Skip Navigation


Cardiovascular Research Advance Access originally published online on October 8, 2009
Cardiovascular Research 2009 84(3):343-344; doi:10.1093/cvr/cvp330
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
84/3/343    most recent
cvp330v2
cvp330v1
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 Similar articles in this journal
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 Brown, D. A.
Right arrow Articles by Cascio, W. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brown, D. A.
Right arrow Articles by Cascio, W. E.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

‘Leaky’ ryanodine receptors and sudden cardiac death

David A. Brown1 and Wayne E. Cascio2,*

1 Departments of Physiology, Brody School of Medicine and the East Carolina Heart Institute, East Carolina University, Greenville, NC, USA
2 Cardiovascular Sciences, Brody School of Medicine and the East Carolina Heart Institute, East Carolina University, 115 Heart Drive, Mail Stop #651, Greenville NC, 27834, USA

* Corresponding author. Tel: +1 252 744 0083, fax: +1 252 744 5884. E-mail address: casciow@ecu.edu

This editorial refers to ‘Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death’ by A.E. Belevych et al., pp. 387–395, this issue.

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

Sudden cardiac death is a significant cause of mortality in the industrialized world, accounting for as much as 30% of deaths in high-risk populations.1 Despite the high incidence, the cellular mechanisms leading to fatal ventricular arrhythmias are not fully understood, thereby hindering the development of novel therapeutic strategies to mitigate this adverse outcome of myocardial infarction. Repolarization heterogeneities have been implicated as substrates for re-entrant arrhythmia, ultimately leading to ventricular fibrillation . . . [Full Text of this Article]


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

Related Article

Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death
Andriy E. Belevych, Dmitry Terentyev, Serge Viatchenko-Karpinski, Radmila Terentyeva, Arun Sridhar, Yoshinori Nishijima, Lance D. Wilson, Arturo J. Cardounel, Kenneth R. Laurita, Cynthia A. Carnes, George E. Billman, and Sandor Gyorke
Cardiovasc Res 2009 84: 387-395. [Abstract] [Full Text] [PDF]