Preeclampsia doubles the risk of venous thromboembolic events, stroke, and ischemic heart disease in women, driven by defective uteroplacental vascular remodeling and systemic inflammation.
Understanding the molecular pathways linking defective uteroplacental vascular remodeling in preeclampsia to systemic inflammation and angiogenic imbalance is crucial for developing strategies to prevent long-term cardiovascular disease in affected women.
Preeclampsia is a complex hypertensive disorder in pregnancy which can be lethal and is responsible for more than 70,000 maternal deaths worldwide every year. Besides the higher risk of unfavorable obstetric outcomes in women with preeclampsia, another crucial aspect that needs to be considered is the association between preeclampsia and the postpartum cardiovascular health of the mother. Currently, preeclampsia is classified as one of the major risk factors of cardiovascular disease (CVD) in women, which doubles the risk of venous thromboembolic events, stroke, and ischemic heart disease. In order to comprehend the pathophysiology behind the linkage between preeclampsia and the development of postpartum CVD, a thorough understanding of the abnormal uteroplacental vascular remodeling in preeclampsia is essential. Therefore, this review aims to summarize the current knowledge of the defective process of spiral artery remodeling in preeclampsia and how the resulting placental damage leads to excessive angiogenic imbalance and systemic inflammation in long term CVD. Key molecular factors in the pathway-including novel findings of microRNAs-will be discussed with suggestions of future management strategies of preventing CVD in women with a history of preeclampsia.
Hong et al. (Mon,) conducted a review in Preeclampsia. Preeclampsia was evaluated. Preeclampsia doubles the risk of venous thromboembolic events, stroke, and ischemic heart disease in women, driven by defective uteroplacental vascular remodeling and systemic inflammation.