Demonstration of Patient-Specific Simulations to Assess Left Atrial Appendage Thrombogenesis Risk
Abstract
Atrial fibrillation (AF) alters left atrial (LA) hemodynamics, which can lead to thrombosis in the left atrial appendage (LAA), systemic embolism and stroke. A personalized risk-stratification of AF patients for stroke would permit improved balancing of preventive anticoagulation therapies against bleeding risk. We investigated how LA anatomy and function impact LA and LAA hemodynamics, and explored whether patient-specific analysis by computational fluid dynamics (CFD) can predict the risk of LAA thrombosis. We analyzed 4D-CT acquisitions of LA wall motion with an in-house immersed-boundary CFD solver. We considered six patients with diverse atrial function, three with either a LAA thrombus (removed digitally before running the simulations) or a history of transient ischemic attacks (LAAT/TIA-pos), and three without a LAA thrombus or TIA (LAAT/TIA-neg). We found that blood inside the left atrial appendage of LAAT/TIA-pos patients had marked alterations in residence time and kinetic energy when compared with LAAT/TIA-neg patients. In addition, we showed how the LA conduit, reservoir and booster functions distinctly affect LA and LAA hemodynamics. Finally, fixed-wall and moving-wall simulations produced different LA hemodynamics and residence time predictions for each patient. Consequently, fixed-wall simulations risk-stratified our small cohort for LAA thrombosis worse than moving-wall simulations, particularly patients with intermediate LAA residence time. Overall, these results suggest that both wall kinetics and LAA morphology contribute to LAA blood stasis and thrombosis.
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BibTeX
@article{garciavillalba2026demonstration,
title = {{Demonstration of Patient-Specific Simulations to Assess Left Atrial Appendage Thrombogenesis Risk}},
author = {Manuel García-Villalba and Lorenzo Rossini and Alejandro Gonzalo and Davis Vigneault and Pablo Martinez-Legazpi and Eduardo Durán and Oscar Flores and Javier Bermejo and Elliot Mcveigh and Andrew M. Kahn and Juan C. Del Álamo},
journal = {Frontiers in Physiology},
year = {2026},
month = oct,
doi = {10.3389/fphys.2021.596596},
url = {https://hal.science/hal-05781418v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Demonstration of Patient-Specific Simulations to Assess Left Atrial Appendage Thrombogenesis Risk
AU - Manuel García-Villalba
AU - Lorenzo Rossini
AU - Alejandro Gonzalo
AU - Davis Vigneault
AU - Pablo Martinez-Legazpi
AU - Eduardo Durán
AU - Oscar Flores
AU - Javier Bermejo
AU - Elliot Mcveigh
AU - Andrew M. Kahn
AU - Juan C. Del Álamo
PY - 2026
DA - 2026/10/06
JO - Frontiers in Physiology
DO - 10.3389/fphys.2021.596596
UR - https://hal.science/hal-05781418v1
AB - Atrial fibrillation (AF) alters left atrial (LA) hemodynamics, which can lead to thrombosis in the left atrial appendage (LAA), systemic embolism and stroke. A personalized risk-stratification of AF patients for stroke would permit improved balancing of preventive anticoagulation therapies against bleeding risk. We investigated how LA anatomy and function impact LA and LAA hemodynamics, and explored whether patient-specific analysis by computational fluid dynamics (CFD) can predict the risk of LAA thrombosis. We analyzed 4D-CT acquisitions of LA wall motion with an in-house immersed-boundary CFD solver. We considered six patients with diverse atrial function, three with either a LAA thrombus (removed digitally before running the simulations) or a history of transient ischemic attacks (LAAT/TIA-pos), and three without a LAA thrombus or TIA (LAAT/TIA-neg). We found that blood inside the left atrial appendage of LAAT/TIA-pos patients had marked alterations in residence time and kinetic energy when compared with LAAT/TIA-neg patients. In addition, we showed how the LA conduit, reservoir and booster functions distinctly affect LA and LAA hemodynamics. Finally, fixed-wall and moving-wall simulations produced different LA hemodynamics and residence time predictions for each patient. Consequently, fixed-wall simulations risk-stratified our small cohort for LAA thrombosis worse than moving-wall simulations, particularly patients with intermediate LAA residence time. Overall, these results suggest that both wall kinetics and LAA morphology contribute to LAA blood stasis and thrombosis.
SN - 1664-042X
ER -