Motivation
The phenomenon of changing cardiac electrophysiology by mechanical stimulation is addressed as mechanoelectrical feedback (MEF). Various works label stretch-activated currents (ISAC) as the origin of this mechanoelectrical interaction. ISAC’s can be found in various types of myocytes. In ventricular and atrial myocytes specifically, they are proven to alter the cardiac action potential duration and its propagation. It is assumed that these alterations may have an effect on inducing arrhythmias. Atrial Fibrillation (AF) can be considered as the most common cardiac arrythmia. Therefore, it is of great interest to gain a detailed understanding about all aspects contributing to the initiation and perpetuation of AF.

Project
We focus on a more detailed understanding about the influence of ISAC on AF by performing a simulative study on an electromechanically coupled whole heart model. For this purpose, we hypothesize that the presence of ISAC can trigger extrasystoles in the atria. In order to validate this hypothesis, the contributing conditions to the presence of extrasystoles or repetitive firing in the atria must be identified. First of all, literature research must be carried out to investigate the relevant non-selective cation currents as well as experimentally confirmed tissue properties that promote the occurrence of AF considering these channels. Subsequently, the necessary adaptations regarding remodeling must be implemented in order to perform large-scale whole-heart simulations following single-cell simulations. As for now, we plan on using Courtemanche et al. to model atrial electrophysiology and the Land model to describe the mechanics.