Published online Nov 10, 2015. doi: 10.5317/wjog.v4.i4.77
Peer-review started: June 3, 2015
First decision: August 4, 2015
Revised: September 3, 2015
Accepted: October 1, 2015
Article in press: October 8, 2015
Published online: November 10, 2015
Processing time: 164 Days and 23 Hours
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.
Core tip: The conventional paradigm is that preeclampsia (PE) is solely due to placental dysfunction. However not all cases of placental dysfunction result in the syndrome of PE. Equally, placental dysfunction - as evidenced by impaired uterine artery Doppler indices, low birth weight and abnormal histology - is not always present in PE. Therefore, the heterogeneity observed in PE cannot be solely explained by placental dysfunction. There is now strong evidence supporting the role of the maternal cardiovascular system in PE. In this mini-review, we evaluate the evidence supporting a dual aetiology of PE, involving both the placenta and the maternal cardiovascular system.