In-Silico study on the Dynamics of Atrial Fibrillation: Evaluating the Effects of Different Fibrotic Remodelling in Low Voltage Areas.
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Background: Personalized computational models integrate the influences of personalised anatomy and atrial fibrillation (AF) remodelling, including fibrosis, for analysing patient-specific AF causes and testing therapy response. Additionally, there is still uncertainty regarding the meaning of areas in electroanatomic mapping data that indicates the presence of fibrosis, such as low voltage areas occurring at different pacing rates. We aim to explore the impact of fibrosis types on AF properties by comparing patient-specific models including slow conduction velocity (CV), ionic channel changes, or replacement fibrosis in low voltage areas identified through omnipolar mapping at various pacing rates. Methods: Patients undergoing ablation for persistent AF provided data on voltage, left atrial (LA) anatomy, and local activation times (LATs). LATs were acquired at pacing intervals of 250ms and 600ms, using coronary sinus pacing in sinus rhythm. An automated Python process generated personalised anatomical models for 10 cases to conduct electrophysiological simulations. Low CV was assigned to peak omnipolar voltage (OV) locations less than 0.5mV in conductivity models. Ionic properties in fibrotic areas (peak OV < 0.5mV) were adjusted for ionic changes. In simulations where replacement fibrosis was included through a probabilistic percolation method, percolation was modelled using a random number generator to remove elements of low voltage. Pulmonary vein isolation was simulated in each model after 5s of AF, and wavefront propagation patterns were analysed in 7 anatomical segments (Figure A). Results: Figure B illustrates an example where rotational activity is higher at CS250ms compared to CS600ms, the anterior wall displayed the highest rotational activity in 7 cases for CS250ms and 9 cases for CS600ms in models with conductivity fibrotic remodelling. Combined percolation and conductivity remodelling resulted in rotational activity on the anterior wall in 9 cases at CS250ms and 7 cases at CS600ms. In simulations with replacement fibrosis (percolation), the roof and anterior wall exhibited the highest rotational activity in 5 cases at CS250ms, while at CS600ms, the posterior wall showed most of the rotational activity in 7 cases (Figure C). All fibrosis models with ionic changes terminated in over half of the cases for both pacing rates. Conclusion: The complex impacts on AF dynamics are caused by low voltage’s impact on fibrotic remodelling.