“…The hypothesis that late-pregnancy changes in UtA-PI are caused by maternal hemodynamic changes and related to the subsequent development of HDP are supported by the finding that pre-eclampsia is associated with heart remodeling and significant impairment of cardiac function [37][38][39][40] . The latter hypothesis is consistent with emerging evidence that maternal cardiovascular profile may play an important role in determining whether women will develop pre-eclampsia 37,[41][42][43] .…”
“…The hypothesis that late-pregnancy changes in UtA-PI are caused by maternal hemodynamic changes and related to the subsequent development of HDP are supported by the finding that pre-eclampsia is associated with heart remodeling and significant impairment of cardiac function [37][38][39][40] . The latter hypothesis is consistent with emerging evidence that maternal cardiovascular profile may play an important role in determining whether women will develop pre-eclampsia 37,[41][42][43] .…”
“…This volume expansion, probably initiated by placental hormones, seems to be dependent on normal adaptive endothelial and vascular function. Failure to accommodate these alterations may identify women at high risk of pregnancy‐related complications and may be the true cause of late pre‐eclampsia, rather than placental issues. Early changes in arterial stiffness and endothelial function may thus provide useful information regarding maternal and fetal risks during pregnancy or later in life.…”
“…These results imply that the finding of villous and vascular placental lesions is neither sensitive nor specific to the diagnosis of PE. Impartial scientific observation would demand that we question whether these placental lesions could truly play an etiological role in the development of PE, or whether they are a consequence of the disease process [23][24][25] .…”
Section: Clinical and Research Implications Of Study Findingsmentioning
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