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.
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 + ADpatients, 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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