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Preeclampsia(PE)is a pregnancy-specific syndrome,complicating 2%-8% of pregnancies.PE is a major cause of maternal mortality throughout the world with 60000 maternal deaths attributed to hypertensive disorders of pregnancy.PE also results in fetal morbidity due to prematurity and fetal growth restriction.The precise aetiology of PE remains an enigma with multiple theories including a combination of environmental,immunological and genetic factors.The conventional and leading hypotheses for the initial insult in PE is inadequate trophoblast invasion which is thought to result in incomplete remodelling of uterine spiral arteries leading to placental ischaemia,hypoxia and thus oxidative stress.The significant heterogeneity observed in pre-eclampsia cannot be solely explained by the placental model alone.Herein we critically evaluate the clinical(risk factors,placental blood flow and biomarkers)and pathological(genetic,molecular,histological)correlates for PE.Furthermore,we discuss the role played by the(dysfunctional)maternal cardiovascular system in the aetiology of PE.We review the evidence that demonstrates a role for both the placenta and the cardiovascular system in early-and late-onset PE and highlight some of the key differences between these two distinct disease entities.
Preeclampsia (PE) is a pregnancy-specific syndrome, complicating 2% -8% of pregnancies. PE is a major cause of maternal mortality throughout the world with 60000 maternal deaths attributed to hypertensive disorders of pregnancy. PE also results in fetal morbidity due to prematurity and fetal growth restriction. The precise aetiology of PE remains an enigma with multiple claims including a combination of environmental, immunological and genetic factors. the conventional and leading hypotheses for the initial insult in PE is inadequate trophoblast invasion which is thought to result in incomplete remodeling of uterine spiral arteries leading to placental ischaemia, hypoxia and thus oxidative stress. The significant heterogeneity observed in pre-eclampsia can not be solely solely explained by the placental model alone. Herein we critically evaluate the clinical (risk factors, placental blood flow and biomarkers) and pathological (genetic, molecular, histological) correlates for PE. Futurertherm, we discuss the role played by the (dysfunctional) maternal cardiovascular system in the aetiology of PE.We review the evidence that demonstrated a role for both the placenta and the cardiovascular system in early-and late-onset PE and highlight some of the key differences between these two distinct disease entities.