Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in Ischemia
Forskningsoutput: Tidskriftsbidrag › Artikel i vetenskaplig tidskrift
Standard
Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in Ischemia. / Tsvetkova, Alena S.; Azarov, Jan E.; Bernikova, Olesya G.; Ovechkin, Alexey O.; Vaykshnorayte, Marina A.; Demidova, Marina M.; Platonov, Pyotr G.
I: Frontiers in Physiology, Vol. 11, 568021, 30.09.2020.Forskningsoutput: Tidskriftsbidrag › Artikel i vetenskaplig tidskrift
Harvard
APA
CBE
MLA
Vancouver
Author
RIS
TY - JOUR
T1 - Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in Ischemia
AU - Tsvetkova, Alena S.
AU - Azarov, Jan E.
AU - Bernikova, Olesya G.
AU - Ovechkin, Alexey O.
AU - Vaykshnorayte, Marina A.
AU - Demidova, Marina M.
AU - Platonov, Pyotr G.
PY - 2020/9/30
Y1 - 2020/9/30
N2 - 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.
AB - 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.
KW - activation time
KW - ECG
KW - ischemia
KW - J-wave
KW - repolarization
KW - ventricular fibrillation
U2 - 10.3389/fphys.2020.568021
DO - 10.3389/fphys.2020.568021
M3 - Article
C2 - 33101054
AN - SCOPUS:85092693637
VL - 11
JO - Frontiers in Physiology
JF - Frontiers in Physiology
SN - 1664-042X
M1 - 568021
ER -