Liu Shin-Huei, Lo Li-Wei, Chou Yu-Hui, Lin Wei-Lun, Tsai Tseng-Ying, Cheng Wen-Han, Yamada Shinya, Chen Shih-Ann
Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine and Cardiovascular Research Institute, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine and Cardiovascular Research Institute, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Heart Rhythm. 2021 Sep;18(9):1596-1604. doi: 10.1016/j.hrthm.2021.05.014. Epub 2021 May 13.
The electrophysiological (EP) effects and safety of renal artery denervation (RDN) in chronic kidney disease (CKD) are unclear.
The purpose of this study was to investigate the arrhythmogenicity of RDN in a rabbit model of CKD.
Eighteen New Zealand white rabbits were randomized to control (n = 6), CKD (n = 6), and CKD-RDN (n = 6) groups. A 5/6 nephrectomy was selected for the CKD model. RDN was applied in the CKD-RDN group. All rabbits underwent cardiac EP studies for evaluation. Immunohistochemistry, myocardial fibrosis, and renal catecholamine levels were evaluated.
The CKD group (34.8% ± 9.2%) had a significantly higher ventricular arrhythmia (VA) inducibility than the control (8.6% ± 3.8%; P <.01) and CKD-RDN (19.5% ± 6.3%; P = .01) groups. In the CKD-RDN group, ventricular fibrosis was significantly decreased compared to the CKD group (7.4% ± 2.0 % vs 10.4% ± 3.7%; P = .02). Sympathetic innervation in the CKD group was significantly increased compared to the control and CKD-RDN groups [left ventricle: 4.1 ± 1.8 vs 0.8 ± 0.5 (10 μm/mm), P <.01; 4.1 ± 1.8 vs 0.9± 0.6 (10 μm/mm), P <.01; right ventricle: 3.6 ± 1.0 vs 1.0 ± 0.4 (10 μm/mm), P <.01; 3.6 ± 1.0 vs 1.0 ± 0.5 (10 μm/mm), P <.01].
Neuromodulation by RDN demonstrated protective effects with less structural and electrical remodeling, leading to attenuated VAs. In a rabbit model of CKD, RDN plays a therapeutic role by lowering the risk of VA caused by autonomic dysfunction.
肾动脉去神经支配术（RDN）在慢性肾脏病（CKD）中的电生理（EP）效应及安全性尚不清楚。
本研究旨在探讨RDN在CKD兔模型中的致心律失常性。
将18只新西兰白兔随机分为对照组（n = 6）、CKD组（n = 6）和CKD-RDN组（n = 6）。采用5/6肾切除术建立CKD模型。CKD-RDN组接受RDN治疗。所有兔子均接受心脏EP研究以进行评估。评估免疫组织化学、心肌纤维化和肾脏儿茶酚胺水平。
CKD组（34.8%±9.2%）的室性心律失常（VA）诱发率显著高于对照组（8.6%±3.8%；P<.01）和CKD-RDN组（19.5%±6.3%；P =.01）。与CKD组相比，CKD-RDN组的心室纤维化显著降低（7.4%±2.0%对10.4%±3.7%；P =.02）。与对照组和CKD-RDN组相比，CKD组的交感神经支配显著增加[左心室：4.1±1.8对0.8±0.5（10μm/mm），P<.01；4.1±1.8对0.9±0.6（10μm/mm），P<.01；右心室：3.6±1.0对1.0±0.4（10μm/mm），P<.01；3.6±1.0对1.0±0.5（10μm/mm），P<.01]。
RDN进行的神经调节显示出保护作用，结构和电重构较少，导致VA减轻。在CKD兔模型中，RDN通过降低自主神经功能障碍引起的VA风险发挥治疗作用。
