: Activation delay in ischemic myocardium has been found to contribute to J-wave appearance and to predict ventricular fibrillation (VF) in experimental myocardial infarction. However, the role of ischemia-related repolarization abnormalities in J-wave generation remains unclear. : The objective of our study was to assess a contribution of myocardial repolarization changes to J-wave generation in the body surface ECG and VF in a porcine acute myocardial infarction model. : In 22 anesthetized pigs, myocardial ischemia was induced by occlusion of the left anterior descending coronary artery (LAD, = 14) and right coronary artery (RCA, = 8). Body surface ECGs were recorded simultaneously with intramyocardial unipolar electrograms led from flexible electrodes positioned across the left ventricular (LV) wall, interventricular septum (IVS), and right ventricular (RV) wall at apical, middle and basal levels of the ventricles (a total of 48 leads). Local activation times (ATs) and activation-repolarization intervals (ARIs, differences between dV/dt maximum during T-wave and dV/dt minimum during QRS) were measured. : J-waves appeared in left precordial leads (in 11 out of 14 animals with LAD occlusion) and right precordial leads (in six out of eight animals with RCA occlusion). During ischemic exposure, ATs prolonged, and the activation delay was associated with J-wave development (OR = 1.108 95% CI 1.072-1.144; < 0.001) and VF incidence (OR = 1.039 95% CI 1.008-1.072; = 0.015). ARIs shortened in the ischemic regions (in the IVS under LAD-occlusion and the lateral RV base under RCA-occlusion). The difference between maximal ARI in normal zones and ARI in the ischemic zones (ΔARI) was associated with J-wave appearance (OR = 1.025 95% CI 1.016-1.033, < 0.001) independently of AT delay in multivariate logistic regression analysis. : Both AT delay and increase of ΔARIs contributed to the development of J-wave in body surface ECG. However, only AT delay was associated with VF occurrence.
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http://dx.doi.org/10.3389/fphys.2020.568021 | DOI Listing |
Heart Rhythm
October 2024
Research and Development, Tachikawa Medical Center, Nagaoka, Japan. Electronic address:
Pacing Clin Electrophysiol
December 2024
Department of Cardiology, Anjo Kosei Hospital, Anjo, Japan.
Digit Health
September 2024
Department of Medical Engineering, Chiba University, Chiba City, Chiba Prefecture, Japan.
Objective: A ballistocardiogram (BCG) is a vibration signal generated by the ejection of the blood in each cardiac cycle. The BCG has significant variability in amplitude, temporal aspects, and the deficiency of waveform components, attributed to individual differences, instantaneous heart rate, and the posture of the person being measured. This variability may make methods of extracting J-waves, the most distinct components of BCG less generalizable so that the J-waves could not be precisely localized, and further analysis is difficult.
View Article and Find Full Text PDFHeart Rhythm
July 2024
Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Background: In patients with Brugada syndrome, myocardial fibrosis can be identified through epicardial biopsy or cardiac magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE). However, the myocardial alterations in patients with early repolarization syndrome (ERS) remain poorly elucidated.
Objective: The objective of this study was to investigate the presence of myocardial fibrosis in patients with ERS by LGE in CMR.
Cureus
May 2024
Department of Community Emergency Medicine, Ehime University Graduate School of Medicine, Ehime, JPN.
The 12-lead electrocardiographic findings in hypothermia include the presence of J waves; prolongation of the PR, QRS, and QT intervals; and atrial and ventricular dysrhythmias. Among these findings, the J wave, known as the Osborn wave, is considered pathognomonic. In 1953, the J wave was reported as a specific response to hypothermia in dogs, representing the current at the site of injury instead of a widening of the QRS complex that occurs caused by a conduction delay.
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