LncRNA Gaplinc promotes the pyroptosis of vascular endothelial cells through SP1 binding to enhance NLRP3 transcription in atherosclerosis.

Pyroptosis, characterized by activation of the Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and its downstream effector inflammatory factors, has been shown to play a crucial role in atherosclerosis development. Long noncoding RNAs (lncRNAs) are involved in the progression of pyroptosis. However, the role and mechanism of the novel lncRNA gastric adenocarcinoma associated, positive CD44 regulator (Gaplinc), in endothelial cell pyroptosis during atherosclerosis development remain unexplored. Bioinformatics was performed to evaluate dysregulated lncRNAs in atherosclerotic mice fed a high-fat diet. The effect of Gaplinc on atherosclerosis progression in vivo was assessed via Oil Red O staining and fluorescence in situ hybridization. Its function in oxidized low-density lipoprotein (ox-LDL)-induced pyroptosis of endothelial cells was determined through ectopic expression. Additionally, RNA pull-down and immunoprecipitation (RIP) assays were performed to determine Gaplinc and transcription factor SP1 interactions. Then the pyroptosis pathway proteins were analyzed via immunofluorescence and western blotting. We found that lncRNA Gaplinc was highly expressed in ox-LDL-induced endothelial cells as well as in the plaque and plasma of high-fat diet-treated ApoE-/- mice. Gaplinc silencing significantly inhibited endothelial cell pyroptosis and atherosclerotic plaque formation. Mechanistically, Gaplinc could interact with SP1 to bind to the NLRP3 promoter and upregulate the target gene expression of NLRP3, facilitating endothelial cell pyroptosis and atherosclerotic plaque enlargement in high- fat diet-fed mice. In conclusion, our results revealed the underlying mechanism of the lncRNA Gaplinc /SP1/NLRP3 axis in endothelial cell pyroptosis, which may provide new potential targets for the treatment of atherosclerosis.

Upregulation of microRNA-34a enhances myocardial ischemia-reperfusion injury via the mitochondrial apoptotic pathway.

Mitochondrial oxidative injury can result in many cardiovascular diseases including cardiac ischemia-reperfusion (I/R) injury. This study was designed to investigate whether microRNA-34a (miR-34a) influences cardiac I/R or hypoxia/reoxygenation (H/R) injury by regulating the mitochondrial apoptotic pathway from oxidative injury.In vivo, myocardial infarction size was examined by Evan blue/TTC staining. Apoptosis was assessed by TUNEL assay. Heart function was measured by echocardiography. Lactate dehydrogenase (LDH) and creatine kinase (CK) were evaluated. In vitro, H9c2 cardiomyocytes were exposed to H/R stimulation. Cell viability was assessed by the CCK-8 assay and apoptosis was detected by Annexin V/PI staining. Mitochondrial superoxide, mitochondrial membrane potential (MMP) and ATP production was evaluated by detection kits, and related proteins were detected by western blotting analysis. We observed that the level of miR-34a was significantly upregulated in I/R rats compared to the sham group. Injection of adenovirus inhibiting miR-34a into the left ventricular anterior wall improved heart function and decreased I/R injury. H9c2 cardiomyocytes exposed to H/R stimulation displayed an obvious increase in miR-34a expression. In addition, miR-34a inhibitor alleviated, whereas miR-34a mimic aggravated H/R-induced mitochondrial injury. Bcl-2 was identified as a target gene of miR-34a by dual-luciferase reporter gene detection. Knockdown of Bcl-2 abolished the cardioprotection of the miR-34a inhibitor in H9c2 cells. In summary,our study demonstrates that inhibition of miR-34a exhibits therapeutic potential in treatment of myocardial I/R injury by restraining mitochondrial apoptosis.

[Protective effect of ginsenoside Rg_1 on hypoxia/reoxygenation injury and its mechanism].

