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Interruptions in nonlinear wave propagation, commonly referred to as wavebreaks, are typical of many complex excitable systems. In the heart they leadto fatal rhythm disorders, the so-called arrhythmias, which are one of the maincauses of sudden death in the industrialized world. Progress in the treatmentand therapy of cardiac arrhythmias requires a detailed understanding of thetriggers and dynamics of these wave breaks. In particular, two very importantquestions are: 1) What determines the potential of a wave break to initiatere-entry? and 2) How do these breaks evolve such that the system is able tomaintain spatiotemporally chaotic electrical activity? Here we approach thesequestions numerically using optogenetics in an in silico model of human atrialtissue that has undergone chronic atrial fibrillation (cAF) remodelling. In thelesser known sub-threshold illumination r\'egime, we discover a new mechanismof wave break initiation in cardiac tissue that occurs for gentle slopes of therestitution characteristics. This mechanism involves "conditioning" orreshaping the wave profile from front to back, such that, removal of theexternal light source causes rapid recovery of cells at the waveback, leadingto the creation of vulnerable windows for sustained re-entry in spatiallyextended systems.

A mechanism for electric turbulence in cardiac tissue with optogenetic modification