title: Ventriculovascular physiology of the growth-restricted fetus.
abstract: OBJECTIVE
  To examine the mechanisms by which intrauterine growth restriction may influence later cardiovascular risk by comparing the ventriculovascular physiology of gestational age- and weight-matched growth-restricted and normal fetuses.
  
  
  METHODS
  A prospective longitudinal observational study of 20 normal fetuses studied from 20 weeks to term at monthly intervals was compared with a growth-restricted cohort examined in the interval between diagnosis and delivery. The last values before delivery of the growth-restricted cohort were compared with the normal cohort in two analyses matched for weight and for gestation. Arterial and venous vessel wall physiology and aortic pulse wave velocity were examined longitudinally in the thoracic descending aorta and inferior vena cava using an ultrasonic phase-locked echo-tracking system. Serial echocardiographic examinations were performed assessing structure, ventricular dimensions, function and Doppler flows.
  
  
  RESULTS
  There was a linear increase in cardiac preload and relative pulse amplitude in the inferior vena cava with gestation. In normal fetuses, the aortic pulse wave velocity, maximum incremental and late decremental velocities increased with gestation whilst the relative pulse amplitude decreased reflecting falling distal impedance. In both age- and weight-matched analyses, the growth-restricted fetuses showed significantly reduced values reflecting the chronic fetal ventriculovascular responses to increased placental impedance. Pulse wave velocity increased with gestation and was significantly less in the growth-restricted cohort.
  
  
  CONCLUSIONS
  Growth restriction is associated with abnormal ventriculovascular physiology that represents a successful adaptive response to raised placental impedance and reduction in wall stress as evidenced by the lower fetal pulse wave velocity in growth-restricted fetuses. However, whilst fetal adaptive mechanisms may aid survival they may result in cerebral and vascular abnormalities that prejudice later cardiovascular health.
authors.affiliation: Division of Paediatrics, Obstetrics & Gynaecology, Imperial College School of Medicine, Royal Brompton and Queen Charlotte's Hospitals, London, UK. H.Gardiner@rbh.nthames.nhs.uk
authors.forename: H
authors.initials: H
authors.lastname: Gardiner
authors.forename: J
authors.initials: J
authors.lastname: Brodszki
authors.forename: K
authors.initials: K
authors.lastname: Marsál
mesh_terms: D001013:Aorta, Thoracic / Q000000981:diagnostic imaging* / Q000196:embryology* / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D011247:Pregnancy; D011446:Prospective Studies; D011674:Pulse; D012039:Regional Blood Flow; D018615:Ultrasonography, Doppler, Color; D016216:Ultrasonography, Prenatal; D014682:Vena Cava, Inferior / Q000000981:diagnostic imaging* / Q000196:embryology* / Q000502:physiology*