  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.
