A survey of pathways for mechano-electric coupling in the atria

Abstract

Mechano-electric coupling (MEC) in atrial tissue has received sparse investigation to date, despite the well-known association between chronic atrial dilation and atrial fibrillation (AF). Of note, no fewer than six different mechanisms pertaining to stretch-activated channels, cellular capacitance and geometric effects have been identified in the literature as potential players. In this mini review, we briefly survey each of these pathways to MEC. We then perform computational simulations using single cell and tissue models in presence of various stretch regimes and MEC pathways. This allows us to assess the relative significance of each pathway in determining action potential duration, conduction velocity and rotor stability. For chronic atrial stretch, we find that stretch-induced alterations in membrane capacitance decrease conduction velocity and increase action potential duration, in agreement with experimental findings. In the presence of time-dependent passive atrial stretch, stretch-activated channels play the largest role, leading to after-depolarizations and rotor hypermeandering. These findings suggest that physiological atrial stretches, such as passive stretch during the atrial reservoir phase, may play an important part in the mechanisms of atrial arrhythmogenesis.

Interactions between calcium‐induced arrhythmia triggers and the electrophysiological–anatomical substrate underlying the induction of atrial fibrillation

“…No other features were required to locate focal excitations to the PVs, demonstrating that these RMP differences in combination with cellular SCRE are sufficient conditions to promote AF triggers in the PVs. Other features, such as local innervation (Chen et al, 2014;Linz et al, 2014) or stretch (Egorov et al, 2019;Gottlieb et al, 2023;Varela et al, 2021), may or may not be more important for the induction of AF, but they are not required to reproduce our observations.…”