Offspring of preeclamptic mothers are predisposed to hypoxic pulmonary hypertension

Abstract

Adverse events in utero may predispose to cardiovascular disease in adulthood. In preeclampsia, the diseased placenta releases circulating vasculotoxic factors that cause maternal endothelial dysfunction. These factors may pass the placental barrier, and leave a persistent vascular imprint that may predispose to a pathological response in later life. Endothelial dysfunction plays a major role in the pathogenesis of hypoxic pulmonary hypertension. We hypothesized that offspring of pre-eclampsia may be predisposed to pulmonary hypertension at high altitude. To test this hypothesis, we measured systolic pulmonary-artery pressure (echocardiography) in 11 young (age, 7 1 years, X SE) healthy Bolivian offspring of preeclampsia, and in 13 sex- and age-matched offspring of normal pregnancies in La Paz (3600 m). The major new finding was that systolic pulmonary-artery pressure was roughly 33 percent higher in offspring of preeclamptic mothers than in control subjects (36 2 vs. 27 1 mmHg, P 0.001). This exaggerated hypoxic pulmonary vasoconstriction was not related to more severe hypoxemia or exaggerated polyglobulia. These findings provide the very first evidence that preeclampsia leaves a persistent and potentially fatal imprint in the pulmonary circulation of the offspring, which predisposes them to exaggerated hypoxic pulmonary hypertension in later life.