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Late sodium current in cardiac cells is very small compared with the fast component, but as it flows throughout the action potential it may make a substantial contribution to sodium loading during each cardiac cycle. Late sodium current may contribute to triggering arrhythmia in two ways: by causing repolarisation failure (early after depolarisations); and by triggering late after depolarisations attributable to calcium oscillations in sodium-calcium overload conditions. Reduction of late sodium current would therefore be expected to have therapeutic benefits, particularly in disease states such as ischaemia in which sodium-calcium overload is a major feature.

Original publication

DOI

10.1136/hrt.2005.078782

Type

Journal article

Journal

Heart

Publication Date

07/2006

Volume

92 Suppl 4

Pages

iv1 - iv5

Keywords

Arrhythmias, Cardiac, Calcium, Calcium Channels, Humans, Myocardial Contraction, Myocardium, Myocytes, Cardiac, Sodium, Sodium Channels, Sodium-Calcium Exchanger, Tetrodotoxin