Castillo-Fenoy A, Thébaut J F, Achard F, de Langenhagen B
Arch Mal Coeur Vaiss. 1980 Jul;73(7):805-15.
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.
本临床研究的目的是通过心腔内心电技术记录窦房结电位，以确定自发性心房停搏的电生理机制，自发性心房停搏定义为心房周期突然延长至其基础值的10倍以上。对31例患者记录的65次心房停搏进行研究，获得了满意的窦房结电位记录（18例无窦房结功能障碍，13例有窦房结疾病）。结果表明，短于两个基础心房周期的心房停搏对应于窦性心律的中度减慢，以及窦性心律恢复时窦房传导时间有时非常显著的延长。长于两个基础心房周期的停搏总是由于窦房阻滞，有时发生在窦性活动明显个体化的患者中，有时发生在窦性活动缓慢持续的患者中。在这些长停搏期间窦性周期不变，窦性心律恢复时窦房传导正常。窦性电位持续时间增加是这些停搏期间的一个恒定发现，与窦房内传导缺陷有关。这表明窦房阻滞的首要原因是窦房内阻滞，它阻止了足够数量的基本窦房结电位的快速募集，从而使合成电位变得阈下，因此无法通过窦房交界区。对额外刺激或心房刺激反应正常的短暂性心房停搏，其电生理特征是窦房传导时间延长而无窦房结电位阻滞，可能与窦性结功能障碍的病理性反应的长时间心房停搏相反，后者的电生理特征是窦房结冲动阻滞。在实践中，通过心房刺激诱发长停搏（窦房阻滞）以揭示窦房内或窦房传导的潜在疾病，可能是窦房结功能障碍的一个重要生理标志。
