Hypertension in pregnancy is currently defined as a systolic blood pressure (BP) of 140 mmHg or more, or a diastolic BP of 90 mmHg or more. This level of BP warrants antihypertensive therapy. Treating to a target BP of 135/85 mmHg halves the risk of severe hypertension that is itself associated with adverse maternal and perinatal outcomes, similar in magnitude to preeclampsia. While based on the results of the Control of Hypertension in Pregnancy Study (CHIPS) trial, this finding is consistent with all antihypertensive trials to date. Also, in the CHIPS trial, "tight" BP control also halved the risk of progression to thrombocytopenia and elevated liver enzymes for the mother, without adverse effects for the fetus or newborn. This was true regardless of the gestational age at which BP control was instituted. While methyldopa, labetalol, and nifedipine are the most commonly-recommended oral antihypertensives, it is not clear that one antihypertensive agent has advantages over the others for treatment of non-severe hypertension in pregnancy. No antihypertensives, including renin-angiotensin-aldosterone system (RAAS) inhibitors, have been shown to be teratogenic, although there may be an increase in malformations associated with the underlying condition of chronic hypertension. Atenolol and RAAS inhibitors should not be used once pregnancy is diagnosed, based on fetotoxicity. At present, BP treatment targets used in clinic are the same as those used at home as the differences are quite variable among hypertensive women. For treatment of acute severe hypertension, the most commonly-recommended antihypertensives are oral nifedipine, IV labetalol, and IV hydralazine, although oral agents have also been shown to be effective in the majority of women; while concerns raised about IV hydralazine-induced maternal hypotension and its consequences have not been confirmed, this medication may be an inferior antihypertensive to oral nifedipine. While treatment recommendations are based on evidence, women should be engaged in decision-making, as their values may alter target BP and antihypertensive choice. Future work will clarify the optimal target BP based on home BP measurements; whether BP targets should be lowered further if the definition of hypertension is based on a lower BP; which, if any, antihypertensive medication for non-severe hypertension is better with regards to maternal and perinatal outcomes; and whether factors beyond BP level (such as variability, race, and other physiological variables) should inform antihypertensive therapy in pregnancy.

Preeclampsia remains associated with an increased risk of maternal and perinatal morbidity and mortality, and the burden of that excess risk is largely borne by pregnant women and their families in low- and middle-income countries (LMICs). Therefore, the Bill & Melinda Gates Foundation funded the PREeclampsia - Eclampsia Monitoring, Prevention, and Treatment (PRE-EMPT) initiative to accelerate progress. From PRE-EMPT, and related activity, have come a number of impactful findings. First, there is increasing global support for broadening the definition of preeclampsia to include women with hypertension and either significant proteinuria or evidence of target organ damage or fetoplacental compromise (including evidence angiogenic imbalance). Second, using blood pressure (BP) data from the Community-Level Interventions for Preeclampsia trials in India, Mozambique, and Pakistan, acquired on validated-for-pregnancy, semi-automated, low-cost BP devices, there are now population-level, rather than facility-based, estimates for the burden of pregnancy hypertension (sub-categorized into preeclampsia (4%-6%), gestational hypertension (7%-12%), and chronic hypertension (0.3%-0.6%)). Third, there is an identified need to understand biological pathways that underlie the causation of preeclampsia in LMICs. Fourth, the Community-Level Interventions for Preeclampsia trials have shown that providing at least eight antenatal contacts, in this case using digital health-supported community health workers, cost-effectively reduces the burden of maternal (by 60%), fetal (60%), and neonatal (40%) mortality. Fifth, what is the utility and cost-effectiveness of routine proteinuria screening of normotensive pregnant women? Sixth, clinical risk factor-based prediction of preeclampsia remains most relevant for most women in LMICs; calcium replacement (≥1 g/day) and low-dose aspirin (100-175 mg/day) are the most useful directly preventative interventions. However, achieving sustainable development goals (SDGs) not directly related to health are more likely to reduce the global burden of preeclampsia and its consequences. Seventh, should a woman develop preeclampsia, personalized maternal time-of-disease risk estimates are available through the PIERS (Preeclampsia Integrated Estimate of RiSk) models, either with (fullPIERS) or without (miniPIERS) access to laboratory testing. Assessment of perinatal risks in LMICs is largely driven by gestational age; however, evidence of significant angiogenic imbalance may identify risk of intrauterine fetal death. Eighth, Control of Hypertension in Pregnancy Study trial data show that women with non-severe pregnancy hypertension (systolic BP 140-159 mmHg or diastolic BP (dBP) 90-109 mmHg) should receive an antihypertensive medication for a target dBP of 85 mmHg. Ninth, for women with severe pregnancy hypertension (systolic BP ≥160 mmHg or dBP ≥110 mmHg), oral antihypertensive management with either nifedipine, labetalol, or, less so, methyldopa will lower BP into the non-severe hypertension range. Tenth, magnesium sulfate remains the sole agent of choice for preventing and treating eclamptic seizures. Eleventh, corticosteroids should be administered to women at risk of delivery <35 +0 weeks’ gestation. Twelfth, although delivery of the placenta initiates resolution of the maternal syndrome of preeclampsia, decisions to initiate delivery should be guided by gestational age and maternal and fetal status. Many women will experience significant postpartum deterioration; delivery should not be equated with "cure" . Thirteenth, whether the development of preeclampsia identifies women at increased risk for early-onset cardiovascular disease in LMICs must be determined.

