The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

Sebastiani, Giorgia; Garcia-Beltran, Cristina; Pié, Sandrine; Guerra, Anna; López‐Bermejo, Abel; Toledo, José Sánchez de; Zegher, Francis de; Roses, Ferran; Ibáñez, Lourdes

doi:10.1111/ijpo.12476

Cited by 9 publications

(8 citation statements)

References 49 publications

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“…While we found significantly increased diastolic mitral E- and A-wave peak inflow velocities, and an increased septal E / E ′ ratio in the SGA group, possibly indicating differences in ventricular filling, these differences were minor. Previous studies report both increased [ 6 ] and similar [ 12 ] E / E ′ ratios in SGA children during early childhood, while in the neonate stage, we found the E / E ′ ratio to be decreased in SGA and increased in LGA [ 13 ]. The increased left atrial volume observed in the LGA group suggests that diastolic function could potentially be affected by high birth weight.…”

Section: Discussionsupporting

confidence: 61%

“…Birth weight associates with ventricular mass in early childhood [ 8 ] and adolescence [ 9 ], with higher birth weight associated with changes in diastolic function [ 10 ]. Recent studies have, however, demonstrated that SGA children show size-appropriate cardiovascular dimensions in early childhood [ 11 , 12 ], suggesting a limited impact of altered fetal growth. We have previously demonstrated cardiac morphology of SGA and LGA neonates to be appropriate for body size, with no evidence of altered geometry [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

“…We have previously discussed that adjusting for BSA could lead to over-adjusting cardiac dimensions in the presence of adiposity [ 13 ], and shown LBM to be the strongest predictor of left ventricular mass during childhood [ 18 ]. Taking current body size into account is especially important when examining children born SGA and LGA, as both SGA [ 12 ] and LGA [ 19 ] are associated with changes in body composition.…”

Section: Introductionmentioning

confidence: 99%

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Childhood cardiovascular morphology and function following abnormal fetal growth

et al. 2022

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Studies examining the link between abnormal fetal growth and cardiac changes in childhood have presented conflicting results. We studied the effect of abnormal fetal growth on cardiac morphology and function during childhood, while controlling for body size, composition and postnatal factors. We report on the follow-up of 90 children (median age 5.81 years, IQR 5.67; 5.95) born appropriate for gestational age (AGA, N = 48), small for gestational age (SGA, N = 23), or large for gestational age (LGA, N = 19); SGA and LGA defined as birth weight Z-score < − 2 and > + 2, respectively. We examined the heart using echocardiography, including Doppler and strain imaging, in relation to anthropometrics, body composition, blood pressure, physical activity, and diet. Although groupwise differences in body size decreased during the first year after birth, LGA remained larger at follow-up, with higher lean body mass and BMI, while SGA were smaller. Slight changes in left ventricular diastolic function were present in SGA and LGA, with SGA showing increased mitral diastolic E- and A-wave peak flow velocities, and increased septal E/E′ ratio, and LGA showing larger left atrial volume adjusted for sex and lean body mass. In univariate analyses, lean body mass at follow-up was the strongest predictor of cardiac morphology. We found no groupwise differences at follow-up for ventricular sphericity, cardiac morphology adjusted for lean body mass and sex, or blood pressure, diet, or physical activity. Cardiac morphology is predicted by lean body mass during childhood, even in the setting of abnormal fetal growth. Our results are consistent with a limited effect of fetal programming on cardiac dimensions during childhood. Minor changes in diastolic function are present in both SGA and LGA children, however, the clinical significance of these changes at this stage is likely small.

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Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Childhood cardiovascular morphology and function following abnormal fetal growth

et al. 2022

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“…Increased carotid IMT has, in contrast to our findings, been linked with SGA during early childhood [ 9 ]. However, studies are inconclusive, as both increased carotid IMT [ 26 – 29 ] and normal carotid IMT [ 30 ], and increased [ 29 ] and normal [ 26 ] aortic IMT have been reported in SGA children, along with normal carotid IMT in LGA children [ 31 ]. We speculate that this could be due to limitations in conventional ultrasound axial resolution applied in earlier studies.…”

Section: Discussionmentioning

confidence: 99%

Arterial health during early childhood following abnormal fetal growth

et al. 2022

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Background Abnormal fetal growth is associated with increased cardiovascular risk in adulthood. We investigated the effect of fetal programming on arterial health and morphology during early childhood. Methods We examined 90 children (median age 5.81 years, interquartile range: 5.67; 5.95), born small for gestational age with fetal growth restriction, large or appropriate for gestational age (SGA, N = 23, LGA, N = 19, AGA N = 48). We measured body composition, anthropometrics, blood pressure, pulse wave velocity (PWV), lipids, glucose and inflammatory markers, and assessed carotid, brachial, radial and femoral arterial morphology and stiffness using very-high resolution ultrasound (46–71 MHz). Results LGA showed increased anthropometry, lean body mass and body mass index. SGA displayed decreased anthropometry and lean body mass. Blood pressure, PWV, carotid artery stiffness and blood work did not differ groupwise. Differences in lumen diameters, intima-media thicknesses (IMT) and adventitia thicknesses disappeared when adjusted for lean body mass and sex. In multiple regression models arterial dimensions were mainly predicted by lean body mass, with birth weight remaining associated only with carotid and brachial lumen dimensions, and not with IMTs. Carotid-femoral PWV was predicted by height and blood pressure only. No independent effect of adiposity was observed. Conclusions Arterial dimensions in childhood associate with current anthropometrics, especially lean body mass, and sex, explaining differences in arterial layer thickness. We found no signs of fetal programming of cardiovascular risk or arterial health in early childhood.

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“…Compared to AGA infants, those infants born small for-gestational age (SGA) were shown to have lower %BF by ADP at term birth [ 55 ]. According to Zegher et al, the greater levels of circulating preadipocyte factor 1 (Pref-1) found in SGA than in AGA newborns may partially explain the impaired intrauterine AT development [ 56 ], as Pref-1 has a role in suppressing adipocyte differentiation [ 57 ].…”

Section: Adipose Tissue Developmentmentioning

confidence: 99%

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

et al. 2020

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Prevalence rates of pediatric obesity continue to rise worldwide. Adipose tissue (AT) development and expansion initiate in the fetus and extend throughout the lifespan. This paper presents an overview of the AT developmental trajectories from the intrauterine period to adolescence; factors determining adiposity expansion are also discussed. The greatest fetal increases in AT were observed in the third pregnancy trimester, with growing evidence suggesting that maternal health and nutrition, toxin exposure, and genetic defects impact AT development. From birth up to six months, healthy term newborns experience steep increases in AT; but a subsequent reduction in AT is observed during infancy. Important determinants of AT in infancy identified in this review included feeding practices and factors shaping the gut microbiome. Low AT accrual rates are maintained up to puberty onset, at which time, the pattern of adiposity expansion becomes sex dependent. As girls experience rapid increases and boys experience decreases in AT, sexual dimorphism in hormone secretion can be considered the main contributor for changes. Eating patterns/behaviors and interactions between dietary components, gut microbiome, and immune cells also influence AT expansion. Despite the plasticity of this tissue, substantial evidence supports that adiposity at birth and infancy highly influences its levels across subsequent life stages. Thus, a unique window of opportunity for the prevention and/or slowing down of the predisposition toward obesity, exists from pregnancy through childhood.

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The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

Cited by 9 publications

References 49 publications

Childhood cardiovascular morphology and function following abnormal fetal growth

Childhood cardiovascular morphology and function following abnormal fetal growth

Arterial health during early childhood following abnormal fetal growth

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

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