Matiukas Arvydas, Pertsov Arkady M, Kothari P, Cram A, Tolkacheva Elena G
Department of Pharmacology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Annu Int Conf IEEE Eng Med Biol Soc. 2009;2009:6321-4. doi: 10.1109/IEMBS.2009.5333176.
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 532 nm, 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 (S(max)), 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, S(max) 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, S(max) 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.
心脏电活动的实时光学记录有助于研究心律失常的发生机制,尤其是由于整体缺血导致的机制。众所周知,整体缺血会增加心脏的电不均一性。然而,缺血期间右心室(RV)和左心室(LV)之间的心室间差异及其与心律失常发生的关系仍知之甚少。我们使用Langendorff灌注兔心脏的高分辨率光学映射(di-4-ANEPPS,532nm激发,640±50nm发射)来量化周期性起搏和心室颤动期间心脏的心室间不均一性。使用两台快速电荷耦合器件(CCD)相机记录对照、整体缺血(20分钟)和再灌注期间右心室和左心室的电活动。心脏以逐渐缩短(从300毫秒到100毫秒)的基础周期长度进行起搏,并通过短阵起搏诱发心室颤动,并在整体缺血前和再灌注后进行记录。测量左心室和右心室表面的动作电位时程(APD)、APD恢复曲线的最大斜率(S(max))以及心室颤动的平均主导频率(DF)。在对照心脏中未观察到APD不均一性。整体缺血在APD中诱导了心室间不均一性(右心室:109±21毫秒,左心室:89±23毫秒;p<0.01),再灌注后这种不均一性消失。然而,右心室(对照:0.94±0.25,缺血:0.36±0.12;p<0.01)和左心室(对照:0.99±0.24,缺血:0.43±0.21;p<0.01)的S(max)均一致降低,且再灌注后未恢复。此外,再灌注期间右心室心室颤动的DF显著降低(从8.6±1.3赫兹降至6.2±1.1赫兹;p<0.05),而左心室则保持不变(9.0±0.8赫兹对8.5±1.0赫兹)。因此,我们的结果表明,整体缺血在周期性起搏期间诱导了APD的心室间不均一性。尽管这种效应在再灌注后消失,但S(max)未恢复,表明心脏电特性存在残余变化。因此,再灌注揭示了心室颤动动态过程中存在心室间不均一性。