Hypertension in pregnancy is currently defined as a systolic blood pressure (BP) of 140 mmHg or more, or a diastolic BP of 90 mmHg or more. This level of BP warrants antihypertensive therapy. Treating to a target BP of 135/85 mmHg halves the risk of severe hypertension that is itself associated with adverse maternal and perinatal outcomes, similar in magnitude to preeclampsia. While based on the results of the Control of Hypertension in Pregnancy Study (CHIPS) trial, this finding is consistent with all antihypertensive trials to date. Also, in the CHIPS trial, "tight" BP control also halved the risk of progression to thrombocytopenia and elevated liver enzymes for the mother, without adverse effects for the fetus or newborn. This was true regardless of the gestational age at which BP control was instituted. While methyldopa, labetalol, and nifedipine are the most commonly-recommended oral antihypertensives, it is not clear that one antihypertensive agent has advantages over the others for treatment of non-severe hypertension in pregnancy. No antihypertensives, including renin-angiotensin-aldosterone system (RAAS) inhibitors, have been shown to be teratogenic, although there may be an increase in malformations associated with the underlying condition of chronic hypertension. Atenolol and RAAS inhibitors should not be used once pregnancy is diagnosed, based on fetotoxicity. At present, BP treatment targets used in clinic are the same as those used at home as the differences are quite variable among hypertensive women. For treatment of acute severe hypertension, the most commonly-recommended antihypertensives are oral nifedipine, IV labetalol, and IV hydralazine, although oral agents have also been shown to be effective in the majority of women; while concerns raised about IV hydralazine-induced maternal hypotension and its consequences have not been confirmed, this medication may be an inferior antihypertensive to oral nifedipine. While treatment recommendations are based on evidence, women should be engaged in decision-making, as their values may alter target BP and antihypertensive choice. Future work will clarify the optimal target BP based on home BP measurements; whether BP targets should be lowered further if the definition of hypertension is based on a lower BP; which, if any, antihypertensive medication for non-severe hypertension is better with regards to maternal and perinatal outcomes; and whether factors beyond BP level (such as variability, race, and other physiological variables) should inform antihypertensive therapy in pregnancy.

Preeclampsia remains associated with an increased risk of maternal and perinatal morbidity and mortality, and the burden of that excess risk is largely borne by pregnant women and their families in low- and middle-income countries (LMICs). Therefore, the Bill & Melinda Gates Foundation funded the PREeclampsia - Eclampsia Monitoring, Prevention, and Treatment (PRE-EMPT) initiative to accelerate progress. From PRE-EMPT, and related activity, have come a number of impactful findings. First, there is increasing global support for broadening the definition of preeclampsia to include women with hypertension and either significant proteinuria or evidence of target organ damage or fetoplacental compromise (including evidence angiogenic imbalance). Second, using blood pressure (BP) data from the Community-Level Interventions for Preeclampsia trials in India, Mozambique, and Pakistan, acquired on validated-for-pregnancy, semi-automated, low-cost BP devices, there are now population-level, rather than facility-based, estimates for the burden of pregnancy hypertension (sub-categorized into preeclampsia (4%-6%), gestational hypertension (7%-12%), and chronic hypertension (0.3%-0.6%)). Third, there is an identified need to understand biological pathways that underlie the causation of preeclampsia in LMICs. Fourth, the Community-Level Interventions for Preeclampsia trials have shown that providing at least eight antenatal contacts, in this case using digital health-supported community health workers, cost-effectively reduces the burden of maternal (by 60%), fetal (60%), and neonatal (40%) mortality. Fifth, what is the utility and cost-effectiveness of routine proteinuria screening of normotensive pregnant women? Sixth, clinical risk factor-based prediction of preeclampsia remains most relevant for most women in LMICs; calcium replacement (≥1 g/day) and low-dose aspirin (100-175 mg/day) are the most useful directly preventative interventions. However, achieving sustainable development goals (SDGs) not directly related to health are more likely to reduce the global burden of preeclampsia and its consequences. Seventh, should a woman develop preeclampsia, personalized maternal time-of-disease risk estimates are available through the PIERS (Preeclampsia Integrated Estimate of RiSk) models, either with (fullPIERS) or without (miniPIERS) access to laboratory testing. Assessment of perinatal risks in LMICs is largely driven by gestational age; however, evidence of significant angiogenic imbalance may identify risk of intrauterine fetal death. Eighth, Control of Hypertension in Pregnancy Study trial data show that women with non-severe pregnancy hypertension (systolic BP 140-159 mmHg or diastolic BP (dBP) 90-109 mmHg) should receive an antihypertensive medication for a target dBP of 85 mmHg. Ninth, for women with severe pregnancy hypertension (systolic BP ≥160 mmHg or dBP ≥110 mmHg), oral antihypertensive management with either nifedipine, labetalol, or, less so, methyldopa will lower BP into the non-severe hypertension range. Tenth, magnesium sulfate remains the sole agent of choice for preventing and treating eclamptic seizures. Eleventh, corticosteroids should be administered to women at risk of delivery <35 +0 weeks’ gestation. Twelfth, although delivery of the placenta initiates resolution of the maternal syndrome of preeclampsia, decisions to initiate delivery should be guided by gestational age and maternal and fetal status. Many women will experience significant postpartum deterioration; delivery should not be equated with "cure" . Thirteenth, whether the development of preeclampsia identifies women at increased risk for early-onset cardiovascular disease in LMICs must be determined.