Key result
Passive atrial stretch promotes after-depolarizations and alters conduction dynamics in computational models.
Why the study?
Mechano-electric coupling in atrial tissue has received sparse investigation despite its association with chronic atrial dilation and atrial fibrillation, with multiple potential mechanisms identified.
Does not yet support changes in AF management; extends computational evidence on stretch effects while leaving clinical implications open.
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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Varela et al. (2020) conducted a review in Atrial Fibrillation (Mechano-electric coupling). Mechano-electric coupling pathways and atrial stretch regimes vs. Baseline (no stretch) was evaluated on Action potential duration, conduction velocity, and rotor stability. Computational models showed time-dependent passive atrial stretch caused after-depolarizations and rotor hypermeandering, while chronic stretch decreased conduction velocity and increased APD.
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