Objective To analyze the impact factors on the occurrence of in-hospital adverse cardiovascular events(MACE)after percutaneous coronary intervention(PCI)in elderly patients with coronary heart disease(CHD),and to construct a prediction model in the form of a column-line diagram and to evaluate the effectiveness of the model.Methods The clinical data of 304 elderly coronary heart disease patients who underwent PCI from February 2021 to March 2024 in our hospital were collected.Patients were divided into MACE group(n=81)and non-MACE group(n=223)based on the occurrence of in-hospital MACE.The optimal cutoff values of each fac-tor were obtained by receiver operating characteristic(ROC)curve analysis.Logistic multiple regression modeling was used to investigate the risk factors of in-hospital MACE after PCI in elderly patients with CHD and a predictive model with columnar graphs was constructed.The correction curve was used for the internal validation of the column chart model and the decision curve was used for evaluating the pre-diction efficacy of the column chart model.Results The proportion of angina pectoris,Gensini score,the proportion of the implanted stent number＞2,and the levels of PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were higher in the MACE group than in the non MACE group,and the difference was statistically significant(P＜0.05).The results of ROC curve analysis showed that the optimal cut-off val-ues for Gensini integral,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were 21 points,38.64％,96.92μmol/L,8.56mg/L,247.67μg/L and 475.14mg/L,respectively.The results of Logistic multiple regression modeling showed that the number of implanted stents,Gensi-ni score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were risk factors for the occurrence of in-hospital MACE after PCI in elderly pa-tients with CHD.Internal validation shows that the C-index of the column-line graph model constructed in this study was 0.991(0.982-0.999).The observed values aligned well with the predicted values.The column-line diagram model with a threshold＞0.08 provided net clinical benefits above the number of implanted stent,Gensini score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a).Conclu-sion In this study,the column-line graph prediction model constructed based on the number of implantated stent,Gensini score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)had good predictive value for the occurrence of in-hospital MACE after PCI in elderly patients with CHD,which may provide a basis for targeted clinical interventions to reduce the occurrence of in-hospital MACE.

Objective To explore the related factors between Helicobacter pylori(Hp)infection and upper gastrointestinal bleeding in the patients with acute myocardial infarction.Methods A total of 180 pa-tients with acute myocardial infarction hospitalized in the department of cardiovascular medicine of Shaanxi Provincial People's Hospital from May 2021 to May 2023 were selected as the study subjects.The general condition of the patients was recorded,the relevant blood biochemical indexes of the patient were recorded,the 3C urea breath test was used to detect Hp,and the expression levels of VEGF,VCAM-1 and CTRP9 were de-termined by ELISA.All study subjects were followed up in 3 months after discharge,and the major adverse cardiac events(MACE)and upper gastrointestinal bleeding events during the follow-up period were recorded.Results Among the 180 study subjects,78 cases(43.33％)were Hp-negative and 102 cases(56.67％)were Hp-positive.The Hb level in Hp-positive patients was lower than that in Hp-negative patients,the levels of IL-6,IL-8,TNF-α,and C-reactive protein were higher than those in Hp-negative patients,and the differences were statistically significant(P＜0.05).The levels of VEGF and VCAM-1 in Hp-positive patients were high-er than those in Hp-negative patients,the level of CTRP9 was lower than that in Hp-negative patients,and the differences were statistically significant(P＜0.05).The results of logistic regression analysis showed that Hb,IL-6,IL-8,TNF-α and C-reactive proteins were the independent influencing factors in predicting Hp infec-tion(P＜0.05).The incidence rate of upper gastrointestinal bleeding events in Hp-positive patients was high-er than that in Hp-negative patients,and the difference was statistically significant(P＜0.05).Hp positivity,Hb and C-reactive protein were the independent influencing factors in predicting the occurrence of upper gas-trointestinal bleeding(P＜0.05).Conclusion The incidence rate of Hp infection in the patients with acute myocardial infarction is high,and the Hp positivity could promote the changes in the levels of various cyto-kines and further aggravate coronary artery injury.Hp infection may increase the incidence rate of upper gas-trointestinal bleeding in the patients with acute myocardial infarction.

