Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts.
Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts.
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DOI：
10.1016/j.jacep.2022.01.018
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发表时间：
2022-04
影响因子：
7
通讯作者：
Vaseghi, Marmar
中科院分区：
文献类型：
--
作者：
Hoang, Jonathan D.;Yamakawa, Kentaro;Rajendran, Pradeep S.;Chan, Christopher A.;Yagishita, Daigo;Nakamura, Keijiro;Lux, Robert L.;Vaseghi, Marmar
关键词：
交感神经兴奋增加室性快速性心律失常（VT）的风险。迷走神经刺激（VNS）在缺血性心律失常的情况下具有抗心律失常作用，但尚不清楚它是否能克服慢性心肌梗死（MI）情况下交感兴奋的电生理效应。本研究的目的是评估间歇性VNS是否减少交感神经兴奋过程中的电不均匀性和心律失常。在慢性MI后的约克郡猪中，进行胸骨切开术，在心室上放置56电极套（n=17），并在左心室中放置篮状导管（n=6）。获得来自袜和篮阵列的连续单极电描记图，以分析激动恢复间期（ARI），即动作电位持续时间的替代物。进行双极电压标测以确定瘢痕、边界区或存活心肌。在交感神经兴奋与双侧星状神经节刺激（BSS）和BSS与间歇性VNS的组合过程中，评价了血流动力学和电参数以及VT诱导。在BSS期间，整体心外膜阿里斯从384±59 ms缩短至297±63 ms，心内膜阿里斯从359±36 ms缩短至318±40 ms。所有区域的阿里斯离散度均增加，在瘢痕和边缘区观察到最大增加。VNS减轻了BSS对边界区阿里斯（从−18.3±6.3%降至−2.1±14.7%）和ARI色散（从104 ms2 [1，1108]降至−108 ms2 [−588，30]）的影响。迷走神经刺激使交感兴奋时诱发的室性心动过速减少（从75%降至40%，p<0.05）。在慢性心肌梗死后，VNS通过减少由交感神经刺激加剧的电生理异质性，减少VT诱导，克服交感神经兴奋的不利影响。交感神经兴奋在室性心律失常的发生中起重要作用。在这项研究中，交感神经刺激显着恶化的全球和区域心室电生理异质性在慢性梗死猪心。值得注意的是，迷走神经刺激显著减轻了交感神经兴奋对瘢痕和边缘区的电生理效应，增加了交感神经刺激期间的心室有效不应期，并使诱发的室性心律失常减少了50%。这项研究强调了即使在交感神经张力升高的状态下，VNS在急性降低VT发生率方面的疗效。迷走神经刺激可减轻慢性梗死猪心边缘区和瘢痕区交感神经介导的促心律失常作用。#EPPeeps #JACCCEP #JACCCEP Twitter
Sympathoexcitation increases risk of ventricular tachyarrhythmias (VT). Vagal nerve stimulation (VNS) has been anti-arrhythmic in the setting of ischemia-driven arrhythmias, but it is unclear if it can overcome the electrophysiological effects of sympathoexcitation in the setting of chronic myocardial infarction (MI). The goal of this study was to evaluate whether intermittent VNS reduces electrical heterogeneities and arrhythmia inducibility during sympathoexcitation. In Yorkshire pigs after chronic MI, a sternotomy was performed, a 56-electrode sock was placed over the ventricles (n=17), and a basket catheter was positioned in the left ventricle (n=6). Continuous unipolar electrograms from sock and basket arrays were obtained to analyze activation recovery interval (ARI), a surrogate of action potential duration. Bipolar voltage mapping was performed to define scar, border zone, or viable myocardium. Hemodynamic and electrical parameters, and VT inducibility were evaluated during sympathoexcitation with bilateral stellate ganglia stimulation (BSS) and during combined BSS with intermittent VNS. During BSS, global epicardial ARIs shortened from 384±59 to 297±63 ms and endocardial ARIs from 359±36 to 318±40 ms. Dispersion in ARIs increased in all regions, with the greatest increase observed in scar and border zone regions. VNS mitigated the effects of BSS on border zone ARIs (from −18.3±6.3% to −2.1±14.7%) and ARI dispersion (from 104 ms2 [1, 1108] to −108 ms2 [−588, 30]). VNS reduced VT inducibility during sympathoexcitation (from 75% to 40%, p<0.05). After chronic myocardial infarction, VNS overcomes the detrimental effects of sympathoexcitation by reducing electrophysiological heterogeneities exacerbated by sympathetic stimulation, decreasing VT inducibility. Sympathetic activation plays a significant role in occurrence of ventricular arrhythmias. In this study, sympathetic stimulation significantly worsened global and regional ventricular electrophysiological heterogeneities in chronically infarcted porcine hearts. Notably, vagal nerve stimulation significantly mitigated the electrophysiological effects of sympathoexcitation on scar and border zone regions, increased ventricular effective refractory period during sympathetic stimulation, and reduced ventricular arrhythmia inducibility by 50%. This study highlights the efficacy of VNS in acutely reducing incidence of VT even during states of elevated sympathetic tone. Vagal nerve stimulation mitigates sympathetically mediated pro-arrhythmic effects on border zones and scar regions in chronically infarcted porcine hearts. #EPPeeps #JACCCEP #CardioTwitter
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