[Comparative analysis of clinical effects according to syndrome differentiation of Qili Qiangxin Capsules on ischemic heart failure: Meta-analysis].

Databases including CNKI,Wan Fang,CBM,VIP,PubMed and Cochrane Library were searched to collect qualified researches,and the quality of articles was evaluated according to scales. Meta-analysis including subgroup analysis was performed by using Rev Man 5. 3 software and Meta-regression test was performed by using Stata 12. 0 software. All of these methods were used to systematically evaluate the safety and clinical efficacy of Qili Qiangxin Capsules in treatment of ischemic heart failure under two circumstances( with or without syndrome differentiation). A total of 22 randomized controlled trials( RCTs) involving 1 942 patients were included,with generally low quality. RESULTS: of Meta-analysis showed that as compared with the routine Western treatment alone,additional use of Qili Qiangxin Capsules could improve the clinical efficacy( RR = 1. 21,95%CI[1. 16,1. 27],P<0. 000 01) in treatment of ischemic heart failure,with its combined effect of syndrome differentiation group greater than that of non-syndrome differentiation group( P= 0. 03,I~2= 78. 9%),Meta-regression( sig = 0. 9,P = 0. 057); left ventricular ejection fraction( WMD = 7. 28,95% CI[5. 18,9. 38],P<0. 000 01),with combined effect of syndrome differentiation group greater than that of non-syndrome differentiation group( P= 0. 01,I2= 83. 2%),Meta-regression( I~2= 81. 09%,R2= 29. 08%,sig = 0. 47,P = 0. 029); 6-minute walk test( WMD = 33. 20,95%CI[24. 70,41. 70 ],P < 0. 000 01); left ventricular end diastolic diameter( WMD =-4. 61,95% CI[-5. 38,-3. 84 ],P <0. 000 01); left ventricular end diastolic volume( WMD =-34. 43,95%CI[-38. 81,-30. 05],P< 0. 000 01); and left ventricular end systolic volume( WMD =-9. 60,95% CI[-13. 16,-6. 05],P < 0. 000 01). Adverse effects were reported in 11 patients taking Qili Qiangxin Capsules and in 20 patients with routine treatment group,tolerable in both groups. None of the patients had obvious abnormality in liver and kidney function. Qili Qiangxin Capsules were effective and safe in the treatment of ischemic heart failure,which can further improve clinical efficacy as compared with routine treatment alone. Qili Qiangxin Capsules with syndrome differentiation showed more significant effects than those without syndrome differentiation,indicating better efficacy of clinical syndrome differentiation. However,these conclusions still need to be verified with more high-quality and large-sample literature.

Suxiao Jiuxin pill promotes exosome secretion from mouse cardiac mesenchymal stem cells in vitro.

Cardiac mesenchymal stem cells (C-MSCs) are endogenous cardiac stromal cells that play a role in heart repair after injury. C-MSC-derived exosomes (Exo) have shown protective effects against apoptosis induced by acute myocardial ischemia/reperfusion. Suxiao Jiuxin pill (SJP) is a traditional Chinese medicine (TCM) formula used in China for the treatment of acute myocardial ischemia, which contains tetramethylpyrazine (TMP) and borneol (BOR) as major components. In this study, we investigated whether SJP treatment affected exosome release from C-MSCs in vitro. C-MSCs prepared from mice were treated with SJP (62.5 µg/mL), TMP (25 µg/mL) or BOR (15 µg/mL). Using an acetylcholinesterase activity assay, we found that both SJP and TMP treatment significantly increased exosome secretion compared to the control ethanol treatment. The neutral sphingomyelinase 2 (nSMase2) pathway was important in exosome formation and packaging. But neither the level of nSMase2 mRNA nor the level of protein changed following SJP, TMP or BOR treatment, suggesting that SJP stimulated exosome release via an nSMase2-independent pathway. The Rab27a and Rab27b GTPases controlled different steps of the exosome secretion pathway. We showed that SJP treatment significantly increased the protein levels of Rab27a, SYTL4 (Rab27a effector) and Rab27b compared with the control treatment. SJP treatment also significantly upregulated the mRNA level of Rab27b, rather than Rab27a. Moreover, SJP-induced increase of C-MSC-exosome release was inhibited by Rab27b knockdown, suggesting that SJP promotes exosome secretion from C-MSCs via a GTPase-dependent pathway. This study reveals a novel mechanism for SJP in modulating cardiac homeostasis.

