Samson A Odukoya1,2, Jagidesa Moodley3, Thajasvarie Naicker4. 1. Optics and Imaging Center, Doris Duke Medical Research Institute, College of Health Sciences, University of Kwa-Zulu Natal, Durban, South Africa. ayoodukoya75@gmail.com. 2. Department of Anatomy and Cell Biology, College of Health Sciences, Obafemi Awolowo University, Ife, Nigeria. ayoodukoya75@gmail.com. 3. Department of Obstetrics and Gynaecology, College of Health Sciences, University of Kwa-Zulu Natal, Durban, South Africa. 4. Optics and Imaging Center, Doris Duke Medical Research Institute, College of Health Sciences, University of Kwa-Zulu Natal, Durban, South Africa.
Abstract
PURPOSE OF REVIEW: Cardiovascular diseases (CVD), including pre-eclampsia (PE), remain the major cause of death and morbidity in women. This review elucidates the current knowledge, state of research and scientific information available on the post-event implications and complications of PE regarding maternal and foetal cardiovascular health. Does PE expose, predispose or aggravate a predilection to maternal and foetal CVD later in life? RECENT FINDINGS: Women with a history of PE are reported to have stiffer arteries and are more likely to develop cardiovascular problems with time, especially aortic stenosis and mitral regurgitation, which were not hitherto linked with hypertensive pregnancy. Foetal cells persistence in the mother long after pregnancy, now clearly established in the lungs of mice postpartum, is suggested to portend an overexpression of STOX1, which may potentiate later life CVD. Moreover, the conventional theories of in utero stress and developmental reprogramming may not adequately explain the risk of later life CVD predilection in offspring born to mothers with pre-eclampsia as recent data has shown that siblings of offspring born from pre-eclamptic pregnancies are also at higher risk of hypertension later in life, irrespective of whether subsequent pregnancies were pre-eclamptic or normotensive. The mechanism involved in adverse cardiovascular outcome in offspring of pre-eclamptic pregnancies is most likely an intricate interaction of foetal programming, environmental and genetic factors. In light of available evidence, the question of whether PE is just a pointer or predisposing factor to maternal development of CVDs in later life begs for answers to facilitate definitive clinical solutions and preventive approaches.
PURPOSE OF REVIEW: Cardiovascular diseases (CVD), including pre-eclampsia (PE), remain the major cause of death and morbidity in women. This review elucidates the current knowledge, state of research and scientific information available on the post-event implications and complications of PE regarding maternal and foetal cardiovascular health. Does PE expose, predispose or aggravate a predilection to maternal and foetal CVD later in life? RECENT FINDINGS:Women with a history of PE are reported to have stiffer arteries and are more likely to develop cardiovascular problems with time, especially aortic stenosis and mitral regurgitation, which were not hitherto linked with hypertensive pregnancy. Foetal cells persistence in the mother long after pregnancy, now clearly established in the lungs of mice postpartum, is suggested to portend an overexpression of STOX1, which may potentiate later life CVD. Moreover, the conventional theories of in utero stress and developmental reprogramming may not adequately explain the risk of later life CVD predilection in offspring born to mothers with pre-eclampsia as recent data has shown that siblings of offspring born from pre-eclamptic pregnancies are also at higher risk of hypertension later in life, irrespective of whether subsequent pregnancies were pre-eclamptic or normotensive. The mechanism involved in adverse cardiovascular outcome in offspring of pre-eclamptic pregnancies is most likely an intricate interaction of foetal programming, environmental and genetic factors. In light of available evidence, the question of whether PE is just a pointer or predisposing factor to maternal development of CVDs in later life begs for answers to facilitate definitive clinical solutions and preventive approaches.
Authors: Cees B M Oudejans; Marie van Dijk; Marjet Oosterkamp; Augusta Lachmeijer; Marinus A Blankenstein Journal: Hum Genet Date: 2006-09-26 Impact factor: 4.132
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