Pre-eclampsia: contribution of maternal constitutional factors and the consequences for cardiovascular health.
1. Pre-eclampsia is a serious complication of pregnancy that is potentially life threatening for both the mother and baby. It encompasses a number of abnormalities that may be present in other clinical conditions. 2. A placenta is essential for the development of pre-eclampsia and can be important in the pathogenesis of pre-eclampsia. Normal pregnancy is associated with remodelling of the maternal spiral arteries, which deliver blood to the placental villous space. Remodelling involves invasion by placental cytotrophoblasts that cause the maternal spiral arteries to lose their smooth muscle and become capacitance vessels; this process, known as placentation, is complete by 20 weeks of pregnancy. Poor placentation is associated with small-for-gestational-age fetuses and some cases of pre-eclampsia. It is thought that poor placentation can result in a hypoxic placenta that releases 'toxic substances' into the maternal circulation, contributing to the maternal syndrome. A number of candidate 'toxic substances' have been proposed, but none is universally raised in pre-eclampsia. 3. Although the placenta is necessary for the development of pre-eclampsia, the extent to which placental abnormalities contribute to the condition varies. It is becoming apparent that maternal constitutional factors may also be important in this syndrome. Underlying hypertension, diabetes and obesity strongly predispose to pre-eclampsia. However, a continuum of risk may exist for blood pressure, bodyweight, glucose and lipids, which, in combination with each other and some degree of placental abnormalities, may lead to the development of pre-eclampsia. 4. The present review will focus on the maternal constitutional factors that define the metabolic syndrome and examine their contribution to pre-eclampsia and the long-term consequences for cardiovascular health.
Barden
Anne
A
School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia. anne.barden@uwa.edu.au
D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000150:complications; D002320:Cardiovascular Physiological Phenomena; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008431:Maternal-Fetal Exchange / Q000502:physiology; D018384:Oxidative Stress; D010920:Placenta / Q000502:physiology; D011225:Pre-Eclampsia / Q000209:etiology*; D011247:Pregnancy; D012307:Risk Factors
D015415:Biomarkers; D008055:Lipids