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<p><b>BACKGROUND</b>Although thrombolytic therapy with rescue percutaneous coronary intervention (PCI) is a common treatment strategy for ST-segment elevation acute myocardial infarction (STEMI), scant data are available on its efficacy relative to primary PCI, and comparison was therefore the aim of this study.</p><p><b>METHODS</b>This multicenter, open-label, randomized, parallel trial was conducted in 12 hospitals on patients (age < or = 70 years) with STEMI who presented within 12 hours of symptom onset (mean interval > 3 hours). Patients were randomized to three groups: primary PCI group (n = 101); recombinant staphylokinase (r-Sak) group (n = 104); and recombinant tissue-type plasminogen activator (rt-PA) group (n = 106). For all patients allocated to the thrombolytic therapy arm, coronary angiography was performed at 90 minutes after drug therapy to confirm infarct-related artery (IRA) patency; rescue PCI was performed in cases with TIMI flow grade < or = 2. Bare-metal stent implantation was planned for all patients.</p><p><b>RESULTS</b>After randomization it required an average of 113.4 minutes to start thrombolytic therapy (door-to-needle time) and 141.2 minutes to perform first balloon inflation in the IRA (door to balloon time). Rates of IRA patency (TIMI flow grade 2 or 3) and TIMI flow grade 3 were significantly lower in the thrombolysis group at 90 minutes after drug therapy than in the primary PCI group at the end of the procedure (70.5% vs. 98.0%, P < 0.0001, and 53.0% vs. 85.9%, P < 0.0001, respectively). Rescue PCI with stenting was performed in 117 patients (55.7%) in the thrombolytic therapy arm. Rates of patency and TIMI flow grade 3 were still significantly lower in the rescue PCI than in the primary PCI group (88.9% vs. 97.9%, P = 0.0222, and 68.4% vs. 85.0%, P = 0.0190, respectively). At 30 days post-therapy, mortality rate was significantly higher in the thrombolysis combined with rescue PCI group than in primary PCI group (7.1% vs. 0, P = 0.0034). Rates of death/MI and bleeding complications were significantly higher in the thrombolysis with rescue PCI group than in the primary PCI group (10.0% vs. 1.0%, P = 0.0380, and 28.10% vs. 8.91%, P = 0.0001, respectively).</p><p><b>CONCLUSIONS</b>Thrombolytic therapy with rescue PCI was associated with significantly lower rates of coronary patency and TIMI flow grade 3, but with significantly higher rates of mortality, death/MI and hemorrhagic complications at 30 days, as compared with primary PCI in this group of Chinese STEMI patients with late presentation and delayed treatments.</p>
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Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Angioplastia Coronaria con Balón , Angiografía Coronaria , Fibrinolíticos , Usos Terapéuticos , Infarto del Miocardio , Quimioterapia , Terapéutica , Terapia TrombolíticaRESUMEN
<p><b>BACKGROUND</b>Nitric oxide (NO) is a biologically active molecule which has been reported to protect the heart against ischemia and reperfusion injury in different species. This study aimed to test the hypothesis that nitric oxide may induce the expression of heat shock protein 72 (HSP72) which may protect the heart against ischemia.</p><p><b>METHODS</b>Rabbits were given intravenous saline or S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, or Zaprinast, an inhibitor of cyclic guanosine monophosphate (GMP)-phosphodiesterase, which may increase myocardial cyclic GMP content. Twenty-four hours later, the rabbits were either sampled to measure HSP72, or induced with a 30-minute coronary occlusion followed by a 120-minute reperfusion, and then the infarct size was measured. Meanwhile, chelerythrine (CHE, an inhibitor of protein kinase C) was given intravenously 5 minutes before SNAP injection and the effect on HSP72 expression and infarct size was determined.</p><p><b>RESULTS</b>Twenty-four hours after pretreatment, immunoblotting showed HSP72 expression increased in the SNAP group compared with control groups, and this was blocked by CHE. Myocardial infarct size in the SNAP group was smaller than that of the control group ((32.4 +/- 5.8)% vs (51.1 +/- 4.7)%, P < 0.05). Pretreated with CHE abolished the infarct size-limiting effect of SNAP ((46.0 +/- 5.1)%). Pretreatment with Zaprinast neither induced HSP72 expression nor reduced infarct size ((55.4 +/- 5.4)%).</p><p><b>CONCLUSION</b>NO induced HSP72 expression and a delayed protection to the heart via the activities of protein kinase C by a cyclic GMP-independent pathway.</p>
Asunto(s)
Animales , Masculino , Conejos , Benzofenantridinas , Farmacología , GMP Cíclico , Metabolismo , Proteínas del Choque Térmico HSP72 , Hemodinámica , Infarto del Miocardio , Metabolismo , Isquemia Miocárdica , Metabolismo , Óxido Nítrico , Metabolismo , Donantes de Óxido Nítrico , Farmacología , Inhibidores de Fosfodiesterasa , Farmacología , Proteína Quinasa C , Metabolismo , Purinonas , Farmacología , S-Nitroso-N-Acetilpenicilamina , FarmacologíaRESUMEN
Objective: To determine the molecular weight and p urity of porcine platelet-derived growth factor (pPDGF) and to investigate its effect on DNA synthesis of human umbilical vein endothelial cells. Metho ds: In the present experiment, the high performance liquid chromatograph y was used and the molecular weight and purity of pPDGF were studied. Human umbi lical vein endothelial cells was cultured and effects of pPDGF on DNA synthesis of endothelial cells was observed by 3H-TdR incorporation in vitro. Results: The findings of high performance liquid chromatography showed that the molecular weight of pPDGF was 29 120 and the purity was 89.46%, a nd pPDGF significantly promoted DNA synthesis of quiescent endothelial cells wit h a maximal response at a concentration of 40 ng/ml at 48 h. Conclusion: The molecular weight of pPDGF is 29 120, and it can promote DNA synthes is of cultured human umbilical vein endothelial cells.
