Key result
Simulated acute AF expands LAA low shear strain to ~86%, indicating increased thromboembolic risk.
Why the study?
Most thrombi causing ischemic complications in AF originate in the LAA, which has large interindividual morphological variability.
Do patient-specific morphological features of the LAA affect hemodynamic thromboembolic risk under atrial fibrillation?
Do patient-specific morphological features of the LAA affect hemodynamic thromboembolic risk under atrial fibrillation?
Local LAA topological features such as sudden bends, trabeculae, and lobes are more directly associated with thromboembolic risk than the global shape of the appendage.
Local LAA morphology may modulate thromboembolic risk in AF; animal data leaves translation to patients open.
Background: A large majority of thrombi causing ischemic complications under atrial fibrillation (AF) originate in the left atrial appendage (LAA), an anatomical structure departing from the left atrium, characterized by a large morphological variability between individuals. This work analyses the hemodynamics simulated for different patient-specific models of LAA by means of computational fluid-structure interaction studies, modeling the effect of the changes in contractility and shape resulting from AF. Methods: Three operating conditions were analyzed: sinus rhythm, acute atrial fibrillation, and chronic atrial fibrillation. These were simulated on four patient-specific LAA morphologies, each associated with one of the main morphological variants identified from the common classification: chicken wing, cactus, windsock, and cauliflower. Active contractility of the wall muscle was calibrated on the basis of clinical evaluations of the filling and emptying volumes, and boundary conditions were imposed on the fluid to replicate physiological and pathological atrial pressures, typical of the various operating conditions. Results: The LAA volume and shear strain rates were analyzed over time and space for the different models. Globally, under AF conditions, all models were well aligned in terms of shear strain rate values and predicted levels of risk. Regions of low shear rate, typically associated with a higher risk of a clot, appeared to be promoted by sudden bends and focused at the trabecule and the lobes. These become substantially more pronounced and extended with AF, especially under acute conditions. Conclusion: This work clarifies the role of active and passive contraction on the healthy hemodynamics in the LAA, analyzing the hemodynamic effect of AF that promotes clot formation. The study indicates that local LAA topological features are more directly associated with a thromboembolic risk than the global shape of the appendage, suggesting that more effective classification criteria should be identified.
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Musotto et al. (2022) studied Atrial Fibrillation (n=4). Simulated acute and chronic atrial fibrillation vs. Simulated sinus rhythm was evaluated on Percentage of left atrial appendage area exposed to shear strain rate below 5 s-1 for the entire cycle. Simulated acute atrial fibrillation expanded regions of low shear strain rate (<5 s-1) to 55-86% of the left atrial appendage area compared to 0-4% in sinus rhythm, indicating increased thromboembolic risk.
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