This project aimed to explore the protective effect of ginsenoside Rg_1 on hypoxia/reoxygenation(H/R)-induced H9 c2 cardiomyocyte injury and its underlying signaling pathway. The H/R model of H9 c2 cardiomyocytes was established and then the cells were divided into different treatment groups. CCK-8(cell counting kit-8) was used to detect the activity of cardiomyocytes; Brdu assay was used to detect the proliferation of H9 c2 cells; the caspase-3 activity was tested, and then the protein expression was assessed by Western blot. Flow cytometry was used to evaluate the apoptosis level of cardiomyocytes. Ginsenoside Rg_1 inhibited H/R-induced cardiomyocyte apoptosis and caspase-3 activity, promoted nuclear transcription of nuclear factor erythroid-2 related factor 2(Nrf2), and enhanced the expression of the downstream heme oxygenase-1(HO-1). Ginsenoside Rg_1 could increase Nrf2 nuclear transcription and HO-1 expression with the increase of concentration(10, 20, 40, 60 µmol·L~(-1)). However, the protective effect of ginsenoside Rg_1 on cardiomyocytes was significantly weakened after the transfection of Nrf2-siRNA. Ginsenoside Rg_1 could protect cardiomyocytes by activating the Nrf2/HO-1 pathway.

Risk factors for pulmonary nodules in north China: A prospective cohort study.

OBJECTIVES: Pulmonary nodules have become common incidental findings with the widespread use of computed tomography (CT) technology. Such nodules have the potential to become early lung cancer lesions, so understanding more about factors that may be associated with them is important. MATERIALS AND METHODS: The present work was based on a large prospective cohort comprising 32,438 participants in Hebei Province (China) between January 2014 and March 2016. Participants aged 40-75 years completed a questionnaire, underwent low-dose CT (LDCT), and were followed up to March 2017. Grouped by the results of LDCT, normal participants and those with pulmonary nodules were included in the data analysis. RESULTS: In total 7752 subjects were included in this study, of whom 2040 (26.32%) were pulmonary nodule patients. Older age, current smoking status (hazard ratio (HR) = 1.43, 95% confidence interval (95%CI): 1.21, 1.68), exposure to second-hand smoke (SHS) at work (HR = 1.17, 95%CI: 1.01, 1.35), dust exposure (HR = 1.49, 95%CI: 1.06, 2.11), history of lung disease (HR = 1.44, 95%CI: 1.16, 1.77), and family history of cancer (HR = 1.28, 95%CI: 1.12, 1.48) were associated with pulmonary nodules. However, consumption of vegetables (HR = 0.82, 95%CI: 0.68, 0.99), tea (HR = 0.88, 95%CI: 0.78, 0.99) and legumes reduced the risk. Approximately 10.09% and 8.58% of pulmonary nodule incidences were attributed to tobacco smoking and low fruit intake, respectively. An estimated 6.36% and 3.88% of patients with pulmonary nodules attributable to family history of cancer and history of lung disease were detected. CONCLUSION: The results of this study suggest that age, smoking, SHS, dietary factors, occupational exposures, history of disease and family history of cancer may affect the incidence of pulmonary nodules.

Research progress on the relationship between zinc deficiency, related microRNAs, and esophageal carcinoma.

Esophageal cancer (EC) is a common malignant tumor of the gastrointestinal tract with a high incidence in China. Zinc (Zn) deficiency is a key risk factor for the occurrence and development of EC and affects progression by regulating microRNA (miRNA, miR) expression. In addition, the dysregulation of miRNAs is accompanied by the dysregulation of their target genes in EC. In this paper, we review the potential molecular mechanisms between Zn deficiency and EC with the aim of providing new strategies and methods for early diagnosis, targeted therapy, and prognostic evaluation.

The role of miR-19b in the inhibition of endothelial cell apoptosis and its relationship with coronary artery disease.

The biological effects of microRNAs (miRNAs) and TNF-α in atherosclerosis have been widely studied. The circulating miR-17-92 cluster has been recently shown to be significantly downregulated in patients with injured vascular endothelium. However, it remains unclear whether the miR-17-92 cluster plays a significant role in vascular endothelial repair. The aim of this study was to investigate the relationship between the miR-17-92 cluster and TNF-α-induced endothelial cell apoptosis. We determined that the down-regulation of miR-19b level among patients with coronary artery disease was consistent with miRNA expression changes in endothelial cells following 24 h of TNF-α treatment. In vitro, the overexpression of miR-19b significantly alleviated the endothelial cells apoptosis, whereas the inhibition of miR-19b significantly enhanced apoptosis. The increased levels of Afap1 and caspase7 observed in our apoptosis model could be reduced by miR-19b, and this effect could be due to miR-19b binding 3'-UTRs of Afap1 and caspase7 mRNA. Therefore our results indicate that miR-19b plays a key role in the attenuation of TNF-α-induced endothelial cell apoptosis and that this function is closely linked to the Apaf1/caspase-dependent pathway.

The lncRNA MALAT1 protects the endothelium against ox-LDL-induced dysfunction via upregulating the expression of the miR-22-3p target genes CXCR2 and AKT.

