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  1 / 192497 MEDLINE  
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[PMID]:29353043
[Au] Autor:Tanaka M; Ishihara Y; Mizuno S; Ishida A; Vogel CF; Tsuji M; Yamazaki T; Itoh K
[Ad] Endereço:Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, 739-8521, Japan; Laboratory for Pharmacotherapy and Experimental Neurology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Kagawa, 769-2193, Japan.
[Ti] Título:Progression of vasogenic edema induced by activated microglia under permanent middle cerebral artery occlusion.
[So] Source:Biochem Biophys Res Commun;496(2):582-587, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain edema is a severe complication that accompanies ischemic stroke. Increasing evidence shows that inflammatory cytokines impair tight junctions of the blood-brain barrier, suggesting the involvement of microglia in brain edema. In this study, we examined the role of microglia in the progression of ischemic brain edema using mice with permanent middle cerebral artery occlusion. The intensity of T2-weighted imaging (T2WI) in the cerebral cortex and the striatum was elevated 3 h after occlusion and spread to peripheral regions of the ischemic hemisphere. Merged images of 2,3,5-triphenyl tetrazolium chloride staining and T2WI revealed the exact vasogenic edema region, which spread from the ischemic core to outside the ischemic region. Microglia were strongly activated in the ischemic region 3 h after occlusion and, notably, activated microglia were observed in the non-ischemic region 24 h after occlusion. Pretreatment with minocycline, an inhibitor of microglial activation clearly suppressed not only vasogenic edema but also infarct formation. We demonstrated in this study that vasogenic edema spreads from the ischemic core to the peripheral region, which can be elicited, at least in part, by microglial activation induced by ischemia.
[Mh] Termos MeSH primário: Edema Encefálico/etiologia
Encéfalo/patologia
Infarto da Artéria Cerebral Média/complicações
Microglia/patologia
[Mh] Termos MeSH secundário: Animais
Edema Encefálico/patologia
Progressão da Doença
Infarto da Artéria Cerebral Média/patologia
Masculino
Camundongos Endogâmicos ICR
Água/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
059QF0KO0R (Water)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


  2 / 192497 MEDLINE  
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[PMID]:28464839
[Au] Autor:Pavlic K; Perme MP
[Ad] Endereço:University of Ljubljana, Faculty of Medicine, Institute for Biostatistics and Medical Informatics, Vrazov trg 2, Ljubljana, 1000, Slovenia.
[Ti] Título:On comparison of net survival curves.
[So] Source:BMC Med Res Methodol;17(1):79, 2017 May 02.
[Is] ISSN:1471-2288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Relative survival analysis is a subfield of survival analysis where competing risks data are observed, but the causes of death are unknown. A first step in the analysis of such data is usually the estimation of a net survival curve, possibly followed by regression modelling. Recently, a log-rank type test for comparison of net survival curves has been introduced and the goal of this paper is to explore its properties and put this methodological advance into the context of the field. METHODS: We build on the association between the log-rank test and the univariate or stratified Cox model and show the analogy in the relative survival setting. We study the properties of the methods using both the theoretical arguments as well as simulations. We provide an R function to enable practical usage of the log-rank type test. RESULTS: Both the log-rank type test and its model alternatives perform satisfactory under the null, even if the correlation between their p-values is rather low, implying that both approaches cannot be used simultaneously. The stratified version has a higher power in case of non-homogeneous hazards, but also carries a different interpretation. CONCLUSIONS: The log-rank type test and its stratified version can be interpreted in the same way as the results of an analogous semi-parametric additive regression model despite the fact that no direct theoretical link can be established between the test statistics.
[Mh] Termos MeSH primário: Infarto do Miocárdio/mortalidade
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Simulação por Computador
Interpretação Estatística de Dados
Feminino
Seres Humanos
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Análise de Regressão
Risco
Fatores Sexuais
Análise de Sobrevida
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12874-017-0351-3


