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  • Journal of Developmental Origins of Health and Disease, Volume 2, Issue 4
  • August 2011, pp. 218-225

Aortic growth arrest after preterm birth: a lasting structural change of the vascular tree

  • U. Schubert (a1), M. Müller (a2), A.-K. Edstedt Bonamy (a3), H. Abdul-Khaliq (a2) and M. Norman (a1)
  • DOI: http://dx.doi.org/10.1017/S2040174411000274
  • Published online: 01 August 2011
Abstract

Young people who are born very preterm exhibit a narrower arterial tree as compared with people born at term. We hypothesized that such arterial narrowing occurs as a direct result of premature birth. The aim of this study was to compare aortic and carotid artery growth in infants born preterm and at term. Observational and longitudinal cohort study of 50 infants (21 born very preterm, all appropriate for gestational age, 29 controls born at term) was conducted. Diameters of the upper abdominal aorta and common carotid artery were measured with ultrasonography at three months before term, at term and three months after term-equivalent age. At the first assessment, the aortic end-diastolic diameter (aEDD) was slightly larger in very preterm infants as compared with fetal dimensions. Fetal aortic EDD increased by 2.6 mm during the third trimester, whereas very preterm infants exhibited 0.9 mm increase in aEDD during the same developmental period (P < 0.001 for group difference). During the following 3-month period, aortic growth continued unchanged (+0.9 mm) in very preterm infants, whereas postnatal growth in term controls slowed down to +1.3 mm (P < 0.001 v. fetal aortic growth). At the final examination, aEDD was 22% and carotid artery EDD was 14% narrower in infants born preterm compared with controls, also after adjusting for current weight (P < 0.01). Aortic and carotid artery growth is impaired after very preterm birth, resulting in arterial narrowing. Arterial growth failure may be a generalized vascular phenomenon after preterm birth, with implications for cardiovascular morbidity in later life.

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Corresponding author
*Address for correspondence: U. Schubert, Neonatal Research Unit B79, Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Huddinge, S-141 86 Stockholm, Sweden. (Email ulfschubert@gmx.de)
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  • EISSN: 2040-1752
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