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【Objective】 Coronary no-reflow during percutaneous conranary intervention (PCI) often results in the failure of ischemic myocardial reperfusion and major adverse cardiovascular events (MACE). The present study sought to evaluate whether the GRACE risk score can predict coronary no-reflow in STEMI patients undergoing PCI. 【Methods】 We consecutively recruited 1 118 patients with STEMI who were admitted to Gansu Provincial People’s Hospital and The First Affiliated Hospital of Xi’an Jiaotong University from January 2009 to December 2011. Main demographic data, cardiovascular risk factors, blood lipid and other biochemical indicators were recorded. Coronary angiography was performed by a radial artery approach using the standard Judkins technique. Coronary no-reflow was evaluated by at least two independent experienced cardiologists. The GRACE risk score was calculated with a computer program. All the cases were followed up by medical records, face-to-face interviews or telephone calls. Finally, we analyzed the predictive value of the GRACE risk score for coronary non-reflow and MACE in STEMI patients undergoing PCI. 【Results】 During a median period of 36 months, 58 of the 1 118 patients (5.2%) were lost to follow-up. Of the remaining 1 060 patients, 118 (11.1%) had no-reflow and 147 (13.9%) had MACE. The GRACE score was higher in patients with no-reflow than those without no-reflow. Multivariate logistic regression established that the GRACE score was an independent predictor for coronary no-reflow (OR=1.034; P=0.002). And multivariate Cox analysis showed the GRACE score was an independent predictor of MACE. The area under the ROC curve for coronary no-reflow and MACE was 0.719 and 0.697, respectively. Kaplan-Meier analysis showed that the probability of rehospitalization for heart failure, reinfarction, all-cause death and cumulative cardiovascular events increased with the increase of the GRACE risk score. 【Conclusion】 The GRACE risk score is a readily available predictive scoring system for coronary no-reflow and MACE in STEMI patients.
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To compare the efficacy of 40 mg and 10 mg atorvastatin on serum levels of 8-Hydroxy-Guanin [8-OHdG] and the cardiac function in patients with ischemic cardiomyopathy [ICM]. One hundred twenty three hospitalized ICM patients and 120 healthy controls were included in this study. All subjects were randomly divided into two groups: 10 mg/d atorvastatin group [n=62] and 40 mg/d atorvastatin group [n=61]. Serum levels of C-reactive protein [CRP], creatine kinase, glutamic-pyruvic transaminase, lipids and B-type natriuretic peptide [BNP] were tested in all subjects both at the initial phase and the terminal phase of this study. Adverse drug reaction events were recorded in this study. Echocardiographic method was applied to compare the cardiac function before and after treatment in the double blind study. Serum 8-OHdG levels were tested by enzyme-linked immunosorbent assay [ELISA] before and after treatment, and the results in atorvastatin treatment groups were compared with the healthy controls. Serum 8-OHdG levels in ICM patients were significantly higher than that in normal control groups [p<0.05]. There was significant difference of Serum 8-OHdG levels in 40 mg/d atorvastatin group [p<0.05], but was no significant difference in 10 mg/d atorvastatin group before and after the treatment. The 8-OHdG level in 40 mg/d atorvastatin group was significantly lower than that in 10 mg/d atorvastatin group before the treatment as well as after the treatment [p<0.05]. The systolic and diastolic function improved significantly in 40 mg/d atorvastatin group before and after treatment, as well as in comparison with 10 mg/d atorvastatin group [p<0.05]. Serum 8-OHdG possibly plays an important role in the pathogenesis of ICM. Atorvastatin is safe and effective in ICM treatment; furthermore atorvastatin which also has independent lipid lowering effect, is significantly better in the dose of 40 mg/day
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Embryonic stem cells (ESCs) show potential prospect of wide application in establishing cardiac pharmacological model system, forming three-dimensional cardiac tissues and constructing biological pacemaker. The process of ESCs differentiating into cardiomyocytes is to simulate heart growth and development in vitro. The cases of transplanting ESCs into animal models confirm that the cardiac function is improved. Moreover, the research and exploitation of tissue engineered cardiac muscle tissue with vessel system brings hope for clinical cardiac muscle restoration. ESC-derived pacemaker can functionally integrate with quiescent ventricular muscle cells to induce rhythmic electrical and contractile activities in vitro. However, the immunological rejection limits its clinical application. Although ESCs have strong differentiation potential, the problems such as the differentiation process towards cardiomyocytes, ESC induction and signal regulatory pathway, and whether induced cardiomyocytes can substitute in vivo cardiomyocytes still need exploration.
