Calkins H, el-Atassi R, Kalbfleisch S, Langberg J, Morady F
Division of Cardiology, University of Michigan Medical Center, Ann Arbor.
Pacing Clin Electrophysiol. 1992 Nov;15(11 Pt 1):1674-80. doi: 10.1111/j.1540-8159.1992.tb02954.x.
Contraction-excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction-excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 +/- 3 mmHg to 15 +/- 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 +/- 5.2 and 6.2 +/- 3.5 msec, respectively (P < 0.001). Similar results were obtained during autonomic blockade. these findings confirm the presence of contraction-excitation feedback in normal human atria.
收缩-兴奋反馈在哺乳动物心室中已得到广泛研究。相比之下，关于哺乳动物心房的收缩-兴奋反馈却知之甚少。本研究的目的是探讨通过改变房室（AV）间期诱导的心房压力急性改变对心房不应期的影响。20例无结构性心脏病的患者参与了本研究。在每例患者中，在500毫秒的周期长度和120毫秒的AV间期进行AV起搏时，测量心房有效不应期（ERP）和绝对不应期（ARP）。在驱动序列的最后两搏同时起搏心房和心室，诱导心房压力急性升高。ERP定义为用两倍刺激阈值的额外刺激电流强度未能夺获的最长额外刺激耦联间期。ARP以类似方式定义，额外刺激电流强度为10毫安。使用递增额外刺激技术确定ERP和ARP。一部分患者在自主神经阻滞期间进行起搏方案。随着驱动序列最后两搏的AV间期从120毫秒缩短至0毫秒，右心房峰值压力从7±3毫米汞柱增加至15±5毫米汞柱（P<0.001）。心房和心室同时起搏相关的心房压力升高分别导致心房ERP和ARP缩短7.3±5.2毫秒和6.2±3.5毫秒（P<0.001）。在自主神经阻滞期间获得了类似结果。这些发现证实了正常人心房存在收缩-兴奋反馈。
