Objective      To evaluate the effects of atrial fibrosis on atrial remodeling and inflammation in an atrial fibrillation (AF) canine model.       Methods      We studied 30 canines

randomly divided into 3 groups: group A (n=6)

group B (n=12) and group C (n=12). A pacemaker was implanted in group A

and provided atrial tachypacing (ATP) for 8 weeks. Group B received ATP and atrial structural remodeling. Besides ATP and left atrial injection

oral hydronidone was administ

ered for the pacing period in group C. We performed C-reactive protein (CRP)

tumor necrosis factor-α (TNF-α)

and interleukin-6 (IL-6) expression detection

echocardiography

AF vulnerability study and atrial fibrosis measurement at baseline

and 4 and 8 weeks after ATP.       Results      Compared to group A

group B showed significant elevation in collagen volume fraction

left atrial diameters

AF duration and percent of burst attempts leading to AF episodes. There was no significant difference between group C and group A. The elevation of CRP in group B was greater than that in group A in 4 weeks after ATP (434.99±135.26 vs 346.67±81.09 ng/mL

P

0.05). Eight weeks after ATP

group B had more significant increases in CRP

IL-6 and TNF-α than other groups. There was no significant difference between group A and group C in any inflammatory factor. The inflammatory factor levels had positive associations with left atrial diameter and collagen volume fraction.       Conclusion      Atrial fibrosis contributes to atrial remodeling and elevation in inflammation

whereas hydronidone attenuates such effects

implicating that hydronidone may play an important role in the management of AF.