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Fibrinogen and factor VII in male neonates

P van der Salm1, H M Ubachs, J W van Wersch

  • 1Department of Gynaecology, De Wever Hospital, Heerlen, The Netherlands.

Thrombosis Research
|February 15, 1994
PubMed

Insights

Early life growth restriction may not program male neonates for adult cardiovascular disease via fibrinogen or factor VII. Fetal growth indicators like placenta/birth weight ratio showed limited correlation with these clotting factors.

Area of Science:

  • Cardiovascular disease research
  • Neonatal health
  • Hemostasis and thrombosis

Background:

  • Studies link retarded fetal growth to adult male cardiovascular disease.
  • Associations between hemostatic variables (fibrinogen, factor VII) and placenta/birth weight ratio are implicated.
  • Clotting factor levels can be influenced by various factors throughout life.

Purpose of the Study:

  • To investigate the relationship between fetal growth and neonatal hemostatic variables.
  • To determine if fibrinogen and factor VII levels in cord blood are associated with fetal growth indicators.
  • To assess the potential programming of adult cardiovascular disease risk in males based on early life factors.

Main Methods:

  • Measurement of fibrinogen and clotting factor VII levels in cord blood of male neonates.
  • Calculation and analysis of the placenta/birth weight ratio.
  • Correlation analysis between hemostatic variables and fetal growth indicators.

Main Results:

  • The placenta/birth weight ratio did not correlate with birth weight for gestational age.
  • Placenta/birth weight ratio was a minor indicator of overall fetal growth.
  • No significant association found between fetal growth indicators and neonatal fibrinogen or factor VII levels.

Conclusions:

  • Fetal growth, as indicated by the placenta/birth weight ratio, does not appear to program male neonates for adult cardiovascular disease through elevated fibrinogen or factor VII levels.
  • The proposed link between early growth and adult cardiovascular disease via these specific hemostatic markers in males is unlikely.
  • Further research may be needed to explore other potential pathways linking early life factors to cardiovascular health outcomes.

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