Base de dados : MEDLINE
Pesquisa : D27.505.954.411 [Categoria DeCS]
Referências encontradas : 11115 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1112 ir para página                         

  1 / 11115 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29203734
[Au] Autor:Skochko OV; Kaidashev IP
[Ad] Endereço:Department Of Internal Medicine No 3 With Phthisiology, Higher State Educational Establishment Of Ukraine "Ukrainian Medical Stomatological Academy", Poltava, Ukraine.
[Ti] Título:Effect of pioglitazone on insulin resistance, progression of atherosclerosis and clinical course of coronary heart disease.
[So] Source:Wiad Lek;70(5):881-890, 2017.
[Is] ISSN:0043-5147
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Pioglitazone, a medication of thiazolidinedione group, is capable of triggering the peroxisome proliferator-activated receptors (PPAR-γ). Activation of receptor PPAR-γ regulates carbohydrate and lipid metabolism, immune and inflammatory responses in heart tissues. THE AIM: Our aim was to study the effect of pioglitazone on insulin resistance, the clinical course of atherosclerosis and coronary heart disease (CHD). MATERIALS AND METHODS: The study included 43 patients with coronary artery disease. Patients were divided into the main group - 20 patients, in whom pioglitazone (Pioglar, Ranbaxy, India) was included in the combined therapy at a dose of 15 mg 1 time per day in the morning, and the comparison group - 23 patients receiving standard complex drug therapy over 6 months. Patients underwent clinical examination, ultrasound of neck vessels, study of carbohydrate and lipid metabolism. RESULTS: Joining pioglitazone to standard therapy resulted in the reduction of systolic (p<0.05) and diastolic (p<0.05) blood pressure; decrease in the duration of pain attacks (p<0.05); reduction in the frequency of angina attacks (p<0.05); regression of atherosclerosis of the carotid vessels (p<0.05), decrease in the thickness of the intima-media complex (p<0.05). The decline in oral glucose tolerance test (p<0.05), hyperglycemic factor (p<0.05), total cholesterol (p<0.05), and low density lipoproteins (p<0.05) were observed, as well as increased high-density lipoprotein (p<0.05). CONCLUSION: Long-term treatment with pioglitazone at low doses against the background of standard therapy contributes to functional and clinical condition of patients, promotes the prevention of atherosclerosis and reduction of insulin resistance, thereby improving the clinical manifestations of coronary heart disease.
[Mh] Termos MeSH primário: Aterosclerose/tratamento farmacológico
Hipoglicemiantes/administração & dosagem
Resistência à Insulina
Tiazolidinedionas/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Aterosclerose/diagnóstico por imagem
Fármacos Cardiovasculares/administração & dosagem
Quimioterapia Combinada
Feminino
Seres Humanos
Masculino
Meia-Idade
Resultado do Tratamento
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Hypoglycemic Agents); 0 (Thiazolidinediones); X4OV71U42S (pioglitazone)
[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:171206
[St] Status:MEDLINE


  2 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453725
[Au] Autor:Nonhoff J; Ricke-Hoch M; Mueller M; Stapel B; Pfeffer T; Kasten M; Scherr M; von Kaisenberg C; Bauersachs J; Haghikia A; Hilfiker-Kleiner D
[Ad] Endereço:Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany.
[Ti] Título:Serelaxin treatment promotes adaptive hypertrophy but does not prevent heart failure in experimental peripartum cardiomyopathy.
[So] Source:Cardiovasc Res;113(6):598-608, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Peripartum cardiomyopathy (PPCM) is a systolic left ventricular dysfunction developing in the peripartum phase in previously healthy women. Relaxin-2 is a pregnancy hormone with potential beneficial effects in heart failure patients. We evaluated Relaxin-2 as a potential diagnostic marker and/or a therapeutic agent in PPCM. Methods and results: In healthy peripartum women, serum Relaxin-2 levels (measured by ELISA in the second half of pregnancy) were elevated showing a decreasing trend in the first postpartum week and returned to non-pregnant levels thereafter. In PPCM patients diagnosed in the first postpartum week, serum Relaxin-2 levels were lower compared to healthy postpartum stage-matched controls. In PPCM patients diagnosed later (0.5-10 months postpartum) Relaxin-2 levels were in the range of non-pregnant controls and not different from healthy postpartum stage-matched controls. In mice, serum Relaxin-1 (functional equivalent of human Relaxin-2) was increased late in pregnancy and rapidly cleared in the first postpartum week. In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or ß-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5. In vitro analyses showed that Prolactin induces cardiomyocyte hypertrophy via activation of STAT5. Conclusion: Although Relaxin-2 levels seemed lower in PPCM patients diagnosed early postpartum, we observed a high pregnancy-related variance of serum Relaxin-2 levels peripartum making it unsuitable as a biomarker for this condition. Supplementation with sRlx may contribute to angiogenesis and compensatory hypertrophy in the diseased heart, but the effects are not sufficient to prevent heart failure in an experimental PPCM model.
[Mh] Termos MeSH primário: Cardiomegalia/patologia
Cardiomiopatias/tratamento farmacológico
Fármacos Cardiovasculares/farmacologia
Insuficiência Cardíaca/prevenção & controle
Miócitos Cardíacos/efeitos dos fármacos
Período Pós-Parto/sangue
Relaxina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Animais
Biomarcadores/sangue
Cardiomegalia/sangue
Cardiomegalia/fisiopatologia
Cardiomiopatias/sangue
Cardiomiopatias/patologia
Cardiomiopatias/fisiopatologia
Estudos de Casos e Controles
Modelos Animais de Doenças
Feminino
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Camundongos Knockout
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Gravidez
Prolactina/sangue
Ratos
Proteínas Recombinantes/farmacologia
Sistema de Registros
Relaxina/sangue
Fator de Transcrição STAT3/deficiência
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT5/metabolismo
Transdução de Sinais/efeitos dos fármacos
Volume Sistólico
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiovascular Agents); 0 (RLN2 protein, human); 0 (Recombinant Proteins); 0 (Rln1 protein, mouse); 0 (STAT3 Transcription Factor); 0 (STAT5 Transcription Factor); 0 (Stat3 protein, mouse); 0 (relaxin-3 protein, mouse); 0 (serelaxin protein, human); 9002-62-4 (Prolactin); 9002-69-1 (Relaxin)
[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/cvw245


  3 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468954
[Au] Autor:Mahmoud AN; Barakat AF; Elgendy AY; Schneibel E; Mentias A; Abuzaid A; Elgendy IY
[Ad] Endereço:From the Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville (A.N.M., A.Y.E., E.S., I.Y.E.); Department of Medicine, Cleveland Clinic Foundation, OH (A.F.B.); Division of Cardiovascular Medicine, Department of Medicine, University of Iowa Carver College of
[Ti] Título:Long-Term Efficacy and Safety of Everolimus-Eluting Bioresorbable Vascular Scaffolds Versus Everolimus-Eluting Metallic Stents: A Meta-Analysis of Randomized Trials.
[So] Source:Circ Cardiovasc Interv;10(5), 2017 May.
