[Study of the mechanism of an atrial pause using endocavitary recording of the sinus node potential in man].

The aim of this clinical study was to determine the electrophysiological mechanism of spontaneous atrial standstill, defined as a sudden lengthening of the trial cycle to over 10 p. 100 of its basal value, by recording the sinus node potential by endocavitary electrocardiological techniques. Satisfactory recordings of the sinus potential were obtained for the study of 65 atrial pauses recorded in 31 patients (18 without sinus node dysfunction and 13 with sinus node disease). It was shown that atrial pauses, shorter than two basal atrial cycles correspond to a moderate slowing of the sinus rhythm and to a sometimes very significant lengthening of the sinoatrial conduction time when sinus rhythm resumed. Pauses longer than two basal atrial cycles were always due to sinoatrial block which sometimes occured in patients with clearly individualised sinus activity, and sometimes with a slow continuous sinus activity. The sinus period did not change during these long pauses and sinoatrial conduction was normal when sinus rhythm resumed. The increased duration of the sinus potential, a constant finding during these pauses, is related to an intrasinusal conduction defect. This suggest that the primum movens of sinoatrial block is intrasinusal block which prevents rapid recruitment of a sufficient number of elemental sinus potentials so that the resultant potential becomes subliminal and therefore incapable of passing the sinoatrial junction. Short-lasting atrial pauses with a normal response to extrastimulus or atrial stimulation and characterised electrophysiologically by an increased sinoatrial conduction time without block of the sinus potential may be opposed to long atrial pauses with the pathological response of sinus node dysfunction characterised electrophysiologically by block of the sinus impulse. In practice the ability to induce a long pause by atrial stimulation (sinoatrial block) revealing latent disease of intrasinusal or sinoatrial conduction, may constitute an essential physiological sign of sinus node dysfunction.