We present a new phenomenological model of human ventricular epicardial cells and we test its reentry dynamics. The model is derived from the Rogers-McCulloch formulation of the FitzHugh-Nagumo equations and represents the total ionic current divided into three contributions corresponding to the excitatory, recovery and transient outward currents. Our model reproduces the main characteristics of human epicardial tissue, including action potential amplitude and morphology, upstroke velocity, and action potential duration and conduction velocity restitution curves. The reentry dynamics is stable, and the dominant period is about 270 ms, which is comparable to clinical values. The proposed model is the first phenomenological model able to accurately resemble human experimental data by using only 3 state variables and 17 parameters. Indeed, it is more computationally efficient than existing models (i.e., almost two times faster than the minimal ventricular model). Beyond the computational efficiency, the low number of parameters facilitates the process of fitting the model to the experimental data.

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In this work, we reported a computational study to quantitatively determine the individual contributions of three candidate arrhythmic factors associated with Brugada Syndrome. In particular, we focused our analysis on the role of structural abnormalities, dispersion of repolarization, and size of the diseased region. We developed a human phenomenological model capable of replicating the action potential characteristics both in Brugada Syndrome and in healthy conditions. Inspired by physiological observations, we employed the phenomenological model in a 2D geometry resembling the pathological RVOT coupled with healthy epicardial tissue. We assessed the insurgence of sustained reentry as a function of electrophysiological and structural abnormalities. Our computational study indicates that both structural and repolarization abnormalities are essential to induce sustained reentry. Furthermore, our results suggest that neither dispersion of repolarization nor structural abnormalities are sufficient on their own to induce sustained reentry. It should be noted how our study seems to explain an arrhythmic mechanism that unifies the classic repolarization and depolarization hypotheses of the pathophysiology of the Brugada Syndrome. Finally, we believe that this work may offer a new perspective on the computational and clinical investigation of Brugada Syndrome and its arrhythmic behaviour.

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