Tachycardia-dependent augmentation of "notched J waves" in a general patient population without ventricular fibrillation or cardiac arrest: Not a repolarization but a depolarization abnormality?

Yoshifusa Aizawa, Masahito Sato, Hitoshi Kitazawa, Yoshiyasu Aizawa, Seiji Takatsuki, Eiji Oda, Masaaki Okabe, Keiichi Fukuda

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)376-383
Number of pages8
JournalHeart Rhythm
Volume12
Issue number2
DOIs
Publication statusPublished - 2015 Feb 1

Fingerprint

Ventricular Fibrillation
Heart Arrest
Tachycardia
Atrial Premature Complexes
Population
Electrophysiology
Sudden Cardiac Death
Population Characteristics
Bradycardia

Keywords

  • Conduction delay
  • Earlyrepolarization
  • J waves
  • Ratedependency

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Tachycardia-dependent augmentation of "notched J waves" in a general patient population without ventricular fibrillation or cardiac arrest : Not a repolarization but a depolarization abnormality? / Aizawa, Yoshifusa; Sato, Masahito; Kitazawa, Hitoshi; Aizawa, Yoshiyasu; Takatsuki, Seiji; Oda, Eiji; Okabe, Masaaki; Fukuda, Keiichi.

In: Heart Rhythm, Vol. 12, No. 2, 01.02.2015, p. 376-383.

Research output: Contribution to journalArticle

@article{dd259c8e7780485eb8e2905af4104cda,
title = "Tachycardia-dependent augmentation of {"}notched J waves{"} in a general patient population without ventricular fibrillation or cardiac arrest: Not a repolarization but a depolarization abnormality?",
abstract = "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.",
keywords = "Conduction delay, Earlyrepolarization, J waves, Ratedependency",
author = "Yoshifusa Aizawa and Masahito Sato and Hitoshi Kitazawa and Yoshiyasu Aizawa and Seiji Takatsuki and Eiji Oda and Masaaki Okabe and Keiichi Fukuda",
year = "2015",
month = "2",
day = "1",
doi = "10.1016/j.hrthm.2014.11.010",
language = "English",
volume = "12",
pages = "376--383",
journal = "Heart Rhythm",
issn = "1547-5271",
publisher = "Elsevier",
number = "2",

}

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

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

UR - http://www.scopus.com/inward/record.url?scp=84921033693&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84921033693&partnerID=8YFLogxK

U2 - 10.1016/j.hrthm.2014.11.010

DO - 10.1016/j.hrthm.2014.11.010

M3 - Article

C2 - 25460863

AN - SCOPUS:84921033693

VL - 12

SP - 376

EP - 383

JO - Heart Rhythm

JF - Heart Rhythm

SN - 1547-5271

IS - 2

ER -