关键词: 心肌梗死, 房颤, 利拉鲁肽, 心肌电活动

Abstract: Objective To investigate the effects of liraglutide on myocardial inflammation and cardiac function in rats with acute myocardial infarction (AMI), and to further explore its effects on susceptibility to atrial fibrillation and the underlying mechanisms. Methods The rats were divided into the sham operation group (sham group), the AMI group(using the method of coronary arteryligation), and the liraglutide group (AMI+LIR group). Rats in the AMI + LIR group were intraperitoneally injected with liraglutide at a dose of 250 μg/ (kg·d).The sham group and the AMI group were injected with an equal amount of normal saline. Four weeks later, echocardiography was used to evaluate the cardiac structure and function of the rats; electrocardiogram was collected and electrophysiological detection was performed to evaluate the susceptibility to atrial fibrillation; HE staining and Masson staining were used to detect the morphology of myocardial cells and the degree of myocardial fibrosis; the enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18); Western blot was used to detect the protein expressions of NLRP3, Caspase-1, and GSDMD in the myocardial tissues. Results Compared with the sham group, the degree of myocardial fibrosis and the infiltration of inflammatory cells in the myocardial tissue of the rats in the AMI group increased significantly; the left atrial diameter (LAD), the left ventricular posterior wall thickness after diastole (LVPWd), and the left ventricular end-diastolic diameter (LVEDd) were significantly increased, while the left ventricular fractional shortening (FS) and the left ventricular ejection fraction (LVEF) were significantly decreased (P＜0.05); The P-wave duration (PWD), PR interval (PRI), and maximum absolute fibrillation duration (MAFD) increased, while the atrial effective refractory period (AERP)was decreased; the levels of inflammatory factors IL-6, IL-18, IL-1β and the protein expressions of NLRP3, Caspase-1, and GSDMD were significantly increased (P＜0.05). Compared with the AMI group, the myocardial fibrosis and inflammatory infiltration in the AMI+LIR group were improved; the LAD, LVPWd, and LVEDd were significantly decreased, while the FS and LVEF were significantly increased; the levels of inflammatory factors IL-6, IL-18, IL-1β and the protein expressions of NLRP3, Caspase-1, and GSDMD were significantly decreased(P＜0.05). Conclusions Liraglutide can reduce myocardial fibrosis and inflammation, improve cardiac function, and decrease the susceptibility to atrial fibrillation in rats with AMI.

Key words: myocardial infarction, atrial fibrillation, liraglutide, myocardial electrical activity