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Aim To investigate the effects of cyclosporin A (CsA) on growth and collagen synthesis of cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP). Methods CFs of neonatal Sprague-Dawley rats were isolated by trypsinization and cultured; growth-arrested CFs were stimulated with 1×10-7 mol·L-1 AVP in the presence or absence of CsA (0.05, 0.5 and 5 μmol·L-1). MTT and flow cytometry techniques were adopted to measure cell number and analyze cell cycle respectively. Collagen synthesis was determined by measurement of hydroxyproline content in culture supernatant with colorimetry. Calcineurin activity was estimated by chemiluminescence. Trypan blue staining to test the viability of CFs. Results 0.05, 0.5 and 5 μmol·L-1 CsA inhibited the increase of CFs number induced by 1×10-7 mol·L-1 AVP in a dose-dependent manner, with the inhibitory rates by 12%, 24% and 29%, respectively (P＜0.05). Furthermore, cell cycle analysis showed 0.5 μmol·L-1 CsA decreased the S stage percentage and proliferation index of CFs stimulated by AVP (P＜0.05). In culture medium, the hydroxyproline content induced by AVP decreased by 0.5 and 5 μmol·L-1 CsA (P＜0.05), with the inhibitory rates of 29% and 33%, respectively. CsA completely inhibited the increment of calcineurin activity induced by AVP (P＜0.01), but CsA itself had no effect on the baseline of calcineurin activity and CFs viability. Conclusion CsA inhibits proliferation and collagen synthesis of CFs by virtue of blocking calcineurin signaling pathway and might provide a novel target for prevention and treatment to cardiac fibrosis.
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BACKGROUND: Radiofrequency catheter ablation (RFCA) in dog triggers myocardial nerve sprouting and sympathetic hyperinnevation. It is possible that RFCA in humans has the same effect. Nerve growth factor (NGF) is a neurons nurture that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, it is hypothetic that RFCA can increases plasma NGF concentration in humans.OBJECTIVE: To test the hypothesis that RFCA increases plasma NGF concentration in humans.DESIGN: Self-control experiment.SETTING: Department of Cardiology, Tangdu Hospital, the Fourth Military Medical University of Chinese PLA.PARTICIPANTS: Forty-three patients were selected from the Cardiological Department of Tangdu Hospital, the Fourth Military Medical University of Chinese PLA from January to June 2005, including atrioventricular nodal reentrant tachycardia (AVNRT) (n=18), right-sided accessory pathways (RSAP) (n=13) and left-sided accessory pathways (LSAP) (n=12), 20 males and 23 females, ages 28-65 years, all agreed to participate in the study voluntarily.METHODS: Blood samples were obtained from the peripheral veins before ablation and at 6 hours, 1, 3, 5, 7 days after ablation. The plasma concentration of NGF was determined with enzyme-linked immunosorbent assay (ELISA).MAIN OUTCOME MEASURES: The plasma concentration of NGF was determined with ELISA before RFCA and at 6 hours, 1, 3, 5, 7 days after RFCA in each patient.RESULTS: Total 43 patients who were referred for ablation therapy for AVNRT, RSAP and LSAP were involved in the result analysis without loss. Plasma NGF increased at 6 hours after RFCA. Increased NGF continued to 7 days in the RFCA treated patients. The plasma NGF concentrations at 6 hours, 1, 3, 5, 7 days after RFCA in AVNRT, RSAP and LSAP ablations treated patients were (29.72±7.04), (30.94±5.68),(31.39 ±4.92), (31.06 ±4.56), (29.11 ±4.59), (31.77 ±6.25), (30.69 ±5.10),(31.46±4.96), (30.15±4.01), (30.43±3.14), (31.42±6.75), (31.00±5.20),(32.08±4.62), (30.67±3.71), (29.27±2.75) μg/L, respectively, and