Cardiovascular Changes in Infants of Preeclampsia Mother
Study Details
Study Description
Brief Summary
Preeclampsia (hypertension during pregnancy) is a common problem affecting 2-8% of pregnancies worldwide and is typically diagnosed by increased blood pressure and proteinuria. The rate of preeclampsia has increased since the 1980s with higher rates at extreme maternal ages as well as during the first pregnancy. Pre-eclampsia is a serious hypertensive disorder of pregnancy affecting outcomes for both mother and infants. These infants not only have increased risk of neonatal complications including preterm birth, intrauterine growth restriction, abnormal Doppler parameters, feed intolerance, intestinal problem, poor growth, and long term lung condition but also have increased risk of cerebral palsy, abnormal neurodevelopmental outcomes, cardiovascular disease, stroke, and mental disorders during childhood and adulthood.
| Condition or Disease | Intervention/Treatment | Phase |
|---|---|---|
|
N/A |
Detailed Description
Preeclampsia is diagnosed according to the International Society for the Study of Hypertension in Pregnancy (ISSHP) criteria: BP > 140/90 on two occasions in previous normotensive mother after 20 weeks of gestation and one of the following; proteinuria in urine > 0.3 gram/kg/day or acute kidney or liver dysfunction or signs of uterine dysfunction. The onset of preeclampsia can be early before 34 weeks of pregnancy (Early-onset preeclampsia) or late after 34 weeks of pregnancy (Late-onset preeclampsia). Early-onset preeclampsia, especially between 28-32 weeks gestation, is characterized by a high prevalence of microvascular changes in the placenta that makes mothers and their infants are more liable to complication. The pathogenesis of preeclampsia is unclear.
Preeclampsia affects hematopoiesis and the fetal myeloid lineage leading to thrombocytopenia, neutropenia, decrease phagocytic function, decrease T regulatory cells, and an increase in cytotoxic natural killer cells in neonates. Innate and adaptive immunity are regulated by myeloid cells and the immune changes in infants of preeclampsia mothers could lead to increased incidence of neonatal sepsis and the development of chronic inflammatory conditions.
Study Design
Arms and Interventions
| Arm | Intervention/Treatment |
|---|---|
| Active Comparator: study group new-born infants born from preeclampsia mother |
Other: Cardiovascular and immunological changes
performing cardiac ultrasound, vascular doppler, and immunological study on cord blood sample
|
| Other: control group new-born infants born from mothers with normal pregnancy matched with the same gestational age, sex and race |
Other: Cardiovascular and immunological changes
performing cardiac ultrasound, vascular doppler, and immunological study on cord blood sample
|
Outcome Measures
Primary Outcome Measures
- Cardiac changes [within 72 hours after birth]
cardiac output will be presented by ml/minute
- Cardiac function changes [within 72 hours after birth]
Fractional shortening and ejection fraction will be presented by percentage
- Vascular changes in superior mesenteric and anterior cerebral arteries [72 hours after birth]
Doppler parameters( peak-systolic velocity, end-diastolic velocity, and mean velocity. All will be measured in meter/second
Secondary Outcome Measures
- Feeding problem [3 months after birth]
rate of necrotizing enterocolitis and feeding intolerance
- oval all outcomes [3 months]
Rate of long term lung condition, sepsis, intraventricular hemorrhage and overall mortality
- immunological changes [cord blood at birth]
interleukins level
Eligibility Criteria
Criteria
Inclusion Criteria:
- Infants born from Pregnant women with preeclampsia, their mother willing to give consent.
Exclusion Criteria:
-
1-Infant with a major heart problem.
-
Infants with major congenital and genetic anomalies.
Contacts and Locations
Locations
No locations specified.Sponsors and Collaborators
- Assiut University
Investigators
None specified.Study Documents (Full-Text)
None provided.More Information
Publications
- Ananth CV, Keyes KM, Wapner RJ. Pre-eclampsia rates in the United States, 1980-2010: age-period-cohort analysis. BMJ. 2013 Nov 7;347:f6564. doi: 10.1136/bmj.f6564.
- Bujold E, Chaiworapongsa T, Romero R, Gervasi MT, Espinoza J, Goncalves LF, Berman S, Yoon BH, Kim YM. Neonates born to pre-eclamptic mothers have a higher percentage of natural killer cells (CD3-/CD56+16+) in umbilical cord blood than those without pre-eclampsia. J Matern Fetal Neonatal Med. 2003 Nov;14(5):305-12.
- Hansen AR, Barnés CM, Folkman J, McElrath TF. Maternal preeclampsia predicts the development of bronchopulmonary dysplasia. J Pediatr. 2010 Apr;156(4):532-6. doi: 10.1016/j.jpeds.2009.10.018. Epub 2009 Dec 14.
- Marins LR, Anizelli LB, Romanowski MD, Sarquis AL. How does preeclampsia affect neonates? Highlights in the disease's immunity. J Matern Fetal Neonatal Med. 2019 Apr;32(7):1205-1212. doi: 10.1080/14767058.2017.1401996. Epub 2017 Nov 20. Review.
- Ness RB, Sibai BM. Shared and disparate components of the pathophysiologies of fetal growth restriction and preeclampsia. Am J Obstet Gynecol. 2006 Jul;195(1):40-9. Epub 2006 Apr 21. Review.
- cardiovascularpreeclampsia