Current research
Maternal-Fetal Congenital Heart Disease
(CHD)
Maternal
Significant advancements in medical care have allowed pregnant people with cardiovascular disease, specifically congenital heart disease (CHD), to survive to childbearing age, resulting in an increased prevalence of cardiovascular disease in pregnancy. Although pregnancy and its associated hemodynamic changes may be well tolerated in some, pregnancy may increase the risk of volume overload, development of arrhythmias, and progressive cardiac dysfunction in others. The presence of maternal CHD is also a major determinant for neonatal morbidity. Overall, pregnancies complicated by maternal CHD are at an increased risk for adverse maternal and neonatal outcomes compared to the general obstetric population. Our translational team focuses on optimizing both delivery coordination and planning for this high-risk population as well as understanding molecular mechanisms that underlie normal and abnormal physiological changes of the cardiovascular system in pregnancy.​​
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Fetal
Fetal congenital heart disease. Congenital heart defects (CHDs) are the most common cause of congenital anomaly, occurring in ~1% of newborns. The etiology(ies) of CHD remain elusive making intervention purely mechanical. 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 arisesfrom 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.
​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. ​​​​​​​​​​​​​​
Across ten years, women who have had Fontan procedures to treat their univentricular hearts were observed to see how such procedures may have impacted their pregnancies. Their babies showed higher rates of being smaller than what is expected by their gestational age, being born prematurely, and being admitted to the NICU.
In pregnancies by older mothers, vascular resistance was found to be associated with weight percentile at birth.
Correlations were found between various maternal hemodynamic metrics. Ultimately, the best predictor for middle cerebral artery pulsatility index was central systolic blood pressure. Thus, maternal hemodynamic metrics can serve as a proxy for fetal cardiac health.
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.
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.
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