Volume-Constrained Wall Motion Alters Left Atrial Appendage Hemodynamic Descriptors: A CFD Sensitivity Study

Rigid-wall left atrium (LA) and left atrial appendage (LAA) computational fluid dynamics (CFD) models are practical but suppress deformation-driven transport, whereas image-derived wall motion is data- and processing-intensive. We evaluated whether a reduced-order, volume-constrained wall-motion prescription changes computed LA/LAA hemodynamic descriptors relative to a static-wall approximation. A patient-specific LA/LAA geometry was combined with literature-informed phasic volumes and boundary conditions to simulate healthy dynamic, grade-II diastolic dysfunction (DD II) dynamic, and DD II static configurations. The healthy-DD II comparison represents a composite disease-state contrast; the DD II dynamic-static pair isolates wall-motion sensitivity within the same DD II setup. Numerical verification supported the intermediate mesh, Δt = 10⁻³ s, five simulated cycles, and the laminar model for the monitored WSS waveform. Suppressing DD II wall motion reduced mean LAA time-averaged wall shear stress (TAWSS) from 0.05 to 0.01 Pa and increased the analyzed atrial surface fraction with TAWSS < 0.1 Pa from 14.4% to 22.4%. Complete-wall, area-weighted medians changed consistently: TAWSS decreased from 0.570 to 0.349 Pa, whereas oscillatory shear index, relative residence time, and endothelial cell activation potential increased from 0.121 to 0.190, 2.52 to 5.02 Pa⁻¹, and 0.217 to 0.539 Pa⁻¹, respectively. At u_c = 0.10 m s⁻¹, mean persistent volume stasis was similar in the two DD II cases, but the volume with low velocity during at least 90% of the cycle increased from 28.5% to 33.8%. Thus, suppressing prescribed deformation shifted the computed LA/LAA environment toward lower shear, greater shear-directional oscillation, and more spatially persistent low velocity. Volume-constrained motion is therefore useful as an engineering sensitivity tier when image-derived kinematics are unavailable; it is not a validated surrogate for regional atrial motion or a patient-specific predictor of thrombosis. .