Feld G K, Shahandeh-Rad F
Division of Cardiology, University of California, San Diego.
J Am Coll Cardiol. 1992 Aug;20(2):441-51. doi: 10.1016/0735-1097(92)90115-4.
This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model.
In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall.
Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system.
At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation.
本研究旨在定位并描述一种新的犬类模型中心房扑动折返环以及右心房挤压伤的电生理效应。
在先前的研究中，通过在右心房游离壁施加线性挤压伤后进行快速心房起搏，在犬类心脏中诱发了持续性心房扑动。
使用64通道计算机标测系统对8只犬（第1组）进行研究，这些犬在右心房、左心房和巴赫曼束上有三个电极片，另外7只犬（第2组）在右心房有一个高密度电极片。
在基线状态下，窦性心律以及右心房和左心房起搏期间，激动均匀传播，无缓慢传导区域。挤压伤在窦性心律期间产生明显的传导延迟或完全阻滞，与对照值相比，损伤部位两侧的激动时间平均差异增加（第1组，31±4毫秒对14±5毫秒，p<0.01；第2组，28±10毫秒对7±2毫秒，p<0.01）。在挤压伤上方和下方进行快速心房起搏（S1S1 200毫秒）显示出一条完全阻滞线，相邻电极记录到明显不同的激动时间（差异分别为33±5毫秒和38±12毫秒），激动波阵面围绕该阻滞线传播，并在刺激电极相对处碰撞。第1组诱发的11次发作和第2组诱发的14次发作的平均心房扑动周期长度分别为157±16毫秒和140±16毫秒（p=无显著性差异）。激动标测显示所有发作中右心房围绕挤压伤处存在一个折返环。尽管折返环不包含离散的缓慢传导区域，但挤压伤下方的激动时间长于上方（第1组分别为92±14毫秒对66±8毫秒，第2组分别为82±12毫秒对59±9毫秒，两组p均<0.01）。快速心房起搏或早搏刺激在挤压伤与三尖瓣环之间产生进行性传导延迟和单向阻滞，在25次发作中有9次直接诱发心房扑动。在16次发作中，心房扑动在短暂诱发心房颤动后发生。
1）该模型中的心房扑动是由于右心房内的折返；2）挤压伤起到解剖学障碍物的作用，围绕其可能发生折返；3）折返环不包含离散的缓慢传导区域，而是在挤压伤下方通常传导较慢。
