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dc.contributor.authorAune, Arleen
dc.contributor.authorKokorina, Marina Victorovna
dc.contributor.authorGrytaas, Marianne Aa.
dc.contributor.authorMidtbø, Helga Bergljot
dc.contributor.authorLøvås, Kristian
dc.contributor.authorGerdts, Eva
dc.date.accessioned2022-04-12T09:36:32Z
dc.date.available2022-04-12T09:36:32Z
dc.date.created2021-07-07T13:30:33Z
dc.date.issued2021
dc.identifier.issn0803-7051
dc.identifier.urihttps://hdl.handle.net/11250/2991040
dc.description.abstractPurpose: We tested the sex-specific associations between primary aldosteronism (PA), left ventricular (LV) hypertrophy and LV systolic myocardial function. Material and methods: Conventional and speckle tracking echocardiography was performed in 109 patients with PA and 89 controls with essential hypertension (EH). LV hypertrophy was identified if LV mass index exceeded 47.0 g/m2.7 in women and 50.0 g/m2.7 in men. LV systolic myocardial function was assessed by global longitudinal strain (GLS) and midwall shortening. Results: PA patients had higher prevalence of LV hypertrophy (52 vs. 21%, p < 0.001) than EH patients in both sexes, while GLS did not differ by sex or hypertension aetiology. In multivariable analyses, presence of LV hypertrophy was associated with PA and obesity in both sexes, while lower systolic myocardial function, whether measured by GLS or midwall shortening, was not associated with PA, but primarily with higher body mass index and LV mass index, respectively, in both sexes (all p < 0.05). Conclusion: Having PA was associated with higher prevalence of LV hypertrophy both in women and men, compared to EH. PA was not associated with LV systolic myocardial function in either sex.en_US
dc.language.isoengen_US
dc.publisherTaylor & Francisen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titlePreclinical cardiac disease in women and men with primary aldosteronismen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2021 The Author(s)en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.1080/08037051.2021.1904775
dc.identifier.cristin1920717
dc.source.journalBlood Pressureen_US
dc.source.pagenumber230-236en_US
dc.identifier.citationBlood Pressure. 2021, 30 (4), 230-236.en_US
dc.source.volume30en_US
dc.source.issue4en_US


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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