheart.00290.2014. Epub 2014 Dec 24.
Aging has a profound influence on arterial wall structure and function. We have previously reported the relationship among pulse wave velocity, age, and blood pressure in hypertensive subjects. In the present study, we aimed for a quantitative interpretation of the observed changes in wall behavior with age using a constitutive modeling approach. We implemented a model of arterial wall biomechanics and fitted this to the group-averaged pressure-area (P-A) relationship of the "young" subgroup of our study population. Using this model as our take-off point, we assessed which parameters had to be changed to let the model describe the "old" subgroup's P-A relationship. We allowed elastin stiffness and collagen recruitment parameters to vary and adjusted residual stress parameters according to published age-related changes. We required wall stress to be homogeneously distributed over the arterial wall and assumed wall stress normalization with age by keeping average "old" wall stress at the "young" level. Additionally, we required axial force to remain constant over the cardiac cycle. Our simulations showed an age-related shift in pressure-load bearing from elastin to collagen, caused by a decrease in elastin stiffness and a considerable increase in collagen recruitment. Correspondingly, simulated diameter and wall thickness increased by about 20 and 17%, respectively. The latter compared well with a measured thickness increase of 21%. We conclude that the physiologically realistic changes in constitutive properties we found under physiological constraints with respect to wall stress could well explain the influence of aging in the stiffness-pressure-age pattern observed.
衰老对动脉壁结构和功能有深远影响。我们之前报道过高血压患者脉搏波速度、年龄和血压之间的关系。在本研究中，我们旨在使用本构模型方法对观察到的动脉壁行为随年龄的变化进行定量解释。我们实施了一个动脉壁生物力学模型，并将其拟合到我们研究人群中“年轻”亚组的组平均压力-面积（P-A）关系。以该模型为出发点，我们评估了哪些参数必须改变才能使模型描述“老年”亚组的P-A关系。我们允许弹性蛋白刚度和胶原蛋白募集参数变化，并根据已发表的与年龄相关的变化调整残余应力参数。我们要求壁应力在动脉壁上均匀分布，并通过将“老年”壁平均应力保持在“年轻”水平来假定壁应力随年龄归一化。此外，我们要求轴向力在心动周期中保持恒定。我们的模拟显示，由于弹性蛋白刚度降低和胶原蛋白募集显著增加，压力负荷承受从弹性蛋白向胶原蛋白发生了与年龄相关的转变。相应地，模拟直径和壁厚分别增加了约20%和17%。后者与测量到的21%的厚度增加相当吻合。我们得出结论，在生理约束下我们发现的关于壁应力的本构特性的生理现实变化，能够很好地解释衰老对观察到的刚度-压力-年龄模式的影响。
