Meta analysis of the efficacy of western medicine combined with Qiliqiangxin capsule versus western medicine alone in the treatment of chronic heart failure

Objective: To compare the clinical efficacy of conventional Western medicine combined with Qiliqiangxin capsule and western medicine alone in the treatment of chronic heart failure, and to prove that Qiliqiangxin capsule combined treatment has more advantages, providing reference for clinical decision-making in the treatment of chronic heart failure. Methods: Randomized controlled trials (RCTs) of conventional Western medicine treatment and Western medicine combined with Qiliqiangxin capsule in the treatment of chronic heart failure were searched in databases such as PubMed, Embase, Webofscience, CNKI, WanFang, VIP, and CBM. The bias risk assessment was conducted using the RCT tool recommended by Cochrane, and then the meta-analysis was performed using RevMan5.4 and Stata17 software. Compare the efficacy evaluation of cardiac function, left ventricular ejection fraction (LVEF), left ventricular end diastolic diameter (LVEDD), cardiac stroke output (SV), 6-minute walking test (6MWT), and N-terminal proBNP in the conventional western medicine combined with Qiliqiangxin capsule group (hereinafter referred to as the treatment group) and the conventional western medicine group (hereinafter referred to as the control group). Results: A total of 20 RCTs meeting the criteria were included, including 2953 patients, including 1508 in the treatment group and 1445 in the control group. The results of meta-analysis showed that the treatment group had significantly better cardiac function evaluation, LVEF, LVEDD, SV, 6MWT, and NT-proBNP improvement than the control group. Its central functional efficacy evaluation (OR=2.09,95% CI: 1.71-2.55, P<0.001), LVEF (WMD=7.05,95% CI: 5.30-8.79, P<0.00001), LVEDD (WMD=6.73, 95% CI: 3.18-10.29, P=0.0002), SV (WMD=6.73, 95% CI: 3.18-10.29, P=0.0002), 6MWT (SMD=0.70,95% CI: 0.54-0.87, P<0.00001), NT-proBNP (SMD=-1.95,95% CI: -2.5 2 to 1.38 (P<0.0001), with statistically significant differences. Conclusion: Conventional western medicine combined with Qiliqiangxin capsule can significantly improve the clinical efficacy of heart failure, improve LVEF, LVEDD, SV, and NT-proBNP index, and improve exercise tolerance. It is worth using for reference in the treatment.

Mechanism of Qiliqiangxin capsule on the regulation of IP3Rs/GRP75/VDAC1 gene in myocardial infarction rat heart

Objective:To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca^(2+)related genes in rats with myocardial infarction(MI).Methods:The rat model of MI was established by ligation of the left anterior descending coronary artery.After operation,the rats were randomly assigned to the model group,the Qiliqiangxin group and the captopril group;a sham-operated group was also available as a control.After four weeks of treatment,the extent of infarction in rats was observed by gross cardiac structure and the morphological changes of myocardial histopathology were observed by HE staining.Detection of mitochondrial Ca^(2+)transport-related genes such as inositol-1,4,5-trisphosphate receptor 2(IP3R2),glucose regulated protein 75(GRP75),voltage-dependent anion channel 1(VDAC1),and mitofusion 2(Mfn2)and mitochondrial apoptosis-related genes such as B-cell lymphoma-2(Bcl-2)and Bcl-2 related X protein(Bax)mRNA expression changes was measured by RT-PCR in the infarct margins of the heart;Western blot was used to detect changes in Bcl-2,Bax protein expression in myocardial tissue.The rate of apoptosis in cardiac myocardial tissue was detected by TUNEL staining.Results:Compared with the sham group,the anterior left ventricular wall of the model group showed a large area of infarction,and the structure of myocardial tissue was disordered.The mRNA expression level of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly increased(P<0.05,P<0.01);The mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were significantly decreased(P<0.01),while the mRNA and protein expression of Bax were significantly increased(P<0.01);and apoptosis rate was significantly increased(P<0.01).Compared with the model group,the infarct size of cardiac gross specimens in the Qiliqiangxin group and the captopril group was reduced and myocardial fibers were relatively well ordered;The mRNA expression of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly reduced(P<0.01);the mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were increased(P<0.05,P<0.01),and the mRNA and protein expression of Bax were significantly decreased(P<0.05,P<0.01).and apoptosis rate was significantly decreased(P<0.01).Conclusion:Qiliqiangxin Capsule can improve the morphological structure of the heart of rats with MI,and its mechanism is related to regulation of the gene expression of mitochondrial Ca^(2+)transport complex IP3R2/GRP75/VDAC1,thereby inhibiting apoptosis.

