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OBJECTIVES: To investigate the long-term outcome of patients with acute ST-segment elevation myocardial infarction (STEMI) and a chronic total occlusion (CTO) in a non-infarct-related artery (IRA) and the risk factors for mortality. METHODS: The enrolled cohort comprised 323 patients with STEMI and multivessel diseases (MVD) that received a primary percutaneous coronary intervention between January 2008 and November 2013. The patients were divided into two groups: the CTO group (n = 97) and the non-CTO group (n = 236). The long-term major adverse cardiovascular and cerebrovascular events (MACCE) experienced by each group were compared. RESULTS: The rates of all-cause mortality and MACCE were significantly higher in the CTO group than they were in the non-CTO group. Cox regression analysis showed that an age ≥ 65 years (OR = 3.94, 95% CI: 1.47-10.56, P = 0.01), a CTO in a non-IRA(OR = 5.09, 95% CI: 1.79 ~ 14.54, P < 0.01), an in-hospital Killip class ≥ 3 (OR = 4.32, 95% CI: 1.71 ~ 10.95, P < 0.01), and the presence of renal insufficiency (OR = 5.32, 95% CI: 1.49 ~ 19.01, P = 0.01), stress ulcer with gastraintestinal bleeding (SUB) (OR = 6.36, 95% CI: (1.45 ~ 28.01, P = 0.01) were significantly related the 10-year mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 (OR = 2.97,95% CI:1.46 ~ 6.03, P < 0.01) and the presence of renal insufficiency (OR = 5.61, 95% CI: 1.19 ~ 26.39, P = 0.03) were significantly related to the 10-year mortality of patients with STEMI and a CTO. CONCLUSIONS: The presence of a CTO in a non-IRA, an age ≥ 65 years, an in-hospital Killip class ≥ 3, and the presence of renal insufficiency, and SUB were independent risk predictors for the long-term mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 and renal insufficiency were independent risk predictors for the long-term mortality of patients with STEMI and a CTO.
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Oclusión Coronaria/fisiopatología , Intervención Coronaria Percutánea , Infarto del Miocardio con Elevación del ST/terapia , Factores de Edad , Anciano , Enfermedad Crónica , Oclusión Coronaria/diagnóstico por imagen , Oclusión Coronaria/mortalidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Úlcera Péptica Hemorrágica/mortalidad , Intervención Coronaria Percutánea/efectos adversos , Intervención Coronaria Percutánea/mortalidad , Insuficiencia Renal/mortalidad , Estudios Retrospectivos , Medición de Riesgo , Factores de Riesgo , Infarto del Miocardio con Elevación del ST/diagnóstico por imagen , Infarto del Miocardio con Elevación del ST/mortalidad , Infarto del Miocardio con Elevación del ST/fisiopatología , Factores de Tiempo , Resultado del TratamientoRESUMEN
Myocardial infarction is one of the common types of coronary heart disease in the clinic. Its morbidity, lethality and disability are high, and it has become a serious threat to human health. At present, it is shown that in the early stage of acute myocardial infarction, myocardial cells are mainly apoptotic, suggesting that effectively blocking myocardial apoptosis in the early stage of myocardial infarction is of great significance for reducing tissue necrosis in the infarcted area. Recent studies have shown that NG nano-protein complexes have a better therapeutic effect on acute myocardial infarction and can inhibit left ventricular remodeling in patients with acute myocardial infarction. However, there are few studies on the effect of NG nano-protein complexes on myocardial cell apoptosis after ischemia. This study used a rat model of acute myocardial infarction to analyze its effect on apoptotic proteins of myocardial cells in rats with acute myocardial infarction in order to provide a certain theoretical basis for its clinical application. In this study, 45 SD rats were randomly divided into a sham operation group, a myocardial infarction group, and a NG nano-protein complex group, with 15 in each group. The sham operation group only underwent thoracotomy, and received normal saline gavage postoperatively; the myocardial infarction group and the NG nano-protein complex group were ligated to the left anterior descending coronary artery of the rat to establish an acute myocardial infarction model, and were performed separately treatment with saline and NG nanoprotein complexes. Finally, we conclude that this nano-protein complex can significantly reduce the expression level of myocardial apoptosis-related proteins in rats with acute myocardial infarction, and is of great significance in inhibiting the apoptosis of acute myocardial infarction cells.
