Myocardial function in offspring 5–8 years after pregnancy complicated by preeclampsia
Introduction
The foetal origin hypothesis; “DOHaD — Developmental Origin of Health and Disease” has evolved after Barker identified a relationship between birth weight and increased risk of arterial hypertension, carotid arteriosclerosis and mortality by coronary heart disease or stroke in adulthood more than 20 years ago [1]. The “Barker hypothesis” suggested that cardiovascular disease and type 2 diabetes arise through a series of interactions between environmental influences and the pathways of development that precede them [2]. Not only foetal undergrowth and placental inadequacy [2], [3], but also increased birth weight [4] are factors associated with later metabolic diseases. The relationship is likely to be U-shaped, with increased risk at both ends of the birth-weight curve [5].
Preeclampsia (PE) and diabetes mellitus (DM) during pregnancy share many pathophysiological features [6], [7], resulting in changes in metabolism and hormones that may lead to alterations in tissue and organ development later in life [8]. Epigenetic mechanisms may cause long-term functional and structural changes [9], [10].
Adequate placental vascular growth is important for normal foetal cardiovascular development [11]. The foetal heart must provide sufficient cardiac output to the different organs throughout gestation, and the fraction of the foetal cardiac output circulating to the placenta remains nearly constant through gestation [12]. Increased impedance of the placental flow may lead to adaptations in the foetal heart due to the increased resistance and afterload [11]. The exact mechanisms underlying the placental origins of adult cardiovascular disease are not known, nor at which age may the diseases be of importance.
Global myocardial function has been measured with ultrasound by fractional shortening [13], [14]. New indices, directly measuring the motion and deformation of the myocardial walls, may be more sensitive for measuring both global and regional myocardial function. These include annular velocities and annular displacement, as well as strain and strain rate that can be obtained by analysis of tissue Doppler images (TDI). The aim of this study was to investigate whether altered myocardial function assessed by tissue Doppler echocardiography could be detected already at the age of 5–8 years in offspring after pregnancies complicated by PE, DM type 1 and gestational diabetes mellitus (GDM).
Section snippets
Study population
In the years 2001–2004, 176 pregnant women with PE, DM type 1, GDM and a control group — i.e. uncomplicated pregnancies delivered at Oslo University Hospital, were enrolled prior to delivery in a pregnancy biobank study, described previously [15]. The women signed a written consent for the pregnancy study and also accepted being contacted again regarding participation in later studies. In 2008, we contacted 149 of these women again by postal invitation for recruitment to a study of both mother
Demographic data
Table 1 shows the demographic data. Some of these have been presented previously [16]. Most of the children in the PE group were prematurely delivered (87% prior to gestational age week 37 and 65% prior to week 34), as compared to the diabetic groups (15% prior to week 37 and 10% prior to week 34) and none in the control group. In the PE group, 57% of the children were born small for gestational age (defined here as below the 10th percentile), compared to 10% in the diabetic groups and none in
Discussion
In this study, we have focused on the global systolic and diastolic longitudinal myocardial function of the left ventricular lateral wall, septum and right ventricular lateral wall. With conventional ultrasound examinations, no differences were found between the offspring of PE, DM type 1, GDM and control group, except for the end-diastolic length of the left ventricle when comparing the PE group with all the three other groups combined. LV length seems to be more sensitive measure of LV size
Acknowledgment
We thank Professor Leiv Sandvik, Centre for Clinical Research, Oslo University Hospital, Ullevål, for valuable advice with the statistics. We are grateful for the administrative and technical help of CHASE coordinator Marie Jeanette Le for contribution to recruitment and follow-up of patients.
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2020, American Journal of Obstetrics and GynecologyCitation Excerpt :However, this association became statistically insignificant in the sex-specific analysis and was not present in the sibling analyses. Our findings are consistent with those of previously published studies on the association between in utero exposure to HDP and cardiovascular morbidity.9–26 These CVD risks can be identified early in life, as demonstrated by Fugelseth et al,9 who showed an excess CVD incidence in exposed offspring at 5–8 years of age.