Preeclampsia is a pregnancy-specific disorder complicating 2%-8% of pregnancies worldwide and characterized by de novo development of hypertension and proteinuria. Current understanding of the pathophysiology of preeclampsia is limited. A main feature is disrupted spiral artery remodeling in the placenta, which restricts the blood flow to the placenta, which in turn leads to decreased uteroplacental perfusion. Impaired blood flow through the placenta might result in fetal growth restriction and secretion of several factors by the placenta-mainly pro-inflammatory cytokines and anti-angiogenic factors-which spread into the maternal circulation, leading to endothelial dysfunction, which subsequently results in disrupted maternal hemodynamics. To date, no treatment options are available apart from termination of pregnancy. Despite normalization of the maternal vascular disturbances after birth, it has become apparent that formerly preeclamptic women experience an increased risk to develop cardiovascular and kidney disease later in life. One well-accepted concept is that the development of preeclampsia is an indicator of maternal susceptibility to develop future cardiovascular conditions, although the increased risk might also be the result of organ damage caused during preeclampsia. Given the associations between preeclampsia and long-term complications, preeclampsia is acknowledged as woman-specific risk factor for cardiovascular disease. Current research focuses on finding effective screening and prevention strategies for the reduction of cardiovascular disease in women with a history of preeclampsia.
Keywords: Anti-angiogenic factor; Endoglin; Fetal growth restriction; Gestational hypertension; Maternal hemodynamics; Placental dysfunction; Placentation; Preeclampsia; Pro-inflammatory cytokines; Renal function; Renin-angiotensin aldosterone system; Syncytiotrophoblast; Uteroplacental perfusion; s-Flt1.