Abstract

Cardiovascular disease (CVD) is the major global killer, for women and men alike, and also the non-communicable disease that removes most days of life. Pregnancy is an underused stress test to identify women at high risk for CVD at a young age. In this overview, the associations between preeclampsia and other placenta-related pregnancy complications, and future maternal CVD are summarized. Large population based studies and meta-analyses concluded that women with a history of preeclampsia are at increased risk for later CVD and premature death compared to women with healthy pregnancies. The likelihood of CVD after preeclampsia increases with repeated disease, premature delivery and fetal growth restriction. Women with previous pregnancy induced hypertension (without proteinuria or other preeclampsia-associated features) or late-onset preeclampsia also have increased risk for CVD, but the risk is lower than after a prematurely preeclampsia delivery. Several mechanisms may underlie these epidemiological associations, and established as well as more novel hypotheses will be presented. The most widely held hypothesis focuses on common risk factors, such as obesity, diabetes mellitus, insulin resistance and hyperglycemia, dyslipidemia, hypertension, a family history of CVD, the metabolic syndrome, as well as common genetic risk factors. A second hypothesis, not rejecting the first, suggests that pregnancy in general, and preeclampsia (and other placental dysfunction disorders) in particular, worsen preexisting, subclinical CVD risk factors or even induce de novo risk factors. The latter includes potentially altered inflammatory and metabolic factors following pregnancies with preeclampsia and dysfunctional placentas, as well as effects on the maternal cardiovasculature. Whatever the mechanisms for the associations, a cost-efficient strategy for follow-up of women with previous preeclampsia for CVD is warranted, in order to avoid or postpone clinical detrimental disease.

Full Text
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