Objective: To study the effects of Total Saponins of Panax Pseudoginseng injection on unstable angina pectoris (UAP) . Methods :Forty-eight cases of UAP patients were randomly divided into Total Saponins of Panax Pseudoginseng injection treatment group and routine treatment group. The serum levels of plasminogen activator inhibitor (PAI), soluble intercellular adhesion molecule-1 (SICAM-1) and C-reactive protein (CRP) after two weeks treatment in two groups were observed. Results:The total effective rate was significantly higher in Total Saponins of Panax Pseudoginseng injection treatment group than in control group. The indexes of PAI after Total Saponins of Panax Pseudoginseng injection treatment were lower. The levels of SICAM-1 and CRP were lower in Total Saponins of Panax Pseudoginseng injection treatment group than those in control group. Conclusion:Total Saponins of Panax Pseudoginseng injection is an effective drug for UAP, and it obviously improves fibrinolytic activity and relieves inflammatory reaction.

Objective To investigate the clinical value of the variety of serum levels of soL-CXCL16 and NT-proBNP peripercutaneous coronary intervention(PCI) in patients with acute myocardial infarction (AMI).Methods A total of 77 cases received PCI were selected to research group.And the contemporaneous 30 healthy persons were chosen to control group.The serum levels of soL-CXCL16,NT-proBNP and cTnT were detected by ELISA.The relationships of soL-CXCL16 and NT-proBNP to cTnT were detected by Pearson linear correlation analysis.Results Compared to pre-PCI,the serum levels of CXCL16 were rising to the peak point at 0.5 h post-PCI,and were decreasing from 2.0 h post-PCI,then the serum levels of CXCL16 were declining to the levels of pre-PCI at 24.0 h post-PCI (P＜0.05).And the serum levels of NT-proBNP were rising from 0.5 h post-PCI,and the peak point was at 24.0 h post-PCI (P＜0.05).The postive relationships of the serum levels of CXCL16 and NT-proBNP to the serum levels of cTnT were confirmed by Pearson linear correlation analysis(P＜0.01).Conclusion Monitoring of soL-CXCL16 and NT-proBNP for patients with percutaneous coronary stenting could provide foundation for prognosis evaluation of PCI.

Objective:To evaluate the feasibility of implanting a new self-expanding valved stent for aortic valve implantation and its influence on coronary blood flow. Methods:We designed a self-expanding valved stent made from super-elastic memory nitinol alloy,with a tubular shape and a wide mesh in the cavate middle part. A valvular ring made of nitinol wire was sutured on the lower part. Fresh porcine pericardium was decellularized,treated with 0. 6% glutaraldehyde solution for 36 h,trimmed into leaflets,and sutured by hand into the valvular ring. The valved stent was pulled into a 14-French sheath by a silk and positioned in the left ventricle of isolated pig heart via the ascending aorta,and then deployed over the native aortic valves by pulling back the outer sheath. Water was injected into the ascending aorta by a silicon tube to evaluate the competence of the prosthetic heart valves and its effect on coronary flow. Results:The prepared valved aortic stent could be stably positioned over the native valves and could be removed after deployment. The prosthetic heart valves showed a satisfactory function and had no influence on coronary flow and mitral valve motion. Conclusion:This self-expanding valved stent is well-designed and allows for aortic valve implantation over the native valves without interfering the coronary flow; it can be evaluated further in vivo.

Objective To evaluate the significance of myocardial bridge and find a reasonable diagnosis and treatment strategy.Methods Sixty-three myocardial bridge patients and sixty-three patients with negative results of coronary artery angiography were reviewed.The clinical data of symptoms,electrocardiogram,exercise tests,coronary artery angiography,therapeutics and the serum levels of C-reactive protein(CRP)were analyzed.Results The symptoms of chest distress and chest pain were found in myocardial bridge patients.Myocardial consumption of oxygen augmentation causes the symptoms of aggravation.Positive results of electrocardiogram and exercise tests in many of myocardial bridge patients were examined.There were no relationship with severity of myocardial bridge artery stenosis.Most of myocardial bridge were discovered in anterior descending branch.At present,the main treatment of myocardial bridge was drug therapeutics.After treatment,the serum levels of CRP was significantly decreased.Conclusion Myocardial bridge was anatomy abnormality with important clinical significance.The serum levels of CRP can be used to evalue the therapeutic efficacy of myocardial bridge.

