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Arnott C, Skilton MR, Ruohonen S, et al. Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study. Open Heart. 2015;2(1):e000265doi: 10.1136/openhrt-2015-000265.
Arnott, C., Skilton, M. R., Ruohonen, S., Juonala, M., Viikari, J. S., Kähönen, M., Lehtimäki, T., Laitinen, T., Celermajer, D. S., & Raitakari, O. T. (2015). Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study. Open heart, 2(1), e000265. https://doi.org/10.1136/openhrt-2015-000265
Arnott, Clare, et al. "Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study." Open heart vol. 2,1 (2015): e000265. doi: https://doi.org/10.1136/openhrt-2015-000265
Arnott C, Skilton MR, Ruohonen S, Juonala M, Viikari JS, Kähönen M, Lehtimäki T, Laitinen T, Celermajer DS, Raitakari OT. Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study. Open Heart. 2015 Aug 28;2(1):e000265. doi: 10.1136/openhrt-2015-000265. eCollection 2015. PMID: 26339495; PMCID: PMC4555072.
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Open Heart. 2015 Aug 28;2(1):e000265. doi: 10.1136/openhrt-2015-000265. eCollection 2015.

Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study.

Open heart

Clare Arnott, Michael R Skilton, Saku Ruohonen, Markus Juonala, Jorma S A Viikari, Mika Kähönen, Terho Lehtimäki, Tomi Laitinen, David S Celermajer, Olli T Raitakari

Affiliations

  1. Faculty of Medicine , University of Sydney , Sydney , Australia ; Department of Cardiology , Royal Prince Alfred Hospital , Sydney , Australia ; Department of Cardiology , Prince of Wales Hospital , Sydney , Australia.
  2. Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, University of Sydney , Sydney , Australia.
  3. Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku , Turku , Finland.
  4. Division of Medicine , Turku University Hospital , Turku , Finland ; Department of Medicine , University of Turku, Finland and Murdoch Children's Research Institute , Melbourne , Australia.
  5. Department of Medicine, University of Turku and Division of Medicine , Turku University Hospital , Turku , Finland.
  6. Department of Clinical Physiology , University of Tampere and Tampere University Hospital , Tampere , Finland.
  7. Department of Clinical Chemistry , Fimlab Laboratories and University of Tampere School of Medicine , Tampere , Finland.
  8. Department of Clinical Physiology and Nuclear Medicine , Kuopio University Hospital and University of Eastern Finland , Finland.
  9. Department of Cardiology , Royal Prince Alfred Hospital , Sydney , Australia ; Faculty of Medicine , University of Sydney , Sydney , Australia.
  10. Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku , Turku , Finland ; Department of Clinical Physiology and Nuclear Medicine , Turku University Hospital , Turku , Finland.

PMID: 26339495 PMCID: PMC4555072 DOI: 10.1136/openhrt-2015-000265

Abstract

BACKGROUND AND OBJECTIVES: Impaired fetal growth is associated with increased cardiovascular morbidity and mortality in adulthood. We sought to determine whether adults born with intrauterine growth restriction have primary maladaptive changes in cardiac structure.

METHODS: Study participants were adults (34-49 years) who attended the 31-year follow-up of the Cardiovascular Risk in Young Finns Study (longitudinal cohort). Transthoracic echocardiograms and demographic and cardiovascular risk surveys were completed for 157 adults born small for gestational age (SGA, birth weight <10th population centile) and 627 born average for gestational age (average for gestational age (AGA), birth weight 50th-90th population centile).

RESULTS: Those born growth restricted had subtly enlarged hearts with indexed left ventricular (LV) end-systolic and end-diastolic diameters slightly greater in the SGA individuals than the AGA group (LVESD 18.7 mm/m(2) SGA vs 18.1 mm/m(2) AGA, p<0.01; LVEDD 27.5 mm/m(2) SGA vs 26.6 mm/m(2) AGA, p<0.01); LV base-to-apex length (47.4 mm/m(2) SGA vs 46.0 mm/m(2) AGA, p<0.01); LV basal diameter (26.4 mm/m(2) SGA vs 25.7 mm/m(2) AGA, p<0.01); and right ventricular base-to-apex length (40.1 mm/m(2) SGA vs 39.2 mm/m(2) AGA, p=0.02). LV stroke volume was greater in those born AGA (74.5 mL SGA vs 78.8 mL AGA, p<0.01), with no significant difference in cardiac output (5 L/min SGA vs 5.2 L/min AGA, p=0.06), heart rate, diastolic indices or sphericity index.

CONCLUSIONS: Adults born SGA have some statistically significant but subtle changes in cardiac structure and function, which are less marked than have been described in childhood, and are unlikely to play a pathogenic role in their elevated cardiovascular risk.

Keywords: CARDIAC FUNCTION

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