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Objective To investigate the relationship between mean platelet volume(MPV)and saphenous vein graft restenosis in patients receiving coronary artery bypass grafting(CABG),and to analyze the clinical significance of MPV in the prediction of restenosis after CABG.Methods A total of 354 patients admitted into Tianjin chest hospital from September 2009 to September 2014 with suspected myocardial ischemic events 3 to 5 years after CABG treatment was enrolled for a retrospective analysis.According to the coronary angiography(CAG)results,patients were divided into the vein bridge vascular lesion group(saphenous vein graft diseases,SVGD)(n=233)and the venous bridge vascular patency group(saphenous vein graft,SVG)(n=121).Paired t test was used to analyze the relationship between different factors and the bridge vascular patency.The binary logistic regression was used to analyze the effects of MPV and other factors on bridge vascular patency.Venous bridge stenosis ＞ 50％ was considered to be clinically significant and to damage myocardial blood supply.Results The MPV was higher in the SVGD group than the SVG group [(10.2±1.5)fl vs.(9.6±1.5)fl,P＜0.01].The logistic regression analysis showed that MPV(OR =1.268,95％CI:1.053-1.570,P=0.014),age(OR =1.007,95％CI:1.038-1.117,P=0.000),gender (OR=0.452,95％CI:0.250-0.816,P=0.008),diabetes mellitus(OR=2.319,95％CI:1.221-4.405,P =0.010)were the independent risk factors for venous bridge stenosis in the two groups,gender(OR=0.495,95％CI:0.251-0.976,P=0.042),diabetes mellitus(OR =2.237,95％CI:1.105-4.527,P =0.025),MPV(OR=1.334,95％CI;1.050 1.694,P=0.018),fibrinogen(OR=1.654,95％CI:1.020-2.682,P =0.041)were the independent risk factors for venous bridge stenosis in non-elderly patients,and age(OR =1.178,95％CI:1.116-1.244,P =1.178)was an independent risk factor for vein graft stenosis in elderly patients.The restenosis rate was higher in patients with MPV ≥ 12 fl(92.6％ or 25/27) than in the patients with MPV ＜ 12 fl(63.6％ or 208/327).The receiver operating characteristics(ROC) curve showed that the areas under the curve of MPV,age,gender,diabetes,fibrinogen were 0.610,0.657,0.394,0.626,0.654,respectively,and the area under the curve of joint diagnosis was 0.796,showing that joint prediction value was higher than any single prediction value(P＜0.01).Conclusions MPV level is an independent risk factor for vein graft stenosis,and has higher predictive value in combination with age,gender,diabetes and fibrinogen.
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Objective To explore the relationship between serum levels of osteoprotein (OPG), soluble nuclear factor-κB receptor activator ligand (sRANKL), inflammatory factors and coronary heart disease (CHD) and its severity. Methods The patients who underwent coronary angiography (CAG) due to chest pain admitted to department of cardiology of Tianjin Chest Hospital from April 2017 to December 2018 were enrolled, and they were divided into CHD group and non-CHD group according to the CAG results. The gender, age, history of hypertension, smoking history, diabetes, the levels of cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein AI (apoAI), apolipoprotein B (apoB), lipoprotein (a) [Lp (a)], MB isoenzyme of creatine kinase (CK-MB) and other clinical data of patients were collected. The serum levels of OPG, sRANKL, matrix metalloproteinase-9 (MMP-9), monocyte chemotactic protein-1 (MCP-1), insulin-like growth factor-1 (IGF-1) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay (ELISA). According to the results of CAG, the patients with