Articles producció científica> Medicina i Cirurgia

Parallel evolution of circulating FABP4 and NT-proBNP in heart failure patients.

  • Datos identificativos

    Identificador: PC:554
    Autores:
    Masana, L.Bardají, A.Bonet, G.Lázaro, I.Valdovinos, P.Cabré, A.
    Resumen:
    Abstract Background: Circulating adipocyte fatty acid-binding protein (FABP4) levels are considered to be a link between obesity, insulin resistance, diabetes, and cardiovascular (CV) diseases. In vitro, FABP4 has exhibited cardiodepressant activity by suppressing cardiomyocyte contraction. We have explored the relationship between FABP4 and the N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) as a clinical parameter of heart failure (HF). Methods: We included 179 stable HF patients who were referred to a specialized HF unit, 108 of whom were prospectively followed for up to 6 months. A group of 163 non-HF patients attending a CV risk unit was used as the non-HF control group for the FABP4 comparisons. Results: In the HF patients, FABP4 and NT-proBNP were assayed, along with a clinical and functional assessment of the heart at baseline and after 6 months of specialized monitoring. The FABP4 levels were higher in the patients with HF than in the non-HF high CV risk control group (p<0.001). The FABP4 levels were associated with the NT-proBNP levels in patients with HF (r=0.601, p<0.001), and this association was stronger in the diabetic patients. FABP4 was also associated with heart rate and the results of the 6-minute walk test. After the follow-up period, FABP4 decreased in parallel to NT-proBNP and to the clinical parameters of HF. Conclusions: FABP4 is associated with the clinical manifestations and biomarkers of HF. It exhibits a parallel evolution with the circulating levels of NT-proBNP in HF patients. Keywords: FABP4, Heart failure, NT-proBNP, Obesity, Diabetes
  • Otros:

    Autor según el artículo: Masana, L. Bardají, A. Bonet, G. Lázaro, I. Valdovinos, P. Cabré, A.
    Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
    Departamento: Medicina i Cirurgia
    e-ISSN: 1475-2840
    URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
    Autor/es de la URV: Anna Cabré, Pilar Valdovinos, Iolanda Lázaro, Gil Bonet, Alfredo Bardají and Lluís Masana
    Resumen: Abstract Background: Circulating adipocyte fatty acid-binding protein (FABP4) levels are considered to be a link between obesity, insulin resistance, diabetes, and cardiovascular (CV) diseases. In vitro, FABP4 has exhibited cardiodepressant activity by suppressing cardiomyocyte contraction. We have explored the relationship between FABP4 and the N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) as a clinical parameter of heart failure (HF). Methods: We included 179 stable HF patients who were referred to a specialized HF unit, 108 of whom were prospectively followed for up to 6 months. A group of 163 non-HF patients attending a CV risk unit was used as the non-HF control group for the FABP4 comparisons. Results: In the HF patients, FABP4 and NT-proBNP were assayed, along with a clinical and functional assessment of the heart at baseline and after 6 months of specialized monitoring. The FABP4 levels were higher in the patients with HF than in the non-HF high CV risk control group (p<0.001). The FABP4 levels were associated with the NT-proBNP levels in patients with HF (r=0.601, p<0.001), and this association was stronger in the diabetic patients. FABP4 was also associated with heart rate and the results of the 6-minute walk test. After the follow-up period, FABP4 decreased in parallel to NT-proBNP and to the clinical parameters of HF. Conclusions: FABP4 is associated with the clinical manifestations and biomarkers of HF. It exhibits a parallel evolution with the circulating levels of NT-proBNP in HF patients. Keywords: FABP4, Heart failure, NT-proBNP, Obesity, Diabetes
    Entidad: Universitat Rovira i Virgili.
    Año de publicación de la revista: 2013
    Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
    Página inicial: 72
    Volumen de revista: 12