Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
JACC Case Rep ; 3(11): 1393-1395, 2021 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-34505081

RESUMO

A 72-year-old patient presented S/P defibrillation for ventricular fibrillation cardiac arrest. We present an interesting teaching electrocardiogram that demonstrates alternating right and left bundle branch blocks, as well as an atrioventricular block that illustrates this patient's complex conduction system disease. (Level of Difficulty: Intermediate.).

2.
ESC Heart Fail ; 8(4): 3119-3129, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34137193

RESUMO

AIMS: Heart failure in constrictive pericarditis (CP) is attributed to impaired biventricular diastolic filling. However, diseases that cause CP due to myocardial infiltration and fibrosis can also impair biventricular systolic function (sf) and contribute to heart failure. This study of patients with CP examined biventricular sf and the effect of myocardial infiltration by pericardial diseases and the resulting fibrosis on ventricular sf. METHODS AND RESULTS: Histopathologic examinations of right ventricular (RV) and left ventricular (LV) myocardia and pericardia were performed on three autopsied hearts of patients with pericardial diseases. Additionally, in 40 adults with clinical heart failure and 40 healthy adults (controls), sf of both ventricles was examined by echocardiography, including strain measurements, and biventricular diastolic filling and pulmonary artery pressures were assessed by cardiac catheterization. Cardiac histopathology indicated thickening of the pericardium with fibrosis, disease infiltrating the myocardium, greater infiltration of the RV than the LV, and an association of pericardial thickness with myocardial infiltrations. Functional analysis indicated that RVsf was impaired on all echo indices, including strain measurement, but LVsf was preserved. CONCLUSIONS: Diseases causing CP are not restricted to the pericardium but also infiltrate the biventricular myocardium and affect the thin-walled RV more than the thick-walled LV, resulting in depressed RVsf. The present results help explain clinical heart failure in the presence of restricted diastolic filling in CP. Depression of RVsf due to progression of fibrosis in the RV myocardium may increase the risk of delayed pericardiectomy.


Assuntos
Insuficiência Cardíaca , Pericardite Constritiva , Adulto , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/diagnóstico , Humanos , Pericardiectomia , Pericardite Constritiva/complicações , Pericardite Constritiva/diagnóstico , Sístole , Função Ventricular Direita
3.
Cell Tissue Res ; 358(1): 229-38, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24859220

RESUMO

Receptors for advanced glycation end-products (RAGE) are members of the immunoglobulin superfamily of cell-surface receptors implicated in mechanisms of pulmonary inflammation. In the current study, we test the hypothesis that RAGE mediates inflammation in primary alveolar macrophages (AMs) exposed to diesel particulate matter (DPM). Quantitative RT-PCR and immunoblotting revealed that RAGE was up-regulated in Raw264.7 cells, an immortalized murine macrophage cell line and primary AMs exposed to DPM for 2 h. Because DPM increased RAGE expression, we exposed Raw264.7 cells and primary AMs isolated from RAGE null and wild-type (WT) mice to DPM prior to the assessment of inflammatory signaling intermediates. DPM led to the activation of Rat sarcoma GTPase (Ras), p38 MAPK and NF-κB in WT AMs and, when compared to WT AMs, these intermediates were diminished in DPM-exposed AMs isolated from RAGE null mice. Furthermore, cytokines implicated in inflammation, including IL-4, IL-12, IL-13 and TNFα, were all significantly decreased in DPM-exposed RAGE null AMs compared to similarly exposed WT AMs. These results demonstrate that diesel-induced inflammatory responses by primary AMs are mediated, at least in part, via RAGE signaling mechanisms. Further work may show that RAGE signaling in both alveolar epithelial cells and resident macrophages is a potential target in the treatment of inflammatory lung diseases exacerbated by environmental pollution.


Assuntos
Poluentes Atmosféricos/toxicidade , Regulação da Expressão Gênica/efeitos dos fármacos , Pulmão/metabolismo , Macrófagos Alveolares/metabolismo , Receptores Imunológicos/biossíntese , Transdução de Sinais/efeitos dos fármacos , Emissões de Veículos/toxicidade , Animais , Linhagem Celular , Citocinas/biossíntese , Citocinas/genética , Regulação da Expressão Gênica/genética , Inflamação/induzido quimicamente , Inflamação/metabolismo , Inflamação/patologia , Pulmão/patologia , Macrófagos Alveolares/patologia , Camundongos , Camundongos Mutantes , Receptor para Produtos Finais de Glicação Avançada , Receptores Imunológicos/genética , Transdução de Sinais/genética
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...