Tsvetkova Alena S, Azarov Jan E, Bernikova Olesya G, Ovechkin Alexey O, Vaykshnorayte Marina A, Demidova Marina M, Platonov Pyotr G
Department of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, Syktyvkar, Russia.
Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden.
Front Physiol. 2020 Sep 30;11:568021. doi: 10.3389/fphys.2020.568021. eCollection 2020.
: 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.
在实验性心肌梗死中，已发现缺血心肌的激活延迟会导致J波出现，并可预测心室颤动（VF）。然而，缺血相关复极异常在J波产生中的作用仍不清楚。
我们研究的目的是评估在猪急性心肌梗死模型中，心肌复极变化对体表心电图J波产生及心室颤动的影响。
在22只麻醉猪中，通过闭塞左前降支冠状动脉（LAD，n = 14）和右冠状动脉（RCA，n = 8）诱导心肌缺血。在心室的心尖、中间和基底水平，从横跨左心室（LV）壁、室间隔（IVS）和右心室（RV）壁放置的柔性电极记录心内膜单极电图的同时，记录体表心电图。测量局部激活时间（ATs）和激活 - 复极间期（ARIs，T波期间dV/dt最大值与QRS期间dV/dt最小值之间的差异）。
J波出现在左胸前导联（14只LAD闭塞动物中的11只）和右胸前导联（8只RCA闭塞动物中的6只）。在缺血暴露期间，ATs延长，激活延迟与J波形成相关（OR = 1.108，95%CI 1.072 - 1.144；P < 0.001）和心室颤动发生率相关（OR = 1.039，95%CI 1.008 - 1.072；P = 0.015）。缺血区域的ARIs缩短（LAD闭塞时IVS及RCA闭塞时RV外侧基底）。在多因素逻辑回归分析中，正常区域最大ARIs与缺血区域ARIs之间的差异（ΔARI）与J波出现相关（OR = 1.025，95%CI 1.016 - 1.033，P < 0.001），独立于AT延迟。
AT延迟和ΔARIs增加均有助于体表心电图J波的形成。然而，只有AT延迟与心室颤动的发生相关。
