Department of Mechanical and Aerospace Engineering, University of California San Diego, La Jolla, California, USA.
Department of Mechanical Engineering, University of Washington, Seattle, Washington, USA.
Int J Numer Method Biomed Eng. 2022 Jun;38(6):e3597. doi: 10.1002/cnm.3597. Epub 2022 Apr 7.
The lack of mechanically effective contraction of the left atrium (LA) during atrial fibrillation (AF) disturbs blood flow, increasing the risk of thrombosis and ischemic stroke. Thrombosis is most likely in the left atrial appendage (LAA), a small narrow sac where blood is prone to stagnate. Slow flow promotes the formation of erythrocyte aggregates in the LAA, also known as rouleaux, causing viscosity gradients that are usually disregarded in patient-specific simulations. To evaluate these non-Newtonian effects, we built atrial models derived from 4D computed tomography scans of patients and carried out computational fluid dynamics simulations using the Carreau-Yasuda constitutive relation. We examined six patients, three of whom had AF and LAA thrombosis or a history of transient ischemic attacks (TIAs). We modeled the effects of hematocrit and rouleaux formation kinetics by varying the parameterization of the Carreau-Yasuda relation and modulating non-Newtonian viscosity changes based on residence time. Comparing non-Newtonian and Newtonian simulations indicates that slow flow in the LAA increases blood viscosity, altering secondary swirling flows and intensifying blood stasis. While some of these effects are subtle when examined using instantaneous metrics like shear rate or kinetic energy, they are manifested in the blood residence time, which accumulates over multiple heartbeats. Our data also reveal that LAA blood stasis worsens when hematocrit increases, offering a potential new mechanism for the clinically reported correlation between hematocrit and stroke incidence. In summary, we submit that hematocrit-dependent non-Newtonian blood rheology should be considered when calculating patient-specific blood stasis indices by computational fluid dynamics.
左心房（LA）在心房颤动（AF）期间缺乏机械有效的收缩，扰乱了血流，增加了血栓形成和缺血性中风的风险。血栓最有可能发生在左心耳（LAA），这是一个血液容易停滞的小而狭窄的囊袋。缓慢的血流促进了 LAA 中红细胞聚集的形成，也称为红细胞缗钱状，导致粘度梯度，这些梯度在患者特定的模拟中通常被忽略。为了评估这些非牛顿效应，我们构建了源自患者 4D 计算机断层扫描的心房模型，并使用 Carreau-Yasuda 本构关系进行了计算流体动力学模拟。我们检查了六名患者，其中三名患有 AF 和 LAA 血栓形成或短暂性脑缺血发作（TIA）病史。我们通过改变 Carreau-Yasuda 关系的参数化并根据停留时间调节非牛顿粘度变化来模拟血细胞比容和红细胞缗钱状形成动力学的影响。比较非牛顿和牛顿模拟表明，LAA 中的缓慢血流会增加血液粘度，改变二次旋流并加剧血液停滞。虽然使用剪切率或动能等瞬时指标检查时，这些影响有些微妙，但它们在血液停留时间上表现出来，该停留时间在多个心跳中积累。我们的数据还表明，当血细胞比容增加时，LAA 中的血液停滞会恶化，为临床上报告的血细胞比容与中风发生率之间的相关性提供了一个潜在的新机制。总之，我们认为，在通过计算流体动力学计算患者特定的血液停滞指数时，应考虑依赖血细胞比容的非牛顿血液流变学。
