TY - JOUR
T1 - Tachycardia-dependent augmentation of "notched J waves" in a general patient population without ventricular fibrillation or cardiac arrest
T2 - Not a repolarization but a depolarization abnormality?
AU - Aizawa, Yoshifusa
AU - Sato, Masahito
AU - Kitazawa, Hitoshi
AU - Aizawa, Yoshiyasu
AU - Takatsuki, Seiji
AU - Oda, Eiji
AU - Okabe, Masaaki
AU - Fukuda, Keiichi
N1 - Publisher Copyright:
© 2015 Published by Elsevier Inc.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Background J waves can be observed in individuals of the general population, but electrocardiographic characteristics are poorly understood. Objective The purpose of this study was to examine the J-wave dynamicity in a general patient population. Methods The responses of J waves (>0.1 mV above the isoelectric line in 2 contiguous leads) to varying RR intervals were analyzed. Patients with aborted sudden cardiac death, documented ventricular fibrillation, or a family history of sudden cardiac death were excluded. The J-wave amplitude was measured at baseline, in beats with short RR intervals in conducted atrial premature beats (APBs) or atrial stimulation during the electrophysiology study, and in the beats next to APBs with prolonged RR intervals. Results Mainly notched J waves were identified in 94 of 701 (24.5%) general patients (13.4%), and APBs were present in 23 of 94 (24.5%) patients. The mean baseline amplitude of J waves was 0.20 ± 0.06 mV at the baseline RR interval of 853 ± 152 ms, 0.25 ± 0.11 mV at the RR interval in the conducted APB of 545 ± 133 ms (P =.0018), and 0.19 ± 0.08 mV at the RR interval of 1146 ± 314 ms (P =.3102). The clinical characteristics were not different between patients with and without tachycardia-dependent augmentation of J waves. Augmentation of J waves was confirmed by the electrophysiology study: 0.28 ± 0.12 mV vs 0.42 ± 0.11 mV at baseline and in the beats of atrial stimulation, respectively (P =.0001). However, no bradycardia-dependent augmentation (>0.05 mV) was observed. Such tachycardia-dependent augmentation can represent depolarization abnormality rather than repolarization abnormality. Conclusion J waves in a general patient population were augmented at shorter RR intervals, but not at prolonged RR intervals. Mechanistically, conduction delay is most likely responsible for this.
AB - Background J waves can be observed in individuals of the general population, but electrocardiographic characteristics are poorly understood. Objective The purpose of this study was to examine the J-wave dynamicity in a general patient population. Methods The responses of J waves (>0.1 mV above the isoelectric line in 2 contiguous leads) to varying RR intervals were analyzed. Patients with aborted sudden cardiac death, documented ventricular fibrillation, or a family history of sudden cardiac death were excluded. The J-wave amplitude was measured at baseline, in beats with short RR intervals in conducted atrial premature beats (APBs) or atrial stimulation during the electrophysiology study, and in the beats next to APBs with prolonged RR intervals. Results Mainly notched J waves were identified in 94 of 701 (24.5%) general patients (13.4%), and APBs were present in 23 of 94 (24.5%) patients. The mean baseline amplitude of J waves was 0.20 ± 0.06 mV at the baseline RR interval of 853 ± 152 ms, 0.25 ± 0.11 mV at the RR interval in the conducted APB of 545 ± 133 ms (P =.0018), and 0.19 ± 0.08 mV at the RR interval of 1146 ± 314 ms (P =.3102). The clinical characteristics were not different between patients with and without tachycardia-dependent augmentation of J waves. Augmentation of J waves was confirmed by the electrophysiology study: 0.28 ± 0.12 mV vs 0.42 ± 0.11 mV at baseline and in the beats of atrial stimulation, respectively (P =.0001). However, no bradycardia-dependent augmentation (>0.05 mV) was observed. Such tachycardia-dependent augmentation can represent depolarization abnormality rather than repolarization abnormality. Conclusion J waves in a general patient population were augmented at shorter RR intervals, but not at prolonged RR intervals. Mechanistically, conduction delay is most likely responsible for this.
KW - Conduction delay
KW - Earlyrepolarization
KW - J waves
KW - Ratedependency
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U2 - 10.1016/j.hrthm.2014.11.010
DO - 10.1016/j.hrthm.2014.11.010
M3 - Article
C2 - 25460863
AN - SCOPUS:84921033693
SN - 1547-5271
VL - 12
SP - 376
EP - 383
JO - Heart Rhythm
JF - Heart Rhythm
IS - 2
ER -