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Cardiovascular Research 2005 65(1):10-12; doi:10.1016/j.cardiores.2004.10.028
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Copyright © 2004, European Society of Cardiology

Less Na+/H+-exchanger to treat heart failure: a simple solution for a complex problem?

Mark A. Stagg and Cesare M.N. Terracciano*

Harefield Heart Science Centre, Laboratory of Cellular Electrophysiology, Imperial College London, National Heart and Lung Institute, Harefield Hospital, Harefield, Middlesex, London UB9 6JH, United Kingdom

* Corresponding author. Tel.: +44 1895 453 874; fax: +44 1895 828 900. Email address: c.terracciano@imperial.ac.uk

Received 18 October 2004; accepted 21 October 2004

The first 10% of the full text of this article appears below.

See article by Baartscheer et al. [1] (pages 83–92) in this issue.


   1. Understanding heart failure: a complex challenge
 
Heart failure is one of the major causes of mortality and morbidity in the western world. Enormous investments have been made for researching the treatment of this disease with the aim of reconstructing the chain of events at the organ, cellular, and molecular levels that leads to cardiac hypertrophy and/or heart failure. This challenge is extremely complex because almost every cellular and molecular system is affected in heart failure. These modifications can be a cause or a consequence of heart failure, can be compensatory or detrimental, or can be simply epiphenomena.

The ideal target for heart failure research . . . [Full Text of this Article]


   2. Inhibiting the Na+/H+ exchanger in heart failure: a simple solution
 

   3. Ca2+ and Na+ regulatory mechanisms: a complex interaction
 

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