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 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,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 TAWSSPa 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, and 0.217 to 0.539 Pa, respectively. Atm s, 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.