Infants with fetal growth restriction show lasting subtle heart muscle dysfunction at one year

Infants who experience fetal growth restriction may appear to recover fully within their first year of life, with their bodies catching up in weight, length, and head circumference and their hearts growing to sizes comparable with those of healthy peers. Yet a prospective longitudinal study published in Pediatric Research suggests that this apparent normalization conceals a subtler problem. Using speckle-tracking echocardiography, an advanced imaging technique sensitive to minute deformations of the heart muscle, researchers found that markers of myocardial function remained significantly impaired in infants with fetal growth restriction throughout the first twelve months, even as conventional echocardiographic measures returned to normal.

Fetal growth restriction, commonly defined as an estimated fetal weight below the tenth percentile for gestational age, affects roughly ten to fifteen percent of pregnancies worldwide and is distinct from simply being small for gestational age, which may reflect a constitutionally small but healthy fetus. The predominant mechanism is placental dysfunction, which deprives the fetus of oxygen and nutrients and triggers adaptive cardiovascular remodeling. This process of fetal programming has been linked to an increased lifetime risk of cardiovascular and metabolic disease, and emerging evidence indicates that the resulting structural and functional myocardial changes can be detected early in life, although conventional echocardiographic parameters often fail to identify subtle impairment.

The study, conducted between February 2021 and 2025, enrolled 128 neonates with fetal growth restriction and 64 appropriate-for-gestational-age controls. Of these, 39 infants with early-onset fetal growth restriction, 47 with late-onset disease, and all 64 controls completed the one-year follow-up. Fetal growth restriction was diagnosed antenatally using estimated fetal weight below the tenth percentile together with abnormal Doppler flow patterns in both the middle cerebral artery and the umbilical artery. Neonates with complex congenital heart disease, suspected or confirmed chromosomal abnormalities, or multiple gestations were excluded, and controls were matched to cases by gestational age at delivery.

Each child underwent echocardiography at birth, six months, and twelve months. The protocol combined conventional M-mode and Doppler measurements, tissue Doppler imaging of annular myocardial velocities, and two-dimensional speckle-tracking analysis of global longitudinal strain and strain rates, which capture how the heart muscle shortens, thickens, and lengthens during each beat. All examinations were performed by a single trained investigator using a Vivid IQ system, with no sedation, and Bland–Altman analysis of fifteen randomly selected studies demonstrated good intra- and inter-observer agreement for ejection fraction, myocardial performance index, and global longitudinal strain.

At birth, the differences between groups were striking. Infants with fetal growth restriction weighed substantially less than controls, with early-onset cases averaging 1,818 grams and late-onset cases 1,934 grams, compared with 2,464 grams in the appropriate-for-gestational-age group. Their hearts were also smaller, with reduced interventricular septal thickness, posterior wall thickness, and left ventricular end-diastolic and end-systolic dimensions. Over the following year, both affected groups showed significant catch-up growth in weight, head circumference, abdominal circumference, and body mass index, and most cardiac structural measurements recovered progressively, approaching those of controls by twelve months.

Conventional functional indices told a partly reassuring story. Left ventricular ejection fraction and fractional shortening were reduced in both fetal growth restriction groups at birth and six months, with fractional shortening becoming comparable to controls by one year, a pattern the authors describe as transient impairment of global systolic function. Tricuspid annular plane systolic excursion, a measure of right ventricular function, was reduced at birth but normalized by six months. The left ventricular myocardial performance index and pulmonary artery pressure did not differ significantly across the three time points, suggesting the limited sensitivity of these conventional parameters to subtle myocardial dysfunction.

Speckle-tracking analysis, however, revealed abnormalities that persisted throughout follow-up. Left ventricular global longitudinal strain was significantly impaired in infants with fetal growth restriction at birth and, although it improved over time, the recovery failed to match the steeper physiological improvement seen in controls, leaving a persistent and widening gap by twelve months. Early and late diastolic strain rates were also significantly lower in the affected infants at six and twelve months, indicating that the relaxation phase of the cardiac cycle remained inefficient long after structural dimensions had normalized.

The right ventricle showed a distinctive trajectory. Right ventricular global longitudinal strain was similar across groups at birth and six months, but by twelve months it was significantly reduced in infants with early-onset fetal growth restriction compared with controls, while late-onset cases showed near-normalization. The authors suggest this progressive emergence of right ventricular dysfunction reflects the greater severity and chronicity of intrauterine hemodynamic stress in the early-onset phenotype, and they note it as a novel finding warranting further longitudinal study given the known persistence of pulmonary vascular remodeling in this population.

General linear models confirmed that study group, not sex, was independently associated with one-year weight, abdominal circumference, height, left ventricular ejection fraction, and both left and right ventricular global longitudinal strain, with no significant group-by-sex interaction. Despite catch-up growth, the affected infants remained behind controls at twelve months, reflecting incomplete recovery. The authors caution that attrition during follow-up may have introduced selection bias, that the single-centre design limits generalizability, that detailed maternal and perinatal covariates were unavailable for adjusted analyses, and that whether the observed dysfunction persists beyond infancy remains unknown.

The findings carry a clear message for clinical interpretation: conventional echocardiographic normalization should not be read as true myocardial recovery in infants with fetal growth restriction. Advanced deformation imaging unmasked persistent subclinical abnormalities that standard indices missed, and prior work in preadolescents and school-age children with a history of fetal growth restriction has documented lasting strain impairment and globular ventricular geometry, placing the infancy findings on a continuum of cardiovascular remodeling. The authors argue that these results underscore the value of speckle-tracking echocardiography in long-term cardiac surveillance of this vulnerable group.

Subject of Research: Longitudinal echocardiographic assessment of cardiac structure and function in infants with fetal growth restriction during the first year of life

Article Title: Persistent subclinical myocardial dysfunction among infants with Fetal growth restriction at one year of age

Article References: Nayak, V., Samanth, J., Nayak, K., Lewis, L. E., A J, A., K S, R., Nayak, R., Naik, V., & Poojary, S. M. (2026). Persistent subclinical myocardial dysfunction among infants with Fetal growth restriction at one year of age. Pediatric Research. https://doi.org/10.1038/s41390-026-05429-y

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05429-y

Keywords: fetal growth restriction, speckle-tracking echocardiography, global longitudinal strain, right ventricular dysfunction, early-onset FGR, catch-up growth, infant cardiac development, tissue Doppler imaging, prospective cohort, pediatric cardiology, Persistent, subclinical