Sporton, Simon Charles Edwin; (2000) QT dispersions : Moving from risk stratification towards underlying mechanisms. Doctoral thesis (M.D), UCL (University College London).

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Abstract

Experimental studies have shown that when pathological processes disrupt the normal orderly sequence of electrical recovery following activation, the conditions favouring the development of reentrant arrhythmias are created. Comparatively little is known about the role of so-called increased dispersion of repolarisation in human arrhythmias, due in part to the difficulty in measuring this process. QT dispersion, defined as the difference between the longest and shortest QT intervals measured from the surface electrocardiogram, has been proposed as just such a measure. A fundamental assumption in the use of QT dispersion is that interlead variations in QT dispersion do indeed reflect regional variations in ventricular repolarisation time. Comparatively few data exist to support this hypothesis and the relationship is explored in this thesis. The last decade has seen a proliferation of studies testing the association between increased QT dispersion and the development of life threatening arrhythmias or sudden death in a variety of cardiac and noncardiac disease states. In the largest group of patients at risk of such events - those with ischaemic heart disease - these studies have so far failed to demonstrate the predictive value of QT dispersion. This may in part be explained by the way in which the methodology has been applied. Dispersion of repolarisation is a dynamic process that may change on a beat to beat basis. A single measure of QT dispersion from a resting electrocardiogram may therefore fail to reflect an individual's capacity to develop the substrate for life threatening arrhythmias. This thesis concerns an exploration of the factors contributing to increased QT dispersion in individuals with heart disease. In particular the influence of acute ischaemia and premature beats, separately and in combination, have been studied as conditions predisposing to arrhythmia development and associated in experimental studies with increased dispersion of repolarisation.

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