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The remodeling of gap junctions may affect their conduction properties and contribute to the maintenance of atrial fibrillation. The significance of the role of angiotensin-II receptor blockers (ARBs) in upstream therapy is not clear. This study was performed to investigate the effects of ARBs on atrial remodeling in a heart failure model. A model of heart failure was established or sham surgery performed in 24 Sprague-Dawley male rats. The rats were divided into sham, heart failure and heart failure-ARB groups. In the ARB group, 30 mg/kg of losartan was administered each day for 4 weeks. Echocardiography was performed at the baseline and 4 weeks following the surgery. An atrial fibrillation induction study and histological and immunohistochemical evaluation were performed 4 weeks after surgery. The increase in the left atrial diameter of the heart failure-ARB group was smaller than that of the heart failure group (P=0.028). The atrial fibrillation inducibility and duration of induced atrial fibrillation were not different between the heart failure and heart failure-ARB groups. Masson's trichrome staining revealed less fibrosis in the heart failure-ARB group compared with the heart failure group. Immunohistochemical staining and western blot analysis for connexin 43 showed a lower expression level in the heart failure-ARB group compared with that in the heart failure group. In a rat model of ischemic heart failure the ARB losartan had structural and histological atrial reverse-remodeling effects. However, its role as an electrical stabilizer requires further study.

Beneficial effects of an angiotensin-II receptor blocker on structural atrial reverse-remodeling in a rat model of ischemic heart failure