Mechano-electric coupling (MEC) in the 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 conductance 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  single cell and tissue simulations in presence of various combination of the mechanisms and applied stretch , in order to assess the relative significance of each mechanism in determining action potential duration, conduction velocity and rotor stability. For chronic  stretch, we find that stretch-induced alterations in membrane capacitance decrease conduction velocity and increase action potential duration  . In the presence of  passive atrial stretch, stretch-activated channels play the largest role, leading to after-depolarizations and rotor hypermeandering  .
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 .
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the
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conductance
capacitance
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computational simulations using
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simulations
models
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combination of the mechanisms and applied stretch , in order
stretch regimes and MEC pathways. This allows us
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mechanism
pathway
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atrial
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, in agreement with experimental findings
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time-dependent
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. 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