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Cardiovascular Research Advance Access originally published online on April 7, 2009
Cardiovascular Research 2009 82(3):390-391; doi:10.1093/cvr/cvp112
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

MinK: a double-hearted partner in cardiac repolarization

Antoni C.G. van Ginneken*

Department of Physiology, Heart Failure Research Centre, Academic Medical Centre, Meibergdreef 15, 1105 AZ, Amsterdam, the Netherlands; Department of Experimental Cardiology, Heart Failure Research Centre, Academic Medical Centre, Meibergdreef 15, 1105 AZ, Amsterdam, the Netherlands

* Corresponding author. Tel: +3120-5664644. E-mail address: a.c.vanginneken@amc.uva.nl

This editorial refers to ‘MinK-dependent internalization of the IKs potassium channel’ by X. Xu et al.,12 pp. 430–438, this issue.

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

Tight control of the cardiac repolarization process is essential to ensure adequate action potential duration. When cardiac repolarization is disturbed—e.g. by ion-channel mutations, drugs, or disease-related defects—rhythm disturbances may ensue. Thus, a delay in repolarization, apparent in the ECG as a long QT interval, may induce early afterdepolarizations that give rise to Torsades de Pointes and can lead to life-threatening arrhythmias.1 On the other hand, a premature repolarization, resulting in a short QT interval, has also been associated with a high rate of sudden cardiac death.2

Two important players in controlling repolarization and duration of the cardiac action . . . [Full Text of this Article]


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Related Article

MinK-dependent internalization of the IKs potassium channel
Xianghua Xu, Vikram A. Kanda, Eun Choi, Gianina Panaghie, Torsten K. Roepke, Stephen A. Gaeta, David J. Christini, Daniel J. Lerner, and Geoffrey W. Abbott
Cardiovasc Res 2009 82: 430-438. [Abstract] [Full Text] [PDF]