CHD were divided into single-, double-, triple-branch coronary artery lesion groups, and the relationship between the levels of serum OPG, sRANKL, inflammatory factors and the degree of coronary artery lesions was observed. Multivariate Logistic regression was used to analyze the risk factors of CHD, and receiver operating characteristic (ROC) curve was plotted to analyze the predictive value of main risk factors for CHD. Results A total of 472 patients were enrolled in the final analysis during the study period, including 264 patients in the CHD group, 208 patients in the non-CHD group, 79 patients in the CHD group with single-branch disease, 75 patients with double-branch disease, and 110 patients with three-branch disease. ① Compared with the non-CHD group, the CHD group had more older male patients, as well as higher proportion of hypertension and diabetes, the levels of serum Lp (a) and CK-MB were significantly increased, and the levels of serum HDL-C and apoAI were significantly lowered. There was no statistically significant difference in serum TC, LDL-C, or apoB between the two groups. The levels of serum OPG, MMP-9, MCP-1, IGF-1 and IL-6 in the CHD group were significantly higher than those in the non-CHD group [OPG (μg/L): 1.79±0.50 vs. 1.50±0.30, MMP-9 (μg/L): 57.91 (33.50, 130.46) vs. 38.33 (29.43, 109.78), MCP-1 (μg/L):298.30 (207.96, 537.16) vs. 252.73 (165.22, 476.01), IGF-1 (μg/L): 734.03±486.11 vs. 217.75±126.45, IL-6 (ng/L):64.76±40.25 vs. 48.60±15.80, all P < 0.05], and the levels of serum sRANKL was significantly lower than that in the non-CHD group (ng/L: 344.31±122.14 vs. 378.74±109.27, P < 0.05). ② The serum OPG level showed a slight upward tendency with the increase in the number of coronary artery lesions, and the sRANKL level showed a slight downward tendency [OPG (μg/L) in the single-, double-, triple-branch coronary artery lesion groups was 1.74±0.49, 1.76±0.50, 1.85±0.52, and sRANKL (ng/L) was 354.96±116.64, 340.05±124.24, 339.57±125.03, respectively) without statistically significant differences (all P > 0.05). The levels of IGF-1 and IL-6 were increased with the number of coronary artery lesions [IGF-1 (μg/L) in the single-, double- and triple-branch coronary artery lesions groups was 372.13±258.42, 676.06±350.29, 1 033.47±468.06, and IL-6 (ng/L) was 48.87±16.72, 65.36±18.84, 75.76±22.72, respectively], and the differences among different lesion groups were statistically significant (all P < 0.01). Correlation analysis showed that IGF-1 level was significantly positively correlated with the number of coronary artery lesions (r = 0.612, P < 0.01), while IL-6 was not correlated with the number of coronary artery lesions (r = 0.185, P > 0.05).③ Multivariate Logistic regression analysis showed that elevated serum OPG and IGF-1 levels were risk factors for CHD [OPG: odds ratio (OR) = 1.995, 95% confidence interval (95%CI) = 1.936-2.067, P = 0.012; IGF-1: OR = 1.009, 95%CI = 1.004-1.015, P = 0.001]. ④ ROC curve analysis showed that the area under ROC curve (AUC) of OPG and IGF-1 was 0.716 and 0.867, respectively. When the cut-off value of OPG was 1.13 μg/L, the sensitivity was 81.7%, the specificity was 58.1%; when the cut-off value of sRANKL was 401.20 μg/L, the sensitivity was 69.7%, the specificity was 95.7%. Conclusions CHD was associated with increased in OPG, related inflammatory cytokines including MMP-9, MCP-1, IGF-1 and IL-6, and decreased in sRANKL. The level of IGF-1 was positively correlated with the severity of CHD. The serum levels of OPG and IGF-1 were risk factors for CHD, which had good predictive value for CHD.
