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Polycystic ovary syndrome is the most common endocrine disorder in women of reproductive age and is characterized by hyperandrogenism, ovulatory dysfunction, and a high prevalence of insulin resistance. During pregnancy, these features interact with the physiological metabolic adaptations of gestation and may contribute to an increased risk of gestational diabetes, hypertensive disorders, preterm birth, and altered fetal growth. At the same time, Doppler ultrasonography and fetal echocardiography allow the uteroplacental circulation, fetal vascular resistance, and fetal cardiac function to be assessed in a noninvasive manner, raising the question of how the maternal metabolic profile is reflected in fetal hemodynamic parameters. This review aimed to analyze the relationship between the maternal metabolic and endocrine profile in pregnant women with polycystic ovary syndrome and uteroplacental and fetal hemodynamic parameters, as well as the implications of this relationship for prenatal surveillance. This is a narrative literature review, guided by a structured question based on the PICo strategy and directed at studies on polycystic ovary syndrome in pregnancy, insulin resistance, hyperandrogenism, placental function, Doppler velocimetry, and fetal cardiac function. The evidence indicates that women with the syndrome present higher insulin resistance, higher androgen concentrations, and a greater frequency of obstetric complications, partly independent of body mass index, and that placental structural and functional changes may act as the link between the maternal environment and the fetus. However, studies with standardized Doppler assessment in pregnancies without additional complications have not demonstrated consistent differences in uterine, umbilical, or fetal cerebral pulsatility indices, suggesting that hemodynamic repercussions become more evident when the metabolic disorder progresses to gestational diabetes, hypertensive disease, or fetal growth restriction. It is concluded that prenatal care for these women should integrate early metabolic screening, phenotype characterization, and hemodynamic surveillance guided by risk, rather than routine assessment based solely on the diagnosis of the syndrome.
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Pasqual et al. (2026) studied this question.
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