Aizawa Yoshifusa, Sato Masahito, Kitazawa Hitoshi, Aizawa Yoshiyasu, Takatsuki Seiji, Oda Eiji, Okabe Masaaki, Fukuda Keiichi
Tachikawa Medical Center, Niigata University, Nagaoka, Niigata, Japan.
Department of Cardiology, Tachikawa General Hospital, Nagaoka, Japan.
Heart Rhythm. 2015 Feb;12(2):376-83. doi: 10.1016/j.hrthm.2014.11.010. Epub 2014 Nov 11.
J waves can be observed in individuals of the general population, but electrocardiographic characteristics are poorly understood.
The purpose of this study was to examine the J-wave dynamicity in a general patient population.
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.
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.
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.
普通人群中可观察到J波,但对其心电图特征了解甚少。
本研究旨在探讨普通患者人群中J波的动态变化。
分析J波(在两个连续导联中高于等电线0.1 mV以上)对不同RR间期的反应。排除心脏性猝死未遂、记录到室颤或有心脏性猝死家族史的患者。在基线、电生理研究期间传导的房性早搏(APB)或心房刺激时RR间期短的搏动以及RR间期延长的APB之后的搏动中测量J波振幅。
701例普通患者中有94例(24.5%)主要表现为有切迹的J波(13.4%),94例患者中有23例(24.5%)存在APB。J波的平均基线振幅在基线RR间期853±152 ms时为0.20±0.06 mV,在传导的APB的RR间期545±133 ms时为0.25±0.11 mV(P = 0.0018),在RR间期1146±314 ms时为0.19±0.08 mV(P = 0.3102)。有和无J波心动过速依赖性增强的患者临床特征无差异。电生理研究证实了J波增强:基线时为0.28±0.12 mV,心房刺激搏动时为0.42±0.11 mV(P = 0.0001)。然而,未观察到心动过缓依赖性增强(>0.05 mV)。这种心动过速依赖性增强可能代表去极化异常而非复极化异常。
普通患者人群中的J波在RR间期较短时增强,但在RR间期延长时不增强。从机制上讲,传导延迟最可能对此负责。