all more than that before RFCA [(14.89±2.84), (15.00±2.71), (15.51±2.75) μg/L, P ＜ 0.01]. However, there were no significant differences in the NGF levels at 6 hours, 1, 3, 5 and 7 days after RFCA (P ＞ 0.05). The plasma NGF concentration was not significant different among AVNRT, RSAP and LSAP ablation patients at any given time (P ＞ 0.05). The number of RFCA applications, the procedure time and the total energy have no correlation with NGF concentration at any given time instance.CONCLUSION: RFCA increases plasma NGF concentration in humans and lasts for at least 7 days. The number of RFCA applications, the procedure time and the total energy have no correlation with NGF concentration at any given time instance.
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Background Cardiac mast cell-derived chymase is involved in myocardial fibrosis,but the underlying mechanisms remain unclear. Objective To investigate the effect of chymase on the collagen synthesis and its relationship with transforming growth factor-?1 (TGF-?1)/Smad pathway in rat cardiac fibroblasts (CFs). Methods CFs,from neonatal SD rats,were isolated by trypsinization. The collagen synthesis of CFs was determined by 3H-proline incorporation. The protein expressions of TGF-?1,phosphorylated Smad2/3 (P-Smad2/3) and total Smad2/3 were determined by immunoblotting in CFs. Results Chymase (15,30 and 60 ?g/L) increased the 3H-proline incorporation in a concentration-dependent manner. 30 ?g/L chymase stimulation increased the protein expressions of TGF-?1 and P-Smad2/3 in a time-dependently,while little effect on Smad2/3 protein expression was found. The stimulatory effect of chymase on 3H-proline incorporation elicited by 30 ?g/L chymase was blocked in the presence of TGF-?1 antibody or staurosporine,a P-Smad2/3 inhibitor. Conclusion Chymase promotes collagen synthesis of rat CFs,TGF-?1/Smad might be involved into the signal pathway.
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To study the electrophysiological mechanism of atrial fibrillation induced by acetylcholine(Ach). The results showed that:①Ach decreased ERP of four atrial sites.When the concentration of Ach was incseased, ERP of 4 sites became shorter but COVERP became bigger.②As the concentration of Ach was increased, the percent of AF induced by Ach and AF was increased with the duration prolonged( P 0 05).③There was a significant correlation between atrial vulnerability with ERP and COVERP( P
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Objective To investigate the synergistic effect of retinol and leukemia inhibitory factor (LIF) on maintaining pluripotency of murine embryonic stem cells (mESCs). Methods The mESCs were randomly divided into two groups, and they were all cultured with the same LIF concentration (100U/ml). Retinol was added into mESCs medium in experimental group, and retinol was not added in control group. 14 days after culturing, the changes in cell morphology were observed under an inverted microscope with alkaline phosphatase staining. The mRNA expression of Oct4 and Nanog was analyzed by RT-PCR, and the proteins for Oct4 and Nanog were determined by Western-blot for the assessment of the pluripotency of mESCs. Results 14 days after culturing, 78% of mESCs in the experimental group formed good cell colonies with good stereoscopic appearance, and they showed strong alkaline phosphatase (AKP) staining. While in the control group, only 35% of mESCs were in undifferentiated mode, and the cells were weakly positive with AKP staining. The quantity of undifferentiated mESCs in experimental group (7.02?0.34) was higher than that in control group (4.28?0.37, P