  3 / 192497 MEDLINE  
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[PMID]:29268650
[Au] Autor:Quitt J; Fassl J
[Ad] Endereço:1 Departement für Anästhesiologie, operative Intensivmedizin, Schmerztherapie und präklinische Notfallmedizin, Universitätsspital Basel, Basel.
[Ti] Título:Kardiovaskuläres Risiko..
[So] Source:Ther Umsch;74(7):351-360, 2017.
[Is] ISSN:0040-5930
[Cp] País de publicação:Switzerland
[La] Idioma:ger
[Mh] Termos MeSH primário: Testes de Função Cardíaca/métodos
Monitorização Intraoperatória/métodos
Infarto do Miocárdio/diagnóstico
Infarto do Miocárdio/prevenção & controle
Assistência Perioperatória/métodos
Complicações Pós-Operatórias/diagnóstico
Complicações Pós-Operatórias/prevenção & controle
[Mh] Termos MeSH secundário: Medicina Baseada em Evidências
Seres Humanos
Prognóstico
Medição de Risco/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1024/0040-5930/a000926


  4 / 192497 MEDLINE  
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[PMID]:29489691
[Au] Autor:Murayama K; Suzuki S; Matsukiyo R; Takenaka A; Hayakawa M; Tsutsumi T; Fujii K; Katada K; Toyama H
[Ad] Endereço:Department of Radiology, Fujita Health University.
[Ti] Título:Preliminary study of time maximum intensity projection computed tomography imaging for the detection of early ischemic change in patient with acute ischemic stroke.
[So] Source:Medicine (Baltimore);97(9):e9906, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Noncontrast computed tomography (NCCT) has been used for the detection of early ischemic change (EIC); however, correct interpretation of NCCT findings requires much clinical experience. This study aimed to assess the accuracy of time maximum intensity projection computed tomography technique (tMIP), which reflects the maximum value for the time phase direction from the dynamic volume data for each projected plane, for detection of EIC, against that of NCCT.Retrospective review of NCCT, cerebral blood volume in CT perfusion (CTP-CBV), and tMIP of 186 lesions from 280 regions evaluated by Alberta Stroke Program Early CT Score (ASPECTS) in 14 patients with acute middle cerebral artery stroke who had undergone whole-brain CTP using 320-row area detector CT was performed. Four radiologists reviewed EIC on NCCT, CTP-CBV, and tMIP in each ASPECTS region at onset using the continuous certainty factor method. Receiver operating characteristic analysis was performed to compare the relative performance for detection of EIC. The correlations were evaluated.tMIP-color showed the best discriminative value for detection of EIC. There were significant differences in the area under the curve for NCCT and tMIP-color, CTP-CBV (P < .05). Scatter plots of ASPECTS showed a positive significant correlation between NCCT, tMIP-gray, tMIP-color, and the follow-up study (NCCT, r = 0.32, P = .0166; tMIP-gray, r = 0.44, P = .0007; tMIP-color, r = 0.34, P = .0104).Because tMIP provides a high contrast parenchymal image with anatomical and vascular information in 1 sequential scan, it showed greater accuracy for detection of EIC and predicted the final infarct extent more accurately than NCCT based on ASPECTS.
[Mh] Termos MeSH primário: Isquemia Encefálica/diagnóstico por imagem
Infarto da Artéria Cerebral Média/diagnóstico por imagem
Acidente Vascular Cerebral/diagnóstico por imagem
Tomografia Computadorizada por Raios X/estatística & dados numéricos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Área Sob a Curva
Encéfalo/irrigação sanguínea
Circulação Cerebrovascular
Feminino
Seguimentos
Seres Humanos
Masculino
Curva ROC
Estudos Retrospectivos
Fatores de Tempo
Tomografia Computadorizada por Raios X/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009906


  5 / 192497 MEDLINE  
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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


