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Objective To evaluate the value of the TIMI risk index in predicting 30-day and one-yosr mortality and incidence of heart failure in patients with ST-elevation myocardial infarction (STEMI).Method Data of 229 patients with STEM1 from August 1999 to March 2006 in the First Affiliated Hospital,Sun Yat-sen University,were retrospeclively collected,analyzed and scored with TIMI risk index.When categorized into quintiles(≤12.5,12.5～17.5,17.5～22.5,22.5～30,>30) and modeled as a continuous variable,difference of prediction of 30day and one-year mortality and 30-day incidence of heart failure of patients were compared respectively.Results When categorized into quintilos and modeled as a continuous variable,30-day and one-year mortality and 30-day incidence of heart failure were increasing with increasing score of risk index (P<0.05).The area under the recewer operating characteristic curve were 0.65,0.68,0.67 and 0.70,0.72,0.70,respectively.Conclusions The TIM1 risk index can be used as a simple,rapid and practical tool to risk-stratify patients with STEMI.
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AIM:To evaluate complement activation in patients with all forms of acute coronary syndromes(ACS)and to examine the relationship between the degree of complement activation and myocardial injury.METHODS:The subjects were divided into 2 groups:110 ACS patients(group ACS)and 18 healthy persons(group control).One hundred and ten patients with ACS were divided into 3 sub-group:51 patients with ST-segment elevated myocardial infarction(STEMI),28 patients with non-ST-segment elevated myocardial infarction(NSTEMI)and 31 patients with unstable angina(UA).Complement 3(C3),complement 4(C4),troponin T(TnT)as well as creatine kinase MB(CK-MB)were evaluated.RESULTS:Plasma C3 and C4 peak levels were significantly higher in patients with STEMI [(1 525?302)mg/L and(423?123)mg/L] and NSTEMI [(1 516?289)mg/L and(396?68)mg/L] than those in patients with UA [(1 275?172)mg/L and(356?91)mg/L] and the control subjects [(1 072?196)mg/L and(182?73)mg/L](P
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AIM: To investigate the effect of angiotensinⅡon Cx43 gap junction in cultured neonatal rat cardiac myocytes and its mechanism. METHODS: The cardiomyocytes were treated with AngⅡ for 24 h, which were pretreated with valsartan or PD98059 for 60 min before AngⅡ treatment. The controls were treated with equal amount of DMSO. The Cx43 expression, synthesis and gap junction in cardiomyocytes were characterized by Western blotting, metabolic labeling and immunoprecipitation assay, and electron microscope. RESULTS: Western blotting analysis revealed that Cx43 content concentration-dependently increased in cells treated with 10 -9-10 -6 mol/L AngⅡfor 24 h. Phosphorylated extracellular signal regulated kinase (P-ERK) 1/2 activity increased in cells treated with 0.1 ?mol/L AngⅡ for 24 h (P
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AIM: To investigate the effects of granulocyte colony-stimulating factor (G-CSF)-mobilized bone marrow stem cells on treatment of the myocardial infarction in experimental rats. METHODS: Three hours after injected with isoprenaline(ISO) interaperitoneally to develop acute ischemic model, rats' bone marrow stem cells were mobilized by G-CSF and migrated to the site of myocardial infarction. The hearts were harvested from 24 hours to 2 weeks after administration of ISO for histopathological examination. RESULTS: 24 hours after administration of ISO , myocardial infarct zones scattered in the pallium of the control group ,there were a large amoumt of inflammatory cells infiltration around the infarct zones and majority of them were neutrophils. The infarction in the G-CSF treatment group was milder, majority of the infiltrative cells were monocytoid; 48 hours after administration of ISO, infarct zones expanded greatly in control group, while that of the G-CSF treatment group increased just mildly; 2 weeks after administration of ISO, there was no significant scar in the G-CSF treatment group. We also found the regeneration of myocytes in the pallium. CONCLUSION: G-CSF treatment protected the ischemic myocardium and it may be used to treat the acute myocardial infarction.