Objective To investigate the protective effect and mechanism of RhoE overexpression in angiotensin Ⅱ-induced myo-cardial fibrosis.Methods Primary cardiomyocytes were cultured in vitro using angiotensin Ⅱ-induced myocardial fibrosis model,and transfected with M-RhoE-carrying overexpressing adenovirus and overexpressing RhoE according to subgroup.α-SMA and Smad3 ex-pression distribution in primary cardiomyocytes were detected by immunofluorescence.The protein expression levels of RhoE,GAPDH,α-SMA,Smad3 and p-Smad3 in primary cells were detected by Western blotting.Results Ang Ⅱ interferes with primary cardiomyo-cytes.Western-blot analysis showed that compared with the control group,the expression levels of p-Smad3 and α-SMA in Ang Ⅱgroup were increased,while the expression levels of RhoE were decreased(P＜0.05).After transfection of RhoE overexpressing adenovi-rus,Western blot results showed that the α-SMA expression level in Ang Ⅱ group was increased compared with that in the control group(P＜0.05).Compared with Ang Ⅱ group α-SMA expression level in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence detection showed that the α-SMA fluorescence intensity in Ang Ⅱ group was increased compared with that in control group(P＜0.05).Compared with Ang Ⅱ group α-SMA fluorescence intensity in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Effects of overexpression of RhoE gene on TGF-β1/Smad3 pathway.Western blot results showed that compared with the control group,the p-Smad3/Smad3 ratio in Ang Ⅱ group was increased(P＜0.05).Compared with Ang Ⅱ group,the p-Smad3/Smad3 ratio in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence nuclear translocation showed that compared with the control group,the red fluorescence in myocardial nucleus of Ang Ⅱ group was significantly increased(P＜0.05).Compared with Ang Ⅱ group,the red fluorescence in myocardial nucleus of Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Conclusion The process of Ang Ⅱ-induced myocardial fibrosis is accompanied by the activation of TGF-β1/Smad3 sig-naling pathway,and RhoE can inhibit Ang Ⅱ-induced myocardial fibrosis by inhibiting TGF-β1/Smad3 signaling pathway.

Objective To investigate the protective effect and mechanism of RhoE overexpression in angiotensin Ⅱ-induced myo-cardial fibrosis.Methods Primary cardiomyocytes were cultured in vitro using angiotensin Ⅱ-induced myocardial fibrosis model,and transfected with M-RhoE-carrying overexpressing adenovirus and overexpressing RhoE according to subgroup.α-SMA and Smad3 ex-pression distribution in primary cardiomyocytes were detected by immunofluorescence.The protein expression levels of RhoE,GAPDH,α-SMA,Smad3 and p-Smad3 in primary cells were detected by Western blotting.Results Ang Ⅱ interferes with primary cardiomyo-cytes.Western-blot analysis showed that compared with the control group,the expression levels of p-Smad3 and α-SMA in Ang Ⅱgroup were increased,while the expression levels of RhoE were decreased(P＜0.05).After transfection of RhoE overexpressing adenovi-rus,Western blot results showed that the α-SMA expression level in Ang Ⅱ group was increased compared with that in the control group(P＜0.05).Compared with Ang Ⅱ group α-SMA expression level in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence detection showed that the α-SMA fluorescence intensity in Ang Ⅱ group was increased compared with that in control group(P＜0.05).Compared with Ang Ⅱ group α-SMA fluorescence intensity in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Effects of overexpression of RhoE gene on TGF-β1/Smad3 pathway.Western blot results showed that compared with the control group,the p-Smad3/Smad3 ratio in Ang Ⅱ group was increased(P＜0.05).Compared with Ang Ⅱ group,the p-Smad3/Smad3 ratio in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence nuclear translocation showed that compared with the control group,the red fluorescence in myocardial nucleus of Ang Ⅱ group was significantly increased(P＜0.05).Compared with Ang Ⅱ group,the red fluorescence in myocardial nucleus of Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Conclusion The process of Ang Ⅱ-induced myocardial fibrosis is accompanied by the activation of TGF-β1/Smad3 sig-naling pathway,and RhoE can inhibit Ang Ⅱ-induced myocardial fibrosis by inhibiting TGF-β1/Smad3 signaling pathway.

