Lee J J, Kamjoo K, Hough D, Hwang C, Fan W, Fishbein M C, Bonometti C, Ikeda T, Karagueuzian H S, Chen P S
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Circ Res. 1996 Apr;78(4):660-75. doi: 10.1161/01.res.78.4.660.
The mechanisms of Wiggers' stage II ventricular fibrillation (VF) are poorly understood. Using computerized mapping techniques, we studied the patterns of activation during Wiggers' stage II VF in 13 open-chest dogs. In 7 of the 13 dogs, the right ventricular Purkinje fibers and adjacent subendocardial myocytes were ablated with Lugol solution. VF was induced electrically, and 3 to 5 seconds of data were obtained beginning approximately 2.5 seconds after the onset of VF. Dynamic displays of the activation patterns and isochronal maps revealed the presence of reentrant wave fronts in 17 of 33 runs of VF in ablated ventricles and in 12 of 45 runs of VF in intact ventricles. The incidence of reentry was not different between the subendocardium-ablated group versus the nonablated group (1.7 +/- 1.6 versus 1.2 +/- 1.6 rotations per episode of VF, P = .19). There were no differences in the core size (25 +/- 19 versus 29 +/- 18 mm2), life span (3.4 +/- 1.1 versus 3.2 +/- 1.2 rotations), or cycle length (111 +/- 12 versus 107 +/- 8 ms) in ablated ventricles versus intact ventricles, respectively. The core was unstable as it meandered within the mapped area displacing the entire reentrant wave front. In all episodes, the reentrant wave fronts were spontaneously initiated by an interaction between two propagating wave fronts roughly perpendicular to each other. The second wave front met the tail of the first wave front 69 +/- 11 ms (range, 40 to 90 ms) after its latest activation, indicating that the interaction occurred during a vulnerable period. The reentrant wave fronts terminated spontaneously (n = 7), as the result of interference by an invading wave front (n = 19 or meandered off the mapped region (n = 3). We conclude the following: (1) Reentrant activities with short life spans and meandering cores are present during Wiggers' stage II VF in dogs. (2) New reentrant wave fronts are generated when one wave front interacts with another wave front during its vulnerable period. (3) The reentrant wave fronts terminate spontaneously or as the result of interference. (4) Chemical subendocardial ablation does not affect the incidence, life span, cycle length, or core size of the reentrant wave fronts.
维格斯二期室颤(VF)的机制目前尚不清楚。我们运用计算机标测技术,对13只开胸犬的维格斯二期室颤激活模式进行了研究。在13只犬中,7只犬的右心室浦肯野纤维和相邻的心内膜下心肌细胞用卢戈氏溶液进行了消融。通过电刺激诱发室颤,并在室颤发作约2.5秒后开始获取3至5秒的数据。激活模式的动态显示和等时图显示,在消融心室的33次室颤发作中有17次、完整心室的45次室颤发作中有12次存在折返波前。心内膜下消融组与未消融组之间折返的发生率无差异(每次室颤发作的旋转次数分别为1.7±1.6次与1.2±1.6次,P = 0.19)。消融心室与完整心室的核心大小(分别为25±19平方毫米与29±18平方毫米)、寿命(分别为3.4±1.1次旋转与3.2±1.2次旋转)或周期长度(分别为111±12毫秒与107±8毫秒)均无差异。核心不稳定,因为它在标测区域内蜿蜒移动,使整个折返波前移位。在所有发作中,折返波前均由两个大致相互垂直传播的波前之间的相互作用自发引发。第二个波前在其最晚激活后69±11毫秒(范围为40至90毫秒)遇到第一个波前的尾部,表明这种相互作用发生在易损期。折返波前自发终止(n = 7),是由于侵入波前的干扰(n = 19)或蜿蜒离开标测区域(n = 3)。我们得出以下结论:(1)犬维格斯二期室颤期间存在寿命短且核心蜿蜒的折返活动。(2)当一个波前在其易损期与另一个波前相互作用时会产生新的折返波前。(3)折返波前自发终止或因干扰而终止。(4)化学性心内膜下消融不影响折返波前的发生率、寿命、周期长度或核心大小。