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Contribution of Increased Angiotensin II Sensitivity to Microvascular Dysfunction in Women With a History of Preeclampsia.

See related article, pp 382–389 

Preeclampsia is a pregnancy disorder characterized by gestational hypertension concomitant with proteinuria and is the leading cause of maternal–fetal morbidity and mortality in the United States and worldwide.1 Preeclampsia affects ≈5% of pregnancies1; yet, there are no accepted strategies to prevent the development of preeclampsia in pregnant women who might be at risk for preeclampsia. Further, women who have had preeclamptic pregnancies demonstrate an increased incidence of cardiovascular disease (CVD) later in life. It is, therefore, key to explore the extent to which cardiovascular dysfunction persists beyond pregnancy and to protect women who have had preeclamptic pregnancies from future CVD and hypertension. The greater risk for future CVD after preeclamptic pregnancies may be explained in 2 ways. One hypothesis is that the cardiovascular sequelae of preeclampsia incur structural or functional damage predisposing affected women to future morbidity and mortality. A second hypothesis, by no means exclusive of the first, suggests that pregnancy serves as a cardiovascular stress test for women and that the development of preeclampsia occurs because of the presence of previously unobserved cardiovascular dysfunction.2 Critically, both hypotheses underscore the importance for the screening of cardiovascular risk factors in women early in pregnancy, especially women who have had at least one pregnancy complicated by preeclampsia. These risk factors have yet to be completely defined as they relate to preeclampsia and the subsequent risk for CVD,3 supporting the need for studies, such as the present one by Stanhewicz et al.4

This excellent article by Stanhewicz et al4 demonstrated that compared with women with normal pregnancies, peripheral microvascular sensitivity …