Universal mechanisms for self-termination of rapid cardiac rhythm

Abstract

Excitable media sustain circulating waves. In the heart, sustained circulating waves can lead to serious impairment or even death. To investigate factors affecting the stability of such waves, we have used optogenetic techniques to stimulate a region at the apex of a mouse heart at a fixed delay after the detection of excitation at the base of the heart. For long delays, rapid circulating rhythms can be sustained, whereas for shorter delays, there are paroxysmal bursts of activity that start and stop spontaneously. By considering the dependence of the action potential and conduction velocity on the preceding recovery time using restitution curves, as well as the reduced excitability (fatigue) due to the rapid excitation, we model prominent features of the dynamics including alternation of the duration of the excited phases and conduction times, as well as termination of the bursts for short delays. We propose that this illustrates universal mechanisms that exist in biological systems for the self-termination of such activities.

Optogenetic manipulation of cardiac electrical dynamics using sub-threshold illumination: dissecting the role of cardiac alternans in terminating rapid rhythms

“…Paradoxically, electrical alternans has also been observed before spontaneous termination of re-entrant rhythms [15]. In a recent study, Biasci and coauthors developed a simplified mathematical model capable of reproducing the electrical dynamics occurring in re-entrant rhythms and demonstrated how alternans are involved in generating non-sustained bursting rhythms [1]. Briefly, when CT and APD oscillate between beats, a stimulus delivered after a beat with a short CT and long APD will encounter a much shorter recovery time than the preceding stimulus.…”

A space-fractional bidomain framework for cardiac electrophysiology: 1D alternans dynamics

“…Understanding the complex dynamics underlying the multiscale features of excitable biological media is becoming of paramount importance in cardiac modelling, especially for personalised medical treatment [2,3]. The enormous effort that has been made to this day in theoretical, experimental, and clinical research in cardiac electrophysiology still has not been able to fully elucidate important issues and underlying mechanisms, such as cell-cell communication, emerging behaviors, irregular rhythms (alternans), and arrhythmias onset [4,5]. Cardiac alternans, in particular, are due to increased dispersion of repolarisation leading to large variations in refractory period and conduction velocity that, in turn, can induce arrhythmias onset (see, e.g., [6,7,8,9] and references therein).…”