CXCR2 plays a key role in protecting the integrity of the endothelium. Emerging evidence has demonstrated that the long ncRNAs (lncRNA) Human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) participates in the regulation of the pathophysiological processes. However, whether there is crosstalk between CXCR2 and MALAT1 remains unknown. In this study, we demonstrated that MALAT1 was upregulated in patients with unstable angina. MALAT1 silencing significantly downregulated the expression of the miR-22-3p target gene CXCR2 via reversing the effect of the miR-22-3p, resulting in the aggravation of Oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury; this process was associated with the AKT pathway. Thus, MALAT1 protects the endothelium from ox-LDL-induced endothelial dysfunction partly through competing with miR-22-3p for endogenous RNA.

A metabolomic study of rats with doxorubicin-induced cardiomyopathy and Shengmai injection treatment.

Doxorubicin-induced cardiomyopathy (DOX-CM) is a severe complication of doxorubicin (DOX) chemotherapy. Characterized by cumulative and irreversible myocardial damage, its pathogenesis has not been fully elucidated. Shengmai Injection (SMI), a Traditional Chinese Medicine, may alleviate myocardial injury and improve heart function in the setting of DOX-CM. As a result of its multi-component and multi-target nature and comprehensive regulation, the pharmacological mechanisms underlying SMI's effects remain obscure. The emerging field of metabolomics provides a potential approach with which to explore the pathogenesis of DOX-CM and the benefits of SMI treatment. DOX-CM was induced in rats via intraperitoneal injections of DOX. Cardiac metabolic profiling was performed via gas chromatography/mass spectrometry and ultra-performance liquid chromatography/tandem mass spectrometry. A bioinformatics analysis was conducted via Ingenuity Pathway Analysis (IPA). Eight weeks following DOX treatment, significant cardiac remodeling, dysfunction and metabolic perturbations were observed in the rats with DOX-CM. The metabolic disturbances primarily involved lipids, amino acids, vitamins and energy metabolism, and may have been indicative of both an energy metabolism disorder and oxidative stress secondary to DOX chemotherapy. However, SMI improved cardiac structure and function, as well as the metabolism of the rats with DOX-CM. The metabolic alterations induced via SMI, including the promotion of glycogenolysis, glycolysis, amino acid utilization and antioxidation, suggested that SMI exerts cardioprotective effects by improving energy metabolism and attenuating oxidative stress. Moreover, the IPA revealed that important signaling molecules and enzymes interacted with the altered metabolites. These findings have provided us with new insights into the pathogenesis of DOX-CM and the effects of SMI, and suggest that the combination of metabolomic analysis and IPA may represent a promising tool with which to explore and better understand both heart disease and TCM therapy.

Shengmai injection improved doxorubicin-induced cardiomyopathy by alleviating myocardial endoplasmic reticulum stress and caspase-12 dependent apoptosis.

BACKGROUND: Apoptosis plays vital roles in the progression of doxorubicin-induced cardiomyopathy (DOX-CM). Endoplasmic reticulum stress (ER stress) could induce specific apoptosis by caspase-12 dependent pathway. Shengmai Injection (SMI), a famous Traditional Chinese Medicine, could alleviate the heart damage via inhibiting myocardial apoptosis. However, it is unknown whether SMI can alleviate ER stress and its specific apoptosis in the setting of DOX-CM. OBJECTIVE: To explore the effects of SMI on heart function, myocardial ER stress, and apoptosis of DOX-CM rats. METHODS: Rats with DOX-CM were treated by SMI. Heart function was assessed by echocardiography and brain natriuretic peptide. Myocardial apoptosis was detected by TUNEL assay. ER stress was assessed by detecting the expressions of GRP78 and caspase-12. RESULTS: At the end of eight-week, compared to control, significant heart dysfunction happened in DOX group. The ratio of apoptotic cardiomyocytes and the expressions of GRP78 and caspase-12 increased significantly (P < 0.05). Compared to DOX group, the apoptotic ratio and the expressions of GRP78 and caspase-12 significantly decreased in DOX + SMI group (P < 0.05), accompanied with improved heart function. CONCLUSION: SMI could alleviate myocardial ER stress and caspase-12 dependent apoptosis, which subsequently helped to improve the heart function of rats with DOX-CM.

Efficacy and safety of cangrelor for patients with coronary artery disease: a meta-analysis of four randomized trials.

