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脂肪组织重新分布与心房颤动患者的左心房重塑及功能障碍相关。

Redistribution of adipose tissue is associated with left atrial remodeling and dysfunction in patients with atrial fibrillation.

作者信息

Chen Qian, Chen Xiuzhen, Wang Jiafu, Zhong Junlin, Zhang Hui, Wu Bingyuan, Zheng Zhenda, Xie Xujing, Zhu Jieming, Tang Xixiang, Li Suhua

机构信息

Department of Cardiovascular Medicine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Department of Radiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

出版信息

Front Cardiovasc Med. 2022 Aug 11;9:969513. doi: 10.3389/fcvm.2022.969513. eCollection 2022.

DOI:10.3389/fcvm.2022.969513
PMID:36035916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9403614/
Abstract

OBJECTIVE

Adipose tissue is recognized as a crucial regulator of atrial fibrillation (AF). However, the effect of epicardial adipose tissue (EAT) on the pathophysiology of AF might be different from that of other adipose tissues. The purpose of this study was to explore the distribution features of different adipose tissues in AF patients and their relationships with left atrial (LA) remodeling and function.

METHODS

A total of 205 participants (including 112 AF and 93 non-AF patients) were recruited. Color doppler ultrasound was used to measure the thickness of subcutaneous, extraperitoneal, and intra-abdominal adipose tissue. Cardiac CT scan was performed to measure the mean thickness of EAT surrounding the whole heart (total-EAT) and specific regions, including left atrium (LA-EAT), left ventricle, right ventricle, interventricular groove, and atrioventricular groove. LA anatomical remodeling and function were measured by echocardiography, while electrical remodeling was evaluated by P-wave duration and dispersion using Electrocardiography (obtained after cardioversion or ablation in AF patients). Relationship between the thickness of different adipose tissues and LA remodeling and function was analyzed.

RESULTS

The thickness of subcutaneous, extraperitoneal, and intra-abdominal adipose tissue was similar between AF and non-AF patients, and had no or only weak association with LA remodeling and dysfunction. However, compared to non-AF participants, total-EAT thickness significantly increased in both paroxysmal and persistent AF patients (non-AF vs. paroxysmal AF vs. persistent AF: 6.31 ± 0.63 mm vs. 6.76 ± 0.79 mm vs. 7.01 ± 1.18 mm, < 0.001), which was positively correlated with the LA size and P-wave duration and dispersion, and negatively correlated with LA ejection fraction and peak strain rate. More interestingly, EAT thickness in AF patients did not increase uniformly in different regions of the heart. Compared to EAT surrounding the other regions, LA-EAT was found to accumulate more greatly, and had a closer relationship to LA remodeling and dysfunction. Multivariate logistic regression analysis also showed that LA-EAT was significantly correlated with the presence of AF (OR = 4.781; 95% CI 2.589-8.831, < 0.001).

CONCLUSION

Rather than other adipose tissues, accumulation and redistribution of EAT, especially surrounding the LA, is associated with LA remodeling and dysfunction in AF patients.

摘要

目的

脂肪组织被认为是心房颤动(AF)的关键调节因子。然而,心外膜脂肪组织(EAT)对AF病理生理学的影响可能与其他脂肪组织不同。本研究的目的是探讨AF患者不同脂肪组织的分布特征及其与左心房(LA)重塑和功能的关系。

方法

共招募了205名参与者(包括112名AF患者和93名非AF患者)。使用彩色多普勒超声测量皮下、腹膜外和腹腔内脂肪组织的厚度。进行心脏CT扫描以测量围绕全心(总EAT)和特定区域(包括左心房(LA-EAT)、左心室、右心室、室间沟和房室沟)的EAT平均厚度。通过超声心动图测量LA解剖重塑和功能,同时使用心电图通过P波持续时间和离散度评估电重塑(在AF患者复律或消融后获得)。分析不同脂肪组织厚度与LA重塑和功能之间的关系。

结果

AF患者和非AF患者的皮下、腹膜外和腹腔内脂肪组织厚度相似,与LA重塑和功能障碍无关联或仅有微弱关联。然而,与非AF参与者相比,阵发性和持续性AF患者的总EAT厚度均显著增加(非AF vs.阵发性AF vs.持续性AF:6.31±0.63mm vs.6.76±0.79mm vs.7.01±1.18mm,<0.001),这与LA大小、P波持续时间和离散度呈正相关,与LA射血分数和峰值应变率呈负相关。更有趣的是,AF患者心脏不同区域的EAT厚度并非均匀增加。与围绕其他区域的EAT相比,发现LA-EAT积累更多,并且与LA重塑和功能障碍关系更密切。多因素逻辑回归分析还显示,LA-EAT与AF的存在显著相关(OR = 4.781;95%CI 2.589-8.831,<0.001)。

结论

与其他脂肪组织不同,EAT的积累和重新分布,尤其是围绕LA的EAT,与AF患者的LA重塑和功能障碍有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/4ff00d576110/fcvm-09-969513-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/300e963d774b/fcvm-09-969513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/393de57ad4ba/fcvm-09-969513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/c108ab316882/fcvm-09-969513-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/f53467281505/fcvm-09-969513-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/42c90f770a4b/fcvm-09-969513-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/4ff00d576110/fcvm-09-969513-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/300e963d774b/fcvm-09-969513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/393de57ad4ba/fcvm-09-969513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/c108ab316882/fcvm-09-969513-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/f53467281505/fcvm-09-969513-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/42c90f770a4b/fcvm-09-969513-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a3c/9403614/4ff00d576110/fcvm-09-969513-g006.jpg

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