Why the study?
Post-myocardial infarction slow conducting channels promote ventricular tachycardia, but non-invasively stratifying their arrhythmogeneity using MRI imaging features remains difficult.
Arrhythmic3D significantly reduces the computational time required to simulate ventricular arrhythmias in 3D models compared to traditional biophysical solvers, potentially enabling clinical translation.
Patients that have suffered a myocardial infarction are at lifetime high risk for sudden cardiac death (SCD). The so-called slow conducting channels (SCC) that extend throughout the infarct scar region are known to help in the initiation and maintenance of ventricular tachycardias (VT). However, it is difficult to stratify non-invasively their arrhythmogeneity based on imaging features from MRI. We have developed Arrhythmic3D, an automata-based solver which allows to simulate cardiac activation sequences in 3D models, and takes into account action potential duration (APD) restitution, conduction velocity restitution, APD memory, electrotonic-effects and source-sink electrical effects (safety factor). We carried out a simulation study in a patient-specific ventricular model that included a segmented scar and reproduced the clinical monomorphic VT supported by SCC using both a biophysical and the automata solvers. Using a mesh of 2.6 Million elements to compare both solvers, a simulation of 1200ms took 7h in the biophysical solver, versus 76s on Arrhythmic3D, which makes it transferable to clinical environments.
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Serra et al. (2021) studied this question.
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