神经节丛消融对心室不应期和室性心律失常发生的影响

Effects of ganglionated plexus ablation on ventricular refractory period and ventricular arrhythmogenesis

目的研究心脏神经节丛（GP）消融对心室不应期和室性心律失常发生的影响。方法24只杂种犬随机分为GP消融组（n=12）和对照组（n：12）。在左、右心室表面分别缝一10极冠状静脉窦电极导管记录心底部至心尖部4个不同部位电图，分别测量各个部位GP消融前和消融后伴或不伴迷走神经刺激时的有效不应期（ERP），测量ERP的空间离散度。随后结扎冠状动脉左前降支，持续体表心电图记录1h，观察室性心律失常发生率和持续时间。实验结束后以s，s，快速右心室心尖部起搏测量心室颤动（室颤）阈值。室颤阈值定义为能诱发持续性室颤的最小刺激电压。对照组不进行GP消融。结果迷走神经刺激和GP消融均显著延长各个部位的ERP（P〈0．05）。与基础状态相比，GP消融并未明显增加ERP的空间离散度（0．11±0．02对0．12＋0．01，P〉0．05）。GP消融后，迷走神经刺激不再延长心室ERP。冠状动脉结扎1h，GP消融组室性早搏的发生率（184_＋106）次／h显著高于对照组（94＋91）次／h（P〈0．05）。GP消融组和对照组分别发生10阵，平均（2．5±1．4）S和4阵，平均（1．5±O．8）S的室性心动过速（P〈0．05）。GP消融组和对照组分别有8只和2只犬发生自发性室颤（P〈0．05）。GP消融组室颤阈值较对照组显著降低[（9．5±1．7）V对（10．5±2．3）V，P〈0．05）]。结论在正常心脏，GP消融延长心室ERP但不增加ERP的空间离散度。在急性心肌梗死心脏，GP消融显著增加室性心律失常发生率和降低室颤阈值，提示合并冠心病的患者GP消融可能增加室性心律失常发生的风险。

Objective To investigate the effects of ganglionated plexus （GP） ablation on ventricular refractory period and ventricular arrhythmogenesis. Methods Twenty-four anesthetized dogs receiving GP abla- tion （n = 12 ） or not （control group, n = 12） were included. Two multiple electrode catheters were sutured at left and right ventricles, respectively, for recording 4 different sites from the apex to the base. Effective refractory period （ERP） was measured with and without vagal nerve stimulation （VNS） before and after GP ablation. The spatial dispersion of ERP was also detected. The incidence of ventricular arrhythmias and the ventricular fibrillation threshold （VFr） were determined after the ligation of left anterior descending coronary artery for 1 h. The measurement of VFT was carried out by rapid ventricular pacing at twice the diastolic threshold. VFT was de- fined as the longest pacing cycle length at which VF could be steadily induced. Results Both VNS and GP ab- lation prolonged the ERP at each site （P〈O. 05 for all）. GP ablation did not increase the spatial dispersion of ventricular ERP when compared with baseline （0. 11＋0. 02 vs. 0. 12＋0. 01 ,P〉0. 05）. After GP ablation,VNS no longer prolonged ventricular ERP. Coronary artery ligation induced a significant increase in the incidence of ventricular premature contraction（ 184＋106）/h vs. （94_＋91）/h, （P〈0. 05 ）. Ten short episodes （mean dura-tion （ 2. 5±1.4） s of VT occurred in GP ablation group while 4 [ mean duration （ 1.5 ±0. 8 ） s 3 in control group （P〈0. 05 ）. Spontaneous VF occurred in 8 and 2 dogs in GP ablation group and control group, respectively （P〈 O. 05 ）. VFT in GP ablation group （9. 5±1.7） V was significantly decreased compared with control group （ 10. 5± 2. 3 ）V（ P〈0.05 ）. Conclusions GP ablation prolonged ventricular ERP but did not increase the spatial dispersion of ERP in structurally normal heart. In acute myocardial infarction hearts, GP ablation significantly increased the incidence of ventricular arrhythmias and decreased the VFT, indicating that GP ablation during acute mvocardialischemia may increase the risk of ventricular arrhythmias.