Josephson M E, Kastor J A
J Clin Invest. 1978 Jan;61(1):171-7. doi: 10.1172/JCI108915.
The pattern of retrograde His-Purkinje conduction was evaluated in 28 patients using ventricular extrastimuli. In each patient progressive prolongations of His-Purkinje conduction (S2H2) which appeared as ventricular extrastimuli were induced at closer coupling intervals (S1S2). There was an inverse linear relationship of S2H2 to S1S2 which was cycle length-dependent: i.e., at any S1S2 interval the resultant S2H2 was less at shorter drive cycle lengths. The degree of S2H2 delay varied widely (from 30 to 340 ms) and was unrelated to the presence of bundle branch block, H-V intervals, or capability of ventriculoatrial conduction. Prolongation of S2H2 was independent of intraventricular (muscle) conduction delay; such delay was usually absent at most, and occasionally all, S1S2 coupling intervals during which S2H2 was lengthening. Furthermore, in two patients both left and right ventricles were activated before the timed depolarization of the His bundle occurred, demonstrating that under the stress of extrastimuli, the impulse conducts through ventricular muscle with less delay than through the His-Purkinje system. We conclude that the His-Purkinje system typically displays slow conduction response to ventricular stress. The site of this conduction delay is probably at the distal "gate".
利用心室期外刺激评估了28例患者的逆行希氏-浦肯野传导模式。在每例患者中,随着心室期外刺激在更短的联律间期(S1S2)诱发,希氏-浦肯野传导(S2H2)逐渐延长。S2H2与S1S2呈负线性关系,且这种关系依赖于周期长度:即,在任何S1S2间期,较短驱动周期长度时的S2H2结果较小。S2H2延迟程度差异很大(30至340毫秒),且与束支阻滞的存在、H-V间期或室房传导能力无关。S2H2延长与心室内(心肌)传导延迟无关;在大多数S1S2联律间期(在此期间S2H2延长),通常最多偶尔所有情况下都不存在这种延迟。此外,在2例患者中,希氏束定时去极化之前左、右心室均已激活,这表明在期外刺激的应激下,冲动通过心室肌传导的延迟比通过希氏-浦肯野系统的延迟少。我们得出结论,希氏-浦肯野系统通常对心室应激表现出缓慢传导反应。这种传导延迟的部位可能在远端“门控”处。