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Browsing by Autor "Heath-Freudenthal, Alexandra"

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    Surviving birth at high altitude.
    (2024) Heath-Freudenthal, Alexandra; Estrada, Alejandra; von Alvensleben, Inge; Julian, Colleen G
    This Symposium Review examines challenges to surviving birth and infancy at high altitudes. Chronic exposure to the environmental hypoxia of high altitudes increases the incidence of maternal vascular disorders of pregnancy characterized by placental insufficiency, restricted fetal growth and preterm delivery, and impairs pulmonary vascular health during infancy. While each condition independently contributes to excess morbidity and mortality in early life, evidence indicates vascular disorders of pregnancy and infantile pulmonary vascular dysfunction are intertwined. By integrating our recent scientific and clinical observations in Bolivia with existing literature, we propose potential avenues to reduce the infant mortality burden at high altitudes and reduce pulmonary vascular disease in highland neonates, and emphasize the need for further research to address unresolved questions.
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    Use of a ductal occluder device as a test and then permanent closure of a large ductus arteriosus with increased pulmonary vascular resistance: a case report.
    (2025) Fabiani, Nelly; Heath-Freudenthal, Alexandra; Von Alvensleben, Inge; Echazú, Gabriel; Freudenthal, Franz; Rothman, Abraham
    A 3-year-old girl with a large ductus arteriosus had increased pulmonary vascular resistance at cardiac catheterisation. Test occlusion of the ductus arteriosus with a Nit-Occlud PDA-R device and hyperoxia decreased the pulmonary arterial pressure to < 50% of systemic level. The ductus was closed with the same device. Two years later, an echocardiogram showed normal pulmonary arterial pressure.
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    Vascular Disorders of Pregnancy Increase Susceptibility to Neonatal Pulmonary Hypertension in High-Altitude Populations.
    (2022) Heath-Freudenthal, Alexandra; Toledo-Jaldin, Lilian; von Alvensleben, Inge; Lazo-Vega, Litzi; Mizutani, Rodrigo; Stalker, Margaret; Yasini, Hussna; Mendizabal, Fanny; Dorado Madera, Jesus; Mundo, William; Castro-Monrroy, Melany; Houck, Julie A; Moreno-Aramayo, Any; Miranda-Garrido, Valquiria; Su, Emily J; Giussani, Dino A; Abman, Steven H; Moore, Lorna G; Julian, Colleen G
    BACKGROUND: Preeclampsia and fetal growth restriction increase cardiopulmonary disease risk for affected offspring and occur more frequently at high-altitude (≥2500 m). Retrospective studies indicate that birth to a preeclampsia woman at high altitude increases the risk of pulmonary hypertension (PH) in later life. This prospective study asked whether preeclampsia with or without fetal growth restriction exaggerated fetal hypoxia and impaired angiogenesis in the fetal lung, leading to neonatal cardiopulmonary circulation abnormalities and neonatal or infantile PH. METHODS AND RESULTS: We studied 79 maternal-infant pairs (39 preeclampsia, 40 controls) in Bolivia (3600-4100 m). Cord blood erythropoietin, hemoglobin, and umbilical artery and venous blood gases were measured as indices of fetal hypoxia. Maternal and cord plasma levels of angiogenic (VEGF [vascular endothelial growth factor]) and antiangiogenic (sFlt1 [soluble fms-like tyrosine kinase]) factors were determined. Postnatal echocardiography (1 week and 6-9 months) assessed pulmonary hemodynamics and PH. Preeclampsia augmented fetal hypoxia and increased the risk of PH in the neonate but not later in infancy. Pulmonary abnormalities were confined to preeclampsia cases with fetal growth restriction. Maternal and fetal plasma sFlt1 levels were higher in preeclampsia than controls and positively associated with PH. CONCLUSIONS: The effect of preeclampsia with fetal growth restriction to increase fetal hypoxia and sFlt1 levels may impede normal development of the pulmonary circulation at high altitude, leading to adverse neonatal pulmonary vascular outcomes. Our observations highlight important temporal windows for the prevention of pulmonary vascular disease among babies born to highland residents or those with exaggerated hypoxia in utero or newborn life.

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