Ventricular tachyarrhythmias can be dangerous. They may result from cardiovascular disease, principally ischaemic heart disease, or they may be an unwanted effect of drug treatment. The surface electrocardiogram has been investigated for its ability to predict either the occurrence of these arrhythmias or their clinical outcome, sudden death. Holter monitoring seemed the most promising of these electrocardiographic techniques with analysis of the frequency and timing of extrasystoles and more recently of heart rate variability. Signal averaging also contributes by identifying abnormalities of QRS duration and configuration. These techniques are useful but they are neither sensitive nor specific. They are applied to conduction abnormalities, autonomic disturbances, and trigger phenomena but they provide no information on what may be the most important arrhythmogenic factor-the heart's recovery of ventricular excitability. Currently, the only routine assessment of ventricular recovery is the traditional measurement of a single QT interval. This measurement is not standardised. Recommendations for QT measurement have not defined a specific lead(s), have suggested a single defined lead (lead II or the lead with the largest T wave), or have proposed a mean QT derived from an arbitrary subset of leads. This lack of a systematic approach may explain the variation in sensitivity and specificity claimed for single lead measurement of QT interval in predicting life threatening ventricular arrhythmias. QT dispersion after myocardial infarction The clinical and research potential of QT dispersion (and other subtle aspects of the QT interval) has yet to be fully established but evidence from studies after myocardial infarction and from its use in the assessment of antiarrhythmic drug treatment suggest an important role. In 1985 Mirvis, using body surface mapping, first showed considerable regional differences in QT intervals over the chest wall in patients 24 hours after acute myocardial infarction compared with controls.4 Cowan et al confirmed the increased dispersion of the surface 12 lead QT interval in patients with one day old myocardial infarction (anterior infarcts, mean (SD) 70 (30)ms; inferior infarcts, 73 (32) ms) compared with a group of patients without cardiac disease (48 (18) ms) and suggested that this increase in dispersion reflected underlying dispersion of repolarisation caused by infarction.2 New data suggest that QT dispersion is greatest in the early hours of infarction, falls with time and successful thrombolysis, and may be highest in patients in whom ventricular fibrillation develops.56QT dispersion and assessment of antiarrhythmic drug treatment QT dispersion changes after acute myocardial infarction are interesting, but as yet they have no clinical application. In the context of antiarrhythmic drug efficacy and safety, however, they are already useful. Day et al found increased QT dispersion in arrhythmia patients with long QT intervals but normal or reduced levels of dispersion in patients with lon...

Objective-To evaluate changes in QT dispersion and components of the QT interval in patients admitted with unstable angina and acute myocardial infarction and to study the dynamics of these changes in patients with infarction. (Br Heart J 1995;73:32-36)

Objective-Terodiline, an antimuscarinic and calcium antagonist drug, was used to treat detrusor instability but was withdrawn in 1991 after provoking serious ventricular arrhythmias associated with increases in the corrected QT interval (QTc). This research was performed to relate drug induced electrocardiographic changes in asymptomatic recipients to plasma concentrations of the R( +) and S(-) terodiline enantiomers. (443 (33) and 42 (17) ms'12, paired t tests, P < 0-002 and P < 0 01 respectively) in the 12 patients in sinus rhythm. The mean (95% confidence interval) drug induced increases were 48 (23 to 74) Ms112 for QTc and 42 (13 to 70) ms'12 for QTd. These increases correlated with total plasma terodiline (QTc: r = 0-77, P < 0-006, QTd: r = 0*68, P < 0.025) and with plasma concentrations of both terodiline enantiomers.Conclusions-Terodiline increases QTc and QTd in a concentration dependent manner. It is not clear whether this is a stereoselective effect and, if so, which enantiomer is responsible. The results suggest that drug induced torsade de pointes is a type A (concentration dependent) adverse drug reaction. (Br HeartJ7 1995;74:53-56)

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Objective-To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion. Design-Prospective cohort study. Setting-Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period. Patients-All had acute myocardial infarction according to World Health Organization criteria. Interventions-For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction. Many techniques have been studied in an eVort to identify those patients most at risk of ventricular fibrillation. One such technique is the QT dispersion measurement, defined by Cowan and colleagues in 1988 as the diVerence between the maximum and minimum QT interval measurements on the standard 12 lead ECG. 1 We have previously shown this simple and non-invasive measurement to be a marker for inhomogeneity of ventricular recovery.2 In that study we showed a strong (r = 0.84) and highly significant (p < 0.001) correlation between QT dispersion and the dispersion of ventricular recovery time from simultaneous epicardial mapping during cardiac surgery. Similar work by Hardman and associates has confirmed the association between QT dispersion and dispersion of endocardial monophasic action potentials by catheter mapping. Increased QT dispersion has been shown to be associated with increased risk of cardiac death in patients with non-insulin dependent diabetes mellitus 4 and those awaiting heart transplantation, 5 and with risk of arrhythmia in patients with congenital long QT syndromes. 6 However, there is debate over whether increased QT dispersion predicts the occurrence of primary ventricular fibrillation early after myocardial infarction. Our pilot study showed a significant diVerence between admission QT dispersion in patients developing ventricular fibrillation or not developing it following acute myocardial infarction (mean (SD), 105 (17) ms, 95% confidence interval (CI) 74 to 136 ms, v 87 (15) ms, 95% CI 81 to 93 ms, respectively).7 This has been repeated by other researchers without agreement (fig 1). In this paper we present a prospective cohort study specifically designed to test this association and we show new data to account for the lack of consensus.The aims of the study were to show whether QT dispersion is increased in patients who develop early ventricular fibrillation following acute myocardial infarction, and to determine the nature of time related changes in QT dispersion measurements.