Exosomes from Suxiao Jiuxin pill-treated cardiac mesenchymal stem cells decrease H3K27 demethylase UTX expression in mouse cardiomyocytes in vitro.

Suxiao Jiuxin pill (SJP) is a traditional Chinese medicine for the treatment of acute coronary syndrome in China, which contains two principal components, tetramethylpyrazine (TMP) and borneol (BOR). Thus far, however, the molecular mechanisms underlying the beneficial effects of SJP on the cardiac microenvironment are unknown. Cardiac mesenchymal stem cells (C-MSCs) communicate with cardiomyocytes (CMs) through the release of microvesicles (exosomes) to restore cardiac homeostasis and elicit repair, in part through epigenetic regulatory mechanisms. In this study, we examined whether SJP treatment altered C-MSC-derived exosomes (SJP-Exos) to cause epigenetic chromatic remodeling in recipient CMs. C-MSC isolated from mouse hearts were pretreated with SJP (SJP-Exos), TMP (TMP-Exos) or BOR (BOR-Exos). Then, HL-1 cells, a mouse cardiomyocyte line, were treated with exosomes from control C-MSCs (Ctrl-Exos), SJP-Exos, TMP-Exos or BOR-Exos. Treatment with SJP-Exos significantly increased the protein levels of histone 3 lysine 27 trimethylation (H3K27me3), a key epigenetic chromatin marker for cardiac transcriptional suppression, in the HL-1 cells. To further explore the mechanisms of SJP-Exo-mediated H3K27me3 upregulation, we assessed the mRNA expression levels of key histone methylases (EZH1, EZH2 and EED) and demethylases (JMJD3 and UTX) in the exosome-treated HL-1 cells. Treatment with SJP-Exo selectively suppressed UTX expression in the recipient HL-1 cells. Furthermore, PCNA, an endogenous marker of cell replication, was significantly higher in SJP-Exo-treated HL-1 cells than in Ctrl-Exo-treated HL-1 cells. These results show that SJP-Exos increase cardiomyocyte proliferation and demonstrate that SJP can modulate C-MSC-derived exosomes to cause epigenetic chromatin remodeling in recipient cardiomyocytes; consequently, SJP-Exos might be used to promote cardiomyocyte proliferation.

Bornyl acetate: A promising agent in phytomedicine for inflammation and immune modulation.

BACKGROUND: Bornyl acetate (BA), as a bicyclic monoterpene, is an active volatile component widely found in plants across the globe. BA can be used as essence and food flavor agent and is widely used in perfumes and food additives. It remains a key component in several proprietary Chinese medicines. PURPOSE: This review summarized the pharmacological activity and research prospects of BA, making it the first of its kind to do so. Our aim is to provide a valuable resource for those pursuing research on BA. METHODS: Databases including PubMed, Web of Science, and CNKI were used based on search formula "(bornyl acetate) NOT (review)" from 1967 to 2022. For the relevant knowledge of TCM, we quoted Chinese literature. Articles related to agriculture, industry, and economics were excluded. RESULTS: BA showed rich pharmacological activities: It inhibits the NF-κB signal pathway via affecting the phosphorylation of IKB and the production of IKKs, inhibits the MAPK signal pathway via inhibiting the phosphorylation of ERK, JNK, and p38, down-regulates pro-inflammatory cytokines such as TNF-α, IL-1ß, IL-6, up-regulates IL-11, reduces NO production, regulates immune response via up-regulating CD86+, decreases catecholamine secretion, and reduces tau protein phosphorylation. In addition to the pharmacological activities of BA, its toxicity and pharmacokinetics were also discussed in this paper. CONCLUSION: BA has promising pharmacological properties, especially anti-inflammatory and immunomodulatory effects. It also has sedative properties and potential for use in aromatherapy. Compared to traditional NSAIDs, it has a more favorable safety profile while maintaining efficacy. BA has potential for developing novel drugs for treating various conditions.

Single-nucleus ribonucleic acid-sequencing and spatial transcriptomics reveal the cardioprotection of Shexiang Baoxin Pill (SBP) in mice with myocardial ischemia-reperfusion injury.

