QT dispersion, describing the range of QT intervals, was first proposed as an index of the spatial dispersion of ventricular recovery times in 1990, by Day et al. As it was thought that the different electrocardiographic (ECG) leads magnified the ECG signal from different myocardial regions, QT dispersion became an almost direct measure of the heterogeneity of myocardial repolarization. Many studies have aimed not only at establishing reference values but also at evaluating QT dispersion as a predictor of ventricular arrhythmia or other adverse events in cardiac disease. The results remain inconclusive in either case.
Retrospective analyses have found that patients with acute or previous myocardial infarction with ventricular arrhythmias have significantly higher QT dispersion than patients without arrhythmias. However, the first prospective study in postinfarction patients, by Zabel et al, showed that none of the 26 ventricular dispersion indices tested had any predictive value. Newer studies have been inconclusive.
Several studies show significant correlation between QT dispersion and outcome in heart failure. The Evaluation of Losartan In The Elderly (ELITE) study, in which sudden cardiac death was decreased in heart failure patients treated with the angiotensin II antagonist losartan vs captopril, showed an increase in QT dispersion on captopril but not on losartan. However, the much larger, double-blind, randomized controlled ELITE II study failed to confirm these results: losartan patients showed no significant differences in all-cause mortality, sudden death, or resuscitated cardiac arrest vs patients treated with captopril.
Substudies of the Danish Investigations of Arrhythmia of Mortality ON Dofetilide-Congestive Heart Failure (DIAMOND-CHF), the United Kingdom Heart Failure Evaluation and Assessment of Risk Trial (UK-HEART), and other large prospective studies failed to show any power of QT dispersion in predicting outcome in heart failure.
In long QT syndrome, the diagnostic value of increased QT dispersion seems undisputed. On the other hand, although Priori et al found significantly higher QT dispersion in (3-blocker nonresponders vs responders, no other data presently available suggest that QT dispersion has any prognostic value in patients with long QT syndrome.
The reasons for such a different range of results and opinions are various:
QT dispersion does not directly and quantifiably reflect the dispersion and heterogeneity of ventricular recovery times. The standard 12-lead ECG contains information about regional electrical phenomena, but this information cannot be extracted by such a simple technique as QT dispersion assessment.
Not only the magnitude of dispersion of recovery times, but the distance over which they are dispersed is important for arrhythmogenesis. Dispersion of recovery times in adjacent areas must be distinguished from that over large areas and possibly from dispersion between the ventricles. Such a scale is clearly beyond the resolution of the standard surface ECG.
The idea of detecting and quantifying dispersion only at the end of repolarization, ie, dispersion of the complete recovery time, also seems questionable. Action potentials of different duration usually have very different shape, particularly during phase 3.
An important point is the effect of drugs on QT dispersion and the risk of torsade de pointes tachycardia. Quinidine increases QT dispersion, and increased QT dispersion seems to have some predictive value for development of torsades de pointes during quinidine therapy. Both sotalol and amiodarone have been shown to decrease, or not to change, QT dispersion, even if cases of induction of torsades de pointes by amiodarone have been reported.
Thus, the jury remains out as to the prognostic meaning of QT dispersion in cardiac disease. In practice, in the individual patient, only grossly abnormal values clearly outside any possible measurement error, eg, >100 ms,
may be useful indicators of abnormal repolarization. Clinical use is therefore likely to be limited to diseases and syndromes in which such values are encountered (Figure), eg, drug-induced torsade de pointes.
Figure. QT dispersion (ms, mÂ±sd) in studies in normal subjects, post-myocardial infarction, left ventricular hypertrophy, heart failure and dilated cardiomyopathy, hypertrophic cardiomyopathy, acute myocardial infarction, and long QT syndrome.
After: Priori SG, Napolitano C, Diehl L, Schwartz PJ. Dispersion of the QT interval. A marker of therapeutic efficacy in idiopathic long QT syndrome. Circulation. 1994;89:1681-1689. Copyright Â© 1994, American Heart Association.
instrumental finding; ECG; QT interval dispersion; electrophysiology; prognosis; torsade de pointes; arrhythmia risk; arrhythmogenic marker