[Is] ISSN:1941-7632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Data regarding the long-term efficacy and safety of everolimus-eluting bioresorbable vascular scaffolds (BVS) compared with everolimus-eluting stents are limited. This meta-analysis aimed to compare the long-term outcomes with both devices. METHODS AND RESULTS: Randomized trials reporting clinical outcomes beyond 1 year and comparing BVS with everolimus-eluting stents were included. Summary estimates risk ratios (RRs) were constructed. The primary efficacy outcome was target lesion failure, defined as cardiac death, target vessel myocardial infarction, and ischemia-driven target lesion revascularization, and the primary safety outcome was definite or probable stent/scaffold thrombosis. Six trials with 5392 patients were included (mean follow-up, 25 months). BVS had a higher rate of target lesion failure (RR, 1.33; 95% confidence interval [CI], 1.11-1.58) driven by the higher rates of target vessel myocardial infarction (RR, 1.65; 95% CI, 1.26-2.17) and target lesion revascularization (RR, 1.39; 95% CI, 1.08-1.78). The risk of definite or probable stent/scaffold thrombosis (RR, 3.22; 95% CI, 1.89-5.49) and very late stent/scaffold thrombosis (>1 year; RR, 4.78; 95% CI, 1.66-13.8) was higher with BVS. The risk of cardiac and all-cause mortality was similar in both groups. CONCLUSIONS: Compared with everolimus-eluting stents, BVS is associated with increased risk of target lesion failure driven by the increased rates of target vessel myocardial infarction and ischemia-driven target lesion revascularization in these studies (mean follow-up, 25 months). The risk of definite or probable stent/scaffold thrombosis and very late stent/scaffold thrombosis seems to be higher with BVS. Further information from randomized trials is critical to evaluate clinical outcomes with BVS on complete resolution of the scaffold.
[Mh] Termos MeSH primário: Implantes Absorvíveis
Fármacos Cardiovasculares/administração & dosagem
Materiais Revestidos Biocompatíveis
Doença da Artéria Coronariana/terapia
Stents Farmacológicos
Everolimo/administração & dosagem
Metais
Intervenção Coronária Percutânea/instrumentação
[Mh] Termos MeSH secundário: Idoso
Fármacos Cardiovasculares/efeitos adversos
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/mortalidade
Trombose Coronária/etiologia
Everolimo/efeitos adversos
Feminino
Seres Humanos
Masculino
Meia-Idade
Infarto do Miocárdio/etiologia
Razão de Chances
Intervenção Coronária Percutânea/efeitos adversos
Intervenção Coronária Percutânea/mortalidade
Desenho de Prótese
Ensaios Clínicos Controlados Aleatórios como Assunto
Medição de Risco
Fatores de Risco
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Coated Materials, Biocompatible); 0 (Metals); 9HW64Q8G6G (Everolimus)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  4 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28464141
[Au] Autor:Larkin I; Ang D; Steinhart J; Chao M; Patterson M; Sah S; Wu T; Schoenbaum M; Hutchins D; Brennan T; Loewenstein G
[Ad] Endereço:University of California, Los Angeles.
[Ti] Título:Association Between Academic Medical Center Pharmaceutical Detailing Policies and Physician Prescribing.
[So] Source:JAMA;317(17):1785-1795, 2017 May 02.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: In an effort to regulate physician conflicts of interest, some US academic medical centers (AMCs) enacted policies restricting pharmaceutical representative sales visits to physicians (known as detailing) between 2006 and 2012. Little is known about the effect of these policies on physician prescribing. Objective: To analyze the association between detailing policies enacted at AMCs and physician prescribing of actively detailed and not detailed drugs. Design, Setting, and Participants: The study used a difference-in-differences multivariable regression analysis to compare changes in prescribing by physicians before and after implementation of detailing policies at AMCs in 5 states (California, Illinois, Massachusetts, Pennsylvania, and New York) that made up the intervention group with changes in prescribing by a matched control group of similar physicians not subject to a detailing policy. Exposures: Academic medical center implementation of policies regulating pharmaceutical salesperson visits to attending physicians. Main Outcomes and Measures: The monthly within-drug class market share of prescriptions written by an individual physician for detailed and nondetailed drugs in 8 drug classes (lipid-lowering drugs, gastroesophageal reflux disease drugs, diabetes drugs, antihypertensive drugs, hypnotic drugs approved for the treatment of insomnia [sleep aids], attention-deficit/hyperactivity disorder