Key result
In silico substitution of Kv1.4 for Kv4.3 disrupts action potential restitution and enhances alternans.
Why the study?
To determine how the transient outward K+ current (Ito) contributes to electrophysiological instability, action potential duration restitution, and alternans in sinus rhythm and chronic AF.
Does substitution of Kv1.4 for native Kv4.3 alter the action potential waveform and enhance alternans in human atrial myocyte models?
Does substitution of Kv1.4 for native Kv4.3 alter the action potential waveform and enhance alternans in human atrial myocyte models?
In silico modeling demonstrates that an isoform switch from Kv4.3 to Kv1.4 in human atrial myocytes alters the action potential waveform and enhances alternans, suggesting a mechanism for AF initiation.
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Hypothesis-generating for Kv isoform switching in AF; leaves open in vivo validation and clinical relevance.
Ni et al. (2018) studied Atrial fibrillation. In silico deletion of 50% of native Ito (Kv4.3) and replacement with Kv1.4 vs. Baseline mathematical models of human atrial myocyte action potential was evaluated on Action potential duration restitution and alternans. In silico substitution of Kv1.4 for the native current Kv4.3 produced discontinuities in the initial slope of the action potential duration restitution curve and enhanced alternans.
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