Articles producció científica> Medicina i Cirurgia

Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel.

  • Datos identificativos

    Identificador: imarina:5251672
    Autores:
    Ference B.A., Ginsberg H.N., Graham I., Ray K.K., Packard C.J., Bruckert E., Hegele R.A., Krauss R.M., Raal F.J., Schunkert H., Watt G.F., Borén J., Fazio S., Horton J.D., Masana L., Nicholls S.J., Nordestgaard B.G., Van De Sluis B., Taskinen M.R., Tokgözo?lu L., Landmesser U., Laufs U., Wiklund O., Stock J.K., Chapman M.J., Catapano A.L.
    Resumen:
    To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150?000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.Consistent evidence from numerous and
  • Otros:

    Autor según el artículo: Ference B.A., Ginsberg H.N., Graham I., Ray K.K., Packard C.J., Bruckert E., Hegele R.A., Krauss R.M., Raal F.J., Schunkert H., Watt G.F., Borén J., Fazio S., Horton J.D., Masana L., Nicholls S.J., Nordestgaard B.G., Van De Sluis B., Taskinen M.R., Tokgözo?lu L., Landmesser U., Laufs U., Wiklund O., Stock J.K., Chapman M.J., Catapano A.L.
    Departamento: Medicina i Cirurgia
    Autor/es de la URV: Masana Marín, Luis
    Palabras clave: Statin therapy Statin Risk Retention Recommendations Pcsk9 Mendelian randomization Low-density lipoprotein Ldl cholesterol General-population Familial hypercholesterolemia Ezetimibe Coronary-heart-disease Clinical trials Causality Cardiovascular disease Atherosclerosis Association recommendations pcsk9 mendelian randomization low-density lipoprotein ezetimibe clinical trials causality cardiovascular disease atherosclerosis
    Resumen: To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150?000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.© The Author 2017. Published on behalf of the European Society of Cardiology
    Áreas temáticas: Saúde coletiva Nutrição Medicina iii Medicina ii Medicina i Interdisciplinar General medicine Farmacia Educação física Direito Ciências biológicas ii Ciências biológicas i Cardiology and cardiovascular medicine Cardiac & cardiovascular systems
    Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 15229645
    Direcció de correo del autor: luis.masana@urv.cat
    Identificador del autor: 0000-0002-0789-4954
    Fecha de alta del registro: 2024-09-07
    Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
    Enlace a la fuente original: https://academic.oup.com/eurheartj/article/38/32/2459/3745109
    URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referencia al articulo segun fuente origial: European Heart Journal. 38 (32): 2459-2472
    Referencia de l'ítem segons les normes APA: Ference B.A., Ginsberg H.N., Graham I., Ray K.K., Packard C.J., Bruckert E., Hegele R.A., Krauss R.M., Raal F.J., Schunkert H., Watt G.F., Borén J., F (2017). Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel.. European Heart Journal, 38(32), 2459-2472. DOI: 10.1093/eurheartj/ehx144
    DOI del artículo: 10.1093/eurheartj/ehx144
    Entidad: Universitat Rovira i Virgili
    Año de publicación de la revista: 2017
    Tipo de publicación: Journal Publications
  • Palabras clave:

    Cardiac & Cardiovascular Systems,Cardiology and Cardiovascular Medicine
    Statin therapy
    Statin
    Risk
    Retention
    Recommendations
    Pcsk9
    Mendelian randomization
    Low-density lipoprotein
    Ldl cholesterol
    General-population
    Familial hypercholesterolemia
    Ezetimibe
    Coronary-heart-disease
    Clinical trials
    Causality
    Cardiovascular disease
    Atherosclerosis
    Association
    recommendations
    pcsk9
    mendelian randomization
    low-density lipoprotein
    ezetimibe
    clinical trials
    causality
    cardiovascular disease
    atherosclerosis
    Saúde coletiva
    Nutrição
    Medicina iii
    Medicina ii
    Medicina i
    Interdisciplinar
    General medicine
    Farmacia
    Educação física
    Direito
    Ciências biológicas ii
    Ciências biológicas i
    Cardiology and cardiovascular medicine
    Cardiac & cardiovascular systems
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