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The electrocardiographic QT interval can contain information on the risk of dying suddenly.
A prolonged QT interval signifies a delay in the ventricular repolarisation phase, which renders the heart vulnerable to malignant arrhythmias such as torsade de pointes ventricular tachycardia. This sign of disease is sometimes subtle and may avoid recognition unless meticulously sought. In this issue of Heart, Malik and colleagues1 draw attention to methodological difficulties in the measurement of the QT interval.
The action potential duration of the myocardium, reflected as the QT interval on the surface ECG, depends on heart rate which hampers estimation of the intrinsic myocardial repolarisation time. The relation of the QT interval and heart rate, or cardiac cycle length, is modified by a number of physiologic processes. The mechanism causing the change in heart rate may variably influence ventricular repolarisation. For example, an equal increase in heart rate shortens the QT interval less during sympathetic stimulation by cold pressor test2 and during cardiac pacing3 compared to physical exercise. Furthermore, the response of the QT interval to a change in rate is not instantaneous, full adaptation taking 1–3 minutes.
CONTINUING DEBATE ON RATE CORRECTION OF QT INTERVAL
Several mathematical formulae have been utilised for rate correction of the QT interval. An inherent limitation is that they take only heart rate into consideration and miss all other determinants of the QT interval. Attempts to overcome this problem have included standardising the conditions under which the ECGs are undertaken. Different reference values have been proposed for diurnal periods and for the exercise test or its recovery period.4, 5 Analysis has also been limited to ECGs sampled only from periods of stable heart rate.6 Even these attempts to eliminate confounders may be futile as Malik and colleagues1 now report that the …