Key result
Atorvastatin attenuated atrial fibrillation in a goat model of aseptic pericarditis by inhibiting inflammation, prolonging the effective refractory period, and reducing the duration of atrial fibrillation.
Why the study?
Does atorvastatin reduce inflammation and attenuate atrial fibrillation in a goat model of aseptic pericarditis?
Does atorvastatin reduce inflammation and attenuate atrial fibrillation in a goat model of aseptic pericarditis?
In a goat model of aseptic pericarditis, atorvastatin attenuated atrial fibrillation by inhibiting inflammation, suggesting a potential role in preventing postoperative AF.
Atorvastatin attenuated AF in this goat model; leaves open translation to human postoperative AF prevention.
The present study was designed to determine the association between atrial fibrillation (AF) and inflammation in a goat sterile pericarditis model and to assess the effect of atorvastatin, a cholesterol‑reducing drug, on AF. A total of 15 adult male goats were randomly divided into control, untreated pericarditis and atorvastatin‑treated pericarditis groups. Pericarditis was induced via thoracotomy and atorvastatin was administered orally (60 mg/day) to the goats in the latter group for the duration of the study, commencing 1 week prior to surgery. The levels of high‑sensitivity C‑reactive protein (hs‑CRP), interleukin(IL)‑6 and tumor necrosis factor‑α (TNF‑α) were significantly elevated following surgery in the untreated pericarditis and atorvastatin groups compared with the control group (P<0.05). However, lower levels of hs‑CRP, IL‑6 and TNF‑α were observed in the atorvastatin group compared with the untreated pericarditis group (P<0.05). Additionally, the animals in the atorvastatin‑treated pericarditis group had a longer effective refractory period (ERP) and a higher rate adaptation of the ERP compared with those in the untreated pericarditis group (P<0.05). There was a significant negative correlation between the levels of ERP and hs‑CRP in the untreated pericarditis group. The inducibility of AF in the left atrium and the duration of AF in the untreated pericarditis and atorvastatin‑treated groups increased significantly following surgery (P<0.05). The pericarditis group, however, had a longer duration of AF compared with the atorvastatin group (P<0.05). Thus, inflammation may promote AF by shortening atrial ERP and by reducing the rate adaptation of ERP. These results suggested that atorvastatin can attenuate AF by inhibiting inflammation and may assist in preventing the occurrence and recurrence of AF following cardiac surgery.
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Zhang et al. (2014) studied Atrial fibrillation and aseptic pericarditis (n=15). Atorvastatin vs. Untreated pericarditis was evaluated on Left atrial effective refractory period (ERP) at 72 hours post-surgery (BCL 500 ms) (p=<0.05). Atorvastatin attenuated atrial fibrillation in a goat model of aseptic pericarditis by inhibiting inflammation, prolonging the effective refractory period, and reducing the duration of atrial fibrillation.
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