Kamakura Tsukasa, Wada Mitsuru, Ishibashi Kohei, Inoue Yuko Y, Miyamoto Koji, Okamura Hideo, Nagase Satoshi, Noda Takashi, Aiba Takeshi, Yasuda Satoshi, Shimizu Wataru, Kamakura Shiro, Kusano Kengo
Division of Arrhythmia and Electrophysiology, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan.
Division of Arrhythmia and Electrophysiology, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan.
Heart Rhythm. 2017 Apr;14(4):553-561. doi: 10.1016/j.hrthm.2016.11.027. Epub 2016 Nov 23.
The pathophysiological mechanism of J wave in anterior leads (A-leads) and inferolateral leads (L-leads) remains unclear.
We investigated the onset mode and circadian distribution of ventricular tachyarrhythmia (VTA) episodes between patients with early repolarization syndrome (ERS) and Brugada syndrome (BrS).
The study enrolled 35 patients with ERS and 52 patients with type 1 BrS with spontaneous ventricular fibrillation who were divided into 4 groups: ERS(A+L) (n = 15), patients with ERS who had a non-type 1 Brugada pattern electrocardiogram in any A-leads (second to fourth intercostal spaces) in control and/or after drug provocation tests; ERS(L) (n = 20), patients with ERS with J wave only in L-leads; BrS(A) (n = 24), patients with BrS without J wave in L-leads; and BrS(A+L) (n = 28), patients with BrS with J wave in L-leads. The onset mode of 206 VTAs obtained from electrocardiograms or implantable cardioverter-defibrillators and the circadian distribution of 352 VTAs were investigated in the 4 groups.
Three groups with J wave in A-leads, ERS(A+L), BrS(A), and BrS(A+L), had higher incidences of nocturnal (63%, 43%, and 47%, respectively) and sudden onset VTAs (67%, 97%, and 86%, respectively) with longer coupling intervals of premature ventricular contractions (388.8, 397.3, and 385.6 ms, respectively) than the ERS(L) group with J wave only in L-leads (25%, P = .0019; 19%, P < .0001; and 330.6 ms, P = .0004, respectively), the last of which mainly displayed VTAs with a short-long-short sequence.
The onset mode of VTAs was different between patients with J wave in A-leads and patients with J wave in only L-leads. The underlying mechanism of J wave may differ between A-leads and L-leads.
前壁导联（A导联）和下侧壁导联（L导联）出现J波的病理生理机制尚不清楚。
我们调查了早期复极综合征（ERS）和Brugada综合征（BrS）患者室性快速心律失常（VTA）发作的起始模式和昼夜分布情况。
该研究纳入了35例ERS患者和52例1型BrS伴自发性室颤患者，将其分为4组：ERS（A+L）组（n = 15），即ERS患者在对照和/或药物激发试验后，任何A导联（第二至第四肋间）心电图呈非1型Brugada模式；ERS（L）组（n = 20），即仅L导联有J波的ERS患者；BrS（A）组（n = 24），即L导联无J波的BrS患者；BrS（A+L）组（n = 28），即L导联有J波的BrS患者。对4组患者通过心电图或植入式心律转复除颤器获得的206次VTA发作的起始模式以及352次VTA发作的昼夜分布情况进行了调查。
A导联有J波的3组，即ERS（A+L）组、BrS（A）组和BrS（A+L）组，夜间VTA发作发生率较高（分别为63%、43%和47%），且发作突然（分别为67%、97%和86%），室性早搏的联律间期较长（分别为388.8、397.3和385.6毫秒），而仅L导联有J波的ERS（L）组夜间VTA发作发生率为25%（P = 0.0019），发作突然的比例为19%（P < 0.0001），联律间期为330.6毫秒（P = 0.0004），ERS（L）组主要表现为短-长-短序列的VTA发作。
A导联有J波的患者与仅L导联有J波的患者VTA发作的起始模式不同。A导联和L导联J波的潜在机制可能不同。
