Treatment of combined aortic regurgitation and systemic hypertension : insights from an animal model study.

Élément Dublin CoreValeurLangue
dc.contributor.authorCouët, Jacques-
dc.contributor.authorGaudreau, Martin-
dc.contributor.authorLachance, Dominic-
dc.contributor.authorPlante, Éric-
dc.contributor.authorRoussel, Élise-
dc.contributor.authorDrolet, Marie-Claude-
dc.contributor.authorArsenault, Marie-
dc.date.accessioned2017-11-14T19:15:27Z-
dc.date.available2017-11-14T19:15:27Z-
dc.date.issued2006-08-01-
dc.identifier.issn0895-7061fr
dc.identifier.urihttp://hdl.handle.net/20.500.11794/15844-
dc.description.abstractBackground : Hypertension (HT) and aortic valve regurgitation (AR) often coexist but the specific impacts of AR + HT on the left ventricle (LV) are still unknown. The best treatment strategy for this combination of diseases is also unclear. The objectives of this study were 1) to evaluate LV function, remodeling and 2) to assess the effects of the angiotensin-converting enzyme (ACE) inhibitor captopril (C) in rats with AR ± HT in spontaneously hypertensive rats (SHR). Methods : Animals were grouped as follows: normotensive (NT) Wistar-Kyoto, NT + AR, hypertensive SHR (HT), and HT + AR receiving or not captopril (150 mg/kg/d). Hearts were evaluated in vivo by echocardiography and harvested for tissue analysis after 6 months of evolution. Results : The HT + AR rats had the worst LV hypertrophy (LVH), subendocardial fibrosis, and lowest ejection fraction. Captopril normalized BP in HT and HT + AR, but could not prevent LVH in HT + AR as well as it did in isolated HT. The LV ejection fraction remained below normal in HT + AR + captopril compared to HT alone + captopril. Cardiomyocyte hypertrophy remained in HT + AR + captopril but was normalized in HT + captopril. Subendocardial fibrosis was reduced by captopril in HT + AR. Conclusions : The AR + HT rats had the most severe myocardial abnormalities. High dose captopril was effective to slow LVH and preserve normal LV ejection fraction in isolated HT or AR, but was less effective when both pathologies were combined. Prohypertrophic stimuli clearly remain active in HT + AR despite ACE inhibition. These results suggest that a very aggressive medical treatment strategy may be required to optimize LV protection when AR and HT co-exist.fr
dc.languageengfr
dc.publisherOxford University Pressfr
dc.subjectHypertensionfr
dc.subjectAortic valve regurgitationfr
dc.subjectRatfr
dc.subjectRenin-angiotensin systemfr
dc.subjectCaptoprilfr
dc.titleTreatment of combined aortic regurgitation and systemic hypertension : insights from an animal model study.fr
dc.title.alternativeHypertension and aortic valve regurgitation in ratsfr
dc.typeCOAR1_1::Texte::Périodique::Revue::Contribution à un journal::Article::Article de recherchefr
dcterms.bibliographicCitationAmerican journal of hypertension, Vol. 19 (8), 843-850 (2006)fr
dc.identifier.doi10.1016/j.amjhyper.2006.01.021fr
dc.identifier.pubmed16876685fr
dc.subject.rvmCœur -- Valvules -- Maladies -- Traitementfr
dc.subject.rvmHypertension artérielle -- Traitementfr
dc.subject.rvmRats (Animaux de laboratoire)fr
dc.subject.rvmSystème rénine-angiotensinefr
dc.subject.rvmCaptoprilfr
rioxxterms.versionAccepted Manuscriptfr
rioxxterms.version_of_recordhttps://doi.org/10.1016/j.amjhyper.2006.01.021fr
rioxxterms.project.funder_nameCanadian Institutes of Health Researchfr
rioxxterms.project.funder_nameHeart and Stroke Foundation of Quebecfr
rioxxterms.project.funder_nameQuebec Heart Institute Foundationfr
bul.rights.periodeEmbargo12 moisfr
Collection :Articles publiés dans des revues avec comité de lecture

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