Pharmacologic Approach to Sinoatrial Node Dysfunction.

Pharmacologic Approach to Sinoatrial Node Dysfunction.
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DOI:
10.1146/annurev-pharmtox-031120-115815
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发表时间:
2021-01-06
影响因子:
12.5
通讯作者:
Mangoni ME
Mangoni ME
中科院分区:
医学1区
文献类型:
--
作者:
Mesirca P;Fedorov VV;Hund TJ;Torrente AG;Bidaud I;Mohler PJ;Mangoni ME

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窦房结的自发活动引起心跳。窦房结功能障碍(SND)和病态窦房综合征是由心脏不能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,继发于心脏起搏器组织的退行性纤维化。然而,也存在其他形式的SND,包括遗传性的特发性原发性SND,以及继发于心血管或全身性疾病的SND。在接下来的半个世纪里,普通人群中SND的发病率预计会增加,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的病理生理机制的了解有了很大的进展。本文综述了目前SND机制方面的知识,并讨论了引入新的药物治疗SND的可能性。
The spontaneous activity of the sinoatrial node initiates the heartbeat. Sinoatrial node dysfunction (SND) and sick sinoatrial 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 sinoatrial 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.
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