| Literature DB >> 31786987 |
Kristin Kräker1,2,3,4,5, Jamie M O'Driscoll6,7,8, Till Schütte2,3,9, Florian Herse1,4,5, Olga Patey6,7, Michaela Golic1,2,3,4,5, Sabrina Geisberger1,2,3,4,5, Stefan Verlohren10, Anna Birukov1,2,3,4,5, Arnd Heuser5, Dominik N Müller1,2,3,4,5, Basky Thilaganathan6,7, Ralf Dechend1,2,3,4,11, Nadine Haase1,2,3,4,5.
Abstract
Preeclampsia 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.Entities:
Keywords: animals; humans; pravastatin; preeclampsia; pregnancy
Year: 2019 PMID: 31786987 DOI: 10.1161/HYPERTENSIONAHA.119.13219
Source DB: PubMed Journal: Hypertension ISSN: 0194-911X Impact factor: 10.190