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(Circulation. 2000;101:e235.)
© 2000 American Heart Association, Inc.

Circulation Electronic Pages

The Electrophysiological Basis of QT Dispersion: Global or Local Repolarization?

Markus Zabel, MD

Klinikum Benjamin Franklin Division of Cardiology, Free University of Berlin, Department of Medicine, Division of Cardiology, Hindenburgdamm 30, 12200 Berlin, Germany, MZabel@csi.com

Michael R. Franz, MD, PhD

VA Medical Center Division of Cardiology, Washington, DC

	Introduction

 
To the Editor:

Kors et al¹ present a very interesting article on the genesis of QT dispersion (QTD) in the 12-lead surface ECG. The authors provide support for the hypothesis that differences in the QT interval on the surface ECG are due to different projections of a common T-wave vector. Although the article is an important methodological contribution and it fuels a necessary rethinking of the clinical and diagnostic value of QTD, we would like to caution against a mechanistic view of its main conclusion.

Many arguments may still be made for the widely appreciated "local" hypothesis of QTD genesis, which we supported after reporting a significant correlation between local myocardial measurements and the surface ECG.^{2 3} Although it is notoriously difficult, if not impossible, to explain local myocardial repolarization by means of surface ECG recordings (the unsolved "inverse" problem of electrocardiography), a common T-wave vector may reflect some simplification of the electric forces during ventricular repolarization. The vectorcardiographic calculation itself presumes that the T wave can be explained by an electric dipole and that it will average existing local differences in repolarization forces.

Importantly, by using the technique of body surface potential mapping, a large number of elaborate studies spanning decades have proven that the nature of repolarization has nondipolar contents as well (recently reviewed by Taccardi et al⁴ ). Under certain arrhythmogenic clinical situations, it may be exactly this local deviation from dipolarity that may reveal the arrhythmogenic substrate. In addition, viewing repolarization as a global electric dipole also . . . [Full Text of this Article]

Jan A. Kors; Gerard van Herpen; Jan H. van Bemmel

Institute of Medical Informatics, Faculty of Medicine and Health Sciences, Erasmus University, PO Box 1738, 3000 DR Rotterdam, The Netherlands, kors@mi.fgg.eur.nl