Fetal cardiovascular remodeling persists at 6 months in infants with intrauterine growth restriction.
OBJECTIVES
Intrauterine growth restriction is associated with increased cardiovascular risk later in life but the link between fetal disease and postnatal risk is not well-documented. We evaluated longitudinally the association between cardiovascular remodeling in small-for-gestational-age (SGA) fetuses and at 6 months of age.


METHODS
A cohort of 80 SGA fetuses (defined by estimated fetal and birth weights < 10(th) centile) delivered > 34 weeks' gestation was compared with 80 normally grown age-matched control fetuses, with follow-up at 6 months of corrected age (i.e. 6 months from estimated date of delivery according to first-trimester crown-rump length). Cardiovascular evaluation included a comprehensive echocardiographic assessment in both fetuses and infants and blood pressure and aortic intima-media thickness (aIMT) measurement in infants. Parameters were adjusted by linear regression analysis for gender, gestational age at delivery, pre-eclampsia, prenatal glucocorticoid exposure, Cesarean delivery, admission to neonatal intensive care unit and body surface area.


RESULTS
Both pre- and postnatally, when compared with controls, the SGA group showed a more globular cardiac shape (left sphericity index: controls 2.06 vs SGA 1.87 (P = 0.022) prenatally and 1.92 vs 1.67 (P = 0.007) postnatally), as well as signs of systolic longitudinal dysfunction (systolic annular peak velocity (S'): 7.2 vs 6.3 cm/s (P = 0.003) prenatally and 7.9 vs 6.4 cm/s (P < 0.001) postnatally; tricuspid annular plane systolic excursion: 7.2 vs 6.8 mm (P = 0.015) prenatally and 16.0 vs 14.2 mm (P < 0.001) postnatally) and diastolic dysfunction (left isovolumetric relaxation time: 46 vs 52 ms (P < 0.001) prenatally and 50 vs 57 ms (P = 0.034) postnatally). In addition, infants in the SGA group had increased mean blood pressure (mean: 61 vs 70 mmHg, P < 0.001) and maximum aIMT (0.57 vs 0.66 mm; P < 0.001).


CONCLUSIONS
Primary cardiovascular changes are already present in the SGA fetus and persist at 6 months of age. These data support prenatal cardiovascular remodeling as a mechanistic pathway of increased risk later in life in cases of SGA, regardless of Doppler abnormalities. Copyright © 2015 ISUOG. Published by John Wiley & Sons Ltd.
['Cruz-Lemini|M|M|', 'Crispi|F|F|', 'Valenzuela-Alcaraz|B|B|', 'Figueras|F|F|', 'Sitges|M|M|', 'Bijnens|B|B|', 'Gratacós|E|E|']
D000328:Adult D002318:Cardiovascular Diseases D002319:Cardiovascular System D059168:Carotid Intima-Media Thickness D018568:Crown-Rump Length D005260:Female D005317:Fetal Growth Retardation D005865:Gestational Age D006801:Humans D007223:Infant D007231:Infant, Newborn D007236:Infant, Small for Gestational Age D008137:Longitudinal Studies D008297:Male D011247:Pregnancy D011446:Prospective Studies D012307:Risk Factors D016216:Ultrasonography, Prenatal D066253:Vascular Remodeling D020257:Ventricular Remodeling
cardiovascular remodeling cardiovascular risk fetal echocardiography fetal programming