BACKGROUND: The efficacy and safety of new intravenous P2Y12 inhibitor (cangrelor) for patients with coronary artery disease (CAD) remain unclear. METHODS AND RESULTS: Trials were identified in PubMed, Web of Science, Embase, and Cochrane Database searches. We included four randomized, placebo-controlled reports in the meta-analysis. The database consisted of 36, 081 patients on cangrelor compared with clopidogrel or placebo. Major adverse cardiac events (MACE) were defined as the primary efficacy endpoint and major or severe bleeding at 48 hours was defined as the primary safety endpoint. Cangrelor significantly decreased risk of MACE (OR: 0.87, P = 0.002) and stent thrombosis (OR: 0.53, P < 0.001). However, at the same time, an increase in TIMI minor bleeding (OR: 1.49, P = 0.04) and in GUSTO moderate bleeding (OR: 1.43, P = 0.04) were observed by cangrelor. CONCLUSIONS: Intravenous administration of cangrelor is benefit to reduce risk of MACE and stent thrombosis in patients with CAD excepting for increased minor bleeding events.

Oxidized low-density lipoprotein and C-reactive protein have combined utility for better predicting prognosis after acute coronary syndrome.

It has been shown that the elevated concentrations of oxidized low-density lipoprotein (Ox-LDL) or high-sensitivity C-reactive protein (hs-CRP) are predictive of future cardiovascular events for acute coronary syndrome (ACS) patients. But, the combined value of Ox-LDL and hs-CRP for predicting cardiovascular events is still unknown. Serum concentrations of Ox-LDL, hs-CRP, and cTnT were measured in a prospective cohort of 425 selective ACS patients followed 3-5 years for the occurrence of acute myocardial infarction (AMI) or death (AMI/death). Among 425 enrolled patients, 124 patients demonstrated AMI/death. Baseline levels of Ox-LDL, hs-CRP, and cTnT were significantly higher in AMI/death group than the event-free survival group. Kaplan-Meier survival analyses supported that elevations in Ox-LDL or hs-CRP predicted increased cardiovascular events risks. However, the strongest risk prediction was achieved by assessing Ox-LDL and hs-CRP together. Patients with high levels of Ox-LDL and hs-CRP were more likely to experience AMI or death than those with either Ox-LDL or hs-CRP elevated. Receiver-operating characteristic curves showed that Ox-LDL and hs-CRP have higher sensitivity and specificity than those of cTnT for predicting AMI or death. This was reflected by the AUC values for Ox-LDL, hs-CRP, and cTnT, which were 0.891, 0.834, and 0.626, respectively. The combined use of Ox-LDL and hs-CRP may improve prognosis after ACS with high-sensitivity and specificity.

Fosinopril attenuates the doxorubicin-induced cardiomyopathy by restoring the function of sarcoplasmic reticulum.

Fosinopril, an angiotensin-converting enzyme inhibitor, is known to attenuate cardiomyopathy induced by doxorubicin (DOX); however, the mechanisms of this cardioprotection are not fully elucidated yet. In the present study, experimental cardiomyopathy was induced in rats by administration of DOX with or without co-treatment with fosinopril. Fosinopril was utilized on day 1 or 14 of the treatment with DOX to compare efficacies of early versus late co-treatments. We observed that fosinopril attenuated changes induced by DOX (e.g., less increased heart and left ventricular weights, diminished lung congestion and ascites, attenuated LVEDP and LVSP, and less decreased +dP/dt and -dP/dt). Further, fosinopril diminished the levels of markers of cardiac toxicity (i.e., plasma levels and activities of cardiac enzymes and proteins AST, LDH, CPK, cTnI, and BNP). Fosinopril also prevented DOX-induced decreases in Ca(2+) uptake and restored activity of Ca(2+)-stimulated ATPase in left ventricular sarcoplasmic reticulum. We next tested whether the improved Ca(2+) transport activity in sarcoplasmic reticulum was due to modulation of SERCA2 and phospholamban expressions by fosinopril. Fosinopril attenuated the decrease in SERCA2 and phospholamban expressions caused by DOX. In conclusion, cardioprotective effects of fosinopril in the DOX-induced cardiomyopathy appear to be due to its ability to prevent remodeling of the cardiac sarcoplasmic reticulum membrane.

Elevated levels of oxidized low-density lipoprotein correlate positively with C-reactive protein in patients with acute coronary syndrome.

