Delise P, D'Este D, Di Pede F, Raviele A, Bonso A, Allibardi P, Pascotto P, Piccolo E
G Ital Cardiol. 1984 Jan;14(1):1-11.
Experimental and clinical studies have demonstrated the existence of phase 3 and phase 4 functional blocks. In this report six cases are presented in which the electrophysiological study demonstrated the existence of a functional intraventricular block different from phase 3 and phase 4 blocks. In these cases the occurrence of the block was related to the presence in mid-diastole of a zone of block preceded and followed by intervals of unimpaired conduction. In two of 6 cases the functional block (infrahisian block) was not present in the basal tracing; it occurred during programmed atrial stimulation in a range of critical H1H2 coupling intervals delivered late in diastole, and did not appear after earlier stimuli. In the remaining four cases the conduction disturbance (2 RBBB, 2 infrahisian blocks) was present in the basal tracing, but disappeared both during early and late supraventricular extrastimuli, the first having short H1H2 intervals, the latter having H1H2 intervals longer than H1H1 basal cycle length. The width of the mid-diastolic zone of block varied from a few msec to hundreds of sec, and increased as heart rate increased. Two hypotheses are put forward in order to explain the electrophysiological mechanism responsible for the phenomenon: 1) a longitudinal dissociation in the conducting system, generating two different ways, one having a long refractory period, the other having a phase 4 spontaneous depolarization; they would be responsible of phase 3 and phase 4 blocks respectively. The early and late zones of conduction could be explained by an alternate conduction in one of the two ways, while the mid-diastolic zone of block could be due to a simultaneous block in both ways; 2) the existence of a diastolic oscillatory potential (late after-depolarization). In the latter case we can suppose that the mid-diastolic block was due to the stimulation of the cells of the conducting system before the restoration of the normal diastolic potential. Our electrophysiological data offer a new contribution to the understanding of intermittent intraventricular blocks. However further experimental and clinical studies are needed to confirm our electrophysiological hypotheses.
实验和临床研究已证实存在3相和4相功能性阻滞。在本报告中，介绍了6例病例，其电生理研究显示存在一种不同于3相和4相阻滞的功能性室内阻滞。在这些病例中，阻滞的发生与舒张中期存在一个阻滞区有关，该阻滞区之前和之后是传导未受损的间期。6例中有2例，基础心电图中不存在功能性阻滞（希氏束下阻滞）；它发生在舒张晚期给予的一系列临界H1H2耦合间期的程控心房刺激过程中，且在较早刺激后未出现。在其余4例中，基础心电图中存在传导障碍（2例右束支传导阻滞，2例希氏束下阻滞），但在早期和晚期室上性期外刺激时均消失，早期刺激的H1H2间期短，晚期刺激的H1H2间期长于基础H1H1周期长度。舒张中期阻滞区的宽度从几毫秒到数百毫秒不等，并随心率增加而增加。为解释该现象的电生理机制提出了两种假说：1）传导系统中的纵向分离，产生两种不同的路径，一种具有长不应期，另一种具有4相自发去极化；它们分别负责3相和4相阻滞。早期和晚期传导区可用两种路径之一的交替传导来解释，而舒张中期阻滞区可能是由于两种路径同时阻滞所致；（2）存在舒张期振荡电位（晚期后除极）。在后一种情况下，我们可以假设舒张中期阻滞是由于在正常舒张电位恢复之前对传导系统细胞的刺激所致。我们的电生理数据为理解间歇性室内阻滞提供了新的贡献。然而，需要进一步的实验和临床研究来证实我们的电生理假说。
