Elvan A, Wylie K, Zipes D P
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, USA.
Circulation. 1996 Dec 1;94(11):2953-60. doi: 10.1161/01.cir.94.11.2953.
We assessed the effects of pacing-induced chronic atrial fibrillation (AF) on sinus node function, intra-atrial conduction, and atrial refractoriness.
In 15 mongrel dogs (20 to 30 kg), AV nodal block was produced by radiofrequency catheter ablation, and a ventricular-inhibited (VVI) pacemaker (Minix 8330, Medtronic) was implanted and programmed to pace at 80 pulses per minute. In 11 of these dogs, right atrial endocardial pacing leads were connected to a pulse generator (Itrel 7432, Medtronic) and set at a rate of 20 Hz to induce AF. Corrected sinus node recovery time, P-wave duration, 24-hour Holter ECG to assess AF duration, maximal heart rate in response to isoproterenol (10 micrograms/min), intrinsic heart rate after administration of atropine (0.04 mg/kg) and propranolol (0.1 mg/kg), and atrial effective refractory periods (ERPs) were obtained at baseline (EPS-1) and after 2 to 6 weeks (EPS-2) of VVI pacing alone (n = 4) or VVI pacing and rapid atrial pacing (n = 11). At EPS-2, corrected sinus node recovery time and P-wave duration were prolonged, maximal heart rate and intrinsic heart rate were decreased, atrial ERPs were shortened, and the duration of AF was increased significantly compared with EPS-1. These changes partially reversed toward baseline 1 week after conversion to sinus rhythm. Sinus node function and AF inducibility observed in the control dogs that underwent ventricular pacing alone (n = 4) did not change.
Pacing-induced chronic AF induces sinus node dysfunction, prolongs intra-atrial conduction time, shortens atrial refractoriness, and perpetuates AF, changes that reverse gradually after termination of AF.
我们评估了起搏诱导的慢性心房颤动(AF)对窦房结功能、心房内传导和心房不应期的影响。
在15只杂种犬(体重20至30千克)中,通过射频导管消融产生房室结阻滞,并植入心室抑制型(VVI)起搏器(美敦力Minix 8330),并将其编程为以每分钟80次脉冲起搏。在这些犬中的11只中,右心房内膜起搏导线连接到脉冲发生器(美敦力Itrel 7432),并设置为20赫兹的频率以诱发房颤。在基线(EPS-1)以及单独进行VVI起搏2至6周后(EPS-2)(n = 4)或VVI起搏与快速心房起搏(n = 11)后,获取校正的窦房结恢复时间、P波持续时间、用于评估房颤持续时间的24小时动态心电图、对异丙肾上腺素(10微克/分钟)反应的最大心率、给予阿托品(0.04毫克/千克)和普萘洛尔(0.1毫克/千克)后的固有心率以及心房有效不应期(ERP)。在EPS-2时,与EPS-1相比,校正的窦房结恢复时间和P波持续时间延长,最大心率和固有心率降低,心房ERP缩短,房颤持续时间显著增加。在恢复窦性心律1周后,这些变化部分恢复至基线水平。单独进行心室起搏的对照犬(n = 4)中观察到的窦房结功能和房颤诱导性未发生变化。
起搏诱导的慢性房颤会诱发窦房结功能障碍,延长心房内传导时间,缩短心房不应期,并使房颤持续存在,这些变化在房颤终止后会逐渐逆转。