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Cardiovascular Research 2002 55(2):229-232; doi:10.1016/S0008-6363(02)00486-8
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Pharmacological rescue of mutant ion channels

Connie R Bezzinaa,* and Hanno L Tana,b

aExperimental and Molecular Cardiology Group, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
bDepartment of Cardiology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

c.r.bezzina@amc.uva.nl

* Corresponding author. Tel.: +31-20-566-3265; fax: +31-20-697-5458

Received 13 May 2002; accepted 13 May 2002

The first 150 words of the full text of this article appear below.

See article by Valdivia et al. [1] (pages 279–289) in this issue.

The congenital Long QT (LQT) syndrome [1] is a disorder that probably affects 1 per 5000 to 10 000 individuals. The disorder presents clinically with syncope, seizures and a torsade de pointes ventricular tachycardia. It is a repolarization abnormality caused by a decrease in net outward current during the repolarization phase of the cardiac action potential, thereby prolonging action potential duration. Six genes have thus far been linked to the disorder. Mutations in the potassium channel subunits KCNQ1 (LQT1) and KCNE1 (LQT5) affect the slowly activating component of the delayed rectifier current (IKs), while mutations in the potassium channel subunits KCNH2 (LQT2) and KCNE2 (LQT6) affect the rapidly activating component of this current (IKr). Mutations in SCN5A (the gene that encodes the cardiac sodium [Na+] channel) are associated with one of the least . . . [Full Text of this Article]


   1. Gain-of-function and loss-of-function defect for the M1766L mutant channel
 

   2. Augmentation of M1766L current by mexiletine
 

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H. L Tan, C. R Bezzina, J. P.P Smits, A. O Verkerk, and A. A.M Wilde
Genetic control of sodium channel function
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[Abstract] [Full Text] [PDF]