Aim: The Shexiang Baoxin Pill (SBP) has been extensively used to treat cardiovascular diseases in China for four decades, and its clinical efficacy has been widely approved. However, the mechanism by which this is achieved remains largely unexplored. Research attempting to understand the underlying mechanism is ongoing, but the findings are controversial. Here, we aimed to explore the possible mechanism of SBP in myocardial ischemia-reperfusion (I/R) injury using heart single-nucleus and spatial ribonucleic acid (RNA) sequencing. Methods: We established a murine myocardial I/R injury model in C57BL/6 mice by ligating and recanalizing the left coronary artery anterior descending branch. Subsequently, single-nucleus RNA-seq and spatial transcriptomics were performed on mice cardiac tissue. We initially assessed the status of cell types and subsets in the model administered with or without SBP. Results: We used single-nucleus RNA sequencing to comprehensively analyze cell types in the cardiac tissue of sham, I/R, and SBP mice. Nine samples from nine individuals were analyzed, and 75,546 cells were obtained. We classified the cells into 28 clusters based on their expression characteristics and annotated them into seven cell types: cardiomyocytes, endothelial cells, fibroblasts, myeloid cells, smooth muscle cells, B cells, and T cells. The SBP group had distinct cellular compositions and features than the I/R group. Furthermore, SBP-induced cardioprotection against I/R was associated with enhanced cardiac contractility, reduced endocardial cell injury, increased endocardial-mediated angiogenesis, and inhibited fibroblast proliferation. In addition, macrophages had active properties. Conclusion: SBP improves the early LVEF of I/R mice and has a cardioprotective effect. Through sequencing analysis, we observed that SBP can increase the gene expression of Nppb and Npr3 in the infarct area of the heart. Npr3 is related to vascular generation mediated by endocardial cells and requires further research. In addition, SBP increases the number of fibroblasts, inhibits the expression of genes related to fibroblast activation and proliferation, and increases the transformation of endothelial cells into fibroblasts. These findings will help to indicate directions for further research.

Nomogram based on multimodal echocardiography for assessing the evolution of diabetic cardiomyopathy in diabetic patients with normal cardiac function.

Background: Diabetic cardiomyopathy (DCM) remains asymptomatic for many years until progression to asymptomatic left ventricular diastolic dysfunction (ALVDD), a subclinical cardiac abnormality present in early-stage DCM. Because LV function in patients with type 2 diabetes mellitus (T2DM) may be subtly altered long before the onset of ALVDD, quantitative assessment of the risk of progression to early-stage DCM in T2DM patients with normal hearts is critical for delaying or even reversing DCM. Objective: This study aimed to establish a nomogram with the aid of DCM characteristics revealed by multimodal echocardiography to assess the likelihood of the progression to early-stage DCM in T2DM patients with normal cardiac function. Methods: Of the 423 T2DM patients enrolled, 302 were included in the training cohort and 121 in the validation cohort. The clinical characteristics, biochemical data, and multimodal echocardiographic parameters were collected. In the training cohort, the screened correlates of ALVDD were utilized to develop a nomogram for estimating the risk coefficient for early-stage DCM. This model was validated both in the training and validation cohorts. Results: ALVDD was independently correlated with the number of comorbidities [with one comorbidity: odds ratio (OR) = 3.009; with two comorbidities: OR = 4.026], HbA1c (OR = 1.773), myocardial blood flow (OR = 0.841), and global longitudinal strain (OR = 0.856) (all P < 0.05). They constituted a nomogram to visualize the likelihood of DCM development in T2DM patients with normal cardiac function. The model was validated to present strong discrimination and calibration, and obtained clinical net benefits both in the training and validation cohorts. Conclusion: We constructed and validated a nomogram to estimate the likelihood of developing early-stage DCM in T2DM patients with normal cardiac function. The alteration of the nomogram-predicted risk coefficient is expected to be proposed as a therapeutic target to slow or stop DCM progression.

Efficacy and safety of Suxiao Jiuxin Pill in the treatment of stable angina (Qi stagnation and blood stasis syndrome): study protocol of a randomized, double-blind, placebo-controlled, multi-center clinical trial.