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Infarto del Miocardio , Animales , Apoptosis , Humanos , Infarto del Miocardio/tratamiento farmacológico , Miocardio , Miocitos Cardíacos , Ratas , Ratas Sprague-DawleyRESUMEN
Sciatic nerves in adult male rats were transected and reunited via a silicone chamber. This was followed by a focal injection of recombinant ciliary neurotrophic factor (CNTF). To evaluate the effect of this therapeutic approach and to explore its possible mechanisms, nerve regeneration was traced by horseradish peroxidase retrograde labeling. Functional recovery was evaluated by functional assessment of the hind feet and the expression of a number of proteins was detected using immunohistochemistry. The results showed that a single administration of CNTF could promote regeneration of motor axons, with improved functional recovery in adult rats. Growth associated protein (GAP)-43, S100, CD68 and major histocompatibility complex class II immunoreactivity in the regenerative and distal nerves suggested that CNTF could promote axon regeneration, Schwann cell migration, monocyte infiltration and activation. CNTF might also indirectly promote axonal regeneration by further activating the JAK-STAT3 pathway and subsequently upregulating phosphotyrosine, GAP-43 and S100 expression to enhance proliferation, growth and migration of Schwann cells. CNTF has suggested important targets for pharmacological intervention in peripheral nerve disease and injury.
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Factor Neurotrófico Ciliar/farmacología , Expresión Génica/efectos de los fármacos , Regeneración Nerviosa/efectos de los fármacos , Implantación de Prótesis/métodos , Neuropatía Ciática/tratamiento farmacológico , Neuropatía Ciática/cirugía , Animales , Antígenos CD/metabolismo , Antígenos de Diferenciación Mielomonocítica/metabolismo , Movimiento Celular/efectos de los fármacos , Movimiento Celular/fisiología , Modelos Animales de Enfermedad , Proteína GAP-43/metabolismo , Expresión Génica/fisiología , Conos de Crecimiento/efectos de los fármacos , Conos de Crecimiento/metabolismo , Conos de Crecimiento/patología , Antígenos de Histocompatibilidad Clase II/metabolismo , Inmunohistoquímica , Janus Quinasa 1/metabolismo , Masculino , Neuronas Motoras/efectos de los fármacos , Neuronas Motoras/metabolismo , Neuronas Motoras/patología , Regeneración Nerviosa/fisiología , Prótesis e Implantes , Ratas , Ratas Sprague-Dawley , Proteínas S100/metabolismo , Factor de Transcripción STAT3/metabolismo , Células de Schwann/efectos de los fármacos , Células de Schwann/metabolismo , Neuropatía Ciática/metabolismo , Siliconas/uso terapéuticoRESUMEN
OBJECTIVE: To explore the effect of low-dose folate on plasma homocysteinemia (Hcy) and chemokine levels in patients with hyperhomocysteinemia (HHcy). METHODS: Forty HHcy patients were treated with 0.8 mg/d folate for 6 months. Plasma levels of Hcy, monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured before and after folate treatment. RESULTS: Plasma level of Hcy significantly decreased after folate treatment [(57.1 +/- 18.0) micromol/L vs (25.8 +/- 12.0) micromol/L, P <0.05]. However, the plasma levels of MCP-1, IL-8, SOD, and MDA were not changed after folate treatment. CONCLUSION: Folate treatment can decrease the plasma Hcy level in HHcy patients; however, it has no obvious effects on the chemokine levels.
