Skip Navigation

Cardiovascular Research 2003 57(2):289-293; doi:10.1016/S0008-6363(02)00835-0
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 Wolk, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wolk, R.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Calcineurin, myocardial hypertrophy, and electrical remodeling

Robert Wolka,b,*

aDepartment of Medicine, Division of Cardiovascular Diseases and Division of Hypertension, Mayo Clinic, Rochester, MN 55902, USA
b1st Department of Cardiology, Silesian Medical School, Silesian Center of Heart Disease, Zabrze, Poland

* Present address: Mayo Foundation, St. Mary's Hospital, DO-4-350, 1216 Second St. SW, Rochester, MN 55902, USA. Tel.: +1-507-255-1144; fax: +1-507-255-7070. wolk.robert@mayo.edu

Received 28 November 2002; accepted 2 December 2002

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

See article by Dong et al. [7] (pages 320–332) in this issue.

The pathogenesis of cardiac ventricular hypertrophy (CVH), both compensated and that associated with cardiac dysfunction, has attracted a lot of attention and this field still continues to expand. This huge clinical and scientific interest is related to the fact that CVH has been identified as a powerful risk factor for total and cardiovascular mortality. Interestingly, the Framingham study also demonstrated that CVH significantly increases the risk of sudden cardiac death, both in men and in women [1]. Subsequent studies provided evidence that cardiac arrhythmias are an important mechanism contributing to the high mortality and sudden death in patients with CVH [2–4]. Not surprisingly, a lot of effort has been expended to characterize the electrophysiological phenotype and to elucidate the mechanisms of arrhythmias in CVH.

New research tools have been provided with the advent of modern molecular . . . [Full Text of this Article]


    1. Calcineurin—a common pathway for electrical remodeling?
 
1.1 Repolarizing currents
1.2 Depolarizing currents

    2. Electrical heterogeneity in the heart
 

    3. Arrhythmogenic mechanisms
 

    4. Conclusions
 

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


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
R. B. Vega, R. Bassel-Duby, and E. N. Olson
Control of Cardiac Growth and Function by Calcineurin Signaling
J. Biol. Chem., September 26, 2003; 278(39): 36981 - 36984.
[Full Text] [PDF]