Objective To establish human heart valve interstitial cells calcification culture model in vitro,and observe the effect of bone morphogenetic protein-2 (BMP-2) on calcification of human heart valve interstitial cells.Methods Human heart valve interstitial cells were cultured in vitro,and divided into control group:cells were cultured in conventional media plus recombinant human BMP-2 treatmnent and experimental group:besides above treaments,calcification inducers (recombinant hunan BMP-2,β-glycerophosphate,L-ascorbic acid,dexamethasone) were added to the culture media.The two group of cells were cultured for 14 days and were stained by Von Kossa,then the cell calcification was observed in this valvular interstitial cells calcification culture model in vitro.Protein expression of intercellular adhesion molecule 1 (ICAM-1),interleukin 8,BMP-2 and BMP-4 was determined by Western blot and BMP-2 secretion was measured by ELISA.Results In the control group,the structure of human heart valve interstitial cells was clear,and the spindle and radial growth shaped cellular morphology was visible,and Von Kossa staining was negative.In the experimental group,the nuclei become darker in color,and granular sediment distribution was seen surrounding cells,and Von Kossa staining was positive,the cells were forming nodules of calcification.The protein expression of ICAM-1,interleukin 8,BMP-2 and BMP-4 in the experimental was significantly higher than that of the control group (all P ＜ 0.05).The expression of BMP-2 in the experimental group was also significantly higher than that in control group ((92.5 ±4.9) pg/ml vs.(22.2 ± 1.9) pg/ml,P ＜ 0.05).Conclusion Human BMP-2,β-glycerophosphate,L-ascorbic acid,and dexamethasone can induce human heart valve interstitial cells calcification and enhance inflammation in vitro by stimulating the secretion of BMP-2.

Objective To observe the protein expression of Notch 1 in the cultured calcified human heart valve interstitial cells (hVICs) in vitro and related mechanisms.Methods hVICs were divided into two groups:control hVICs were cultured in conventional media for 14 days and calcified hVICs were cultured with calcification inducers:[3-glycerophosphate (500 μl),ascorbic acid (200 μl),dexamethasone (100 μl) for 7 days.The calcified hVICs were further divided into calcified hVICs group and inhibited calcified hVICs by adding specific Notch1 inhibitor DAPT (50 μmol/L(4 μl/hole))groups and cultured for another 7 days.Inflammatory response of all groups were induced by lipopolysaccharide (LPS) for 8 to 12 hours.Western blot was used to detect the protein expression of Notch1,phosphorylation nuclear transcription factor κB (p-NF-κB),bone morphogenetic protein-2/4(BMP-2/4).ELISA was applied to detect the content of BMP-2 secretion of the groups.Von Kossa staining was used to observe of cellular calcification.Results (1)Von Kossa staining is positive in the induced calcification group,the expression of Notch1,p-NF-κB,BMP-2 and BMP-4 is significantly higher in the induced calcification group than in the control group (all P ＜ 0.05).The expression of BMP-2 is significantly higher in the induced calcification group than in control group ((88.23 ± 3.28) pg/ml vs.(25.41 ± 3.68) pg/ml,P =0.02).(2) After treatment with DAPT,the calcification and the expression of Notch1,p-NF-κB,BMP-2 and BMP-4 were significantly decreased compared to calcification group (all P ＜ 0.05).The expression of BMP-2 is (26.74 ± 4.62) pg/ml in the calcification inhibition group and (80.41 ± 2.96) pg/ml in calcified control group (P =0.02).Conclusions Upregulated Notch 1 expression promotes BMP-2/4 secretion in LPS stimulated hVICs,and contributes to osteogenic changes in hVICs.Inhibiting Notch1 can decrease the BMP-2/4 secretion and calcification in hVICs,which may serve as a novel therapeutic option for treating calcific valve disease.

Objective: To evaluate the prevalence and risk factors of aortic valve calcification among the elderly (≥65 years old) resident of Wuxi city, Jiangsu province. Methods: The household registration population aged ≥65 years old in Wuxi city was selected as the research subject by stratified sampling method from August 2017 to December 2018. Echocardiography was performed to assess the aortic valve calcification, and the participants were divided into calcification group and non-calcification group. Multivariate logistic regression analysis was used to explore the related risk factors of aortic valve calcification. Results: The age of the respondents was (73.6±7.1) years old, of which 48.8% (461 cases) were males.The prevalence rate of aortic valve calcification was 22.0% (208/944) in the elderly (≥ 65 years old) residents in Wuxi city. The prevalence rate in 65-69 years old, 70-74 years old, 75-79 years old, 80-84 years old and ≥85 years old was 16.7% (58/347),16.7% (41/245),16.2% (26/161),23.3% (24/103), and 67.0% (59/88),respectively. There were significant differences in age, weight, abdominal circumference, hip circumference, high-salt diets, exercise, hypertension, hyperlipidemia, diabetes, coronary heart disease, cerebrovascular disease, and carotid atherosclerosis between the non-calcified group (736 cases) and the calcified group (208 cases) (P<0.01 or 0.05).Multivariate logistic regression analysis showed that age (OR=1.077, 95%CI 1.053-1.101, P<0.001), diabetes mellitus (OR=1.697, 95%CI 1.174-2.453, P=0.005), and coronary heart disease (OR=1.964, 95%CI 1.378-2.799, P<0.001) were the risk factors of aortic valve calcification. Conclusions The prevalence of aortic valve calcification in the elderly (≥65 years old) residents in Wuxi city of Jiangsu province increases with aging. Age, diabetes mellitus and coronary heart disease are the risk factors of aortic valve calcification in this population cohort.

