Search

Preeclampsia is associated with decreased maternal low-density lipoprotein cholesterol (LDL-c), which is essential for fetal growth. The underlying mechanisms for decreased LDL-c in preeclampsia remain unknown. Proprotein convertase subtillisin/kexin type 9 (PCSK9) regulates serum LDL-c via LDL receptor (LDL-R) degradation. We describe the possible role of PCSK9 in lipid metabolism in all compartments of the parturient (maternal blood, placental tissue, and fetal blood) in pregnancies with and without preeclampsia.This is an observational study examining PCSK9 levels in maternal sera, umbilical cord blood, and PCSK9 protein content in placental tissue in three different locations (maternal placental interface, fetal placental interface, and umbilical cord) in women with and without preeclampsia at23 weeks gestation.68 parturients with preeclampsia and 55 without preeclampsia were enrolled. Maternal serum LDL-c (116.6 ± 48.9 mg/dL vs 146.1 ± 47.1 mg/dL, p = 0.0045) and PCSK9 (83 [61.8127.6] ng/mL vs 105.3 [83.5142.9] ng/mL, p = 0.011) were also reduced in the preeclamptics versus controls. There were no differences in PCSK9 protein content between preeclamptics and controls at comparative placental interfaces. However, PCSK9 protein content increased between the preeclampsia maternal placental interface (1.87 ± 0.62) and the preeclampsia umbilical cord (2.67 ± 1.08, p = 0.0243).PCSK9 levels are lower in maternal sera in preeclampsia when compared to controls. Placental PCSK9 protein content in preeclampsia increases from the maternal interface to the umbilical cord; however, this is not seen in controls. This suggests a potential compensatory mechanism for PCSK9 which allows for higher circulating fetal LDL-c levels in preeclampsia.

INTRODUCTION: Women with preeclampsia are more likely to have abnormal echocardiographic parameters at the time of diagnosis and are more likely to have hypertension and other cardiovascular diseases (CVD) later in life. Screening for future CVD in preeclamptic women would assist in appropriately risk stratifying and identifying high risk women for preventive management; however, the timing of screening and the screening factors are unknown. OBJECTIVE: The objectives of this project are to 1) assess incidence of essential hypertension 4 years after pregnancy in preeclampsia with severe features (PEC) 2) identify predictive echocardiographic variables at the time of PEC diagnosis and 3) assess the rate of echocardiographic abnormalities 4 years after developing PEC. STUDY DESIGN: This is a prospective longitudinal study observing the incidence of essential hypertension in women within 4 years of a pregnancy complicated by PEC. We further looked at echocardiographic variables at the time of PEC diagnosis and at 4 years after PEC pregnancy in women with and without subsequent incident essential hypertension. The primary outcome measure is the incidence of essential hypertension within 4 years of PEC pregnancy, defined as a systolic blood pressure ≥ 130 mmHg or a diastolic blood pressure ≥ 80 mmHg. Secondary imaging outcomes include the persistence of abnormal echocardiographic parameters. Clinical secondary outcomes are new diagnoses of severe CVD, including coronary artery disease, stroke, arrhythmia, heart failure, or inpatient hospital admission for CVD. RESULTS: Of the 33 enrolled women with PEC, 48% (16/33) developed incident essential hypertension within 4 years of delivery. These women had thicker left ventricular posterior walls on their initial antenatal echocardiogram when compared to the 52% (17/33) who did not develop hypertension (1.0 cm [0.9–1.1 cm] vs 0.9 cm [0.7–0.9 cm]. p < 0.016). However, these abnormal echocardiographic variables resolved in the 16 women who underwent 4-year follow-up echocardiography. CONCLUSION: Women who develop PEC have a high incidence of essential hypertension within 4 years of delivery. The group who develops essential hypertension are more likely to have evidence of adverse cardiac remodeling at the time of PEC diagnosis; however, neither group have cardiac echocardiographic abnormalities 4 years postpartum. Because this is a small study, larger long-term cohort studies are needed to confirm these echocardiographic and clinical findings.