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Quimiocinas/sangre , Ácido Fólico/uso terapéutico , Homocisteína/sangre , Hiperhomocisteinemia/sangre , Hiperhomocisteinemia/tratamiento farmacológico , Anciano , Femenino , Ácido Fólico/administración & dosificación , Humanos , Masculino , Persona de Mediana Edad , Resultado del TratamientoRESUMEN
OBJECTIVE: To evaluate the effectiveness and safety of subcutaneous low molecular weight heparin (LMWH) used in acute management of patients with non-ST segment elevation acute coronary syndrome (ACS). METHODS: A total of 102 patients with non-ST segment elevation ACS were treated for at least 48 hours ( > or =5 times) with subcutaneous nadroparin (1 mg/kg each 12 hours). All 102 patients underwent coronary angiographies (CAG) within 8 hours after LMWH injection, followed by immediate percutaneous coronary intervention (PCI). RESULTS: Anti-Xa activity at the time of catheterization was (0.62 +/- 0.18) IU/ml, and 90% of the patients had anti-Xa activity > 0.5 IU/ml. No death, myocardial infarction relapse or emergent revascularization occurred after PCI. Thrombosis and/or embolism occurred in 2 patients (3.5%) during PCI. Mild hemorrhage was observed in 4 patients (3.9%) of PCI group and in 2 patients (4.4%) in CAG group. No major hemorrhage occurred. CONCLUSION: PCI within 8-12 hours of the last dose after > or =48 hours nadroparin subcutaneous injection seems to be effective and safe.
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Síndrome Coronario Agudo/terapia , Anticoagulantes/uso terapéutico , Nadroparina/uso terapéutico , Síndrome Coronario Agudo/sangre , Angioplastia de Balón , Anticoagulantes/efectos adversos , Inhibidores del Factor Xa , Humanos , Nadroparina/efectos adversosRESUMEN
PURPOSE: Effective therapy for visual loss caused by optic nerve injury or diseases has not been achieved even though the optic nerve has the regeneration potential after injury. This study was designed to modify amniotic epithelial cells (AECs) with basic fibroblast growth factor (bFGF) gene, preliminarily investigating its effect on transected optic nerve. METHODS: A human bFGF gene segment was delivered into rat AECs (AECs/hbFGF) by lentiviral vector, and the gene expression was examined by RT-PCR and ELISA. The AECs/hbFGF and untransfected rat AECs were transplanted into the transected site of the rat optic nerve. At 28 days post transplantation, the survival and migration of the transplanted cells was observed by tracking labeled cells; meanwhile retinal ganglion cells (RGCs) were observed and counted by employing biotin dextran amine (BDA) and Nissl staining. Furthermore, the expression of growth associated protein 43 (GAP-43) within the injury site was examined with immunohistochemical staining. RESULTS: The AECs/hbFGF was proven to express bFGF gene and secrete bFGF peptide. Both AECs/hbFGF and AECs could survive and migrate after transplantation. RGCs counting implicated that RGCs numbers of the cell transplantation groups were significantly higher than that of the control group, and the AECs/hbFGF group was significantly higher than that of the AECs group. Moreover GAP-43 integral optical density value in the control group was significantly lower than that of the cell transplantation groups, and the value in the AECs/hbFGF group was significantly higher than that of the AECs group. CONCLUSIONS: AECs modified with bFGF could reduce RGCs loss and promote expression of GAP-43 in the rat optic nerve transected model, facilitating the process of neural restoration following injury.
