Heyansh Kreiselukas*
Preeclampsia remains a significant cause of maternal and perinatal morbidity and mortality globally, characterized by hypertension and proteinuria arising after 20 weeks of gestation. This comprehensive review explores the intricate interplay between perinatal cardiovascular features and alterations in the Renin-Angiotensin System (RAS) in maternal preeclampsia. Preeclamptic pregnancies are marked by systemic vascular dysfunction, including impaired vasodilation and increased vascular resistance, which contribute to elevated maternal blood pressure and compromised placental perfusion. Mechanistically, dysregulation of the RAS, with heightened angiotensin II levels and altered expression of angiotensin receptors, plays a pivotal role in the pathophysiology of preeclampsia. The review synthesizes current evidence on the association between maternal preeclampsia and fetal programming of cardiovascular health, emphasizing the role of RAS dysregulation in shaping perinatal outcomes. Understanding these complex interactions is crucial for developing targeted interventions aimed at mitigating the impact of preeclampsia on maternal and fetal cardiovascular health, thereby improving both short-term and long-term pregnancy outcomes.
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