不同部位起搏对正常和心力衰竭犬心室跨壁复极梯度的影响

Alterations in the transmural gradient of ventricular repolarization with different pacing sites in normal and heart failure canines

跨壁复极梯度的改变可能导致跨壁复极离散度的增加和室速的增多,跨壁复极离散可能在左室心外膜起搏相关猝死中发生重要作用。本研究对心力衰竭(心衰)犬进行心室不同部位起搏,观察左心室跨壁复极梯度的变化。选用8条健康杂种犬,随机分成健康对照组和心衰组(n=4),心衰组4条健康犬经快速右心室心内膜心尖部(right ventricular apical endocardium,RVEndo)起搏4~5周建立慢性充血性心衰模型。健康对照组和心衰组分别在右心房(right atrium, RA)起搏、RVEndo起搏、左心室心外膜(left ventricular lateral epicardium, LVEpi)起搏及双心室(biventricular, Biv)同步起搏的条件下,应用自制的跨室壁单相动作电位(monophasic action potential, MAP)记录电极,于左心室同步记录和测量三层心肌(内层、中层、外层)的MAP时程(MAP duration, MAPD)。结果显示,健康对照组窦性心律时左心室三层心肌MAPD比较:中层>内层>外层,各层之间比较均有统计学差异(均P <0.05);RVEndo、LVEpi、Biv起搏时MAPD仍为中层>内层>外层,心外膜层与心内膜层MAPD比较无统计学差异(P> 0.05);每种起搏时中层与心外膜层及心内膜层的MAPD比较均有统计学差异(均P <0.05)。与健康对照组比较,心衰组不同起搏模式(RA起搏、RVEndo起搏、LVEpi起搏、Biv起搏)时左心室心肌各层的MAPD均延长(均P <0.05)。心衰组RA、RVEndo、LVEpi及Biv起搏时左心室三层心肌MAPD均表现为中层>内层>外层,但各层心肌MAPD均无统计学差异(均P> 0.05)。通过应用改良标测导管记录MAP的方法,我们发现健康犬RA起搏时左心室心内膜层、中层及心外膜层存在明显的跨壁梯度,RVEndo、LVEpi、Biv起搏时左心室心内膜与心外膜间跨壁梯度消失;然而心衰犬左心室的三层心肌在RA、RVEndo、LVEpi、Biv起搏时均不存在跨壁梯度,这些结果有助于加深对心衰患者室性心律失常发生机制的理解。

Alterations of the transmural gradient of repolarization may contribute to the increase of transmural dispersion of repolarization and ventricular arrhythmias. The transmural gradient of repolarization may play an important role in sudden death associated with left ventricular epicardial pacing. To investigate the changes of transmural gradient dispersion of ventricular repolarization with different pacing sites in heart failure(HF) canines, 8 mongrel dogs were randomized into healthy group and HF group(n = 4). We mapped the monophasic action potential duration(MAPD) in the subendocardial, subepicardial and mid-myocardial layers of the left ventricle(LV) in canines of healthy and HF groups during right atrium(RA) pacing, right ventricular apical endocardial(RVEndo) pacing, left ventricular lateral epicardial(LVEpi) pacing and biventricular(Biv) pacing respectively. The results showed that in the healthy group, the MAPDs were significantly different among the three layers during RA pacing(all P < 0.05). The MAPD was longer in the mid-myocardial layer compared with those in the subepicardial and subendocardial layers during RVEndo, LVEpi or Biv pacing(P < 0.05). However, there was no significant difference in MAPD between the subendocardial and subepicardial layers during RVEndo, LVEpi or Biv pacing(P > 0.05). In the HF group, the MAPDs in all three layers were prolonged compared with those in the same locations in the healthy group(all P < 0.05). However, there were no differences in MAPD among the three layers during RA, RVEndo, LVEpi or Biv pacing(all P > 0.05). By MAP recording with our new mapping electrode, we found a transmural MAPD gradient among the three layers of the LV during RA pacing and the gradient between the subendocardial and subepicardial layers vanished during RVEndo, LVEpi or Biv pacing in healthy dogs. In contrast, there was no transmural MAPD gradient during RA, RVEndo, LVEpi or Biv pacing in HF dogs. These results are helpful to understand the mechanism of ventricular arrhythmias in patients with HF.