Elsevier

Early Human Development

Volume 87, Issue 8, August 2011, Pages 531-535
Early Human Development

Myocardial function in offspring 5–8 years after pregnancy complicated by preeclampsia

https://doi.org/10.1016/j.earlhumdev.2011.04.006Get rights and content

Abstract

Introduction

Preeclampsia and diabetic pregnancies share pathophysiological features suggested to influence epigenetic changes during foetal life with importance for later development and metabolic and cardiovascular diseases.

Aim

Our objective was to study the myocardium in offspring after pregnancy complications.

Methods

Forty-five children (age 5–8 years) delivered from pregnancies complicated by preeclampsia (n = 25), diabetes mellitus type 1 (n = 8) or gestational diabetes mellitus (n = 12) were included. Fifteen children from uneventful pregnancies served as controls. Myocardial functions of right and left ventricle were examined by conventional Doppler and tissue Doppler imaging (TDI).

Results

No major differences were found in the myocardial function between offspring of pregnancy complications and control group. However, the preeclampsia group had smaller hearts, increased heart rate and increased late diastolic velocity (A′-wave) at mitral valve attachments shown by both pulsed wave and colour TDI compared to the control and diabetic groups together (p  0.01).

Conclusion

Children born after preeclampsia may show effects of a negative impact on the heart already at the age of 5 to 8 years. The numbers of examined children were, however, limited.

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.

References (30)

  • D.J. Barker et al.

    Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease

    BMJ

    (Mar 4, 1989)
  • T. Forsen et al.

    Growth in utero and during childhood among women who develop coronary heart disease: longitudinal study

    BMJ

    (Nov 27, 1999)
  • C.M. Boney et al.

    Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus

    Pediatrics

    (Mar 2005)
  • P.D. Gluckman et al.

    Effect of in utero and early-life conditions on adult health and disease

    N Engl J Med

    (Jul 3, 2008)
  • M.T. Schram et al.

    Vascular risk factors and markers of endothelial function as determinants of inflammatory markers in type 1 diabetes: the EURODIAB Prospective Complications Study

    Diabetes Care

    (Jul 2003)
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