Current research
Prenatal Vascular Phenotype & Fetal Congenital Heart Disease
Congenital heart defects (CHDs) are the most common cause of congenital anomaly, occurring in ~1% of newborns. These neonates generally survive in-utero; however, there is lifetime morbidity related to vascular sequalae. The etiology(ies) of CHD remain elusive making intervention purely mechanical. Upstream and/or downstream signaling alterations in endothelial mechano-transduction throughout their life due to the abnormal flow patterns, remains a unifying phenotype. We have termed this the prenatal vascular phenotype.
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​To understand and target the mechanisms underlying the vascular phenotype, we aim to integrate data through the life course -- the prenatal and postnatal sequalae. We couple prenatal maternal-fetal imaging, underlying genetic predispositions, and developmental endothelial flow dynamics. Ultimately, this may improve treatment that arise from loss of vascular integrity. Despite being born with a morbid CHD, we have a chance to understand downstream complications and interventions that can improve quality of life in these patients with lifelong sequelae related to an abnormal endothelial cell and vascular phenotype.
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To standardize practices and improve outcomes for congenital heart disease, a standardized clinical assessment and management plan (SCAMP) was used for more than 400 patients. It was found to have decreased early and cesarean delivery.
Twins that share one placenta have a significantly greater chance of congenital heart disease than pregnancies with one fetus or with twins that have two individual placentas. However, no significant association was found between identified risk factors and the development of CHD.
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