Fetal progamming of cardiovascular dysfunction in intrauterine growth restriction.

• Autores: Fátima Crispi Brillas
• Directores de la Tesis: Eduardo Gratacós Solsona (dir. tes.)
• Lectura: En la Universitat de Barcelona ( España ) en 2009
• Idioma: inglés
• Tribunal Calificador de la Tesis: Torvid Kiserud (presid.), Josep M. Martínez Crespo (secret.), Jan Deprest (voc.)
• Materias:
  • Ciencias médicas
    • Ciencias clínicas
      • Ginecología
    • Medicina interna
      • Cardiología
    • Patología
      • Patología cardiovascular
• Enlaces
  • Tesis en acceso abierto en:  TDX  Dipòsit Digital de la UB 
• Resumen

  • BACKGROUNDFetal growth restriction (FGR), with a prevalence of 5-10% in newborns, is associated with increased cardiovascular mortality in adulthood, but the pathophysiological links of this relationship are only partially understood. The main hypothesis of this thesis was that FGR induces primary cardiac dysfunction and remodelling in utero that persists postnatally and leads to increased cardiovascular risk in adulthood. METHODSCardiovascular function was assessed in a cohort of FGR fetuses and correlated to the severity stages of FGR, presence of preeclampsia and also perinatal data in order to evaluate its potential utility in the clinical management of these fetuses. Finally, cardiac and vascular function was also assessed in childhood.RESULTSIn utero, FGR fetuses showed signs of subclinical cardiac dysfunction measured by echocardiography (increased E/A ratios and isovolumic times with normal cardiac output) from early stages. Cardiac dysfunction deteriorated further with the progression of fetal compromise, together with the appearance of biochemical signs of cell damage (increased heart-fatty acid binding protein concentrations in cord blood). Preeclampsia per se was not associated to cardiac function in FGR fetuses. Cardiac function parameters, such as ductus venosus and myocardial performance index, were independently associated with perinatal death in preterm FGR. Therefore, a combination cardiac parameters may be useful in the clinical management of preterm FGR by stratifying the estimated probability of death. Children with FGR showed changes in cardiac shape (more globular morphology), subclinical cardiac dysfunction (increased heart rate and reduced stroke volume and myocardial peak velocities) and vascular remodelling (increased blood pressure and carotid intima-media thickness). CONCLUSIONSFGR present cardiovascular dysfunction in utero that persists postnatlly. These findings suggest that fetal growth restriction induces primary cardiac changes which could explain the increased predisposition to cardiovascular disease in adult life. Given its high prevalence in the general population, this might have to be taken into account in assessing cardiovascular risk factors and treatment.