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  • Title: [Secondary pauses following high frequency atrial stimulation: incidence and possible underlying mechanisms].
    Author: Schmidt G, Mashima S, Ulm K, Wirtzfeld A.
    Journal: Z Kardiol; 1985 May; 74(5):287-93. PubMed ID: 4013463.
    Abstract:
    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)
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