Disorganization of gap junction distribution in dilated atria of patients with chronic atrial fibrillation

Susumu Takeuchi, Toshiaki Akita, Yoshiko Takagishi, Eiichi Watanabe, Chieko Sasano, Haruo Honjo, Itsuo Kodama

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Background: Atrial fibrillation (AF) is an arrhythmia associated with functional and morphological remodeling of atria. We investigated the distribution and the expression of connexins in atrial tissues from patients with chronic AF and left atrial dilatation (AD). Methods and Results: Immunohistochemistry was performed in atrial tissues obtained during cardiac surgery from patients with chronic AF+AD (n=11), sinus rhythm (SR, n=11) and SR+AD (n=4). In SR patients (control), the connexin (Cx) 43 labeling of the intercalated disks seen en-face was characterized by small central spots surrounded by larger spots at the periphery. In the left atria from AF+AD patients, the area of the intercalated disk was significantly enlarged. Although peripheral Cx43 labeling was preserved, there was a striking loss of central labeling spots. The area occupied by gap junctions was slightly but significantly larger than that of the control. The left atria from patients with SR+AD showed gap junction disorganization analogous to AF+AD. The labeling patterns of Cx40 were essentially similar to those of Cx43. Conclusions In chronic AF with AD, gap junctions at the intercalated disk are disorganized, resulting most likely from AD but not from AF itself. This gap junction remodeling might be involved in altered atrial conduction properties, but its potential arrhythmogenic role remains unclear.

Original languageEnglish
Pages (from-to)575-582
Number of pages8
JournalCirculation Journal
Volume70
Issue number5
DOIs
Publication statusPublished - 04-05-2006

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Gap Junctions
Atrial Fibrillation
Dilatation
Connexin 43
Heart Atria
Atrial Remodeling
Connexins
Thoracic Surgery
Cardiac Arrhythmias
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Takeuchi, Susumu ; Akita, Toshiaki ; Takagishi, Yoshiko ; Watanabe, Eiichi ; Sasano, Chieko ; Honjo, Haruo ; Kodama, Itsuo. / Disorganization of gap junction distribution in dilated atria of patients with chronic atrial fibrillation. In: Circulation Journal. 2006 ; Vol. 70, No. 5. pp. 575-582.
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Disorganization of gap junction distribution in dilated atria of patients with chronic atrial fibrillation. / Takeuchi, Susumu; Akita, Toshiaki; Takagishi, Yoshiko; Watanabe, Eiichi; Sasano, Chieko; Honjo, Haruo; Kodama, Itsuo.

In: Circulation Journal, Vol. 70, No. 5, 04.05.2006, p. 575-582.

Research output: Contribution to journalArticle

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AU - Takeuchi, Susumu

AU - Akita, Toshiaki

AU - Takagishi, Yoshiko

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AU - Sasano, Chieko

AU - Honjo, Haruo

AU - Kodama, Itsuo

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N2 - Background: Atrial fibrillation (AF) is an arrhythmia associated with functional and morphological remodeling of atria. We investigated the distribution and the expression of connexins in atrial tissues from patients with chronic AF and left atrial dilatation (AD). Methods and Results: Immunohistochemistry was performed in atrial tissues obtained during cardiac surgery from patients with chronic AF+AD (n=11), sinus rhythm (SR, n=11) and SR+AD (n=4). In SR patients (control), the connexin (Cx) 43 labeling of the intercalated disks seen en-face was characterized by small central spots surrounded by larger spots at the periphery. In the left atria from AF+AD patients, the area of the intercalated disk was significantly enlarged. Although peripheral Cx43 labeling was preserved, there was a striking loss of central labeling spots. The area occupied by gap junctions was slightly but significantly larger than that of the control. The left atria from patients with SR+AD showed gap junction disorganization analogous to AF+AD. The labeling patterns of Cx40 were essentially similar to those of Cx43. Conclusions In chronic AF with AD, gap junctions at the intercalated disk are disorganized, resulting most likely from AD but not from AF itself. This gap junction remodeling might be involved in altered atrial conduction properties, but its potential arrhythmogenic role remains unclear.

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