Statins Reverse Postpartum Cardiovascular Dysfunction in a Rat Model of Preeclampsia

Journal article

Kräker, Kristin, O’Driscoll, Jamie M., Schütte, Till, Herse, Florian, Patey, Olga, Golic, Michaela, Geisberger, Sabrina, Verlohren, Stefan, Birukov, Anna, Heuser, Arnd, Müller, Dominik N., Thilaganathan, Basky, Dechend, Ralf and Haase, Nadine 2019. Statins Reverse Postpartum Cardiovascular Dysfunction in a Rat Model of Preeclampsia. Hypertension. 75 (1), pp. 202-210. https://doi.org/10.1161/hypertensionaha.119.13219
AuthorsKräker, Kristin, O’Driscoll, Jamie M., Schütte, Till, Herse, Florian, Patey, Olga, Golic, Michaela, Geisberger, Sabrina, Verlohren, Stefan, Birukov, Anna, Heuser, Arnd, Müller, Dominik N., Thilaganathan, Basky, Dechend, Ralf and Haase, Nadine
AbstractPreeclampsia is associated with increased cardiovascular long-term risk; however, the underlying functional and structural mechanisms are unknown. We investigated maternal cardiac alterations after preeclampsia. Female rats harboring the human angiotensinogen gene [TGR(hAogen)L1623] develop a preeclamptic phenotype with hypertension and albuminuria during pregnancy when mated with male rats bearing the human renin gene [TGR(hRen)L10J] but behave physiologically normal before and after pregnancy. Furthermore, rats were treated with pravastatin. We tested the hypothesis that statins are a potential therapeutic intervention to reduce cardiovascular alterations due to simulated preeclamptic pregnancy. Although hypertension persists for only 8 days in pregnancy, former preeclampsia rats exhibit significant cardiac hypertrophy 28 days after pregnancy observed in both speckle tracking echocardiography and histological staining. In addition, fibrosis and capillary rarefaction was evident. Pravastatin treatment ameliorated the remodeling and improved cardiac output postpartum. Preeclamptic pregnancy induces irreversible structural changes of cardiac hypertrophy and fibrosis, which can be moderated by pravastatin treatment. This pathological cardiac remodeling might be involved in increased cardiovascular risk in later life.
KeywordsInternal Medicine
Year2019
JournalHypertension
Journal citation75 (1), pp. 202-210
PublisherOvid Technologies (Wolters Kluwer Health)
ISSN0194-911X
1524-4563
Digital Object Identifier (DOI)https://doi.org/10.1161/hypertensionaha.119.13219
Official URLhttps://doi.org/10.1161/HYPERTENSIONAHA.119.13219
Publication dates
Print2020
Publication process dates
Accepted02 Dec 2019
Deposited18 Dec 2019
Accepted author manuscript
Output statusPublished
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