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Objective To explore the polymorphisms of T149C and T950C gene in osteoprotectin (OPG) promoter sites and the levels of serum OPG and soluble nuclear factor-κB receptor activator ligand (sRANKL) and the incidence of coronary heart disease (CHD). Methods 528 patients in Tianjin suspected of CHD and underwent coronary angiography (CAG) who admitted to the department of cardiology of Tianjin Chest Hospital from April 2017 to December 2018 were enrolled. According to the CAG results, they were divided into two groups: CHD group (n = 302) and non-CHD group (n = 226). The gender, age, history of hypertension, family history of CHD, diabetes, levels of blood lipid parameters in serum and other clinical data of patients were recorded. The levels of serum OPG and sRANKL were measured by enzyme-linked immunosorbent assay (ELISA). T149C and T950C gene polymorphisms were analyzed by polymerase chain reaction-restriction endonuclease fragment length polymorphism (PCR-RFLP) methods. Hardy-Weinberg genetic balance test was performed for alleles. Binomial classification multivariate non-conditional Logistic regression method was used to analyze the relationship between T149C and T950C gene polymorphisms, serum levels of OPG and sRANKL and CHD. Results All patients were enrolled in the final analysis. The serum level of OPG in CHD group was significantly higher than that in non-CHD group (μg/L: 1.76±0.49 vs. 1.47±0.29, P < 0.01), the serum level of sRANKL was significantly lower than that in non-CHD group (ng/L: 342.14±121.38 vs. 376.63±108.66, P < 0.05). Logistic regression analysis showed that after adjusting for age, gender, blood lipid parameters, diabetes and other factors, the increase in serum OPG level was an independent risk factor for CHD [odds ratio (OR) = 1.995, 95% confidence interval (95%CI) = 1.935-2.066, P = 0.012]. PCR-RFLP results showed that TT, TC and CC genotypes were found in T149C and T950C of OPG promoter. According to Hardy-Weinberg equilibrium test, the polymorphisms of OPG T149C and T950C accorded with Hardy-Weinberg law, achieving genetic balance with representative of the population. The frequencies of TT, TC, CC and alleles T and C in T149C genotypes of non-CHD group were 53.5%, 42.9%, 3.6%, 75.0% and 25.0%, respectively, and they were 43.1%, 50.3%, 6.6%, 68.2% and 31.8%, respectively in CHD group. There were statistically significant differences in genotype and allele frequencies between the two groups (all P < 0.05). It was shown by Logistic regression analysis that the risk of CHD in TC+CC genotype of T149C was 1.86 of TT genotype (OR = 1.86, 95%CI = 1.24-2.78, P = 0.003). It was suggested that C allele might be a susceptible gene for CHD. In non-CHD group, the frequencies of TT, TC, CC, and alleles T and C in T950C genotypes were 39.8%, 46.5%, 13.7%, 63.1% and 36.9%, respectively. They were 39.4%, 43.4%, 17.2%, 61.1% and 38.9%, respectively in CHD group. There were no significant differences in genotype and allele frequencies between the two groups (all P > 0.05). Logistic regression analysis showed that TC+CC genotype of T950C was not related with CHD. Conclusions The increased level of serum OPG was closely related with CHD and could be used as a risk factor for CHD. The cases carried OPG T149C TC+CC genotype might have the risk suffering CHD. C allele is might be a susceptible gene.
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Objective Mouse models of sepsis-induced myocardial injury by intraperitoneal injection of lipopolysaccharide (LPS) was established in order to provide a reliable method for the research of pathogenesis of sepsis-induced myocardial injury. Methods According to the method of random number table, a total of 150 male C57BL/6 mice were divided into five groups: NC group, sham group, and LPS 10, 12, 15 mg/kg groups, with 30 in each group. Septic myocardial injury was induced by intraperitoneal injection LPS in mice; sham group was injected with equal 0.9% saline; while there was no treatment in mice of NC group. Fifteen of the 30 mice in each group were used to observe the general status of mice before and after LPS or saline injection. Twenty-four hours after LPS or saline injection, the left ventricular function was assessed by echocardiography, serum level of cardiac troponin (cTnI) was determined by enzyme linked immunosorbent assays (ELISA), and the cardiac histomorphology and ultrastructure were observed; the other 15 mice were used to monitor the 7-day mortality after LPS or saline injection. Results The mice challenged to LPS displayed symptoms of sepsis, such as depression, ruffled fur, and diarrhea. Compared with NC group, left ventricular ejection fraction (LVEF), left ventricular fraction shortening (LVFS) were significantly decreased at 24 hours after LPS administration in LPS 10, 12, 15 mg/kg groups [LVEF: 0.459±0.044, 0.432±0.034, 0.348±0.064 vs. 0.588±0.019, LVFS: (22.36±2.60)%, (20.78±1.91)%, (16.27±3.31)% vs. (30.55±1.30)%, all P < 0.01], and cTnI levels were significantly increased (ng/L: 270.40±43.50, 281.14±41.79, 298.39±42.05 vs. 192.59±16.90, all P <0.01). Myocardium injury was observed in three LPS groups, myocardial fibrosis, interstitial edema, erythrocyte leakage and infiltrating inflammatory cells were observed under light-microscope; ultrastructural changes disorderly arranged in cardiac muscle fibers, mitochondrial swelling and even partly missing mitochondria cristae were found under transmission electron microscope (TEM), and the higher of the dose, the more sever of the damage. There was no significant difference between sham group and NC group. The 7-day mortality in LPS 10, 12, 15 mg/kg groups were 33.3%, 53.3% and 86.7%, respectively, while no death in the NC group and sham group. Conclusion For establishing the mouse model of sepsis-induced myocardial injury, intraperitoneal injection with 12 mg/kg LPS is a preferable choice in our research.
