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Cardiovascular Research 2006 70(3):404-406; doi:10.1016/j.cardiores.2006.04.006
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Copyright © 2006, European Society of Cardiology

Low penetrance, subclinical congenital LQTS: Concealed LQTS or silent LQTS?

Andras Varróa,* and Julius Gy. Pappa,b

aDepartment of Pharmacology and Pharmacotherapy, University of Szeged, H-6720 Szeged, Dóm tér 12, PO Box 427, Hungary
bDivision for Cardiovascular Pharmacology, Hungarian Academy of Sciences, Szeged, Hungary

* Corresponding author. Email address: a.varro@phcol.szote.u-szeged.hu

Received 20 March 2006; accepted 5 April 2006

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

See article by Boulet et al. [1] (pages 466–474) in this issue.


   1. ‘Silent long QT syndrome’
 
The paper by Boulet et al. in this issue [1] describes the electrophysiological basis of an ion channel malfunction reported in ‘a silent LQTS’ patient. This patient, a 40-year-old woman, had a documented syncopal event, palpitations, recurrent chest discomfort, tachycardia, and since diagnosis has been asymptomatic on β-blocker therapy [2].

Genetic analysis revealed a loss-of-function mutation in the KCNQ1 gene underlying the {alpha} subunit of the IKs potassium channel. It is important and interesting that this patient had a QTc interval of 430 ms, which is well within the normal range in women. Although there is . . . [Full Text of this Article]


   2. Repolarization reserve
 

   3. Congenital long QT syndromes and IKs
 

   4. Downregulation and pharmacological block of IKs as a possible link to decreased repolarization reserve
 

   5. Implication
 

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