BACKGROUND: Coronary heart disease (CHD) has become one of the biggest health problems in the world. Stable angina is a common clinical type of CHD with poor prognosis and high mortality. Although there are various interventions for stable angina, none of them can significantly reduce mortality. Both basic and clinical research have shown that Suxiao Jiuxin Pill (SJP) can relieve the symptoms of angina pectoris and improve the clinical efficacy, but there is a lack of high-quality clinical research to provide research-based evidence. We design a randomized, double-blind, placebo-controlled trial to evaluate the efficacy of SJP for stable angina. METHODS/DESIGN: This is a prospective, randomized, double-blind, placebo-controlled, and multicenter trial. The trial will enroll 324 participants with chronic stable angina (Qi Stagnation and Blood Stasis syndrome). All participants will have received the conventional therapy of chronic stable angina. Participants will be randomized into two groups, conventional therapy plus SJP group and conventional therapy plus placebo group. Eligible participants will receive either SJP or placebo (five pills administered orally, three times daily) in addition to conventional treatment for 24 weeks. The primary outcomes are the symptom improvement rate of angina from baseline to 4 weeks after inclusion and major adverse cardiovascular events (MACE). The secondary outcomes are angina classification (CCS), improvement of traditional Chinese medicine (TCM) syndromes, Seattle Angina Scale score, the dosage of emergency drugs and the stopping rate, and electrocardiogram (EKG) efficacy. Adverse events will be monitored throughout the trial. DISCUSSION: Integrated traditional Chinese and Western Medicine is commonly used for angina in China. This study will evaluate the clinical effectiveness and safety of SJP for angina. The results of the trial will provide high-level clinical research-based evidence for the application of SJP instable angina. TRIAL REGISTRATION: This study protocol was registered on 14 March 2019. The registration number is ChiCTR1900021876 on the Chinese Clinical Trial Registry.

Efficacy and safety of Qi-Jing Hui-Xin Decoction in the treatment of coronary microvascular angina: study protocol for a randomized, controlled, multi-center clinical trial.

BACKGROUND: With the increased understanding of heart disease, microvascular angina (MVA) is receiving greater attention from clinicians. Studies have shown that patients with MVA have significantly higher major cardiovascular events and all-cause mortality than the control population, and the search for effective treatments is of great clinical importance. Both basic and clinical studies have shown that Qi-Jing Hui-Xin Decoction (QJHX) can relieve angina symptoms and improve clinical efficacy, but there is a lack of high-quality clinical studies to provide a research basis. This article introduces the evaluation protocol of QJHX for the adjunctive treatment of MVA. METHODS/DESIGN: This is a prospective randomized controlled trial. The trial will enroll 150 patients with MVA. On the basis of Western drug treatment, patients will be randomized into two groups, and the experimental group will receive QJHX treatment for 12 weeks and follow-up at 24 week. The primary indicators are the clinical efficacy of angina pectoris and the evidence of traditional Chinese medicine (TCM) efficacy. Secondary indicators are the Seattle Angina Scale score, serum lipid levels, electrocardiogram, and echocardiogram diagnosis. Additional indicators are endothelial function and immunoinflammatory factors. Adverse events will be monitored throughout the trial. DISCUSSION: Integrated traditional Chinese and Western medicine is commonly used for angina in China. This study will evaluate the clinical effectiveness and safety of adding QJHX based on standardized Western medications. The results of the trial will provide high-level clinical research-based evidence for the application of QJHX in MVA. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR1900027015 . Registered on 28 October 2019.

Shengmai Injection Suppresses Angiotensin II-Induced Cardiomyocyte Hypertrophy and Apoptosis via Activation of the AMPK Signaling Pathway Through Energy-Dependent Mechanisms.

Shengmai injection (SMI), a traditional Chinese herbal medicine extracted from Panax ginseng C.A. Mey., Ophiopogon japonicus (Thunb.) Ker Gawl., and Schisandra chinensis (Turcz.) Baill., has been used to treat acute and chronic heart failure. This study aimed to further clarify the effects of SMI on energy metabolism. SMI could improve cell-survival rate and also reduce myocardial cell hypertrophy and apoptosis. Mitochondria are important sites of cellular energy metabolism, and SMI protects mitochondrial function which was evaluated by mitochondrial ultrastructure, mitochondrial respiratory control ratio (RCR), and mitochondrial membrane potential (ΔΨm) in this study. The expression levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), and phosphocreatine (PCr) increased. The expression levels of free fatty acid oxidation [carnitine palmitoyltransferase-1 (CPT-1)], glucose oxidation [glucose transporter-4 (GLUT-4)], and mitochondrial biogenesis-related genes (peroxisome proliferator-activated receptor-γ coactivator-1α [PGC-1α]) were upregulated after SMI treatment. AMP-activated protein kinase (AMPK) is an important signaling pathway regulating energy metabolism and also can regulate the above-mentioned indicators. In the present study, SMI was found to promote phosphorylation of AMPK. However, the effects of SMI on fatty acid, glucose oxidation, mitochondrial biogenesis, as well as inhibiting apoptosis of hypertrophic cardiomyocytes were partly blocked by AMPK inhibitor-compound C. Moreover, decreased myocardial hypertrophy and apoptosis treated by SMI were inhibited by AMPK knockdown with shAMPK to a certain degree and AMPK knockdown almost abolished the SMI-induced increase in the expression of GLUT-4, CPT-1, and PGC-1α. These data suggest that SMI suppressed Ang II-induced cardiomyocyte hypertrophy and apoptosis via activation of the AMPK signaling pathway through energy-dependent mechanisms.

