Key result
Amiodarone therapy did not change QT dispersion, and QT dispersion on amiodarone was not associated with subsequent arrhythmic events.
Why the study?
Does amiodarone alter QT dispersion and does QT dispersion predict subsequent arrhythmic events in patients with ventricular tachyarrhythmias?
Cohort (n=52)
Does amiodarone alter QT dispersion and does QT dispersion predict subsequent arrhythmic events in patients with ventricular tachyarrhythmias?
Amiodarone increases QT and QTc intervals but does not significantly alter QT dispersion, and QT dispersion on amiodarone is not a useful marker for predicting subsequent arrhythmic events.
Answers are grounded in this paper and cite their sources.
QT dispersion should not guide arrhythmic risk assessment on amiodarone; leaves open need for reliable markers in ventricular tachyarrhythmia cohorts.
BACKGROUND AND HYPOTHESIS: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization. The purpose of the present study was twofold: (1) to analyze the effect of amiodarone on QT dispersion measured in the 12-lead standard ECG, and (2) to examine the association between QT dispersion on amiodarone and subsequent arrhythmic events. METHODS: To determine the effect of amiodarone on QT dispersion and its clinical significance for subsequent arrhythmic events, QT dispersion was measured in the 12-lead standard electrocardiogram (ECG) in 52 patients before and after administration of empiric amiodarone for ventricular tachyarrhythmias. RESULTS: QT intervals increased from 401 +/- 44 ms before amiodarone to 442 +/- 53 ms after amiodarone therapy, and rate corrected QT intervals (QTc) increased from 452 +/- 43 ms to 477 +/- 37 ms, respectively (p < 0.01). QT dispersion, QTc dispersion, and adjusted QTc dispersion, which take account of the number of leads measured, were not significantly different before and after initiation of amiodarone therapy (58 +/- 24 ms vs. 61 +/- 26 ms, 68 +/- 29 vs. 66 +/- 26 ms, and 22 +/- 8 vs. 22 +/- 8 ms, respectively, p = NS). During 31 +/- 25 months follow-up after initiation of amiodarone therapy, arrhythmic events defined as sustained ventricular tachycardia, ventricular fibrillation, or sudden death occurred in 11 of 52 study patients (21%). QT dispersion, QTc dispersion, and adjusted QTc dispersion on amiodarone were not different between patients with and without arrhythmic events during follow-up (65 +/- 14 vs. 59 +/- 29 ms, 73 +/- 15 vs. 64 +/- 28 ms, and 25 +/- 6 vs. 21 +/- 8 ms, respectively, p = NS). CONCLUSIONS: We conclude that (1) amiodarone increases QT intervals and QTc intervals during sinus rhythm but does not significantly change measures of QT dispersion; and (2) QT dispersion measured in the 12-lead standard ECG after initiation of amiodarone therapy does not appear to be a useful marker for subsequent arrhythmic events.
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Grimm et al. (1997) conducted a cohort in Ventricular tachyarrhythmias (n=52). Amiodarone vs. Baseline (before amiodarone) was evaluated on QT dispersion (p=NS). Amiodarone therapy did not change QT dispersion, and QT dispersion on amiodarone was not associated with subsequent arrhythmic events.
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