Jordan J, Yamaguchi I, Mandel W J, McCullen A E
Am Heart J. 1977 Mar;93(3):367-74. doi: 10.1016/s0002-8703(77)80256-1.
Recent evidence has suggested a difference in response to overdrive pacing dependent on the location of the pacemaker within the A-V conduction system. To test this hypothesis, the effects of overdrive pacing were evaluated in five anesthetized dogs with experimentally induced A-V block and in seven patients with advanced A-V block. In the animals, sinoatrial node recovery times were studied over wide ranges of rates (130 to 210 beats per minute) and durations (30 to 180 seconds) of atrial pacing. All sinus node recovery times were less than 600 msec. with a mean maximum pause of 0.540+/-0.043 seconds (M.+/-S.E.M.). In contrast, after ventricular pacing (rates 90 to 150 beats per minute; durations 30 to 180 seconds), subsidiary pacemaker recovery times were significantly greater (p less than 0.025) with a mean maximum recovery time of 28.4+/-8.3 seconds. In the seven patients studied, all sinus node recovery times were less than 1,400 msecs. with a mean maximum pause of 0.954+/-0.051 seconds. As seen with the experimental animals, a significantly longer (p less than 0.025 mean maximum subsidiary pacemaker recovery time of 3.55+/-0.92 seconds was observed. The present studies in both experimental animals and in man without evidence of sinus node dysfunction showed that sinus node recovery time was independent of both rate and duration of atrial overdrive pacing. In contrast, subsidiary pacemaker recovery time was correlated with both rate and duration of ventricular overdrive pacing. In both experimental protocols, subsidiary pacemaker recovery time was shown to exceed sinus node recovery time at all rates and at all durations of pacing. Postrecovery sinus node acceleration was consistently observed after atrial overdrive pacing. In contrast, postrecovery subsidiary pacemaker "depression" characterized ventricular overdrive pacing. It is concluded that subsidiary pacemakers are significantly more susceptible to overdrive suppression than the sinoatrial node, a feature of substantial clinical significance.
最近有证据表明，根据起搏器在房室传导系统中的位置不同，对超速起搏的反应也存在差异。为了验证这一假设，我们对5只实验性诱发房室传导阻滞的麻醉犬和7例晚期房室传导阻滞患者进行了超速起搏效应的评估。在动物实验中，研究了在较宽的心房起搏频率范围（每分钟130至210次搏动）和持续时间（30至180秒）下的窦房结恢复时间。所有窦房结恢复时间均小于600毫秒，平均最大停顿时间为0.540±0.043秒（平均值±标准误）。相比之下，心室起搏后（频率为每分钟90至150次搏动；持续时间为30至180秒），次级起搏器恢复时间显著延长（p<0.025），平均最大恢复时间为28.4±8.3秒。在研究的7例患者中，所有窦房结恢复时间均小于1400毫秒，平均最大停顿时间为0.954±0.051秒。与实验动物的情况一样，观察到次级起搏器平均最大恢复时间显著延长（p<0.025），为3.55±0.92秒。目前在无窦房结功能障碍证据的实验动物和人类中的研究表明，窦房结恢复时间与心房超速起搏的频率和持续时间均无关。相反，次级起搏器恢复时间与心室超速起搏的频率和持续时间均相关。在两个实验方案中，在所有起搏频率和持续时间下，次级起搏器恢复时间均超过窦房结恢复时间。心房超速起搏后始终观察到恢复后窦房结加速。相比之下，恢复后次级起搏器“抑制”是心室超速起搏的特征。结论是，次级起搏器比窦房结更容易受到超速抑制，这一特征具有重要的临床意义。
