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Related Experiment Video

Updated: Jun 9, 2026

Murine Fetal Echocardiography

Murine Fetal Echocardiography

Published on: February 15, 2013

Cardiac function in trisomy 21 fetuses.

S A B Clur¹, K Oude Rengerink, J Ottenkamp

¹Department of Pediatric Cardiology of the Emma Children's Hospital, Academic Medical Centre, Amsterdam, The Netherlands. s.a.clur@amc.nl

Ultrasound in Obstetrics & Gynecology : the Official Journal of the International Society of Ultrasound in Obstetrics and Gynecology

|September 4, 2010

Summary

This summary is machine-generated.

Cardiac function is altered in fetuses with trisomy 21, showing abnormalities regardless of congenital heart defects. This study reveals early signs of cardiac dysfunction and loading in trisomy 21 pregnancies.

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Area of Science:

Fetal Cardiology
Genetics
Prenatal Diagnosis

Background:

Trisomy 21 (Down syndrome) is linked to increased nuchal translucency (NT), abnormal ductus venosus (DV) flow, and congenital heart defects (CHD).
Cardiac dysfunction is hypothesized as a potential link between these trisomy 21-associated findings.

Purpose of the Study:

To investigate alterations in cardiac function in fetuses with trisomy 21.
To determine if cardiac dysfunction is present irrespective of structural heart defects or increased NT.

Main Methods:

Echocardiography was performed on 46 trisomy 21 fetuses and 191 controls between 11-35 weeks' gestation.
Measurements included atrioventricular and semilunar valve velocities, myocardial performance index (MPI), stroke volume (SV), cardiac output, and DV pulsatility index for veins (PIV).
Data were analyzed across three gestational age groups: 11-13+6, 14-21+6, and 22-35 weeks.

Main Results:

Trisomy 21 fetuses showed reduced tricuspid valve A-wave and aortic valve peak velocities.
Early in gestation (11-14 weeks), increased DV pulsatility index (PIV), altered atrioventricular valve ratios, and evidence of left ventricular (LV) systolic dysfunction (reduced SV, increased MPI) were observed.
Later in gestation, trisomy 21 fetuses with normal hearts exhibited reduced mitral valve A-wave velocity and E/TVI ratio compared to controls with increased NT.

Conclusions:

Cardiac function is significantly altered in trisomy 21 fetuses, even without overt congenital heart defects.
Findings suggest evidence of increased cardiac loading (preload and afterload) and both systolic and diastolic dysfunction in trisomy 21 fetuses.
These cardiac functional changes may represent an underlying mechanism linking various trisomy 21-associated phenotypes.