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药物治疗病态窦房结综合征。

Pharmacologic Approach to Sinoatrial Node Dysfunction.

机构信息

Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email:

LabEx Ion Channels Science and Therapeutics (ICST), 06560 Nice, France.

出版信息

Annu Rev Pharmacol Toxicol. 2021 Jan 6;61:757-778. doi: 10.1146/annurev-pharmtox-031120-115815. Epub 2020 Oct 5.

DOI:10.1146/annurev-pharmtox-031120-115815
PMID:33017571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7790915/
Abstract

The spontaneous activity of the sinoatrial node initiates the heartbeat. Sino-atrial node dysfunction (SND) and sick sinoatrial (sick sinus) syndrome are caused by the heart's inability to generate a normal sinoatrial node action potential. In clinical practice, SND is generally considered an age-related pathology, secondary to degenerative fibrosis of the heart pacemaker tissue. However, other forms of SND exist, including idiopathic primary SND, which is genetic, and forms that are secondary to cardiovascular or systemic disease. The incidence of SND in the general population is expected to increase over the next half century, boosting the need to implant electronic pacemakers. During the last two decades, our knowledge of sino-atrial node physiology and of the pathophysiological mechanisms underlying SND has advanced considerably. This review summarizes the current knowledge about SND mechanisms and discusses the possibility of introducing new pharmacologic therapies for treating SND.

摘要

窦房结的自发性活动启动心跳。窦房结功能障碍（SND）和病态窦房结（病态窦房结）综合征是由于心脏无法产生正常的窦房结动作电位引起的。在临床实践中，SND 通常被认为是一种与年龄相关的病理学，继发于心脏起搏器组织的退行性纤维化。然而，其他形式的 SND 也存在，包括原发性 SND，这是遗传性的，以及继发于心血管或系统性疾病的形式。预计在未来半个世纪，SND 在普通人群中的发病率将会增加，这将增加对植入电子起搏器的需求。在过去的二十年中，我们对窦房结生理学和 SND 病理生理机制的认识有了很大的提高。这篇综述总结了目前关于 SND 机制的知识，并讨论了引入新的药物治疗 SND 的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/3d1edbc9008d/nihms-1636884-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/b7e95d9a0482/nihms-1636884-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/1af993ec262c/nihms-1636884-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/5b1f66076fb5/nihms-1636884-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/3d1edbc9008d/nihms-1636884-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/b7e95d9a0482/nihms-1636884-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/1af993ec262c/nihms-1636884-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/5b1f66076fb5/nihms-1636884-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7b/7790915/3d1edbc9008d/nihms-1636884-f0004.jpg

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本文引用的文献

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Sci Rep. 2020 Jun 17;10(1):9835. doi: 10.1038/s41598-020-66673-8.
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Heritable arrhythmia syndromes associated with abnormal cardiac sodium channel function: ionic and non-ionic mechanisms.遗传性心律失常综合征与心脏钠通道功能异常相关：离子和非离子机制。
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Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node.神经元钠通道功能障碍导致人心房结内传导阻滞和折返性心律失常。
Nat Commun. 2020 Jan 24;11(1):512. doi: 10.1038/s41467-019-14039-8.
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Cardiac Pacemaker Activity and Aging.心脏起搏器活动与衰老。
Annu Rev Physiol. 2020 Feb 10;82:21-43. doi: 10.1146/annurev-physiol-021119-034453. Epub 2019 Nov 22.
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