drugs, antidepressant drugs, and antipsychotic drugs) comparing the 10- to 36-month period before implementation of the detailing policies with the 12- to 36-month period after implementation, depending on data availability. Results: The analysis included 16 121 483 prescriptions written between January 2006 and June 2012 by 2126 attending physicians at the 19 intervention group AMCs and by 24 593 matched control group physicians. The sample mean market share at the physician-drug-month level for detailed and nondetailed drugs prior to enactment of policies was 19.3% and 14.2%, respectively. Exposure to an AMC detailing policy was associated with a decrease in the market share of detailed drugs of 1.67 percentage points (95% CI, -2.18 to -1.18 percentage points; P < .001) and an increase in the market share of nondetailed drugs of 0.84 percentage points (95% CI, 0.54 to 1.14 percentage points; P < .001). Associations were statistically significant for 6 of 8 study drug classes for detailed drugs (lipid-lowering drugs, gastroesophageal reflux disease drugs, antihypertensive drugs, sleep aids, attention-deficit/hyperactivity disorder drugs, and antidepressant drugs) and for 9 of the 19 AMCs that implemented policies. Eleven of the 19 AMCs regulated salesperson gifts to physicians, restricted salesperson access to facilities, and incorporated explicit enforcement mechanisms. For 8 of these 11 AMCs, there was a significant change in prescribing. In contrast, there was a significant change at only 1 of 8 AMCs that did not enact policies in all 3 areas. Conclusions and Relevance: Implementation of policies at AMCs that restricted pharmaceutical detailing between 2006 and 2012 was associated with modest but significant reductions in prescribing of detailed drugs across 6 of 8 major drug classes; however, changes were not seen in all of the AMCs that enacted policies.
[Mh] Termos MeSH primário: Centros Médicos Acadêmicos/estatística & dados numéricos
Conflito de Interesses
Indústria Farmacêutica
Prescrições de Medicamentos/estatística & dados numéricos
Política Organizacional
Médicos/estatística & dados numéricos
Medicamentos sob Prescrição/uso terapêutico
[Mh] Termos MeSH secundário: Anticolesterolemiantes/uso terapêutico
Antidepressivos/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Antipsicóticos/uso terapêutico
California
Fármacos Cardiovasculares/uso terapêutico
Seres Humanos
Hipnóticos e Sedativos/uso terapêutico
Hipoglicemiantes/uso terapêutico
Illinois
Relações Interprofissionais
Massachusetts
New York
Pennsylvania
Análise de Regressão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Antidepressive Agents); 0 (Antihypertensive Agents); 0 (Antipsychotic Agents); 0 (Cardiovascular Agents); 0 (Hypnotics and Sedatives); 0 (Hypoglycemic Agents); 0 (Prescription Drugs)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.4039


  5 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453734
[Au] Autor:Hausenloy DJ; Garcia-Dorado D; Bøtker HE; Davidson SM; Downey J; Engel FB; Jennings R; Lecour S; Leor J; Madonna R; Ovize M; Perrino C; Prunier F; Schulz R; Sluijter JPG; Van Laake LW; Vinten-Johansen J; Yellon DM; Ytrehus K; Heusch G; Ferdinandy P
[Ad] Endereço:The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London WC1E 6HX, UK; The National Institute of Health Research University College London Hospitals Biomedical Research Centre, 149 Tottenham Court Road London, W1T 7DN, UK; Cardiovascular and Metabolic Disorders Program
[Ti] Título:Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart.
[So] Source:Cardiovasc Res;113(6):564-585, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ischaemic heart disease and the heart failure that often results, remain the leading causes of death and disability in Europe and worldwide. As such, in order to prevent heart failure and improve clinical outcomes in patients presenting with an acute ST-segment elevation myocardial infarction and patients undergoing coronary artery bypass graft surgery, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury (IRI). During the last three decades, a wide variety of ischaemic conditioning strategies and pharmacological treatments have been tested in the clinic-however, their translation from experimental to clinical studies for improving patient outcomes has been both challenging and disappointing. Therefore, in this Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart, we critically analyse the current state of ischaemic conditioning in both the experimental and clinical settings, provide recommendations for improving its translation into the clinical setting, and highlight novel therapeutic targets and new treatment strategies for reducing acute myocardial IRI.
