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; Takatsuki, Seiji; Oda, Eiji; Okabe, Masaru; Fukuda, Keiichi

doi:10.1016/j.hrthm.2014.11.010

Cited by 38 publications

(35 citation statements)

References 30 publications

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“…[16][17][18]20 The subjects with J waves in our control group showed different responses of the J waves to changes in the heart rate compared with the IVF patients. In our previous study, 15 the J-wave amplitude is augmented when A pause-dependent attenuation of the J-wave amplitude was not clear, but a positive correlation of the J-wave amplitude with increasing heart rate was suggested (Figures 1 and 2). The most likely mechanism for the tachycardia-dependent augmentation of J waves would be conduction delay.…”

Section: J-wave Dynamicity In the Non-ivf Patientsmentioning

confidence: 80%

“…[11][12][13] Because J waves are augmented at a slower rate, it is natural to expect that J waves are attenuated at higher rates, although this has rarely been confirmed in the literature. [11][12][13] On the basis of the gap in earlier reports, 11,15 we hereby present the results of atrial pacing in IVF patients to show the tachycardia-dependent attenuation of J waves. The results from IVF patients were compared with those from non-IVF subjects.…”

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confidence: 89%

“…The most likely mechanism for the tachycardia-dependent augmentation of J waves would be conduction delay. 15 It is well known that activation delay occurs at longer coupling intervals during premature stimulation of the heart after a healed myocardial infarction. 21 Discontinuity in the myocardial bundle or nonuniform anisotropy from fibrosis would be responsible for such conduction delay.…”

Section: J-wave Dynamicity In the Non-ivf Patientsmentioning

confidence: 99%

“…The age of IVF and non-IVF subjects was different, and the results need to be confirmed in a study with a larger number of patients of the same age. However, including the previous 11,15 it is likely that there are different mechanisms of J-wave genesis. There are subjects in whom we are unable to determine the response of J waves to heart rate on the surface ECG.…”

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confidence: 99%

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Tachycardia-Induced J-Wave Changes in Patients With and Without Idiopathic Ventricular Fibrillation

Takatsuki

Nishiyama

Kimura

et al. 2017

Circ: Arrhythmia and Electrophysiology

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Among 48 patients diagnosed with J-wave-associated IVF, J waves were studied in 8 patients during atrial pacing. In 1 patient, © 2017 American Heart Association, Inc. Original Article Circ Arrhythm ElectrophysiolBackground-To know the underlying mechanisms of J waves, the response to atrial pacing was studied in patients with idiopathic ventricular fibrillation (IVF) and patients with non-IVF. Methods and Results-In 8 patients with IVF, the J-wave amplitude was measured before, during, and after atrial pacing.All patients had episodes of ventricular fibrillation without structural heart disease. The responses of J waves were compared with those of the 17 non-IVF control subjects who revealed J waves but no history of cardiac arrest and underwent electrophysiological study. The IVF patients were younger than the non-IVF patients (28±10 versus 52±14 years, respectively; P=0.002) and had larger J waves with more extensive distribution. J waves decreased from 0.35±0.26 to 0.22±0.23 mV (P=0.025) when the RR intervals were shortened from 782±88 to 573±162 ms (P=0.001). A decrease (≥0.05 mV) in the J-wave amplitude was observed in 6 of the 8 patients. In addition, 1 patient showed a distinct reduction of J waves in the unipolar epicardial leads. In contrast, J waves were augmented in the 17 non-IVF subjects from 0.27±0.09 to 0.38±0.10 mV (P<0.001): augmented in 9 and unchanged in the 8 subjects. The different response patterns of J waves to rapid pacing suggest different mechanisms: early repolarization in IVF patients and conduction delay in non-IVF patients. Conclusions-The Aizawa et al Different Mechanisms of J-Wave Genesisa pause-dependent augmentation was analyzed in earlier study. 12 As the entry criteria, all patients were admitted after experiencing cardiac arrest because of out-of-hospital VF and being resuscitated by emergency medical personnel. All of them showed normal findings in complete blood counts, blood chemistry panels, and serological tests after admission and echocardiography, and cardiac catheterization excluded structural heart diseases. A provocation test using acetylcholine or ergonovine maleate was negative for coronary spasms. Coexistence of Brugada syndrome was studied by Pilsicainide, a class Ic antiarrhythmic drug. All patients underwent atrial pacing during electrophysiological study (EPS) or at bedside to control VF. The atrial pacing was performed at steady rate at ≥1 peced cycle lengths. None was on any medication. Non-IVF PatientsAs a control group, the response of J waves to atrial pacing was also studied in 17 consecutive male subjects who presented with J waves among 220 patients who had undergone EPS in the preceding 2 years: 8 patients were common to the previous study, and 9 patients were new. 16The entry criteria were identical to those for the IVF patients, and none of the patients in the control group had a past history and a family history of sudden cardiac death or cardiac arrest. All patients denied having a history of structural heart disease, and they lacked the signs ...

