Optical mapping of electrical heterogeneities in the heart during global ischemia.
Optical mapping of electrical heterogeneities in the heart during global ischemia.
复制标题
DOI：
10.1109/iembs.2009.5333176
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Tolkacheva EG
中科院分区：
文献类型：
--
作者：
Matiukas A;Pertsov AM;Kothari P;Cram A;Tolkacheva EG
心脏电活动的实时光学记录允许心律失常机制的研究，特别是由于全局缺血。众所周知，全身缺血会增加心脏电的不均匀性。然而，缺血时右心室（RV）和左心室（LV）的心室间差异及其与心律失常的关系仍然知之甚少。我们使用高分辨率光学成像（di-4-ANEPPS， 532nm激发，640±50 nm发射）对langendorff灌注兔心脏进行定量，以量化周期性起搏和心室颤动期间心脏的室间异质性。两台快速CCD摄像机记录左室和左室在控制、全脑缺血（20分钟）和再灌注期间的电活动。心脏起搏逐渐减少（从300 ms到100 ms）基本周期长度，并在全缺血前和再灌注后记录猝发起搏引起的心室颤动。测定左室和右室表面的动作电位持续时间（APD）、APD恢复曲线最大斜率（Smax）和心室颤动的平均优势频率（DF）。对照心脏APD不存在异质性。全脑缺血引起的apd心室间异质性（RV: 109±21 ms, LV: 89±23 ms, p<0.01）在再灌注后消除。然而，左心室（对照组：0.94±0.25，缺血：0.36±0.12,p<0.01）和左心室（对照组：0.99±0.24，缺血：0.43±0.21,p<0.01）的Smax均下降，再灌注后未恢复。此外，心室颤动再灌注时的DF在RV组显著降低（从8.6±1.3 Hz降至6.2±1.1 Hz, p<0.05），而在LV组保持不变（9.0±0.8 Hz vs 8.5±1.0 Hz）。因此，我们的研究结果表明，在周期性起搏期间，全脑缺血导致APD的心室间异质性。虽然这种影响在再灌注时被消除，但Smax并没有恢复，这表明心脏电特性存在残余变化。因此，再灌注显示心室颤动动力学中存在室间异质性。
Real-time optical registration of electrical activity in the heart allows the study of arrhythmogenic mechanisms, in particular due to global ischemia. It is known that global ischemia increases electrical heterogeneity in the heart. However, inter-ventricular differences between the right (RV) and left ventricle (LV) during ischemia and their relationship to arrhythmogenesis remains poorly understood. We used high resolution optical mapping (di-4-ANEPPS, excitation at 532nm, emission at 640±50 nm) of Langendorff-perfused rabbit hearts to quantify inter-ventricular heterogeneity in the heart during periodic pacing and ventricular fibrillation. Two fast CCD cameras were used to record electrical activity from the RV and LV during control, global ischemia (20 min), and reperfusion. Hearts were paced at progressively reduced (from 300 ms to 100 ms) basic cycle lengths and ventricular fibrillation was induced by burst pacing and recorded before the global ischemia, and after the reperfusion. The action potential durations (APD), maximum slopes of APD restitution curves (Smax), and mean dominant frequency (DF) of ventricular fibrillation were measured for both LV and RV surfaces. No APD heterogeneity was observed in control hearts. Global ischemia induced inter-ventricular heterogeneity in APDs (RV: 109±21 ms, LV: 89±23 ms; p<0.01) that was abolished upon reperfusion. However, Smax was uniformly decreased in both RV (control: 0.94±0.25, ischemia: 0.36±0.12; p<0.01) and LV (control: 0.99±0.24, ischemia: 0.43±0.21; p<0.01) and did not recover upon reperfusion. In addition, the DF of ventricular fibrillation during reperfusion decreased significantly in RV (from 8.6±1.3 Hz to 6.2±1.1 Hz; p<0.05) but remained the same in LV (9.0±0.8 Hz vs 8.5±1.0 Hz). Thus, our results demonstrate that global ischemia induces inter-ventricular heterogeneity in APD during periodic pacing. Although this effect was abolished upon reperfusion, Smax did not recover, indicating the presence of residual changes in electrical properties of the heart. Therefore, reperfusion reveals the presence of inter-ventricular heterogeneities in the dynamics of ventricular fibrillation.