Strickberger S A, Weiss R, Daoud E G, Goyal R, Bogun F, Man K C, Morady F
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109, USA.
Circulation. 1996 Sep 1;94(5):1023-6. doi: 10.1161/01.cir.94.5.1023.
Radiofrequency catheter modification of AV conduction can be used to control the ventricular rate during atrial fibrillation both in the baseline state and during exercise. Slow-pathway ablation has been suggested to be the mechanism for this response. The purpose of this study was to determine the effect of slow-pathway ablation on the ventricular rate in atrial fibrillation during autonomic blockade and sympathetic stimulation in patients with AV nodal reentrant tachycardia (AVNRT).
Thirty-five patients undergoing slow-pathway radiofrequency ablation for AVNRT were assigned to autonomic blockade (0.2 mg/kg propranolol and 0.04 mg/kg atropine; n = 14) or isoproterenol (2 micrograms/min; n = 21). Atrial fibrillation was induced before and after slow-pathway radiofrequency ablation. During autonomic blockade, the mean ventricular cycle length (448 +/- 34 versus 525 +/- 103 ms, P < .01) and maximum ventricular cycle length (640 +/- 105 versus 798 +/- 226 ms, P = .04) were prolonged after ablation, whereas the minimum ventricular cycle length did not change significantly (361 +/- 42 versus 403 +/- 83 ms, P = .05). During isoproterenol infusion, the mean ventricular cycle length (375 +/- 52 versus 390 +/- 61 ms, P = .2), maximum ventricular cycle length (520 +/- 88 versus 537 +/- 106 ms, P = .3), and minimum ventricular cycle length (307 +/- 59 versus 298 +/- 33 ms, P = .4) did not change significantly after slow-pathway ablation.
Slow-pathway ablation slows the ventricular rate during atrial fibrillation under conditions of autonomic blockade but not during sympathetic stimulation. Therefore, slow-pathway ablation alone cannot account for the clinical results obtained with radiofrequency modification of AV conduction in patients with atrial fibrillation.
房室传导的射频导管改良可用于在基线状态和运动期间控制房颤时的心室率。有人提出慢径路消融是这种反应的机制。本研究的目的是确定在房室结折返性心动过速（AVNRT）患者中，自主神经阻滞和交感神经刺激期间慢径路消融对房颤时心室率的影响。
35例因AVNRT接受慢径路射频消融的患者被分为自主神经阻滞组（0.2mg/kg普萘洛尔和0.04mg/kg阿托品；n = 14）或异丙肾上腺素组（2μg/min；n = 21）。在慢径路射频消融前后诱发房颤。在自主神经阻滞期间，消融后平均心室周期长度（448±34对525±103ms，P<.01）和最大心室周期长度（640±105对798±226ms，P =.04）延长，而最小心室周期长度无显著变化（361±42对403±83ms，P =.05）。在输注异丙肾上腺素期间，慢径路消融后平均心室周期长度（375±52对390±61ms，P =.2）、最大心室周期长度（520±88对537±106ms，P =.3）和最小心室周期长度（307±59对298±33ms，P =.4）均无显著变化。
慢径路消融在自主神经阻滞条件下可减慢房颤时的心室率，但在交感神经刺激时则不然。因此，单纯慢径路消融不能解释房颤患者房室传导射频改良所获得的临床结果。