The relationship between oxidized low-density lipoprotein (Ox-LDL) and C-reactive protein (CRP) in patients with acute coronary syndrome (ACS) is unknown. We, therefore, measured serum levels of Ox-LDL and high-sensitivity (hs)-CRP in 90 ACS patients, 45 stable angina pectoris (SAP) patients, and 66 healthy controls using sandwich ELISA. ACS patients were subdivided into: (1) acute myocardial infarction (AMI; n = 45); (2) unstable angina pectoris (UAP; n = 45) groups. In AMI patients, Ox-LDL (177.5 mmol/l) and hs-CRP (25.40 mg/l) levels were significantly higher (P < 0.01) than in UAP (Ox-LDL:107.5 mmol/l, hs-CRP:10.7 mg/l) and SAP (Ox-LDL:82.3 mmol/l, hs-CRP:2.10 mg/l) patients as well as controls (Ox-LDL:41.4 mmol/l, hs-CRP:1.76 mg/l). Ox-LDL/hs-CRP levels in UAP patients were significantly higher (P < 0.01) than in SAP patients and controls. Importantly, a positive correlation was found between Ox-LDL and CRP (r = 0.622; P < 0.01) levels. Serum levels of total, HDL, and LDL cholesterol did not differ among these patient groups. In conclusion, our data show that Ox-LDL and hs-CRP levels correlate positively in ACS patients, supporting the hypothesis that Ox-LDL and CRP may play a direct role in promoting the inflammatory component of atherosclerosis in these individuals. We suggest that Ox-LDL/CRP elevated levels may serve as markers of the severity of the disease in evaluation and management of ACS patients.

Artemisinin inhibits extracellular matrix metalloproteinase inducer (EMMPRIN) and matrix metalloproteinase-9 expression via a protein kinase Cδ/p38/extracellular signal-regulated kinase pathway in phorbol myristate acetate-induced THP-1 macrophages.

1. Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN) and matrix metalloproteinases (MMPs) by monocytes/macrophages has been proposed to play a significant role in atherosclerotic plaque progression and rupture. The aim of the present study was to explore whether artemisinin, a natural extract from Artemisia annua, could decrease EMMPRIN and MMP-9 expression in phorbol myristate acetate (PMA)-induced macrophages by regulating the protein kinase (PK) Cδ/c-Jun N-terminal kinase (JNK)/p38/extracellular signal-regulated kinase (ERK) pathway. 2. Human monocytic THP-1 cells were pretreated with 20-80 µg/mL artemisinin for 4 h or 1-10 µmol/L rottlerin for 1 h prior to stimulation with PMA (100 nmol/L) for another 48 h. Cells were collected to analyse the induction of EMMPRIN and MMP-9. Upstream pathway analysis using the PKCδ inhibitor rottlerin detected activation of the PKCδ/JNK/p38/ERK pathway. 3. Artemisinin (20-80 µg/mL) significantly inhibited the induction of EMMPRIN and MMP-9 at both the transcriptional and translational levels in a dose-dependent manner in PMA-induced macrophages. In addition, artemisinin (20-80 µg/mL) strongly blocked PKCδ/JNK/p38/ERK MAPK phosphorylation. The PKCδ inhibitor rottlerin (1-10 µmol/L) also significantly inhibited JNK/p38/ERK phosphorylation and decreased EMMPRIN and MMP-9 mRNA and protein expression. 4. The results of the present study suggest that artemisinin inhibits EMMPRIN and MMP-9 expression and activity by suppressing the PKCδ/ERK/p38 cascade in PMA-induced macrophages.

Influence of shengmai capsule on recovery of living capacity in patients after myocardial infarction.

OBJECTIVE: To observe the effect of long-term application of Shengmai Capsule (SMC) on recovery of patients after myocardial infarction. METHODS: A total of 120 myocardial infarction patients were: assigned into two groups. Changes of angina pectoris, electrocardiogram (ECG), living capacity and heart function in patients were observed after 6-month treatment. RESULTS: The total effective rate in alleviating angina: pectoris was 90.0% and that in improving ECG figure was 93.3% in the treatment group, both were significantly higher than those in the control group, 73.4% and 70.0% respectively (P<0.05). The Karnofsky Performance Status scores of heart function were increased and the Activity of Daily Living scores in living capacity decreased in both groups, but the improvements were better in the treatment group (P<0.01 and P<0.05). The parameters of cardiac function, including cardiac output, stroke volume, cardiac index and ejection fraction, were increased in both groups, but the increments in the treatment group were more significant (P<0.01 or P<0.05). CONCLUSION: Long-term application of SMC could effectively prevent and treat angina pectoris, improve the living capacity and accelerate the recovery of heart function in patients after myocardial infarction.

