肺静脉电隔离对犬急性心房电重构影响的实验研究

Impact of pulmonary veins isolation on the short-time atrial electrical remodeling in dogs

目的肺静脉电隔离（PVI）是治疗心房颤动（房颤）的重要手段，心房电重构是房颤发生和维持的重要因素。本研究旨在研究PVI对急性心房电重构的影响并揭示其可能机制。方法选取成年杂种犬18只，随机分为对照组和PVI组。应用硫代巴比妥钠麻醉后分离并结扎双侧颈交感迷走神经干。两组犬均行房间隔穿刺并以600次／min起搏右心房30min构建急性心房电重构模型，PVI组穿间隔后即行环肺静脉口部电隔离。快速心房电刺激前后于右心耳（RAA）及左心耳（LAA）处测量基础状态下（非迷走神经刺激）及颈部迷走神经干刺激时的心房有效不应期（ERP）和房颤易感窗口（VW）。结果（1）对照组快速心房电刺激后基础状态下（RAA处P〈0．01，LAA处P〈0．001）和迷走神经刺激时（RAA处P〈0．05，LAA处P〈0．05）测得的ERP均明显缩短。快速心房电刺激前后基础状态下均不能诱发房颤；快速心房电刺激后，RAA（P〈0．01）和LAA处（P〈0．05）的VW在迷走神经刺激时明显增宽。（2）PVI组快速心房电刺激后基础状态下（RAA处P=0．451，LAA处P=0．197）和迷走神经刺激时（RAA处P=0．104，LAA处P=0．231）测得的ERP较快速心房电刺激前无明显变化。快速心房电刺激前后基础及迷走神经刺激下均不能诱发房颤。（3）对照组快速心房电刺激后ERP缩短值较PVI组明显增加（基础状态时LAA处P〈0．05，RAA处P〈0．05；迷走神经刺激时LAA处P〈0．01，RAA处P〈0．05）。结论心房电重构伴随着迷走神经对心房电生理特性调节活动增强，肺静脉电隔离能减轻心房电重构，其机制可能为心房去迷走神经效应。

Objective Pulmonary vein isolation（PVI）has been proved to be effective on atrial fibrillation（AF）. However,the mechanism of AF is still on contraversy. This study aimed to investigate the effect of PVI on atrial electrical remodeling （AER） and to explore the intrinsic mechanism. Methods Eighteen adult mongrel dogs under general anesthesia were randomized to control group and PVI group. Bilateral cervical sympathovagal trunks were decentralized and the sympathetic effect was blocked by metoprolol administration. AER was performed by rapid right atriql pacing at the rate of 600bpm for 30 minutes. PVI was achieved via trans-septal procedures in PVI group. Atrial effective refractory period （ERP） , vulnerability window （VW）of AF were measured at baseline（without vagal stimulation）and vagal stimulation at right atrial appendage（RAA） and left atrial appendage（LAA） before and after rapid atrial pacing. Results （ 1 ） In control group, ERP decreased significantly at baseline and vagal stimulation after AER（P 〈0. 01 at LAA and P 〈0. 01 at RAA at baseline;P 〈 0. 05 at LAA and P 〈 0. 05 at RAA during vagal stimulation）. AF was rarely induced at baseline before and after AER（ VW close to 0 ）, while VW during vagal stimulation increased significantly after AER （P 〈 0. 05 at LAA and P 〈0. 01 at RAA）. （2）In PVI group,ERP remained unchanged at baseline and during vagal stimulation before and after rapid atrial pacing（P = 0. 197 at LAA and P = 0. 451 at RAA at baseline;P = 0. 231 at LAA and P = 0. 104 at RAA during vagal stimulation）. AF was rarely induced both at baseline and during vagal stimulation before and after rapid atrial pacing（ VW close to 0）. （3）After rapid atrial pacing, shortening of ERP in control group increased significantly than that in PVI group（ P 〈 0. 05 at LAA and P 〈0. 05 at RAA at baseline;P 〈 0. 01 at LAA and P 〈 0. 05 at RAA during vagal stimulation ）. Conclusions PVI releases the atrial electrical remodeling thereby suppresses AF,which maybe contribute to the vagal dennervation. It indicates that PVI not only eradicates triggered foci, but also modifies substrates of AF.