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.
Keywords cardiac; cytokines; pregnancy; VEGF
Clinical significance of the hypertensive disorders of pregnancyPreeclampsia (PE) is a pregnancy-specific syndrome characterized by new-onset hypertension and proteinuria manifesting after 20 weeks of gestation, which may progress and cause injury to the blood vessels of major organs, such as the liver and the brain. The hepatic and neuro logical complications of PE make it a potentially deadly disease, especially when tertiary obstetrical care is lacking. Consequently, PE remains a considerable obstetric problem and a significant source of maternal and neonatal morbidity and mortality [1].