[Mh] Termos MeSH primário: Cardiologia/métodos
Fármacos Cardiovasculares/uso terapêutico
Ponte de Artéria Coronária/efeitos adversos
Insuficiência Cardíaca/prevenção & controle
Precondicionamento Isquêmico/métodos
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Intervenção Coronária Percutânea/efeitos adversos
Infarto do Miocárdio com Supradesnível do Segmento ST/terapia
Pesquisa Médica Translacional/métodos
[Mh] Termos MeSH secundário: Animais
Cardiologia/normas
Fármacos Cardiovasculares/efeitos adversos
Ponte de Artéria Coronária/normas
Modelos Animais de Doenças
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Pós-Condicionamento Isquêmico/métodos
Precondicionamento Isquêmico/efeitos adversos
Precondicionamento Isquêmico/normas
Precondicionamento Isquêmico Miocárdico/métodos
Traumatismo por Reperfusão Miocárdica/etiologia
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Intervenção Coronária Percutânea/normas
Fatores de Proteção
Fatores de Risco
Infarto do Miocárdio com Supradesnível do Segmento ST/complicações
Infarto do Miocárdio com Supradesnível do Segmento ST/patologia
Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia
Pesquisa Médica Translacional/normas
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; PRACTICE GUIDELINE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx049


  6 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Registro de Ensaios Clínicos
Texto completo
[PMID]:27774758
[Au] Autor:Ielasi A; Varricchio A; Campo G; Leoncini M; Cortese B; Vicinelli P; Brugaletta S; di Uccio FS; Latib A; Tespili M
[Ad] Endereço:Cardiology Division, Bolognini Hospital Seriate, Seriate, BG, Italy.
[Ti] Título:A prospective evaluation of a standardized strategy for the use of a polymeric everolimus-eluting bioresorbable scaffold in ST-segment elevation myocardial infarction: Rationale and design of the BVS STEMI STRATEGY-IT study.
[So] Source:Catheter Cardiovasc Interv;89(7):1129-1138, 2017 Jun 01.
[Is] ISSN:1522-726X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To assess the feasibility and the clinical results following a prespecified bioresorbable vascular scaffold (Absorb BVS) implantation strategy in ST-elevation myocardial infarction (STEMI) patients. BACKGROUNDS: Concerns raised about the BVS safety in STEMI setting because a not negligible thrombosis rate was reported within 30 days and 12 months after implantation. Technical procedural issues related to the structural BVS features were advocated as probable causes for the thrombotic events. METHODS: This is an investigators-owned and -directed, prospective, nonrandomized, single-arm multicenter registry intended to obtain data from 500 consecutive STEMI patients undergoing primary PCI with BVS (1.1 or GT1) following a prespecified implantation protocol. The study is recorded in ClinicalTrials.gov with the identifier: NCT02601781. RESULTS: The primary endpoint is a device-oriented composite end-point (DOCE) of cardiac death, any myocardial infarction clearly attributable to the intervention culprit vessel and ischemic-driven target lesion revascularization within 30 days after the index procedure. The DOCE will be assessed even at 6-month, 1-, 3-, and 5-year follow-up. CONCLUSIONS: This will be the first study investigating the feasibility and the early- and long-term clinical impact of a prespecified BVS implantation protocol in thrombotic lesions causing STEMI. Here, we describe the rationale and the design of the study. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Implantes Absorvíveis
Fármacos Cardiovasculares/administração & dosagem
Materiais Revestidos Biocompatíveis
Trombose Coronária/terapia
Everolimo/administração & dosagem
Intervenção Coronária Percutânea/instrumentação
Polímeros/química
Infarto do Miocárdio com Supradesnível do Segmento ST/terapia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Fármacos Cardiovasculares/efeitos adversos
Angiografia Coronária
Trombose Coronária/diagnóstico por imagem
Trombose Coronária/mortalidade
Everolimo/efeitos adversos
Estudos de Viabilidade
Feminino
Seres Humanos
Itália
Masculino
Meia-Idade
Intervenção Coronária Percutânea/efeitos adversos
Intervenção Coronária Percutânea/mortalidade
Estudos Prospectivos
Desenho de Prótese
Recidiva
Sistema de Registros
Projetos de Pesquisa
Fatores de Risco
Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem
Infarto do Miocárdio com Supradesnível do Segmento ST/mortalidade
Fatores de Tempo
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Coated Materials, Biocompatible); 0 (Polymers); 9HW64Q8G6G (Everolimus)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1002/ccd.26801


  7 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468832
[Au] Autor:Gut P; Reischauer S; Stainier DYR; Arnaout R
[Ad] Endereço:Nestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, C
[Ti] Título:LITTLE FISH, BIG DATA: ZEBRAFISH AS A MODEL FOR CARDIOVASCULAR AND METABOLIC DISEASE.
