Skip Navigation

Cardiovascular Research 2002 54(2):315-324; doi:10.1016/S0008-6363(02)00222-5
© 2002 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 Brundel, B. J.J.M.
Right arrow Articles by Crijns, H. J.G.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brundel, B. J.J.M.
Right arrow Articles by Crijns, H. J.G.M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Molecular mechanisms of remodeling in human atrial fibrillation

Bianca J.J.M. Brundela,*, Robert H. Henningb, Harm H. Kampingaa, Isabelle C. Van Gelderc and Harry J.G.M. Crijnsd

aDepartment of Radiation and Stress Cell Biology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
bDepartment of Clinical Pharmacology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
cDepartment of Cardiology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
dDepartment of Cardiology, University of Maastricht, Maastricht, The Netherlands

* Corresponding author. Tel.: +31-50-363-2911; fax: +31-50-363-2913 B.J.J.M.Brundel{at}med.rug.nl

An important acknowledgement of the last several years is that atrial fibrillation (AF) modifies the electrical properties of the atrium in a way that promotes its occurrence and maintenance. This arrhythmogenic electrophysiological remodeling is well established, but can not explain by itself that ‘AF begets AF’. This review describes molecular changes involving rapid functional alterations and slower changes in protein expression that cause electrical remodeling and contractile dysfunction in AF. An important molecular feature of AF is the reduction in L-type Ca2+ channel function and protein expression. This reduction may serve to protect the cell against a potentially lethal Ca2+ overload resulting from the increased activation rate in AF. Further, the review discusses the possible role of proteolytic systems, notably the calpains, as a mechanism linking Ca2+ overload to reduced protein expression. Thus, it appears that the elaborate molecular changes in AF are directed primarily at protecting the myocyte from cellular stress. However, such early protection occurs at the expense of electrophysiological changes that promote the long-term maintenance of AF.

KEYWORDS Ion channels; Contractile function; Arrhythmia (mechanisms)


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
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Etzion, M. Mor, A. Shalev, S. Dror, O. Etzion, A. Dagan, O. Beharier, A. Moran, and A. Katz
New insights into the atrial electrophysiology of rodents using a novel modality: the miniature-bipolar hook electrode
Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1460 - H1469.
[Abstract] [Full Text] [PDF]

Home page
 Journal of Renin-Angiotensin-Aldosterone SystemHome page
R. Laszlo, C. Eick, N. Rueb, S. Weretka, H.-J. Weig, J. Schreieck, and R. F Bosch
Inhibition of the renin-angiotensin system: effects on tachycardia-induced early electrical remodelling in rabbit atrium
Journal of Renin-Angiotensin-Aldosterone System, September 1, 2008; 9(3): 125 - 132.
[Abstract] [PDF]

Home page
 J Am Coll CardiolHome page
E. I. Skalidis, M. I. Hamilos, I. K. Karalis, G. Chlouverakis, G. E. Kochiadakis, and P. E. Vardas
Isolated Atrial Microvascular Dysfunction in Patients With Lone Recurrent Atrial Fibrillation
J. Am. Coll. Cardiol., May 27, 2008; 51(21): 2053 - 2057.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al.
ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society
J. Am. Coll. Cardiol., August 15, 2006; 48(4): e149 - e246.
[Full Text] [PDF]

Home page
 Cardiovasc ResHome page
B. J.J.M Brundel, H. H Kampinga, and R. H Henning
Calpain inhibition prevents pacing-induced cellular remodeling in a HL-1 myocyte model for atrial fibrillation
Cardiovasc Res, June 1, 2004; 62(3): 521 - 528.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. Nattel, M. Allessie, and M. Haissaguerre
Spotlight on atrial fibrillation--the 'complete arrhythmia'
Cardiovasc Res, May 1, 2002; 54(2): 197 - 203.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.