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Cardiovascular Research 2007 76(3):379-380; doi:10.1016/j.cardiores.2007.10.001
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Copyright © 2007, European Society of Cardiology

Penetrance of monogenetic cardiac conduction diseases. A matter of conduction reserve?

Harold V.M. van Rijena,* and Jacques M.T. de Bakkera,b,c

aDepartment of Medical Physiology, Division Heart and Lungs, University Medical Center Utrecht, The Netherlands
bInteruniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
cHeart Failure Research Center Amsterdam, Academic Medical Center, Amsterdam, The Netherlands

*Corresponding author. Department of Medical Physiology, Division Heart and Lungs, University Medical Center Utrecht, The Netherlands. Tel.: +31 30 253 8900; fax: +31 30 253 9036. h.v.m.vanrijen@med.uu.nl

Received 27 September 2007; accepted 2 October 2007

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

See article by Tan et al. [3] (pages 409–417) in this issue.

Loss-of-function mutations in the SCN5a gene coding for the human Nav1.5 cardiac sodium channel, which lead to decreased peak sodium current, are associated with cardiac conduction defects (CCD), progressive cardiac conduction disease [1] or Brugada syndrome [2]. However, despite the strong linkage of sodium channel mutations to the disease in probands, the same mutation is often found in non-affected family members. The . . . [Full Text of this Article]


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