Key result
Adding EAT effects nearly doubles simulated atrial reentry inducibility compared to fibrosis alone.
Why the study?
The contribution of left atrial epicardial adipose tissue to atrial fibrillation mechanisms is rarely included in computational models, limiting understanding of its pro-arrhythmic role.
Does incorporating epicardial adipose tissue (EAT)-associated electrophysiological effects into fibrosis-based atrial computational models alter reentrant arrhythmia inducibility?
Does incorporating epicardial adipose tissue (EAT)-associated electrophysiological effects into fibrosis-based atrial computational models alter reentrant arrhythmia inducibility?
Incorporating epicardial adipose tissue (EAT) effects into computational models of atrial fibrillation significantly increases the inducibility of functional reentry, particularly in areas where fibrosis and EAT overlap.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“The AF substrate is complex and fibrotic remodeling, while essential, is only one piece of the puzzle. In this study, patient-specific simulations showed that the rare regions where fibrosis and epicardial adipose tissue overlap were the most likely to sustain reentry. A more integrated view of the atrial substrate, combining imaging with mechanistic modeling, is essential to understanding it.”
EAT incorporation into fibrosis models may heighten reentry inducibility; leaves open whether EAT-targeted interventions improve ablation outcomes in persistent AF.
BACKGROUND: Computational models of atrial fibrillation (AF) help clarify arrhythmia mechanisms, but the contribution of left atrial (LA) epicardial adipose tissue (EAT) is rarely included. OBJECTIVE: To assess whether incorporating EAT-associated effects into fibrosis-based atrial models alters reentrant arrhythmia inducibility, and to characterize the pro-arrhythmic properties of EAT-affected tissue. METHODS: LA fibrosis and EAT were quantified by LGE and Dixon MRI in 19 patients with persistent AF. For each patient, three anatomically identical image-personalized models were built (fibrosis only; fibrosis plus half-epicardial EAT effects, 0.5 mm; fibrosis plus full-epicardial EAT effects, 1.0 mm), yielding 855 simulations. In EAT regions, inward rectifier K RESULTS: Sustained reentry occurred in 370 simulations (43.3%), of which 306 had a functional (rotor-driven) component. Functional reentry inducibility rose from 22.8% (fibrosis only) to 41.4% (half-EAT) and 43.2% (full-EAT). At least one functional reentry was inducible in 12/19 fibrosis-only models, 18/19 half-EAT models, and 19/19 full-EAT models. Median inducible simulations per patient increased from 4 to 6 (p=0.004) and 7 (p=0.003), without significant difference between half- and full-EAT (p=0.895). Fibrosis/EAT overlap regions comprised only 2.1% of the LA wall but were the most arrhythmogenic, with a median 65.5% of their volume harboring reentry versus 8.8% (non-substrate), 37.3% (fibrosis), and 42.8% (EAT) (all p<0.001). In an exploratory analysis of PVI-only ablation patients (n=13), fibrosis-EAT overlap outside the PVI region was associated with 1-year recurrence (log-rank p=0.007). CONCLUSION: Adding EAT effects to fibrosis-based models increased sustained functional reentry, with transmural depth contributing only modestly. Reentry anchored preferentially where fibrosis and EAT effects coexisted.
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Chahine et al. (2026) studied Persistent atrial fibrillation (n=19). Epicardial adipose tissue (EAT) electrophysiological effects vs. Fibrosis-only models was evaluated on Functional (rotor-driven) reentry inducibility. Adding full epicardial adipose tissue (EAT) effects to fibrosis-based atrial computational models increased functional reentry inducibility from 22.8% to 43.2%.
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