Liu Shaowen, Olsson S Bertil, Yang Yanzong, Hertervig Eva, Kongstad Ole, Yuan Shiwen
Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
J Cardiovasc Electrophysiol. 2004 Feb;15(2):144-9. doi: 10.1046/j.1540-8167.2004.03301.x.
Both concealed conduction and dual pathway physiology are important electrophysiologic characteristics of the AV node. The interaction of AV nodal concealment and duality, however, is not clearly understood.
The properties of AV conduction curves in the presence and absence of a conditioning blocked impulse were prospectively studied during premature atrial stimulation in 20 patients with AV nodal reentrant tachycardia before and after slow pathway ablation and in 14 control patients. AV nodal duality in the control conduction curve in the absence of a conditioning impulse was observed in 19 (95%) of 20 patients with AV nodal reentrant tachycardia. However, AV nodal duality in the modulated conduction curve in the presence of a blocked impulse was only identified in 2 (10%) of 20 patients (2/20 vs 19/20, P < 0.0001). The modulated curve was characterized by a significantly longer AV nodal effective and functional refractory periods compared to the control curve (P < 0.0001) in both patients with and without AV nodal reentry and in AV nodal reentry patients after successful slow pathway ablation. The maximum AH interval (AH(max)) of the modulated curve was significantly shorter than the control curve in both patients with (217 +/- 74 ms vs 347 +/- 55 ms, P < 0.0001) and without AV nodal reentry (178 +/- 50 ms vs 214 +/- 54 ms, P = 0.02). AH(max) of the control curve was significantly longer in AV nodal reentry patients than in controls (P < 0.0001). AH(max) of the modulated curve, however, was not significantly different between the two groups. After slow pathway ablation, AH(max) of the control curve was significantly reduced (347 +/- 55 ms vs 191 +/- 40 ms, P < 0.0001). Significant reduction in AH(max) of the modulated curve was not observed.
An interaction of AV nodal concealed conduction and dual pathway physiology was demonstrated by our data. Slow pathway conduction of the AV node was prevented by the concealed beat in both patients with and without AV nodal reentry.
隐匿性传导和双径路生理特性均为房室结重要的电生理特征。然而，房室结隐匿性与双径路之间的相互作用尚不清楚。
前瞻性研究了20例房室结折返性心动过速患者在慢径路消融前后以及14例对照患者在房性早搏刺激期间，存在和不存在条件性阻滞冲动时的房室传导曲线特性。在20例房室结折返性心动过速患者中，19例（95%）在无条件性冲动的对照传导曲线中观察到房室结双径路现象。然而，在存在阻滞冲动的调制传导曲线中，仅20例患者中的2例（10%）发现房室结双径路现象（2/20对比19/20，P<0.0001）。在有和无房室结折返的患者以及慢径路消融成功后的房室结折返患者中，调制曲线的特点是与对照曲线相比，房室结有效不应期和功能不应期显著延长（P<0.0001）。在有房室结折返的患者（217±74毫秒对比347±55毫秒，P<0.0001）和无房室结折返的患者（178±50毫秒对比214±54毫秒，P=0.02）中，调制曲线的最大AH间期（AH(max)）均显著短于对照曲线。房室结折返患者对照曲线的AH(max)显著长于对照组（P<0.0001）。然而，两组之间调制曲线的AH(max)无显著差异。慢径路消融后，对照曲线的AH(max)显著缩短（347±55毫秒对比191±40毫秒，P<0.0001）。未观察到调制曲线的AH(max)有显著缩短。
我们的数据表明了房室结隐匿性传导与双径路生理特性之间存在相互作用。在有和无房室结折返的患者中，隐匿性搏动均阻止了房室结的慢径路传导。
