Key result
QTc intervals were significantly prolonged in the 10 beats preceding triggering supraventricular extrabeats compared to nontriggering extrabeats (470.1 vs 436.7 ms; P=0.006) before AF onset.
Why the study?
The QT interval can serve as an indirect marker of atrial repolarization, and this study aimed to verify whether QT interval variations precede the onset of AF.
Does QT prolongation and variability precede the onset of atrial fibrillation triggered by supraventricular extrabeats?
Observational (n=21)
Does QT prolongation and variability precede the onset of atrial fibrillation triggered by supraventricular extrabeats?
QT prolongation and increased QT variability precede the onset of atrial fibrillation, suggesting they represent a relevant substrate marker for AF genesis.
QT prolongation may precede AF onset via extrabeats; hypothesis-generating for substrate markers and requires prospective validation.
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.
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Magnano et al. (2019) conducted an observational in Atrial fibrillation (n=21). Triggering supraventricular extrabeats (TSVEB) vs. Nontriggering supraventricular extrabeats (NTSVEB) was evaluated on QTc interval in the 10 beats preceding extrabeats (p=0.006). QTc intervals were significantly prolonged in the 10 beats preceding triggering supraventricular extrabeats compared to nontriggering extrabeats (470.1 vs 436.7 ms; P=0.006) before AF onset.
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