Effect of atorvastatin applied to atrial tachypacing rabbits on electrical remodeling / 中国病理生理杂志

ABSTRACT

AAIM:To investigate the effect of atorvastatin ( ATO) on electrical remodeling, atrial ion channel protein expression and cardiac function in atrial tachypacing rabbits, and to explore the potential electrical mechanism of ATO in the prevention of atrial fibrillation.METHODS:The rabbits were subjected to atrial tachypacing at 600 min-1 in the absence or presence of treatment with atorvastatin (ATP and ATO groups) for 48 h, and the other 10 as sham group without pacing ( NP group) .The tachypacing model was performed by attaching pacing and testing electrodes to left atrial and connecting with custom animal cardiac pacemaker in the open-chest situation.The animals in ATO group were pretrea-ted with ATO for 7 d and continued during tachypacing.Serial atrial effective refractory period ( AERP) was measured in each rabbit at baseline, 8 h, 16 h, 24 h, 32 h, 40 h and 48 h with different cycle lengths.The changes of cardiac func-tions and cardiac structure were observed by cardiac ultrasonic cardiogram before and after atrial tachypacing.The expres-sion of atrial ion channel proteins CaLα1 and Kv4.3 was detected by Western blotting.RESULTS:Compared with NP group, AERP at cycle lengths of 150 and 200 ms, the adaption of AERP, and the levels of CaLα1 and Kv4.3 expression were all decreased in ATP and ATO group, especially in ATP group.Left atrial dimension ( LAD) was increased in pacing groups as compared with NP group (P<0.05) after pacing delivery for 48 h, while no difference between the formers was observed.No significant change of the left ventricular dimension ( LVD) and ejection fraction ( LVEF) among groups be-fore and after pacing was found.CONCLUSION:Atrial tachypacing significantly shorten AERP, resulting in poor adap-tion of AERP, while ATO pretreatment significantly attenuates the atrial electrical remodeling in rabbits, but had no effect on cardiac structure.ATO suppresses the down-regulation of atrial ion channel proteins CaLα1 and Kv4.3 expression after 48 h, which may be the potential ionic mechanism of atrial electrical remodeling for ATO.