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Objective To investigate the prognosis in risk of ventricular arrhythmia in coronary heart disease with heart rate variability (H RV), left ventricular ejection fraction (LVEF) and other clinical background dat a. Methods A total of 81 patients were divided into ventricular premature beats (VPBs)≥30/h group and VPBs<30/h group. Their LVEF, HRV and cli nical data were studied and analyzed. Results The age and blood pressure between 2 groups had no significant difference. LVEF, standard deviati on of all normal RR intervals (SDNN), SD of the average of NN interval (SDANN) a nd HRV triangular index (HRVI) were significant less in VPBs≥30/h group than in VPBs<30/h group (43.29±15.38 vs 67.33±11.47,P<0.01;90.05±22.2 9 vs 117.90±30.32,P<0.05;77.43±17.78 vs 105.69±28.79,P<0.05 ;24.54±8.70 vs 32.70±10.87,P<0.05, respectively). Incidence of myo cardial infarction (MI) was larger in VPBs≥30/h group than VPBs<30/h group. LVE F was the independent predictable factor in risk of ventricular arrhythmia with multinomial regression logistic analysis(B=0.119, P=0.032). Co nclusion Our findings indicate that LVEF is an independent predictable factor i n risk of ventricular arrhythmia in coronary heart disease. Although HRV and MI history can not be used to predict VPB, significant difference is found between 2 groups. High-risk patients could be selected successfully when these data are considered in combination.
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Objective: To determine the molecular weight and p urity of porcine platelet-derived growth factor (pPDGF) and to investigate its effect on DNA synthesis of human umbilical vein endothelial cells. Metho ds: In the present experiment, the high performance liquid chromatograph y was used and the molecular weight and purity of pPDGF were studied. Human umbi lical vein endothelial cells was cultured and effects of pPDGF on DNA synthesis of endothelial cells was observed by 3H-TdR incorporation in vitro. Results: The findings of high performance liquid chromatography showed that the molecular weight of pPDGF was 29 120 and the purity was 89.46%, a nd pPDGF significantly promoted DNA synthesis of quiescent endothelial cells wit h a maximal response at a concentration of 40 ng/ml at 48 h. Conclusion: The molecular weight of pPDGF is 29 120, and it can promote DNA synthes is of cultured human umbilical vein endothelial cells.
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Objective To investigate the prognosis in risk of ventricular arrhythmia in coronary heart disease with heart rate variability (H RV), left ventricular ejection fraction (LVEF) and other clinical background dat a. Methods A total of 81 patients were divided into ventricular premature beats (VPBs)≥30/h group and VPBs<30/h group. Their LVEF, HRV and cli nical data were studied and analyzed. Results The age and blood pressure between 2 groups had no significant difference. LVEF, standard deviati on of all normal RR intervals (SDNN), SD of the average of NN interval (SDANN) a nd HRV triangular index (HRVI) were significant less in VPBs≥30/h group than in VPBs<30/h group (43.29±15.38 vs 67.33±11.47,P<0.01;90.05±22.2 9 vs 117.90±30.32,P<0.05;77.43±17.78 vs 105.69±28.79,P<0.05 ;24.54±8.70 vs 32.70±10.87,P<0.05, respectively). Incidence of myo cardial infarction (MI) was larger in VPBs≥30/h group than VPBs<30/h group. LVE F was the independent predictable factor in risk of ventricular arrhythmia with multinomial regression logistic analysis(B=0.119, P=0.032). Co nclusion Our findings indicate that LVEF is an independent predictable factor i n risk of ventricular arrhythmia in coronary heart disease. Although HRV and MI history can not be used to predict VPB, significant difference is found between 2 groups. High-risk patients could be selected successfully when these data are considered in combination.