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Cardiovascular Research 2004 62(1):1-3; doi:10.1016/j.cardiores.2004.01.037
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure?

Stéphane Hatem*

INSERM Unité de Recherche 621, Faculté de Médecine Pitié-Salpêtrière, 91 Boulevard de l'Hôpital, 75013 Paris, France

* Tel.: +33-1-40-25-86-00; fax: +33-1-40-25-86-02. Email address: hatem@bichat.inserm.fr

Received 28 January 2004; accepted 30 January 2004

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

See article by Louch et al. [1] (pages 63–73) in this issue.


   1. Introduction
 
Congestive heart failure (CHF) is the leading cause of death in developed countries. This syndrome is due to the incapacity of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. Very often CHF is caused by a defect in myocardial contraction. Thereby, a better understanding of the cellular and molecular basis of the altered contractility of failing heart is a major research topic of many laboratories in the hopes of identifying new targets for the treatment of CHF. The manuscript of Louch et al. [1] in the current issue of Cardiovascular Research examines the possibility that . . . [Full Text of this Article]


   2. T-tubules synchronize Ca2+ release
 

   3. Cellular models to study cardiac myocyte T-tubular network
 

   4. Is there a reduction of T-tubules in the failing human myocardium?
 

   5. Conclusion and perspectives
 

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