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The placenta and preeclampsia: villain or victim?

Journal

AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 226, Issue 2, Pages S954-S962

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2020.10.024

Keywords

cardiovascular function; change in partner; etiology; ovum donation; parity; placentation; preeclampsia; spiral artery transformation; uterine Doppler

Funding

  1. European Union [765274]

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Preeclampsia is a disease that has remained unchanged in its characteristics for 150 years, with little consensus on its true etiology. Emerging evidence suggests that suboptimal maternal cardiovascular performance may be the cause of secondary placental dysfunction in preeclampsia. The clinical presentation of preeclampsia is dominated by cardiovascular signs and symptoms, which may persist into the postnatal period.
Preeclampsia is a disease whose characterization has not changed in the 150 years since the cluster of signs associated with the disorder were first described. Although our understanding of the pathophysiology of preeclampsia has advanced considerably since then, there is still little consensus regarding the true etiology of preeclampsia. As a consequence, preeclampsia has earned the moniker disease of theories, predominantly because the underlying biological mechanisms linking clinical epidemiologic findings to observed organ dysfunction in preeclampsia are far from clear. Despite the lack of cohesive evidence, expert consensus favors the hypothesis that preeclampsia is a primary placental disorder. However, there is now emerging evidence that suboptimal maternal cardiovascular performance resulting in uteroplacental hypoperfusion is more likely to be the cause of secondary placental dysfunction in preeclampsia. Preeclampsia and cardiovascular disease share the same risk factors, preexisting cardiovascular disease is the strongest risk factor (chronic hypertension, congenital heart disease) for developing preeclampsia, and there are now abundant data from maternal echo-cardiography and angiogenic marker studies that cardiovascular dysfunction precedes the development of preeclampsia by several weeks or months. Importantly, cardiovascular signs and symptoms (hypertension, cerebral edema, cardiac dysfunction) predominate in preeclampsia at clinical presentation and persist into the postnatal period with a 30% risk of chronic hypertension in the decade after birth. Placental malperfusion caused by suboptimal maternal cardiovascular performance may lead to preeclampsia, thereby explaining the preponderance of cardiovascular drugs (aspirin, calcium, statins, metformin, and antihypertensives) in preeclampsia prevention strategies. Despite the seriousness of the maternal and fetal consequences, we are still developing sensitive screening, reliable diagnostic, effective therapeutic, or improvement strategies for postpartum maternal cardiovascular legacy in preeclampsia. The latter will only become clear with an acceptance and understanding of the cardiovascular etiology of preeclampsia.

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