Literature DB >> 30915593

Circulating primary bile acid is correlated with structural remodeling in atrial fibrillation.

Xin-Hua Wang1, Zheng Li2, Min-Hua Zang2, Tian-Bao Yao2, Jia-Liang Mao2, Jun Pu3.   

Abstract

BACKGROUND: Circulating primary bile acid was involved in the regulation of cardiac ionic channel currents and ventricular myocyte apoptosis, but it was unknown whether or not it played a role in structural remodeling of AF. This study was aimed to testify the hypothesis that elevated chenodeoxycholic acid (CDCA) concentration correlated with left atrial low voltage area (LVA) and could induce apoptosis of atrial myocytes in AF. METHODS AND
RESULTS: Serum concentrations of 12 types of bile acids were determined in patients with paroxysmal (n = 21), persistent AF (n = 20), and type A pre-excitation and paroxysmal supraventricular tachycardia (PSVT) (n = 19) and were correlated with LVA in AF, which was obtained by electroanatomical mapping during ablation. Additionally, the impact of CDCA incubation on apoptosis of mouse atrial myocytes was evaluated. Serum levels of CDCA and cholic acid were significantly higher in AF than in PSVT. CDCA serum concentration was significantly higher in persistent AF than in paroxysmal AF. CDCA serum level was positively correlated with the size (r = 0.78, P < 0.05) and proportion of LVA (r = 0.89, P < 0.05) in AF patients. CDCA (75 μM, 100 μM) promoted atrial myocyte apoptosis in a concentration-dependent manner.
CONCLUSIONS: The higher circulating level of CDCA in AF than in PSVT, positive correlation of CDCA with LVA in AF, and incubation dose-dependent increase of mouse atrial myocyte apoptosis indicated that CDCA might play a significant role in the progress of structural remodeling of AF.

Entities:  

Keywords:  Atrial fibrillation; Chenodeoxycholic acid; Low voltage area; Primary bile acid; Structural remodeling

Mesh:

Substances:

Year:  2019        PMID: 30915593     DOI: 10.1007/s10840-019-00540-z

Source DB:  PubMed          Journal:  J Interv Card Electrophysiol        ISSN: 1383-875X            Impact factor:   1.900


  8 in total

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