Introduction Preeclampsia is a pregnancy-related condition affecting up to 8 % of pregnancies worldwide []. The incidence varies according to geographical, social, economic and racial differences []. It has been estimated that preeclampsia or complications of the condition account for more than 50,000 maternal deaths worldwide each year []. Clinical manifestations appear after 20 weeks of gestation. Although the diagnostic criteria are clear, [] it has been difficult to find a way to predict the disease in early pregnancy or to predict which women that will develop severe preeclampsia and/or eclampsia. The details of the pathophysiology remain elusive but recent research has improved the understanding of the condition markedly. Preeclampsia is described to develop in two stages [, ]. The stage is characterized by a defect placentation []. The extravillous trophoblast cells do not remodel the spiral arteries in the maternal decidua properly and consequently fail to create a low-resistance even utero-placental blood flow [, ]. Uneven perfusion leads to oxidative stress in the placenta that contributes to the damage of the blood-placenta barrier and subsequent leakage between the fetal and maternal circulation. In fact, cell-free fetal DNA [, ], micro-particles [] and cell-free fetal hemoglobin [, ] have been described in the maternal circulation of women with preeclampsia [, ]. The second stage of preeclampsia is characterized by the clinical manifestations, e.g. increased blood pressure and proteinuria detected after 20 weeks of gestation [, ]. The link between the stages 1 and 2 is still a main focus of modern preeclampsia research. Maternal constitutional factors such as obesity are important risk factors for late onset preeclampsia in particular. Furthermore, a new focus area is the role of maternal cardiac strain in the development of preeclampsia [].
Introduction Preeclampsia is a pregnancy-related condition affecting up to 8 % of pregnancies worldwide []. The incidence varies according to geographical, social, economic and racial differences []. It has been estimated that preeclampsia or complications of the condition account for more than 50,000 maternal deaths worldwide each year []. Clinical manifestations appear after 20 weeks of gestation. Although the diagnostic criteria are clear, [] it has been difficult to find a way to predict the disease in early pregnancy or to predict which women that will develop severe preeclampsia and/or eclampsia. The details of the pathophysiology remain elusive but recent research has improved the understanding of the condition markedly. Preeclampsia is described to develop in two stages [, ]. The stage is characterized by a defect placentation []. The extravillous trophoblast cells do not remodel the spiral arteries in the maternal decidua properly and consequently fail to create a low-resistance even utero-placental blood flow [, ]. Uneven perfusion leads to oxidative stress in the placenta that contributes to the damage of the blood-placenta barrier and subsequent leakage between the fetal and maternal circulation. In fact, cell-free fetal DNA [, ], micro-particles [] and cell-free fetal hemoglobin [, ] have been described in the maternal circulation of women with preeclampsia [, ]. The second stage of preeclampsia is characterized by the clinical manifestations, e.g. increased blood pressure and proteinuria detected after 20 weeks of gestation [, ]. The link between the stages 1 and 2 is still a main focus of modern preeclampsia research. Maternal constitutional factors such as obesity are important risk factors for late onset preeclampsia in particular. Furthermore, a new focus area is the role of maternal cardiac strain in the development of preeclampsia [].