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Section: J-wave Dynamicity In the Non-ivf Patientsmentioning

confidence: 80%

mentioning

confidence: 89%

Section: J-wave Dynamicity In the Non-ivf Patientsmentioning

confidence: 99%

mentioning

confidence: 99%

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Tachycardia-Induced J-Wave Changes in Patients With and Without Idiopathic Ventricular Fibrillation

Takatsuki

Nishiyama

Kimura

et al. 2017

Circ: Arrhythmia and Electrophysiology

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“…[Yan 1996;Gussak 2000, Koncz 2013, Gurabi 2013 (2) Depolarization hypothesis maintains that regional conduction delay is the cause underlying the electrographic manifestation of a J wave [Hoogendijk 2013, Meiborg 2016. In this sense, ERP is considered to be a distinctly fragmented QRS complex, so thus J wave is actually an r' or R' wave [Huikuri 2015, Aizawa 2015.…”

Section: I14 Cellular Electrophysiologymentioning

confidence: 99%

Cellular mechanisms underlying the effects of cilostazol, milrinone, isoproterenol and ajmaline on electrographic and arrhythmic manifestations of early repolarization syndrome, and comparative analysis of the cardiac electrophysiological effects of the optical isomers of mexiletine

Patocskai¹

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Electrocardiographic features of the presence of occult myocardial disease in patients with VPD‐induced cardiomyopathy

Gwag

Park

et al. 2020

Journal of Arrhythmia

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Background: Frequent ventricular premature depolarizations (VPDs) can cause reversible cardiomyopathy (CMP). However, many patients maintain a normal left ventricular (LV) function with a high VPD burden. The electrocardiographic characteristics of VPD-induced CMP have not been elucidated. Methods:One hundred and eighty (91 men, age; 51 ± 15 years) patients with frequent idiopathic VPDs (>10% VPDs/day or >10 000 VPDs/day) were studied. All patients underwent successful ablation and were then divided into two groups according to the echocardiographic findings before and after the ablation procedure.Results: Group A (n = 139) had a normal LV function with VPD frequencies, and Group B (n = 41) had reversible LV dysfunction after ablation. The VPD QRS duration (QRSd) was wider in patients with CMP (Group A vs Group B; 137.2 ± 12.0 milliseconds vs 159.7 ± 5.3 milliseconds, P < .001). VPDs with a terminal QRS delay marked by a notch followed by a discrete lower amplitude signal after the peak R wave in any precordial lead were identified. The incidence of terminal signals was higher in the CMP group (Group A vs Group B; 2.1% vs 53.6%, P < .001). Conclusions:The wider VPD QRSd and terminal QRS delay in patients with VPDinduced CMP suggest subclinical cell-to-cell conduction abnormalities as a potential factor predisposing VPD-induced CMP. K E Y W O R D Scardiomyopathy, electrocardiogram, ventricular premature depolarization

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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?

Cited by 38 publications

References 30 publications

Tachycardia-Induced J-Wave Changes in Patients With and Without Idiopathic Ventricular Fibrillation

Tachycardia-Induced J-Wave Changes in Patients With and Without Idiopathic Ventricular Fibrillation

Cellular mechanisms underlying the effects of cilostazol, milrinone, isoproterenol and ajmaline on electrographic and arrhythmic manifestations of early repolarization syndrome, and comparative analysis of the cardiac electrophysiological effects of the optical isomers of mexiletine

Electrocardiographic features of the presence of occult myocardial disease in patients with VPD‐induced cardiomyopathy

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