One-year vascular adaptations following pregnancies complicated by hypertension.

Abstract

It has been postulated that elevated blood pressure in pregnancy is associated with increased risk of cardiovascular disease later in life. The postpartum burden of incident disease among hypertension-complicated pregnancies is extremely wide and includes arterial hypertension, diabetes mellitus, cardiovascular events, and chronic kidney disease. However, it is still debated whether discrete phenotypes of hypertension disorders in pregnancy (ie, gestational hypertension, preeclampsia, chronic hypertension in pregnancy, and superimposed preeclampsia) are equally associated with future cardiovascular complications and the extent of such associations. Also, it is unclear whether hypertension disorders in pregnancy constitute an intermediate surrogate of cardiovascular events later in life in women with or without early clustering of cardiovascular risk factors or if they really represent an etiological lever for adverse cardiovascular prognosis.1, 2 To address this clinically meaningful question, a retrospective evaluation of cardiovascular events among women with a history of normotensive or hypertension-complicated pregnancies and women without a history of pregnancy (ie, nulliparity), taking also into consideration the use of contraceptive pills, should be performed. Beyond the questioned role of hypertension-complicated pregnancies in future cardiovascular health, it is also important to examine postpartum vascular changes in normotensive and hypertension-complicated pregnancies. This pathophysiological insight might enable us to better understand the extent of vascular deterioration in women with a pregnancy complicated by hypertension. In the current issue of The Journal of Clinical Hypertension, Ehrenthal and colleagues3 in a prospective case-control study demonstrate that pregnancies complicated by hypertensive disorders (ie, gestational hypertension or preeclampsia) are accompanied by increased blood pressure levels and arterial wave reflections 1 year after delivery. By contrast, carotid-femoral pulse wave velocity did not differ among women with either normotensive or hypertension-complicated pregnancies during the same postpartum period. These find-ings taken together reflect that endothelial dysfunction related to hypertensive pregnancy–induced disorders does not resolve after delivery but it persists for at least the following year. Arterial wall changes as assessed by pulse wave velocity measurements were not significant in the same postpartum timeframe, suggesting that mid-term vascular adaptations might not be accompanied by substantial structural damage. However, it remains unknown whether endothelial dysfunction is further deteriorated after the first year postdelivery and whether arterial stiffness is becoming more pronounced under the effects of both long-standing systolic blood pressure increase and potential perpetuation of endothelial dysfunction. Although the findings by Ehrenthal and colleagues3 are of pathophysiological interest, their clinical repercussion is limited by the short postpartum follow-up period, the absence of vascular and blood pressure measurements at booking (ie, prepregnacy), and the possibility that some women became pregnant by assisted reproductive techniques.4 Also, two additional groups of nonpregnant women matched for age and body mass index with normotension or hypertension would have refined the effects of hypertension disorders in pregnancy on vascular changes during the follow-up period. More studies are needed to evaluate the impact of each phenotype among hypertensive disorders in pregnancy on both vascular effects and clinical outcomes later in life. None. None.