Objective:To investigate the correlation between serum growth differentiation factor 11 (GDF11) level and coronary artery lesions in patients with ST-segment elevation myocardial infarction (STEMI), and the predictive efficacy of nomogram risk prediction model based on GDF11 combined with traditional risk factors on the occurrence of STEMI.Methods:This study was a retrospective cross-sectional study. Patients hospitalized in the Department of Cardiology of the 904th Hospital of Joint Logistic Support Force of People′s Liberation Army of China from 2016 to 2018 were selected and divided into control group and STEMI group. The demographic data, blood lipid level, laboratory indicators of blood and GDF11 level were collected. Logistic regression analysis screened out independent correlated factors for the occurrence of STEMI. Spearman correlation analysis clarified the correlation of each indicator with the SYNTAX or Gensini scores. A nomogram risk prediction model for the risk of STEMI occurrence and the receiver operating characteristic curve was used to compare the prediction efficiency of each model.Results:A total of 367 patients were enrolled, divided into control group ( n=172) and STEMI group ( n=195), age (66.5±11.8), male 222 (60.49%). The serum GDF11 level of STEMI group was significantly lower than that of the control group (36.20 (16.60, 70.75) μg/L vs. 85.00 (53.93, 117.10) μg/L, P<0.001). The results of multivariate logistic regression analysis showed serum GDF11( OR=0.98, 95% CI: 0.97-0.99) and traditional independent risk factors such as smoking, diabetes, C-reactive protein, homocysteine, lipoprotein (a) and apolipoprotein A1/B were independent correlate factors for the occurrence of STEMI ( P<0.05). Spearman correlation analysis showed that serum GDF11 was negatively correlated with SYNTAX score and Gensini score ( P<0.05). The nomogram model constructed by serum GDF11 combined with traditional independent risk factors (AUC=0.85, 95% CI: 0.81-0.89) had better predictive value for the occurrence of STEMI than the traditional nomogram model constructed by independent risk factors(AUC=0.80, 95% CI:0.75-0.84) or serum GDF11 (AUC=0.76, 95% CI: 0.72-0.81), all P<0.01. Conclusions:Serum GDF11 is an independent correlate factor in the occurrence of STEMI and is negatively correlated with the severity of coronary artery lesions in patients with STEMI. The nomogram model constructed based on GDF11 combined with traditional risk factors can be a good predictor for the occurrence of STEMI.

Objective To explore the effect of adeno-associated virus sense transfection up-regulating the expression level of the growth and differential factor 11 (GDF11) in vivo on aortic injury in type 2 diabetic mellitus rats (T2DM).Methods Nine-week-old male SD rats were randomly selected to establish a T2DM model by using high-sugar and high-fat chow plus small-dose streptozotocin (STZ) combined induction.Both normal rats and dia-betic model rats were randomly divided into five groups:blank control group (Control group) , negative virus con-trol group (NC group), GDF11 adeno-associated virus group (GDF11 group), diabetic group (DM group), and diabetic + GDF11 adeno-associated virus group (DM+GDF11 group) .After 8 weeks of feeding, the serum con-centrations of insulin (INS) , advanced glycosylation end products (AGES) , recombinant growth transforming fac-tor 11 (GDF11), total cholesterol (T-CHO), triglycerides (TG), low-density lipoproteins (LDL-C), high-densi-ty lipoproteins (HDL-C) , asymmetric dimethylarginine (ADMA) , and malondialdehyde (MDA) were assayed in the rats;periodic acid-schiff stain(PAS stain) was used to observe the sites of glycogen deposition, and hematoxy-lin-eosin staining (HE) was used to observe vascular damage.Scanning electron microscopy was used to observe the damage of vascular endothelial cells and vascular elastic fibers, and protein blotting and immunohistochemistry were used to detect the expression levels of vascular injury-related proteins.Protein blotting and immunohistochem-istry were used to detect the expression levels of vascular injury-related proteins.Results The biochemical inde-xes showed that the serum concentrations of AGES, T-CHO, TG, LDL-C and MDA were higher in the DM group than those in the Control group (P<0.05), the concentrations of INS, GDF11, HDL-C and ADMA were signifi-cantly lower than those in the Control group (P<0.05) , and the concentrations of AGES and HDL-C were not sig-nificantly lower in the DM+GDF11 group compared with the DM group (P<0.05) .HDL-C was not significantly different from the DM group, and several other data were improved (P<0.05) .Pathological staining suggested that PAS staining in the DM group suggested that glycogen particles deposited in the endothelium and subendotheli-um of the aorta, HE staining observed thickening of the aortic mesentery, endothelial cells and elastic fibers broke off in an irregular alignment, and electron microscopy observed endothelial damage in the vasculature and elastic fi-bers broke off in the DM group, and these changes attenuated in the DM+GDF11 group.Protein blotting and im-munohistochemistry indicated that the expression of endothelial cell-associated proteins decreased in the DM group (P<0.05) , and mesenchymal markers elevated in the DM group (P<0.05) , these proteins were regressed in the DM+GDF11 group, and the difference was statistically significant (P <0.05).Conclusion Increasing the expression level of GDF11 in vivo can improve aortic vascular injury caused by diabetes mellitus, which is inferred that it may be related to the inhibition of endothelial mesenchymal transition to protect the function of vascular endo-thelial cells and thus improve vascular injury.