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Células Epiteliales/trasplante , Factor 2 de Crecimiento de Fibroblastos/genética , Regeneración Nerviosa/fisiología , Traumatismos del Nervio Óptico/terapia , Nervio Óptico/metabolismo , Amnios/citología , Animales , Biomarcadores/metabolismo , Recuento de Células , Diferenciación Celular , Supervivencia Celular , Células Epiteliales/citología , Células Epiteliales/metabolismo , Factor 2 de Crecimiento de Fibroblastos/metabolismo , Proteína GAP-43/genética , Proteína GAP-43/metabolismo , Expresión Génica , Vectores Genéticos , Humanos , Lentivirus/genética , Masculino , Nervio Óptico/patología , Nervio Óptico/cirugía , Traumatismos del Nervio Óptico/metabolismo , Traumatismos del Nervio Óptico/patología , Ratas , Ratas Sprague-Dawley , Células Ganglionares de la Retina/citología , Células Ganglionares de la Retina/metabolismo , Transducción Genética , TransgenesRESUMEN
There are numerous parallels between the heamatolymphopoietic and nervous systems in terms of the mechanisms regulating their development. We proposed that neural stem cells (NSCs) may respond to the microenvironmental signals provided by bone marrow stromal cells (BMSCs) which regulate the differentiation and maturation of hematolymphopoietic stem cells. First, we isolated and proliferated BMSCs from the femur and tibia, and NSCs from the midbrain of Sprague-Dawley (SD) rats, and then investigated the effects of BMSCs on the differentiation of NSCs into neurons, astrocytes and oligodendrocytes by directly plating neurospheres on BMSC monolayers in serum-free conditions. The results confirmed that BMSCs induced NSCs to differentiate selectively into neurons. The percentage of neurons significantly increased in 7 days in vitro co-cultures of NSCs and BMSCs as compared to NSCs cultures alone. When the duration of the cultures was extended to 12 days in vitro, BMSCs enhanced the survival of neurons derived from these NSCs; our investigation then focused on the underlying mechanism for this effect of BMSCs. NSCs were cultured with BMSC conditioned-medium and co-cultured with membrane fragments of live BMSCs or paraformaldehyde fixed BMSCs, the inducing activity of BMSCs was solely detectable in BMSC conditioned-medium, indicating that soluble factors secreted by BMSCs were responsible for its effect on the neuronal differentiation of NSCs. Therefore, BMSCs may provide a powerful tool for therapeutic neurological applications.
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Células de la Médula Ósea/citología , Diferenciación Celular/fisiología , Mesencéfalo/citología , Proteínas del Tejido Nervioso , Neuronas/citología , Células Madre/citología , Células del Estroma/fisiología , 2',3'-Nucleótido Cíclico Fosfodiesterasas/metabolismo , Animales , Animales Recién Nacidos , Antígenos CD/metabolismo , Antígenos de Diferenciación de Linfocitos B/metabolismo , Recuento de Células , Diferenciación Celular/efectos de los fármacos , Membrana Celular/metabolismo , Supervivencia Celular , Células Cultivadas , Técnicas de Cocultivo , Medios de Cultivo Condicionados/farmacología , Proteína Ácida Fibrilar de la Glía/metabolismo , Inmunoquímica , Proteínas de Filamentos Intermediarios/metabolismo , Proteínas Asociadas a Microtúbulos/metabolismo , Nestina , Neuronas/efectos de los fármacos , Neuronas/fisiología , Ratas , Ratas Sprague-Dawley/crecimiento & desarrollo , Ratas Sprague-Dawley/metabolismo , Receptores de Transferrina , Células Madre/fisiología , Células del Estroma/metabolismo , Factores de TiempoRESUMEN
The GFRalpha1 cDNA was amplified by RT-PCR from fetal rat hippocampus. The soluble recombinant GFRalpha1 and its mutants were obtained from an Escherichia coli expression system. The biological activity of soluble GFRalpha1 and its mutants were evaluated in PC12 cells. The results suggest that the central domain of GFRalpha1 is a crucial determinant for ligand binding. This established a solid basis for further study to find the key amino acid mediating the binding of GDNF and GFRalpha1.
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Proteínas Proto-Oncogénicas/genética , Proteínas Proto-Oncogénicas/metabolismo , Proteínas Tirosina Quinasas Receptoras/genética , Proteínas Tirosina Quinasas Receptoras/metabolismo , Secuencia de Aminoácidos , Animales , Diferenciación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Cartilla de ADN/genética , Escherichia coli/metabolismo , Eliminación de Gen , Receptores del Factor Neurotrófico Derivado de la Línea Celular Glial , Hipocampo/química , Humanos , Modelos Moleculares , Células PC12 , Unión Proteica , Estructura Secundaria de Proteína , Estructura Terciaria de Proteína/genética , Proteínas Proto-Oncogénicas/farmacología , Proteínas Proto-Oncogénicas c-ret , Ratas , Proteínas Tirosina Quinasas Receptoras/farmacología , Proteínas Recombinantes/química , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo , Proteínas Recombinantes/farmacología , Relación Estructura-ActividadRESUMEN
The ciliary neurotrophic factor (CNTF) plays a very important role in the development and regeneration of the nervous system. In this study, the prediction of secondary structure and the hydrophobicity analysis of human CNTF were performed according to the amino acid sequence deduced from the nucleotide sequence of the cDNA. Based on the results of the prediction of structure, the human CNTF gene was modified by insertion and deletion mutagenesis. The various mutants were all highly expressed in E. coli. The recombinant proteins were purified from bacterial via DEAE A-50 and Sephacryl S-200 chromatography, and their survival-promoting activities were determined by using cultures of the dorsal root ganglion neurons of embryonic chick. The results showed that the alpha-helixes in CNTF were critical for the biological activity and the flexible C-terminus of human CNTF was not essential. Our data also indicated that the middle and the tail part of the D-helix might play crucial roles in the biological functions of CNTF.
