BACKGROUND: QT dispersion is considered an index of spatial inhomogeneity of repolarization duration and increased dispersion of ventricular repolarization is supposed to increase the risk of ventricular arrhythmia. Circadian variation in QT dispersion was investigated. METHODS: Three different modes of lead selection was used: all 12-leads (QTdisp 12), only precordial leads (QTdisp 6), and one pair of preselected leads (QTdisp 2) in a 24-hour Holter recording every fourth hour each comprising 10 consecutive measurements in 54 healthy subjects, 29 patients with coronary artery disease (CAD), and 29 patients with heart failure (HF). RESULTS: A significant circadian variation was observed in healthy subjects when modes QTdisp 12 and QTdisp 6 were used (Mean +/- SD 35.58 +/- 16.48 ms; P < 0.0001; and 28.82 +/- 16.02 ms; P < 0.0001, respectively), and in patients with CAD (Mean +/- SD 37.86 +/- 17.87 ms; P < 0.01; and 28.72 +/- 17.06 ms; P < 0.0001, respectively), whereas no circadian variation was observed in QTdisp 2. No circadian variation was observed in patients with HF irrespectively of lead selection. Patients with CAD without myocardial infarction (MI) had a circadian variation in QTdisp 12 (Mean +/- SD 33.13 +/- 14.86 ms; P < 0.05), whereas no circadian variation was observed in patients with MI (Mean +/- SD 40.35 +/- 18.80 ms; P = NS). CONCLUSIONS: Circadian variation of QT dispersion was detected in healthy subjects and in patients with uncomplicated CAD, but not in those who had suffered a previous MI and in patients with HF. The number of leads among which selection of the longest and shortest QT intervals took place was critical for the disclosure of circadian variation of QT dispersion.
BACKGROUND: QT dispersion is considered an index of spatial inhomogeneity of repolarization duration and increased dispersion of ventricular repolarization is supposed to increase the risk of ventricular arrhythmia. Circadian variation in QT dispersion was investigated. METHODS: Three different modes of lead selection was used: all 12-leads (QTdisp 12), only precordial leads (QTdisp 6), and one pair of preselected leads (QTdisp 2) in a 24-hour Holter recording every fourth hour each comprising 10 consecutive measurements in 54 healthy subjects, 29 patients with coronary artery disease (CAD), and 29 patients with heart failure (HF). RESULTS: A significant circadian variation was observed in healthy subjects when modes QTdisp 12 and QTdisp 6 were used (Mean +/- SD 35.58 +/- 16.48 ms; P < 0.0001; and 28.82 +/- 16.02 ms; P < 0.0001, respectively), and in patients with CAD (Mean +/- SD 37.86 +/- 17.87 ms; P < 0.01; and 28.72 +/- 17.06 ms; P < 0.0001, respectively), whereas no circadian variation was observed in QTdisp 2. No circadian variation was observed in patients with HF irrespectively of lead selection. Patients with CAD without myocardial infarction (MI) had a circadian variation in QTdisp 12 (Mean +/- SD 33.13 +/- 14.86 ms; P < 0.05), whereas no circadian variation was observed in patients with MI (Mean +/- SD 40.35 +/- 18.80 ms; P = NS). CONCLUSIONS: Circadian variation of QT dispersion was detected in healthy subjects and in patients with uncomplicated CAD, but not in those who had suffered a previous MI and in patients with HF. The number of leads among which selection of the longest and shortest QT intervals took place was critical for the disclosure of circadian variation of QT dispersion.
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