Cardiovascular Center, Taichung Veterans General Hospital and Chiayi Branch, Taichung and Chiayi, Taiwan.
Department of Internal Medicine, Faculty of Medicine, Institute of Clinical Medicine, Cardiovascular Research Center, National Yang-Ming University School of Medicine, Taipei, Taiwan.
PLoS One. 2020 Feb 21;15(2):e0228818. doi: 10.1371/journal.pone.0228818. eCollection 2020.
High beat-to-beat morphological variation (divergence) on the ventricular electrogram during programmed ventricular stimulation (PVS) is associated with increased risk of ventricular fibrillation (VF), with unclear mechanisms. We hypothesized that ventricular divergence is associated with epicardial wavebreaks during PVS, and that it predicts VF occurrence.
Langendorff-perfused rabbit hearts (n = 10) underwent 30-min therapeutic hypothermia (TH, 30°C), followed by a 20-min treatment with rotigaptide (300 nM), a gap junction modifier. VF inducibility was tested using burst ventricular pacing at the shortest pacing cycle length achieving 1:1 ventricular capture. Pseudo-ECG (p-ECG) and epicardial activation maps were simultaneously recorded for divergence and wavebreaks analysis, respectively. A total of 112 optical and p-ECG recordings (62 at TH, 50 at TH treated with rotigaptide) were analyzed. Adding rotigaptide reduced ventricular divergence, from 0.13±0.10 at TH to 0.09±0.07 (p = 0.018). Similarly, rotigaptide reduced the number of epicardial wavebreaks, from 0.59±0.73 at TH to 0.30±0.49 (p = 0.036). VF inducibility decreased, from 48±31% at TH to 22±32% after rotigaptide infusion (p = 0.032). Linear regression models showed that ventricular divergence correlated with epicardial wavebreaks during TH (p<0.001).
Ventricular divergence correlated with, and might be predictive of epicardial wavebreaks during PVS at TH. Rotigaptide decreased both the ventricular divergence and epicardial wavebreaks, and reduced the probability of pacing-induced VF during TH.
在程控心室刺激（PVS）期间，心室电图上的高逐搏形态变化（发散）与室颤（VF）风险增加相关，其机制尚不清楚。我们假设心室发散与 PVS 期间的心外膜波破裂有关，并且可以预测 VF 的发生。
Langendorff 灌注兔心（n = 10）进行 30 分钟的治疗性低温（30°C），然后用缝隙连接调节剂罗替戈汀（300 nM）处理 20 分钟。使用最短起搏周期长度达到 1:1 心室夺获的突发心室起搏来测试 VF 的诱导性。同时记录伪 ECG（p-ECG）和心外膜激活图，分别用于发散和波破裂分析。共分析了 112 个光学和 p-ECG 记录（62 个在 TH 时，50 个在 TH 时用罗替戈汀处理）。添加罗替戈汀可降低心室发散，从 TH 时的 0.13±0.10 降低到 0.09±0.07（p = 0.018）。同样，罗替戈汀降低了心外膜波破裂的数量，从 TH 时的 0.59±0.73 降低到 0.30±0.49（p = 0.036）。VF 的诱导性降低，从 TH 时的 48±31%降低到罗替戈汀输注后的 22±32%（p = 0.032）。线性回归模型表明，在 TH 期间，心室发散与心外膜波破裂相关（p<0.001）。
在 TH 期间，心室发散与 PVS 期间的心外膜波破裂相关，并且可能具有预测性。罗替戈汀降低了心室发散和心外膜波破裂的数量，并降低了 TH 期间起搏诱导的 VF 的可能性。
