Haissaguerre M, Warin J F, Lemétayer P, Guillem J P, Blanchot P
Service de cardiologie, hôpital Saint-André, Bordeaux.
Arch Mal Coeur Vaiss. 1988 Mar;81(3):293-300.
The electrocardiographic expression of preexcitation results from the electrophysiological behaviour of the 2 conduction pathways: the normal pathway and the accessory pathway (AP). Its interpretation can only be deductive since the electrical activities of these 2 pathways are not recorded simultaneously. The validation of a K potential likely to represent Kent's bundle activation is based on criteria of exclusion of other origins (atrium, His bundle, ventricle). The K potential could be obtained in 16 of 32 consecutive studies. In 2 cases the unusual behaviour of the AP could be reliably studied owing to recording of the K potential. In case n. 1 a 35 ms increment in conduction was reproducibly observed by atrial extrastimulation at the atrium-Kent's bundle interface. In case n. 2 preexcitation was expressed on ECG only when the atrial rate was 70 to 100/mn. With lower atrial rates conduction in the AP was impaired by a 1st degree block with an atrium-Kent's bundle delay of 100 ms. Atrial acceleration reduced this delay to 40 ms, showing that this improvement in conduction reflected an initial block on the AP in phase IV. With higher atrial rates a block was observed on the AP in phase III either as an abrupt rupture of the atrium-Kent's bundle conduction, or as a block following progressive increment of the Luciani-Wenckebach type. Injection of ATP 20 mg produced and anterograde block on the AP at the atrium-Kent's bundle interface. Retrograde conduction seemed to be lacking in the AP since atrial activity was completely dissociated from induced ventriculograms.(ABSTRACT TRUNCATED AT 250 WORDS)
正常途径和旁路(AP)。由于这两条途径的电活动并非同时记录,其解读只能是推断性的。对可能代表肯特束激活的K电位的验证基于排除其他起源(心房、希氏束、心室)的标准。在32项连续研究中的16项中可获得K电位。在2例中,由于记录到K电位,得以可靠地研究AP的异常行为。在病例1中,通过在心房 - 肯特束界面进行心房额外刺激,可重复性地观察到传导增加35毫秒。在病例2中,仅当心房率为70至100次/分钟时,心电图才表现出预激。心房率较低时,AP传导受一度阻滞影响,心房 - 肯特束延迟100毫秒。心房加速使该延迟减少至40毫秒,表明这种传导改善反映了AP在第IV期的初始阻滞。心房率较高时,在第III期观察到AP阻滞,表现为心房 - 肯特束传导突然中断,或为Luciani - Wenckebach型逐渐增加后的阻滞。注射20毫克ATP在心房 - 肯特束界面产生AP的前向阻滞。由于心房活动与诱发的心室造影完全分离,AP似乎缺乏逆向传导。(摘要截断于250字)