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QT dispersion: Measurement and interpretation

Authors
Velislav Batchvarov, MD
A John Camm, MD
Section Editor
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor
Brian C Downey, MD, FACC

INTRODUCTION

QT dispersion (maximum QT interval minus minimum QT interval) was originally proposed as an index of the spatial dispersion of ventricular recovery times. In reality, QT dispersion is a crude and approximate measure of a general abnormality of repolarization [1].

Attempts to characterize and quantify the inhomogeneity of ventricular repolarization from the surface electrocardiogram (ECG) using precise mathematical methods, such as principal component analysis of the T wave, can be traced back to the 1960s [2]. In clinical practice, however, the ECG assessment of ventricular repolarization has been limited to the measurement of the QT interval and its heart rate-corrected value (QTc) and to the description of the ST-T morphology, often using vague terms such as "non-specific ST-T wave changes."

The QT interval duration varies between leads on the standard ECG, Frank orthogonal leads, and body surface potential maps [3-8]. These interlead differences, called QT interval dispersion or QT range, were proposed as an index of the spatial dispersion of the ventricular recovery times [9]. This measurement was an attempt to distinguish between myocardium that is homogeneous from myocardium that displays inhomogeneity, which is accompanied by increased dispersion of the ventricular recovery times and prolongation of repolarization.

However, there has been much concern about the validity of the concept and the methodology of the measurement. Despite ongoing controversy, there are a number of reasonable conclusions about the reliability and applicability of the technique [1,10]. The pathophysiology and measurement of QT dispersion will be reviewed here. The clinical applications of QT dispersion are discussed separately. (See "QT dispersion: Clinical applications".)

PATHOPHYSIOLOGY OF QT DISPERSION

The initial concept that QT dispersion is an index of inhomogeneity was supported by the link between the dispersion of ventricular recovery times and the genesis of arrhythmias [11-15]. It was generally believed that the standard 12-lead electrocardiogram (ECG) contained information about regional ventricular repolarization; thus, when increased QT dispersion was seen in cardiac diseases in which ventricular recovery times were known to be heterogeneous, it was assumed that increased QT dispersion was a direct reflection of the disparity of ventricular recovery times [16].

          

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