Disentangling the Hemodynamic Effects of A-Wave Loss and Cardiac Output Reduction in Atrial Fibrillation

Atrial fibrillation (AF) increases thromboembolic risk, yet the relative hemodynamic contributions of A-wave loss, cardiac output (CO) reduction, and patient-specific atrial geometry remain incompletely understood. This study aimed to isolate the hemodynamic consequences of A-wave removal and CO reduction on left atrial (LA) flow and stasis.

Five patient-specific LA geometries were evaluated using transient laminar CFD simulations. For each geometry, the sinus rhythm transmitral waveform was used as the baseline and modified to represent AF with compromised and conserved CO. Hemodynamic endpoints included LA velocity, time-averaged wall shear stress (TAWSS), relative residence time (RRT), oscillatory shear index (OSI), divergence of the average wall shear stress (AWSS), and threshold-defined blood stasis metrics.

Analysis of the pooled spatial distributions across the 5 patient geometries showed that AF-compromised CO conditions resulted in decreased LA velocity, decreased TAWSS (0.788 to 0.508 Pa), increased RRT, and increased blood stasis regions based on velocity (61.8%), TAWSS (86.7%), and RRT (88.5%). When CO was conserved under AF conditions, peak velocity and pooled TAWSS were partially restored (0.508 to 0.827 Pa), with reductions in pooled RRT and threshold-defined stasis ratios (velocity: 42.5%; TAWSS: 59.8%; RRT: 71.7%); however, flow organization, near-wall transport patterns, and several stasis-related metrics remained altered relative to sinus rhythm despite CO restoration. Changes in AWSS indicated altered near-wall flow organization following A-wave removal.

Waveform modifications representing AF-related alterations promoted hemodynamic conditions associated with increased flow stasis, with the magnitude of these effects depending on CO and patient anatomy. CO restoration alone did not fully normalize atrial flow organization, suggesting that A-wave loss contributes to impaired LA washout and altered near-wall hemodynamics independent of bulk flow restoration.