[1]郑涛,综述,凌智瑜,等.心外膜脂肪组织与心房颤动[J].心血管病学进展,2016,(4):372-375.[doi:10.16806/j.cnki.issn.1004-3934.2016.04.012]
　ZHENG Tao,LING Zhiyu.Epicardial Adipose Tissue and Atrial Fibrillation[J].Advances in Cardiovascular Diseases,2016,(4):372-375.[doi:10.16806/j.cnki.issn.1004-3934.2016.04.012]
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心外膜脂肪组织与心房颤动()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2016年4期
页码:
372-375
栏目:
综述
出版日期:
2016-08-15

文章信息/Info

Title:
Epicardial Adipose Tissue and Atrial Fibrillation
作者:
郑涛1; 综述; 凌智瑜1; 2; 审校
1.重庆医科大学研究生院,重庆400010; 2.重庆医科大学附属第二医院心血管内科,重庆 400010
Author(s):
ZHENG Tao1;  LING Zhiyu1; 2
1. Chongqing Medical University Graduate School,Chongqing 400010,China; 2.Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
关键词:
心外膜脂肪组织;  心房颤动;  神经节;  炎性介质
Keywords:
Epicardial adipose tissue;  Atrial fibrillation;  Ganglionated plex;  Inflammatory mediator
分类号:
R541.7+5
DOI:
10.16806/j.cnki.issn.1004-3934.2016.04.012
文献标志码:
A
摘要:
心房颤动是临床上常见的心律失常,其发生机制尚未完全阐明。近年的研究发现,心外膜脂肪组织与心房颤动的发生发展密切相关。心外膜脂肪组织导致心房颤动的机制可能为:(1)心外膜脂肪组织中存在大量的自主神经节,心外膜脂肪组织增加可导致自主神经活动紊乱,神经节内的交感神经元兴奋,释放更多的去甲肾上腺素,引起神经节附近的肺静脉及心房内的心肌细胞钙负荷增加,诱发早期后除极,从而形成肺静脉及心房内的异常放电,并可导致心房有效不应期缩短,使心房组织产生电重构。(2)心外膜脂肪组织是心房组织局部炎性介质的源泉,心外膜脂肪组织的增加可导致炎性介质过度表达促使心房肌纤维化的进展,并导致心房产生结构重构,为心房颤动的发生及维持提供了基质。
Abstract:
Atrial fibrillation is one of the most common arrhythmias encountered in clinical practice, however its mechanism is not yet fully understood. Recent studies have shown that epicardial adipose tissue(EAT)plays an important role in the occurrence and development of atrial fibrillation. There are two potential mechanisms explaining for how EAT impacts the atria:(1)EAT contains abundant ganglionated plexi, and an increase in EAT may provoke abnormal autonomic nervous activity and increase the secretion of noradrenaline. This may cause calcium overload nearby pulmonary veins of the left atria, leading to the development of early after depolarizations, and resulting in abnormal electric activities in the pulmonary vein and atria. Additionally it can shorten the effective refractory period and lead to the electrical remodeling of atria.(2)Mechanism is that EAT is also the source of inflammatory medium, and an increase of EAT may cause the overexpression of inflammatory biomarkers and prompt the progress of the atrial fibrosis, which can result in structural remodeling of the atria, and provide the substrate for initiation and maintenance of atrial fibrillation.

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备注/Memo

备注/Memo:
基金项目:重庆市卫生局重点课题(2011-1-045) 作者简介:郑涛(1990—),在读硕士,主要从事心律失常、心力衰竭的治疗研究。Email:cardiologzhengtao@163.com 通信作者:凌智瑜(1977—),副教授,硕士生导师,博士,主要从事心律失常、心力衰竭、冠心病等的哈治疗研究。Email:13512362075@163.com
更新日期/Last Update: 2016-07-25