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Cardiovascular Research 2001 51(4):627-629; doi:10.1016/S0008-6363(01)00389-3
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

LQT genotype–phenotype relationships: patients and patches

Arthur A.M. Wildea,* and Denis Escandeb

aExperimental and Molecular Cardiology Group, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, and the Interuniversity Cardiology Institute, The Netherlands
bLaboratoire de Physiopathologie et de Pharmacologie Cellulaires et Moléculaires, INSERM 4533, Hotel-Dieu, Nantes, France

* Corresponding author. Tel.: +31-20-566-3265; fax: +31-20-697-5458 a.a.wilde@amc.uva.nl

accepted 4 July 2001

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

See article by Huang et al. [14] (pages 670–680) in this issue.

The electrophysiological basis of the congenital long QT syndrome (LQTS), including both the Romano–Ward (RW) and the Jervell and Lange–Nielsen syndrome (JLN), relates to dysfunctioning ion channels, secondary to genetic aberrancies in their encoding genes (for review see Roden and Spooner [1]). Because these ion channels have different time and voltage characteristics gene-specific elements in clinical presentation have been searched for. Indeed, a gene-differentiating potential has been demonstrated, initially in small series and later confirmed in larger patient populations, for the morphology of ST-T segments [2–4] and for symptoms-related triggers [5–7]. To some extent also the clinical course including prognosis relies on the underlying gene defect [8]. Based on these data and other, more subtle differences [9], correct prediction of the genotype of clinically affected patients is feasible with reasonable accuracy. At present this . . . [Full Text of this Article]


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