房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Impact of slow pathway ablation on vagal innervation and vulnerability to atrial fibrillation

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性，慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬，全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管，经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管），经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min，P〉0．05]，提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms，P〉0．05]，CSd分别为[（55±30）ms对（42±32）ms，P=0．08]，IRA分别为[（66±24）ms对（19±21）ms，P〈0．001]，CSp分别为[（46±24）ms对（7±18）ms，P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响，对CSd区域的迷走神经调节功能有一定的影响，而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后，HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms，P〉0．05]，CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms，P=0．07]，CSp及IRA的VW明显降低[CSp：（1±3）ms对（49±36）ms，P〈0．005；IRA：（10±12）ms对（45±34）ms，P〈0．05]。提示慢径区域消融导致了CSp及IRA局部区域去迷走神经效应，降低了该区域早搏刺激诱发迷走神经介导房颤的易感性。结论慢径区域消融没有直接改变窦房结区域及HRA的迷走神经支配。部分削弱了CSd的迷走神经功能。导致了IRA及CSp区域的去迷走神经效应。降低了IRA及CSp区域早搏刺激诱发迷走神经介导房颤的易感性。

Objective Atrioventricular node reentrant tachycardia （AVNRT） ablation may effect the vagal response, which is indicated by sinus tachycardia. On the other hand, atrial fibrillation （AF）, which was found to be associated with vagal innervation,often coexists with AVNRT. However,little is known about the impact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympathovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was performed from coronary sinus （CS） ostium to the middle area of Koch triangle. Atrial effective refractory period （ERP） ,vulnerability window （VW） of AF, and sinus rhythm cycle length （SCL） were measured at high right atrium （HRA） ,low right atrium （LRA）, distal （CSd） and proximal CS （CSp） at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results （ 1 ） SCL during vagal stimulation remained unchanged before and after ablation （ 107 ± 19 ） bpm vs （ 108±8） bpm （ P 〉 0. 05 ）. （2） After ablation, ERP during vagal stimulation remained unchanged at HRA （55 ± 34） ms vs （69 ± 37） ms （ P 〉 0.05 ） , and decreased slightly at CSd （42 ± 32 ） ms vs （ 55± 30） ms （ P = 0.08 ）. However, at LRA and CSp, ERP was significantly decreased after ablation （ 19 ± 21 ） ms vs （66 ±＋ 24 ） ms （P 〈 0. 001 ） ; and （7 ±18） ms vs （46 ±24） ms （P 〈0. 001 ） ,respectively. （3） AF was difficult to be induced at baseline before and after ablation in all sites （ VW close to 0）. While during vagal stimulation ,after ablation VW of AF significantly decreased at LRA （1 ±3） ms vs （49±36） ms （P〈0. 005） and CSp （10±12） ms vs （45 ±34） ms （P〈 0. 05 ）, decreased slightly at CSd after ablation （ 35± 37 ） ms vs （ 57 ±28 ） ms （ P = 0. 07 ）, and remained unchanged at HRA （ 63 ±31 ） ms vs （ 63 ± 25 ） ms （ P 〉 0. 05 ）. （ 4 ） The altered architecture of individual ganglia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS, thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL, ERP shortening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.