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  1. Fibrinogen, plasminogen activator inhibitor-1, and carotid intima-media wall thickness in the NHLBI family heart study.

    Article - En anglais

    Several studies have linked higher plasma fibrinogen and plasminogen activator inhibitor (PAI-1) concentrations with increased risk of cardiovascular disease.

    We studied whether members of families with increased occurrence of coronary heart disease (CHD) have increased levels of fibrinogen and PAI-1 and whether subclinical carotid atherosclerosis is associated with these two hemostatic factors.

    Contrary to our hypothesis, fibrinogen and PAI-1 antigen levels were not different between high CHD risk families versus random families.

    Adjusted for age and family type, fibrinogen and PAI-1 were both associated positively with carotid intima-media thickness assessed by B-mode ultrasound.

    However, adjustment for lifestyle and medical covariates essentially eliminated these associations.

    These data suggest 1) elevated fibrinogen and PAI-1 do not explain clustering of CHD in families and 2) fibrinogen and PAI-1 may partly mediate the effects of other risk factors on carotid atherosclerosis, though the data are also consistent with them playing no causal role.

    Mots-clés Pascal : Cardiopathie coronaire, Fibrinogène, Facteur coagulation, Inhibiteur plasminogen activator 1, Facteur risque, Epidémiologie, Athérosclérose, Carotide, Paroi vasculaire, Epaisseur paroi, Intima, Média, Etats Unis, Amérique du Nord, Amérique, Homme, Appareil circulatoire pathologie, Vaisseau sanguin pathologie

    Mots-clés Pascal anglais : Coronary heart disease, Fibrinogen, Coagulation factor, Plasminogen activator inhibitor 1, Risk factor, Epidemiology, Atherosclerosis, Carotid, Vascular wall, Wall thickness, Intima, Media, United States, North America, America, Human, Cardiovascular disease, Vascular disease

    Logo du centre Notice produite par :
    Inist-CNRS - Institut de l'Information Scientifique et Technique

    Cote : 98-0121439

    Code Inist : 002B12A03. Création : 22/06/1998.