Toyama J, Niimi N, Ishikawa T, Wada M, Oguri H, Okajima M, Yamada K
Adv Cardiol. 1978;21:77-81. doi: 10.1159/000400427.
The relationship between the lack of electromotive force in myocardial infarction and body surface potential distribution was investigated on maps reconstructed from a simulated heart model and transfer impedance vectors of human torso model. The heart model, a cluster of 3-mm cubic blocks, was stored in the memory of a computer. Transfer impedance vectors between 81 lead points on the human torso model and 392 positions covering ventricular areas in the torso were measure. Body surface potential values were calculated mathematically by summing up scalar products between the electromotive force of the heart model and the measured transfer impedance vectors. Thus, reconstructed maps changed in their patterns with the alternation in lacation and/or extent of infarcted region in the heart model. In particular, the appearance of the abnormal potential minimum, which projects the infarcted region in the heart model onto the torso surface, was characteristic in both transmural and subendocardial infarction. In addition, delayed activation in the intact layer of the epicardium overlying the infarcted region produced a potential maximum on the same place as the abnormal potential minimum appeared previously.
基于模拟心脏模型重建的地图以及人体躯干模型的转移阻抗矢量，研究了心肌梗死中电动势缺失与体表电位分布之间的关系。心脏模型由3毫米见方的小块组成，存储在计算机内存中。测量了人体躯干模型上81个导联点与躯干中覆盖心室区域的392个位置之间的转移阻抗矢量。通过将心脏模型的电动势与测量的转移阻抗矢量之间的标量积相加，以数学方式计算体表电位值。因此，随着心脏模型中梗死区域位置和/或范围的变化，重建地图的模式也会改变。特别是，异常电位最小值的出现具有特征性，它将心脏模型中的梗死区域投射到躯干表面，在透壁性梗死和心内膜下梗死中均如此。此外，梗死区域上方完整的心外膜层的延迟激活在先前出现异常电位最小值的同一位置产生了一个电位最大值。