Objective To analyze the impact factors on the occurrence of in-hospital adverse cardiovascular events(MACE)after percutaneous coronary intervention(PCI)in elderly patients with coronary heart disease(CHD),and to construct a prediction model in the form of a column-line diagram and to evaluate the effectiveness of the model.Methods The clinical data of 304 elderly coronary heart disease patients who underwent PCI from February 2021 to March 2024 in our hospital were collected.Patients were divided into MACE group(n=81)and non-MACE group(n=223)based on the occurrence of in-hospital MACE.The optimal cutoff values of each fac-tor were obtained by receiver operating characteristic(ROC)curve analysis.Logistic multiple regression modeling was used to investigate the risk factors of in-hospital MACE after PCI in elderly patients with CHD and a predictive model with columnar graphs was constructed.The correction curve was used for the internal validation of the column chart model and the decision curve was used for evaluating the pre-diction efficacy of the column chart model.Results The proportion of angina pectoris,Gensini score,the proportion of the implanted stent number＞2,and the levels of PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were higher in the MACE group than in the non MACE group,and the difference was statistically significant(P＜0.05).The results of ROC curve analysis showed that the optimal cut-off val-ues for Gensini integral,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were 21 points,38.64％,96.92μmol/L,8.56mg/L,247.67μg/L and 475.14mg/L,respectively.The results of Logistic multiple regression modeling showed that the number of implanted stents,Gensi-ni score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)were risk factors for the occurrence of in-hospital MACE after PCI in elderly pa-tients with CHD.Internal validation shows that the C-index of the column-line graph model constructed in this study was 0.991(0.982-0.999).The observed values aligned well with the predicted values.The column-line diagram model with a threshold＞0.08 provided net clinical benefits above the number of implanted stent,Gensini score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a).Conclu-sion In this study,the column-line graph prediction model constructed based on the number of implantated stent,Gensini score,PAG,Scr,hs-CRP,Lp-PLA2 and Lp(a)had good predictive value for the occurrence of in-hospital MACE after PCI in elderly patients with CHD,which may provide a basis for targeted clinical interventions to reduce the occurrence of in-hospital MACE.

【Objective】 To evaluate the effects of miR-148a-3p on calreticulin (CRT) expression and mitochondrial function in cardiomyocytes incubated with high glucose. 【Methods】 miR-148a-3p minic and inhibitor were used to intervene the H9c2 cardiomyocytes of rats. The expression of CRT protein was detected. Then the cells were divided into control group, high-glucose group (HG), HG +miR-148a-3p minic group, HG + miR-148a-3p minic + TG (CRT agonist) group, HG + miR-148a-3p inhibitor group, and HG + miR-148a-3p inhibitor + CRT- (CRT-siRNA) group. The content of adenosine triphosphate (ATP) and the level of reactive oxygen species (ROS), the activity of mitochondrial respiratory chain complex enzyme and apoptotic rate were detected. 【Results】 miR-148a-3p minic significantly inhibited the expression of CRT protein in cardiomyocytes, while miR-148a inhibitor increased the expression of CRT. miR-148a-3p minic inhibited the decrease of ATP production, the increase of ROS production and cell apoptosis, and the inactivity of mitochondrial respiratory chain complex enzyme in cardiomyocytes induced by high glucose, while TG weakened the above effects of miR-148a-3p minic. miR-148a inhibitor aggravated the mitochondrial injury and apoptosis of cardiomyocytes induced by high glucose, but the effects of miR-148a-3p inhibitor were partially blocked by CRT-siRNA. 【Conclusion】 miR-148a-3p negatively regulates the expression of CRT in cardiomyocytes and protects the mitochondrial injury and apoptosis induced by high-glucose through inhibiting CRT.

