QT dispersion--what does it mean?

Abstract

S ince the recognition of the high frequency of unexpected cardiac arrest as a mode of cardiac deaths, medical scientists and clinicians have sought methods to predict and prevent its occurrence. Several reports have raised the optimistic notion that sudden arrhythmic death can be predicted by methods potentially useful for widespread screening programs [1]. However, none of these methods are on routine clinical use at the moment, because of methodological problems of the tests and methods and because of their relatively low overall accuracy in risk stratification. A test or method that is ideal for risk stratification should be inexpensive, it should be easily available, easy to perform and interpret. In this respect, standard 12lead electrocardiogram (ECG) is an excellent tool. Attempts to characterise abnormalities of ventricular repolarisation from 12-lead surface ECG have long been used in risk stratification. Measurement of QT interval (or heart rate corrected QTc interval) has most commonly been used in the assessment of abnormalities of myocardial repolarisation. Despite the clinical utility of this simple measurement in specific situations, such as in diagnosis of congenital or acquired long QT syndromes, the epidemiological literature suggests that the QTc interval is an imprecise marker of cardiovascular disease [2]. It also provides only limited prognostic information in various patient populations. In 1990, it was proposed that measurement of interlead difference in the QT interval from standard 12-lead ECG might provide more powerful diagnostic information than the measurement of only the maximum QT interval [3]. It was hypothesised that the difference between the maximum and minimum QT intervals, defined as QT dispersion, might reflect inhomogeneity in ventricular repolarisation and thereby provide information on the risk for ventricular tachyarrhythmias. This idea was welcomed by the scientists and clinicians, and since then a large number of articles have been published dealing with QT dispersion [4]. After initial enthusiasm, a lot of criticism has been presented against the theory behind QT dispersion and the clinical value of measurement of QT dispersion. Recent studies have suggested that QT dispersion may not reflect inhomogeneity in ventricular recovery times, but may in fact be due to variable projections of T wave loops into individual ECG leads [5]. Another criticism deals with methodological aspects. Most of the problems are related to the difficulty in defining exactly the offset of T wave. Interand intraobserver variability in the manual QT dispersion measurement has been reported to be relatively large [4]. The shorter the QT dispersion in the study population, the larger is the measurement variability. Despite some problems in the methodology, majority of studies has suggested that increased QT dispersion is a risk marker for future adverse clinical events [4]. In particular, broad QT dispersion seems to predict the occurrence of drug induced Torsade de Pointes [4]. Role of QT dispersion as a risk marker in other patient populations, e.g. in patients with a recent or prior myocardial infarction, is more controversial [6–8]. In this issue, Kontouris et al. report on the effects of trimetazidine, an anti-ischaemic agent, on QT dispersion among the patients surviving an acute myocardial infarction [9]. The authors conclude that trimetazidine decreases QT dispersion of post-infarction patients. This study provides a nice piece of evidence that reduction of ischaemia burden and infarct size by antiischaemic medication may have favourable effects on preventing abnormalities in ventricular repolarisation. Unfortunately, after considering the conceptual and methodological limitations of QT dispersion measurement and its controversial prognostic power in postinfarction patients, the clinical significance of this study remains obscure. It remains to be established whether the observed effects of this new drug on QT dispersion have any clinical meaning. After identifying a risk marker, a next step in research is to find a drug or intervention that is able to modify it. If such a drug or other mode of therapy is found, an intervention trial is needed to prove that this modification has a positive, beneficial effect on the outcome of patients. This schema has nicely been followed in the antihypertensive treatment of patients with elevated blood pressure and lipid-lowering treatment of patients with elevated cholesterol levels. Because sudden arrhythmic death accounts for approximately 50% of all cardiovascular mortality, and most of the lifethreatening cardiac arrhythmias arise from abnormalities of myocardial repolarisation, it will be a challenge