Gmeiner R, Ng C K, Hammer I, Becker A E
Eur Heart J. 1984 Mar;5(3):233-42. doi: 10.1093/oxfordjournals.eurheartj.a061642.
Paroxysmal tachycardia with widened QRS complexes was recorded in an eleven-year old boy who had suffered from brain damage, which had resulted from an episode of ventricular fibrillation. Atrial stimulation produced an increased AV conduction, sudden disappearance of the His bundle deflection and a complete left bundle branch block pattern. Tachycardias of this morphology were initiated by early atrial and ventricular premature beats. The findings suggested the presence of a macro re-entry circuit, utilizing a slow AV node- nodoventricular bypass tract as the anterograde limb and the His-Purkinje system--fast AV node as the retrograde limb. This supposition found further support by serial sectioning of the AV junctional area of the heart, which revealed a nodoventricular tract, which originated from the posterior extension of the compact part of the atrioventricular node and inserted into the crest of the ventricular septum.
一名11岁男孩记录到阵发性心动过速伴QRS波群增宽，该男孩曾因心室颤动发作导致脑损伤。心房刺激导致房室传导增加、希氏束波突然消失及完全性左束支传导阻滞图形。这种形态的心动过速由房性和室性早搏诱发。这些发现提示存在一个大折返环路，其顺行支利用缓慢的房室结-结室旁路，逆行支利用希氏-浦肯野系统-快速房室结。对心脏房室交界区进行连续切片进一步支持了这一推测，切片显示一条结室束，它起源于房室结致密部的后延伸部分并插入室间隔嵴。
