Endothelial dysfunction: a link among preeclampsia, recurrent pregnancy loss, and future cardiovascular events?

We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease.

[Ultrasound assessment of endothelial function in Chilean children and adults].

Background: Endothelial dysfunction is an important pathogenetic mechanism in the development of atherosclerosis.

Aim: To evaluate endothelial function in Chilean children and adult subjects and to provide normal values of flow mediated dilatation (FMD) in the Chilean population.

Subjects And Methods: Flow mediated dilation of the brachial artery was measured by high resolution ultrasonography in healthy children (n=32) and adults (n=69) of both gender, in a group of 8 healthy women during 4 periods of pregnancy and late postpartum, and in 22 men and women with a history of stroke or coronary heart disease.