Open AccessAtrial Fibrillation Promotion in a Rat Model of Rheumatoid Arthritis
Author(s) -
Dai Hui,
Wang Xiaoyu,
Yin Shuangli,
Zhang Yun,
Han Yu,
Yang Ning,
Xu Jicheng,
Sun Li,
Yuan Yue,
Sheng Li,
Gong Yongtai,
Li Yue
Publication year - 2017
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.117.007320
Subject(s) - medicine , atrial fibrillation , rheumatoid arthritis , arthritis , cardiology , effective refractory period , heart failure , fibrosis
Background The prevalence of atrial fibrillation ( AF ) is significantly higher in rheumatoid arthritis ( RA ) patients, but the underlying mechanisms remain poorly understood. The goal of this study was to assess the effects of RA on AF susceptibility and atrial arrhythmogenic remodeling in a rat model of RA . Methods and Results Collagen‐induced arthritis was induced in rats by immunization with type II collagen in Freund's incomplete adjuvant. Among the rats that developed arthritis, AF susceptibility and atrial remodeling were examined 8 weeks after the primary immunization. AF inducibility and duration were substantially increased in collagen‐induced arthritis rats, and AF duration was significantly and positively correlated with the serum IL ‐6 and TNF ‐α levels. Rats with collagen‐induced arthritis showed prolonged atrial conduction time with no changes in the atrial effective refractory period. Atrial conduction delay was accompanied by significantly increased atrial fibrosis. In addition, atrial structural and autonomic remodeling, including left atrial dilation, apoptosis and autophagy of atrial myocytes, and atrial heterogeneous sympathetic hyperinnervation, was observed. Interestingly, we found that collagen‐induced arthritis had no significant effects on connexins, Nav1.5, and the main ion channels' protein expressions in atria. Conclusions We demonstrated that RA increased AF susceptibility by inducing AF ‐promoting atrial remodeling. This study may provide insights into mechanisms underlying RA ‐induced AF and validate a model that is suitable for further mechanistic and therapeutic exploration.