REENTRANT VENTRICULAR ARRHYTHMIAS IN THE LATE MYOCARDIAL-INFARCTION PERIOD .14. MECHANISMS OF RESETTING, ENTRAINMENT, ACCELERATION, OR TERMINATION OF REENTRANT TACHYCARDIA BY PROGRAMMED ELECTRICAL-STIMULATION
REENTRANT VENTRICULAR ARRHYTHMIAS IN THE LATE MYOCARDIAL-INFARCTION PERIOD .14. MECHANISMS OF RESETTING, ENTRAINMENT, ACCELERATION, OR TERMINATION OF REENTRANT TACHYCARDIA BY PROGRAMMED ELECTRICAL-STIMULATION
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DOI：
10.1111/j.1540-8159.1987.tb05974.x
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发表时间：
1987-03-01
影响因子：
1.8
通讯作者：
RESTIVO, M
中科院分区：
文献类型：
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作者：
ELSHERIF, N;GOUGH, WB;RESTIVO, M
在犬梗死后模型中研究了程控电刺激重置、夹带、加速或终止折返性室性心动过速的机制。在该模型中，折返回路位于覆盖梗死的心外膜层，并可通过多路复用技术进行详细标测。折返回路具有特征性的8字形构型，其形式为围绕功能性传导阻滞弧的两个循环波前，其合并成缓慢的共同折返波前。折返性心动过速的终止发生在刺激波阵面较早到达慢传导区近端部分的战略位置区域时，在远端不应期结束之前，导致传导阻滞。决定刺激波是否能及时到达该区而发生传导阻滞的三个因素是：（1）刺激周期长度;（2）刺激搏动次数;（3）刺激部位。刺激终止折返的最佳情况是施加到靠近慢传导区近端侧的缺血区的临界耦合单一刺激，其局部捕获并过早传导到传导阻滞的战略区。当一个单一的刺激波前未能终止再入，一个或多个后续波前成功。然而，受刺激的列车必须在中断再入的节拍之后终止。否则，随后的刺激搏动可能重新启动相同的折返回路或诱导不同的回路。新的回路可能具有更短的旋转时间，导致心动过速加速，偶尔退化为心室颤动。超速终止折返需要一个关键的周期长度的刺激和一个关键数量的心跳刺激列车。另外，刺激串可以在折返通路中建立一个新的不应性和传导速度的平衡。这可能会使折返过程在刺激序列的较短周期长度下持续下去，并且自发折返将在序列终止时恢复（夹带）。该研究提供了更好地了解程序电刺激对折返性室性心动过速的作用机制。
The mechanisms of resetting, entrainment, acceleralion, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post‐infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure‐eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachycardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefrout could reach this zone in time for conduction block were: (1) the cycle length of stimulation; (2) the number of stimulated beats, and (3) the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration, and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new balance of refractoriness and conduction velocity in the reentrant pathway. This could perpetuate the reentrant process at the shorter cycle length of the stimulated train and spontaneous reentry would resume on termination of the train (entrainment). The study provides better understanding of the mechanisms of action of programmed electrical stimulation on reentrant ventricular tachycardia.