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Objective To investigate the protective effects of MicroRNA-214 on myocardial injury induced by myocardial ischemia and reperfusion,as well as the regulation mechanism of PI3K and its downstream protein kinase B(AKT)and FoxO1(PI3K / AKT / FoxO1).Methods Wistar rats were randomly divided into 4 groups:sham operation group(Sham group),myocardial ischemia reperfusion injury(IRI)group(IRI group),microRNA-214+sham operation group(MS group),microRNA-214+IRI group(MI group),(n=10,each).The cardiac function was detected at 6 h after ischemia-reperfusion operation.And blood lactate dehydrogenase(LDH),creatine kinase(CK),creatine phosphate kinase isoforms MB(CK-MB),cardiac troponin T(cTnT),serum B natriuretic peptide(pro-BNP)in plasma were detected by enzyme-linked immunosorbent assay(ELISA).Interleukin 10(IL-10),Interleukin 6(IL-6)and tumor necrosis factor α(TNF-α)were assayed.Pathological changes of myocardial tissue were detected by HE and Masson.The expression of microRNA-214 was detected by RT-PCR.The expression of Bax,Caspase-3,BCl2,PI3K,Akt,FoxO1 was detected by Western Blot.Results Compared with Sham group,IRI group showed a significantly increases in myocardial injury parameters of LDH,CK,IL-6 and TNF concentration in plasma,and a significantly reduced concentration of IL-10(P<0.05).And compared with Sham group,MI group showed a significantly increased expression of microRNA-214(P<0.05)and showed a significantly increased myocardial parameters of Bax,Caspase-3,PI3K,Akt protein,and a decreased level of BCl2,FoxO1(P<0.05).Compared with IRI group,microRNA-21 group showed a reduced myocardial ischemia-reperfusion-induced myocardial injury in rats and a reduced plasma concentration of LDH,CK,IL-6 and TNF-alpha,a inhibited expression of caspase-3,Bax,myocardial PI3K and Akt,and a promoted expression of BCl2 and FoxO1 protein(P<0.05).Conclusions MicroRNA-214 reduces the myocardial injury induced by myocardial ischemia-reperfusion through PI3K/Akt signaling pathway.
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Objective To investigate the effect of rhBNP in treating pulmonary hypertension after mitral value replacement (MVR) compared with PGE1.Methods 60 patients with pulmonary hypertension after MVR were randomly divided into 3 groups(control group, PGE1 group and rhBNP group).Hemodynamic factors(MAP, CVP, mPAP, etc.) were monitored before and after taking medicine at 1 h, 6 h, 24 h, respectively including drug withdrawal 2 h.TXA2 and cGMP were analyzed by ELISA.To observe the levels of TXA2 and cGMP in plasma before and after treatment with rhBNP and PGE1 for three times (24 h, 1 week and 3 months).Information about patients'mechanical ventilation time was also recorded.Results Patients' mechanical ventilation time in PGE1 group was the shortest.MAP, mPAP, PRVI, PAWP were reduced after treatment by medicine 1 h for in PGE1 group.However, these indexes were rebound after drug withdrawal.mPAP, PRVI, PAWP in rhBNP group decreased after treatment by medicine at 6 h.The decreased level of mPAP was less than that in PGEI group.In control group, TXA2 went down and cGMP went up after operation.After taking medicine at 24 h, TXA2 decreased and cGMP increased in both PGE1 and rhBNP group.The increased level in rhBNP group was higher than that of control group.With medicine, the decreased level of TXA2 in PGE1 was also higher than that in rhBNP group.The going-up of cGMP in rhBNP was higher than that in PGE1.Conclusion Both rhBNP and PGE1 can reduce pulmonary artery pressure, PGE1 is more effective than that of rhBNP.
