Non‐Newtonian blood rheology impacts left atrial stasis in patient‐specific simulations

• Published in: International journal for numerical methods in biomedical engineering 2022-06, Vol.38 (6), p.e3597-n/a
• Main Authors: Gonzalo, Alejandro, García‐Villalba, Manuel, Rossini, Lorenzo, Durán, Eduardo, Vigneault, Davis, Martínez‐Legazpi, Pablo, Flores, Oscar, Bermejo, Javier, McVeigh, Elliot, Kahn, Andrew M., del Alamo, Juan C.
• Format: Article
• Language: English
• Subjects: Atria; Atrial Appendage; Atrial Fibrillation; Blood flow; blood viscosity; Computational fluid dynamics; Computed tomography; Computer applications; Constitutive relationships; Erythrocytes; Fibrillation; Fluid dynamics; Heart Atria; Hematocrit; Humans; Hydrodynamics; Ischemia; Kinetic energy; left atrium; Parameterization; Residence time distribution; Rheological properties; Rheology; Rheology - methods; Shear rate; Simulation; Stroke; Swirling; Thromboembolism; Thrombosis; Thrombosis - complications; Viscosity
• ISSN: 2040-7939; 2040-7947
• DOI: 10.1002/cnm.3597

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. The left atrial appendage (LAA) is the most frequent site of intracardiac thrombosis, a major cause of ischemic stroke. Slow blood flow causes viscosity gradients in the LAA but these non‐Newtonian effects have been neglected so far in hemodynamic simulations. We built patient‐specific atrial models from 4D‐CT images simulated blood flow using non‐Newtonian constitutive laws that incorporate the effects of hematocrit and rouleaux formation kinetics. Our simulations reveal important hematocrit‐dependent effects in patient‐specific indices of blood stasis like residence time.