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. 2013 Jan 19;98(2):286–296. doi: 10.1093/cvr/cvt012

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©The Author 2013. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial use, distribution, and reproduction in any medium, provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oup.com

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Possible hypotheses to explain how I_Na can contribute to wave initiation and propagation. (A) Entry of Na⁺ ions occurs via I_Na and an alteration of wave properties may result from changes in [Na⁺]_i, particularly in the sub-sarcolemmal space. In this proposed mechanism (1) increased fuzzy space [Na⁺] provides a milieu that enhances the probability of (2) Ca²⁺ sparks leading to (3) the activation and firing of an adjacent RyR cluster to result in (4) wave initiation and propagation throughout the cell. (B) Alternatively Na_v1.5 channels may be involved in wave propagation per se in the intact cardiomyocyte. Such involvement could comprise (1) spontaneous SR Ca²⁺ release in the form of a spark resulting in (2) local Ca²⁺ efflux by NCX causing (3) local depolarization of the sarcolemma, which (4) subsequently results in local activation of I_Na and I_Ca assisting the rise in local (‘fuzzy space’) [Ca²⁺]_i that can lead to (5) adjacent RyR clusters firing and (6) wave propagation.