Placental ischemia and cardiovascular dysfunction in preeclampsia and beyond: Making the connections

Jeffrey S. Gilbert, Mark J. Nijland, Penny Knoblich

Research output: Contribution to journalReview articlepeer-review

30 Scopus citations


Hypertensive disorders of pregnancy continue to be a significant source of maternal and fetal morbidity and mortality, and recent evidence suggests that the incidence of preeclampsia (PE) is increasing Recent epidemiological studies indicate that the effects of PE may persist long after pregnancy, in both the mother and the offspring, as increased incidence of cardiovascular disease. The last decade has produced new insights into the pathogenesis of PE. The initiating event in PE appears to be impaired placental perfusion and subsequent placental ischemia, which results in the elaboration of numerous factors. Factors such as soluble fms-like tyrosine kinase-1, soluble endoglin and the angiotensin II type-1 receptor autoantibodies contribute to maternal endothelial and cardiovascular dysfunction, marked by increased reactive oxygen species and decreased bioavailable VEGF, nitric oxide and prostacyclin. However, the importance of the various endothelial and humoral factors that mediate these changes during PE remain to be elucidated.

Original languageEnglish (US)
Pages (from-to)1367-1377
Number of pages11
JournalExpert Review of Cardiovascular Therapy
Issue number10
StatePublished - Nov 2008


  • Cardiac
  • Cytokines
  • Pregnancy
  • VEGF

ASJC Scopus subject areas

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine


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