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目的探讨房室结慢径区域消融对心房迷走神经调节功能及心房颤动易感性的影响。方法11条成年杂种犬,全麻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(Hallo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。测量慢径路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(LRA)、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窦性周长的变化:消融前、后迷走神经刺激导致的SCL缩短值的差异无统计学意义[(107±19)比(108±8)次／min,P>0．05]。②有效不应期的变化: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、(55±34)ms,两者间差异无统计学意义(P>0．05);CSd分别为(55±30)ms及(42±32)ms,LRA分别为(66±24) ms及(19±21)ms,CSp分别为(46±24)及(7±18) mS,差异均有统计学意义(P值分别<0．05、0．01)。③心房易感窗口的变化:消融前后基础状态下各个部位刺激均较难诱发心房颤动(VW接近0)。消融前、后HRA迷走神经刺激诱发心房颤动能力的差异无统计学意义[(63±31) ms比(63±25) ms,P>0．05],CSd的VW有一定程度的降低[(35±37) ms比(57±28) ms,P=0．07],LRA及CSp的VW明显降低(LRA:(1±3)ms比(49±36) ms;CSp:(10±12) ms比(45±34)ms,P值均<0．05)。结论慢径区域消融未直接改变窦房结区域及高位右心房的迷走神经支配,部分削弱了冠状静脉窦远端的迷走神经功能。导致了低位右心房及冠状静脉窦口区域的去迷走神经效应。降低了低位右心房及冠状静脉窦区域早搏刺激诱发迷走神经介导房颤的易感性。
Objective To investigate the effect of regional ablation of atrioventricular nodal slow pathway on atrial vagus nerve modulation and atrial fibrillation susceptibility. Methods 11 adult mongrel dogs underwent cervical sympathetic vagus nerve trunk stripping under general anesthesia. Coronary sinus catheters were placed through the right internal jugular vein puncture. Right ventricular catheter and right atrial standard electrode (Hallo catheter) were punctured through the left femoral vein. The ablation catheter and His bundle catheter were placed through the right femoral vein. Intravenous metoprolol blocks sympathetic activity. The changes of sinusoidal circumference (SCL), high right atrium (HRA), low right atrium (LRA), coronary sinus (CSp), and distal coronary sinus (CSd) under basal and vagal stimulation before and after ablation were measured in slow pathway areas. Effective refractory period (ERP) and atrial susceptibility window (VW). Results ① The changes of sinus circumference: There was no significant difference in shortening of SCL caused by vagus nerve stimulation before and after ablation (107 ± 19) vs (108 ± 8) times / min, P> 0.05]. (2) The changes of effective refractory period: The ERP shortening values of vagal stimulation before and after ablation were (69 ± 37) ms and (55 ± 34) ms, respectively. There was no significant difference between the two groups (P> 0. 05). CSd was (55 ± 30) ms and (42 ± 32) ms respectively. LRA was (66 ± 24) ms and (19 ± 21) ms respectively. CSp was (46 ± 24) and ) mS, the differences were statistically significant (P values were <0.05, 0.01). ③ changes in atrial susceptibility window: before and after ablation of all parts of the foundation state stimulation are more difficult to induce atrial fibrillation (VW close to 0). There was no significant difference in the ability of HRA vagus nerve stimulation to induce atrial fibrillation before and after ablation [(63 ± 31) ms vs (63 ± 25) ms, P> 0.05]. The VW of CSd was decreased to a certain extent (57 ± 28) ms, P = 0.07]. The VW of LRA and CSp was significantly decreased (49 ± 36 ms vs 49 ± 36 ms for LRA: (10 ± 12) ms vs ms (45 ± 34) ms, P <0.05). Conclusions Slow regional ablation did not directly change the vagal innervation of the sinoatrial node area and the superior right atrium and partially attenuated the vagal function distal to the coronary sinus. Leading to vagal denervation in the lower right atrium and coronary sinus ostium. Reduced susceptibility to vagal-mediated atrial fibrillation by premature beats in the lower right atrium and coronary sinus area.