Lai W T, Lee C S, Sheu S H, Hwang Y S, Sung R J
Department of Internal Medicine, Kaohsiung Medical College, Taiwan, Republic of China.
Circulation. 1995 Jul 1;92(1):66-76. doi: 10.1161/01.cir.92.1.66.
Although AV nodal reentrant tachycardia (AVNRT) is a well-known rhythm disorder, its anatomic substrate and electrophysiological mechanism remain to be defined. Previously, the description of the excitable gap (EG) of AVNRT was based on electrical stimulation performed from sites remote from the reentrant circuit. In the present study, we characterized the EG of AVNRT by atrial extrastimulation close to the putative reentrant circuit in the AV junction.
In 16 patients (3 men, 13 women; mean age, 45 +/- 13 years) with inducible slow-fast AVNRT (mean cycle length, 353 +/- 52 ms), single extrastimuli with a 10-ms decrement in the premature coupling interval were delivered from the anterosuperior interatrial septum (fast pathway area) and the posteroinferior interatrial septum (slow pathway area) from late diastole until atrial refractoriness. An EG was considered present when resetting or termination of AVNRT was induced by single atrial extrastimulation. The study showed that the duration of the EG of AVNRT was wide, measuring 121 +/- 56 and 123 +/- 47 ms and occupying 33 +/- 11% and 34 +/- 9% of the tachycardia cycle length during single extrastimulation from the slow pathway area and the fast pathway area, respectively. The resetting pattern most commonly manifested as the sum of the coupling interval and the return cycle being less than a fully compensatory pause (two times the basic tachycardia cycle length). However, patterns equal to and greater than a fully compensatory pause were also observed. Of note, in 2 of the 16 patients, atrial extrastimulation from either the fast or slow pathway area also affected the preceding tachycardia cycle length (HH interval), indicating alteration of the anterograde input. In all patients, the curve derived from plotting the coupling interval of extrastimuli against the return cycle during resetting exhibited an "increasing" pattern. The mode of tachycardia termination usually occurred when the premature atrial impulse was orthodromically blocked in the anterograde slow pathway.
The EG of slow-fast AVNRT is relatively wide, as demonstrated by single atrial extrastimulation from the interatrial septum near the AV junction. Overall, the electrophysiological manifestations of the EG of AVNRT are very similar to those described in AV reciprocating tachycardia incorporating an accessory connection. These findings lend further support to the notion that, in humans, AVNRT involves a reentrant mechanism with a wide excitable gap.
尽管房室结折返性心动过速（AVNRT）是一种广为人知的节律紊乱，但它的解剖基质和电生理机制仍有待明确。此前，对AVNRT可兴奋间隙（EG）的描述是基于从远离折返环路的部位进行的电刺激。在本研究中，我们通过在房室交界区靠近假定折返环路处进行心房额外刺激来对AVNRT的EG进行特征描述。
在16例（3例男性，13例女性；平均年龄45±13岁）可诱发慢快型AVNRT（平均心动周期长度353±52毫秒）的患者中，从舒张晚期直至心房不应期，从前上房间隔（快径路区域）和后下房间隔（慢径路区域）发放提前偶联间期递减10毫秒的单个额外刺激。当单个心房额外刺激诱发AVNRT的重置或终止时，则认为存在EG。研究表明，AVNRT的EG持续时间较宽，在从慢径路区域和快径路区域进行单个额外刺激时，分别为121±56毫秒和123±47毫秒，分别占心动过速周期长度 的33±11%和34±9%。重置模式最常见的表现是偶联间期与返回周期之和小于完全代偿间歇（基础心动过速周期长度的两倍）。然而，也观察到了等于和大于完全代偿间歇的模式。值得注意的是，在16例患者中的2例，来自快径路区域或慢径路区域的心房额外刺激也影响了先前的心动过速周期长度（HH间期），表明前传输入发生了改变。在所有患者中，在重置期间将额外刺激的偶联间期与返回周期作图得到的曲线呈现“上升”模式。心动过速终止的方式通常发生在房性早搏冲动在前传慢径路中发生正向阻滞时。
通过在房室交界区附近的房间隔进行单个心房额外刺激证明，慢快型AVNRT的EG相对较宽。总体而言，AVNRT的EG的电生理表现与包含附加连接的房室折返性心动过速中所描述的非常相似。这些发现进一步支持了在人类中AVNRT涉及具有宽可兴奋间隙的折返机制这一观点。
