Liebman J, Thomas C, Fraenkel R, Rudy Y
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio.
J Electrocardiol. 1989 Jul;22(3):195-209. doi: 10.1016/0022-0736(89)90030-7.
The authors present electrocardiographic body surface potential maps (BSPMs) of 11 patients with hypoplastic right ventricle (HRV) of three types: type I, HRV with pulmonary atresia; type II, HRV with tricuspid atresia; and type III, HRV with tricuspid artesia and transposition of the great arteries. The BSPMs of all 11 patients demonstrated evidence for epicardial right ventricular breakthrough, indicating conduction through an intact right bundle branch and Purkinje system. Nonetheless, the BSPMs strongly suggested profound morphological, probably embryological, differences among the right ventricles of the three groups. The four patients with type I HRV had no evidence for conduction abnormality. The five patients with type II, HRV however, had very marked conduction abnormality. In four of these five, the standard ECG and VCG had initial forces suggesting left lateral wall myocardial infarction. The BSPMs showed no evidence for infarction but demonstrated very complicated slow initial activation, explaining why the initial QRS vector was to the right and posterior before extending leftward. In addition, in all five the initial positive potentials were unusually inferior and the initial negative potentials unusually superior. After the evidence for epicardial right ventricular breakthrough, the positive and negative potentials rapidly changed positions so that the positive potentials were unusually superior and the negative potentials unusually inferior, consistent with the BSPM of endocardial cushion defects. In four of these five there was marked delay of total ventricular activation time. Of the two patients with type III HRV, one had an initial QRS similar to that of type II. Neither had rapid change of inferior and superior positive and negative potentials after right ventricular breakthrough, and both had intraventricular slowing, one with partial left bundle branch block.
作者展示了11例三种类型右心室发育不全（HRV）患者的体表心电图电位图（BSPM）：I型，伴有肺动脉闭锁的HRV；II型，伴有三尖瓣闭锁的HRV；III型，伴有三尖瓣闭锁及大动脉转位的HRV。所有11例患者的BSPM均显示有心外膜右心室激动的证据，表明激动通过完整的右束支和浦肯野系统传导。尽管如此，BSPM强烈提示三组患者右心室在形态学上可能存在胚胎学差异。4例I型HRV患者无传导异常证据。然而，5例II型HRV患者有非常明显的传导异常。在这5例中的4例，标准心电图和心向量图的初始向量提示左外侧壁心肌梗死。BSPM未显示梗死证据，但显示出非常复杂的缓慢初始激动，解释了为何初始QRS向量在向左扩展之前指向右后方。此外，在所有5例中，初始正电位异常低，初始负电位异常高。在心外膜右心室激动的证据出现后，正电位和负电位迅速换位，使得正电位异常高，负电位异常低，这与心内膜垫缺损的BSPM一致。在这5例中的4例，总心室激动时间明显延迟。2例III型HRV患者中，1例初始QRS与II型相似。两者在右心室激动后下、上正、负电位均无快速变化，且均有室内传导减慢，其中1例伴有部分左束支传导阻滞。
