title: Maternal nonpregnant vascular function correlates with subsequent fetal growth.
abstract: OBJECTIVE
  Evidence is accumulating that fetal growth is influenced by preexisting maternal disorder(s) hampering endothelial function. We tested the hypothesis that in nonpregnant normotensive, formerly preeclamptic women, vascular function predicts the development of fetal growth restriction.
  
  
  METHODS
  In 60 formerly preeclamptic women, we measured central hemodynamic and vascular and clotting function mid follicular phase during the menstrual cycle. Inclusion for final analysis required besides normotension, a subsequent singleton pregnancy, established within 1 year after the prepregnant evaluation and ongoing beyond 16 weeks' gestation. In the ongoing pregnancy we determined birth weight and birth weight percentile.
  
  
  RESULTS
  Among 60 formerly preeclamptic women, 45 (75%) were normotensive. Thirty-one (69%) participants succeeded in establishing an ongoing pregnancy within 1 year and were included for final analysis. Of the 31 subsequent pregnancies, 8 (26%) were complicated by fetal growth restriction. Prepregnant left and right uterine artery pulsatility index (PI) correlated inversely with carotid artery compliance ( r = 0.57, P = .005, r = 0.62, P = .002) and venous compliance ( r = 0.49, P = .02 and r = 0.45, P = .04, respectively). The latter, in turn, correlates with plasma volume ( r = 0.63, P = .001) and total peripheral vascular resistance index ( r = -0.45, P = .02). Finally, prepregnant left and right uterine artery PI correlated inversely with subsequent achieved fetal growth ( r = -0.68, P < .0001 and r = -0.58, P = .001, respectively).
  
  
  CONCLUSIONS
  In nonpregnant normotensive, formerly preeclamptic women, an elevated uterine artery PI predisposes to subsequent restriction in fetal growth.
authors.affiliation: Department of Obstetrics and Gynecology,University Hospital Maastricht and University Hospital Nijmegen, Nijmegen, The Netherlands. m.spaanderman@obgyn.umcn.nl
authors.forename: Marc E A
authors.initials: ME
authors.lastname: Spaanderman
authors.forename: Christine
authors.initials: C
authors.lastname: Willekes
authors.forename: Arnold P G
authors.initials: AP
authors.lastname: Hoeks
authors.forename: Timo H A
authors.initials: TH
authors.lastname: Ekhart
authors.forename: Robert
authors.initials: R
authors.lastname: Aardenburg
authors.forename: Dorette A
authors.initials: DA
authors.lastname: Courtar
authors.forename: Hugo W F
authors.initials: HW
authors.lastname: Van Eijndhoven
authors.forename: Louis L H
authors.initials: LL
authors.lastname: Peeters
mesh_terms: D000328:Adult; D001794:Blood Pressure; D001808:Blood Vessels / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology*; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D010953:Plasma Volume; D011225:Pre-Eclampsia / Q000150:complications*; D011247:Pregnancy; D014655:Vascular Resistance