Shimizu A, Nozaki A, Rudy Y, Waldo A L
Department of Medicine, Case Western Reserve University, University Hospitals of Cleveland, Ohio 44106.
J Am Coll Cardiol. 1991 Apr;17(5):1223-34. doi: 10.1016/0735-1097(91)90857-6.
To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.
为了验证诱发性心房扑动由过渡性节律演变而来这一假说，首先对40只患有无菌性心包炎的犬类中99次持续超过5分钟的诱发性心房扑动发作（平均周期长度135±18毫秒）的起始情况进行了特征描述。在99次发作中的85次（86%），心房扑动之前有一段短暂的（平均1.4±0.9秒，范围0.4至42秒）心房颤动期。然后，在11项开胸研究中，在18次诱发性心房扑动发作（平均周期长度136±16毫秒）起始期间，同时从95对右心房电极记录心房电图。心房扑动通过一串8次的心房起搏刺激诱发，随后是一或两次房性早搏（7次发作）或快速心房起搏（11次发作）。心房起搏诱发的短时间心房颤动（平均周期长度110±7毫秒）通过波阵面激活右心房，产生一个局部缓慢传导区域。然后，在全部或部分缓慢传导区域，波阵面出现一次心跳的单向传导阻滞。这使得未阻滞的波阵面围绕功能性阻滞区域折返，并通过已形成单向传导阻滞的缓慢传导区域返回，从而启动折返环。单向阻滞相对于循环波阵面方向的位置决定了折返运动是顺时针还是逆时针。缓慢传导和单向传导阻滞区域出现在波阵面与心房肌纤维方向垂直交叉的地方，提示各向异性传导起了作用。这些区域包括终沟的右心房上部（10次发作）、终沟的右心房下部（4次发作）和梳状肌区域（4次发作）。得出的结论是，在该模型中，心房扑动的发生需要右心房出现局部缓慢传导区域，随后在短时间心房颤动或快速心房起搏期间该区域产生单向传导阻滞。
