The Effects Of Statins On Autonomic Nervous Function In Rats With Atrial Fibrillation And The Related Mechanisms

Objective: To assess the effect of statins on autonomic nervous function in rats with atrial fibrillation (AF). Methods: 45 SD rats were randomly and equally assigned into control, AF model, and statin treatment groups. The atrial effective refractory period (AERP) was measured using the S1S2 pre-procedure stimulation method, and the AF induction rate was also measured. Heart rhythm variation analysis software was used to reveal the autonomic nervous function. Western blot was adopted to analyze the expressions of tyrosine hydroxylase (TH) and choline acetyl transferase (CHAT) in atrial tissues. ELISA was employed to quantify the expression of the inflammatory cytokines, including transformation growth factor-beta 1 (TGF-beta 1), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP). Results: The expression of nuclear factor-kappa B (NF-kappa B). The AF rats had a shortened AERP and a higher AF induction rate. The autonomic nervous function indexes including SDNN, SDANN, RMSSD, and the SDNNindx were decreased in the AF group, had a higher low frequency (LF)/high frequency (HF) ratio and an enhanced TH but a decreased CHAT expression, and TGF-beta 1, TNF-alpha, CRP, and NF-kappa B were upregulated (P<0.05 compared to the control group). The statin group had an elongated AERP, decreased AF induction, higher SDNN, SDANN, RMSSD and SDNNindx, a decreased LF/HF, lower TH expression but higher CHAT, and TGF-beta 1, TNF-alpha, CRP, and NF-kappa B were downregulated (P<0.05 compared to the AF group). Conclusion: Statin drugs can suppress inflammation to improve the AF condition via suppressing the expression and function of cardiac autonomic nerves.