Inhibition of sodium-dependent calcium overload to treat myocardial ischemia.

Clinical Cardiology
C R Conti

Abstract

Because intracellular sodium and calcium overload play a key role in both mechanical and electrical dysfunction during myocardial ischemia, inhibition of the late sodium current would be expected to decrease the intracellular sodium and calcium overloads and thereby reduce their undesirable effects. Ranolazine selectively inhibits late sodium current relative to peak sodium current, and attenuates the abnormalities of ventricular repolarization and contractility associated with ischemia. This is the currently proposed mechanism (hypothesis) of action of the effects of ranolazine during myocardial ischemia.

References

Jan 22, 2004·JAMA : the Journal of the American Medical Association·Bernard R ChaitmanUNKNOWN Combination Assessment of Ranolazine In Stable Angina (CARISA) Investigators
Apr 20, 2004·Journal of the American College of Cardiology·Bernard R ChaitmanUNKNOWN MARISA Investigators

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Citations

May 12, 2007·International Journal of Clinical Practice·D Q Pham, M Mehta
Jun 17, 2008·American Journal of Physiology. Heart and Circulatory Physiology·Victor A MaltsevAbertas Undrovinas
Jan 22, 2008·American Journal of Physiology. Heart and Circulatory Physiology·Victor A MaltsevAlbertas Undrovinas
Jul 6, 2006·Nature Reviews. Drug Discovery·Jonathan AbramsPeter Kirkpatrick
Feb 1, 2007·Clinical Cardiology·C R Conti

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