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Published on: February 26, 2013
Disentangling the Hemodynamic Effects of A-Wave Loss and Cardiac Output Reduction in Atrial Fibrillation
Hailey LaBonte1, Ahmad Bshennaty1, Ghasaq Saleh2
1Department of Biomedical Engineering, Michigan Technological University, Houghton, MI, USA.
Insights
Atrial fibrillation (AF) increases thromboembolic risk. Reduced cardiac output (CO) and loss of the A-wave in AF worsen left atrial (LA) blood stasis, with CO restoration alone not fully normalizing flow.
Area of Science:
- Cardiovascular Physiology
- Biomedical Engineering
- Computational Fluid Dynamics
Background:
- Atrial fibrillation (AF) is linked to increased thromboembolic risk.
- The specific hemodynamic impacts of AF-related changes like A-wave loss and reduced cardiac output (CO) on left atrial (LA) function are not fully understood.
- Patient-specific atrial geometry also influences these hemodynamic alterations.
Purpose of the Study:
- To isolate and quantify the hemodynamic effects of A-wave loss and CO reduction on LA flow and stasis.
- To investigate the interplay between AF, CO, and patient-specific atrial anatomy in determining LA hemodynamics.
Main Methods:
- Utilized patient-specific computational fluid dynamics (CFD) simulations on five LA geometries.
- Modeled sinus rhythm transmitral waveforms and modified them to represent AF with both compromised and conserved CO.
- Analyzed hemodynamic parameters including LA velocity, time-averaged wall shear stress (TAWSS), relative residence time (RRT), and blood stasis metrics.
Main Results:
- AF with compromised CO significantly increased LA blood stasis (e.g., 86.7% increase in TAWSS-defined stasis regions).
- Conserving CO during AF partially restored velocity and TAWSS but did not normalize flow organization or near-wall transport.
- A-wave removal, independent of CO, altered near-wall flow organization and contributed to impaired LA washout.
Conclusions:
- AF-related waveform changes promote conditions conducive to increased LA flow stasis.
- The severity of stasis is influenced by both CO levels and individual patient anatomy.
- Restoring CO alone is insufficient to fully normalize LA hemodynamics after A-wave loss, highlighting the independent role of A-wave loss in impaired atrial function.
Purpose:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
