Murakawa Y, Sezaki K, Yamashita T, Kanese Y, Omata M
Second Department of Internal Medicine, University of Tokyo, Japan.
Am J Physiol. 1997 Sep;273(3 Pt 2):H1377-85. doi: 10.1152/ajpheart.1997.273.3.H1377.
To investigate the electrophysiological and electrocardiographic characteristics of ventricular arrhythmia due to abnormal repolarization, we studied the three-dimensional activation sequence of cesium-induced ventricular tachycardia (VT) in 10 anesthetized dogs using a 384-channel recording system. Seventeen monomorphic VT (mVT) and eight polymorphic VT (pVT) episodes induced by cesium chloride (2 or 3 mM/kg) were analyzed. Only a single arrhythmogenic focus was detected in most beats of VT, whereas two competing foci were temporarily observed in two episodes of pVT. The site of arrhythmogenic focus of mVT was the endocardium (5 of 17), the midmyocardium (4 of 17), or undetermined (8 of 17). Both endocardial and midmyocardial arrhythmogenic foci were also found in pVT, and most pVT (6 of 8) were associated with the transition of the site of arrhythmogenic focus. These results are consistent with the view that both myocardial muscle fibers and Purkinje cells can cause ventricular arrhythmia due to abnormal repolarization and that changing the site of arrhythmogenic focus is the main mechanism of pVT.
为研究复极异常所致室性心律失常的电生理和心电图特征,我们使用384通道记录系统,对10只麻醉犬氯化铯诱导的室性心动过速(VT)的三维激动顺序进行了研究。分析了由氯化铯(2或3 mM/kg)诱发的17次单形性室性心动过速(mVT)和8次多形性室性心动过速(pVT)发作。在VT的大多数搏动中仅检测到单个致心律失常灶,而在2次pVT发作中暂时观察到2个相互竞争的病灶。mVT的致心律失常灶部位为心内膜(17例中的5例)、心肌中层(17例中的4例)或未确定(17例中的8例)。pVT中也发现了心内膜和心肌中层致心律失常灶,且大多数pVT(8例中的6例)与致心律失常灶部位的转变有关。这些结果与以下观点一致,即心肌纤维和浦肯野细胞均可因复极异常导致室性心律失常,且致心律失常灶部位的改变是pVT的主要机制。