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Updated: Jan 27, 2026

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
Published on: February 14, 2022
Circulating primary bile acid is correlated with structural remodeling in atrial fibrillation
Xin-Hua Wang1, Zheng Li2, Min-Hua Zang2
1Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 1630 Dongfang Rd., Shanghai, 200127, China. ttwwxh@126.com.
Insights
Elevated chenodeoxycholic acid (CDCA) correlates with atrial fibrillation structural remodeling. Higher CDCA levels are linked to low voltage areas and induce atrial myocyte apoptosis.
Area of Science:
- Cardiology
- Biochemistry
- Electrophysiology
Background:
- Primary bile acids regulate cardiac function and myocyte apoptosis.
- The role of bile acids in atrial fibrillation (AF) structural remodeling remains unclear.
Purpose of the Study:
- To investigate the hypothesis that elevated chenodeoxycholic acid (CDCA) concentration correlates with left atrial low voltage areas (LVA) in AF.
- To determine if CDCA induces apoptosis of atrial myocytes.
Main Methods:
- Serum bile acid levels were measured in patients with AF and other arrhythmias.
- Electoanatomical mapping identified LVA in AF patients.
- Mouse atrial myocytes were incubated with CDCA to assess apoptosis.
Main Results:
- Serum CDCA and cholic acid levels were higher in AF patients compared to PSVT patients.
- CDCA levels were significantly higher in persistent AF than paroxysmal AF.
- CDCA serum levels positively correlated with LVA size and proportion in AF patients.
- CDCA promoted atrial myocyte apoptosis in a dose-dependent manner.
Conclusions:
- Elevated circulating CDCA levels are associated with AF.
- CDCA correlates with LVA, suggesting a role in AF structural remodeling.
- CDCA may significantly contribute to the progression of AF structural remodeling via myocyte apoptosis.
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.
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