Anti-apoptotic effect of Suxiao Jiuxin Pills against hypoxia-induced injury through PI3K/Akt/GSK3ß pathway in HL-1 cardiomyocytes.

BACKGROUND: Suxiao Jiuxin Pill (SX), Chinese traditional medicine primarily consisting of tetramethylpyrazine and borneol, has been shown to protect against ischemic heart diseases. Nevertheless, the involved mechanism still remains unclear. The following study aimed to investigate the potential protective effect and molecular mechanisms of SX on apoptosis in HL-1 cardiomyocytes. METHODS: Simulated hypoxia was established by culturing HL-1 cardiomyocytes in DMEM with no glucose or serum in a hypoxic chamber with 95% N2 and 5% CO2 for 24 h. HL-1 cardiomyocytes were divided into 5 groups: control, hypoxic injury, hypoxic injury + insulin (PI3K agonist, 10 µM), hypoxic injury + SX (100 µg/mL), and hypoxic injury + SX + LY294002 (PI3K inhibitor, 10 µM) (n = 3 wells/group). The anti-apoptotic effect of SX was evaluated by Annexin V/PI analysis. Mitochondrial membrane potential (ΔΨm) was detected by JC-1 assay. The protein expression of PI3K, phosphorylated PI3K (p-PI3K), Akt, phosphorylated Akt (p-Akt), GSK3ß and phosphorylated GSK3ß (p-GSK3ß) were detected by western blot. RESULTS: SX exhibited anti-apoptotic effect in HL-1 cardiomyocytes; nonetheless, the effect was blocked by PI3K inhibitor LY294002. Also, the anti-apoptotic effect of SX was mediated by increased mitochondrial membrane potential (ΔΨm). Furthermore, p-PI3K, p-Akt, and p-GSK3ß expressions were significantly increased after SX treatment, while they were all reduced after administration of LY294002. CONCLUSION: SX protects HL-1 cardiomyocytes from apoptosis induced by hypoxia, partly through enhancing the phosphorylation of PI3K/Akt/GSK3ß signaling pathway.

Suxiao Jiuxin Pill protects cardiomyocytes against mitochondrial injury and alters gene expression during ischemic injury.

Suxiao Jiuxin Pill (SX), a traditional Chinese medicine compound consisting primarily of tetramethylpyrazine and borneol, has been reported to protect against ischemic heart disease. However, the effects of SX on mitochondrial injury and gene expression in various signaling pathways are unclear. The aim of the present study was to investigate the effects of SX on mitochondrial injury and to screen the expression of genes potentially altered by SX using a cell culture model of ischemic injury. Simulated ischemia was established by culturing HL-1 cardiomyocytes in Dulbecco's modified Eagle medium without glucose or serum in a hypoxic chamber containing 95% N2 and 5% CO2 for 24 h. HL-1 cardiomyocytes were divided into 3 groups: Control, ischemic injury and ischemic injury + SX (100 µg/ml; n=3 wells/group). Mitochondrial membrane potential was detected by staining with JC-1 dye. The mRNA expression levels of adenylyl cyclase (Adcy) 1-9, adrenoceptor ß1, Akt1, ATPase Na+/K+ transporting subunit ß2, calcium voltage-gated channel auxiliary subunit α2δ (Cacna2d)2, Cacna2d3, calcium channel voltage-dependent γ subunit 8, cytochrome C oxidase subunit 6A2 (Cox6a2), fibroblast growth factor receptor (Fgfr) 4, Fgf8, Fgf12, Gnas complex locus, glycogen synthase kinase 3ß (Gsk3b), mitogen-activated protein kinase (Mapk)11-14, Mapk kinase kinase kinase 1 (Map4k1), Mas1, nitric oxide synthase 3 (Nos3), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (Pik3ca), phospholipase A2 group 4A, rap guanine nucleotide exchange factor 4 and ryanodine receptor 2 were detected using reverse transcription-quantitative polymerase chain reaction. The protein expression levels of phosphoinositide 3-kinase (PI3K), MAS-1 and phosphorylated-endothelial NOS were also examined by immunofluorescence staining. The decrease in mitochondrial membrane potential in the cell culture model of ischemic injury (P<0.001) was significantly attenuated by SX treatment (P<0.001). Furthermore, increases in the mRNA expression levels of Adcy2 (P<0.05), 3 (P<0.01) and 8 (P<0.05) in the ischemic injury model were significantly attenuated by SX treatment (P<0.01), and SX treatment significantly decreased the mRNA expression levels of Adcy1 (P<0.01) and 6 (P<0.05) in ischemic cells. Decreases in the mRNA expression levels of Cox6a2 (P<0.001), Gsk3b (P<0.01) and Pik3ca (P<0.001) in the ischemic injury model were also significantly attenuated by SX treatment (P<0.05, P<0.01 and P<0.001, respectively). In addition, the decrease in the protein expression of PI3K (P<0.001) was significantly attenuated by SX treatment (P<0.001). The present findings indicate that SX may protect cardiomyocytes against mitochondrial injury and attenuate alterations in the gene expression of Adcy2, 3 and 8, Cox6a2, Gsk3b and Pik3ca during ischemic injury.

MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition.

AIMS: Acute myocardial infarction (MI) leads to cardiac remodelling and development of heart failure. Insufficient myocardial capillary density after MI is considered a critical determinant of this process. MicroRNAs (miRs), negative regulators of gene expression, have emerged as important players in MI. We previously showed that miR-532-5p (miR-532) is up-regulated by the ß-arrestin-biased ß-adrenergic receptor antagonist (ß-blocker) carvedilol, which activates protective pathways in the heart independent of G protein-mediated second messenger signalling. Here, we hypothesize that ß2-adrenergic receptor/ß-arrestin-responsive miR-532 confers cardioprotection against MI. METHODS AND RESULTS: Using cultured cardiac endothelial cell (CEC) and in vivo approaches, we show that CECs lacking miR-532 exhibit increased transition to a fibroblast-like phenotype via endothelial-to-mesenchymal transition (EndMT), while CECs over-expressing miR-532 display decreased EndMT. We also demonstrate that knockdown of miR-532 in mice causes abnormalities in cardiac structure and function as well as reduces CEC proliferation and cardiac vascularization after MI. Mechanistically, cardioprotection elicited by miR-532 is in part attributed to direct repression of a positive regulator of maladaptive EndMT, prss23 (a protease serine 23) in CECs. CONCLUSIONS: In conclusion, these findings reveal a pivotal role for miR-532-prss23 axis in regulating CEC function after MI, and this novel axis could be suitable for therapeutic intervention in ischemic heart disease.

Effects of Kanlijian on exercise tolerance, quality of life, and frequency of heart failure aggravation in patients with chronic heart failure.

OBJECTIVE: To observe the effects of conventional therapy combined with Kanlijian (KLJ) on exercise tolerance, quality of life and frequency of heart failure aggravation in patients with chronic heart failure (CHF). METHODS: Sixty CHF patients differentiated as sufferring from the syndrome of Xin-Shen Yang deficiency were included in the study and randomly assigned at the ratio of 2:1 into the KLJ group (n = 39) and the control group (n = 21). All the patients were treated with conventional therapy of Western medicine, but to those in the KLJ group, KLJ was medicated additionally one dose daily with 24 wks as one therapeutic course. The efficacy on TCM syndrome and changes of scores on TCM syndrome were observed after treatment. The indexes, including 6-minute walking distance (6MWD), quality of life (QOL, accessed by LHFQ scoring), NYHA grade, hemodynamic indexes and reducing/withdrawal rate of diuretic and digoxin before and after treatment were recorded and compared. Also the frequency of re-admission due to aggravation of heart failure in one year's time were observed. RESULTS: (1) The efficacy on TCM syndrome, improvement on scores of TCM syndrome, therapeutic effects on 6MWD, QOL, and NYHA grade in the KLJ group were superior to those in the control group. (2) Hemodynamic indexes after treatment, left ventricular fractional shortening (LVFS) and E peak/A peak (E/A), between the two groups had no significant difference, while left ventricular ejection fraction (LVEF) was increased significantly in the KLJ group, but with no obvious change in the control group. (3) The reducing/withdrawal rate of diuretic and digoxin in the KLJ group was significantly higher than that in the control group. (4) The 1-year frequency of re-admission significantly decreased in the KLJ group. CONCLUSION: The adjuvant treatment of KLJ on the basis of Western conventional therapy can significantly improve CHF patients' exercise tolerance, quality of life and cardiac function, reduce the dosage of diuretic and digoxin needed, and decrease the re-admission frequency due to aggravation of heart failure.