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CLINICAL STATEMENTS AND GUIDELINES

September 16, 2025 Circulation. 2025;152:e114–e218. DOI: 10.1161/CIR.0000000000001356 e174

fetotoxic in the second and third trimesters of preg­ nancy due to their effects on the developing renal system, leading to oligohydramnios and AKI.10,13,14 Adverse effects in the first trimester may be second­ ary to hypertension or medications. Based on the mechanism of action and data from animal studies, fetal exposure to spironolactone may cause feminiza­ tion of a male fetus or growth restriction and is gener­ ally not recommended,29–32 even for individuals with primary aldosteronism. The feminizing effects appear to be dose-dependent. There are few human data on nitroprusside safety in pregnancy, but data from ani­ mal studies show that nitroprusside crosses the pla­ centa and may lead to fetal cyanide toxicity. Following delivery, many antihypertensive medications can be safely used again. LactMed33 is a searchable data­ base of medication safety for lactating individuals.34,35

5.5.1 Gestational Hypertension

Synopsis

Gestational hypertension is the de novo development of hypertension after 20 weeks’ gestation in the absence of new proteinuria or target organ damage (Table 20).1 Gestational hypertension is associated with an increased risk of maternal and fetal/neonatal adverse events, and up to 30% of women with gestational hypertension ul­ timately develop preeclampsia.2 Following delivery, indi­ viduals with gestational hypertension have an increased risk of future hypertension and CVD. Most RCTs examin­ ing BP targets for pregnant individuals with gestational hypertension have been small and of poor to moderate quality. The highest-quality randomized trial that included women with nonproteinuric hypertension examined tight versus less-tight DBP targets (85 mm Hg and 100 mm Hg, respectively) and demonstrated a reduction in severe maternal hypertension with tight DBP control.3,4 There were no other significant differences in maternal, fetal, or neonatal complications or pregnancy loss between treatment groups. In post-hoc analyses, the develop­ ment of severe hypertension was also associated with an increased risk of pregnancy loss, neonatal intensive care unit admission, preterm delivery, and low birth­ weight.4 Current treatment recommendations by ACOG in the 2020 Practice Bulletin advocate that individuals with gestational hypertension who present with severerange blood pressures, which is defined as persistent SBP ≥160 mm Hg or DBP ≥110 mm Hg, be managed with the same approach as those with preeclampsia and severe-range blood pressures, highlighting the overlap in risks associated with both of these HDP (Table 23).

5.5.2 Preeclampsia and Eclampsia, Including

Preeclampsia Superimposed on Chronic Hypertension Synopsis

Preeclampsia, a multiorgan system inflammatory syn­ drome, is an HDP characterized by hypertension, as well as proteinuria or target organ dysfunction (Table 24).1 Preeclampsia also develops in 20% to 50% of individuals with chronic hypertension and is termed su­ perimposed preeclampsia in that scenario, which often presents as an increase in baseline hypertension or proteinuria. In an individual with preeclampsia, the de­ velopment of severe features or hemolysis, elevated liv­ er enzymes, and low platelet count (HELLP) syndrome are associated with increased rates of maternal and fetal/neonatal morbidity and mortality. Eclampsia, the occurrence of convulsive seizures, is one of the most severe forms of preeclampsia. Both preeclampsia and eclampsia can occur before, during, or after delivery, and magnesium sulfate in addition to antihypertensive medications are the mainstay of treatment. Low-dose aspirin is the only routinely recommended intervention that has been demonstrated to reduce the risk of pre­ eclampsia and its sequelae when taken from 12 weeks of gestation in pregnant people at moderate and great­ er risk.2–4 Pravastatin has been investigated in small studies as a potential therapy for the treatment of pre­ eclampsia, but larger prospective studies are needed to confirm safety and efficacy.5 The measurement of the antiangiogenic markers soluble fms-like tyrosine kinase -1 (sFlt-1), placental growth factor (PlGF), and their ratio is emerging as a diagnostic test with high

Table 20.  Classification of Hypertensive Disorders of Pregnancy20 Condition Definition Chronic hypertension Diagnosis prior to pregnancy or at <20 wks’ gesta­ tion Gestational hyper­ tension De novo hypertension at ≥20 wks’ gestation in the absence of proteinuria or other signs of pre­ eclampsia Preeclampsia Gestational hypertension with proteinuria or other maternal end-organ dysfunction including neurologic findings, pulmonary edema, hematologic findings, acute kidney injury, hepatic dysfunction (Section 5.5.2 “Preeclampsia and Eclampsia, Including Pre­ eclampsia Superimposed on Chronic Hypertension”) Preeclampsia superimposed on chronic hypertension Preeclampsia in a woman with a history of hyper­ tension before pregnancy or before 20 weeks’ gestation Table 21.  ACOG Diagnostic Criteria for Hypertension in Pregnancy20

Condition Definition Hypertension in pregnancy SBP ≥140 mm Hg and/or DBP ≥90 mm Hg Severe-range hypertension SBP ≥160 mm Hg and/or DBP ≥110 mm Hg ACOG indicates American College of Obstetricians and Gynecologists; DBP, diastolic blood pressure; and SBP, systolic blood pressure.

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