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.