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The glial cell line-derived neurotrophic factor(GDNF) plays a very important role in the regeneration of the nervous system. Based on the results of the X-ray structure analysis of rat GDNF, human GDNF gene was modified with deletion and insertion mutagenesis by using PCR methods. The various mutants were all highly expressed in E.coli. The recombinant proteins were purified and their survival-promoting activities were determined by using cultures of the spinal cord neurons of embryonic mouse. The results showed that the "cystine knot motif" was critical for the maintenance of GDNF structure the alpha-helix, finger 1 and finger 2 region were critical for GDNF neurotrophic activity and the N-terminus of human GDNF was not essential for its biological functions.
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The human persephin (PSP) was expressed in Tn-5B1-4 insect cells using the Bac to Bac baculovirus expression system. The expressed product amounted for 20% of total cellular soluble proteins. The expressed product was purified by Ni(2+) affinity chromatography and the activity assays showed that it could significantly prolong the survival of spinal cord neurons.
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The human glial cell derived neurotrophic factor (GDNF) was expressed in Tn-5B1-4 insect cells using the Bac to Bac baculovirus expression system, accounting for 30% of total cellular soluble proteins. The expressed product was purified by affinity chromatography and the activity assays showed that it could significantly promote the survival of dopaminergic neurons. The study can be the basis for further structural-functional analysis of GDNF.
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The cDNA encoding the mature human glial cell derived neurotrophic factor(GDNF) was isolated by using RT-PCR method from total RNA extracted of fetal human brain. The expression plasmid pET-GDNF was constructed by inserting GDNF cDNA into plasmid pET-28a(+) containing T7 promoter and transformed into E.coli BL21(DE3). An expression strain BLGDNF was selected. SDS-PAGE analysis revealed that the human GDNF protein was highly expressed and accumulated up to above 30% of the total bacterial proteins in the form of inclusion body after the induction. The antibody to GDNF was prepared by immunization of rat using purified GDNF protein. Purified and refolded GDNF protein could significantly promote the survival of dopaminergic neurons.
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To observe the influence of tumor necrosis factor-alpha (TNF-alpha) on differentiation of rat mesencephalic neural stem cells (NSCs), the numbers of neurons, astrocytes and oligodendrocytes generated from NSCs were analyzed after differentiation for 3 days by using immunocytochemistry technique. The results show that: (1) TNF-alpha enhanced the proportions of neurons and oligodendrocytes in progeny of NSCs; and (2) TNF-alpha induced the proliferation of oligodendrocytes derived from NSCs, but the proliferation of astrocytes was not influenced by TNF-alpha. We conclude that the TNF-alpha could influence the application of NSCs.
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Diferenciación Celular/fisiología , Mesencéfalo/citología , Células-Madre Neurales/citología , Oligodendroglía/citología , Factor de Necrosis Tumoral alfa/fisiología , Animales , Animales Recién Nacidos , Astrocitos/citología , Proliferación Celular , Neuronas/citología , Ratas , Ratas Sprague-DawleyRESUMEN
It is widely accepted that monoamine transmitters are playing an important role in the progress of depression. The functions of monoamine transmitters and their receptors change profoundly during depression and its treatment. This paper is attempted to review the new progress of investigation into serotonin receptors, adrenoceptors and dopamine receptors related with depression mechanism respectively.