Effect of Shengmai injection on vascular endothelial and heart functions in patients with coronary heart disease complicated with diabetes mellitus.

OBJECTIVE: To study the effect of Shengmai injection (, SMI) on vascular endothelial and heart functions in coronary heart disease patients complicated with diabetes mellitus (CHD-DM). METHODS: One hundred and twenty patients with CHD-DM, their diagnosis confirmed by coronary arteriography, were equally randomized into a control group treated with conventional treatment and a treated group treated with conventional treatment plus SMI. The changes in blood levels of nitric oxide (NO), endothelin-1 (ET-1) and angiotensin II (Ang II), as well as endothelium-dependent vascular dilating function and heart function in the patients were observed before treatment and after the 3-week treatment. RESULTS: After being treated with SMI for 3 weeks, in the treated group, blood level of NO was raised significantly from 69.8 + or - 33.1 micro mol/L to 120.1 + or - 50.8 micro mol/L, and ET-1 was lowered from 70.1 + or - 32.1 ng/L to 46.2 + or - 21.3 ng/L, respectively (P<0.01); that of Ang II was lowered from 81.3 + or - 24.3 ng/L to 50.2 + or - 27.3 ng/L (P<0.01); brachial arterial post-congestion blood flow increasing rate was raised from 389.4 + or - 26.3% to 459.3 + or - 27.8% (P<0.01); and the improvement in heart function as seen through the ejection fraction (EF) was increased from 44 + or - 5% to 68 + or - 6% (P<0.01), all the changes being more significant than those in the control group (all P<0.01). CONCLUSION: SMI can improve not only the endothelial function in CHD-DM patients, but also heart contraction significantly.

Effect of Shengmai Injection on cardiac function and inflammatory reaction in patients with acute coronary syndrome.

OBJECTIVE: To confirm the effect of Shengmai Injection (, SMI) in improving cardiac function in patients with acute coronary syndrome (ACS) and to explore its influence on inflammatory reaction in patients. METHODS: Ninety ACS patients were randomized into two groups, the control group treated with conventional therapy and the SMI group treated with SMI. The patients' cardiac function was noted and the content of high sensitive C-reactive protein (hs-CRP) in venous blood was measured before treatment and 1 week and 3 weeks after treatment, so as to observe and compare their changes between the two groups. RESULTS: The cardiac output, stroke volume and ejection fraction in the SMI group after 3 weeks of treatment were all higher than those in the control group (P<0.05). The serum content of hs-CRP was reduced in both groups (P<0.05), but the reduction in the SMI group was more significant than that in the control group (P<0.05). CONCLUSION: SMI could improve the cardiac function and further inhibit the inflammatory reaction in patients with ACS.

[Effect of shengmai injection on hemodynamics in patients with dilated cardiomyopathy].

OBJECTIVE: To observe the effects of Shengmai Injection (SMI) on hemodynamics in patients with dilated cardiomyopathy (DCM), and to explore the clinical effect of SMI in treating patients of DCM with heart failure. METHODS: One hundred patients were divided into two groups. In the 50 cases of the treated group, 10 cases with heart function of II degree, 35 of III degree and 5 of IV degree. The corresponding number of cases in the 50 patients of the control group were 10, 36 and 4. Conventional treatment was given to both groups, and SMI was administered to the treated group additionally. The therapeutic effect and the indexes of heart function before and after treatment were determined and compared. RESULTS: In the treated group, treatment showed markedly effective in 22 cases and effective in 20, the total effective rate being 84%, while in the control group, markedly effective in 14 and effective in 16, the total effective rate being 60%, the comparison between the two groups showed significant difference (chi 2 = 7.14, P < 0.01). In the treated group, cardiac output, stroke volume (SV), cardiac index, eject fraction (EF), lefe ventricular minor axis shortened rate, ventricular wall thickened rate were all increased after treatment and system vascular resistance (SVR) decreased significantly (P < 0.05), while in the control group, insignificant change was found in the above-mentioned parameters after treatment (P > 0.05). Comparison between the two groups after treatment showed that EF and SV were obviously higher and SVR obviously lower in the treated group than those in the control group. CONCLUSION: SMI could markedly improve the heart function of patients with DCM. The effect of conventional treatment would be enhanced in combination therapy with SMI.