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)
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