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Subclinical myocardial injury in small-for-gestational-age neonates
T Chaiworapongsa1, J Espinoza, J Yoshimatsu
1Perinatology Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland, USA.
Insights
A small percentage of small-for-gestational-age (SGA) newborns show signs of heart muscle injury at birth. This early myocardial injury in SGA infants may increase their risk for adult cardiovascular disease.
Area of Science:
- Neonatal Medicine
- Cardiovascular Research
- Pediatric Cardiology
Background:
- Small-for-gestational-age (SGA) infants face increased risks of adult cardiovascular diseases, including myocardial infarction, stroke, hypertension, and diabetes.
- Severe intrauterine growth restriction can lead to subclinical cardiovascular abnormalities detectable via fetal echocardiography.
Purpose of the Study:
- To investigate whether newborns classified as small-for-gestational-age (SGA) exhibit evidence of myocardial injury at birth.
- To assess cardiac troponin I levels in umbilical cord blood of SGA newborns.
Main Methods:
- Umbilical cord venous blood samples were collected at birth from 72 SGA infants and 309 appropriate-for-gestational-age (AGA) infants.
- Cardiac troponin I, a specific biomarker for myocardial injury, was measured using a commercial immunoassay (Immulite 2000).
Main Results:
- Cardiac troponin I was undetectable in all umbilical cord blood samples from AGA infants.
- Detectable levels of cardiac troponin I were found in 4.2% of SGA infants (p = 0.007), indicating myocardial injury.
Conclusions:
- A subset of SGA newborns experiences myocardial injury prior to birth.
- This prenatal cardiac insult may contribute to the development of premature cardiovascular disease and mortality in adulthood.
Objective:
Small-for-gestational-age (SGA) infants are at risk for premature death from cardiovascular disease (myocardial infarction and stroke), hypertension, and diabetes in adult life. Severe intrauterine growth restriction is often associated with subclinical cardiovascular abnormalities detectable during fetal echocardiography. The objective of this study was to determine whether SGA newborns have evidence of myocardial injury at birth.
Study Design:
Cardiac troponin I, a specific marker of myocardial injury widely used for the diagnosis of myocardial infarction in adults, was determined in umbilical cord blood. Umbilical cord venous blood was obtained at the time of birth from 72 SGA newborns (birth weight below the 10th centile for gestational age) and 309 newborns whose birth weights were appropriate for gestational age (AGA). Cardiac troponin I was determined with a commercially available immunoassay (sensitivity 0.2 ng/ml) employed in clinical laboratories (Immulite 2000, Diagnostic Products Corp., Los Angeles, CA).
Results:
Cardiac troponin I was not detectable in any of the blood samples from AGA infants. In contrast, 4.2% (3/72) of SGA infants had detectable cardiac troponin I in umbilical cord blood (Fisher's exact test, p = 0.007).
Conclusion:
A subgroup of SGA newborns undergoes myocardial injury before birth. This insult may predispose to the development of adult premature cardiovascular disease and death.