Antenatal inflammation tied to postpartum cardiac changes in hypertensive pregnancy; mouse study
A pilot study of pregnant women and a mouse model found that antenatal inflammation, not postpartum inflammation, is linked to cardiac dysfunction months after delivery.
A team led by Queen Mary University of London reported, in a paper available via doi.org, a prospective study of women in the third trimester (36–40 weeks) at The Royal London Hospital, paired with a mouse model of hypertensive pregnancy disorders. The cohort included 22 normotensive women and 38 women with hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension nature.com
doi.orgnature.comOpen source ↗. Women with gestational diabetes were excluded.
The authors hypothesized that maternal inflammation drives persistent cardiac maladaptation after such pregnancies. They assessed cardiac function and circulating inflammatory profiles during pregnancy and again 3–6 months postpartum.
Cardiac and hormonal findings
Systolic blood pressure averaged 142.6 ± 18.4 in women with hypertensive disorders versus 115.1 ± 11.6 in normotensive controls (mean ± s.d.). The sFlt1:PlGF ratio was 12-fold higher in the hypertensive cohort. Plasma progesterone was significantly lower in this group, while estriol was not.
Echocardiography showed eccentric hypertrophy in both groups, consistent with physiological pregnancy. A subset of women with hypertensive disorders also had concentric hypertrophy, with left ventricular mass of 136.7 ± 18.9 g versus 106 ± 4.1 g in normotensive women nature.com
doi.orgnature.comOpen source ↗. Diastolic dysfunction was present too: the E/e′ ratio was 9.2 ± 2.6 versus 7.0 ± 2.5.
Inflammation and progesterone in mice
Distinct antenatal inflammatory signatures, including elevated chemokines, correlated with adverse left ventricular structure and function 3–6 months postpartum, even though systemic inflammation had resolved by then, the authors reported.
In the mouse model, reduced antenatal progesterone, also seen in patients, drove inflammation and postpartum cardiac dysfunction. Progesterone given at embryonic day 14.5 prevented postpartum cardiac dysfunction, whereas treatment at postpartum day 28 did not. According to the authors, this points to a possible mechanism and a therapeutic strategy that remain to be tested; the data are from mice and a pilot human cohort.
