Late sodium current in the pathophysiology of cardiovascular disease: consequences of sodium-calcium overload

Heart. 2006 Jul;92 Suppl 4(Suppl 4):iv1-iv5. doi: 10.1136/hrt.2005.078782.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Arrhythmias, Cardiac / drug therapy
  • Arrhythmias, Cardiac / metabolism
  • Arrhythmias, Cardiac / physiopathology*
  • Calcium / metabolism*
  • Calcium Channels / physiology
  • Humans
  • Myocardial Contraction / physiology
  • Myocardium / metabolism
  • Myocytes, Cardiac / metabolism
  • Sodium / metabolism*
  • Sodium Channels / physiology
  • Sodium-Calcium Exchanger / physiology
  • Tetrodotoxin / physiology

Substances

  • Calcium Channels
  • Sodium Channels
  • Sodium-Calcium Exchanger
  • Tetrodotoxin
  • Sodium
  • Calcium