Lee Shih-Huang, Tai Ching-Tai, Chiang Chern-En, Yu Wen-Chung, Cheng Jun-Jack, Ding Yu-An, Chang Mau-Song, Chen Shih-Ann
Division of Cardiology, Department of Medicine, National Yang-Ming University, Veterans General Hospital-Taipei, Taiwan, Republic of China.
J Cardiovasc Electrophysiol. 2003 Dec;14(12):1337-41. doi: 10.1046/j.1540-8167.2003.03198.x.
The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia.
In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 +/- 0.25 mV vs 0.16 +/- 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 +/- 19 ms) compared with 2:1 AV block (44 +/- 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 +/- 6 ms, P < 0.01).
The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle.
房室结折返性心动过速期间2:1房室传导阻滞自发转变为1:1房室传导的发生率尚未得到充分报道。在以往的研究中,关于房室结折返性心动过速期间2:1房室传导阻滞的部位也存在争议。
对房室结折返性心动过速期间发生2:1房室传导阻滞的患者,分析2:1房室传导阻滞自发转变为1:1房室传导的发生率以及自发转变过程中电生理特性的变化。在20例房室结折返性心动过速期间发生2:1房室传导阻滞的患者中,8例患者在2:1房室传导阻滞的阻滞搏动中无希氏束电位,4例患者阻滞搏动中希氏束电位的最大振幅与下传搏动中的相同,8例患者阻滞搏动中希氏束电位的最大振幅明显小于下传搏动中的(0.49±0.25mV对0.16±0.07mV,P = 0.007)。20例房室结折返性心动过速期间发生2:1房室传导阻滞的患者中有15例(75%)出现2:1房室传导阻滞自发转变为1:1房室传导。2:1房室传导阻滞自发转变为1:1房室传导与短暂性右束支和/或左束支传导阻滞有关。与2:1房室传导阻滞(44±6ms,P<0.01)和无束支传导阻滞的1:1房室传导(43±6ms,P<0.01)相比,伴有短暂性束支传导阻滞的1:1房室传导与显著的希氏束-心室(HV)间期延长(66±19ms)有关。
房室结折返性心动过速期间的2:1房室传导阻滞是功能性的;在大多数房室结折返性心动过速期间发生2:1房室传导阻滞的患者中,阻滞水平显示在希氏束内或其下方,少数患者可能在房室结与希氏束交界处较高。