By G. Riecker (auth.), Privatdozent Dr. med. Berndt Lüderitz (eds.)
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STEINBECK and B. LODERITZ: 46 Table 1. Results of atrial stimulation studies in 10 controls No. Sex and Age 1 2 3 4 5 6 7 8 9 10 M,32 F,66 F,27 M,50 M,51 F, 33 M,16 F, 19 M,71 M,72 Sinusrate/min 65 85 96 96 65 64 83 80 91 97 82± 13 Max. SNRT/ms SACT/ms Atropine 1 mg Sinusrate/min Max. SNRT/ms SACT/ms 120 600 25 95 895 35 97 815 45 770± 152 35 ± 10 1280 70 60 40 50 60 70 1050 1205 1000 1145 930 50 110 1101±131 63±21 104±13 Table 2. Results of atrial stimulation studies in 18 patients with sinoatrial disease Max.
Strauss, H. , Bigger, J. , Saroff, A. , Giardina, E. G. : Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction. Circulation 53, 763 (1976) 29. Strauss, H. , Svenson, R. , Miller, H. , Wallace, A. : Electrophysiological effects of propranolol on sinus node function in patients with sinus node dysfunction. Submitted for publication 30. Strauss, H. , Saroff, A. , Bigger, J. , Giardina, E. G. : Premature atrial stimulation as a key to the understanding of sinoatrial conduction in man.
In two patients, late APDs that fell in zone I were followed by greater than compensatory A2A3 cycles . Further, the A3A4 cycles in zone I were similarly prolonged, when in 40 H. C. STRAUSS and A. G. WALLACE: all of our other patients, the A3A4 cycles equaled the A1Al cycles in zone I. How then, can we explain the prolongation of the A2A3 and A3A4 cycles in zone I, a zone in which APDs fail to gain access to the sinus node and should therefore be followed by a compensatory response? The most likely explanation would seem to lie in the fact that, in some humans, either the stimulus itself, or the APD, is capable of releasing acetylcholine from nerve terminals, thereby depressing sinus node automaticity and prolonging the A2A3 and A3A4 cycles.
Cardiac Pacing: Diagnostic and Therapeutic Tools by G. Riecker (auth.), Privatdozent Dr. med. Berndt Lüderitz (eds.)