AIMS: QT interval may be considered an indirect marker of atrial repolarization. Aim of our study was to verify if QT interval variations precede the onset of atrial fibrillation (AF). METHODS: We analyzed 21 AF onsets recorded at 24-h Holter ECG. Triggering supraventricular extrabeats (TSVEB) were identified and matched to nontriggering supraventricular extrabeats (NTSVEB) with the same prematurity index. QT and QTc intervals and their variability (max-min QT interval) were measured in the 10 beats preceding TSVEB and NTSVEB. RESULTS: QTc (470.1 ± 56.7 vs. 436.7 ± 25.6 ms; P = 0.006), QT (36.8 ± 13.1 vs. 21.1 ± 10.1 ms; P = 0.001) and QTc variability (41.5 ± 15.8 vs. 23.1 ± 11.9; P = 0.001) significantly varied between TSVEB and NTSVEB. By stratifying AF onsets in vagal (n = 10) and adrenergic (n = 11) according to Heart Rate Variability, significant differences emerged concerning QT (35.20 ± 16.48 vs. 22.70 ± 10.23 ms, P = 0.006) and QTc variability (39.30 ± 18.32 vs. 25.60 ± 12.91 ms, P = 0.029) for vagal onsets and QTc (477.73 ± 57.50 vs. 438.00 ± 28.55 ms, P = 0.045), QT (38.36 ± 9.79 vs. 19.73 ± 10.21 ms, P = 0.005) and QTc variability (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.004) for adrenergic onsets. By stratifying AF onsets in type I (n = 7) or II (n = 14) according to a cycle length variation in the 30 s before the onset greater or smaller than 10% respectively, significant differences were noted concerning QTc (477.73 ± 57.50 vs. 438 ± 28.55 ms, P = 0.045), QT (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.005) and QTc variability (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.004) in type I and QT (35.20 ± 16.48 vs. 22.70 ± 10.23 ms, P = 0.006) and QTc variability (39.30 ± 18.32 vs. 25.60 ± 12.91 ms, P = 0.029) in type II onsets. CONCLUSION: Prolongation and QT variability represent a relevant substrate marker in the genesis of AF, independently of the trigger type.
AIMS: QT interval may be considered an indirect marker of atrial repolarization. Aim of our study was to verify if QT interval variations precede the onset of atrial fibrillation (AF). METHODS: We analyzed 21 AF onsets recorded at 24-h Holter ECG. Triggering supraventricular extrabeats (TSVEB) were identified and matched to nontriggering supraventricular extrabeats (NTSVEB) with the same prematurity index. QT and QTc intervals and their variability (max-min QT interval) were measured in the 10 beats preceding TSVEB and NTSVEB. RESULTS:QTc (470.1 ± 56.7 vs. 436.7 ± 25.6 ms; P = 0.006), QT (36.8 ± 13.1 vs. 21.1 ± 10.1 ms; P = 0.001) and QTc variability (41.5 ± 15.8 vs. 23.1 ± 11.9; P = 0.001) significantly varied between TSVEB and NTSVEB. By stratifying AF onsets in vagal (n = 10) and adrenergic (n = 11) according to Heart Rate Variability, significant differences emerged concerning QT (35.20 ± 16.48 vs. 22.70 ± 10.23 ms, P = 0.006) and QTc variability (39.30 ± 18.32 vs. 25.60 ± 12.91 ms, P = 0.029) for vagal onsets and QTc (477.73 ± 57.50 vs. 438.00 ± 28.55 ms, P = 0.045), QT (38.36 ± 9.79 vs. 19.73 ± 10.21 ms, P = 0.005) and QTc variability (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.004) for adrenergic onsets. By stratifying AF onsets in type I (n = 7) or II (n = 14) according to a cycle length variation in the 30 s before the onset greater or smaller than 10% respectively, significant differences were noted concerning QTc (477.73 ± 57.50 vs. 438 ± 28.55 ms, P = 0.045), QT (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.005) and QTc variability (43.55 ± 13.72 vs. 20.82 ± 11.01 ms, P = 0.004) in type I and QT (35.20 ± 16.48 vs. 22.70 ± 10.23 ms, P = 0.006) and QTc variability (39.30 ± 18.32 vs. 25.60 ± 12.91 ms, P = 0.029) in type II onsets. CONCLUSION: Prolongation and QT variability represent a relevant substrate marker in the genesis of AF, independently of the trigger type.