title: Cardiac dysfunction and cell damage across clinical stages of severity in growth-restricted fetuses.
abstract: OBJECTIVE
  The purpose of this study was to assess cardiac function and cell damage in intrauterine growth-restricted (IUGR) fetuses across clinical Doppler stages of deterioration.
  
  
  METHODS
  One hundred twenty appropriate-for-gestational-age and 81 IUGR fetuses were classified in stages 1/2/3 according umbilical artery present/absent/reversed end-diastolic blood flow, respectively. Cardiac function was assessed by modified-myocardial performance index, early-to-late diastolic filling ratios, cardiac output, and cord blood B-type natriuretic peptide; myocardial cell damage was assessed by heart fatty acid-binding protein, troponin-I, and high-sensitivity C-reactive protein.
  
  
  RESULTS
  Modified-myocardial performance index, blood B-type natriuretic peptide, and early-to-late diastolic filling ratios were increased in a stage-dependent manner in IUGR fetuses, compared with appropriate-for-gestational-age fetuses. Heart fatty acid-binding protein levels were higher in IUGR fetuses at stage 3, compared with control fetuses. Cardiac output, troponin-I, and high-sensitivity C-reactive protein did not increase in IUGR fetuses at any stage.
  
  
  CONCLUSIONS
  IUGR fetuses showed signs of cardiac dysfunction from early stages. Cardiac dysfunction deteriorates further with the progression of fetal compromise, together with the appearance of biochemical signs of cell damage.
authors.affiliation: Department of Maternal-Fetal Medicine, Institut Clínic de Ginecologia, Obstetrícia i Neonatologia, Instituto de Salud Carlos III, Hospital Clinic-University of Barcelona, Barcelona, Spain.
authors.forename: Fatima
authors.initials: F
authors.lastname: Crispi
authors.forename: Edgar
authors.initials: E
authors.lastname: Hernandez-Andrade
authors.forename: Maurice M A L
authors.initials: MM
authors.lastname: Pelsers
authors.forename: Walter
authors.initials: W
authors.lastname: Plasencia
authors.forename: Jesus Andres
authors.initials: JA
authors.lastname: Benavides-Serralde
authors.forename: Elisenda
authors.initials: E
authors.lastname: Eixarch
authors.forename: Ferdinand
authors.initials: F
authors.lastname: Le Noble
authors.forename: Asif
authors.initials: A
authors.lastname: Ahmed
authors.forename: Jan F C
authors.initials: JF
authors.lastname: Glatz
authors.forename: Kypros H
authors.initials: KH
authors.lastname: Nicolaides
authors.forename: Eduard
authors.initials: E
authors.lastname: Gratacos
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002302:Cardiac Output / Q000502:physiology; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005317:Fetal Growth Retardation / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D005318:Fetal Heart / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D011247:Pregnancy; D011673:Pulsatile Flow; D012039:Regional Blood Flow; D012307:Risk Factors; D012907:Smoking / Q000453:epidemiology; D019210:Troponin I / Q000097:blood; D018608:Ultrasonography, Doppler; D016216:Ultrasonography, Prenatal; D014469:Umbilical Arteries / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D019210:Troponin I; D002097:C-Reactive Protein