Efficacy and safety of oral Chinese patent medicine combined with sacubitril/valsartan in the treatment of chronic heart failure:A Metaanalysis

Objective:To systematically evaluate the clinical efficacy of oral Chinese patent medicine combined with sacubitril/valsartan in treating chronic heart failure(CHF).Methods:CNKI,CSPD,CCD,CBM,PubMed,Web of Science,Cochrane Library and EMbase were retrieved to screen out randomized controlled trials Chinese patent medicine and Western medicine in treating CHF.Manual retrieval was also applied as a supplement.The Cochrane Reviewers Handbook 5.1.0 was used to evaluate the bias risk of the included studies and RevMan 5.4 software was used for Meta-analysis.Results:A total of 1301 patients enrolled in the 13 RCTs were included.According to the results of Meta-analysis,a combination of oral Chinese patent medicine and sacubitril/valsartan could further improve total effectiveness rate(RR=1.23,95%CI[1.16,1.30],P<0.001),increase 6 minutes’walk distance(MD=53.04,95%CI[33.43,72.64],P<0.001),improve left ventricular ejection fraction(MD=6.67,95%CI[5.15,8.19],P<0.001)and stroke volume(MD=7.56,95%CI[3.94,11.18],P<0.001),reduce left ventricular end-diastolic dimension(MD=-3.68,95%CI[-4.57,-2.78],P<0.001)and N terminal pro B type natriuretic peptide(MD=-434.08,95%CI[-518.95,-349.22],P<0.001)and no statistically significant difference in drug safety was found between the sacubitril/valsartan-only group and the combined treatment group(RR=0.73,95%CI[0.32,1.65],P=0.45).Conclusion:It’s indicated that a combination of traditional Chinese patent medicine and sacubitril/valsartan had a good clinical efficacy in the treatment of CHF,which had certain guiding significance for clinical practice.

Effects of Qili Qiangxin capsule on lung structural remodeling in heart failure rats after myocardial infarction and its mechanism

Objective To observe the effect of Qili Qiangxin Capsule(QQC)in improving lung structural remodeling on heart failure(HF)rats after myocardial infarction(MI)and to study its possible mechanism.Methods The proximal left anterior descending branch of coronary artery was ligated using a terylene suture to establish

Mechanism of Qili Qiangxin Capsule for Heart Failure Based on miR133a-Endoplasmic Reticulum Stress

Objective:To investigate the pharmacological mechanism of Qili Qiangxin Capsule(QLQX)improvement of heart failure(HF)based on miR133a-endoplasmic reticulum stress(ERS)pathway.Methods:A left coronary artery ligation-induced HF after myocardial infarction model was used in this study.Rats were randomly assigned to the sham group,the model group,the QLQX group[0.32 g/(kg·d)],and the captopril group[2.25 mg/(kg·d)],15 rats per group,followed by 4 weeks of medication.Cardiac function such as left ventricular ejection fraction(EF),fractional shortening(FS),left ventricular systolic pressure(LVSP),left ventricular end diastolic pressure(LVEDP),the maximal rate of increase of left ventricular pressure(+dp/dt max),and the maximal rate of decrease of left ventricular pressure(–dp/dt max)were monitored by echocardiography and hemodynamics.Hematoxylin and eosin(HE)and Masson stainings were used to visualize pathological changes in myocardial tissue.The m RNA expression of mi R133a,glucose-regulated protein78(GRP78),inositol-requiring enzyme 1(IRE1),activating transcription factor 6(ATF6),X-box binding protein1(XBP1),C/EBP homologous protein(CHOP)and Caspase 12 were detected by RT-PCR.The protein expression of GRP78,p-IRE1/IRE1ratio,cleaved-ATF6,XBP1-s(the spliced form of XBP1),CHOP and Caspase 12 were detected by Western blot.Td T-mediated d UTP nick-end labeling(TUNEL)staining was used to detect the rate of apoptosis.Results:QLQX significantly improved cardiac function as evidenced by increased EF,FS,LVSP,+dp/dt max,-dp/dt max,and decreased LVEDP(P<0.05,P<0.01).HE staining showed that QLQX ameliorated cardiac pathologic damage to some extent.Masson staining indicated that QLQX significantly reduced collagen volume fraction in myocardial tissue(P<0.01).Results from RT-PCR and Western blot showed that QLQX significantly increased the expression of mi R133a and inhibited the m RNA expressions of GRP78,IRE1,ATF6 and XBP1,as well as decreased the protein expressions of GRP78,cleaved-ATF6 and XBP1-s and decreased p-IRE1/IRE1 ratio(P<0.05,P<0.01).Further studies showed that QLQX significantly reduced the expression of CHOP and Caspase12,resulting in a significant reduction in apoptosis rate(P<0.05,P<0.01).Conclusion:The pharmacological mechanism of QLQX in improving HF is partly attributed to its regulatory effect on the mi R133a-IRE1/XBP1 pathway.