Behrens S, Li C, Knollmann B C, Franz M R
Cardiology Division, Veterans Affairs Medical Center, Washington, D.C. 20422, USA.
Pacing Clin Electrophysiol. 1998 Jan;21(1 Pt 1):100-7. doi: 10.1111/j.1540-8159.1998.tb01067.x.
Dispersion of ventricular repolarization, assessed as QT dispersion in the ECG or by multiple monophasic action potential (MAP) recordings, is defined as the difference between the earliest and latest repolarization. It is thus measured in the time domain. However, myocardial refractoriness is primarily a function of the membrane potential during phase 3 repolarization. The purpose of this study, therefore, was to measure dispersion of ventricular repolarization in the voltage domain and to study its relation to VF inducibility. To further validate this concept, the effect of chronic amiodarone treatment on the voltage dispersion were assessed. MAPs were recorded simultaneously at 10 epicardial and endocardial sites in isolated rabbit hearts, both under baseline conditions (n = 8) and after chronic amiodarone treatment (n = 8). Repolarization dispersion in the voltage domain was calculated as the difference between the highest and lowest repolarization level of all 10 MAPs at 10-ms steps, starting from the MAP plateau level to complete repolarization. Plotting these voltage differences along the time axis resulted in a dispersion curve, which rose during early repolarization, reached a peak during phase 3 repolarization, and thereafter declined toward zero. There was a close correlation between VF vulnerability in response to electrical field stimuli and the time during which voltage dispersion was maximal (r = 0.828, P < 0.0001). Amiodarone caused a right-ward shift of both the dispersion curve (P = 0.007) and VF vulnerability (P = 0.025), but did not change the magnitude nor the shape of the voltage dispersion curve and its relation to VF vulnerability. Repolarization dispersion in the voltage domain describes an alternate approach for evaluating the heterogeneity of ventricular repolarization and may help to characterize arrhythmia susceptibility under experimental conditions.
心室复极离散度，通过心电图中的QT离散度或多个单相动作电位（MAP）记录来评估，定义为最早和最晚复极之间的差异。因此，它是在时域中测量的。然而，心肌不应期主要是第3期复极期间膜电位的函数。因此，本研究的目的是测量电压域中的心室复极离散度，并研究其与室颤易感性的关系。为了进一步验证这一概念，评估了慢性胺碘酮治疗对电压离散度的影响。在离体兔心脏的10个心外膜和心内膜部位同时记录MAP，分别在基线条件下（n = 8）和慢性胺碘酮治疗后（n = 8）进行。电压域中的复极离散度计算为从MAP平台期水平到完全复极，以10 ms步长，所有10个MAP的最高和最低复极水平之间的差异。将这些电压差异沿时间轴绘制得到一条离散度曲线，该曲线在早期复极期间上升，在第3期复极期间达到峰值，此后降至零。对电场刺激的室颤易感性与电压离散度最大时的时间之间存在密切相关性（r = 0.828，P < 0.0001）。胺碘酮使离散度曲线（P = 0.007）和室颤易感性（P = 0.025）均向右移位，但未改变电压离散度曲线的幅度和形状及其与室颤易感性的关系。电压域中的复极离散度描述了一种评估心室复极异质性的替代方法，可能有助于在实验条件下表征心律失常易感性。
