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Published on: June 29, 2013
Persistence of Cardiac Remodeling in Preadolescents With Fetal Growth Restriction
Sebastian Imre Sarvari1, Merida Rodriguez-Lopez1, Marta Nuñez-Garcia1
1From the Cardiology Department, Cardiovascular Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Spain (S.I.S., M.S.); Department of Cardiology, Oslo University Hospital, Rikshospitalet, University of Oslo, Norway (S.I.S.); Fetal i+D Fetal Medicine Research Center, IDIBAPS (M.R.-L., A.S.-M., E.G., F.C.) and BCNatal | Barcelona Center for Maternal Fetal and Neonatal Medicine, Hospital Clínic and Hospital Sant Joan de Déu (M.R.-L., A.S.-M., E.G., F.C.), Universitat de Barcelona, Spain; PhySense, Department of Information and Communication Technologies (DTIC), Universitat Pompeu Fabra, Barcelona, Spain (M.N.-G., O.C., C.B., B.B.); Centro de Investigación Biomédica en Red en Enfermedades Raras, Spain (E.G., F.C.); and ICREA, Barcelona, Spain (B.B.).
Insights
Fetal growth restriction (FGR) leads to lasting cardiac changes, including altered heart shape and function, persisting into preadolescence. These findings suggest primary cardiac programming contributes to adult cardiovascular risk in FGR individuals.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Developmental Biology
Background:
- Fetal growth restriction (FGR) affects 5-10% of newborns.
- FGR is linked to increased adult cardiovascular mortality.
- Prenatal cardiovascular changes in FGR require further investigation into long-term effects.
Purpose of the Study:
- To determine if cardiovascular changes observed in fetuses with FGR persist into preadolescence.
- To investigate the long-term cardiac remodeling in individuals with a history of FGR.
- To explore the link between FGR and lifelong cardiovascular health.
Main Methods:
- A cohort study followed 58 FGR and 94 control individuals from fetus to preadolescence (8-12 years).
- Echocardiography and 3D computational shape analysis were used to assess cardiac structure and function.
- Statistical analysis adjusted for various confounding factors including parental ethnicity, smoking, and gestational age.
Main Results:
- FGR preadolescents exhibited distinct cardiac shapes (more spherical, smaller hearts) compared to controls.
- FGR individuals showed decreased longitudinal myocardial motion and impaired relaxation.
- Global longitudinal strain was reduced in FGR, compensated by increased circumferential strain, with higher postsystolic shortening prevalence.
Conclusions:
- Cardiac remodeling due to FGR persists into preadolescence, mirroring prenatal and childhood findings.
- The study supports the hypothesis of primary cardiac programming in FGR.
- These persistent cardiac alterations may explain the association between low birth weight and adult cardiovascular risk.
Background:
Fetal growth restriction (FGR) affects 5% to 10% of newborns and is associated with increased cardiovascular mortality in adulthood. We evaluated whether prenatal cardiovascular changes previously demonstrated in FGR persist into preadolescence.
Methods And Results:
A cohort study of 58 FGR (defined as birth weight below 10th centile) and 94 normally grown fetuses identified in utero and followed-up into preadolescence (8-12 years of age) by echocardiography and 3-dimensional shape computational analysis. Compared with controls, FGR preadolescents had a different cardiac shape, with more spherical and smaller hearts. Left ventricular ejection fraction was similar among groups, whereas FGR had decreased longitudinal motion (decreased mitral annular systolic peak velocities: control median, 0.11 m/s [interquartile range, 0.09-0.12] versus FGR median 0.09 m/s [interquartile range, 0.09-0.10]; P<0.01) and impaired relaxation (isovolumic relaxation time: control, 0.21 ms [interquartile range, 0.12-0.35] versus FGR, 0.35 ms [interquartile range, 0.20-0.46]; P=0.04). Global longitudinal strain was decreased (control mean, -22.4% [SD, 1.37] versus FGR mean, -21.5% [SD, 1.16]; P<0.001) compensated by an increased circumferential strain and with a higher prevalence of postsystolic shortening in FGR as compared with controls. These differences persisted after adjustment for parental ethnicity and smoking, prenatal glucocorticoid administration, preeclampsia, gestational age at delivery, days in intensive care unit, sex, age, and body surface area at evaluation.
Conclusions:
This study provides evidence that cardiac remodeling induced by FGR persists until preadolescence with findings similar to those reported in their prenatal life and childhood. The findings support the hypothesis of primary cardiac programming in FGR for explaining the association between low birth weight and cardiovascular risk in adulthood.
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