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Objective:To investigate the effect of chronic alcohol consumption on both left ventricular myocardial collagen and diastolic function in rats,and their relationship thereof.Methods:Twenty-four male Wistar rats were randomly divided into 2 groups:control group(n=12)and ethanol group(n=12).The changes in cardiac diastolic function were evaluated by echocardiography and tissue Doppler imaging(TDI).The value of myocardial hydroxyproline content was determined by hydroxyproline reagent kit.The expressions of collagen Ⅰ and collagen Ⅲ mRNA were detected by RT-PCR analysis.Results:It was found that mitral E and mitral annulus Ea were decreased,mitral annulus Aa was increased,and isovolumic relaxation time(IVRT)was prolonged in the ethanol group compared with those in control group(P＜0.05).The value of Ea/Aa ratio was greater than 1 in control group and less than 1 in ethanol group(P＜0.01).It was found that myocardial hydroxyproline content,collagen Ⅰ,collagen Ⅲ mRNA expression and their ratio significantly increased in ethanol group compared with those in the control group(P＜0.01).There was positive correlation between hydroxyproline content,collagen Ⅰ,collagen Ⅲ mRNA expression,and collagen Ⅰ /collagen Ⅲ mRNA ratio with IVRT(P＜0.05),and negative correlation between hydroxyproline content,collagen Ⅰ,collagen Ⅲ mRNA expression,and collagen Ⅰ /collagen Ⅲ mRNA ratio with the Ea/Aa ratio(P＜0.01).Conclusion:Chronic ethanol consumption can induce increase in left ventricular myocardial collagen synthesis and impairment in diastolic function in rats.Left ventricular diastolic dysfunction correlates with increase in myocardial collagen synthesis positively.
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Objective:To investigate the role of serum inflammatory cytokines in the development of acute coronary syndrome (ACS). Methods: All of enrolled patients were diagnosed by clinical and coronary angiographic features and divided into four groups, the acute myocardial infarction (AMI) group, unstable angina pectoris (UAP) group, stable angina pectoris (SAP) group and control group. The values of high-sersitivity C-reactive protein(hs-CRP), matrix metallopeptidase 9(MMP-9) and tumor necrosis factor-a (TNF-a) in serum were measured by cytokine detection equipment system (B10-RAD Biological Technology Co.Ltd, USA) and analysed in four groups with statistics. Results: Compared with SAP and the control groups, the levels of TNF-a and MMP-9 were increased significantly in AMI group(P 0.05). It was found that there was positive relation between hs-CRP, MMP-9 and TNF-a by Pearson correlation analysis. Conclusion:There was obvious relation between coronary heart disease and inflammation. The cytokines characterized by the increases of hs-CRP, TNF-a and MMP-9 were involved in the formation and progression of atherosclerosis and served as markers of unstable plagues.
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Objective To investigate the association of monocyte chemoattractant protein-1 (MCP-1) promoter -2518A/G gene polymorphism with coronary lesions and in stent restenosis in Tianjin Chinese population. Methods Two hundred and seventy six patients who underwent percutaneous coronary intervention (PCI) and coronary angiography during follow-up were enrolled in the study. The MCP-1 gene promoter polymorphism at position -2518 was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results The frequencies of three genotypes of MCP-1-2518A/G polymorphism were 21.0% AA, 34. 1% GG,44.9% AG, respectively. There were no statistical differences in the number and the mean degree of stenosis vessels before PCI among 3 genotype groups (all P＞0.05). 113 cases developed in-stent restenosis and 163 cases were free from restenosis. In restenosis group, the AA, AG and GG genotype frequencies were 23.9%, 40.7%, 35.4%, against 19.0%, 47.9% and 33.1% in nonrestenosis group (P = 0. 446) . The frequencies of -2518A and G allele were 44.2%, 55.8% in restenosis group versus 42.9%, 57. 1% in non-restenosis group(P=0. 761). Conclusions The polymorphism of MCP-1-2518 A/G gene may be associated with neither atherosclerosis nor the in-stent restenosis.