Copyright © 2005, European Society of Cardiology
The molecular genetics of arrhythmias
aExperimental and Molecular Cardiology Group, Academic Medical Center, Amsterdam, The Netherlands
bDepartment of Clinical Genetics, Academic Medical Center, Amsterdam, The Netherlands
cDepartment of Medicine and Pharmacology, Oates Institute for Experimental Therapeutics and Division of Clinical Pharmacology, Vanderbilt, Nashville, Tennessee, USA
* Corresponding author. Experimental and Molecular Cardiology Group, Academic Medical Center, Amsterdam, The Netherlands. Tel.: +31 20 566 3265; fax: +31 20 697 5458. Email address: C.R.Bezzina@amc.uva.nl
Received 13 June 2005; accepted 14 June 2005
| The first 150 words of the full text of this article appear below. |
It was only ten years ago that mutations in ion channel genes were first described in patients with the long QT syndrome (LQTS) [1]. Since then, mutations in a total of eight different sarcolemmal ion channel subunit genes (KCNQ1, KCNH2, KCNE1, KCNE2, SCN5A, KCNJ2, HCN4, CACNA1C), two genes encoding sarcoplasmic reticulum (SR) Ca2+ handling proteins (RYR2, CASQ2), and an anchoring protein gene (ANK2) have been linked to a range of primary arrhythmia syndromes. The recognition of abnormal function of these genes in the inherited arrhythmia syndromes has provided remarkable insight into mechanisms of arrhythmias not only in these uncommon syndromes, but has also had very important implications for arrhythmia mechanisms and management more generally. It is therefore very opportune that Cardiovascular Research dedicates this spotlight issue to this topic. In this issue, a series of
| 1. Monogenic arrhythmia disorders |
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| 2. Modifier genes and polygenic arrhythmia disorders |
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| 3. Research tools |
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| 4. The future |
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