Personalized cardiac electrophysiology simulations have demonstrated great potential to study cardiac arrhythmias and help in therapy planning of radio-frequency ablation. Its application to analyze vulnerability to ventricular tachycardia and sudden cardiac death in infarcted patients has been recently explored. However, the detailed multi-scale biophysical simulations used in these studies are very demanding in terms of memory and computational resources, which prevents their clinical translation. In this work, we present a fast phenomenological system based on cellular automata (CA) to simulate personalized cardiac electrophysiology. The system is trained on biophysical simulations to reproduce cellular and tissue dynamics in healthy and pathological conditions, including action potential restitution, conduction velocity restitution and cell safety factor. We show that a full ventricular simulation can be performed in the order of seconds, emulate the results of a biophysical simulation and reproduce a patient’s ventricular tachycardia in a model that includes a heterogeneous scar region. The system could be used to study the risk of arrhythmia in infarcted patients for a large number of scenarios.

Reinforcement learning is one of the most promising machine learning techniques to get intelligent behaviors for embodied agents in simulations. The output of the classic Temporal Difference family of Reinforcement Learning algorithms adopts the form of a value function expressed as a numeric table or a function approximator. The learned behavior is then derived using a greedy policy with respect to this value function. Nevertheless, sometimes the learned policy does not meet expectations, and the task of authoring is difficult and unsafe because the modification of one value or parameter in the learned value function has unpredictable consequences in the space of the policies it represents. This invalidates direct manipulation of the learned value function as a method to modify the derived behaviors. In this paper, we propose the use of Inverse Reinforcement Learning to incorporate real behavior traces in the learning process to shape the learned behaviors, thus increasing their trustworthiness (in terms of conformance to reality). To do so, we adapt the Inverse Reinforcement Learning framework to the navigation problem domain. Specifically, we use Soft Q-learning, an algorithm based on the maximum causal entropy principle, with MARL-Ped (a Reinforcement Learning-based pedestrian simulator) to include information from trajectories of real pedestrians in the process of learning how to navigate inside a virtual 3D space that represents the real environment. A comparison with the behaviors learned using a Reinforcement Learning classic algorithm (Sarsa($\lambda$)) shows that the Inverse Reinforcement Learning behaviors adjust significantly better to the real trajectories.

In silico models offer a promising advancement for studying cardiac arrhythmias and their clinical implications. However, existing detailed mathematical models often suffer from prolonged computational time compared to diagnostic needs. This study introduces a Cellular Automaton (CA) model tailored to replicate atrial electrophysiology in different stages of Atrial Fibrillation (AF), including persistent AF (PsAF). The CA, using a finite set of states, has been trained using biophysical simulations on a reduced domain for a large set of pacing conditions. Fine-tuning included tissue heterogeneity and anisotropic propagation through pacing simulations. Characterized by Action Potential Duration (APD), Diastolic Interval (DI) and Conduction Velocity (CV) for varying levels of electrical remodeling, the biophysical simulations introduced restitution curves or surfaces into the CA. Validation involved a comprehensive comparison with realistic 2D and 3D atrial models, evaluating healthy and pro-arrhythmic behaviors. Comparisons between CA and biophysical solver revealed striking proximity, with a Cycle Length difference of <10 ms in self-sustained re-entry and a 4.66±0.57 ms difference in depolarization times across the complete atrial geometry. Notably, the CA model exhibited a 80% accuracy, 96% specificity and 45% sensitivity in predicting AF inducibility under different pacing sites and substrate conditions. Additionally, the CA allowed for a 64-fold decrease in computing time compared to the biophysical solver. CA emerges as an efficient and valid model for simulation of atrial electrophysiology across different stages of AF, with potential as a general screening tool for rapid tests. While biophysical tests are recommended for investigating specific mechanisms, CA proves valuable in clinical applications for personalized therapy planning through digital twin simulations.

This study presents a novel methodology for stratifying post-myocardial infarction patients at risk of ventricular arrhythmias using patient-specific 3D cardiac models derived from late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) images. The method integrates imaging and computational simulation with the fast electrophysiology solver, Arritmic3D, enabling rapid and accurate ventricular arrhythmias (VA) risk assessment in clinical timeframes. Applied to 51 patients, the solver generated thousands of personalized simulations exploring ranges of values for several parameters to evaluate arrhythmia inducibility and predict VA risk. Key findings include the identification of slow conduction channels (SCCs) within scar tissue as critical to reentrant arrhythmias and the localization of high-risk zones for potential intervention. The Arrhythmic Risk Score (ARRISK), developed from simulation results, demonstrated strong concordance with clinical outcomes and outperformed traditional imaging-based risk stratification. The methodology is fully automated, requiring minimal user intervention, and offers a promising tool for improving precision medicine in cardiac care by enhancing patient-specific arrhythmia risk assessment and guiding treatment strategies.