Vagal Nerve Stimulation Reduces Ventricular Arrhythmias and Mitigates Adverse Neural Cardiac Remodeling Post-Myocardial Infarction.
Vagal Nerve Stimulation Reduces Ventricular Arrhythmias and Mitigates Adverse Neural Cardiac Remodeling Post-Myocardial Infarction.
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迷走神经刺激可减少心室心律不齐，并减轻心肌后梗死后神经心脏重塑。
DOI：
10.1016/j.jacbts.2023.03.025
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发表时间：
2023-09
影响因子：
9.7
通讯作者：
Ardell, Jeffrey L.
中科院分区：
文献类型：
--
作者：
Hadaya, Joseph;Dajani, Al-Hassan;Cha, Steven;Hanna, Peter;Challita, Ronald;Hoover, Donald B.;Ajijola, Olujimi A.;Shivkumar, Kalyanam;Ardell, Jeffrey L.
关键词：
迷走神经刺激已成为一种有前途的治疗方法，以打击所观察到的副交感神经张力的撤回，并抵消反射介导的交感神经兴奋与缺血性心脏病。与MI猪相比，以神经生理学引导的方式递送的反应性cVNS导致MI + cVNS猪的心脏机械功能显著改善和室性心律失常显著减少。cVNS稳定了瘢痕边缘区MI诱导的电异质性，减少了各向异性电传播和传导阻滞，并使心肌复极正常化-体内室性心律失常的关键驱动因素。cVNS减少了瘢痕边缘区和主要交感传出和传入神经节（星状和T1背根神经节）的异常结构重塑。cVNS保留了MI后心脏的交感神经控制。本研究旨在评价慢性迷走神经刺激（cVNS）对心肌梗死（MI）后心脏和心外神经结构/功能的影响。组为对照组、MI组和MI + cVNS组; cVNS在MI后2天开始。MI后6周进行终末实验。MI损害左心室机械功能，诱发各向异性电传导，增加室性心动过速和颤动的易感性，改变星状神经节和背根神经节中的神经元和神经胶质表型，包括神经胶质激活。cVNS改善心脏机械功能，减少MI后室性心动过速/室颤，部分通过稳定边缘区的激活/复极化。心肌梗死相关的心外神经重塑，特别是神经胶质细胞活化，减轻了cVNS。
Vagal nerve stimulation has emerged as a promising therapeutic approach to combat the observed withdrawal of parasympathetic tone and to counteract the reflex-mediated sympathoexcitation associated with ischemic heart disease. Reactive cVNS, delivered in a neurophysiological-guided manner, resulted in a substantial improvement in cardiac mechanical function and dramatic reduction in ventricular arrhythmias in MI + cVNS pigs compared with MI pigs. cVNS stabilized MI-induced electrical heterogeneity in the scar-border zone, reduced anisotropic electrical propagation and conduction block, and normalized myocardial repolarization—key drivers of ventricular arrhythmias in vivo. cVNS reduced aberrant structural remodeling of the scar-border zone and principal sympathetic efferent and afferent ganglia (stellate and T1 dorsal root ganglia). cVNS preserved sympathetic control of the heart after MI. This study sought to evaluate the impact of chronic vagal nerve stimulation (cVNS) on cardiac and extracardiac neural structure/function after myocardial infarction (MI). Groups were control, MI, and MI + cVNS; cVNS was started 2 days post-MI. Terminal experiments were performed 6 weeks post-MI. MI impaired left ventricular mechanical function, evoked anisotropic electrical conduction, increased susceptibility to ventricular tachycardia and fibrillation, and altered neuronal and glial phenotypes in the stellate and dorsal root ganglia, including glial activation. cVNS improved cardiac mechanical function and reduced ventricular tachycardia/ventricular fibrillation post-MI, partly by stabilizing activation/repolarization in the border zone. MI-associated extracardiac neural remodeling, particularly glial activation, was mitigated with cVNS.
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影响因子：
20.1
作者：
Fukuda K;Kanazawa H;Aizawa Y;Ardell JL;Shivkumar K
通讯作者：
Shivkumar K
迷走神经的选择性神经调节。
影响因子：
4.3
作者：
Fitchett A;Mastitskaya S;Aristovich K
通讯作者：
Aristovich K
影响因子：
4
作者：
Hadaya J;Ardell JL
通讯作者：
Ardell JL
影响因子：
37.8
作者：
Ando, M;Katare, RG;Sato, T
通讯作者：
Sato, T
影响因子：
18.2
作者：
Hamann, Jason J.;Ruble, Stephen B.;Sabbah, Hani N.
通讯作者：
Sabbah, Hani N.