Key result
Rosuvastatin prolonged the atrial effective refractory period, reduced the inducibility of atrial fibrillation, and reversed atrial autonomic neural remodeling in rabbits (P < 0.05).
Why the study?
Does rosuvastatin reduce atrial fibrillation inducibility and autonomic neural remodeling in rabbits with rapid-pacing-induced AF?
RCT (n=30)
randomly divided
Does rosuvastatin reduce atrial fibrillation inducibility and autonomic neural remodeling in rabbits with rapid-pacing-induced AF?
In a rabbit model of rapid-pacing-induced AF, rosuvastatin reduced AF inducibility and reversed atrial autonomic neural remodeling.
Rosuvastatin attenuates pacing-induced ANR and AF inducibility in rabbits; leaves open translation to human AF prevention.
BACKGROUND: The study aimed to observe the effects of pacing on the atrial effective refractory period (AERP), inducibility of atrial fibrillation (AF), and changes of atrial autonomic neural remodeling (ANR) by rosuvastatin intervention on the acute model of rapid-pacing-induced AF. METHODS: Thirty rabbits were randomly divided into a control group (C, n = 10), rapid-pacing group (P, n = 10), and rosuvastatin-intervention group (R, n = 10). AERP and inducibility of AF were measured for all groups. The sympathetic and parasympathetic nerves of left atrium, right atrium, and atrial septum labeled with tyrosine hydroxylase (TH) and choline acetyl transferase (ChAT) were detected by immunohistochemistry and Western blot. RESULTS: The AERP in group R was prolonged, and AF could not be induced as easily (P < 0.05). Immunohistochemistry showed that the densities and heterogeneity of TH and ChAT positive nerves of the atrium in group P were significantly higher than those in group C (ranked as right atrium > atrial septum > left atrium), whereas those in group R were decreased (P < 0.05). Western blot showed that TH and ChAT protein expression in group P was significantly increased compared with group C, but decreased in group R (P < 0.05). CONCLUSIONS: Persistent rapid atrial pacing can lead to heterogeneous ANR in different parts of the rabbit atrium and may cause AF, which can be reversed by rosuvastatin. The inhibitory function of rosuvastatin may be associated with its role in reversing atrial ANR.
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Zhang et al. (2016) conducted an RCT in experimental atrial fibrillation (n=30). Rosuvastatin vs. Control group and rapid-pacing group was evaluated on Atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) (p=<0.05). Rosuvastatin prolonged the atrial effective refractory period, reduced the inducibility of atrial fibrillation, and reversed atrial autonomic neural remodeling in rabbits (P < 0.05).
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