  6 / 192497 MEDLINE  
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[PMID]:28453728
[Au] Autor:Vincent A; Sportouch C; Covinhes A; Barrère C; Gallot L; Delgado-Betancourt V; Lattuca B; Solecki K; Boisguérin P; Piot C; Nargeot J; Barrère-Lemaire S
[Ad] Endereço:IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
[Ti] Título:Cardiac mGluR1 metabotropic receptors in cardioprotection.
[So] Source:Cardiovasc Res;113(6):644-655, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: In a previous study using a genome-wide microarray strategy, we identified metabotropic glutamate receptor 1 (mGluR1) as a putative cardioprotective candidate in ischaemic postconditioning (PostC). In the present study, we investigated the role of cardiac mGluR1 receptors during cardioprotection against myocardial ischaemia-reperfusion injury in the mouse myocardium. Methods and results: mGluR1 activation by glutamate administered 5 min before reperfusion in C57Bl/6 mice subjected to a myocardial ischaemia protocol strongly decreased both infarct size and DNA fragmentation measured at 24 h reperfusion. This cardioprotective effect was mimicked by the mGluR1 agonist, DHPG (10 µM), and abolished when glutamate was coinjected with the mGluR1 antagonist YM298198 (100 nM). Wortmannin (100 nM), an inhibitor of PI3-kinase, was able to prevent glutamate-induced cardioprotection. A glutamate bolus at the onset of reperfusion failed to protect the heart of mGluR1 knockout mice subjected to a myocardial ischaemia-reperfusion protocol, although PostC still protected the mGluR1 KO mice. Glutamate-treatment improved post-infarction functional recovery as evidenced by an echocardiographic study performed 15 days after treatment and by a histological evaluation of fibrosis 21 days post-treatment. Interestingly, restoration of functional mGluR1s by a PostC stimulus was evidenced at the transcriptional level. Since mGluR1s were localized at the surface membrane of cardiomyocytes, they might contribute to the cardioprotective effect of ischaemic PostC as other Gq-coupled receptors. Conclusion: This study provides the first demonstration that mGluR1 activation at the onset of reperfusion induces cardioprotection and might represent a putative strategy to prevent ischaemia-reperfusion injury.
[Mh] Termos MeSH primário: Agonistas de Aminoácidos Excitatórios/administração & dosagem
Glutamina/administração & dosagem
Infarto do Miocárdio/prevenção & controle
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miocárdio/metabolismo
Receptores de Glutamato Metabotrópico/agonistas
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Antagonistas de Aminoácidos Excitatórios/farmacologia
Predisposição Genética para Doença
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miocárdio/patologia
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Glutamato Metabotrópico/deficiência
Receptores de Glutamato Metabotrópico/genética
Transdução de Sinais
Fatores de Tempo
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agonists); 0 (Excitatory Amino Acid Antagonists); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor type 1); 0RH81L854J (Glutamine); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx024


  7 / 192497 MEDLINE  
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[PMID]:29397593
[Au] Autor:Committee of Cardio-Cerebro-Vascular Diseases of Gerontological Society of China; Working Group of Chinese Expert Consensus on the Use of Xuezhikang
[Ti] Título:[Chinese expert consensus on the use of Xuezhikang (2017 revised edition)].
[So] Source:Zhonghua Nei Ke Za Zhi;57(2):97-100, 2018 Feb 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Xuezhikang, a Chinese traditional medicine, contains natural statin and is effective on dyslipidemia by inhibiting cholesterol synthesis. Xuezhikang therapy for 8 weeks in patients with hyperlipidemia reduced total cholesterol (TC) by 23%, low density lipoprotein cholesterol (LDL-C) by 28.5% and triglyceride(TG) by 36.5%, and increased high density lipoprotein cholesterol (HDL-C) by 19.6%, respectively. Data from China Coronary Secondary Prevention Study (CCSPS) showed that treatment with Xuezhikang lowered the risks of major coronary events, death from coronary heart disease, and all cause death in patients with myocardial infarction, indicating that Xuezhikang can be used in the primary and secondary prevention of cardiovascular disease.
[Mh] Termos MeSH primário: Consenso
Medicamentos de Ervas Chinesas/uso terapêutico
Dislipidemias/tratamento farmacológico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático
Causas de Morte
China
LDL-Colesterol
Seres Humanos
Infarto do Miocárdio
Prevenção Secundária
Triglicerídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, LDL); 0 (Drugs, Chinese Herbal); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Triglycerides); 0 (xuezhikang)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2018.02.003


