Does polycystic ovary syndrome impair vascular adaptations to pregnancy, affecting arterial elasticity and blood pressure?
PCOS impairs physiological vascular adaptations to pregnancy, leading to increased arterial stiffness, higher blood pressure, and a higher incidence of pregnancy-induced hypertension.
Decreased arterial viscoelasticity has been described in young women with polycystic ovary syndrome (PCOS), as have abnormal arterial vasodilatory responses and increased intima/media thickness in the carotid artery. An association with hypertension is less clearly defined. If, as some have proposed, PCOS is associated with pregnancy-induced hypertensive disorders, including preeclampsia, it is not clear whether PCOS is an independent risk factor. This prospective study tests the hypothesis that PCOS impairs vascular adaptations to pregnancy so as to promote changes in arterial elasticity and blood pressure. Ambulatory blood pressure was monitored at intervals throughout pregnancy in 22 women with PCOS, and the same number of control women matched with the study group for age, body mass index, parity, and ethnicity. Arterial elasticity was estimated by carotid artery ultrasonography. Ambulatory systolic, diastolic, and mean arterial pressures were nearly always higher in all trimesters of pregnancy in women with PCOS than in control subjects. The differences were most marked in late pregnancy. Heart rate did not differ consistently between the 2 groups. In both groups, mean daytime arterial pressures were higher than nighttime values. In each trimester, carotid artery stiffness was greater, and compliance lower, in women with PCOS than in control subjects. PCOS appeared to have reversed the increase in compliance normally observed during pregnancy. Pregnancy-induced hypertension was more frequent in PCOS women, 3 of whom had preeclampsia, and 3 gestational hypertension. Neither of these diagnoses was made in the control group. Birth weights were 11% lower in normotensive women with PCOS compared to matched control subjects, but were unaffected in hypertensive women with PCOS. These findings suggest that PCOS impairs physiological vascular adaptations to pregnancy, resulting in some instances in maternal hypertension and impaired fetal growth. More marked changes may be expected in women with PCOS who conceive after fertility treatment because they tend to have more severe symptoms of PCOS.
Hu et al. (Thu,) studied this question.
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