Skip Navigation


European Heart Journal Advance Access originally published online on April 25, 2007
European Heart Journal 2007 28(9):1054-1056; doi:10.1093/eurheartj/ehm068
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
28/9/1054    most recent
ehm068v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Wehrens, X. H.T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wehrens, X. H.T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Leaky ryanodine receptors cause delayed afterdepolarizations and ventricular arrhythmias

Xander H.T. Wehrens*

Department of Molecular Physiology and Biophysics, and Medicine (in Cardiology), Baylor College of Medicine, One Baylor Plaza, Suite 414-B, Houston, TX 77030, USA

* Corresponding author. Tel: +1 713 798 4261; fax: +1 713 798 3475. E-mail address: wehrens@bcm.edu

This editorial refers to ‘Mutant ryanodine receptors in catecholaminergic polymorphic ventricular tachycardia generate delayed afterdepolarizations due to increased propensity to Ca2+ waves'{dagger} by J. Paavola et al., on page 1135

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

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disease characterized by the absence of structural heart disease, syncope, and sudden cardiac death.1 Typically, acceleration of the heart rate during physical exercise or emotional distress provokes an increasing number of ventricular premature complexes followed by runs of bidirectional or polymorphic ventricular tachycardia (VT). During clinical testing, about 30–50% of the patients will reproducibly develop VT following exercise testing or catecholamine injection.1,2

The ECG morphology of ventricular tachyarrhythmias observed in patients with CPVT resembles that of VTs commonly described in digitalis toxicity (which is associated with cellular calcium overload), and in metabolic disturbances as seen in severe HF (which is associated with high adrenergic tone).3 In conditions of cytoplasmic Ca2+ overload or enhanced ß-adrenergic signalling, cardiac myocytes exhibit greater ectopic activity. It has therefore been suggested that arrhythmias in CPVT are mediated by triggered activity and delayed afterdepolarizations (DADs), . . . [Full Text of this Article]

Clinical evidence for DADs in patients with CPVT

Ionic mechanisms underlying DADs in CPVT

RyR2 defects associated with CPVT-linked mutations


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related articles in EHJ:

Mutant ryanodine receptors in catecholaminergic polymorphic ventricular tachycardia generate delayed afterdepolarizations due to increased propensity to Ca2+ waves
Jere Paavola, Matti Viitasalo, Päivi J. Laitinen-Forsblom, Michael Pasternack, Heikki Swan, Ilkka Tikkanen, Lauri Toivonen, Kimmo Kontula, and Mika Laine
EHJ 2007 28: 1135-1142. [Abstract] [FREE Full Text]