Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5961366 | Heart Rhythm | 2013 | 9 Pages |
Abstract
These data suggest that cytosolic Na+ entry and its modulation of Ca2+ handling are necessary for arrhythmogenesis. During the loss of inward-rectifier K+ current function, not only Na+/Ca2+-exchange dominance but Na+ flux may determine arrhythmia burden. Therefore, selective inhibition of TTX-sensitive Na+ channels may offer a potential therapeutic target to alleviate arrhythmias during states of Ca2+ overload secondary to loss of inward-rectifier K+ current function without compromising the excitability reserve.
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Authors
PrzemysÅaw B. PharmD, PhD, Amara Greer-Short, Steven PhD,