Why the study?
Sustained circulating waves in the heart can cause serious impairment or death, prompting investigation into factors affecting the stability of such waves.
Optogenetic stimulation in mouse hearts demonstrates that action potential restitution and reduced excitability (fatigue) are universal mechanisms for the self-termination of rapid cardiac rhythms.
Suggests restitution and fatigue drive self-termination in mouse hearts; leaves open translation to human arrhythmia mechanisms.
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.
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Biasci et al. (2020) studied this question.
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