Abstract

During normal pregnancy, the maternal cardiovascular system undergoes important anatomic and functional modifications to establish a low-resistance, high-volume state to support fetal demands for nutrients and gas exchange.1 Cardiac output increases by as much as 30% to 40%, resulting from increases in stroke volume and, to a lesser extent, heart rate. Gestational hormones and alterations in the synthesis of, and reactivity to, vasoactive substances result in systemic vasodilatation.2 Despite increases in cardiac output, maternal blood pressure decreases because of a substantial reduction in systemic vascular resistance. Pregnancy is also associated with an increase in venous capacitance and a parallel large expansion of blood volume.3 The purpose of these maternal changes is to promote blood flow to the implantation site to optimize fetal growth, increase maternal renal excretory functions because of excess maternal, placental, and fetal metabolic demand, and to withstand hemorrhage at delivery. Hemodynamic and vascular adaptations that occur in normal pregnancy are disrupted in women who develop preeclampsia (PE), a hypertensive disorder that affects 2% to 8% of all pregnancies worldwide.4 PE is characterized by new-onset hypertension (blood pressure consistently >140/90 mm Hg) after 20 weeks of gestation, accompanied by evidence of organ injury (proteinuria, thrombocytopenia, renal or liver impairment, pulmonary edema, or cerebral/visual symptoms suggesting cerebral cortical dysfunction), as redefined by the American College of Obstetrics and Gynecology in 2013.5 PE can be subdivided into early-onset PE (before 34 weeks of gestation), the more severe subset of the disease with smaller birthweight neonates and a higher rate of recurrence, and late-onset PE (after 37 weeks of gestation).6 Once established, PE often advances until delivery and may persist for some time in the postpartum period.7–10 Recent population-based cohort studies have concluded that women with a history of PE are at …

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