Ehlert F A, Damle R S, Goldberger J J, Kadish A H
Department of Medicine, Northwestern University School of Medicine, Chicago, Illinois.
J Cardiovasc Electrophysiol. 1994 Jun;5(6):485-95. doi: 10.1111/j.1540-8167.1994.tb01289.x.
Prior studies of sinus node function in man stated that the stimulus intensity of overdrive pacing has no effect on the response of the sinus node to overdrive suppression; however, data documenting these statements were lacking. Previous studies have also suggested that drive train stimulus intensity can alter ventricular refractoriness, but similar studies have not been performed on the human atrium. The purpose of this study was to evaluate the effects of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time.
The effect of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time was studied in 42 patients undergoing clinical electrophysiologic tests. The atrial effective refractory period was shorter at 10 mA (221 +/- 20 msec) and 5 mA (232 +/- 25 msec) than at a drive train stimulus intensity of 1.5 times late diastolic threshold (248 +/- 24 msec, P < 0.05 for pairwise comparison). The sinus node recovery time did not demonstrate a similar effect in the baseline state, following beta-adrenergic blockade, or following combined parasympathetic and beta-adrenergic blockade. However, following isolated parasympathetic blockade with atropine, the corrected sinus node recovery time shortened from 88 +/- 51 msec at 1.5 times late diastolic threshold to 48 +/- 55 msec at 10 mA (P < 0.05). Significant variability was present in sinus node recovery time measurements at baseline and following beta blockade; this variability decreased following parasympathetic blockade.
These data suggest that drive train stimulus intensity can affect the electrophysiologic properties of sinus node and atrial tissue. This effect appears to be mediated by local catecholamine and acetylcholine release and provides further evidence that the interaction between pacing stimuli and the cardiac autonomic system may need to be considered in evaluating electrophysiologic effects.
先前关于人类窦房结功能的研究表明，超速起搏的刺激强度对窦房结对超速抑制的反应没有影响；然而，缺乏记录这些说法的数据。先前的研究还表明，驱动序列刺激强度可改变心室不应期，但尚未对人体心房进行类似研究。本研究的目的是评估驱动序列刺激强度对心房有效不应期和窦房结恢复时间的影响。
在42例接受临床电生理检查的患者中，研究了驱动序列刺激强度对心房有效不应期和窦房结恢复时间的影响。心房有效不应期在10 mA（221±20毫秒）和5 mA（232±25毫秒）时比在舒张晚期阈值的1.5倍的驱动序列刺激强度下更短（248±24毫秒，两两比较P<0.05）。在基线状态、β肾上腺素能阻滞剂给药后或副交感神经和β肾上腺素能联合阻滞剂给药后，窦房结恢复时间未显示出类似影响。然而，在用阿托品进行单独的副交感神经阻滞之后，校正的窦房结恢复时间从舒张晚期阈值的1.5倍时的88±51毫秒缩短至10 mA时的48±55毫秒（P<0.05）。在基线和β阻滞剂给药后，窦房结恢复时间测量存在显著变异性；副交感神经阻滞后这种变异性降低。
这些数据表明，驱动序列刺激强度可影响窦房结和心房组织的电生理特性。这种效应似乎是由局部儿茶酚胺和乙酰胆碱释放介导的，并提供了进一步的证据，表明在评估电生理效应时可能需要考虑起搏刺激与心脏自主神经系统之间的相互作用。