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Monoaminas Biogénicas/fisiología , Depresión/metabolismo , Humanos , Receptores Adrenérgicos/fisiología , Receptores de Amina Biogénica/fisiología , Receptores Dopaminérgicos/fisiología , Receptores de Serotonina/fisiologíaRESUMEN
Objective. To examine the effect of electromagnetic fields (EMF) (20 Hz, 8 mT; 5 Hz, 8 mT) on the neuron-orientated differentiation of neural stem cells (NSCs) from midbrains of new-bom rats. Method. Differentiated NSCs were exposed to EMF for 2 x 15 min per day lasting for I d, 5 d, or 10 d. The sham-exposure controls were correspondingly established. Cells were fixed and processed for immunofluorescent staining using the antibody against neuron-specific marker MAP2, then the percentage of MAP2+ cells was calculated. Result. The two EMFs promoted the differentiation of a neuronal fate in different ways. Both of them came into effect even after 1 d exposure. When cells exposed to the 20 Hz EMF, the percentage of neuron-orientated cells gradually increased with longer-term exposure and the most significant effect appeared in 10 d group while that happened in 5 d group under the condition of 5 Hz EMF. The effect contrasted horizontally, significant differences between the two EMFs were observed only at 10 d groups, 20 Hz EMF having more favorable effect than 5 Hz EMF. Conclusion. 20 Hz and 5 Hz EMF could promote the differentiation of midbrain NSCs to a neuronal phenotype in different ways, suggesting that the physical induction might be another strategy to manipulate the differentiation of NSCs.
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Diferenciación Celular/efectos de la radiación , Campos Electromagnéticos , Mesencéfalo/efectos de la radiación , Neuronas/efectos de la radiación , Células Madre/efectos de la radiación , Animales , Animales Recién Nacidos , Diferenciación Celular/fisiología , Células Cultivadas/efectos de la radiación , Mesencéfalo/citología , Neuronas/fisiología , Ratas , Células Madre/fisiología , Factores de TiempoRESUMEN
Despite advances in antibiotic therapy and intensive care, the mortality caused by systemic inflammatory response syndrome and severe sepsis remains high. The use of anti-inflammatory agents to attenuate inflammatory response during acute systemic inflammatory reactions may improve survival rates. Here we show that a newly synthesized 2-pyridone compound (FJU-C4) can suppress the expression of late inflammatory mediators such as iNOS and COX-2 in murine macrophages. The pro-inflammatory cytokines, including TNFα, IL-1ß, and IL-6, were dose-dependently suppressed by FJU-C4 both in mRNA and protein levels. In addition, the expression of TNFα was inhibited from as early as 2 hours after exposure to LPS stimulation. The production of mature pro-inflammatory cytokines was also suppressed by pretreatment with FJU-C4 in either cell culture medium or mice serum when stimulated by LPS. FJU-C4 prolongs mouse survival and prevents mouse death from LPS-induced systemic inflammation when the dose of FJU-C4 is over 5 mg/kg. The activities of ERK, JNK, and p38MAPK were induced by LPS stimulation on murine macrophage cell line, but only p38MAPK signaling was dramatically suppressed by pretreatment with the FJU-C4 compound in a dose-dependent manner. NF-κB activation also was suppressed by FJU-C4 compound. These findings suggest that the FJU-C4 compound may act as a promising therapeutic agent against inflammatory diseases by inhibiting the p38MAPK and NF-κB signaling pathway.
