Gap junction remodelling by chronic pressure overload is related to the increased susceptibility to atrial fibrillation in rat heart

Seung Yong Shin, Won Min Jo, Too Jae Min, Byoung Kwon Kim, Dae Hyun Song, Seong Hyeop Hyeon, Jee Eun Kwon, Wang Soo Lee, Kwang Je Lee, Sang Wook Kim, Tae Ho Kim, Chee Jeong Kim, Sung Il Im, Hong Euy Lim

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Aims Left atrial (LA) fibrosis caused by various pathological stimuli is a common finding. However, the difference of atrial remodelling via haemodynamic change in diverse cardiomyopathy has not been elucidated. Methods and results Male Sprague-Dawley rats (6-8 weeks, n = 180) were randomly assigned to three groups and corresponding sham control groups: (i) ischaemic cardiomyopathy, (ii) left ventricular hypertrophy (LVH), and (iii) dilated cardiomyopathy. At 12 weeks after operation, atrial fibrillation (AF) inducibility and duration were assessed by in vivo burst transoesophageal pacing. Using the Langendorff apparatus, left ventricular (LV) function and pressure were measured. The expression of connexin-43 (Cx43) and alpha-smooth muscle actin (α-SMA) in atrial tissues was assessed by quantitative real-time polymerase chain reaction and immunohistochemical staining. Fibrosis was analysed by Masson's trichrome staining. Compared with controls, the LA weight/heart weight ratio was increased in the LVH group alone, and was significantly correlated with AF duration (P < 0.001, R = 0.388). Atrial fibrillation inducibility and duration were higher and longer only in the LVH group (P = 0.002, 0.079, respectively), and isolated LV diastolic dysfunction and elevated LV pressure were observed. Although α-SMA expression and fibrosis were increased in all three cardiomyopathy models, down-regulation of Cx43 expression in the LA was observed in the LVH group alone. Conclusion Chronic pressure overload in the absence of LV systolic dysfunction resulted in LA hypertrophy and increased susceptibility to AF, which might be related to conduction abnormality via decreased expression and lateral distribution of Cx43 as well as interstitial fibrosis.

Original languageEnglish
Pages (from-to)655-663
Number of pages9
Issue number4
Publication statusPublished - 2015 Apr 1
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2014 Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014.


  • Atrial fibrillation
  • Connexin
  • Fibroblast
  • Fibrosis
  • Gap junction
  • Hypertrophy
  • Pressure overload
  • Remodelling

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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