Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth

Background: Placental health may impact the development and outcomes of congenital heart disease (CHD). CHD fetuses have been shown retrospectively to have decreased placental blood flow. Objectives: The purpose of this study was to determine if CHD fetuses with decreased placental blood flow have p...

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Main Authors: Rebecca Josowitz, MD, PhD, Deborah Y. Ho, MD, MPH, Somya Shankar, BS, Antara Mondal, MS, Alexis Zavez, PhD, Rebecca L. Linn, MD, Zhiyun Tian, MD, J. William Gaynor, MD, Jack Rychik, MD
Format: Article
Language:English
Published: Elsevier 2025-02-01
Series:JACC: Advances
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Online Access:http://www.sciencedirect.com/science/article/pii/S2772963X24008408
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author Rebecca Josowitz, MD, PhD
Deborah Y. Ho, MD, MPH
Somya Shankar, BS
Antara Mondal, MS
Alexis Zavez, PhD
Rebecca L. Linn, MD
Zhiyun Tian, MD
J. William Gaynor, MD
Jack Rychik, MD
author_facet Rebecca Josowitz, MD, PhD
Deborah Y. Ho, MD, MPH
Somya Shankar, BS
Antara Mondal, MS
Alexis Zavez, PhD
Rebecca L. Linn, MD
Zhiyun Tian, MD
J. William Gaynor, MD
Jack Rychik, MD
author_sort Rebecca Josowitz, MD, PhD
collection DOAJ
description Background: Placental health may impact the development and outcomes of congenital heart disease (CHD). CHD fetuses have been shown retrospectively to have decreased placental blood flow. Objectives: The purpose of this study was to determine if CHD fetuses with decreased placental blood flow have placental pathology at birth and if there is a relationship between placental blood flow, placental pathology, and outcomes. Methods: We performed a prospective case-control study of 38 CHD fetuses, including 28 with single ventricle physiology and 36 controls. Demographic, clinical, and postnatal biometric data were collected. Umbilical venous volume flow (UVVF) was measured from 2nd trimester fetal echocardiograms. Placentas underwent standardized pathological analysis. Standard descriptive statistics and regression analyses were performed to analyze the relationship between UVVF, placental defects, and outcomes. Results: CHD fetuses had a 15% decrease in mid-gestational UVVF indexed to fetal weight (P < 0.01), and a 27% reduction in UVVF as a proportion of fetal cardiac output (P < 0.01) compared to controls. CHD fetuses had increased placental maternal vascular malperfusion (MVM) lesions (44% vs 18%, P < 0.05), especially high-grade MVM (39% vs 9.1%, P = 0.05), and a trend toward increased placental fetal vascular malperfusion lesions (42% vs 23%, P = 0.10). Placental MVM but not fetal vascular malperfusion lesions were associated with decreased birth weight in CHD fetuses (P < 0.001). There was no association between UVVF and placental pathologic findings or fetal growth. Conclusions: CHD (particularly single ventricle) fetuses have decreased mid-gestational placental blood flow, increased placental malperfusion defects, and impaired fetal growth. Placental MVM may influence impaired fetal growth in CHD.
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spelling doaj-art-7cb41e7faa1b408db93c799508e3d9b72025-01-18T05:05:38ZengElsevierJACC: Advances2772-963X2025-02-0142101559Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired GrowthRebecca Josowitz, MD, PhD0Deborah Y. Ho, MD, MPH1Somya Shankar, BS2Antara Mondal, MS3Alexis Zavez, PhD4Rebecca L. Linn, MD5Zhiyun Tian, MD6J. William Gaynor, MD7Jack Rychik, MD8Division of Cardiology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USADivision of Pediatric Cardiology, Stanford School of Medicine, Lucile Packard Children’s Hospital, Palo Alto, California, USADivision of Cardiology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USADepartment of Biomedical and Health Informatics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USADepartment of Biomedical and Health Informatics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USADivision of Anatomic Pathology, Department of Pathology and Laboratory Medicine, Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USADivision of Cardiology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USADivision of Cardiothoracic Surgery, Department of Surgery, Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USADivision of Cardiology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; Department of Pediatrics, Perelman School of Medicine at University of Pennsylvania, Philadelphia, Pennsylvania, USA; Address for correspondence: Dr Jack Rychik, Fetal Heart Program Children’s Hospital of Philadelphia, 3401 Civic Center Boulevard, Philadelphia, Pennsylvania 1910, USA.Background: Placental health may impact the development and outcomes of congenital heart disease (CHD). CHD fetuses have been shown retrospectively to have decreased placental blood flow. Objectives: The purpose of this study was to determine if CHD fetuses with decreased placental blood flow have placental pathology at birth and if there is a relationship between placental blood flow, placental pathology, and outcomes. Methods: We performed a prospective case-control study of 38 CHD fetuses, including 28 with single ventricle physiology and 36 controls. Demographic, clinical, and postnatal biometric data were collected. Umbilical venous volume flow (UVVF) was measured from 2nd trimester fetal echocardiograms. Placentas underwent standardized pathological analysis. Standard descriptive statistics and regression analyses were performed to analyze the relationship between UVVF, placental defects, and outcomes. Results: CHD fetuses had a 15% decrease in mid-gestational UVVF indexed to fetal weight (P < 0.01), and a 27% reduction in UVVF as a proportion of fetal cardiac output (P < 0.01) compared to controls. CHD fetuses had increased placental maternal vascular malperfusion (MVM) lesions (44% vs 18%, P < 0.05), especially high-grade MVM (39% vs 9.1%, P = 0.05), and a trend toward increased placental fetal vascular malperfusion lesions (42% vs 23%, P = 0.10). Placental MVM but not fetal vascular malperfusion lesions were associated with decreased birth weight in CHD fetuses (P < 0.001). There was no association between UVVF and placental pathologic findings or fetal growth. Conclusions: CHD (particularly single ventricle) fetuses have decreased mid-gestational placental blood flow, increased placental malperfusion defects, and impaired fetal growth. Placental MVM may influence impaired fetal growth in CHD.http://www.sciencedirect.com/science/article/pii/S2772963X24008408congenital heart diseasefetalmalperfusionplacenta
spellingShingle Rebecca Josowitz, MD, PhD
Deborah Y. Ho, MD, MPH
Somya Shankar, BS
Antara Mondal, MS
Alexis Zavez, PhD
Rebecca L. Linn, MD
Zhiyun Tian, MD
J. William Gaynor, MD
Jack Rychik, MD
Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
JACC: Advances
congenital heart disease
fetal
malperfusion
placenta
title Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
title_full Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
title_fullStr Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
title_full_unstemmed Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
title_short Congenital Heart Disease Fetuses Have Decreased Mid-Gestational Placental Flow, Placental Malperfusion Defects, and Impaired Growth
title_sort congenital heart disease fetuses have decreased mid gestational placental flow placental malperfusion defects and impaired growth
topic congenital heart disease
fetal
malperfusion
placenta
url http://www.sciencedirect.com/science/article/pii/S2772963X24008408
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