Gonzalez-Zuelgaray J, Sheikh S, Akhtar M, Jazayeri M R
Electrophysiology Laboratory, University of Wisconsin Milwaukee Campus, USA.
J Cardiovasc Electrophysiol. 1996 Mar;7(3):248-58. doi: 10.1111/j.1540-8167.1996.tb00522.x.
The mechanism of functional bundle branch block induced at the onset of supraventricular tachycardia (SVT) is well established. However, no data exist to address the underlying mechanism of functional bundle branch block occurring in the second beat of SVT, when the first beat is conducted with a narrow QRS morphology and preceded by ventricular stimulation.
Two patients showing such a phenomenon form the basis of this report. Patient 1 with AV nodal reentrant tachycardia of the common variety persistently demonstrated functional right bundle branch block in the second SVT complex when a short train of ventricular pacing was introduced during SVT. This occurred without any discernible change in the SVT cycle length. Patient 2 had a manifest posteroseptal accessory pathway and inducible orthodromic reentrant tachycardia. Functional bundle branch block during propagation of the second SVT complex invariably occurred either in the left bundle when SVT was induced by a bundle branch reentrant complex during premature ventricular stimulation, or in the right bundle when SVT was induced with a short train of ventricular pacing. The development of functional bundle branch block was preceded by minimal or no cycle length variations in the His-bundle inputs.
These observations suggest that the type of functional bundle branch block occurring in the second SVT complex as a de novo phenomenon may be related to the relative timing of the retrograde penetration of the right versus left bundle during ventricular pacing or bundle branch reentrant complex. Therefore, due to its longest cycle length of activation and refractoriness, the earliest site of retrograde penetration is the most likely site of functional block during propagation of the second SVT complex. This delayed manifestation of retrograde concealment may provide new information regarding the electrophysiologic behavior of the His-Purkinje system.
室上性心动过速(SVT)发作时诱发功能性束支传导阻滞的机制已得到充分证实。然而,尚无数据探讨在SVT的第二个心动周期出现功能性束支传导阻滞的潜在机制,此时第一个心动周期的QRS波形态窄,且先于心室刺激。
本报告基于两名出现此类现象的患者。病例1为常见类型的房室结折返性心动过速,在SVT期间进行短阵心室起搏时,第二个SVT心动周期持续出现功能性右束支传导阻滞。这种情况在SVT周期长度无明显变化的情况下发生。病例2有明显的后间隔旁路且可诱发顺向型折返性心动过速。当在室性早搏刺激期间由束支折返性心动过速诱发SVT时,第二个SVT心动周期传导过程中的功能性束支传导阻滞总是发生在左束支;当用短阵心室起搏诱发SVT时,则发生在右束支。在希氏束输入中,功能性束支传导阻滞出现之前,心动周期长度变化极小或无变化。
这些观察结果表明,作为一种新出现的现象,在第二个SVT心动周期出现的功能性束支传导阻滞类型可能与心室起搏或束支折返性心动过速期间右束支与左束支逆行穿透的相对时间有关。因此,由于其最长的激活和不应期周期长度,最早的逆行穿透部位是第二个SVT心动周期传导过程中最可能发生功能性阻滞的部位。这种逆行隐匿的延迟表现可能为希氏-浦肯野系统的电生理行为提供新的信息。