Key result
Computational modeling indicates that atrial fibrillation aggravates thrombosis, which primarily forms on the left atrial appendage wall before expanding internally.
Why the study?
Remodeling of left atrial morphology and function from AF can exacerbate LA thrombosis and increase stroke risk, prompting investigation into the effect of AF on LA hemodynamics and thrombosis.
Computational modeling of the left atrium demonstrates that atrial fibrillation exacerbates thrombosis, primarily originating on the wall of the left atrial appendage.
Should not yet change AF thrombosis management; hypothesis-generating for LAA wall mechanisms pending clinical validation.
The remodeling of the left atrial morphology and function caused by atrial fibrillation (AF) can exacerbate thrombosis in the left atrium (LA) even spike up the risk of stroke within AF patients. This study explored the effect of the AF on hemodynamic and thrombosis in LA. We reconstructed the patient-specific anatomical shape of the LA and considered the non-Newtonian property of the blood. The thrombus model was applied in the LA models to simulate thrombosis. Our results indicate that AF can aggravate thrombosis which mainly occurs in the left atrial appendage (LAA). Thrombosis first forms on the LAA wall then expands toward the internal LAA. The proposed computational model also shows the potential application of numerical analyses to help assess the risk of thrombosis in AF patients.
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Wang et al. (2020) studied Atrial fibrillation. Atrial fibrillation was evaluated on Thrombosis risk and location in the left atrium. Computational modeling indicates that atrial fibrillation aggravates thrombosis, which primarily forms on the left atrial appendage wall before expanding internally.
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