Abstract:Foetal growth restriction was associated with subtle cardiac morphological changes, whereas both prematurity and FGR were associated with subclinical alterations in diastolic function.
“…Our results disclose that SGA children already display a thicker carotid intima-media at age 1 year and more pre-peritoneal fata surrogate of visceral fat (18)by age 2 years as compared with AGA infants; these differences are not accompanied by altered markers of myocardial or vascular damage, by an abnormal cardiac performance or by changes in cardiac morphometry. The absence of cardiac abnormalities is in accordance with the results reported in a recent study performed in newborns and young infants (24) but appears to be at variance with those reported in other cohorts (7,25); those studies, however, were performed in mixed populations including both preterm and term infants with heterogeneous prenatal and postnatal trajectories and used a broader SGA definition.…”
Summary
Background
The sequence of prenatal growth restraint and postnatal catch‐up growth leads to a thicker intima‐media and more pre‐peritoneal fat by age 3–6 years.
Objectives
To study whether carotid intima‐media thickness (cIMT) and pre‐peritoneal fat differ already between catch‐up small‐for‐gestational‐age (SGA) infants and appropriate‐for‐gestational‐age (AGA) controls in late infancy (ages 1 and 2 years) and whether such differences – if any – are accompanied by differences in cardiac morphology and function.
Methods
Longitudinal assessments included body height and weight; fasting glucose, insulin, Insulin‐like growth factor (IGF‐I), high‐molecular‐weight adiponectin; body composition (by absorptiometry); cIMT, aortic IMT, pre‐peritoneal fat partitioning (by ultrasound); cardiac morphometry and function (by echocardiography) in AGA and SGA infants at birth, at age 1 year (N = 87), and again at age 2 years (N = 68).
Results
Catch‐up SGA infants had already a thicker cIMT than AGA controls at ages 1 and 2 years, and more pre‐peritoneal fat by age 2 years (all p values between <0.01 and <0.0001); all cardiac and endocrine‐metabolic results were similar in AGA and SGA infants at ages 1 and 2 years.
Conclusions
From late infancy onwards, catch‐up SGA infants have a thicker cIMT and more pre‐peritoneal fat than AGA controls, but their cardiac morphology and function remain reassuringly similar.
“…Our results disclose that SGA children already display a thicker carotid intima-media at age 1 year and more pre-peritoneal fata surrogate of visceral fat (18)by age 2 years as compared with AGA infants; these differences are not accompanied by altered markers of myocardial or vascular damage, by an abnormal cardiac performance or by changes in cardiac morphometry. The absence of cardiac abnormalities is in accordance with the results reported in a recent study performed in newborns and young infants (24) but appears to be at variance with those reported in other cohorts (7,25); those studies, however, were performed in mixed populations including both preterm and term infants with heterogeneous prenatal and postnatal trajectories and used a broader SGA definition.…”
Summary
Background
The sequence of prenatal growth restraint and postnatal catch‐up growth leads to a thicker intima‐media and more pre‐peritoneal fat by age 3–6 years.
Objectives
To study whether carotid intima‐media thickness (cIMT) and pre‐peritoneal fat differ already between catch‐up small‐for‐gestational‐age (SGA) infants and appropriate‐for‐gestational‐age (AGA) controls in late infancy (ages 1 and 2 years) and whether such differences – if any – are accompanied by differences in cardiac morphology and function.
Methods
Longitudinal assessments included body height and weight; fasting glucose, insulin, Insulin‐like growth factor (IGF‐I), high‐molecular‐weight adiponectin; body composition (by absorptiometry); cIMT, aortic IMT, pre‐peritoneal fat partitioning (by ultrasound); cardiac morphometry and function (by echocardiography) in AGA and SGA infants at birth, at age 1 year (N = 87), and again at age 2 years (N = 68).
Results
Catch‐up SGA infants had already a thicker cIMT than AGA controls at ages 1 and 2 years, and more pre‐peritoneal fat by age 2 years (all p values between <0.01 and <0.0001); all cardiac and endocrine‐metabolic results were similar in AGA and SGA infants at ages 1 and 2 years.
Conclusions
From late infancy onwards, catch‐up SGA infants have a thicker cIMT and more pre‐peritoneal fat than AGA controls, but their cardiac morphology and function remain reassuringly similar.
“…report that foetal growth restrictions were associated with subtle cardiac morphological changes and subclinical alterations in diastolic function. These alterations may contribute to the increased risk of cardiovascular disease seen in this population . …”
Section: Some Consequences Of Preterm Birth and Foetal Growth Restricmentioning
“…Lifelong cardiovascular risk of children descending from pregnancy-related complications is based on the presence of overweight/obesity (increased body mass index and/or wider waist circumference) [1][2][3][4][5][6][7][8][9][10][11], higher systolic and/or diastolic blood pressures [1,2,[6][7][8][12][13][14][15][16][17][18][19][20][21][22], higher nocturnal systolic and diastolic blood pressures [16], altered lipid profiles [6,21], altered metabolite pattern [23], impaired glucose tolerance [3,[5][6][7]24], alteration in the systemic and the pulmonary circulation [25], altered cardiac geometry and function [26][27][28][29] and the acceleration of pubertal timing [30].…”
The goal was to assess how a history of any kind of pregnancy-related complication altered expression profile of microRNAs played a role in the pathogenesis of diabetes, cardiovascular and cerebrovascular diseases in the peripheral blood leukocytes of children at the age of 3–11 years. The prior exposure to gestational hypertension, preeclampsia, fetal growth restriction, gestational diabetes mellitus, preterm prelabor rupture of membranes or spontaneous preterm birth causes that a significant proportion of children (57.42% to 90.0% specifically) had a substantially altered microRNA expression profile, which might be the origin of a lifelong cardiovascular risk. A total of 23 out of 29 tested microRNAs were upregulated in children born from such complicated gestation. The occurrence of overweight, obesity, valve problems and heart defects even intensified upregulation of microRNAs already present in children exposed to such pregnancy complications. The occurrence of overweight/obesity (miR-92a-3p, and miR-210-3p) and valve problems or heart defects (miR-342-3p) induced microRNA upregulation in children affected with pregnancy complications. Overall, 42.86% overweight/obese children and 27.36% children with valve problems or heart defects had even higher microRNA levels than children with normal clinical findings after complicated pregnancies. In addition, the microRNA expression profile was also able to differentiate between children descending from normal gestation in relation to the occurrence of overweight and obesity. Screening on the base of the combination of 19 microRNAs identified 70.0% overweight/obese children at 90.0% specificity. In general, children after complicated pregnancies, just as children after normal pregnancies, with abnormal findings are at a higher risk of the onset of cardiovascular complications, and their dispensarization, with the aim to implement primary prevention strategies, would be beneficial.
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