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Cardiovascular Research 2001 51(2):194-197; doi:10.1016/S0008-6363(01)00356-X
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Cardiac sodium–calcium exchanger: a double-edged sword

Simon J Conway* and Srinagesh V Koushik

Institute of Molecular Medicine and Genetics, and Department of Cell Biology and Anatomy, Medical College of Georgia, 1120 15th Street, CB2803, Augusta, GA 30912-2640, USA

* Corresponding author. Tel.: +1-706-721-8775; fax: +1-706-721-8732 sconway@mail.mcg.edu

Received 31 May 2001; accepted 31 May 2001

The first 150 words of the full text of this article appear below.

See article by Schäfer et al. [31] (pages 241–250) in this issue.

Development of heart failure is associated with an impairment of intracellular calcium (Ca2+) handling. During the past decade, pharmacological management of heart failure has mainly focused on therapies that are aimed at improving haemodynamics and modulating neurohormonal pathways. However, despite optimal inhibition of these systems with drugs such as ACE inhibitors, beta-blockers, digoxin and, most recently, spironolactone, the mortality rate remains unacceptably high [1]. Recently, the failing cardiomyocyte within the heart itself has become the target for potential therapies — particularly via the regulation of Ca2+ transport. The slower rate of decay of Ca2+ transients within the failing heart, due to the reduced Ca2+ uptake into the sarcoplasmic reticulum (SR), ultimately results in a Ca2+ overload that leads to mechanical and electrical dysfunction of the cardiomyocytes.

Pathological conditions such as coronary artery disease and an inefficient . . . [Full Text of this Article]


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