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通道病中的心脏交感神经去神经支配

Cardiac Sympathetic Denervation in Channelopathies.

作者信息

Dusi Veronica, De Ferrari Gaetano Maria, Pugliese Luigi, Schwartz Peter J

机构信息

Department of Molecular Medicine, Section of Cardiology, University of Pavia, Pavia, Italy.

Cardiac Intensive Care Unit, Arrhythmia and Electrophysiology and Experimental Cardiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.

出版信息

Front Cardiovasc Med. 2019 Mar 26;6:27. doi: 10.3389/fcvm.2019.00027. eCollection 2019.

DOI:10.3389/fcvm.2019.00027
PMID:30972341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6443634/
Abstract

Left cardiac sympathetic denervation (LCSD) is a surgical antiadrenergic intervention with a strong antiarrhythmic effect, supported by preclinical as well as clinical data. The mechanism of action of LCSD in structurally normal hearts with increased arrhythmic susceptibility (such as those of patients with channelopathies) is not limited to the antagonism of acute catecholamines release in the heart. LCSD also conveys a strong anti-fibrillatory action that was first demonstrated over 40 years ago and provides the rationale for its use in almost any cardiac condition at increased risk of ventricular fibrillation. The molecular mechanisms involved in the final antiarrhythmic effect of LCSD turned out to be much broader than anticipated. Beside the vagotonic effect at different levels of the neuraxis, other new mechanisms have been recently proposed, such as the antagonism of neuronal remodeling, the antagonism of neuropeptide Y effects, and the correction of neuronal nitric oxide synthase (nNOS) imbalance. The beneficial effects of LCSD have never been associated with a detectable deterioration of cardiac performance. Finally, patients express a high degree of satisfaction with the procedure. In this review, we focus on the rationale, results and our personal approach to LCSD in patients with channelopathies such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.

摘要

左心交感神经去神经支配术(LCSD)是一种具有强大抗心律失常作用的外科抗肾上腺素能干预措施,有临床前及临床数据支持。LCSD在结构正常但心律失常易感性增加的心脏(如患有离子通道病的患者心脏)中的作用机制并不局限于拮抗心脏中急性儿茶酚胺的释放。LCSD还具有强大的抗纤颤作用,这在40多年前就首次得到证实,这也为其在几乎任何有室颤风险增加的心脏疾病中的应用提供了理论依据。事实证明,LCSD最终抗心律失常作用所涉及的分子机制比预期的要广泛得多。除了在神经轴不同水平的迷走神经作用外,最近还提出了其他新机制,如拮抗神经元重塑、拮抗神经肽Y的作用以及纠正神经元型一氧化氮合酶(nNOS)失衡。LCSD的有益效果从未与可检测到的心脏功能恶化相关联。最后,患者对该手术表达了高度满意度。在本综述中,我们重点关注LCSD在长QT综合征和儿茶酚胺能多形性室性心动过速等离子通道病患者中的理论依据、结果及我们的个人方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1543/6443634/92688687c5a3/fcvm-06-00027-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1543/6443634/ea080b237a26/fcvm-06-00027-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1543/6443634/92688687c5a3/fcvm-06-00027-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1543/6443634/ea080b237a26/fcvm-06-00027-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1543/6443634/92688687c5a3/fcvm-06-00027-g0002.jpg

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