益气复脉注射液联合左西孟旦治疗慢性心力衰竭的效果及对miR-30a、miR-101a表达的影响

Effect of Yiqi Fumai injection combined with levosimendan in the treatment of chronic heart failure and its influences on the expression of miR-30a and miR-101a

目的分析益气复脉注射液联合左西孟旦治疗慢性心力衰竭的效果及对miR-30a、miR-101a表达的影响。方法选取2021年6月至2022年6月收治的80例慢性心力衰竭患者为研究对象,以随机数字表法将其分为对照组(n=40,左西孟旦)和观察组(n=40,益气复脉注射液联合左西孟旦)。比较两组的治疗效果。结果观察组的治疗总有效率高于对照组(P<0.05)。治疗后,观察组的N-末端前脑钠肽(NT-proBNP)、游离脂肪酸(FFA)、激活素A(ACT-A)水平低于对照组(P<0.05)。治疗后,观察组的层粘连蛋白(LN)、透明质酸(HA)以及Ⅲ型前胶原(PCⅢ)水平低于对照组(P<0.05)。治疗后,观察组的miR-30a表达水平低于对照组,miR-101a表达水平高于对照组(P<0.05)。结论益气复脉注射液联合左西孟旦治疗慢性心力衰竭能提高治疗效果,促进心肌损害标志物、心肌纤维化指标水平降低,调节miR-30a、miR-101a表达水平。

Objective To analyze the effect of Yiqi Fumai injection combined with levosimendan in the treatment of chronic heart failure and its influences on the expression of miR-30a and miR-101a.Methods A total of 80 patients with chronic heart failure admitted from June 2021 to June 2022 were selected as the research objects,and the patients were divided into control group(n=40,levosimendan)and observation group(n=40,Yiqi Fumai injection combined with levosimendan)by random number table method.The therapeutic effects of the two groups were compared.Results The total effective rate of treatment in the observation group was higher than that in the control group(P<0.05).After treatment,the levels of N-terminal pro-brain natriuretic peptide(NT-proBNP),free fatty acid(FFA)and activin A(ACT-A)in the observation group were lower than those in the control group(P<0.05).After treatment,the levels of laminin(LN),hyaluronic acid(HA)and procollagenⅢ(PCⅢ)in the observation group were lower than those in the control group(P<0.05).After treatment,the expression level of miR-30a in the observation group was lower than that in the control group,and the expression level of miR-101a was higher than that in the control group(P<0.05).Conclusion Yiqi Fumai injection combined with levosimendan in the treatment of chronic heart failure can improve the therapeutic effect,promote the decrease of myocardial damage markers and myocardial fibrosis indexes,and regulate the expression levels of miR-30a and miR-101a.