Camm A J, Ward D E, Spurrell R A
Br Heart J. 1978 Oct;40(10):1119-26. doi: 10.1136/hrt.40.10.1119.
Of 8 patients with the short PR interval, normal QRS complex syndrome studied recently, 3 reported here displayed gaps in anterograde conduction. Atrial premature beats at decreasing coupling intervals conducted with minimal AH prolongation until a zone within the cardiac cycle was reached where conduction failed at a supra-Hisian level. Conduction resumed at earlier atrial coupling intervals and was associated with a sudden increase in the AH interval and the appearance of atrial echo beats with earliest atrial activation on the proximal coronary sinus electrogram. It is suggested that the failure of anterograde conduction at relatively late atrial coupling intervals was caused by a short AH functional refractoriness produced by the pre-excitation of the lower AV junction by a partial AV nodal bypass. Conduction resumed only when early atrial premature beats found the extranodal pathway refractory and were transmitted with decremental delay through the AV node.
在最近研究的8例短PR间期、QRS波群正常综合征患者中,本文报道的3例显示出顺向传导存在间隙。随着联律间期缩短,房性早搏以最小的AH间期延长进行传导,直到到达心动周期内的一个区域,在此区域希氏束以上水平传导失败。在更早的房性联律间期传导恢复,且与AH间期突然增加以及冠状窦近端电图上最早心房激动的房性回波搏动出现有关。提示相对较晚房性联律间期时顺向传导失败是由部分房室结旁路对房室交界区下部的预激产生的短AH功能不应期所致。仅当早期房性早搏发现结外通路不应期并通过房室结以递减延迟传导时传导才恢复。