Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. The most significant histological property of AF is atrial fibrosis, but the underlying mechanism is not clear. In this study we investigated the expression of miR-133 and miR-30, anti-fibrotic microRNAs (miRNAs), in chronic AF in canines. A total amount of 42 mongrel canines of either gender, weighing between 20 and 28 kg, were randomly assigned to the sham-operated and AF groups. All canines were subjected to weekly physical examinations and electrocardiogram. Alterations in tissue structure were assessed in atrial tissue samples by using hematoxylin and eosin and Masson's trichrome. The expression of miR-133 and miR-30 was determined by TaqMan real-time polymerase chain reaction (RT-PCR) and northern blot analyses of atrial tissue. The data were analyzed using the program SPSS 11.5 for Windows. At follow-up, rapid pacing from the left superior pulmonary vein induced sustained AF in the AF group. In the left atrium, increased interstitial fibrosis and chronic inflammation were observed. RT-PCR and northern blot analyses showed that miR-133 and miR-30 expression was downregulated in the AF group. Our results show that both miR-133 and miR-30 play an important role in controling structural changes in chronic AF.

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