TY - JOUR
T1 - Deep Learning Framework for Real-Time Estimation of in-silico Thrombotic Risk Indices in the Left Atrial Appendage
AU - Morales Ferez, Xabier
AU - Mill, Jordi
AU - Juhl, Kristine Aavild
AU - Acebes, Cesar
AU - Iriart, Xavier
AU - Legghe, Benoit
AU - Cochet, Hubert
AU - De Backer, Ole
AU - Paulsen, Rasmus R
AU - Camara, Oscar
N1 - Copyright © 2021 Morales Ferez, Mill, Juhl, Acebes, Iriart, Legghe, Cochet, De Backer, Paulsen and Camara.
PY - 2021
Y1 - 2021
N2 - Patient-specific computational fluid dynamics (CFD) simulations can provide invaluable insight into the interaction of left atrial appendage (LAA) morphology, hemodynamics, and the formation of thrombi in atrial fibrillation (AF) patients. Nonetheless, CFD solvers are notoriously time-consuming and computationally demanding, which has sparked an ever-growing body of literature aiming to develop surrogate models of fluid simulations based on neural networks. The present study aims at developing a deep learning (DL) framework capable of predicting the endothelial cell activation potential (ECAP), an in-silico index linked to the risk of thrombosis, typically derived from CFD simulations, solely from the patient-specific LAA morphology. To this end, a set of popular DL approaches were evaluated, including fully connected networks (FCN), convolutional neural networks (CNN), and geometric deep learning. While the latter directly operated over non-Euclidean domains, the FCN and CNN approaches required previous registration or 2D mapping of the input LAA mesh. First, the superior performance of the graph-based DL model was demonstrated in a dataset consisting of 256 synthetic and real LAA, where CFD simulations with simplified boundary conditions were run. Subsequently, the adaptability of the geometric DL model was further proven in a more realistic dataset of 114 cases, which included the complete patient-specific LA and CFD simulations with more complex boundary conditions. The resulting DL framework successfully predicted the overall distribution of the ECAP in both datasets, based solely on anatomical features, while reducing computational times by orders of magnitude compared to conventional CFD solvers.
AB - Patient-specific computational fluid dynamics (CFD) simulations can provide invaluable insight into the interaction of left atrial appendage (LAA) morphology, hemodynamics, and the formation of thrombi in atrial fibrillation (AF) patients. Nonetheless, CFD solvers are notoriously time-consuming and computationally demanding, which has sparked an ever-growing body of literature aiming to develop surrogate models of fluid simulations based on neural networks. The present study aims at developing a deep learning (DL) framework capable of predicting the endothelial cell activation potential (ECAP), an in-silico index linked to the risk of thrombosis, typically derived from CFD simulations, solely from the patient-specific LAA morphology. To this end, a set of popular DL approaches were evaluated, including fully connected networks (FCN), convolutional neural networks (CNN), and geometric deep learning. While the latter directly operated over non-Euclidean domains, the FCN and CNN approaches required previous registration or 2D mapping of the input LAA mesh. First, the superior performance of the graph-based DL model was demonstrated in a dataset consisting of 256 synthetic and real LAA, where CFD simulations with simplified boundary conditions were run. Subsequently, the adaptability of the geometric DL model was further proven in a more realistic dataset of 114 cases, which included the complete patient-specific LA and CFD simulations with more complex boundary conditions. The resulting DL framework successfully predicted the overall distribution of the ECAP in both datasets, based solely on anatomical features, while reducing computational times by orders of magnitude compared to conventional CFD solvers.
UR - http://www.scopus.com/inward/record.url?scp=85109978860&partnerID=8YFLogxK
U2 - 10.3389/fphys.2021.694945
DO - 10.3389/fphys.2021.694945
M3 - Journal article
C2 - 34262482
VL - 12
SP - 694945
JO - Frontiers in Physiology
JF - Frontiers in Physiology
SN - 1664-042X
M1 - 694945
ER -