[So] Source:Physiol Rev;97(3):889-938, 2017 Jul 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The burden of cardiovascular and metabolic diseases worldwide is staggering. The emergence of systems approaches in biology promises new therapies, faster and cheaper diagnostics, and personalized medicine. However, a profound understanding of pathogenic mechanisms at the cellular and molecular levels remains a fundamental requirement for discovery and therapeutics. Animal models of human disease are cornerstones of drug discovery as they allow identification of novel pharmacological targets by linking gene function with pathogenesis. The zebrafish model has been used for decades to study development and pathophysiology. More than ever, the specific strengths of the zebrafish model make it a prime partner in an age of discovery transformed by big-data approaches to genomics and disease. Zebrafish share a largely conserved physiology and anatomy with mammals. They allow a wide range of genetic manipulations, including the latest genome engineering approaches. They can be bred and studied with remarkable speed, enabling a range of large-scale phenotypic screens. Finally, zebrafish demonstrate an impressive regenerative capacity scientists hope to unlock in humans. Here, we provide a comprehensive guide on applications of zebrafish to investigate cardiovascular and metabolic diseases. We delineate advantages and limitations of zebrafish models of human disease and summarize their most significant contributions to understanding disease progression to date.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/genética
Descoberta de Drogas/métodos
Doenças Metabólicas/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Fármacos Cardiovasculares/farmacologia
Doenças Cardiovasculares/tratamento farmacológico
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/fisiopatologia
Modelos Animais de Doenças
Predisposição Genética para Doença
Seres Humanos
Doenças Metabólicas/tratamento farmacológico
Doenças Metabólicas/metabolismo
Doenças Metabólicas/fisiopatologia
Fenótipo
Especificidade da Espécie
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00038.2016


  8 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28455405
[Au] Autor:Li Kam Wa ME; Taraborrelli P; Hayat S; Lim PB
[Ad] Endereço:Department of Cardiology, Imperial College Healthcare NHS Trust, London, UK.
[Ti] Título:Respiration driven excessive sinus tachycardia treated with clonidine.
[So] Source:BMJ Case Rep;2017, 2017 Apr 28.
[Is] ISSN:1757-790X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A 26-year-old man presented to our syncope service with debilitating daily palpitations, shortness of breath, presyncope and syncope following a severe viral respiratory illness 4 years previously. Mobitz type II block had previously been identified, leading to a permanent pacemaker and no further episodes of frank syncope. Transthoracic echocardiography, electophysiological study and repeated urine metanepherines were normal. His palpitations and presyncope were reproducible on deep inspiration, coughing, isometric hand exercise and passive leg raises. We demonstrated rapid increases in heart rate with no change in morphology on his 12 lead ECG. His symptoms were resistant to fludrocortisone, flecainide, ß blockers and ivabradine. Initiation of clonidine in combination with ivabradine led to rapid resolution of his symptoms. We suggest that an excessive respiratory sinus arrhythmia was responsible for his symptoms and achieved an excellent response with the centrally acting sympatholytic clonidine, where previous peripherally acting treatments had failed.
