Acute Maternal Hyperoxygenation in CHD
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|ClinicalTrials.gov Identifier: NCT03944837|
Recruitment Status : Recruiting
First Posted : May 10, 2019
Last Update Posted : August 12, 2020
|Condition or disease||Intervention/treatment||Phase|
|Congenital Heart Disease||Other: Oxygen gas||Not Applicable|
This study determines the impact of administering oxygen to mother during the later part of pregnancy on cerebral oxygen delivery in fetuses who were identified with severe forms of Congenital Heart disease (CHD) including the following groups:
- Group 1: Single ventricular (SV) lesions, including hypoplastic left heart syndrome (HLHS); pulmonary atresia with intact ventricular septum (PA/IVS); tricuspid atresia (TA); unbalanced AV septal defect (AVSD); double inlet ventricle (DILV); and severe form of Ebstein's anomaly (EA with pulmonary atresia) of the tricuspid valve; and
- Group 2: Tetralogy of Fallot (TOF),including TOF-like double outlet right ventricle (DORV), pulmonary atresia with ventricular septal defect (PA/VSD)
- Group 3: Bi-ventricular lesions with transposition of the great arteries (TGA), including DORV with TGA
Children with severe CHD experience challenges in multiple developmental domains, impacting executive function, memory, language, and other aspects of cognitive and motor function. It is now well established that brain growth and development are adversely affected by CHD and it is increasingly clear that central nervous system changes that occur in the third trimester play a particularly important role in the pathogenesis of adverse neurodevelopmental outcomes.
Supplemental maternal oxygen will used in the last trimester for a short period of time (acute MH) in pregnant mothers carrying babies with CHD to briefly increase fetal oxygen levels to those reached in the newborn with spontaneous breathing. This study will examine whether and to what degree acute MH will improve the cerebrovascular oxygenation. The rate and duration of MH (10 to 15L/min by mask for up to 30-45 minutes/test) is considered to be safe to the mother and her fetus. Both fetal echocardiography and fetal MRI will be used to determine the effects of acute MH on the fetal-placental circulation and will determine in fetuses with CHD whether acute exposure to MH leads to measurable increases in fetal cerebral oxygenation from baseline. Thus it could potentially become useful as a chronic in-utero treatment strategy to promote brain growth/maturation to birth and to improve postnatal neurodevelopmental outcomes.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||170 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Congenital Heart Disease (CHD): Hemodynamic Effects of Acute Maternal Hyperoxygenation in the Fetus|
|Actual Study Start Date :||April 26, 2019|
|Estimated Primary Completion Date :||December 31, 2022|
|Estimated Study Completion Date :||December 31, 2023|
Experimental: Severe fetal congenital heart disease (CHD)
Mothers whose fetuses have a diagnosis of CHD will be exposed to 10-15 L/minute of oxygen while undergoing echocardiogaphy and MRI scanning
Other: Oxygen gas
Transient maternal oxygen administration during echocardiographic and MRI imaging
- Characterize the hemodynamic effects of acute MH on fetuses with a) SV lesions and biventricular anomalies b) with TOF and c) with TGA. [ Time Frame: Outcome measure obtained during hyperoxygenation while undergoing echocardiography and MRI ]The affect MH has on the cerebral oxygenation from baseline for each type of CHD will be characterized using the MRI variables of cerebral oxygen delivery (cDO2) and cerebral oxygen consumption(cVO2) , which are calculated using fluximetry measurements (ml/min/m2) and the oxymetry of the ascending aorta and the superior vena cava
- Determine the pulmonary and placental vascular response to acute MH for each CHD [ Time Frame: Outcome measure obtained during hyperoxygenation while undergoing echocardiography and MRI ]The pulmonary and placental vascular response to acute MH for each CHD type will be measured using the placenta T2 star variable and the variables related to main pulmonary artery and branch pulmonary artery flow. Pulmonary vaso-reactivity to oxygen by echocardiography defined by a decrease the branch PA PI of ≥10%.
- Assess the relationship between fetal brain volumes and cerebral oxygen delivery [ Time Frame: Outcome measure obtained during hyperoxygenation while undergoing echocardiography and MRI ]The fetal brain volumetry (mL) and rate of cerebral oxygen delivery (cDO2 ml/min/m2) at the time of the baseline fetal MRI will be compared
- To compare the prenatal measurement of placenta and the growth in body and brain size at birth. [ Time Frame: Date of echocardiography/MRI to the date of the infant's birth, when the birth weight, height and head circumference data become available. ]The placental measurement by MRI will be correlated with head circumference and body weight at birth.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03944837
|Contact: Edger Jaeggi, MD, FRCP(C)||(416) email@example.com|
|Contact: Mika Saito, MDfirstname.lastname@example.org|
|The Hospital for Sick Children||Recruiting|
|Toronto, Ontario, Canada, M5G1X8|
|Contact: Edgar Jaeggi, MD 4168137654 email@example.com|
|Principal Investigator:||Edgar Jaeggi, MD, FRCP(C)||The Hospital for Sick Children|