Non-Newtonian Blood Rheology Impacts Left Atrial Stasis in Patient-Specific Simulations

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 (LAA), a narrow sac of varied morphology 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 of blood flow using the Carreau-Yasuda constitutive relation. We examined N=6 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 blood residence time. Comparing non-Newtonian and Newtonian simulations indicates that slow flow in the LAA can trigger increases in blood viscosity, altering secondary swirling flows and intensifying LAA blood stasis. While some of these effects can be subtle when studied by instantaneous metrics such as the shear rate or kinetic energy, they are manifest 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 to explain the clinically reported correlation between hematocrit and stroke incidence. In summary, we submit that hematocrit-dependent non-Newtonian blood rheology should be considered in calculating patient-specific indices of blood stasis by computational fluid dynamics.