[Mh] Termos MeSH primário: Inalação/fisiologia
Síncope/fisiopatologia
Taquicardia Sinusal/complicações
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos alfa 2/administração & dosagem
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Adulto
Benzazepinas/administração & dosagem
Benzazepinas/uso terapêutico
Fármacos Cardiovasculares/administração & dosagem
Fármacos Cardiovasculares/uso terapêutico
Clonidina/administração & dosagem
Clonidina/uso terapêutico
Tosse/complicações
Tosse/etiologia
Quimioterapia Combinada/métodos
Dispneia/diagnóstico
Dispneia/etiologia
Ecocardiografia/métodos
Eletrocardiografia/métodos
Seres Humanos
Masculino
Síncope/etiologia
Taquicardia/etiologia
Taquicardia/fisiopatologia
Taquicardia Sinusal/diagnóstico por imagem
Taquicardia Sinusal/tratamento farmacológico
Taquicardia Sinusal/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Benzazepines); 0 (Cardiovascular Agents); 3H48L0LPZQ (ivabradine); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  9 / 11115 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29320517
[Au] Autor:Psota M; Bandosz P; Gonçalvesová E; Avdicová M; Bucek Psenková M; Studencan M; Pekarcíková J; Capewell S; O'Flaherty M
[Ad] Endereço:Department of Public Health, Faculty of Health Sciences and Social Work, Trnava University in Trnava, Trnava, Slovak Republic.
[Ti] Título:Explaining the decline in coronary heart disease mortality rates in the Slovak Republic between 1993-2008.
[So] Source:PLoS One;13(1):e0190090, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Between the years 1993 and 2008, mortality rates from coronary heart disease (CHD) in the Slovak Republic have decreased by almost one quarter. However, this was a smaller decline than in neighbouring countries. The aim of this modelling study was therefore to quantify the contributions of risk factor changes and the use of evidence-based medical therapies to the CHD mortality decline between 1993 and 2008. METHODS: We identified, obtained and scrutinised the data required for the model. These data detailed trends in the major population cardiovascular risk factors (smoking, blood pressure, total cholesterol, diabetes prevalence, body mass index (BMI) and physical activity levels), and also the uptake of all standard CHD treatments. The main data sources were official statistics (National Health Information Centre and Statistical Office of the Slovak Republic) and national representative studies (AUDIT, SLOVAKS, SLOVASeZ, CINDI, EHES, EHIS). The previously validated IMPACT policy model was then used to combine and integrate these data with effect sizes from published meta-analyses quantifying the effectiveness of specific evidence-based treatments, and population-wide changes in cardiovascular risk factors. Results were expressed as deaths prevented or postponed (DPPs) attributable to risk factor changes or treatments. Uncertainties were explored using sensitivity analyses. RESULTS: Between 1993 and 2008 age-adjusted CHD mortality rates in the Slovak Republic (SR) decreased by 23% in men and 26% in women aged 25-74 years. This represented some 1820 fewer CHD deaths in 2008 than expected if mortality rates had not fallen. The IMPACT model explained 91% of this mortality decline. Approximately 50% of the decline was attributable to changes in acute phase and secondary prevention treatments, particularly acute and chronic treatments for heart failure (≈12%), acute coronary syndrome treatments (≈9%) and secondary prevention following AMI and revascularisation (≈8%). Changes in CHD risk factors explained approximately 41% of the total mortality decrease, mainly reflecting reductions in total serum cholesterol. However, other risk factors demonstrated adverse trends and thus generated approximately 740 additional deaths. CONCLUSION: Our analysis suggests that approximately half the CHD mortality fall recently observed in the SR may be attributable to the increased use of evidence-based treatments. However, the adverse trends observed in all the major cardiovascular risk factors (apart from total cholesterol) are deeply worrying. They highlight the need for more energetic population-wide prevention policies such as tobacco control, reducing salt and industrial trans fats content in processed food, clearer food labelling and regulated marketing of processed foods and sugary drinks.
