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目的探讨碎裂电位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10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静脉窦导管,经左股静脉穿刺放置右心室导管(房室结消融后,行临时右心室起搏)及右心房导管(Hallo导管),经右股静脉穿刺放置房间隔穿刺鞘管,经房间隔穿刺途径放置消融导管及左心房标测导管(Lasso导管)。静脉应用美托洛尔阻断交感神经活性。通过双侧颈部交感-迷走神经干刺激诱发并维持心房颤动,在心房颤动过程中标测并记录碎裂电位的分布部位。测量碎裂电位消融前后基础状态及迷走神经刺激下的窦性周长(SCL)及右心耳(RAA)、左心耳(LAA)、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)。消融后应用甲醛固定心脏标本,对消融区域的心脏标本进行连续切片,应用苏木精-伊红染色观察消融对心房肌的影响,并选择相同区域未消融的犬心脏标本做对照。结果①窦性周长的变化:消融后迷走神经刺激导致的SCL为(18±8)次／min,较消融前[(107±19)次／min]明显缩短(P<0．001)。②有效不应期的变化:消融前、后迷走神经刺激导致的ERP缩短值在右心耳分别为(65±22) ms及(17±24)ms,冠状静脉窦远端分别为(63±23)ms及(9±10)ms,冠状静脉窦近端分别为(61±21) ms及(4±16)ms,左心耳分别为(41±19)ms及(6±14)ms,差异均有统计学意义(P值均<0．001)。③心房易感窗口的变化:消融前、后基础状态下测得的VW的差异无统计学意义(P>0．05)。消融前、后迷走神经刺激诱发心房颤动的能力:右心耳分别为(18±29)、(58±13)ms,冠状静脉窦远端分别为(11±20)、(52±28)ms,冠状静脉窦近端分别为(7±15)、(62±35)ms,左心耳分别为(19±22)、(31±24)ms,差异均有统计学意义(P值均<0．05=。组织病理学分析显示碎裂电位区域心外膜脂肪垫存在大量自主神经纤维的分布,碎裂电位区域消融明显损伤了神经纤维。结论碎裂电位消融能导致迷走神经介导的窦房结抑制、心房不应期缩短效应及心房颤动易感窗口增加效应明显下降。提示碎裂电位的发生与迷走神经密切相关,针对碎裂电位消融能引起心房局部去神经反应,进而减少迷走神经对心房的支配,抑制迷走神经介导的心房颤动的发生。
Objective To investigate the effect of fragmentation potential ablation on atrial vagal modulation and atrial fibrillation susceptibility. Methods Ten adult mongrel dogs underwent cervical sympathetic vagal stripping under general anesthesia. The right venous catheter was placed through the right internal jugular vein, the right ventricular catheter was placed through the left femoral vein (temporary right ventricular pacing after atrioventricular node ablation) and the right atrial catheter (Hallo catheter) Atrial septum puncture sheath, percutaneous transseptal puncture approach placed ablation catheter and left atrial catheter (Lasso catheter). Intravenous metoprolol blocks sympathetic activity. Atrial fibrillation was induced and maintained by bilateral cervical sympathetic-vagus nerve stimulation, and the distribution of fragmentation potential was measured and recorded during atrial fibrillation. The basal state before and after ablation of fragmentation potential and the sinus circumference (SCL) and the efficacy of vagal stimulation (RAA), LAA, CSp and CSd were measured Refractory period (ERP) and atrial susceptibility window (VW). Cardiac specimens were fixed with formaldehyde after ablation, and the heart specimens of the ablation area were serially sectioned. The effect of ablation on atrial myocardium was observed by hematoxylin-eosin staining, and the non-ablated canine heart specimens of the same area were selected for comparison. RESULTS ① Changes of sinus circumference: The SCL induced by vagal stimulation after ablation was (18 ± 8) min / min after ablation, which was significantly shorter than that before ablation (107 ± 19) min / min (P <0.001). The changes of effective refractory period: The shortening value of ERP caused by vagus nerve stimulation before and after ablation were (65 ± 22) ms and (17 ± 24) ms respectively in the right atrial appendage, and the distal ends of coronary sinus were (63 ± 23) (61 ± 21) ms and (4 ± 16) ms, respectively. The left atrial appendage was (41 ± 19) ms and (6 ± 14) ms, respectively There was statistical significance (P <0.001). ③ atrial susceptibility window changes: before and after ablation baseline VW measured no significant difference (P> 0.05). The abilities of atrial fibrillation induced by vagus nerve stimulation before and after ablation were (18 ± 29) and (58 ± 13) ms for the right atrial appendage and (11 ± 20) and (52 ± 28) ms for the distal coronary sinus, respectively (7 ± 15) and (62 ± 35) ms respectively, and the left atrial appendage were (19 ± 22) and (31 ± 24) ms, respectively, with significant difference (P <0.05) Histopathological analysis showed that there was a large number of autonomic nerve fibers distributed in the epicardial fat pad in the fragmentation potential region, and the ablation of fragmentation potential obviously damaged the nerve fibers.Conclusion Fragmentation potential ablation can lead to vagal-mediated sinus node inhibition , The atrial refractory period shortening effect and atrial fibrillation susceptibility window increase effect decreased significantly.It is suggested that the occurrence of fragmentation potential is closely related to the vagus nerve, ablation of fragmentation potential can cause local atrial denervation reaction, thus reducing the vagus nerve atrial control , Inhibit vagal-mediated atrial fibrillation.