Fenofibrate reduces cardiac remodeling and improves cardiac function in a rat model of severe left ventricle volume overload

DC FieldValueLanguage
dc.contributor.authorDhahri, Wahiba-
dc.contributor.authorCouët, Jacques-
dc.contributor.authorRoussel, Élise-
dc.contributor.authorDrolet, Marie-Claude-
dc.contributor.authorArsenault, Marie-
dc.date.accessioned2017-11-14T16:05:34Z-
dc.date.available2017-11-14T16:05:34Z-
dc.date.issued2012-11-07-
dc.identifier.issn0024-3205fr
dc.identifier.urihttp://hdl.handle.net/20.500.11794/15825-
dc.description.abstractAims : Fenofibrate is a peroxisome proliferator-associated receptor alpha agonist (PPARα) used clinically for the management of dyslipidemia and is a myocardial fatty acid oxidation stimulator. It has also been shown to have cardiac anti-hypertrophic properties but the effects of fenofibrate on the development of eccentric LVH and ventricular function in chronic left ventricular (LV) volume overload (VO) are unknown. This study was therefore designed to explore the effects of fenofibrate treatment in a VO rat model caused by severe aortic valve regurgitation (AR) with a focus on cardiac remodeling and myocardial metabolism. Main methods : Male Wistar rats were divided in four groups (13–15 animals/group): Shams (S) treated with fenofibrate (F; 100 mg/kg/d PO) or not (C) and severe AR receiving or not fenofibrate. Treatment was started one week before surgery and the animals were sacrificed 9 weeks later. Key findings : AR rats developed severe LVH (increased LV weight) during the course of the protocol. Fenofibrate did not reduce LV weight. However, eccentric LV remodeling was strongly reduced by fenofibrate in AR animals. Fractional shortening was significantly less affected in ARF compared to ARC group. Fenofibrate also increased the myocardial enzymatic activity of enzymes associated with fatty acid oxidation while inhibiting glycolytic enzyme phosphofructokinase. Significance : Fenofibrate decreased LV eccentric remodeling associated with severe VO and helped maintain systolic function. Studies with a longer follow-up will be needed to assess the long-term effects of fenofibrate in chronic volume overload caused by aortic regurgitation.fr
dc.languageengfr
dc.publisherPergamonfr
dc.subjectCardiomyopathyfr
dc.subjectVolume overloadfr
dc.subjectFenofibratefr
dc.subjectHypertrophyfr
dc.titleFenofibrate reduces cardiac remodeling and improves cardiac function in a rat model of severe left ventricle volume overloadfr
dc.title.alternativeFenofibrate and left ventricle remodeling in volume overloadfr
dc.typeCOAR1_1::Texte::Périodique::Revue::Contribution à un journal::Article::Article de recherchefr
dcterms.bibliographicCitationLife Sciences, Vol. 92 (1), 26–34 (2013)fr
dc.identifier.doi10.1016/j.lfs.2012.10.022fr
dc.subject.rvmFénofibratefr
dc.subject.rvmRemodelage ventriculairefr
dc.subject.rvmCœur -- Ventricule gauche -- Maladiesfr
dc.subject.rvmRats (Animaux de laboratoire)fr
dc.subject.rvmCœur -- Valvules -- Maladiesfr
rioxxterms.versionAccepted Manuscriptfr
rioxxterms.version_of_recordhttps://doi.org/10.1016/j.lfs.2012.10.022fr
rioxxterms.project.funder_nameCanadian Institutes of Health Researchfr
rioxxterms.project.funder_nameQuebec Heart and Stroke Foundationfr
rioxxterms.project.funder_nameQuebec Heart Institute Corporationfr
bul.rights.periodeEmbargo12 moisfr
Collection:Articles publiés dans des revues avec comité de lecture

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