Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin.
Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin.
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左心室起源的特发性室性心动过速夹带期间表现出慢传导区的特征。
DOI：
10.1016/s0002-9149(97)89368-x
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
H. Yasue
中科院分区：
文献类型：
--
作者：
K. Okumura;H. Yamabe;T. Tsuchiya;T. Tabuchi;A. Iwasa;H. Yasue
特发性室性心动过速（VT）伴右束分支阻滞和电轴左偏已被证明是由于折返，但折返回路内慢传导区的性质知之甚少。在7例患者中（平均VT周期长度[CL]：361 ± 49 ms），在VT期间从右心室流出道进行快速起搏，同时记录左心室早期激动部位和右心室心尖部的电描记图;还测量了从起搏部位到这些记录部位的传导时间（分别为St-A和St-B间期）。在所有患者中均观察到持续融合（最后一次起搏搏动除外）和进行性融合，表明VT夹带。起搏CL为351 ± 47 ms时，左室部位被顺向夺获，St-A间期为394 ± 57 ms，右室心尖部被直接夺获，St-B间期为63 ± 19 ms，随着起搏CL的缩短，St-A间期逐渐延长，而St-B间期保持不变。所有患者均在起搏CL为279 ± 39 ms时VT中断。分别在5例和7例患者中检查了静脉注射利多卡因（1 mg/kg）和维拉帕米（1 mg）的效果。两种药物均未终止室性心动过速，但利多卡因组VT-CL增加至369 ± 57 ms（p < 0.05），维拉帕米组VT-CL增加至413 ± 69 ms（p <0.05）（与利多卡因组相比p < 0.05）。利多卡因组和维拉帕米组的St-A间期显著延长（p <0.05），而St-B间期无明显变化。维拉帕米治疗后，ST-A间期和VT-CL的变化之间存在显著相关性（p < 0.001）。结论：该室性心动过速的慢传导区表现为心动过速依赖性传导延迟，其慢传导机制主要为钙通道依赖性传导和部分抑制的钠通道依赖性传导。
Idiopathic ventricular tachycardia (VT) with the right bundle branch block pattern and left-axis deviation has been shown to be due to reentry, but the property of the slow conduction zone within the reentry circuit is little understood. In 7 patients (mean VT cycle length [CL]: 361 ± 49 ms), rapid pacing from the right ventricular outflow tract was performed during VT while recording electrograms at the early activation site in the left ventricle and at the right ventricular apex; also, conduction times from the pacing site to these recording sits (St-A and St-B intervals, respectively) were measured. Both constant fusion (except for the last paced beat) and progressive fusion were seen in all patients, indicating VT entrainment. The left ventricular site was captured orthodromically with an St-A interval of 394 ± 57 ms at the pacing CL of 351 ± 47 ms during entrainment, while the right ventricular apex was captured directly with an St-B interval of 63 ± 19 ms. The St-A interval was gradually prolonged with the shortening of the pacing CL, whereas the St-B interval remained unchanged. VT was interrupted in all patients at the pacing CL of 279 ± 39 ms. The effects of intravenous lidocaine (1 mg/kg) and verapamil (1 mg) were examined in 5 and 7 patients, respectively. Neither drug terminated VT but the VT-CL was increased to 369 ± 57 ms after lidocaine (p < 0.05) and to 413 ± 69 ms after verapamil (p < 0.05) (p < 0.05 vs after lidocaine). The St-A interval was significantly increased after lidocaine (p <0.05) and after verapamil (p <0.05), while the St-B interval remained unchanged. A significant correlation between changes in St-A interval and VT-CL after verapamil was noted (p < 0.001). In conclusion, the slow conduction zone of this VT shows tachycardia-dependent conduction delay, and the mechanism of this slow conduction involves mainly calcium channel-dependent conduction and partly depressed sodium channel-dependent conduction.
证明人类持续性室性心动过速期间存在慢传导：使用心动过速的瞬时夹带。
影响因子：
37.8
作者：
Okumura,K;Olshansky,B;Henthorn,RW;Epstein,AE;Plumb,VJ;Waldo,AL
通讯作者：
Waldo,AL
瞬时夹带的第四个标准：渐进融合的电描记图等效值。
影响因子：
37.8
作者：
Henthorn,RW;Okumura,K;Olshansky,B;Plumb,VJ;Hess,PG;Waldo,AL
通讯作者：
Waldo,AL