Meta-analysis of curative effect of Sacubitril valsartan combined with Qiliqiangxin capsule in the treatment of patients with chronic cardiac failure

Objective:To systematically review the effect of Sacubitril valsartan combined with Qiliqiangxincapsule on clinical effect,serological index,cardiac function,quality of live,and adverse reactions in patients with heart failure.Methods:Search the databases of CNKI,VIP,WanFang,CBM,DuXiu,ChiCTR,Web of science,The Cochrane Library,PubMed and Embase to collect the randomized controlled trial(RCT)of Sacubitril valsartan combined with Qiliqiangxin capsule in the treatment of patients with heart failure,The search time limit is from the establishment of the database to May 2021.After the literatures were screened,evaluated and extracted by two researchers independently,Meta analysis was carried out with Stata 16.1 software.Results:A total of 18 RCTs,were included,including 1613 patients.The results of the Meta-analysis showed that there was statistical significance in improving the effective rate(OR=2.60,95%CI[2.09,3.24],P<0.00001),N-terminal pro-brain natriuretic peptide(MD=-468.36,95%CI[-606.80,-329.92],P<0.00001),left ventricular ejection fraction(MD=5.41,95%CI[4.93,5.89],P<0.00001),left ventricular end-diastolic diameter(MD=-3.27,95%CI[-3.65,-2.90],P<0.00001),left ventricular end-systolic diameter(MD=-3.60,95%CI[-4.99,-2.21],P<0.00001),6-minute walking distance(MD=61.42,95%CI[50.04,72.80],P<0.00001),Minnesota living with heart failure questionnaire(MD=-11.39,95%CI[-14.50,-8.28],P<0.00001),and traditional Chinese medicine syndrome score scale(MD=-3.62,95%CI[-6.45,-0.80],P=0.01),but there was no significant difference in cardiac output(MD=0.26,95%CI[-0.02,0.54],P=0.07)and adverse reactions.Conclusion:The current evidence shows that Sacubitril Valsartan combined with Qiliqiangxin capsule can better improve cardiac function,TCM symptoms and quality of life in patients with heart failure than simple Sacubitril Valsartan.However,there was no significantdifference in improving cardiac output between the two groups.However,higher quality RCTs are needed to verify.

Study on gene regulation mechanism of Qiliqiangxin capsule on myocardial fibrosis in myocardial infarction rats

Objective:To investigate the effect and possible mechanism of Qiliqiangxin capsule on myocardial fibrosis in rats with myocardial infarction(MI).Methods:The rat model of myocardial infarction was established by ligation of anterior descending branch of left coronary artery.The rats were randomly divided into model group,Qiliqiangxin capsule group,captopril group after operation.Rats that without ligation were set as parallel control group,namely,the sham group.Cardiac pathology was observed by hematoxylin eosin(HE)staining after 4 weeks of treatment.Masson staining was used to observe myocardial fibrosis and calculate collagen volume fraction(CVF).The miR-133a and expression levels of transforming growth factor β1(TGF-β1),Smad 2,Smad 3,type Ⅰ collagen(col-Ⅰ),type Ⅲ collagen(col-Ⅲ)mRNA were examined by Real-time PCR.Results:Compared with the sham group,myocardial cells in model group were disordered,CVF was significantly increased(P<0.01),the expression levels of col-Ⅰ,col-ⅢmRNA were increased(P<0.01);besides,the expression level of miR-133a was significantly decreased(P<0.01),the expression levels of TGF-β1,Smad 2 and Smad 3 mRNA were increased(P<0.05,P<0.01).Compared with the model group,the arrangement of myocardial cells in Qiliqiangxin capsule group and captopril group were orderly and CVF was significantly decreased(P<0.05);the expression level of miR-133a was increased(P<0.05,P<0.01);the expression levels of TGF-β1,Smad 2 and Smad 3 mRNA were significantly decreased(P<0.01).Conclusion:Qiliqiangxin capsule can improve myocardial infarction rat myocardial tissue fibrosis,its mechanism may be in related with the regulation on miR-133a/TGF-β1/Smads signal pathway at the genetic level.