[Mh] Termos MeSH primário: Doença das Coronárias/mortalidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Angioplastia/utilização
Fármacos Cardiovasculares/uso terapêutico
Doenças Cardiovasculares/epidemiologia
Colesterol/sangue
Ponte de Artéria Coronária/utilização
Doença das Coronárias/terapia
Diabetes Mellitus/epidemiologia
Dieta
Medicina Baseada em Evidências
Exercício
Feminino
Seres Humanos
Masculino
Metanálise como Assunto
Meia-Idade
Modelos Cardiovasculares
Mortalidade/tendências
Sobrepeso/epidemiologia
Fatores de Risco
Eslováquia/epidemiologia
Fumar/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Cardiovascular Agents); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190090


  10 / 11115 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29305859
[Au] Autor:Zhao Y; Liu Y; Jing Z; Peng L; Jin P; Lin Y; Zhou Y; Yang L; Ren J; Xie Q; Jin X
[Ad] Endereço:Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, Xiamen 361000, PR China.
[Ti] Título:N-oleoylethanolamide suppresses intimal hyperplasia after balloon injury in rats through AMPK/PPARα pathway.
[So] Source:Biochem Biophys Res Commun;496(2):415-421, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cell (VSMC) proliferation and migration are crucial events in the pathological course of restenosis after percutaneous coronary intervention (PCI). N-oleoylethanolamide (OEA) is a bioactive lipid amide released upon dietary fat digestion with many reported actions. However, the effect of OEA on restenosis after vascular injury remains unknown. Here, we investigated the effects of OEA on intimal hyperplasia after balloon injury in vivo, its effect on VSMC proliferation and migration induced by platelet-derived growth factor (PDGF) stimulation in vitro, and the underlying mechanism underlying these effects. The results showed that OEA-treated rats displayed a significant reduction in neointima formation after balloon injury. In cultured VSMCs, treatment with OEA decreased cell proliferation and migration induced by PDGF. OEA treatment both in vivo and in vitro led to an increase in adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and peroxisome proliferator-activated receptor alpha (PPARα), and a decrease in proliferating cell nuclear antigen (PCNA) and cyclinD1 expression. Pharmacological inhibition of AMPK and PPARα reversed the suppressive effects of OEA on VSMC proliferation and migration, suggesting that the suppressive effect of OEA on VSMC proliferation and migration is mediated through the activation of AMPK and PPARα. In conclusion, our present study demonstrated that OEA attenuated neointima formation in response to balloon injury by suppressing SMC proliferation and migration through an AMPK and PPARα-dependent mechanism. Our data suggests that OEA may be a potential therapeutic agent for restenosis after PCI.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/genética
Fármacos Cardiovasculares/farmacologia
Lesões das Artérias Carótidas/tratamento farmacológico
Endocanabinoides/farmacologia
Hiperplasia/prevenção & controle
Neointima/prevenção & controle
Ácidos Oleicos/farmacologia
PPAR alfa/genética
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Animais
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/metabolismo
Lesões das Artérias Carótidas/patologia
Artéria Carótida Primitiva/efeitos dos fármacos
Artéria Carótida Primitiva/metabolismo
Artéria Carótida Primitiva/patologia
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ciclina D1/genética
Ciclina D1/metabolismo
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Hiperplasia/genética
Hiperplasia/metabolismo
Hiperplasia/patologia
Masculino
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Neointima/genética
Neointima/metabolismo
Neointima/patologia
PPAR alfa/metabolismo
Fosforilação
Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Fator de Crescimento Derivado de Plaquetas/farmacologia
Cultura Primária de Células
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Ratos
Ratos Sprague-Dawley
Túnica Íntima/efeitos dos fármacos
Túnica Íntima/metabolismo
Túnica Íntima/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Ccnd1 protein, rat); 0 (Endocannabinoids); 0 (Oleic Acids); 0 (PPAR alpha); 0 (Platelet-Derived Growth Factor); 0 (Proliferating Cell Nuclear Antigen); 0 (oleoylethanolamide); 136601-57-5 (Cyclin D1); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE



página 1 de 1112 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde