Effects of rosuvastatin on atrial nerve sprouting and electrical remodeling in rabbits with myocardial infarction

This study is to investigate the effect of rosuvastatin on atrial nerve sprouting and electrical remodeling after myocardial infarction (MI).

Rabbit MI model was established by anterior descending branch ligation. These models were divided into the sham (n = 9), MI model (n = 7), and rosuvastatin intervention (n = 8) groups. Immunohistochemistry was used to detect the autonomic atrial nerve distribution. Real-time PCR and Western blot analysis were performed to evaluate the mRNA and protein expression levels, respectively.

Our results from immunohistochemistry showed that, compared with the sham group, the densities of tyrosine hydroxylase (TH)- and choline acetyltransferase (CHAT)-positive nerve fibers were significantly elevated in the MI model group. However, TH- and CHAT-positive nerve fibers were significantly decreased by rosuvastatin treatment, suggesting that rosuvastatin could reduce autonomic nerve sprouting in acute MI. Moreover, rosuvastatin decreased the mRNA and protein expression levels of TH in atrial tissues following MI. Compared with the sham group, the mRNA expression level of KCND3 was significantly down-regulated in the MI model group. And, this down-regulation was restored by rosuvastatin treatment. These results suggested that rosuvastatin could inhibit the electrical remodeling in atrium after acute MI.

Atrial nerve sprouting and electrical remodeling occur following MI, which could be suppressed by rosuvastatin treatment. Our findings provide insights into the understanding of the mechanism through which statins decrease the risk of atrium arrhythmia after MI.