Abstract

Objectives: to determine the prevalence of endothelial dysfunction and its association with a history of mild and severe preeclampsia in adolescents. Methods: a cross-sectional study was carried out at the MEAC-UFC with 103 primiparous adolescents postpartum. The assessment of endothelial function was performed by way of flow-mediated dilatation of the brachial artery. Variables (age, body mass index, gestational age at delivery, systolic and diastolic blood pressure and flow-mediated dilation) were compared between groups. p<0.05 was considered to be statistically significant. Results: twenty-four (23.3%) patients had preeclampsia (PE): 11 mild and 13 severe. The overall prevalence of endothelial dysfunction was 23.3% (21.5% of patients with normotensive pregnancies and 29.2% of the PE patients: 18.2% of those with mild PE and 38.5% of those with severe PE). The figures were statistically significant for systolic blood pressure, p=0.007. Conclusions: patients with a history of PE have higher systolic blood pressure than patients with a history of normotensive pregnancy, but did not have more endothelial dysfunction.

Highlights

  • Preeclampsia (PE) remains one of the main causes of maternal death worldwide

  • Endothelial dysfunction is defined as an alteration in vascular relaxation due to a decrease in the bioavailability of the relaxing factors derived from the endothelium, nitric oxide

  • The relationship between PE and endothelial dysfunction has been well established; the fact that ultrasound is a non-invasive technique and the test is reproduced explains why there are so many studies attempting to show the efficacy of flow-mediated dilation (FMD) as a predictor of or factor correlated with PE.[2,9]

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Summary

Introduction

Preeclampsia (PE) remains one of the main causes of maternal death worldwide. Its incidence varies according to region, in some countries maternal death rates of up to 40% have been observed. Roberts et al.[2] were the first to put forward the hypothesis that the soluble factors that induce endothelial cell dysfunction and are responsible for the onset of clinical symptoms such as hypertension, proteinuria and edemas develop during preeclampsia. Endothelial dysfunction is defined as an alteration in vascular relaxation due to a decrease in the bioavailability of the relaxing factors derived from the endothelium, nitric oxide. Studies suggest that this dysfunction occurs in response to abnormal placentation, which may lead to placental ischemia and the release of substances that damage the maternal vascular endothelium.[1,3]

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