Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros

Base de dados
Ano de publicação
Tipo de documento
Intervalo de ano de publicação
1.
Rev Esp Cardiol (Engl Ed) ; 76(4): 238-244, 2023 Apr.
Artigo em Inglês, Espanhol | MEDLINE | ID: mdl-35878779

RESUMO

INTRODUCTION AND OBJECTIVES: Left bundle branch block (LBBB)-induced cardiomyopathy occurs in patients with long-standing LBBB. These patients characteristically exhibit hyperresponsiveness to cardiac resynchronization therapies (CRT). However, there is scarce information on their response to medical treatment. The aim of this study was to assess the change in left ventricular ejection fraction (LVEF) after a 3-month period following titration of guideline-directed medical therapy for heart failure. METHODS: This retrospective analysis included all patients assessed in the heart failure unit of a Spanish University Hospital between 2020 and 2021, who presented with de novo ventricular dysfunction (LVEF <40%) and had a history of long-standing LBBB with no other possible causes of cardiomyopathy. RESULTS: A total of 1497 patients were analyzed, of which 21 were finally eligible. Mean time from first diagnosis of LBBB to first consultation was 4.05± 4.1 years. Mean LVEF from first consultation to end of titration improved from 29.5±5.7% to 32.7±8.6% (P = .172), but none had recovered ventricular function at the end of follow-up. New York Heart Association functional class improved from 1.91±0.46 to 1.81±0.53 (P=.542). After CRT device implantation in 8 patients, LVEF improved by 18.1±6.4% (P=.003). CONCLUSIONS: Guideline-directed medical therapy seems to be ineffective in improving LVEF and functional class in patients with de novo heart failure and LBBB-induced cardiomyopathy. Based on a positive response to CRT on LVEF improvement, early CRT implantation could be a reasonable strategy for these patients.


Assuntos
Terapia de Ressincronização Cardíaca , Cardiomiopatias , Insuficiência Cardíaca , Humanos , Bloqueio de Ramo/etiologia , Bloqueio de Ramo/terapia , Bloqueio de Ramo/diagnóstico , Volume Sistólico/fisiologia , Estudos Retrospectivos , Função Ventricular Esquerda , Resultado do Tratamento , Eletrocardiografia , Cardiomiopatias/complicações , Cardiomiopatias/terapia , Cardiomiopatias/diagnóstico , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/terapia
2.
Oral Surg Oral Med Oral Pathol Oral Radiol ; 121(4): 396-401.e1, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-26899292

RESUMO

OBJECTIVE: To compare the proliferation and the expression of matrix metalloproteinases (MMPs; MMP-2 and MMP-9) in solid and unicystic ameloblastomas with ameloblastic carcinomas. STUDY DESIGN: Five cases of ameloblastic carcinoma (AC), 18 cases of solid ameloblastoma (SA), and seven of unicystic ameloblastoma (UA) were selected. The immunohistochemical expression of MMPs was assessed by the percentage of positive tumor cells and stained stroma. The mean argyrophilic nucleolar organizer region (AgNOR) and the percentage of cells with more than one AgNOR per nucleus were evaluated. RESULTS: Statistically significant higher mean AgNOR was observed in AC than in SA and UA. MMP-2 was expressed similarly in tumor and stroma among groups. MMP-9 was higher in the stroma of SA than that of UA (P = .0484). CONCLUSIONS: The cell proliferation was related to the greater aggressiveness of AC. High expression of MMP-2 and MMP-9 in all lesions highlighted the importance of these enzymes in the biology of ameloblastic tumors.


Assuntos
Ameloblastoma/enzimologia , Neoplasias Mandibulares/enzimologia , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Ameloblastoma/patologia , Biomarcadores Tumorais/metabolismo , Brasil , Proliferação de Células , Criança , Estudos Transversais , Feminino , Humanos , Masculino , Neoplasias Mandibulares/patologia , Pessoa de Meia-Idade , Estudos Retrospectivos
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA