title: First-trimester fetuses with increased nuchal translucency do not show altered intracardiac flow velocities.
abstract: OBJECTIVE
  To study intracardiac flow velocities in first-trimester fetuses with normal nuchal translucency thickness (NT) and those with increased NT.
  
  
  METHODS
  Ultrasound examinations were performed in 85 normal fetuses and 45 fetuses with NT > 95(th) percentile. Follow-up was complete and postmortem examination was performed on terminated pregnancies. Flow velocities during the early (e-wave) and late (a-wave) peaks across the tricuspid and mitral valves were measured and compared, using multilevel analysis, between the fetuses with normal and those with increased NT. In the group with increased NT, fetuses with and without a heart defect irrespective of the karyotype were compared, and in this group, euploid and aneuploid fetuses were compared, irrespective of the presence of a heart defect.
  
  
  RESULTS
  No difference in intracardiac flow velocities was found between fetuses with normal and those with increased NT. Within the group of fetuses with increased NT, there was no difference between the fetuses with and without a cardiac defect. However, comparison of aneuploid with euploid fetuses within the group with increased NT showed that both the e-wave and a-wave peaks were decreased significantly by 3.03 cm/s and 5.95 cm/s, respectively, across the tricuspid valve, and by 3.47 cm/s and 5.92 cm/s, respectively, across the mitral valve (P < 0.05). The most common cardiac malformations were septal defects.
  
  
  CONCLUSIONS
  There is no difference in intracardiac blood flow velocities between normal fetuses and those with increased NT. This contradicts the theory that NT is caused by impaired atrial contraction or cardiac failure. In fetuses with increased NT, those with aneuploidy show a decreased e-wave and a-wave compared with euploid fetuses. This cannot, however, be explained by the presence of cardiac defects, because there is no difference between fetuses with and without a cardiac defect. Therefore, we hypothesize that the relationship between enlarged NT and cardiac defects can only be explained by a developmental process that coexists at this period of gestation and is linked to cardiovascular development.
authors.affiliation: Department of Obstetrics and Gynecology, VU University Medical Center, Amsterdam, The Netherlands. MC.Haak@vumc.nl
authors.forename: M C
authors.initials: MC
authors.lastname: Haak
authors.forename: J W R
authors.initials: JW
authors.lastname: Twisk
authors.forename: M M
authors.initials: MM
authors.lastname: Bartelings
authors.forename: A C
authors.initials: AC
authors.lastname: Gittenberger-de Groot
authors.forename: J M G
authors.initials: JM
authors.lastname: van Vugt
mesh_terms: D001783:Blood Flow Velocity; D016022:Case-Control Studies; D025063:Chromosome Disorders / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005260:Female; D047109:Fetal Development; D005315:Fetal Diseases / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005318:Fetal Heart / Q000000981:diagnostic imaging*; D005500:Follow-Up Studies; D006801:Humans; D007621:Karyotyping; D008943:Mitral Valve; D048208:Nuchal Translucency Measurement; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D012039:Regional Blood Flow; D014261:Tricuspid Valve