Computational simulations of hemodynamic changes within thoracic, coronary, and cerebral arteries following early wall remodeling in response to distal aortic coarctation
Computational simulations of hemodynamic changes within thoracic, coronary, and cerebral arteries following early wall remodeling in response to distal aortic coarctation
复制标题
DOI：
10.1007/s10237-012-0383-x
复制
发表时间：
2013-01-01
影响因子：
3.5
通讯作者：
Figueroa, C. Alberto
中科院分区：
文献类型：
--
作者：
Coogan, Jessica S.;Humphrey, Jay D.;Figueroa, C. Alberto
越来越多的证据表明，大动脉内血压和血流的脉动特征作为血管壁生长和重塑的机械生物刺激发挥着特别重要的作用。然而，更好地理解不断变化的壁几何形状、结构和特性与血流动力学之间的高度耦合相互作用将需要更多的实验数据。计算流体-固体生长模型有望帮助设计和解释此类实验，并确定观察到的动脉适应的候选机械生物学机制。受最近动物主动脉缩窄模型的启发，我们使用计算流固相互作用模型来研究由于远端主动脉缩窄和随后的壁适应空间变化对胸主动脉、冠状动脉、颈动脉和脑动脉内的血流动力学可能产生的局部和全身影响。特别是，我们研究了急性心脏代偿的初始阶段（即维持心输出量），然后是早期动脉壁重塑（即空间变化的壁增厚和硬化）。例如，结果表明，虽然缩窄增加了近端血管的平均压力和脉压，但最接近缩窄的位置的脉压变化最大。此外，在引入空间变化的壁适应后，压力、左心室做功和波速均增加。最后，血管壁应变同样经历了与血管壁适应程度一致的空间变化。
Mounting evidence suggests that the pulsatile character of blood pressure and flow within large arteries plays a particularly important role as a mechano-biological stimulus for wall growth and remodeling. Nevertheless, understanding better the highly coupled interactions between evolving wall geometry, structure, and properties and the hemodynamics will require significantly more experimental data. Computational fluid-solid-growth models promise to aid in the design and interpretation of such experiments and to identify candidate mechanobiological mechanisms for the observed arterial adaptations. Motivated by recent aortic coarctation models in animals, we used a computational fluid-solid interaction model to study possible local and systemic effects on the hemodynamics within the thoracic aorta and coronary, carotid, and cerebral arteries due to a distal aortic coarctation and subsequent spatial variations in wall adaptation. In particular, we studied an initial stage of acute cardiac compensation (i.e., maintenance of cardiac output) followed by early arterial wall remodeling (i.e., spatially varying wall thickening and stiffening). Results suggested, for example, that while coarctation increased both the mean and pulse pressure in the proximal vessels, the locations nearest to the coarctation experienced the greatest changes in pulse pressure. In addition, after introducing a spatially varying wall adaptation, pressure, left ventricular work, and wave speed all increased. Finally, vessel wall strain similarly experienced spatial variations consistent with the degree of vascular wall adaptation.