Imai T, Ohkawa S, Sakai M, Watanabe C, Chida K, Kuramoto K, Ueda K
Division of Cardiology, Tokyo Metropolitan Geriatric Hospital.
Nihon Ronen Igakkai Zasshi. 1993 May;30(5):403-11. doi: 10.3143/geriatrics.30.403.
An electrophysiologic study was performed in a 95-year-old man with bifascicular block (right bundle branch block and left anterior hemiblock). During sinus rhythm (AA interval = 980 ms), every sinus beat was conducted to the ventricle. The AH interval was 130 ms and HV interval was 50 ms. A programmed premature atrial stimulation was performed after 8 paced beats at a slightly shorter cycle length than the sinus cycle length (900 ms). As the atrial coupling interval was shortened, the H1H2 interval also shortened. At an H1H2 interval of 680 ms the premature atrial beat was blocked distal to the recording site of the His potential. The block persisted up to an H1H2 interval of 560 ms. AV conduction resumed paradoxically when the H1H2 interval was further shortened to intervals lasting 540-490 ms. During this period the H2V2 interval was 50 ms. At still shorter H1H2 intervals, H2 was again blocked. The H2V2 intervals during this phase of improved conduction were unchanged compared with those of other conducted beats. Therefore normalization due to the gap phenomenon could be ruled out, and the improved conduction could be explained by a phenomenon of supernormal conduction in the posterior division of left bundle branch.
对一名患有双分支阻滞（右束支阻滞和左前分支阻滞）的95岁男性进行了电生理研究。在窦性心律时（AA间期 = 980毫秒），每一个窦性搏动均下传至心室。AH间期为130毫秒，HV间期为50毫秒。在以略短于窦性周期长度（900毫秒）的周期长度进行8次起搏搏动后，进行了程控心房早搏刺激。随着心房耦合间期缩短，H1H2间期也缩短。当H1H2间期为680毫秒时，心房早搏在希氏束电位记录部位远端发生阻滞。该阻滞持续至H1H2间期为560毫秒。当H1H2间期进一步缩短至540 - 490毫秒时，房室传导反常恢复。在此期间，H2V2间期为50毫秒。在更短的H1H2间期时，H2再次发生阻滞。与其他下传搏动相比，在传导改善的这一阶段，H2V2间期未发生改变。因此，可以排除因裂隙现象导致的传导正常化，而传导改善可由左束支后分支的超常传导现象来解释。
