A mechanism for electric turbulence in cardiac tissue with optogenetic modification

TL;DR

This paper uncovers a novel wave break initiation mechanism in optogenetically modified cardiac tissue, revealing how gentle restitution slopes and wave profile conditioning can promote arrhythmogenic re-entry.

Contribution

It introduces a new wave break initiation mechanism in cardiac tissue under sub-threshold optogenetic stimulation, advancing understanding of arrhythmia triggers.

Findings

Discovered wave break mechanism involving wave profile conditioning.

Identified gentle restitution slopes as critical for wave break initiation.

Showed external light removal can trigger re-entry in cardiac tissue.

Abstract

Interruptions in nonlinear wave propagation, commonly referred to as wave breaks, are typical of many complex excitable systems. In the heart they lead to fatal rhythm disorders, the so-called arrhythmias, which are one of the main causes of sudden death in the industrialized world. Progress in the treatment and therapy of cardiac arrhythmias requires a detailed understanding of the triggers and dynamics of these wave breaks. In particular, two very important questions are: 1) What determines the potential of a wave break to initiate re-entry? and 2) How do these breaks evolve such that the system is able to maintain spatiotemporally chaotic electrical activity? Here we approach these questions numerically using optogenetics in an in silico model of human atrial tissue that has undergone chronic atrial fibrillation (cAF) remodelling. In the lesser known sub-threshold illumination r\'egime, we discover a new mechanism of wave break initiation in cardiac tissue that occurs for gentle slopes of the restitution characteristics. This mechanism involves "conditioning" or reshaping the wave profile from front to back, such that, removal of the external light source causes rapid recovery of cells at the waveback, leading to the creation of vulnerable windows for sustained re-entry in spatially extended systems.