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      Disproportionate cardiac hypertrophy during early postnatal development in infants born preterm

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          Abstract

          Background

          Adults born very preterm have increased cardiac mass and reduced function. We investigated whether a hypertrophic phenomenon occurs in later preterm infants and when this occurs during early development.

          Methods

          Cardiac ultrasound was performed on 392 infants (33% preterm at mean gestation 34±2 weeks). Scans were performed during fetal development in 137, at birth and 3 months of postnatal age in 200, and during both fetal and postnatal development in 55. Cardiac morphology and function was quantified and computational models created to identify geometric changes.

          Results

          At birth, preterm offspring had reduced cardiac mass and volume relative to body size with a more globular heart. By 3 months, ventricular shape had normalized but both left and right ventricular mass relative to body size were significantly higher than expected for postmenstrual age (left 57.8±41.9 vs. 27.3±29.4%, P<0.001; right 39.3±38.1 vs. 16.6±40.8, P=0.002). Greater changes were associated with lower gestational age at birth (left P<0.001; right P=0.001).

          Conclusion

          Preterm offspring, including those born in late gestation, have a disproportionate increase in ventricular mass from birth up to 3 months of postnatal age. These differences were not present before birth. Early postnatal development may provide a window for interventions relevant to long-term cardiovascular health.

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          Most cited references36

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          Rapid transition of cardiac myocytes from hyperplasia to hypertrophy during postnatal development.

          The switch from myocyte hyperplasia to hypertrophy occurs during the early postnatal period. The exact temporal sequence when cardiac myocytes cease dividing and become terminally differentiated is not certain, although it is currently believed that the transition takes place gradually over a 1-2-week period. The present investigation has characterized the growth pattern of cardiac myocytes during the early postnatal period. Cardiac myocytes were enzymatically isolated from the hearts of 1, 2, 3, 4, 6, 8, 10, and 12-day-old rats for the measurements of binucleation, cell volume and myocyte number. Almost all myocytes were mononucleated and cell volume remained relatively constant during the first 3 days of age. Increases in cell volume and binucleation of myocytes were first detected at day 4. Myocyte volume increased 2.5-fold from day 3 to day 12 (1416 +/- 320 compared to 3533 +/- 339 microns 3). The percentage of binucleated myocytes began to increase at day 4 and proceeded at a high rate, reaching the adult level of approximately 90% at day 12. Myocyte number increased 68% during the first 3 days (from 13.6 +/- 3.5 x 10(6) at day 1 to 22.9 +/- 5.6 x 10(10) at day 3) and remained constant thereafter. To confirm that no further myocyte division exists after 4 days, bromodeoxyuridine (Brdu) was administered to 4-day-old rats and the fate of DNA-synthesizing myocytes was examined 2 h and 2, 4, 6 and 8 days after Brdu injection. About 12% of myocytes were labeled with Brdu at 2 h and all were mononucleated at that time. Gradually, these Brdu-labeled myocytes became binucleated. However, the percentage of labeled myocytes in all groups was identical, indicating that DNA-synthesizing myocytes were becoming binucleated without further cell division after 4 days of age. Within 8 days after injection, approximately 82% of total labeled myocytes were binucleated, while the others remained mononucleated. Sarcomeric alpha-actinin was fully disassembled in dividing myocytes of 2-day-old rats, while typical alpha-actinin striations were present in dividing myocytes of 4-day-old rats. The results from this study suggest that a rapid switch from myocyte hyperplasia to hypertrophy occurs between postnatal day 3 and 4 in rat hearts.
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            INTERGROWTH-21st very preterm size at birth reference charts.

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              Epidemiology of preterm birth and its clinical subtypes.

              Preterm birth (<37 weeks) complicates 12.5% of all deliveries in the USA, and remains the leading cause of perinatal mortality and morbidity, accounting for as many as 75% of perinatal deaths. Despite the recent temporal increase in preterm birth, efforts to understand the problem of prematurity have met with little success. This may be attributable to the under-appreciation of the etiologic heterogeneity of preterm birth as well as the heterogeneity in its underlying clinical presentations--spontaneous onset of labor, preterm premature rupture of membranes, and medically indicated preterm birth. In this paper, we review data regarding preterm births with particular focus on its incidence, temporal trends, and recurrence. Studies of births from the USA indicate that the recent temporal increase in the overall preterm birth rate is driven by an impressive concomitant increase in medically indicated preterm birth. However, the largest temporal decline in perinatal mortality has also occurred among medically indicated preterm births (relative to other clinical subtypes), suggesting that these obstetric interventions at preterm gestational ages are associated with a reduction in perinatal mortality. Recent data indicate that spontaneous preterm birth is not only associated with increased recurrence of spontaneous, but also medically indicated, preterm birth, and vice versa. This suggests that the clinical subtypes may share common underlying etiologies. Since medically indicated preterm birth accounts for as many as 40% of all preterm births, efforts to understand the reasons for such interventions and their impact on short- and long-term morbidity in newborns is compelling. Further research is necessary in order to understand the mechanisms and etiology of preterm birth, thus leading to the possibility of effective preventive or therapeutic strategies.
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                Author and article information

                Journal
                Pediatr Res
                Pediatr. Res
                Pediatric Research
                Nature Publishing Group
                0031-3998
                1530-0447
                July 2017
                24 May 2017
                : 82
                : 1
                : 36-46
                Affiliations
                [1 ]Oxford Cardiovascular Clinical Research Facility, Division of Cardiovascular Medicine, University of Oxford , Oxfordshire, UK
                [2 ]Department of Biomedical Engineering, King’s College London , London, UK
                [3 ]Centre for Statistics in Medicine, University of Oxford , Oxford, Oxfordshire, UK
                [4 ]Department of Paediatrics and Neonatology, John Radcliffe Hospital , Oxford, Oxfordshire, UK
                [5 ]Nuffield Department of Obstetrics & Gynaecology, University of Oxford, Oxford , Oxfordshire, UK
                Author notes
                [6]

                The first two authors contributed equally to this work.

                Article
                pr201796
                10.1038/pr.2017.96
                5511508
                28399117
                850f6d81-acbf-43d8-8f53-6ea90701ab74
                Copyright © 2017 The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 15 November 2016
                : 20 March 2017
                Categories
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                Pediatrics
                Pediatrics

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