慢性心肌梗死后心脏去交感神经支配后迷走神经刺激的抗心律失常作用。
Antiarrhythmic effects of vagal nerve stimulation after cardiac sympathetic denervation in the setting of chronic myocardial infarction.
机构信息
Division of Cardiology, David Geffen School of Medicine at University of California, Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, California; Neurocardiology Research Center of Excellence, UCLA, Los Angeles, California.
Neurocardiology Research Center of Excellence, UCLA, Los Angeles, California.
出版信息
Heart Rhythm. 2018 Aug;15(8):1214-1222. doi: 10.1016/j.hrthm.2018.03.012. Epub 2018 Mar 9.
BACKGROUND
Neuraxial modulation with cardiac sympathetic denervation (CSD) can potentially reduce burden of ventricular tachyarrhythmia (VT). However, despite catheter ablation and CSD, VT can recur in patients with cardiomyopathy and the role of vagal nerve stimulation (VNS) in this setting is unclear.
OBJECTIVE
The purpose of this study was to evaluate the electrophysiological effects of VNS after CSD in normal and infarcted hearts.
METHODS
In 10 normal and 6 infarcted pigs, electrophysiological and hemodynamic parameters were evaluated before and during intermittent VNS pre-CSD (bilateral stellectomy and T2-T4 thoracic ganglia removal) as well as post-CSD. The effect of VNS during isoproterenol was also assessed pre- and post-CSD. Multielectrode ventricular activation recovery interval (ARI) recordings, a surrogate of action potential duration, were obtained. VT inducibility was tested during isoproterenol infusion after CSD with and without VNS.
RESULTS
VNS increased the global ARI by 4% ± 4% pre-CSD and by 5% ± 6% post-CSD, with enhanced effects observed during isoproterenol infusion (10% ± 8% pre-CSD and 12% ± 9% post-CSD) in normal animals. In infarcted animals pre-CSD, VNS increased ARI by 6% ± 7% before and by 13% ± 8% during isoproterenol infusion. Post-CSD, VNS increased ARI by 6% ± 5% before and by 11% ± 7% during isoproterenol infusion. VT was inducible in all infarcted animals post-CSD during isoproterenol infusion; this inducibility was reduced by 67% with VNS (P = .01). In all animals, the hemodynamic effects of VNS remained after CSD.
CONCLUSION
After CSD, the beneficial electrophysiological effects of VNS remain. Furthermore, VNS can reduce VT inducibility beyond CSD in the setting of circulating catecholamines, suggesting a role for additional parasympathetic modulation in the treatment of ventricular arrhythmias.
背景
通过心脏交感神经去神经支配（CSD）进行神经轴调制有可能降低室性心动过速（VT）的负担。然而，尽管进行了导管消融和 CSD，心肌病患者的 VT 仍可能复发，而迷走神经刺激（VNS）在这种情况下的作用尚不清楚。
目的
本研究旨在评估 CSD 后 VNS 在正常和梗死心脏中的电生理效应。
方法
在 10 只正常和 6 只梗死猪中，在 CSD 前（双侧星状神经切除术和 T2-T4 胸神经节切除）和 CSD 后评估电生理和血流动力学参数。还评估了 CSD 前后异丙肾上腺素期间 VNS 的作用。获得了替代动作电位持续时间的多电极心室激活恢复间隔（ARI）记录。在 CSD 后用和不用 VNS 在异丙肾上腺素输注期间测试 VT 的可诱导性。
结果
在正常动物中，VNS 在 CSD 前增加了 4%±4%的全局 ARI，在 CSD 后增加了 5%±6%，在异丙肾上腺素输注期间观察到增强效应（CSD 前 10%±8%，CSD 后 12%±9%）。在 CSD 前的梗死动物中，VNS 在异丙肾上腺素输注前增加了 6%±7%的 ARI，在异丙肾上腺素输注期间增加了 13%±8%的 ARI。CSD 后，VNS 在异丙肾上腺素输注前增加了 6%±5%的 ARI，在异丙肾上腺素输注期间增加了 11%±7%的 ARI。在所有梗死动物中，在异丙肾上腺素输注期间 CSD 后均可诱导 VT；在异丙肾上腺素输注期间，VNS 将可诱导性降低了 67%（P=0.01）。在所有动物中，CSD 后 VNS 的血流动力学效应仍然存在。
结论
CSD 后，VNS 的有益电生理效应仍然存在。此外，在循环儿茶酚胺存在的情况下，VNS 可以降低 CSD 后 VT 的可诱导性，这表明额外的副交感神经调节在治疗室性心律失常方面可能发挥作用。
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