Abstract
Background and Aims: Physiological maternal hypercholesterolemia (MPH; total cholesterol (TC)≤280 mg/dL) occurs during pregnancy. However, some women develop supraphysiological maternal hypercholesterolemia (MSPH; TC>280 mg/dL) which associates with increased levels of LDL and leads to fetal endothelial dysfunction and atherosclerosis. Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates LDL levels. It is unknown whether (1) PCSK9 is modulated in MSPH and (2) if MSPH associates with changes in maternal and neonatal lipoproteins functions, favoring a pro-atherogenic profile.
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