Schmidt G, Mashima S, Ulm K, Wirtzfeld A
Z Kardiol. 1985 May;74(5):287-93.
Atrial pacing up to 250 bpm was performed in 88 patients with suspected sick sinus syndrome or syncopes of unknown origin. Measurements were done on the first five return cycles. According to cSNRTmax they were divided in 3 groups (group 1 less than 525 ms, group 2 greater than or equal to 525 ms less than 1000 ms, group 3 greater than or equal to 1000 ms). The return cycle pattern (PSM) was calculated (mean + standard deviation of PSI 1-PS15 at each pacing rate). A "normal" PSM with long PSI1 and gradual shortening of the subsequent cycles was found only at low pacing rates in group 1 and group 2. At higher rates, the PSI1 shortened and PSI2 lengthened, resulting in frequent secondary pauses (SP). Atrial pacing up to 400 bpm was performed in 20 open chest dogs. SP were frequently obtained at pacing rates above 300 bpm. Intravenous application of propranolol and atropine did not diminish SP, neither did bilateral vagotomy. Additional subthreshold stimuli, as well as stimulation with large interpolar distance did not influence the PSM of SP at high frequencies. Simultaneous stimulation of right atrium and right ventricle had no significant effects on SP. Pacemaker shifts occurring frequently after high rate pacing were not necessarily accompanied by SP. The velocity of activation spread over the sinoatrial region was significantly slower in cases of postpacing beats preceding a SP. It was concluded that the PSM of SP provoked by high rate atrial pacing is neither caused by local release of neurotransmitters nor by pacing induced changes of the autonomic tone nor by pacemaker shifts.(ABSTRACT TRUNCATED AT 250 WORDS)
对88例疑似病态窦房结综合征或不明原因晕厥的患者进行了高达250次/分钟的心房起搏。在前五个折返周期进行测量。根据最大校正窦房结恢复时间(cSNRTmax),将他们分为3组(第1组小于525毫秒,第2组大于或等于525毫秒且小于1000毫秒,第3组大于或等于1000毫秒)。计算折返周期模式(PSM)(每个起搏频率下PSI 1 - PS15的平均值+标准差)。仅在第1组和第2组的低起搏频率下发现了具有长PSI1和随后周期逐渐缩短的“正常”PSM。在较高频率下,PSI1缩短而PSI2延长,导致频繁出现继发性停搏(SP)。对20只开胸犬进行了高达400次/分钟的心房起搏。在起搏频率高于300次/分钟时经常出现SP。静脉注射普萘洛尔和阿托品并不能减少SP,双侧迷走神经切断术也不能。额外的阈下刺激以及大极间距刺激在高频时不影响SP的PSM。同时刺激右心房和右心室对SP没有显著影响。高频率起搏后频繁出现的起搏器移位不一定伴有SP。在SP之前的起搏后搏动情况下,窦房区域的激动传播速度明显较慢。得出的结论是,高频率心房起搏诱发的SP的PSM既不是由神经递质的局部释放引起的,也不是由起搏诱导的自主神经张力变化或起搏器移位引起的。(摘要截断于250字)