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Antiinflamatorios no Esteroideos/farmacología , FN-kappa B/genética , Piridonas/farmacología , Síndrome de Respuesta Inflamatoria Sistémica/tratamiento farmacológico , Proteínas Quinasas p38 Activadas por Mitógenos/genética , Animales , Ciclooxigenasa 2/genética , Ciclooxigenasa 2/metabolismo , Femenino , Regulación de la Expresión Génica , Interleucina-1beta/antagonistas & inhibidores , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/antagonistas & inhibidores , Interleucina-6/genética , Interleucina-6/metabolismo , Lipopolisacáridos , MAP Quinasa Quinasa 4/genética , MAP Quinasa Quinasa 4/metabolismo , Ratones , Ratones Endogámicos BALB C , FN-kappa B/antagonistas & inhibidores , FN-kappa B/metabolismo , Óxido Nítrico Sintasa de Tipo II/genética , Óxido Nítrico Sintasa de Tipo II/metabolismo , Transducción de Señal , Síndrome de Respuesta Inflamatoria Sistémica/inducido químicamente , Síndrome de Respuesta Inflamatoria Sistémica/genética , Síndrome de Respuesta Inflamatoria Sistémica/patología , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismoRESUMEN
BACKGROUND: Evidence indicates that early reperfusion therapy in patients with ST-elevation myocardial infarction (STEMI) reduces complications. This study was undertaken to compare the in-hospital delay to primary percutaneous coronary intervention (PPCI) for patients with STEMI between specialized hospitals and non-specialized hospitals in Beijing, China. METHODS: Two specialized hospitals and fifteen non-specialized hospitals capable of performing PPCI were selected to participate in this study. A total of 308 patients, within 12 hours of the onset of symptoms and undergoing PPCI between November 1, 2005 and December 31, 2006 were enrolled. Data were collected by structured interview and review of medical records. RESULTS: The median in-hospital delay was 98 (interquartile range 105 to 180) minutes, and 16.9% of the patients were treated within 90 minutes. Total in-hospital delay and ECG-to-treatment decision-making time were longer in the non-specialized hospitals than in the cardiac specialized hospitals (147 minutes vs. 120 minutes, P < 0.001; 55 minutes vs. 45 minutes, P = 0.035). After controlling the confounding factors, the non-specialized hospitals were independently associated with an increased risk of being in the upper median of in-hospital delays. CONCLUSIONS: There were substantial in-hospital delays between arrival at the hospital and the administration of PPCI for patients with STEMI in Beijing. Patients admitted to the cardiac specialized hospitals had a shorter in-hospital delay than those to the non-specialized hospitals because of a shorter time of ECG-to-treatment decision-making.
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Angioplastia Coronaria con Balón , Hospitales/estadística & datos numéricos , Infarto del Miocardio/terapia , China , Toma de Decisiones , Electrocardiografía , Femenino , Humanos , Masculino , Persona de Mediana Edad , Calidad de la Atención de Salud , Factores de Tiempo , Resultado del TratamientoAsunto(s)
Encéfalo/fisiología , Neuroglía/fisiología , Animales , Antígenos/metabolismo , Antígenos/fisiología , Encéfalo/metabolismo , Estrógenos/metabolismo , Estrógenos/fisiología , Proteína Ácida Fibrilar de la Glía/metabolismo , Humanos , Neuroglía/metabolismo , Progesterona/metabolismo , Progesterona/fisiologíaRESUMEN
OBJECTIVE: To evaluate the effects of socioeconomic status on the distribution of cardiovascular risk factors and clinical treatments of patients with acute myocardial infarction in Beijing. METHODS: In Beijing, a prospective, multi-center, registration study was carried out which including 800 patients who were consecutively hospitalized for ST-segment elevation acute myocardial infarction within 24 hours after event attack in 19 different hospitals in Beijing between November, 2005 and December, 2006. Indicators of socioeconomic status included self-reported personal income (< 500, 500-2000, > 2000 RMB/ month), educational attainment (< or = 12 and > 12 years) and status of medical insurance (yes/no). According to categories of education, patients were categorized into two groups of lower socioeconomic status and higher socioeconomic status. Differences of cardiovascular risk factors and clinical treatments were compared across the two groups respectively. RESULTS: Proportion of diabetes and hyperlipidemia in patients with higher socioeconomic status was much higher than that of patients with lower socioeconomic status (P < 0.05, P < 0.01 respectively). Patients with lower socioeconomic status were more likely to be smokers (P < 0.05). The rates of receiving coronary angiography and PTCA were much lower in patients with lower socioeconomic status. Medical insurance and income were the most important two socioeconomic factors determining the use of PTCA. CONCLUSION: Compared to patients with lower socioeconomic status, patients with higher socioeconomic status had higher rates of hyperlipidemia and diabetes but lower smoking rate among cardiovascular risk factors. The rates of receiving interventional therapies were much lower in patients with lower socioeconomic status.