This editorial highlights basic science evidence that specific arrhythmogenic sodium channel variants mimic CaMKII-induced gating changes, which are enhanced in heart failure.
this issue of Circulation, Koval et al 1 show that 2 arrhythmogenic human cardiac Na channel (hNa V 1.5) variants mimic the altered channel gating effects induced by Ca 2 -calmodulin-dependent protein kinase (CaMKII). They also show that phosphorylation of an adjacent CaMKII target site on Na V 1.5 is enhanced in human heart failure (HF) samples and in the border zone of postinfarcted canine hearts.
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Bers et al. (2012) studied this question.
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