Abstract
J-wave pattern has been recognized as an arrhythmic risk marker, particularly in myocardial infarction patients. Mechanisms underlying J-wave development in ischemia remain unknown. In myocardial infarction model, we evaluated activation time delay as a prerequisite of J-wave appearance and predictor of ventricular fibrillation. Body surface ECGs and myocardial unipolar electrograms were recorded in 14 anesthetized pigs. 48 intramural leads were positioned across ventricular free walls and interventricular septum. Myocardial ischemia was induced by ligation of the left anterior descending coronary artery and the recordings were done during 40-minute coronary occlusion. The local activation times were determined as instants of dV/dt minimum during QRS complex in unipolar electrograms. During occlusion, ventricular local activation time prolonged in the middle portion of the left ventricular free wall, and basal and middle portions of septum, while J-waves appeared in precordial leads in 11 animals. In logistic regression and ROC curve analyses, activation time delay at a given time-point was associated with J-wave development, and a longer activation time was associated with ventricular fibrillation appearance. In experimental coronary occlusion, activation delay in ischemic myocardium was associated with generation of the J waves in the body surface ECG and predicted ventricular fibrillation.
Highlights
The mechanism of the J-wave genesis in acute ischemia remains controversial
Www.nature.com/scientificreports that in patients with an acute ST-elevation myocardial infarction the J-wave amplitude was augmented in tachycardia, which supported the conduction delay-related mechanism of the early repolarization pattern
While the nonischemic areas had stable Local activation time (LAT) during the occlusion period, the areas identified as non-perfused by postmortem investigation and presenting typical ST-segment elevation on local intramyocardial electrograms could have either increased or unchanged LATs (Fig. 2, panel A)
Summary
The mechanism of the J-wave genesis in acute ischemia remains controversial. There are two main lines of evidence suggesting repolarization or depolarization abnormalities to underlie this phenomenon. The direct reason for the J-wave formation has been reported to be a transmural difference in a transient outward current density. This ECG phenomenon has been shown to be accentuated by increased vagal tone and bradycardia[18], an observation supporting the suggested repolarization-related mechanism for the J-wave. LV that in patients with an acute ST-elevation myocardial infarction the J-wave amplitude was augmented in tachycardia, which supported the conduction delay-related mechanism of the early repolarization pattern. Simulation studies[21,22] demonstrated that prolonged activation in ischemic conditions produces an “overlap” of depolarization and repolarization potentials manifesting as the J-wave pattern. We aimed at evaluating activation time delay as a prerequisite of J-wave appearance and predictor of VF in open-chest porcine model of myocardial infarction
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