A Survey of Pathways for Mechano-Electric Coupling in the Atria

TL;DR

This paper reviews and computationally investigates the pathways of mechano-electric coupling in atrial tissue, highlighting their roles in atrial arrhythmogenesis and the effects of stretch on electrical activity.

Contribution

It provides a comprehensive survey of MEC mechanisms in atria and assesses their relative importance through simulations, linking mechanical stretch to electrical disturbances.

Findings

Stretch-induced membrane capacitance changes decrease conduction velocity.

Stretch-activated channels cause after-depolarizations and rotor hypermeandering.

Passive atrial stretch may contribute to atrial arrhythmias.

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.