Immune Markers, Blood Pressure Severity, and Cardiac Remodeling 1 to 2 Years After Hypertensive Disorders of Pregnancy.

Abstract

Background Cardiovascular dysfunction and hypertension can persist postpartum following hypertensive disorders of pregnancy (HDPs). This study hypothesized that activin A, proinflammatory markers and concentric remodeling by echo would be higher 1-2 years postpartum following HDP with persistent hypertension compared to HDP with normalized blood pressure (BP). We further hypothesized correlations between biomarkers with BP and echocardiographic indices. Methods and Results This study enrolled participants with HDPs but no prepregnancy hypertension followed 1 to 2 years after delivery. Activin A and inflammatory cytokines, BP, and echocardiograms were obtained. Biomarker concentrations and echocardiographic parameters were compared between HDP with and without persistent hypertension. Individuals with persistent hypertension at a mean of 1.6 years postpartum had significantly higher activin A concentrations (median[interquartile range 25-75] 230.6 [196.0-260.9] versus 175.3 pg/mL [164.3-188.4]; P<0.01), more concentric left ventricular concentric remodeling (relative wall thickness >0.42, 48% versus 7%; P<0.01), and worse peak left atrial strain (33.4% versus 39.3%; P<0.05) as compared with those whose BP normalized. Higher activin A and interleukin-6 concentrations correlated with higher systolic (activin A: r=0.43, P=0.01) and diastolic BP (activin A: r=0.58, P<0.01; interleukin-6: r=0.36; P<0.05), as well as greater left ventricular thickness (activin A and interventricular septal thickness: r=0.41, interleukin-6 and interventricular septal thickness: r=0.36; both P<0.05). Conclusions Individuals with HDPs and persistent hypertension had significantly higher activin A and greater concentric remodeling compared with those with HDPs and normalized BP at 1 to 2 years postpartum. Activin A was positively correlated with both BP and echocardiographic indices (left ventricular thickness), suggesting overlapping processes between persistent hypertension and cardiac remodeling.