Abstract

Preeclampsia (PE), a multisystem hypertensive disorder affecting 2-8% of pregnancies, has emerged as a novel risk factor for cardiovascular disease (CVD) in affected mothers and in their offspring. Between 10 and 15 years following gestation, women with a history of PE have double the risk of CVD, nearly 4 times the risk of hypertension, and increased all-cause mortality. Offspring exposed to PE in utero carry an increased risk of CVD and congenital heart defects. Due to the multifactorial nature of both PE and CVD, a clear dependency has been difficult to establish. The interplay between CVD and PE is an area of active investigation, likely involving placental, genetic, and epigenetic factors resulting in enduring endothelial, vascular, and immune dysfunction. Fetal developmental programming induced by adverse intrauterine environments, epigenetic changes triggered by oxidative stress, and underlying genetic predisposition play pivotal roles in the development of CVD in offspring exposed to PE. Though the literature has discussed the cardiovascular outcomes associated with PE for nearly a decade, patient risk perception and health care provider awareness remain low, representing a substantial missed opportunity for early intervention in this vulnerable population. This review article will discuss the pathophysiology of preeclampsia, its intersection with CVD, and the long-term cardiovascular consequences for affected mothers and their offspring. Our objective is to increase health care provider awareness and garner greater research interest in this important topic.

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