Zheng Shaohua, Zhang Yujiao, Wang Zhongsu, Li Zhiyuan, Hou Xujuan, Duan Wenchang, Hou Yinglong
Shandong Provincial Qianfoshan Hospital, and the Department of Clinical Medicine, School of Medicine, Shandong University, Jinan City, China.
Pacing Clin Electrophysiol. 2014 Jun;37(6):745-50. doi: 10.1111/pace.12338. Epub 2013 Dec 20.
No evidence has been presented to show whether autonomic neural remodeling occurs in pulmonary vein-left atrium (PV-LA) junction and what an important role it may play in AF. This study aims to find out these issues in a prolonged rapid atrial pacing canine model.
Twelve healthy mongrel dogs were randomly divided into two groups, six in each: the paced group underwent rapid right atrial pacing at 400 beats per minute for 4 weeks, and the control group was not paced. The effective refractory period (ERP) of left superior pulmonary vein-left atrium (LSPV-LA) junction in all animals was determined immediately after 4 weeks. Tissues were removed from 1 cm around all PV-LA junctions. Immunohistochemical staining and western blotting were performed to examine the expression of tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT).
Compared with the control group, ERP of LSPV-LA junction of the paced group was significantly shortened ([83.33 ± 16.33] ms vs [111.67 ± 20.41] ms, P < 0.05). Spontaneous atrial fibrillation developed in two animals in the paced group, but in none of the control group. Immunohistochemistry showed that the average density and heterogeneity of both TH- and ChAT-positive nerves at LSPV-LA junction in the paced group were significantly higher compared to the control group (P < 0.01). Western blotting showed that the expression of TH and ChAT at four PV-LA junctions in the paced group also increased markedly compared with the control group (P < 0.01).
Autonomic neural remodeling did exist in PV-LA junction after prolonged atrial pacing, which may contribute to the initiation of atrial fibrillation and be significant in its treatment by radiofrequency catheter ablation.
尚无证据表明肺静脉-左心房(PV-LA)连接处是否发生自主神经重塑,以及它在房颤中可能发挥何种重要作用。本研究旨在通过延长快速心房起搏犬模型来探究这些问题。
将12只健康杂种犬随机分为两组,每组6只:起搏组以每分钟400次的频率进行右心房快速起搏4周,对照组未进行起搏。4周后立即测定所有动物左上肺静脉-左心房(LSPV-LA)连接处的有效不应期(ERP)。从所有PV-LA连接处周围1 cm处取组织。进行免疫组织化学染色和蛋白质印迹法检测酪氨酸羟化酶(TH)和胆碱乙酰转移酶(ChAT)的表达。
与对照组相比,起搏组LSPV-LA连接处的ERP显著缩短([83.33±16.33]毫秒对[111.67±20.41]毫秒,P<0.05)。起搏组有2只动物发生自发性房颤,而对照组无。免疫组织化学显示,与对照组相比,起搏组LSPV-LA连接处TH和ChAT阳性神经的平均密度和异质性均显著更高(P<0.01)。蛋白质印迹法显示,起搏组4个PV-LA连接处TH和ChAT的表达也较对照组显著增加(P<0.01)。
延长心房起搏后PV-LA连接处确实存在自主神经重塑,这可能有助于房颤的起始,并且在通过射频导管消融治疗房颤中具有重要意义。