  8 / 192497 MEDLINE  
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[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


  9 / 192497 MEDLINE  
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[PMID]:29286056
[Au] Autor:Zaid Iskandar M; Lang CC
[Ad] Endereço:Ninewells Hospital and Medical School, Dundee, Scotland, UK.
[Ti] Título:Sacubitril and valsartan fixed combination to reduce heart failure events in post-acute myocardial infarction patients.
[So] Source:Drugs Today (Barc);53(10):545-551, 2017 Oct.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Heart failure is a term used to define a constellation of symptoms and signs that are commonly attributed to the inability of the heart to produce a cardiac output that meets the demands of the body. It remains a deadly disease, affecting between 1-2% of the population, and is more common in the elderly, with around 6-10% of patients over 65 suffering from the condition. Sacubitril/valsartan (LCZ-696) is a combined neprilysin inhibitor and angiotensin AT1 receptor blocker approved in recent years for the treatment of chronic heart failure with reduced ejection fraction. In an area where there have been limited pharmacological advances in the last 10 years, this drug was a game changer and a much welcomed addition to contemporary heart failure therapy. It is currently being studied in patients with heart failure with preserved ejection fraction and for the reduction of heart failure events post-acute myocardial infarction. Results from the ongoing PARADISE-MI study are awaited by the global cardiology community with great interest.
[Mh] Termos MeSH primário: Aminobutiratos/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Infarto do Miocárdio/complicações
Neprilisina/antagonistas & inibidores
Tetrazóis/administração & dosagem
Valsartana/administração & dosagem
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Ensaios Clínicos como Assunto
Seres Humanos
Tetrazóis/farmacologia
Valsartana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (LCZ 696); 0 (Tetrazoles); 80M03YXJ7I (Valsartan); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.10.2722396


  10 / 192497 MEDLINE  
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[PMID]:29231026
[Au] Autor:Song RY; Ding RT; Cui W
[Ad] Endereço:Medical College of Qingdao University, Qingdao 266000, China.
[Ti] Título:[Impact of Myocardial Infarction and Abnormalities of Cardiac Conduction System on Sudden Cardiac Death].
[So] Source:Fa Yi Xue Za Zhi;33(2):171-174, 2017 Apr.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Sudden cardiac death (SCD), most commonly seen in coronary heart disease, is a kind of sudden death caused by series of cardiac parameters, which usually combines with myocardial infarction. However, some SCDs (including early myocardial infarction) happen suddenly and cause death in a very short time. In these circumstances, typical morphological changes are lack in macroscopic or microscopic fields, which make such SCDs become the emphasis and difficulty in the present research. SCD caused by myocardial infarction and abnormalities of cardiac conduction system (CCS) is related to atherosclerosis of coronary artery closely. This paper reviews cardiac dysfunction caused by myocardial infarction and diseases of CCS from morphology and molecular biology, and explores potential relationship between them. This paper aims to provide clues to the mechanism of myocardial infarction related sudden death and possible assistance for forensic diagnosis of SCD.
[Mh] Termos MeSH primário: Morte Súbita Cardíaca
Sistema de Condução Cardíaco/fisiopatologia
Infarto do Miocárdio/complicações
[Mh] Termos MeSH secundário: Doença das Coronárias
Morte Súbita Cardíaca/etiologia
Seres Humanos
Infarto do Miocárdio/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2017.02.014



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