AJP - Heart Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (June 22, 2007). doi:10.1152/ajpheart.00355.2007
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
293/4/H2024    most recent
00355.2007v1
Right arrow Alert me when this article is cited
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Antzelevitch, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Antzelevitch, C.
Submitted on March 20, 2007
Accepted on June 14, 2007

The Role of Spatial Dispersion of Repolarization in Inherited and Acquired Sudden Cardiac Death Syndromes

Charles Antzelevitch1*

1 Masonic Medical Research Laboratory, Utica, New York, United States

* To whom correspondence should be addressed. E-mail: ca{at}mmrl.edu.

This review examines the role of spatial electrical heterogeneity within ventricular myocardium on the function of the heart in health and disease. The cellular basis for transmural dispersion of repolarization (TDR) is reviewed and the hypothesis that amplification of spatial dispersion of repolarization underlies the development of life-threatening ventricular arrhythmias associated with inherited ion channelopathies is evaluated. The role of TDR in the long QT, short QT and Brugada syndromes as well as catecholaminergic polymorphic ventricular tachycardia are critically examined. In the long QT Syndrome, amplification of TDR is often secondary to preferential prolongation of the action potential duration (APD) of M cells, whereas in the Brugada Syndrome, it is thought to be due to selective abbreviation of the APD of right ventricular epicardium. Preferential abbreviation of APD of either endocardium or epicardium appears to be responsible for amplification of TDR in the short QT syndrome. In catecholaminergic polymorphic VT, reversal of the direction of activation of the ventricular wall is responsible for the increase in TDR. In conclusion, the long QT, short QT, Brugada and catecholaminergic polymorphic VT syndromes are pathologies with very different phenotypes and etiologies, but which share a common final pathway in causing sudden cardiac death.




This article has been cited by other articles:


Home page
 Eur Heart JHome page
N. Gaborit, T. Wichter, A. Varro, V. Szuts, G. Lamirault, L. Eckardt, M. Paul, G. Breithardt, E. Schulze-Bahr, D. Escande, et al.
Transcriptional profiling of ion channel genes in Brugada syndrome and other right ventricular arrhythmogenic diseases
Eur. Heart J., February 2, 2009; 30(4): 487 - 496.
[Abstract] [Full Text] [PDF]

Home page
 Circ Arrhythm ElectrophysiolHome page
C. Patel, J. F. Burke, H. Patel, P. Gupta, P. R. Kowey, C. Antzelevitch, and G.-X. Yan
Is there a significant transmural gradient in repolarization time in the intact heart?: Cellular Basis of the T Wave: A Century of Controversy
Circ Arrhythm Electrophysiol, February 1, 2009; 2(1): 80 - 88.
[Full Text] [PDF]

Home page
 EuropaceHome page
S. Peters
Arrhythmogenic right ventricular dysplasia-cardiomyopathy and provocable coved-type ST-segment elevation in right precordial leads: clues from long-term follow-up
Europace, July 1, 2008; 10(7): 816 - 820.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.