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Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in
Alena S Tsvetkova1, Jan E Azarov1,2,3, Olesya G Bernikova1
1Department of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, Syktyvkar, Russia.
Insights
Activation delay in ischemic heart muscle contributes to J-wave appearance and ventricular fibrillation (VF). Myocardial repolarization changes also play a role in J-wave generation during acute myocardial infarction.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Research
Background:
- Activation delay in ischemic myocardium is linked to J-wave appearance and predicts ventricular fibrillation (VF) in experimental myocardial infarction.
- The precise role of ischemia-related repolarization abnormalities in J-wave generation remains incompletely understood.
Purpose of the Study:
- To investigate the contribution of myocardial repolarization changes to J-wave generation in body surface ECG.
- To assess the role of these changes in ventricular fibrillation (VF) within a porcine acute myocardial infarction model.
Main Methods:
- Myocardial ischemia was induced in 22 pigs via coronary artery occlusion (LAD or RCA).
- Body surface ECGs and intramyocardial electrograms were recorded simultaneously.
- Local activation times (ATs) and activation-repolarization intervals (ARIs) were measured.
Main Results:
- J-waves manifested in precordial leads correlating with occlusion location.
- Prolonged ATs were associated with J-wave development and VF incidence.
- Shortened ARIs in ischemic regions and the difference between normal and ischemic zones (ΔARI) correlated with J-wave appearance, independent of AT delay.
Conclusions:
- Both activation time delay and increased ΔARIs contribute to J-wave formation in the body surface ECG.
- Activation time delay, but not ΔARIs, was significantly associated with the occurrence of ventricular fibrillation.
Abstract:
Background: 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. Objectives: 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. Methods: In 22 anesthetized pigs, myocardial ischemia was induced by occlusion of the left anterior descending coronary artery (LAD, n = 14) and right coronary artery (RCA, n = 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. Results: 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; p < 0.001) and VF incidence (OR = 1.039 95% CI 1.008-1.072; p = 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, p < 0.001) independently of AT delay in multivariate logistic regression analysis. Conclusions: 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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