Objective: To investigate the correlation between serum melatonin level and cardiac function, blood lipid in patients of heart failure with preserved ejection fraction (HFpEF). Methods: One hundred and seventy patients with HFpEF (HFpEF group) in Ninth Hospital of Xi′an City from May 2016 to May 2018 were selected. According to the cardiac function grading of New York Heart Association (NYHA), Ⅱ grade (cardiac function Ⅱ grade) was in 98 cases, and Ⅲ grade (cardiac function Ⅲ grade) was in 72 cases. Then, 32 healthy volunteers were selected as control group. The 2 groups were sampled at 2:00 and 7:00, and the level of melatonin was detected by enzyme-linked immunosorbent assay. The correlation between serum melatonin level and cardiac function, blood lipid were analyzed (Pearson correlation), including triglyeride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), N-terminal precursor brain natriuretic peptide (NTproBNP), hypersensitive C reactive protein (hs-CRP), ejection fraction, left ventricular end-diastolic volume index (LVEDVI), miral diastolic early and end-diastolic maximum blood flow velocity ratio (E/A) and peak value of early diastolic blood flow velocity in the mitral valve and peak value of the early diastolic velocity of the mitral annulus (E/e′). Results: The TG, TC, LDL-C, NTproBNP and hs-CRP in cardiac function Ⅲ grade patients were significantly higher than those in cardiac function Ⅱ grade patients: (1.51 ± 0.69) mmol/L vs. (1.15 ± 0.75) mmol/L, (4.03 ± 1.02) mmol/L vs. (3.47 ± 0.94) mmol/L, (1.42 ± 0.33) mmol/L vs. (1.17 ± 0.31) mmol/L, (3 438.54 ± 553.58) ng/L vs. (3 034.58 ± 557.35) ng/L and (4.26 ± 2.54) mg/L vs. (3.12 ± 2.13) mg/L, the HDL-C, ejection fraction and E/A were significantly lower than those in cardiac function Ⅱ grade patients: (2.44 ± 0.88) mmol/L vs. (2.97 ± 0.94) mmol/L, (56.23 ± 5.26)% vs. (61.11 ± 5.33)% and 0.82 ± 0.18 vs. 0.91 ± 0.17, and there were statistical differences (P<0.01). The melatonin levels at 2:00 and 7:00 in control group and cardiac function Ⅱgrade patients of HFpEF group were significantly higher than those in cardiac function Ⅲ grade patients of HFpEF group: (454.24 ± 123.54) and (432.68 ± 155.68) ng/L vs. (368.85 ± 98.52) ng/L, (483.25 ± 90.54) and (418.54 ± 103.57) ng/L vs. (345.85 ± 98.52) ng/L, the melatonin level at 7:00 in control group was significantly higher than that in cardiac function Ⅱ grade patients of HFpEF group, and there was statistical difference (P<0.01). In cardiac function Ⅱ grade patients of HFpEF group, the melatonin level was correlated with TG, TC, LDL-C and HDL-C (P<0.01); In cardiac function Ⅲ grade patients of HFpEF group, the melatonin level was correlated with NTproBNP, hs-CRP, ejection fraction, LVEDVI, E/A, E/e′, TG, TC, LDL-C and HDL-C (P<0.01 or <0.05). Conclusions The melatonin level is correlated with the level of blood lipid in HFpEF patients. Melatonin level is correlated with cardiac function Ⅲ grade patients, but this phenomenon is not observed in cardiac function Ⅱ grade patients.