Kirchhof C, Chorro F, Scheffer G J, Brugada J, Konings K, Zetelaki Z, Allessie M
Department of Physiology, University of Limburg, Maastricht, The Netherlands.
Circulation. 1993 Aug;88(2):736-49. doi: 10.1161/01.cir.88.2.736.
It recently has been demonstrated that during atrial fibrillation, a short and variable excitable gap exists, allowing regional control of atrial fibrillation by local stimulation. In the present study, we visualized the process of excitation during regional entrainment of atrial fibrillation by rapid pacing.
In six open-chest dogs, the excitation of the left atrial free wall was mapped using a spoon-shaped mapping electrode (248 points). Episodes of atrial fibrillation were induced by burst pacing (50 Hz, 2 seconds). During atrial fibrillation, the electrograms showed rapid irregular activity with a median cycle length of 98 +/- 16 ms (mean +/- SD, n = 6). Rapid pacing in the center of the mapping electrode at intervals slightly shorter or longer than the median atrial fibrillation interval resulted in regional capture of atrial fibrillation. The window of entrainment was 16 +/- 5 ms. Mapping of atrial fibrillation showed that the left atrium was activated by fibrillatory wavelets coming from different directions. During entrainment, a relatively large area with a diameter of about 4 cm was activated by uniform wave fronts propagating away from the site of stimulation. The area of entrainment was limited by intra-atrial conduction block and by collision with fibrillation waves. Regional control of atrial fibrillation was lost by pacing either too slowly or too rapidly. In the first case, retrograde invasion of the area of entrainment by fibrillatory waves resulted in depolarization of the pacing site prior to the stimulus. Pacing too rapidly caused acceleration of atrial fibrillation by induction of local intra-atrial reentry circuits with a revolution time shorter than the pacing interval.
During atrial fibrillation, an area with a diameter of about 4 cm can be entrained by local pacing. The resulting reduction in fibrillating tissue mass was not sufficient to terminate atrial fibrillation. Extension of the area of entrainment was limited by intra-atrial conduction block, whereas entrainment at a too high rate resulted in acceleration of atrial fibrillation by induction of local microreentry.
最近有研究表明，在心房颤动期间，存在一个短暂且可变的可兴奋间隙，这使得通过局部刺激对心房颤动进行区域控制成为可能。在本研究中，我们通过快速起搏观察了心房颤动区域夺获期间的激动过程。
在6只开胸犬中，使用勺形标测电极（248个点）对左心房游离壁的激动进行标测。通过短阵快速起搏（50 Hz，2秒）诱发心房颤动。在心房颤动期间，心电图显示快速不规则活动，平均周期长度为98±16毫秒（平均值±标准差，n = 6）。在标测电极中心以略短或略长于心房颤动平均间隔的间期进行快速起搏，可导致心房颤动的区域夺获。夺获窗为16±5毫秒。心房颤动标测显示，左心房由来自不同方向的颤动波激活。在夺获期间，一个直径约4厘米的相对较大区域由从刺激部位向外传播的均匀波前激活。夺获区域受心房内传导阻滞和与颤动波碰撞的限制。起搏过慢或过快都会导致心房颤动区域控制的丧失。在第一种情况下，颤动波逆行侵入夺获区域导致起搏部位在刺激前发生去极化。起搏过快会通过诱发局部心房内折返环，使折返时间短于起搏间期，从而导致心房颤动加速。
在心房颤动期间，局部起搏可夺获直径约4厘米的区域。由此导致的颤动组织质量减少不足以终止心房颤动。夺获区域的扩展受心房内传导阻滞的限制，而过高频率的夺获会通过诱发局部微折返导致心房颤动加速。
